Exam 1

Heart Structure & Function

• The cardiovascular system is made up of the:

  • Heart

  • Vascular system

• Main purpose:

  • Delivers oxygen and nutrients to tissues.

  • Helps remove waste products.

• The heart is a hollow, muscular organ that pumps blood throughout the body.

• Located in the mediastinum:

  • Between the lungs.

  • Between the sternum and spinal column.

  • Rests on the diaphragm.

  • Extends downward and to the left.

• Apex/Point of Maximum Impulse (PMI):

  • Located at the 5th intercostal space, left midclavicular line.

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Layers of the Heart

• Endocardium

  • Innermost layer.

  • Made of endothelial tissue.

  • Lines the inside of the heart and the valves.

• Myocardium

  • Middle layer.

  • Thickest layer of the heart.

  • Made of muscle fibers.

  • Responsible for the pumping action of the heart.

• Epicardium

  • Outermost layer.

  • Serous layer that protects the heart.

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Pericardium

• The pericardium is a fibrous sac surrounding the heart.

• The serous pericardium has two layers:

  • Visceral pericardium

    • Covers the surface of the heart.

  • Parietal pericardium

    • Lines the pericardial sac.

• The layers produce serous fluid.

• Pericardial space

  • Space between the visceral and parietal pericardium.

  • Contains serous fluid.

  • Allows the layers to move smoothly against one another.

• The parietal pericardium helps anchor the heart within the thorax.

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Heart Chambers

The heart has 4 chambers:

• Right atrium

• Right ventricle

• Left atrium

• Left ventricle

Atria

• Receive blood returning to the heart.

Ventricles

• Receive blood from the atria.

• Pump blood to the lungs and the rest of the body.

Septum

• Band of tissue that separates:

  • Right side of the heart.

  • Left side of the heart.

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🩸 Blood Flow Through the Heart Remember:

Body → Right side → Lungs → Left side → Body

Detailed blood flow:

1. Superior vena cava

   • Brings deoxygenated blood from the head and neck.

2. Inferior vena cava

   • Brings deoxygenated blood from the rest of the body.

3. Right atrium

4. Right ventricle

5. Pulmonary arteries

   • Carry deoxygenated blood to the lungs.

   • Only arteries in the adult vascular system that carry deoxygenated blood.

6. Lungs

   • Blood becomes oxygenated.

7. Pulmonary veins

   • Carry oxygenated blood back to the heart.

   • Only veins in the adult vascular system that carry oxygenated blood.

8. Left atrium

9. Left ventricle

10. Aorta

11. Body

Important

• The left ventricle has a thicker wall than the right ventricle.

• This is because the left ventricle pumps blood to the entire body, requiring more force.

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Heart Valves Main function

• Ensure blood flows in one direction.

• Open and close as blood moves through the heart.

Two Types of Valves Atrioventricular (AV) Valves

Separate the atria from the ventricles.

• Tricuspid valve

  • Between the right atrium and right ventricle.

  • Has 3 leaflets.

• Mitral/Bicuspid valve

  • Between the left atrium and left ventricle.

  • Has 2 leaflets.

Semilunar Valves

• Pulmonic valve

  • Between the right ventricle and pulmonary artery.

• Aortic valve

  • Between the left ventricle and aorta.

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Systole vs. Diastole Systole = Squeeze

• Contraction phase of the cardiac cycle.

• Ventricles contract and pump blood out.

Diastole = Relax

• Relaxation phase.

• Heart chambers fill with blood.

• One complete cardiac cycle = one heartbeat.

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Vascular System

The vascular system includes:

• Arteries

• Arterioles

• Capillaries

• Venules

• Veins

Functions

• Arteries

  • Transport high-pressure blood away from the heart.

• Arterioles

  • Connect arteries to capillaries.

• Capillaries

  • Allow:

    • Gas exchange.

    • Nutrient transfer.

    • Waste removal.

• Venules

  • Connect capillaries to veins.

• Veins

  • Act as a blood reservoir.

  • Carry low-pressure blood back to the heart.

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Coronary Circulation

• The heart muscle requires its own oxygen supply.

• Blood is supplied through the:

  • Right coronary artery (RCA)

  • Left coronary artery (LCA)

• Coronary arteries originate from the base of the aorta, just above the aortic valve.

• Coronary perfusion occurs primarily during diastole.

Important!

• Increased heart rate → shorter diastole → decreased time for coronary perfusion.

Left Coronary Artery Branches

• Left main coronary artery

• Left anterior descending (LAD) artery

  • Supplies the anterior portion of the left ventricle.

• Circumflex artery

  • Supplies the left atrium.

  • Supplies the posterior-lateral portion of the left ventricle.

Right Coronary Artery Branches

• Marginal artery

  • Supplies the lateral part of the right side of the heart.

• Posterior descending artery (PDA)

  • Supplies the posterior part of the heart.

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Cardiac Conduction System ⚡

The heart has its own electrical conduction system.

Order of electrical conduction: SA Node → AV Node → Bundle of His → Right & Left Bundle Branches → Purkinje Fibers SA Node

• Located in the right atrium.

• Known as the heart's natural pacemaker.

• Sets the heart's rate and rhythm.

AV Node

• Receives the impulse from the SA node.

• Causes a slight delay.

• Allows the atria to fully contract and empty into the ventricles.

Bundle of His

• Conducts the impulse into the interventricular septum.

Right and Left Bundle Branches

• Carry the impulse toward the right and left ventricles.

Purkinje Fibers

• Final part of the conduction pathway.

• Stimulation causes ventricular contraction.

• Dysfunction in the conduction pathway can result in dysrhythmias.

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Cardiac Output (CO) Definition

• The total amount of blood ejected from one ventricle per minute.

Normal resting cardiac output

• Approximately 5–6 L/min in a healthy adult.

Formula

Cardiac Output = Heart Rate × Stroke Volume

Stroke Volume

• Amount of blood ejected by one ventricle with each heartbeat.

Three factors affecting stroke volume:

1. Preload

2. Afterload

3. Contractility

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Preload

• The degree of stretching of the ventricular muscle at the end of diastole.

• At the end of diastole:

  • The ventricle contains its greatest volume of blood.

  • Muscle fibers experience the greatest stretch.

• Preload directly affects stroke volume.

• Can be estimated by measuring pulmonary capillary wedge (PCW) pressure.

Easy way to remember:

Preload = volume/stretch before contraction

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Afterload

• The resistance or pressure the ventricle must overcome to eject blood.

• Directly related to:

  • Arterial blood pressure.

  • Diameter of blood vessels.

• Smaller blood vessels = increased afterload.

• Increased afterload can occur with hypertension.

Easy way to remember:

Afterload = resistance against which the heart pumps

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Contractility

• The force generated by the myocardium during contraction.

• Influences stroke volume.

Increases contractility:

• Sympathetic stimulation.

• Positive inotropic medications.

Decreases contractility:

• Hypoxia.

• Negative inotropic medications.

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Heart Sounds 🩺 Normal Heart Sounds S1 = "Lub"

• Closure of:

  • Mitral valve

  • Tricuspid valve

S2 = "Dub"

• Closure of:

  • Aortic valve

  • Pulmonic valve

Remember:

S1 = AV valves close S2 = Semilunar valves close

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Abnormal Heart Sounds S3

• Best heard with the bell of the stethoscope.

• Described as a ventricular gallop.

• Heard as a loud "DUB" following S2.

• Indicates decreased ventricular compliance.

• Can be normal in:

  • Children.

  • Adults up to age 40.

• In adults older than 40, may indicate heart failure.

S4

• Best heard with the bell.

• Described as an atrial gallop.

• Heard as a loud "LUB" immediately before S1.

• Associated with decreased ventricular compliance.

• May occur with:

  • Hypertension.

  • Aortic stenosis.

  • Coronary artery disease.

  • Cardiomyopathy.

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Murmurs & Pericardial Friction Rub Murmur

• Caused by turbulent blood flow through healthy or diseased valves.

• Sounds like "whooshing."

Systolic Murmur

• Heard between S1 and S2.

Diastolic Murmur

• Heard between S2 and S1.

Pericardial Friction Rub

• Abnormal heart sound.

• Usually heard over the left sternal border.

• Caused by:

  • Inflammation.

  • Infection.

  • Infiltration in the pericardial sac.

• Sounds "grating."

• Usually disappears when the underlying cause is treated.

Valvular Dysfunction

Main Function of Heart Valves

• Heart valves ensure blood flows in one direction.

• Valves open to allow forward blood flow.

• Valves close to prevent backflow of blood.

• The 4 valves are:

  • Tricuspid

  • Pulmonic

  • Mitral (bicuspid)

  • Aortic

• AV valves:

  • Tricuspid

  • Mitral

• Semilunar valves:

  • Pulmonic

  • Aortic

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Types of Valvular Dysfunction 1. Stenosis

Stenosis = narrowing of a valve

• Valve does not open completely.

• Blood has difficulty moving forward through the valve.

• The heart must work harder to push blood through the narrowed opening.

• Can lead to:

  • Increased pressure behind the valve.

  • Chamber hypertrophy.

  • Decreased cardiac output.

  • Heart failure.

Easy way to remember:

Stenosis = "stuck closed"

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2. Regurgitation (Insufficiency)

Regurgitation = valve does not close completely

• Blood leaks backward through the valve.

• Causes volume overload in the affected chamber.

• The heart must pump extra blood to maintain adequate cardiac output.

• Can eventually cause:

  • Chamber dilation.

  • Decreased cardiac output.

  • Pulmonary congestion.

  • Heart failure.

Easy way to remember:

Regurgitation = "leaky valve"

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Mitral Valve Dysfunction Mitral Stenosis

• Narrowing of the mitral valve.

• Mitral valve is located between:

  • Left atrium

  • Left ventricle

• Obstruction prevents blood from moving easily from the left atrium to the left ventricle.

• Blood backs up into:

  • Left atrium.

  • Pulmonary circulation.

Possible findings

• Dyspnea.

• Fatigue.

• Pulmonary congestion.

• Crackles.

• Exercise intolerance.

• Increased risk for atrial dysrhythmias.

Think:

Mitral stenosis → blood backs up into the lungs

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Mitral Regurgitation

• Mitral valve does not close completely.

• During ventricular systole:

  • Some blood flows backward from the left ventricle → left atrium.

• Can result in:

  • Left atrial enlargement.

  • Pulmonary congestion.

  • Decreased forward cardiac output.

Possible findings

• Fatigue.

• Dyspnea.

• Pulmonary congestion.

• Heart murmur.

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Aortic Valve Dysfunction Aortic Stenosis

• Narrowing of the aortic valve.

• Makes it difficult for blood to leave the left ventricle.

• Left ventricle must generate more pressure to push blood through the narrowed valve.

Effects

• Increased afterload.

• Left ventricular hypertrophy.

• Decreased cardiac output.

Classic symptoms

SAD

• Syncope

• Angina

• Dyspnea

Important NCLEX concept

• Aortic stenosis can significantly decrease blood flow to the body.

• Severe stenosis may lead to:

  • Heart failure.

  • Dysrhythmias.

  • Syncope.

  • Sudden cardiac death.

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Aortic Regurgitation

• Aortic valve does not close completely.

• Blood flows backward from the:

  • Aorta → left ventricle

• Occurs during diastole.

• Causes increased volume in the left ventricle.

Effects

• Left ventricular dilation.

• Increased workload.

• Decreased cardiac efficiency.

• Possible heart failure.

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Tricuspid Valve Dysfunction Tricuspid Stenosis

• Narrowing of the tricuspid valve.

• Obstructs blood flow from:

  • Right atrium → right ventricle

• Can cause blood to back up into the systemic venous circulation.

Possible findings

• Jugular venous distention (JVD).

• Peripheral edema.

• Hepatomegaly.

• Ascites.

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Tricuspid Regurgitation

• Tricuspid valve does not close completely.

• Blood flows backward from:

  • Right ventricle → right atrium

• Occurs during ventricular systole.

Can cause signs of right-sided heart failure:

• JVD.

• Peripheral edema.

• Hepatomegaly.

• Ascites.

• Weight gain.

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Pulmonic Valve Dysfunction Pulmonic Stenosis

• Narrowing of the pulmonic valve.

• Obstructs blood flow from:

  • Right ventricle → pulmonary artery

• Right ventricle must work harder to pump blood to the lungs.

Possible effects

• Right ventricular hypertrophy.

• Decreased pulmonary blood flow.

• Signs of right-sided heart failure in severe cases.

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Pulmonic Regurgitation

• Pulmonic valve does not close completely.

• Blood flows backward from:

  • Pulmonary artery → right ventricle

• Occurs during diastole.

• Causes volume overload of the right ventricle.

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Murmurs and Valvular Dysfunction

• A murmur is caused by turbulent blood flow.

• Often described as a "whooshing" sound.

• Systolic murmurs occur between:

  • S1 → S2

• Diastolic murmurs occur between:

  • S2 → S1.

Quick Rule for Murmurs Systolic

• Aortic stenosis

• Mitral regurgitation

Diastolic

• Aortic regurgitation

• Mitral stenosis

Easy Memory Trick:

"Stenosis = systolic on the semilunar valves"

• Aortic stenosis

• Pulmonic stenosis

"Regurgitation = diastolic on the semilunar valves"

• Aortic regurgitation

• Pulmonic regurgitation

For the AV valves, the pattern is reversed:

• Mitral/tricuspid regurgitation = systolic

• Mitral/tricuspid stenosis = diastolic

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Signs and Symptoms of Valvular Disease

Depending on the valve affected, watch for:

Decreased Cardiac Output

• Fatigue.

• Weakness.

• Exercise intolerance.

• Dizziness.

• Syncope.

• Hypotension.

Left-Sided Effects

• Dyspnea.

• Orthopnea.

• Crackles.

• Pulmonary edema.

Right-Sided Effects

• Peripheral edema.

• JVD.

• Hepatomegaly.

• Ascites.

• Weight gain.

Valvular Dysfunction

Main Function of Heart Valves

• Heart valves ensure blood flows in one direction.

• Valves open to allow forward blood flow.

• Valves close to prevent backflow of blood.

• The 4 valves are:

  • Tricuspid

  • Pulmonic

  • Mitral (bicuspid)

  • Aortic

• AV valves:

  • Tricuspid

  • Mitral

• Semilunar valves:

  • Pulmonic

  • Aortic

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Types of Valvular Dysfunction 1. Stenosis

Stenosis = narrowing of a valve

• Valve does not open completely.

• Blood has difficulty moving forward through the valve.

• The heart must work harder to push blood through the narrowed opening.

• Can lead to:

  • Increased pressure behind the valve.

  • Chamber hypertrophy.

  • Decreased cardiac output.

  • Heart failure.

Easy way to remember:

Stenosis = "stuck closed"

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2. Regurgitation (Insufficiency)

Regurgitation = valve does not close completely

• Blood leaks backward through the valve.

• Causes volume overload in the affected chamber.

• The heart must pump extra blood to maintain adequate cardiac output.

• Can eventually cause:

  • Chamber dilation.

  • Decreased cardiac output.

  • Pulmonary congestion.

  • Heart failure.

Easy way to remember:

Regurgitation = "leaky valve"

---

Mitral Valve Dysfunction Mitral Stenosis

• Narrowing of the mitral valve.

• Mitral valve is located between:

  • Left atrium

  • Left ventricle

• Obstruction prevents blood from moving easily from the left atrium to the left ventricle.

• Blood backs up into:

  • Left atrium.

  • Pulmonary circulation.

Possible findings

• Dyspnea.

• Fatigue.

• Pulmonary congestion.

• Crackles.

• Exercise intolerance.

• Increased risk for atrial dysrhythmias.

Think:

Mitral stenosis → blood backs up into the lungs

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Mitral Regurgitation

• Mitral valve does not close completely.

• During ventricular systole:

  • Some blood flows backward from the left ventricle → left atrium.

• Can result in:

  • Left atrial enlargement.

  • Pulmonary congestion.

  • Decreased forward cardiac output.

Possible findings

• Fatigue.

• Dyspnea.

• Pulmonary congestion.

• Heart murmur.

---

Aortic Valve Dysfunction Aortic Stenosis

• Narrowing of the aortic valve.

• Makes it difficult for blood to leave the left ventricle.

• Left ventricle must generate more pressure to push blood through the narrowed valve.

Effects

• Increased afterload.

• Left ventricular hypertrophy.

• Decreased cardiac output.

Classic symptoms

SAD

• Syncope

• Angina

• Dyspnea

Important NCLEX concept

• Aortic stenosis can significantly decrease blood flow to the body.

• Severe stenosis may lead to:

  • Heart failure.

  • Dysrhythmias.

  • Syncope.

  • Sudden cardiac death.

---

Aortic Regurgitation

• Aortic valve does not close completely.

• Blood flows backward from the:

  • Aorta → left ventricle

• Occurs during diastole.

• Causes increased volume in the left ventricle.

Effects

• Left ventricular dilation.

• Increased workload.

• Decreased cardiac efficiency.

• Possible heart failure.

---

Tricuspid Valve Dysfunction Tricuspid Stenosis

• Narrowing of the tricuspid valve.

• Obstructs blood flow from:

  • Right atrium → right ventricle

• Can cause blood to back up into the systemic venous circulation.

Possible findings

• Jugular venous distention (JVD).

• Peripheral edema.

• Hepatomegaly.

• Ascites.

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Tricuspid Regurgitation

• Tricuspid valve does not close completely.

• Blood flows backward from:

  • Right ventricle → right atrium

• Occurs during ventricular systole.

Can cause signs of right-sided heart failure:

• JVD.

• Peripheral edema.

• Hepatomegaly.

• Ascites.

• Weight gain.

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Pulmonic Valve Dysfunction Pulmonic Stenosis

• Narrowing of the pulmonic valve.

• Obstructs blood flow from:

  • Right ventricle → pulmonary artery

• Right ventricle must work harder to pump blood to the lungs.

Possible effects

• Right ventricular hypertrophy.

• Decreased pulmonary blood flow.

• Signs of right-sided heart failure in severe cases.

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Pulmonic Regurgitation

• Pulmonic valve does not close completely.

• Blood flows backward from:

  • Pulmonary artery → right ventricle

• Occurs during diastole.

• Causes volume overload of the right ventricle.

---

Murmurs and Valvular Dysfunction

• A murmur is caused by turbulent blood flow.

• Often described as a "whooshing" sound.

• Systolic murmurs occur between:

  • S1 → S2

• Diastolic murmurs occur between:

  • S2 → S1.

Quick Rule for Murmurs Systolic

• Aortic stenosis

• Mitral regurgitation

Diastolic

• Aortic regurgitation

• Mitral stenosis

Easy Memory Trick:

"Stenosis = systolic on the semilunar valves"

• Aortic stenosis

• Pulmonic stenosis

"Regurgitation = diastolic on the semilunar valves"

• Aortic regurgitation

• Pulmonic regurgitation

For the AV valves, the pattern is reversed:

• Mitral/tricuspid regurgitation = systolic

• Mitral/tricuspid stenosis = diastolic

---

Signs and Symptoms of Valvular Disease

Depending on the valve affected, watch for:

Decreased Cardiac Output

• Fatigue.

• Weakness.

• Exercise intolerance.

• Dizziness.

• Syncope.

• Hypotension.

Left-Sided Effects

• Dyspnea.

• Orthopnea.

• Crackles.

• Pulmonary edema.

Right-Sided Effects

• Peripheral edema.

• JVD.

• Hepatomegaly.

• Ascites.

• Weight gain.

Cardiomyopathy

• Cardiomyopathy is a chronic cardiac condition that affects the heart's ability to pump blood efficiently.

• There are 4 main types:

  1. Dilated cardiomyopathy (DCM)

  2. Hypertrophic cardiomyopathy (HCM)

  3. Restrictive cardiomyopathy (RCM)

  4. Arrhythmogenic cardiomyopathy (ACM)

• The direct cause is often unknown, but multiple contributing factors may increase the risk.

• Cardiomyopathy is closely associated with heart failure.

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Types of Cardiomyopathy 1. Dilated Cardiomyopathy (DCM) Pathophysiology

• Most common type of cardiomyopathy.

• Progressive cardiac disorder.

• The ventricles become dilated/stretched out.

• Ventricular muscle fibers become weakened.

• The heart cannot contract effectively.

• Ineffective contractions lead to:

  • ↓ Cardiac output

  • Heart failure

Think:

Dilated = stretched → weak squeeze → ↓ cardiac output

​

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2. Hypertrophic Cardiomyopathy (HCM) Pathophysiology

• Caused by hypertrophy/thickening of:

  • Left ventricular walls

  • Interventricular septum

• Thickened ventricles do not allow adequate blood refilling.

• Results in:

  • ↓ Left ventricular filling

  • ↓ Cardiac output

Think:

Hypertrophic = thick → can't fill

​

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3. Restrictive Cardiomyopathy (RCM) Pathophysiology

• Least common type of cardiomyopathy.

• Typically has a poor prognosis.

• Ventricles become stiff.

• Stiff ventricles cannot fill adequately during diastole.

• Results in:

  • ↓ Diastolic ventricular filling

  • ↓ Cardiac output

Think:

Restrictive = rigid/stiff → can't fill

​

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4. Arrhythmogenic Cardiomyopathy (ACM) Pathophysiology

• Ventricular muscle fibers are replaced with:

  • Fibrous tissue

  • Fatty tissue

• The abnormal tissue causes electrical instability.

• Can lead to lethal dysrhythmias:

  • Ventricular tachycardia (VT)

  • Ventricular fibrillation (VF)

• Can result in sudden cardiac death.

Think:

Arrhythmogenic = abnormal tissue → abnormal electrical activity → lethal dysrhythmias

​

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⭐ Quick Comparison

Type	Main Problem	Effect
DCM	Ventricles are stretched/dilated	Weak contractions
HCM	Ventricular walls/septum are thickened	Decreased filling
RCM	Ventricles are stiff	Decreased diastolic filling
ACM	Muscle replaced with fatty/fibrous tissue	Lethal dysrhythmias

​

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Etiology / Causes DCM

• Not age-specific.

• More typically seen in male clients.

• Possible causes:

  • Viral infections.

  • Autoimmune disorders.

  • Myocarditis.

  • Sarcoidosis.

  • Malnutrition.

  • Endocrine disorders.

  • Inflammatory processes.

  • Alcohol use.

HCM

• Often has a genetic predisposition.

• Associated with mutations to cardiac contractile muscle proteins.

• Can occur in athletes.

RCM

• Cause is usually unknown.

• May be linked to:

  • Amyloidosis.

  • Sarcoidosis.

ACM

• Associated with a genetic defect.

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Impact on Overall Health Psychosocial Effects

• Cardiomyopathy requires ongoing:

  • Lifestyle changes.

  • Management.

  • Modifications to daily life.

• Clients may have an increased risk of depression due to loss of independence.

• Medications such as diuretics and beta blockers may affect:

  • Sexual libido.

  • Mood.

  • Urinary continence.

• The financial burden of multiple medications may contribute to feeling overwhelmed.

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Safety Considerations ⚠

• Clients with arrhythmogenic or restrictive cardiomyopathy have an increased risk of sudden cardiac death.

• Risk is particularly important with competitive recreational sports.

• Other safety considerations are similar to those for heart failure.

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Considerations for Older Adults

• Cognitive deficits may interfere with the client's ability to:

  • Follow self-care recommendations.

  • Manage cardiomyopathy effectively.

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Clinical Manifestations DCM

Common findings:

• Chest discomfort.

• Peripheral edema.

• Progressively increasing fatigue.

• Exertional dyspnea.

​

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HCM

• May be asymptomatic.

• Possible manifestations:

  • Fatigue.

  • Syncope.

  • Chest discomfort.

  • Palpitations.

  • Exhaustion.

  • Dyspnea.

• Increased risk of sudden cardiac death, including in clients without manifestations.

​

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RCM

• Manifestations progress over time.

• Symptoms are similar to heart failure manifestations seen with:

  • DCM

  • HCM

​

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ACM

Manifestations may include:

• Symptoms similar to other cardiomyopathies.

• Ascites

• Increased JVD

• Lethal dysrhythmias:

  • VT

  • VF

​

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Diagnostic Tests 🔬 Chest X-Ray

• Used to identify cardiac enlargement.

Blood Tests

• CBC

• CMP

• Monitor for abnormalities involving:

  • Liver function.

  • Thyroid function.

  • Renal function.

​

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Cardiac Markers Troponin I & Troponin T

• Heart muscle-specific biomarkers.

• Elevation indicates myocardial injury.

NCLEX Question:

What does an elevated troponin I indicate?

➡ Myocardial injury

BNP

• A hormone released when ventricular contraction has weakened due to muscle fiber stretching from excessive fluid overload.

​

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ECG Findings

An ECG may show:

• Irregular heart rhythm.

• Widened QRS complexes.

• Bundle branch block.

• Abnormal P waves.

• Abnormal T waves.

• Absence of P waves.

• Ventricular tachycardia.

• Ventricular fibrillation.

​

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Echocardiogram

Used to evaluate:

• Thickness of the ventricles.

• Ventricular function.

• Movement of the heart valves.

​

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Role of the Nurse 👩‍⚕ ICD Safety

Some clients may have an implantable cardioverter-defibrillator (ICD).

ICD function:

• Monitors for abnormal cardiac rhythms.

• Detects life-threatening rhythms such as:

  • VT

  • VF

• Delivers an electrical shock when indicated.

Nursing Assessment:

• Ask the client:

  • Has the ICD delivered a shock?

  • How often has it delivered shocks?

• Report this information to the healthcare provider.

​

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Individual Assessment

Obtain a complete:

• Medical history.

• Family history.

Assess for factors that may predispose the client to cardiomyopathy.

Determine whether the client can perform ADLs without increased:

• Fatigue.

• Dyspnea.

• Palpitations.

​

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Client Education

Teach the importance of:

• Follow-up appointments.

• Frequent vital sign monitoring.

• Monitoring medication effectiveness.

Lifestyle Modifications

• Reduce dietary sodium.

• Restrict fluids to approximately 2 L/day.

• Eliminate or decrease:

  • Nicotine use.

  • Alcohol use.

• Avoid strenuous activity.

• Participate in low-impact exercise once cleared by the healthcare provider.

• Pace activities.

• Take rest periods as needed.

• Monitor daily for:

  • Weight changes.

  • Lower extremity edema.

​

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Nursing Process 1. Recognize Cues — Assessment

Assess for manifestations of heart failure:

• Lower extremity edema.

• JVD.

• Pulmonary congestion.

Additional assessments:

• Palpate pulses for irregularities that may indicate A-fib.

• Assess for:

  • Liver distention.

  • Ascites.

• Auscultate for:

  • Heart murmurs.

  • Extra heart sounds.

  • Irregular rhythms.

​

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2. Analyze Cues

• Gather all relevant client data.

• Develop a plan of care.

• Provide support and education.

• Reinforce:

  • Medication adherence.

  • Lifestyle modifications.

• Goal: improve the client's quality of life.

​

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3. Priority of Care ⭐ Main priority:

Improve cardiac output and quality of life.

​

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4. Generate Solutions

Collaborate with the interprofessional healthcare team to plan:

• Medication management.

• Dietary restrictions.

• Activity restrictions.

• Education about monitoring manifestations.

​

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5. Take Actions

Treatment may include:

• Lifestyle modifications.

• Medications.

• Surgical interventions.

​

---

6. Evaluate Outcomes

• Clients require frequent follow-up.

• Treatments are complex.

• Regular monitoring is needed to prevent potentially life-threatening complications.

• Evaluate the effectiveness of the plan of care.

​

---

Treatments & Therapies Nonpharmacological Interventions

Teach clients to:

• Reduce sodium intake.

• Reduce fluid intake.

• Maintain or reduce weight as appropriate.

• Avoid:

  • Alcohol.

  • Smoking.

  • Illicit drug use.

• Discontinue strenuous activities.

• Participate in low-impact exercise.

• Consider genetic testing and counseling.

​

---

Pharmacological Interventions 💊 General Treatment

For all four types:

• Diuretics

  • Manage fluid overload.

• Vasodilators

  • Help decrease manifestations of fluid overload.

  • Example: Nitroglycerin

​

---

DCM Medications

• ACE inhibitors

  • Enalapril.

  • Lisinopril.

• ARBs

  • Losartan.

  • Valsartan.

• Beta blockers

  • Metoprolol.

• Mineralocorticoid antagonists

  • Eplerenone.

  • Spironolactone.

​

---

HCM Medications

• Beta blocker.

• Calcium channel blocker:

  • Verapamil

• Used to reduce:

  • Chest discomfort/pressure.

  • Dyspnea.

​

---

RCM Medications ⚠

• The heart may require a higher heart rate to maintain adequate cardiac output.

• Use beta blockers and calcium channel blockers cautiously because they can decrease the heart rate.

​

---

Surgical & Invasive Interventions DCM and RCM

For end-stage heart failure:

Heart Transplantation

• Can improve long-term survival and heart function.

• Finding a compatible donor can take a long time.

LVAD — Left Ventricular Assist Device

• Surgically implanted cardiac device.

• Helps maintain:

  • Heart function.

  • Cardiac output.

• May be used:

  • While waiting for a heart transplant.

  • As a long-term treatment option.

• Following LVAD placement:

  • Clients typically remain in the ICU for 4–5 days while IV medications are weaned.

​

---

HCM Procedures Septal Myectomy

• Invasive procedure similar to open-heart surgery.

• Removes or reduces portions of the hypertrophied ventricular septum.

• Allows increased capacity for diastolic filling.

Alcohol Septal Ablation

• Less invasive procedure.

• Performed with cardiac catheterization.

• Medical alcohol is injected into the thickened septal tissue.

• Eliminates blood flow to the targeted area.

• Tissue death reduces the thickness of the septum.

ICD

• May reduce the high risk of sudden cardiac death.

• Battery life: approximately 6–12 years.

• Clients should be monitored by the healthcare provider at least every 6 months.

​

Heart Failure

• Heart failure (HF) is a complex, progressive clinical syndrome.

• Occurs due to abnormalities in the:

  • Structure of the heart

  • Function of the heart

• These abnormalities lead to:

  • ↓ Cardiac output (CO)

  • ↑ Pressure within the heart

• Can occur:

  • At rest.

  • During stress.

• Heart failure occurs when the heart cannot meet the needs of the systemic circulatory system.

• This happens when:

  • Ventricles do not fill properly.

  • Blood is not effectively ejected into the systemic circulation.

Conditions that contribute to HF:

• Hypertension.

• Coronary artery disease (CAD).

• Uncontrolled arrhythmias.

• Myocardial infarction (MI).

• Valvular disease.

Key Concept 🧠

Heart failure = filling problem, pumping problem, or both.

---

Etiology / Causes Most Common Causes

• CAD

• MI

• Diabetes mellitus

Structural Causes

• Uncontrolled arrhythmias.

• Hypertension.

• Myocarditis.

• Congenital heart disease.

Other Causes

Heart failure can also occur due to:

• Thyrotoxicosis.

• Anemia.

• Thiamine deficiency.

• Pregnancy.

---

Risk Factors

• Family history of heart disease.

• Chronic pulmonary disease.

• CAD.

• Hypertension.

• Chronic infection or inflammation.

• Diabetes mellitus.

• Obesity.

• Metabolic diseases.

• Alcohol abuse.

• Treatment with cardiotoxic agents, such as:

  • Anthracyclines

---

Common Comorbidities

More than half of clients with heart failure also have another comorbid condition.

Cardiac and Noncardiac Comorbidities

• Obesity.

• Atrial fibrillation (A-fib).

• Chronic kidney disease (CKD).

• Diabetes mellitus.

• Hypertension.

• Anemia.

• Iron deficiency.

• Frailty.

---

Impact on Overall Health Physiological Effects

Common manifestations can include:

• Shortness of breath.

• Fatigue.

• Weakness.

• Difficulty sleeping.

• Lower extremity edema.

Psychosocial Effects

• Diminished quality of life.

• Difficulty completing ADLs independently.

• Activity intolerance.

• Increased dependence on caregivers.

• May contribute to:

  • Depression.

  • Hopelessness.

  • Helplessness.

---

Safety Considerations ⚠

• Heart failure is progressive, but manifestations can worsen quickly.

• Clients need to know:

  • How to monitor their manifestations.

  • When to report changes.

Oxygen Safety

If the client uses oxygen:

• Follow proper oxygen administration.

• Post no-smoking signs.

• Keep oxygen at least 6 feet from open flames.

• Use electrical equipment safely.

---

Considerations for Older Adults

• Incidence of heart failure increases with age.

• Adults age 65 and older should be educated about:

  • Manifestations of developing heart failure.

  • Modifiable risk factors.

  • Strategies to reduce risk.

---

Types of Heart Failure Left-Sided Heart Failure 🫁

• Primarily causes blood and fluid to back up toward the lungs.

Manifestations

• Shortness of breath.

• Hypotension with tachycardia.

• Orthopnea.

• Exertional dyspnea.

• Paroxysmal nocturnal dyspnea (PND).

• Lower extremity edema.

• Weight gain.

• Increased abdominal girth.

• Pulmonary congestion.

• Rales.

• Productive cough.

• White or pink blood-tinged sputum.

• Displaced point of maximum impulse (PMI).

Memory Trick:

LEFT = LUNGS

---

Right-Sided Heart Failure 💧

• Associated with systemic fluid buildup.

Manifestations

• JVD.

• Chest discomfort.

• S3 heart sound.

• Heart murmurs.

• Palpitations.

• Ascites.

• Peripheral edema.

• Generalized swelling.

• Enlarged liver.

• Enlarged spleen.

Memory Trick:

RIGHT = REST of the body

---

Biventricular Heart Failure

• Involves both ventricles.

• Client experiences manifestations of both:

  • Left-sided HF.

  • Right-sided HF.

Common findings

• Fluid buildup.

• Dyspnea.

• Pulmonary and systemic congestion.

---

⭐ Left vs. Right Heart Failure

Left-Sided HF	Right-Sided HF
Pulmonary congestion	Systemic congestion
Dyspnea	JVD
Orthopnea	Peripheral edema
PND	Ascites
Rales	Hepatomegaly
Pink/white blood-tinged sputum	Generalized swelling

---

Framingham Diagnostic Criteria

To diagnose heart failure, the client must meet:

• 2 major criteria

OR

• 1 major criterion + 2 minor criteria

Major Criteria

• Acute pulmonary edema.

• Cardiomegaly.

• Hepatojugular reflux.

• Neck vein distention.

• Paroxysmal nocturnal dyspnea.

• Orthopnea.

• Pulmonary rales.

• Third heart sound (S3 gallop).

• Weight loss of 4.5 kg or more in 5 days in response to treatment.

• Central venous pressure greater than 16 cm of water.

• Radiographic cardiomegaly.

Minor Criteria

• Ankle edema.

• Dyspnea on exertion.

• Hepatomegaly.

• Nocturnal cough.

• Pleural effusion.

• Tachycardia:

  • Heart rate greater than 120/min.

• Decrease in vital capacity by one-third of the maximum recorded value.

---

NYHA Functional Classification

Used to classify the severity of heart failure based on manifestations during physical activity.

Class I

• No limitation.

• Able to perform normal activities.

• No manifestations.

Class II

• Slight limitation with normal activity.

• Mild manifestations with activity.

• Comfortable at rest.

Class III

• Moderate limitation.

• Moderate manifestations with decreased activity.

• Comfortable only at rest.

Class IV

• Severe limitation.

• Manifestations with minimal activity.

• Manifestations may be present at rest.

Possible Manifestations

• Chest pain.

• Shortness of breath.

• Fatigue.

• Palpitations.

• Fainting.

Easy Memory 🧠

• I = no symptoms

• II = slight limitation

• III = moderate limitation

• IV = symptoms at rest

---

Diagnostic Tests & Labs 🔬 Complete Laboratory Profile

Used to evaluate:

• Renal function.

• Liver function.

• Anemia.

• Iron deficiency.

• Possible cause and severity of HF.

---

BNP — B-Type Natriuretic Peptide

• Used to help determine whether dyspnea is:

  • Cardiac-related

  • Noncardiac

• Can also monitor effectiveness of treatment.

• BNP levels correspond with the NYHA classification.

• BNP obtained before discharge can help predict:

  • Readmission risk.

  • Risk of death.

NCLEX Pearl ⭐

Dyspnea + suspected heart failure → check BNP

---

Echocardiogram

Used to assess:

• Systolic dysfunction.

• Diastolic dysfunction.

• Wall motion abnormalities.

• Heart valve function.

Systolic Dysfunction

• Left ventricle does not contract normally.

• Not enough blood is pushed into circulation.

Diastolic Dysfunction

• Left ventricle does not relax normally.

• Ventricle does not fill properly during relaxation.

Easy Memory:

Systolic = squeeze problem Diastolic = filling/relaxation problem

---

Chest X-Ray

Used to assess:

• Heart size.

• Degree of pulmonary congestion.

Findings suggestive of HF:

• Pulmonary vascular congestion.

• Enlarged heart.

• Fluid in the base of the lungs.

---

Other Tests ECG

• Helps identify underlying causes.

• Can identify rhythm abnormalities.

Cardiac Catheterization

• May be performed if HF is related to an acute MI.

• May be followed by PCI to restore blood flow.

Stress Test

• Used to help determine the underlying cause.

---

Role of the Nurse 👩‍⚕ Environmental Assessment

During home visits, assess:

• Ability to perform ADLs.

• Meals the client is preparing.

• Safe use of oxygen.

• Ability to ask questions and understand teaching.

---

Individualized Assessment

Assess each client's:

• Manifestations.

• Functional ability.

• Ambulation.

• Mobility.

• Cognition.

• Ability to remain independent safely.

Assess understanding of:

• Manifestations to report.

• How and when to take medications.

• Importance of daily weights.

---

Daily Weight Monitoring ⚖

A weight gain may indicate fluid retention and worsening heart failure.

Report:

• More than 2–3 lb in 1 day

OR

• More than 5 lb in 1 week

How to Weigh

• Use the same scale.

• Weigh at the same time every day.

• Ideally weigh:

  • In the morning.

  • Before eating.

---

Client Education Monitor Daily For:

• Increased shortness of breath.

• Swelling.

• Weight gain.

• Other worsening manifestations.

Lifestyle Changes

• Smoking cessation.

• Limit alcohol.

• Reduce sodium intake to less than 3 g/day.

• Approximately 2 L fluid restriction/day, especially with:

  • Hyponatremia.

  • Advanced symptoms.

• Take medications as prescribed.

• Attend regular follow-up appointments.

• Maintain recommended vaccinations, including:

  • Influenza.

  • Pneumococcal.

---

Nursing Process 1. Recognize Cues — Assessment

Obtain a complete health history:

• Current and past manifestations.

• Other medical conditions.

• Ability to perform ADLs.

Physical Assessment

Assess:

• General appearance.

• Lung sounds.

• Heart sounds.

• JVD.

• Peripheral edema.

• Full set of vital signs.

Review:

• Laboratory results.

• Diagnostic testing.

---

2. Analyze Cues

Look for signs of worsening HF:

• Weight gain.

• Decreased ability to perform activities.

• Edema.

• Rales.

• Evidence of fluid overload.

• Elevated or abnormal BNP findings.

---

3. Priority of Care ⭐ Main Priority:

Reduce fluid overload and improve respiratory and cardiac status.

---

4. Generate Solutions

Collaborate with the interprofessional team.

Goals include:

• Control and monitor manifestations.

• Medication adherence.

• Dietary adherence.

• Daily weight monitoring.

• Improve quality of life.

• Reduce morbidity and mortality.

• Reduce hospital readmissions.

---

5. Take Actions

If the client has respiratory distress:

• Elevate the head of the bed to High-Fowler's.

• Administer O₂ as prescribed.

• Encourage anxiety-relieving techniques:

  • Pursed-lip breathing.

  • Guided imagery.

  • Relaxation.

• Encourage coughing and deep breathing every 2 hours.

• Reassess lung sounds at least every 4 hours, or more frequently as indicated.

Treatment may include:

• Medications.

• Lifestyle modifications.

• Surgical interventions.

---

6. Evaluate Outcomes

Evaluate whether treatment resulted in:

• Maintained weight.

• Decreased edema.

• Improved quality of life.

• Decreased hospital readmissions.

Continue frequent monitoring of manifestations.

---

Nonpharmacological Treatment

Treatment focuses on:

• Correcting the underlying cause when possible.

• Relieving manifestations.

• Slowing disease progression.

• Improving quality of life.

Lifestyle Changes

• Stop smoking.

• Reduce or maintain weight.

• Monitor fluid intake.

• Use alcohol and caffeine in moderation.

• Follow a heart-healthy diet.

• Remain physically active as appropriate.

• Manage stress.

• Control blood pressure.

---

Pharmacological Treatment 💊

Heart failure treatment may involve multiple medications.

Medication Classes

• SGLT-2 inhibitors

  • Reduce HF hospitalizations.

  • Reduce cardiovascular mortality.

• ACE inhibitors

  • Examples:

    • Captopril.

    • Enalapril (Vasotec).

• Angiotensin II receptor blockers (ARBs)

• Angiotensin receptor-neprilysin inhibitors (ARNIs)

• Beta blockers

  • Example: Metoprolol

• Aldosterone antagonists

  • Example: Spironolactone

• Hydralazine and isosorbide dinitrate

• Diuretics

Other Medications

May include:

• Anticoagulants

  • For clients with A-fib.

  • Example: Warfarin.

• Statins

  • For elevated cholesterol or history of MI.

• Digoxin

---

Surgical & Invasive Interventions Cardiac Catheterization + PCI

Used when HF is caused by an acute MI.

Purpose:

• Restore blood flow to cardiac muscle.

• Decrease the extent of myocardial damage.

---

Cardiac Resynchronization Therapy (CRT) Ventricular Desynchrony

• Right and left ventricles do not contract and relax at the same time.

• Different areas of the ventricles may contract at different times.

• Can contribute to dysrhythmias.

CRT with Biventricular Pacemaker

• Used to synchronize ventricular contractions.

• Pacemaker is inserted below the collarbone.

• Three wires are threaded into the ventricles.

• The device detects and corrects rhythm problems.

---

Implantable Cardioverter-Defibrillator (ICD) ⚡

• Clients with LVEF less than 35% are at high risk for dysrhythmias.

• An ICD may be inserted to help prevent sudden cardiac death.

• Device is placed beneath the skin below the collarbone.

• Two wires are threaded into:

  • Right atrium.

  • Right ventricle.

• Detects dysrhythmias.

• Sends an electrical impulse to correct the abnormal rhythm.

---

ICD Discharge Teaching

For approximately 4–6 weeks, follow prescribed activity restrictions.

Incision Care

• Monitor for infection:

  • Redness.

  • Drainage.

  • Increased pain.

• Keep incision dry for 4–5 days.

• After that:

  • Shower as instructed.

  • Gently pat incision dry.

• Avoid:

  • Tub baths.

  • Swimming.

  • Hot tubs.

• Continue avoiding these until the incision is completely healed.

Activity Restrictions

• Wear comfortable clothing that does not rub the incision.

• Do not lift more than 10–15 lb.

• Avoid:

  • Twisting.

  • Pushing.

  • Pulling for 2–3 weeks.

• Do not raise the affected arm above the shoulder for 4–6 weeks.

• Keep follow-up appointments for regular device monitoring.

diuretics

Overview Indications for medications affecting urinary output

• Management of blood pressure.

• Removal of excess/edematous fluid related to:

  • Heart failure.

  • Kidney disease.

  • Liver disease.

• Prevention of kidney failure in certain situations.

Main Types of Diuretics

1. High-ceiling loop diuretics

2. Thiazide diuretics

3. Potassium-sparing diuretics

4. Osmotic diuretics

---

1. High-Ceiling Loop Diuretics 💧 Prototype

• Furosemide (Lasix)

Other Medications

• Ethacrynic acid

• Bumetanide

• Torsemide

---

Expected Pharmacological Action

• Work in the loop of Henle.

• Block reabsorption of:

  • Sodium.

  • Chloride.

• Prevent reabsorption of water.

• Cause extensive diuresis, even with severe renal impairment.

• Increase excretion of:

  • Water.

  • Potassium.

  • Sodium.

  • Chloride.

  • Magnesium.

  • Calcium.

Memory Trick 🧠

Loop diuretics = lose lots of fluid and electrolytes.

---

Therapeutic Uses

Used when there is an emergent need for rapid fluid removal.

• Pulmonary edema caused by heart failure.

• Edema caused by:

  • Liver disease.

  • Cardiac disease.

  • Kidney disease.

• Conditions that do not respond to other diuretics.

• Hypertension:

  • Torsemide.

• Unlabeled use: Hypercalcemia

Routes

• Oral

• IV

• IM

---

Loop Diuretic Complications ⚠ 1. Dehydration Manifestations

• Dry mouth.

• Increased thirst.

• Oliguria.

• Lethargy.

• Weight loss.

Nursing Actions

• Monitor for dehydration.

• Monitor daily weight.

• Report urine output less than 30 mL/hr.

• Notify the provider.

• Medication may need to be withheld.

• Therapy is generally started with a low dose.

---

2. Hypotension / Orthostatic Hypotension Nursing Actions

• Monitor blood pressure.

• Teach the client to:

  • Change positions slowly.

  • Rise slowly from lying or sitting.

Client Education

If light-headedness or dizziness occurs:

• Sit down.

• Lie down.

---

3. Ototoxicity 👂 Important!

• Usually transient with furosemide.

• Can be irreversible with ethacrynic acid.

Nursing Actions

• Avoid combining with other ototoxic medications when possible.

• Example:

  • Aminoglycoside antibiotics such as gentamicin.

Client Education

Report:

• Tinnitus.

• Ringing.

• Buzzing.

• Vertigo.

• Feeling of fullness in the ears.

---

4. Hypokalemia Potassium level:

• K⁺ less than 3.5 mEq/L

Manifestations

• Nausea.

• Vomiting.

• Fatigue.

• Leg cramps.

• General weakness.

Nursing Actions

• Monitor:

  • Potassium.

  • Cardiac status.

• Report K⁺ less than 3.5 mEq/L.

• Monitor ECG if potassium drops below 3.5 mEq/L.

• Client may require a potassium supplement.

Client Education

Eat potassium-rich foods:

• Bananas.

• Potatoes.

• Dried fruits.

• Nuts.

• Spinach.

• Citrus fruits.

---

5. Other Electrolyte Imbalances

Loop diuretics can cause:

• Hyponatremia

• Hypomagnesemia

• Hypochloremia

• Hypocalcemia

Nursing Actions

• Monitor electrolyte levels.

• Report abnormal results.

---

6. Other Adverse Effects

• Hyperglycemia.

• Hyperuricemia.

• ↓ HDL cholesterol.

• ↑ LDL cholesterol.

• ↑ Triglycerides.

Nursing Actions

Monitor:

• Blood glucose.

• Uric acid.

• Lipid levels.

---

Loop Diuretics: Contraindications & Precautions Contraindicated

• Anuria = no urine output.

Use Cautiously With

• Severe liver disease.

• Diabetes mellitus.

• Dehydration.

• Electrolyte depletion.

• Gout.

Use caution with clients taking:

• Digoxin.

• Lithium.

• Ototoxic medications.

• NSAIDs.

• Antihypertensives.

Important

• Hypoproteinemia can increase the risk of ototoxicity.

---

Loop Diuretic Drug Interactions Digoxin + Hypokalemia ⚠

• Hypokalemia increases the risk for digoxin toxicity.

• Can lead to ventricular dysrhythmias.

Nursing Actions

Monitor:

• Cardiac status.

• Potassium levels.

• Digoxin levels.

Important

• Potassium-sparing diuretics may be given with loop diuretics to reduce the risk of hypokalemia.

---

Antihypertensives

• Can cause an additive hypotensive effect.

Nursing Action

• Monitor blood pressure.

---

Lithium

• Hyponatremia caused by loop diuretics can increase lithium levels.

• Can result in lithium toxicity.

Nursing Action

• Monitor lithium levels.

---

NSAIDs

• Decrease blood flow to the kidneys.

• Can decrease the effectiveness of the diuretic.

Nursing Action

Monitor for:

• Decreased urine output.

• Decreased diuretic effectiveness.

---

Loop Diuretic Nursing Administration

Obtain baseline:

• Orthostatic blood pressure.

• Weight.

• Electrolytes.

• Location and extent of edema.

Monitor:

• Blood pressure.

• I&O.

• Daily weight.

Daily Weight

• Weigh at the same time each day.

• Use the same amount of clothing.

• Usually weigh upon awakening.

Administration Timing ⏰

Avoid giving late in the day to prevent nocturia.

Usual dosing:

• 0800

• 1400

IV Furosemide

• May be given:

  • IV bolus.

  • Continuous IV infusion.

• IV bolus should be administered at 20 mg/min or slower.

• Slow administration helps prevent:

  • Abrupt hypotension.

  • Hypovolemia.

Safety

• Initiate fall precautions, especially for older adults.

• Monitor for pain in:

  • Chest.

  • Calves.

  • Pelvis.

• Notify the provider if these occur.

---

Loop Diuretic Effectiveness

Therapy is effective when there is:

• ↓ Pulmonary edema.

• ↓ Peripheral edema.

• Weight loss.

• ↓ Blood pressure.

• ↑ Urine output.

• ↓ Calcium level.

---

2. Thiazide Diuretics 💊 Prototype

• Hydrochlorothiazide (HCTZ)

Other Medications

• Chlorothiazide.

• Methyclothiazide.

Thiazide-Type Diuretics

• Indapamide.

• Chlorthalidone.

• Metolazone.

---

Expected Pharmacological Action

• Work in the early distal convoluted tubule.

• Block reabsorption of:

  • Sodium.

  • Chloride.

• Prevent water reabsorption.

• Promote diuresis when renal function is not impaired.

---

Thiazide Therapeutic Uses

• Often the first choice for essential hypertension.

• Mild to moderate edema caused by:

  • Heart failure.

  • Liver disease.

  • Kidney disease.

• Often combined with other antihypertensive medications.

• Reduce urine production in diabetes insipidus.

• Promote calcium reabsorption.

• Can reduce the risk of postmenopausal osteoporosis.

Memory Trick 🧠

Thiazides hold onto calcium.

---

Thiazide Complications 1. Dehydration & Hyponatremia Manifestations

• Dry mouth.

• Increased thirst.

• Minimal urine output.

• Weight loss.

Nursing Actions

• Monitor:

  • Electrolytes.

  • Weight.

  • Urine output.

• Report urine output less than 30 mL/hr.

• Stop medication and notify the provider as directed.

---

2. Hypokalemia & Hypochloremia Monitor

• Cardiac status.

• Potassium levels.

Report

• K⁺ less than 3.5 mEq/L.

Client Education

Consume potassium-rich foods.

Watch for:

• Nausea.

• Vomiting.

• Weakness.

• Fatigue.

• Leg cramps.

---

3. Hyperglycemia Nursing Action

• Monitor blood glucose.

---

4. Other Effects

• Hyperuricemia.

• Hypomagnesemia.

• Increased lipid levels.

Monitor:

• Uric acid.

• Magnesium.

• Total cholesterol.

• HDL.

• LDL.

• Triglycerides.

Low Magnesium Manifestations

• Weakness.

• Muscle twitching.

• Tremors.

---

Thiazide Contraindications & Precautions Contraindicated

• Renal impairment.

• Lactation.

Pregnancy

• Use cautiously due to risk of:

  • Jaundice in the newborn.

  • Thrombocytopenia in the newborn.

Use Cautiously With

• Cardiovascular disease.

• Diabetes mellitus.

• Hypokalemia.

• Hyperlipidemia.

• Hypomagnesemia.

• Gout.

Use caution with:

• Digoxin.

• Lithium.

• Antihypertensives.

Important

• Thiazides do not cause hearing loss.

• They can be combined with ototoxic medications.

---

Thiazide Nursing Administration

• Chlorothiazide: Oral or IV.

• All other thiazides: Oral.

Obtain baseline:

• Orthostatic BP.

• Weight.

• Electrolytes.

• Location and extent of edema.

Monitor:

• Potassium.

• Blood pressure.

• I&O.

• Daily weight.

Alternate-Day Dosing

• Can help decrease electrolyte imbalances.

If K⁺ is less than 3.5 mEq/L:

• Monitor ECG.

• Notify the provider.

• Potassium supplementation may be needed.

---

Thiazide Client Education Timing

• Take first dose in the morning.

• If prescribed twice daily:

  • Take second dose by 1400.

Prevents:

Nocturia

Daily Weight

• Weigh at the same time every day.

• Wear the same amount of clothing.

• Notify the provider for a weight gain of more than 3 lb in 1 day.

Fluids

• Maintain approximately 1,500 mL/day, unless contraindicated.

GI Upset

• Take with or after meals.

Other Teaching

• Rise slowly.

• Monitor BP.

• Monitor blood glucose if diabetic.

• Report:

  • Significant weight loss.

  • Dizziness.

  • Lightheadedness.

  • GI distress.

  • General weakness.

---

Thiazide Effectiveness

Expected outcomes:

• ↓ Blood pressure.

• ↓ Edema.

• ↑ Urine output.

• ↓ Urine output in diabetes insipidus.

• Preserved bone integrity in postmenopausal clients.

---

3. Potassium-Sparing Diuretics 🥔 Prototype

• Spironolactone

Other Medications

• Triamterene.

• Amiloride.

---

Expected Pharmacological Action

• Block the action of aldosterone.

• Aldosterone normally promotes sodium and water retention.

• Potassium-sparing diuretics:

  • Retain potassium.

  • Increase sodium excretion.

  • Increase water excretion.

Memory Trick 🧠

Potassium-sparing = save the K⁺!

---

Therapeutic Uses

• Often combined with:

  • Loop diuretics.

  • Thiazide diuretics.

• Helps reduce the risk of hypokalemia.

• Used to treat:

  • Hypertension.

  • Edema.

  • Heart failure.

• Used for primary hyperaldosteronism.

Onset

• Therapeutic effects can take 48–72 hours.

Route

• Oral.

---

Potassium-Sparing Complications 1. Hyperkalemia ⚠ High potassium:

• Greater than 5 mEq/L

Manifestations

• Weakness.

• Fatigue.

• Dyspnea.

• Dysrhythmias.

Nursing Actions

• Monitor potassium.

• Initiate cardiac monitoring if K⁺ is greater than 5 mEq/L.

• Monitor electrolytes.

• If hyperkalemia occurs:

  • Discontinue medication.

  • Restrict potassium in diet.

  • May give a potassium-excreting diuretic.

  • May administer IV glucose and insulin to shift potassium into cells.

Do NOT Combine With

• Potassium supplements.

• Other potassium-sparing diuretics.

Use caution with:

• ACE inhibitors.

• ARBs.

• Direct renin inhibitors.

These can all increase potassium levels.

---

2. Endocrine Effects

Spironolactone can cause:

• Deepened voice.

• Impotence.

• Menstrual irregularities.

• Gynecomastia.

• Hirsutism.

Client Education

• Observe for these effects.

• Notify the provider if they occur.

---

3. Drowsiness & Metabolic Acidosis Nursing Actions

Monitor for:

• Drowsiness.

• Restlessness.

Client Education

• Avoid activities requiring alertness until the medication's effects are known.

---

Potassium-Sparing Contraindications

Do not administer to clients who:

• Have hyperkalemia.

• Take potassium supplements.

• Take another potassium-sparing diuretic.

• Have severe kidney failure.

• Have anuria.

Pregnancy

• Associated with fetal harm.

• Wear gloves when handling medication.

Use Cautiously With

• Kidney disease.

• Liver disease.

• Electrolyte imbalances.

• Metabolic acidosis.

---

Potassium-Sparing Drug Interactions

The following increase the risk of hyperkalemia:

• ACE inhibitors.

• ARBs.

• Direct renin inhibitors.

• Potassium supplements.

• Potassium-containing salt substitutes.

• Other potassium-sparing diuretics.

Nursing Actions

• Monitor K⁺.

• Notify the provider if K⁺ is greater than 5.0 mEq/L.

• Avoid concurrent use when indicated.

---

Potassium-Sparing Nursing Administration

Obtain baseline data.

Monitor:

• Daily weight.

• Blood pressure.

• I&O.

• ECG periodically.

• Potassium levels.

---

Potassium-Sparing Client Education Avoid

• Salt substitutes containing potassium.

• Excess potassium-rich foods, such as:

  • Oranges.

  • Bananas.

  • Potatoes.

  • Dates.

Monitor

• Blood pressure.

• Weight.

Keep a log.

Triamterene

• Can cause bluish-colored urine.

Report:

• Cramps.

• Diarrhea.

• Thirst.

• Altered menstruation.

• Deepened voice.

---

Potassium-Sparing Effectiveness

Expected outcomes:

• Potassium maintained between:

  • 3.5–5.0 mEq/L

• Weight loss.

• ↓ Blood pressure.

• ↓ Edema.

---

4. Osmotic Diuretics 🧠👁💧 Prototype

• Mannitol

---

Expected Pharmacological Action

• Raises serum osmolality.

• Draws fluid into the bloodstream.

• Reduces:

  • Intracranial pressure (ICP)

  • Intraocular pressure (IOP)

Memory Trick 🧠

Mannitol = pulls water out of tissues and into the bloodstream.

---

Therapeutic Uses Kidney Protection

Can help prevent kidney failure in:

• Hypovolemic shock.

• Severe hypotension.

Mannitol:

• Is not reabsorbed.

• Remains in the nephron.

• Draws water into the nephron.

• Helps preserve urine flow.

Other Uses

• Decreases ICP caused by cerebral edema.

• Decreases IOP.

• Promotes sodium retention and water excretion in clients with:

  • Hyponatremia.

  • Fluid volume excess.

• Used during the oliguria phase of acute kidney injury.

---

Mannitol Complications ⚠ 1. Heart Failure & Pulmonary Edema

Watch for:

• Dyspnea.

• Weakness.

• Fatigue.

• Distended neck veins.

• Weight gain.

Nursing Action

• Stop the medication immediately.

• Notify the provider.

---

2. Rebound Increased ICP

Monitor for:

• Change in level of consciousness.

• Changes in pupils.

• Headache.

• Nausea.

• Vomiting.

---

3. Fluid & Electrolyte Imbalances

Can cause:

• Electrolyte abnormalities.

• Metabolic acidosis.

Metabolic Acidosis Manifestations

• Drowsiness.

• Restlessness.

Nursing Actions

• Monitor laboratory values.

• Monitor for manifestations of metabolic acidosis.

---

Mannitol Contraindications

Contraindicated in clients with:

• Active intracranial bleeding.

• Anuria.

• Severe pulmonary edema.

• Severe dehydration.

• Renal failure.

Use Extreme Caution With

• Heart failure.

• Pregnancy.

• Breastfeeding.

• Renal insufficiency.

• Electrolyte imbalances.

---

Mannitol Drug Interactions Lithium

• Mannitol increases renal excretion of lithium.

Nursing Action

• Monitor lithium levels.

Cardiac Glycosides

• Increased risk of hypokalemia.

Nursing Actions

• Monitor potassium.

• Monitor ECG.

---

Mannitol Administration Route

• Administer by continuous IV infusion.

Important: Crystals! ⚠

To prevent administration of microscopic crystals:

• Use a filter needle when drawing from the vial.

• Use a filter in the IV tubing.

---

Mannitol Nursing Assessment

Monitor:

• Daily weight.

• I&O.

• Blood electrolytes.

• Blood pressure.

• Dehydration.

• Increased edema.

• Potassium.

If K⁺ falls below 3.5 mEq/L:

• Monitor ECG.

• Notify the provider.

Monitor for increased ICP:

• Change in LOC.

• Pupil changes.

• Headache.

• Nausea/vomiting.

Monitor for metabolic acidosis:

• Drowsiness.

• Restlessness.

---

Mannitol Client Education

• Get up slowly to prevent postural hypotension.

• Monitor blood pressure.

• If dizzy or faint:

  • Sit down.

  • Lie down.

Report:

• Significant weight loss.

• Lightheadedness.

• Dizziness.

• GI distress.

• General weakness.

These can indicate:

• Hypokalemia.

• Hypovolemia.

---

Mannitol Effectiveness

Expected therapeutic outcomes:

Kidney Function

• Urine output at least 30 mL/hr.

• Creatinine:

  • Males: 0.6–1.3 mg/dL

  • Females: 0.5–1.1 mg/dL

• BUN:

  • 10–20 mg/dL

Other indicators:

• ↓ Intracranial pressure.

• ↓ Intraocular pressure.

---

⭐ Quick Comparison of Diuretics

Type	Prototype	Main Site/Action	Potassium Effect	High-Yield Use
Loop	Furosemide	Loop of Henle; massive diuresis	↓ K⁺	Pulmonary edema
Thiazide	Hydrochlorothiazide	Distal convoluted tubule	↓ K⁺	First-line for HTN
Potassium-sparing	Spironolactone	Blocks aldosterone	↑ K⁺ / saves K⁺	HF + prevents hypokalemia
Osmotic	Mannitol	Pulls water into circulation/nephron	Monitor electrolytes	↓ ICP and ↓ IOP

---

🧠 NCLEX High-Yield Points Furosemide

Think: “Fluid out, potassium out.”

Monitor for:

• Dehydration.

• Hypotension.

• Hypokalemia.

• Ototoxicity.

Important

• Report urine output < 30 mL/hr.

• Give early in the day.

• IV furosemide: 20 mg/min or slower.

• Avoid combining with other ototoxic medications.

---

Hydrochlorothiazide

Think: “Thiazides = first-line hypertension + save calcium.”

Monitor for:

• Dehydration.

• Hyponatremia.

• Hypokalemia.

• Hyperglycemia.

• Hyperuricemia.

• Hypomagnesemia.

• Take in the morning.

• Second dose by 1400.

• Can reduce the risk of postmenopausal osteoporosis because it promotes calcium reabsorption.

---

Spironolactone

Think: “Spironolactone spares potassium.”

Monitor for:

• Hyperkalemia.

• Dysrhythmias.

• Endocrine effects.

Avoid:

• Potassium supplements.

• Potassium-containing salt substitutes.

• Excess potassium-rich foods.

Possible endocrine effects:

• Gynecomastia.

• Impotence.

• Menstrual irregularities.

• Hirsutism.

• Deepened voice.

---

Mannitol

Think: “Mannitol moves fluid out of the brain and eyes.”

Used to:

• ↓ ICP.

• ↓ IOP.

• Promote urine flow/prevent kidney failure in specific situations.

Important:

• IV continuous infusion.

• Use a filter needle and filter tubing.

• Monitor for:

  • Pulmonary edema.

  • Heart failure.

  • Rebound increased ICP.

  • Fluid/electrolyte imbalances.

---

Complementary Therapy Interactions 🌿

• Ginkgo biloba + thiazide diuretic

  • Can cause hypertension.

• Licorice + antihypertensives

  • Can contribute to hypokalemia.

cardiac glycosides

• Heart failure (HF) occurs when the heart cannot pump enough blood to meet the body's circulatory needs.

• Results in:

  • ↓ Cardiac output (CO)

  • ↓ Tissue perfusion

  • Fatigue

  • Weakness

  • Shortness of breath

  • Activity intolerance

Important Factors Affected

• Heart rate (HR)

• Stroke volume (SV)

• Preload

• Afterload

• Cardiac output (CO)

Types of Heart Failure

Left-sided HF

• Mainly causes pulmonary manifestations

• Dyspnea

• Cough

• Oliguria

• Pulmonary congestion

Right-sided HF

• Mainly causes systemic venous congestion

• Peripheral edema

• Jugular venous distention (JVD)

• Weight gain

Common Medications for Heart Failure

• Diuretics

• ACE inhibitors

• ARBs

• Beta-adrenergic blockers

• Cardiac glycosides may be used when other medications do not adequately control manifestations.

---

Cardiac Glycosides Prototype Medication: Digoxin Main Actions

Digoxin has two major effects:

1. Positive Inotropic Effect = Stronger Contractions 💪

• ↑ Force of myocardial contraction

• ↑ Efficiency of the heart as a pump

• ↑ Stroke volume

• ↑ Cardiac output

Remember:

Positive inotropic = positive force

---

2. Negative Chronotropic Effect = Slower Heart Rate ❤

• ↓ SA node depolarization

• ↓ Heart rate

• Slows conduction through the heart

• Gives ventricles more time to fill

Overall Result

↓ HR + ↑ contraction strength = ↑ SV and ↑ CO

---

Therapeutic Uses of Digoxin

• Second-line treatment for heart failure

• Can be used for atrial fibrillation

• Helps reduce manifestations

• Does not prolong life

---

Digoxin Complications & Toxicity 🚨 1. Cardiac Effects

• Dysrhythmias

• Bradycardia

• Cardiotoxicity

Risk Factors for Digoxin-Induced Dysrhythmias

• Hypokalemia

• ↑ Digoxin levels

• Heart disease

• Older adult clients

Nursing Actions

• Monitor:

  • Heart rate

  • Heart rhythm

  • ECG

  • Potassium level

  • Digoxin level

Potassium Goal

• K⁺: 3.5–5.0 mEq/L

Important NCLEX Connection

Low potassium = increased risk of digoxin toxicity

Low K⁺ → Digoxin toxicity ↑

---

Digoxin Therapeutic Level

• Expected therapeutic range: 0.8–2.0 ng/mL

• Obtain blood level:

  • At least 6–8 hr after the last dose

  • Preferably just before the next dose

Remember

Do not rely only on the digoxin level.

• Assess the client for manifestations of toxicity.

• Consider:

  • Symptoms

  • Digoxin level

  • Potassium level

  • Cardiac rhythm

---

Digoxin Toxicity 🚨 GI Manifestations

Often the earliest sign:

• Anorexia

• Nausea

• Vomiting

• Abdominal pain

CNS Manifestations

• Fatigue

• Weakness

Visual Changes 👀

• Blurred vision

• Yellow-green vision

• White or yellow-green halos around objects

Easy Memory Trick

Digoxin toxicity = GI + Vision + Heart

• GI: anorexia, nausea, vomiting

• Vision: yellow/green halos, blurred vision

• Heart: bradycardia and dysrhythmias

---

Nursing Administration: Digoxin Check Apical Pulse Before Giving

Notify the provider if:

• Adult HR < 60/min

• Child HR < 70/min

• Infant HR < 90/min

Administration

• Administer at the same time every day

• Do not double doses if a dose is missed.

• Avoid OTC medications unless approved by the provider.

IV Digoxin

• Infuse over at least 5 minutes

• For clients with pulmonary edema:

  • Infuse over 10–15 minutes

• Monitor for dysrhythmias.

---

Client Teaching for Digoxin

• Monitor pulse rate and rhythm.

• Take at the same time every day.

• Do not double a missed dose.

• Report:

  • Anorexia

  • Nausea/vomiting

  • Fatigue

  • Weakness

  • Blurred vision

  • Yellow-green halos

  • Irregular pulse

If Taking a Potassium-Wasting Diuretic

Examples:

• Furosemide

• Hydrochlorothiazide

• Monitor potassium closely.

• May need potassium supplements.

• May be prescribed a potassium-sparing diuretic such as spironolactone.

• Consume potassium-rich foods if appropriate:

  • Bananas

  • Potatoes

  • Green leafy vegetables

---

Digoxin Contraindications & Precautions Contraindicated In

• Ventricular fibrillation

• Ventricular tachycardia

• Second-degree heart block

• Third-degree heart block

Use Cautiously In

• Hypokalemia

• Partial AV block

• Advanced heart failure

• Impaired kidney function

---

Digoxin Drug Interactions Loop & Thiazide Diuretics

Examples:

• Furosemide

• Hydrochlorothiazide

Effect

• Can cause hypokalemia

• Hypokalemia ↑ risk for digoxin dysrhythmias and toxicity

Nursing Action

• Maintain K⁺ between 3.5–5.0 mEq/L

---

ACE Inhibitors & ARBs

• Can cause hyperkalemia

• May decrease the therapeutic effects of digoxin

Nursing Action

• Monitor potassium.

• Use caution with:

  • Potassium supplements

  • Potassium-sparing diuretics

---

Sympathomimetics

Example:

• Dopamine

Effect

• Increased inotropic action

• ↑ Risk for tachydysrhythmias

Nursing Action

• Monitor ECG.

• Monitor pulse.

• Report palpitations.

---

Quinidine

• ↑ Risk for digoxin toxicity

• Displaces digoxin from binding sites.

• ↓ Kidney excretion of digoxin

Nursing Action

• Avoid concurrent use.

---

Verapamil

• ↑ Plasma levels of digoxin

• Can increase risk of toxicity

Nursing Action

• Digoxin dose may need to be decreased.

• Concurrent use is usually avoided.

---

Antacids

• ↓ Absorption of digoxin

• Can decrease effectiveness

Client Teaching

• Talk to the provider before taking antacids.

---

Management of Digoxin Toxicity 🚨

1. Stop digoxin.

2. Stop potassium-wasting diuretics.

3. Monitor potassium.

4. If K⁺ < 3.5 mEq/L:

   • Administer potassium as prescribed.

5. Do not give additional potassium if:

   • K⁺ > 5.0 mEq/L

   • AV block is present

6. Treat dysrhythmias with:

   • Phenytoin

   • Lidocaine

7. Treat bradycardia with:

   • Atropine

8. Severe toxicity may require:

   • Activated charcoal

   • Cholestyramine

   • Digoxin immune Fab

---

Adrenergic Agonists Common Medications Catecholamines

• Epinephrine

• Dopamine

• Dobutamine

• Isoproterenol

• Norepinephrine

Noncatecholamines

• Albuterol

• Ephedrine

---

Adrenergic Receptors Alpha₁ Receptors Effects

• Vasoconstriction

• ↑ Blood pressure

• Mydriasis

Location

• Blood vessels of:

  • Skin

  • Viscera

  • Mucous membranes

  • Veins

---

Beta₁ Receptors ❤ Effects

• ↑ Heart rate

• ↑ Myocardial contractility

• ↑ AV node conduction

• ↑ Cardiac output

Also

• Stimulates renin release from kidneys

Memory Trick

Beta 1 = 1 heart ❤

---

Beta₂ Receptors 🫁 Effects

• Vasodilation

• Bronchodilation

• Uterine relaxation

• Glycogenolysis → ↑ blood glucose

Memory Trick

Beta 2 = 2 lungs 🫁

---

Dopamine Receptors Effects

• Dilate renal blood vessels

• ↑ Renal perfusion

• Can help maintain urine output

---

Epinephrine Alpha₁ Effects

• Vasoconstriction

• ↑ Blood pressure

Uses

• Anaphylactic shock

• Slow absorption of local anesthetics

• Control superficial bleeding

• Decrease nasal congestion

Beta₁ Effects

• ↑ HR

• ↑ Contractility

• ↑ AV node conduction

• ↑ CO

• ↑ Tissue perfusion

Uses

• AV block

• Heart failure

• Shock

• Cardiac arrest

Beta₂ Effects

• Bronchodilation

Use

• Asthma

---

Dopamine Low Dose = Dopamine Receptors 🫘 Effects

• Renal vasodilation

• ↑ Renal perfusion

• ↑ Urine output

Uses

• Shock

• Heart failure

• Acute kidney injury

---

Moderate Dose = Beta₁ Effects ❤

• ↑ HR

• ↑ Contractility

• ↑ AV node conduction

• Maintains renal vasodilation

Uses

• Shock

• Heart failure

---

High Dose = Dopamine + Beta₁ + Alpha₁ Effects

• ↑ HR

• ↑ Contractility

• Vasoconstriction

• Mydriasis

• Renal vasoconstriction

Uses

• Shock

• Heart failure

Easy Way to Remember

Low = kidneys Medium = heart High = blood vessels

---

Dobutamine Primarily Beta₁ Effects

• ↑ Heart rate

• ↑ Contractility

• ↑ Cardiac output

• ↑ AV node conduction

Main Use

• Heart failure

---

Complications of Adrenergic Agonists 🚨 Hypertensive Crisis

• Caused by Alpha₁ stimulation.

• Can lead to cerebral hemorrhage.

Nursing Actions

• Continuous cardiac monitoring

• Continuous blood pressure monitoring

• Report significant vital sign changes.

---

Cardiac Complications

• Dysrhythmias

• Tachycardia

• Increased myocardial workload

• Increased oxygen demand

• Angina

Nursing Actions

• Continuous ECG monitoring

• Monitor HR.

• Monitor for chest pain.

• Monitor urine output.

• Report dysrhythmias.

---

Extravasation → Tissue Necrosis Especially With

• Epinephrine

• High-dose dopamine

Nursing Actions

• Monitor IV site closely.

• Stop infusion if irritation occurs.

• Prefer a central line for high-dose dopamine if possible.

Treatment

Phentolamine

• Alpha blocker

• Injected subcutaneously into the extravasation area

• Counteracts vasoconstriction

---

Contraindications & Precautions Dopamine

Contraindicated in:

• Tachydysrhythmias

• Ventricular fibrillation

Use cautiously with:

• Hypovolemia

• Angina

• History of MI

• Hypertension

• Diabetes

Dobutamine

Use cautiously with:

• Hypovolemia

• Angina

• History of MI

• Hypertension

• Diabetes

Epinephrine

Use cautiously with:

• Hyperthyroidism

• Angina

• Cardiac dysrhythmias

• Hypertension

---

Adrenergic Agonist Interactions MAOIs

• Prolong effects of epinephrine.

• Can cause cardiotoxicity with dopamine and dobutamine.

Avoid concurrent use.

Tricyclic Antidepressants

• Intensify and prolong effects.

• May require lower doses.

General Anesthetics

• Can increase sensitivity of the heart.

• ↑ Risk for dysrhythmias.

Nursing Action

• Continuous ECG monitoring

Alpha Blockers

Example:

• Phentolamine

Used for:

• Epinephrine toxicity

• Extravasation of epinephrine or dopamine

Beta Blockers

Example:

• Propranolol

Can be used to treat:

• Chest pain

• Dysrhythmias

---

Nursing Administration: Adrenergic Agonists

• Administer by continuous IV infusion.

• Use an IV pump.

• Titrate dosage based on blood pressure response.

• Continuously monitor:

  • ECG

  • Blood pressure

  • Heart rate

  • Urine output

  • Peripheral perfusion

  • Cardiac output

  • Pulmonary capillary wedge pressure

  • Central venous pressure

Report

• Chest pain

• Tachycardia

• Dysrhythmias

Clients With Diabetes

Monitor for hyperglycemia with:

• Epinephrine

• Isoproterenol

• Albuterol

---

Effectiveness of Adrenergic Agonists

Improved perfusion is evidenced by:

• Urine output ≥ 30 mL/hr

• Improved mental status

• Systolic BP ≥ 90 mm Hg

---

Angiotensin Receptor-Neprilysin Inhibitor (ARNI) Prototype Medication

Sacubitril/Valsartan

---

Therapeutic Use

• Used for NYHA Class II–IV heart failure

• Used in clients with reduced ejection fraction

• Used to replace an ACE inhibitor or ARB

---

Sacubitril/Valsartan Complications

• Angioedema

• Hyperkalemia

• Hypotension

• Cough

• Dizziness

• Renal failure

Nursing Actions

• Monitor:

  • Renal function

  • Potassium level

  • Blood pressure

---

ARNI Contraindications & Precautions Avoid Use

• During pregnancy

• While breastfeeding

• Severe hepatic impairment

Do Not Combine With

• ACE inhibitors

• ARBs

• Potassium-sparing diuretics

• NSAIDs

• Lithium

Also should not be used by clients with diabetes who are taking:

• Aliskiren

---

ARNI Administration

• Oral tablet

• Monitor:

  • Kidney function

  • Potassium

Expected Effectiveness

• Improved control of heart failure manifestations

---

⭐ High-Yield NCLEX Summary Digoxin

• Positive inotrope → ↑ contraction strength

• Negative chronotrope → ↓ HR

• Check apical pulse for 1 full minute

• Hold and notify provider for adult HR < 60/min

• Therapeutic level: 0.8–2.0 ng/mL

• K⁺ 3.5–5.0 mEq/L

• Hypokalemia = ↑ digoxin toxicity

• Toxicity:

  • Anorexia

  • Nausea/vomiting

  • Fatigue/weakness

  • Blurred vision

  • Yellow-green halos

  • Bradycardia/dysrhythmias

• Severe toxicity antidote: Digoxin immune Fab

Dopamine

• Low dose → kidneys → ↑ urine output

• Moderate dose → Beta₁ → heart stimulation

• High dose → Alpha₁ → vasoconstriction

Extravasation

Adrenergic agonist extravasation → Phentolamine

Sacubitril/Valsartan

• ARNI

• Used for HF with reduced EF

• Monitor K⁺ and renal function

• Can cause:

  • Hypotension

  • Hyperkalemia

  • Angioedema

• Do not combine with ACE inhibitors or ARBs

Meds that increase contractility

• cardiac glycosides

• positive inotrope (increase squeeze), negative chronotrope (decrease HR)

• increase force of myocardial contraction

• improve cardiac output

• slow AV conduction

• ex: digoxin (se: decreased K+ toxicity risk → halos, arrythmias, nausea. check K+ levels, HR, dopamine, dobutamine

meds that decrease contractility

• beta blockers (go low and slow)

• decrease HR + decrease contractility

• block adrenaline

• negative chronotrope

• ex: metoprolol, carvedilol (All HF patients should be discharged with Beta blockers, check HR and BP)

meds that decrease preload

• diuretics

• decrease fluid in system (“reduce circulating blood volume”, lowers pulmonary congestion in turn

• decrease preload

• ex: furosemide, bumex, spironolactone

• loop: watch K+ for hypokalemia

• spironolactone: watch for hyperkalemia

meds that decrease afterload (think BP)

• ace inhibitors, ARBs, ARNIs, direct vasodilators (nitro)

• decrease resistance to overcome

• block ace enzyme from converting angiotensin I to angiotensin II which is a vasoconstrictor

• increase vasodilation

• decrease cardiac workload

• ex: lisinopril, acinopril

• ACEs: assess BP and K+, worry about hyperkalemia, angioedema, cough

HF

heart fails to pump due to damage to muscle or valves

difference between a TTE and TEE

TTE: thoracic echo, noninvasive. looks at functionality of heart, for HF, look at EF

TEE: esophageal echo, invasive, looks at backside of heart

what special considerations are needed for a TEE

make NPO (risk for aspiration), consent form (invasive procedure, from provider), sedation/anesthesia (cardiac/O2 monitor), numbing meds (test gag reflex before eat/drink)

what is a normal EF

55-70%

dry weight for daily weights

daily weight, in morning, after pee, same amount of clothes, record it

when should HF pt call doctor with daily weights

all if gain 2-3 lbs overnight or 5lbs in a week

how does RAAS system make HF so much worse

sympathetic NS activation

What is heart failure?

Heart failure occurs when damage to the heart muscle or valves impairs the heart's ability to function as an effective pump.

The heart functions as what?

A pump.

“squeeze” “forward flow”

goal= pump blood

damage = decreased forward flow efficiency

What can cause heart failure?

Damage to the heart muscle or valves.

What valve diseases are associated with heart failure?

Mitral and/or tricuspid valve disease.

What cardiomyopathies are associated with heart failure?

Hypertrophic cardiomyopathy and dilated cardiomyopathy.

How can the heart compensate for increased workload?

The heart can hypertrophy or dilate. (cardiac remodeling)

Hypertrophic means what?

Stiff and thick.

Dilated means what?

Thin and stretched. and weak

risk factors for HF

• CAD: feeds heart, plaque buildup in arteries = increase workload

• HTN: systemic vascular resistance = afterload, force backs up to heart = HF

• DM

• metabolic syndrome: big abdominal girth, BMI, and triglycerides

• obesity

• smoking: vasoconstriction

• high sodium dietary intake: not alone it doesnt hurt you

• chemo: vasotoxic

• illicit drugs

cardiac output

The amount of blood ejected from the left ventricle each minute.

What is the formula for cardiac output? CO = Heart Rate × Stroke Volume. (SV: blood ejected w/ each contraction)

What is stroke volume? The amount of blood ejected with each contraction.

What three factors affect stroke volume? Preload, afterload, and contractility.

• preload: meds that effect: diuretics (furosemide) blocks sodium reuptake, synonymous with fluid volume

• afterload: systemic vascular resistance

• contractility: the force, how well the pump actually pumps

what things decrease the effects of CO

• HF

• renal disease (increase fluid volume)

• dehydration

• hypovolemia

fluid retention equation

1L of fluid = 1 kg = 2.2 lbs

daily weights

call dr is gain 2-3 Ibs overnight or 5 Ibs in a weeks

Left vs right side HF

• start showing s/s at 6 L thats why daily weights are important

• L = lungs: pulmonary congestion, crackles (bases=little, higher=more), blood tinged sputum, confusion, orthopnea, exertional dyspnea, fatigue

  • pulmonary edema: increase workload on capillary vessels, coughing blood tinges pink frothy sputum

• R = site (what you see): ascites (fluid in belly), enlarged liver and spleen, distended jugular veins, dependent edema (sacral, legs, feeling full)

• babies: poor feeding, irritability

NY heart association functionality classification scale

Class I? No symptoms even with activity.

Class II? Symptoms are present with ordinary exertion, such as ADLs or grocery shopping.

Class III? Symptoms are present with minimal exertion.

Class IV? Symptoms are present at rest

What happens when cardiac output decreases?

The body activates compensatory mechanisms.

What nervous system is activated as compensation for decreased cardiac output? The sympathetic nervous system.

What hormonal system is activated as compensation for decreased cardiac output? The renin-angiotensin-aldosterone system (RAAS).

What BNP level is considered high in these notes?

Greater than 400 pg/mL.

hormone released in response to cardiac muscle stretching

greater the number = greater the HF exacerbation

What does a transthoracic echocardiogram (TTE) assess?

Functionality or problems with the heart's blood flow, chamber walls, and valves.

non invasive

What is another name for a transthoracic echocardiogram? An echo.

TEE: transesophageal echo: echo that is invasive and looks at backside of heart

What is ejection fraction (EF)?

The total volume percentage the heart ejects with each beat.

What is a typical healthy ejection fraction? 55% to 70%.

What is an important education topic for clients with heart failure?

Daily weights and intake and output (I&O) (2-3 Ibs a night or 5Ibs a week → call doctor, med adherance, sodium (1.5 g restriction)

Why are daily weights important for clients with heart failure? They are related to fluid balance and accurate intake and output. if intake is higher than output than you are retaining fluid

What should be considered when teaching clients with heart failure about food? The nutrition content of foods, especially factors relevant to heart failure management such as sodium intake.

ECG Interpretation

Overview

• An ECG (electrocardiogram) records the electrical activity of the heart.

• ECG interpretation can help identify:

  • Dysrhythmias

  • Myocardial infarction (MI)

  • Cardiomyopathy

  • Conduction abnormalities

  • Other cardiac conditions

• ECGs may be interpreted by specially trained:

  • Nurses

  • Physicians

  • Monitor technicians

• Many clinicians interpreting ECGs also have ACLS training.

• If an abnormal rhythm is identified on 3- or 5-lead telemetry, a 12-lead ECG should be obtained for more accurate diagnosis.

• An 18-lead ECG may be used to identify abnormalities not seen on standard ECGs, such as right-sided heart abnormalities.

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Safety Considerations

• Determine whether the client has any allergies.

  • Helps prevent allergic reactions.

• Verify the client's identity according to facility protocol.

  • Ensures the correct procedure is performed on the correct client.

• Use standard and infection-control precautions.

  • Helps prevent transmission of infectious organisms.

  • Additional precautions may be needed based on client history and facility policy.

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Equipment/Supplies

• Rhythm strip at least 6 seconds long

• Calipers

• Ink pen

• Calculator

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General Steps Before ECG Interpretation 1. Review the Client's Medical Record

• Assess for a history of:

  • Chest pain or pressure

  • Palpitations

  • Dysrhythmias

  • Conduction abnormalities

  • Electrolyte abnormalities

  • Previous cardiac surgery

  • Previous cardiac catheterization

  • Coronary artery disease

  • Heart failure

  • Syncope/fainting

  • Previous cardiac arrest

  • Recent changes in heart rhythm or rate

• Reviewing the client's history helps identify:

  • Why the ECG is being performed

  • Which abnormalities may be expected

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2. Understand ECG Graph Paper

• ECG paper measures time horizontally and amplitude vertically.

• 1 small box = 0.04 seconds

• 1 large box = 0.20 seconds

  • 1 large box = 5 small boxes

• 5 large boxes = 1 second

• 25 small boxes = 1 second

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3. Know Normal ECG Components

• Review normal:

  • P waves

  • QRS complexes

  • T waves

  • PR intervals

  • QT intervals

• Knowing expected characteristics helps identify abnormalities.

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PQRST Complex

• P wave

  • Represents atrial depolarization.

• Atrial repolarization

  • Usually hidden within the QRS complex.

• QRS complex

  • Represents ventricular depolarization.

• T wave

  • Represents ventricular repolarization.

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ECG Interpretation Steps Step 1: Gather Supplies

• Bring all necessary equipment to the clinical area.

• Ensure the nurse is prepared before beginning interpretation.

Step 2: Obtain a Rhythm Strip

• Obtain a 6- to 12-second telemetry strip, according to facility policy.

• A standard time period allows calculation of:

  • Heart rate

  • Rhythm regularity

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Step 3: Calculate the Heart Rate

• For the 6-second method:

  • Count the number of QRS complexes in 6 seconds.

  • Multiply by 10.

• Normal adult heart rate: 60-100 beats/minute

• Use calipers for accurate ECG measurements.

Purpose

• Identify:

  • Bradycardia: HR < 60 bpm

  • Tachycardia: HR > 100 bpm

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Step 4: Measure the PR Interval

• Measure from the beginning of the P wave to the beginning of the QRS complex.

• Normal PR interval: 0.12-0.20 seconds

• Equivalent to 120-200 milliseconds.

Abnormal PR Intervals

• Prolonged: > 0.20 seconds

  • May indicate first-degree AV block.

  • May occur with second-degree type I AV block.

• Shortened: < 0.12 seconds

  • May indicate a junctional dysrhythmia.

• PR interval cannot be accurately measured if:

  • No P waves are present.

  • The PR interval varies between beats.

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Step 5: Measure the QRS Complex

• Measure the width of the QRS complex.

• Normal QRS duration: < 0.12 seconds.

• A wide or abnormal QRS may indicate:

  • Bundle branch block (BBB)

  • Ventricular origin of the beat

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Step 6: Measure the QT Interval

• Measure from the beginning of the QRS complex to the end of the T wave.

• Normal QT interval: approximately 0.36-0.44 seconds.

• QT interval varies with:

  • Heart rate

  • Age

  • Gender

• QT interval:

  • Increases with slower heart rates

  • Decreases with faster heart rates

• With a normal heart rate, the QT interval generally should not be more than half of the R-R interval.

Clinical Significance of a Prolonged QT

• May result from:

  • Medication side effects

  • Electrolyte abnormalities

  • Other cardiac abnormalities

• Increases the risk for potentially fatal dysrhythmias.

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Expected Normal ECG Findings

• Heart rate: 60-100 bpm

• A P wave precedes each QRS complex

• PR interval: 0.12-0.20 seconds

• QRS complex: < 0.12 seconds

• QT interval: generally 0.36-0.44 seconds, but varies with heart rate

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Step 8: Determine Rhythm Regularity

• Compare the R-R intervals using calipers.

• Regular rhythm: R-R intervals are consistent.

• Irregular rhythm: R-R intervals vary.

• Regular with occasional irregular beats: rhythm is mostly regular with occasional variations.

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Step 9: Methods for Calculating Ventricular Rate 6-Second Method

• Count QRS complexes in 6 seconds.

• Multiply by 10.

300 Method

• Count the number of large boxes between R waves.

• Divide that number into 300.

• Use only when the rhythm is regular.

1500 Method

• Count the number of small boxes between R waves.

• Divide that number into 1500.

Small-Box Time Method

• Count small boxes in one R-R interval.

• Multiply by 0.04 seconds.

• Use the calculated interval to determine the heart rate.

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Step 10: Evaluate the P Waves

• If no P waves are present, the rhythm is not sinus.

• For a sinus rhythm, P waves should:

  • Be present

  • Occur before each QRS complex

  • Have a similar shape

  • Typically be upright in lead II

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Step 11: Evaluate the PR Interval

• Determine whether PR intervals are:

  • Constant

  • Prolonged

  • Shortened

  • Variable

• Measure using the small boxes between the beginning of the P wave and beginning of the QRS complex.

• Multiply the number of small boxes by 0.04 seconds.

• Document the PR interval on the rhythm strip when measurable.

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Common Supraventricular/Sinus Rhythms Sinus Bradycardia

• Rhythm: Regular

• Rate: < 60 bpm

• PR interval: Normal

• QRS: Normal

Sinus Tachycardia

• Rhythm: Regular

• Rate: > 100 bpm

• PR interval: Normal

• QRS: Normal

Sinus Arrhythmia

• Rhythm: Irregular

• Rate: Usually normal

• Often varies with respiration

• QRS: Normal

Sinus Arrest

• Rhythm: Irregular

• P waves: Normal when present

• PR interval: Normal

• QRS: Normal

• May have occasional missed beats.

Sick Sinus Syndrome

• Rhythm: Irregular

• Rate: May alternate between fast and slow

• PR interval: Variable

• QRS: Usually normal

Premature Atrial Contractions (PACs)

• Rhythm: Irregular

• Rate: Usually normal

• PR interval: Usually normal

• QRS: Normal

• P wave:

  • Occurs early

  • May have an abnormal appearance

Paroxysmal Atrial Tachycardia

• Rhythm: Regular

• Rate: 150-250 bpm

• PR interval: May be abnormal

• QRS: Usually normal

• P and T waves may be abnormal.

Atrial Flutter

• Rhythm: Usually regular

• Atrial rate: Approximately 300 bpm

• Ventricular rate: May be fast or slow

• PR interval: Usually unable to measure

• QRS: Usually normal

• Characteristic finding:

  • Sawtooth waves

  • Clear atrial-to-ventricular conduction ratio

  • T waves may be difficult to distinguish

Atrial Fibrillation

• Rhythm: Irregular

• Rate: Variable

• PR interval: Unable to measure

• QRS: Usually normal

• Characteristic finding:

  • Chaotic or quivering atrial activity

  • Variable ventricular response

Wolff-Parkinson-White (WPW) Syndrome

• Rhythm: Usually regular

• Rate: May be normal

• PR interval: Short, < 0.10 seconds

• QRS: Wide, > 0.10 seconds

• Associated with increased risk for serious dysrhythmias, including torsades de pointes.

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Step 12: Evaluate the QRS Complex

• Determine whether QRS complexes are:

  • Normal in shape

  • Abnormal in shape

  • Narrow

  • Wide

• Normal width: < 0.12 seconds

• A wide/abnormal QRS can suggest:

  • Bundle branch block

  • Ventricular-origin beat

• Check for associated P waves to help determine the origin of the rhythm.

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Ventricular Rhythms Premature Ventricular Contractions (PVCs)

• Rhythm: Irregular

• Rate: Normal or fast

• PR interval:

  • Usually normal for normal beats

  • Not applicable to the PVC itself

• QRS:

  • Wide and abnormal during the ventricular beat

• PVC patterns include:

  • Bigeminy: every second beat is a PVC

  • Trigeminy: every third beat is a PVC

Idioventricular Rhythm (Agonal Rhythm)

• Rhythm: Regular

• Ventricular rate: < 40 bpm

• May be accelerated

• P waves: Usually absent

• QRS: Wide and abnormal

• Occurs when no other functional conduction system is controlling the heart.

Ventricular Tachycardia (VT)

• Rhythm: Regular or irregular

• Rate: > 100 bpm

• P waves: Usually absent

• PR interval: Not measurable

• QRS: Wide and abnormal

• Other findings:

  • Beats originate in the ventricles

  • T waves may be inverted

Torsades de Pointes

• Rhythm: Irregular

• Rate: 150-250 bpm

• P waves: Absent

• QRS:

  • Wide

  • Variable morphology

• Characteristic appearance:

  • QRS complexes appear to twist or rotate around the baseline

Ventricular Fibrillation (VF)

• Rhythm: No organized rhythm

• Rate: None

• P waves: Absent

• QRS: Absent

• Characterized by chaotic electrical activity and quivering of the ventricles.

Asystole

• Rhythm: No rhythm

• Rate: None

• P waves: Absent

• QRS: Absent

• ECG appears nearly as a flat line with no significant electrical activity.

Pulseless Electrical Activity (PEA)

• Rhythm: May appear regular or irregular

• ECG may show normal electrical activity.

• No effective mechanical contractions or pulse are present despite electrical activity.

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Step 13: Evaluate T Waves

• Determine whether T waves are:

  • Present

  • Consistent in appearance

  • Round and smooth

  • Similar in amplitude

• Compare T-wave direction to the QRS complex.

• T waves are typically upright in leads II and III.

• Abnormal T waves may indicate changes affecting ventricular repolarization.

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Step 14: Evaluate the QT Interval

• Measure from the beginning of the QRS/Q wave to the end of the T wave.

• Count the number of small boxes.

• Multiply by 0.04 seconds.

• Determine whether the QT interval is:

  • Normal

  • Prolonged/wide

• Document the QT interval on the ECG strip.

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Step 15: Interpret the Rhythm

• Interpret the ECG based on:

  • Rate

  • Rhythm regularity

  • Presence and appearance of P waves

  • PR interval

  • QRS width and morphology

  • T-wave characteristics

  • QT interval

• Use these findings to identify possible:

  • Electrical abnormalities

  • Conduction problems

  • Structural cardiac abnormalities

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Step 16: Ensure Client Safety

Before leaving the client:

• Place the call light within reach.

• Place personal items within easy reach.

• Lower the bed to the lowest position.

• Ensure the bed brakes are locked.

• Address any individual client safety needs.

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Client Considerations

• Always consider the client's cardiac history when interpreting an ECG.

• ECG interpretation and communication may be urgent, especially when the client:

  • Is experiencing chest pain

  • Is being evaluated for cardiac disease

  • Has a new abnormal rhythm

  • Is in a code situation

• Complete interpretation promptly and communicate urgent findings immediately.

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Documentation

• Document completion of ECG interpretation in the client's chart.

• Notify the provider ASAP of abnormal results.

• Communicate critical findings immediately.

• Educate the client and family about results within the RN's scope of practice.

Quick Normal ECG Values to Memorize

• Heart rate: 60-100 bpm

• PR interval: 0.12-0.20 seconds

• QRS duration: < 0.12 seconds

• QT interval: approximately 0.36-0.44 seconds

• Small box: 0.04 seconds

• Large box: 0.20 seconds

• 5 large boxes: 1 second

• 25 small boxes: 1 second

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lead placement and heart rythms

Overview

• ECG/EKG = noninvasive, painless test that records the heart’s electrical activity.

• Electrodes are attached to the client’s skin and connected to an ECG machine.

• Procedure typically takes 5–10 minutes.

• ECG tracing can be used to:

  • Evaluate heart rhythm.

  • Evaluate pacemaker effectiveness.

  • Identify signs of structural abnormalities.

  • Identify ischemia.

• 18-lead ECG provides additional views not obtained with a 12- or 15-lead ECG.

  • Especially useful for diagnosing:

    • Right-sided myocardial infarction (MI).

    • Posterior MI.

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Delegation

• The nurse may delegate ECG performance to assistive personnel (AP) if:

  • The client has already been assessed by a licensed nurse or provider.

  • The client’s condition is stable.

  • The AP has been trained and competent in the skill.

• AP should report all findings to the nurse.

• Do NOT delegate if:

  • Client’s condition is unknown.

  • Client is unstable.

  • AP has not been trained in the skill.

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Safety Considerations Check for Adhesive Allergies

• Determine whether the client has an allergy or sensitivity to adhesives.

• Helps prevent an allergic reaction from ECG electrodes.

Verify Client Identity

• Use facility protocol to ensure the correct procedure is performed on the correct client.

Infection Control

• Use standard precautions.

• Perform hand hygiene.

• Use gloves/PPE as indicated.

• Follow additional infection-control precautions based on:

  • Client history.

  • Isolation requirements.

  • Facility policy.

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Equipment and Supplies

• ECG machine — records the heart’s electrical activity.

• Alcohol swabs — cleanse skin and improve electrode adhesion.

• Clippers/scissors — remove excess hair if necessary.

  • Use an electronic clipper, not a razor.

• ECG electrodes — adhere to the skin and transmit electrical signals.

• Adhesive remover wipes/disposable wet wipes — remove adhesive residue.

• Nonsterile gloves and other PPE — infection prevention.

• Approved disinfectant wipes — clean ECG machine after use.

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General Steps Before the Procedure 1. Review the Client’s Medical Record and MAR

Review:

• Allergies.

• Medical history.

• Age and gender.

• Medications.

• Previous vital signs.

• Pertinent laboratory values.

• Provider’s prescription/order.

• Previous ECG results.

• Facility policy and procedure manual.

Important considerations:

• Identify contraindications or adhesive allergies.

• Consider anatomical differences, such as an amputated limb.

• Verify the provider’s order and purpose of the ECG.

• Review facility policy before performing an unfamiliar skill.

2. Check the ECG Machine

• Ensure the machine is operational before entering the client’s room.

• Check for malfunction before beginning the procedure.

3. Gather Supplies

• Bring all necessary equipment to the bedside.

• Being prepared helps prevent interruptions during the procedure.

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Step-by-Step Procedure 1. Provide Privacy

• Close the door or curtain.

• Protect the client’s:

  • Confidentiality.

  • Physical privacy.

  • Dignity.

2. Introduce Yourself

• Identify yourself to the client.

• Helps establish a therapeutic nurse-client relationship.

3. Perform Hand Hygiene and Apply PPE

• Perform hand hygiene before client contact.

• Apply nonsterile gloves/PPE as indicated.

4. Identify the Client

• Use two unique identifiers according to facility policy.

5. Confirm Allergies

• Double-check allergy status, especially adhesive allergies.

6. Educate the Client

• Explain:

  • What will happen.

  • Why the ECG is being performed.

• Allow the client to ask questions.

• Verify understanding.

• Education can help decrease anxiety.

7. Position the Client

• Position comfortably, preferably at approximately 45 degrees.

• Raise the bed/stretcher to a comfortable working height.

• Keep the ECG machine within reach.

8. Ensure Proper Grounding

• Verify the third grounding prong is intact.

• Ensure the machine is properly plugged in.

• Helps prevent:

  • Electrical malfunction.

  • Electrical shock.

9. Enter Client Information

• Turn on the ECG machine.

• Enter required client and nurse information according to:

  • Facility policy.

  • Machine instructions.

• Ensures correct identification and proper transmission of results.

10. Expose Necessary Areas

• Assist the client with adjusting clothing to expose:

  • Chest.

  • Arms.

  • Lower limbs.

• Keep the pelvic area and thighs covered.

• Ensure the room is warm enough.

  • Shivering can cause artifact on the ECG.

11. Prepare the Skin

• Clean electrode sites gently with alcohol wipes.

• Remove excess hair with an electronic clipper if needed.

• Promotes good electrode adhesion and accurate electrical conduction.

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ECG Electrode Placement Limb Leads

• RA (Right Arm): Right shoulder or arm.

• LA (Left Arm): Left shoulder or arm.

• RL (Right Leg): Right leg.

• LL (Left Leg): Left leg.

Chest/Precordial Leads

• V1: 4th intercostal space, right sternal border.

• V2: 4th intercostal space, left sternal border.

• V3: Midway between V2 and V4.

• V4: 5th intercostal space, left midclavicular line.

• V5: 5th intercostal space, between V4 and V6.

• V6: 5th intercostal space, just left of the spine.

Special Considerations

• Follow facility policy for variations in placement.

• Some facilities use the wrist for arm leads.

• If the client has an amputation:

  • Place the electrode on the remaining limb or stump.

Key point: Correct electrode placement is essential for an accurate ECG reading.

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Recording the ECG 13. Connect the Cables

• If not already connected:

  • Connect ECG cables to the machine.

  • Attach each cable to the correct electrode.

• Allows electrical signals to travel to the ECG machine.

14. Instruct the Client to Remain Still

• Tell the client to:

  • Relax shoulders.

  • Relax legs.

  • Remain still.

• Muscle movement and tension can cause artifact.

15. Activate and Record the ECG

• Verify:

  • Machine is turned on.

  • Correct client information is entered.

• Follow machine directions to record the ECG.

• Print a copy and/or transfer results to the electronic medical record (EMR) according to facility policy.

16. Review the Tracing Before Removing Electrodes

• Check for:

  • Artifact.

  • Poor-quality tracing.

  • An adequate ECG recording.

• Repeat the ECG if necessary before disconnecting the client.

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After the ECG 17. Remove Electrodes

• Disconnect cords from electrodes.

• Remove electrodes gently.

• Use adhesive remover if needed.

• Remove any remaining adhesive residue.

Purpose: Prevent skin irritation or skin breakdown.

18. Clean Equipment

• Disinfect the ECG machine with a facility-approved disinfectant.

• Dispose of:

  • Used electrodes.

  • Used wipes.

• Store the machine according to facility policy.

19. Provide Post-Procedure Education

Teach the client/family:

• What the next steps are after the ECG.

• An ECG does not measure symptoms such as:

  • Chest pain.

  • Dyspnea/shortness of breath.

• The client should continue reporting symptoms to the healthcare provider.

• Outpatients should continue current treatment recommendations until the provider communicates the ECG results.

20. Ensure Client Safety

Before leaving:

• Position client safely.

• Address individual safety needs.

• Reduce risk of:

  • Falls.

  • Injury.

21. Remove PPE and Perform Hand Hygiene

• Follow facility infection-control policy.

22. Notify the Provider

• Notify the ordering provider that the ECG is complete.

• Report preliminary results provided by the ECG machine as appropriate.

• STAT report abnormal results to ensure prompt treatment.

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Unexpected Outcomes

• Notify the provider of any unexpected outcomes or abnormal findings.

• Prompt communication helps ensure timely treatment.

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Documentation

Document accurately in the client’s MAR and medical record according to facility policy.

Include as indicated:

• Date and time ECG was completed.

• Type of ECG performed.

  • Example: 18-lead instead of 12- or 15-lead.

• Client’s response to the procedure.

• Any unexpected outcomes.

• Education provided to the client and family.

• Provider notification that the ECG was completed.

• Provider notification of unexpected/abnormal outcomes.

​

​

​

ECG Interpretation & Non-Ventricular Dysrhythmia Notes Electrocardiogram (ECG) Overview

• ECG: Noninvasive test that records the heart's electrical activity.

• ECG helps identify:

  • Abnormal electrical conduction

  • Areas of decreased or absent cardiac perfusion

  • Dysrhythmias

  • Myocardial ischemia/injury

• ECG does not visualize actual cardiac structures.

Cardiac Electrical Activity

• Depolarization: Electrical stimulation that causes cardiac muscle contraction.

• Repolarization: Electrical recovery/relaxation as the heart prepares for the next impulse.

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Steps for ECG Analysis

1. Calculate heart rate

2. Determine if rhythm is regular or irregular

3. Assess P waves

4. Measure PR interval

5. Measure QRS duration

6. Assess ST segment

7. Observe T waves

8. Measure QT interval

9. Interpret the rhythm

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ECG Waveform Components P Wave

• Represents atrial depolarization.

• Normally:

  • One P wave before each QRS complex

  • P waves should have a consistent shape

PR Interval

• Measured from the beginning of the P wave to the beginning of the QRS complex.

• Represents conduction of the impulse through the atria and AV node.

• Normal: 0.12–0.20 seconds

• Should be consistent.

QRS Complex

• Represents ventricular depolarization.

• Normal duration: approximately 0.06–0.10 seconds.

• A QRS duration >0.12 seconds may indicate abnormal ventricular conduction.

ST Segment

• Located between the QRS complex and T wave.

• Should remain near the isoelectric baseline.

• Elevation or depression may indicate:

  • Altered cardiac perfusion/ischemia

  • Electrolyte abnormalities

T Wave

• Represents ventricular repolarization.

• Peaked T waves: May indicate hyperkalemia.

• Inverted T waves: May indicate:

  • Ischemia

  • Altered cardiac perfusion

  • Pulmonary embolism

QT Interval

• Measured from the beginning of the QRS complex to the end of the T wave.

• Represents the total time for ventricular depolarization and repolarization.

• Prolonged QT increases the risk for dangerous dysrhythmias.

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ECG Grid Paper & Heart Rate Calculation ECG Paper Measurements

• 1 small box = 0.04 seconds

• 1 large box = 0.20 seconds

• 5 small boxes = 1 large box

• A typical 6-second ECG strip = 30 large boxes

300 Method

• Used for regular rhythms.

• Count the number of large boxes between two R waves.

• 300 ÷ number of large boxes = heart rate

6-Second Method

• Count the number of QRS complexes in 6 seconds.

• Multiply by 10.

• Useful for obtaining an average heart rate.

Determining Regularity

• R-to-R intervals: Determine ventricular rhythm.

• P-to-P intervals: Determine atrial rhythm.

• Equal spacing = regular.

• Unequal spacing = irregular.

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Expected Normal ECG Criteria

• Heart rate: 60–100/min

• Rhythm: Regular

• P waves: One P wave for every QRS

• PR interval: 0.12–0.20 sec

• QRS: 0.06–0.10 sec

• ST segment: No significant elevation or depression

• QT interval:

  • Prepuberty: <0.45 sec

  • Postpubertal males: <0.46 sec

  • Postpubertal females: <0.47 sec

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Normal Sinus Rhythm (NSR) Pathophysiology

• Electrical impulse follows the normal conduction pathway:

  • SA node

  • AV node

  • Bundle of His

  • Right and left bundle branches

  • Purkinje fibers

• Impulse originates in the SA node and travels normally through the heart.

ECG Criteria

• Rate: 60–100/min

• Rhythm: Regular

• P waves: One consistently shaped P wave before every QRS

• PR interval: 0.12–0.20 sec

• QRS: 0.06–0.10 sec

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Sinus Bradycardia Definition

• SA node fires at a rate <60 bpm.

• All other ECG characteristics are generally the same as NSR.

ECG Criteria

• Rate: <60/min

• Rhythm: Regular

• P waves: One consistent P wave before every QRS

• PR interval: 0.12–0.20 sec

• QRS: 0.06–0.10 sec

Causes/Risk Factors

• Well-conditioned athletes

• Normal aging

• Myocardial infarction

• Sleep apnea

• Increased intracranial pressure

• Hypothyroidism

• Eating disorders/decreased metabolic needs

• Hypoxia

• Increased vagal stimulation:

  • Coughing

  • Gagging

  • Straining during bowel movements

• Certain infections

• Medications

Medications That Can Cause Bradycardia

• Parasympathomimetics

• Beta blockers: Metoprolol

• Digoxin

• Calcium channel blockers: Diltiazem

• Amiodarone

• Lithium

Clinical Manifestations

• May be asymptomatic

• If symptomatic:

  • Dizziness

  • Lightheadedness

  • Syncope/near syncope

  • Chest pain

  • Altered mental status

  • Dyspnea

  • Diaphoresis

  • Exercise intolerance/fatigue

Diagnostics

• ECG

• Electrolytes, including magnesium and calcium

• Thyroid hormone testing

• Troponin

• Drug/toxicology screening if indicated

Nursing Priorities

• First priority: Determine if the client is stable or unstable.

• Assess for decreased cardiac output.

• Monitor:

  • Heart rate

  • Blood pressure

  • ECG

  • Mental status

  • Chest pain

  • Oxygenation

• Implement fall precautions if symptomatic.

• Encourage slow position changes.

• Review and potentially hold medications that contribute to bradycardia as directed.

Treatment

• Asymptomatic: Usually observation and treatment of the underlying cause.

• Unstable/symptomatic:

  • Atropine 1 mg IV

  • May repeat every 3–5 minutes

  • Maximum total dose: 3 mg

• If atropine is ineffective:

  • Prepare for transcutaneous pacing

  • A permanent pacemaker may be needed for persistent underlying conduction problems.

NCLEX Key Point

Symptomatic bradycardia = assess perfusion and hemodynamic stability first.

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Sinus Tachycardia Definition

• SA node fires at a rate >100 bpm.

• Usually a response to an underlying physiological or psychological stressor.

• Prolonged tachycardia can decrease cardiac output by reducing ventricular filling time.

ECG Criteria

• Rate: >100 to <150 bpm

• Rhythm: Regular

• P waves: One consistent P wave before every QRS

• PR interval: 0.12–0.20 sec

• QRS: 0.06–0.10 sec

Causes/Risk Factors

• Fever

• Pain

• Anxiety/stress

• Hypovolemia/fluid volume loss

• Fluid volume excess

• MI

• Shock

• Hyperthyroidism

• Anemia

• Physical exertion

• Hypoxia

• Sepsis

• Medications:

  • Atropine

  • Catecholamines

  • Theophylline

• Stimulants:

  • Cocaine

  • Amphetamines

  • Caffeine

  • Nicotine

Clinical Manifestations

• May be asymptomatic

• If symptomatic:

  • Palpitations

  • Chest pain

  • Dyspnea

  • Dizziness/lightheadedness

  • Elevated temperature

Signs of Instability

• Hypotension

• Increased respiratory rate

• Shortness of breath

• Chest pain

• Altered level of consciousness

• Decreased urine output

• Signs of dehydration

Nursing Priorities

• Identify and treat the underlying cause.

• Assess for hemodynamic instability.

• Monitor:

  • ECG

  • Vital signs

  • Perfusion

  • Urine output

  • Mental status

• Implement fall precautions if dizziness is present.

Treatment

• Treat the underlying cause:

  • Fever → reduce temperature

  • Pain → manage pain

  • Hypovolemia → replace fluids as prescribed

  • Anxiety/stress → reduce stressor

• Depending on the clinical situation, treatment may include:

  • Medications such as beta blockers

  • Adenosine in specific tachyarrhythmia evaluation/treatment situations

  • Catheter ablation for persistent cases

Client Education

• Reduce/avoid stimulants that increase heart rate.

• Reduce caffeine and nicotine.

• Avoid illicit drugs.

• Use stress-management techniques:

  • Controlled breathing

  • Meditation

  • Relaxation

NCLEX Key Point

Sinus tachycardia is usually a symptom of another problem—find and treat the cause.

---

Premature Ventricular Contractions (PVCs) Definition/Pathophysiology

• Early ventricular beat caused by an irritable ventricular focus.

• Occurs before the next expected normal SA node impulse.

• PVC QRS complexes are typically wide and abnormal.

ECG Findings

• Underlying rhythm may be normal but slightly irregular.

• Premature beat occurs early.

• Wide QRS >0.12 sec

• P wave associated with the PVC may be absent or hidden.

• PR interval may be unmeasurable.

PVC Patterns

• Unifocal: PVCs have the same shape → originate from one ventricular site.

• Multifocal: PVCs have different shapes → originate from multiple sites.

• Bigeminy: Every other beat is a PVC.

• Trigeminy: Every third beat is a PVC.

• Quadrigeminy: Every fourth beat is a PVC.

Causes/Risk Factors

• May occur in healthy individuals and be benign.

• MI/cardiac muscle damage

• Hypertension

• Cardiomyopathy

• Chronic lung disease/COPD

• Pulmonary hypertension

• Sleep apnea

• Thyroid disorders

• Hypokalemia

• Hypomagnesemia

• Caffeine sensitivity

• Nicotine

• Alcohol

• Illicit drugs

Clinical Manifestations

• Often asymptomatic

• Palpitations

• Feeling like the heart “skipped a beat”

• Lightheadedness

• Chest pain

• Shortness of breath

Diagnostics

• ECG

• Electrolytes:

  • Potassium

  • Magnesium

• Thyroid testing

• Holter/ambulatory monitor: Often worn 24–48 hours

• Echocardiogram to assess structural heart disease

Nursing Priorities

• Assess:

  • Frequency and pattern of PVCs

  • Peripheral pulses

  • Symptoms

  • Cardiac output/perfusion

• Monitor ECG and vital signs.

• Identify and correct triggers.

• Correct electrolyte imbalances as prescribed.

• Implement fall precautions if dizzy or lightheaded.

Treatment

• Asymptomatic/benign PVCs:

  • Often require no specific treatment

  • Manage triggers

• Frequent/persistent symptomatic PVCs:

  • Beta blockers: Metoprolol, carvedilol

  • Antiarrhythmics may be prescribed

• Persistent PVCs may be treated with catheter ablation.

NCLEX Key Point

Frequent PVCs + low potassium or magnesium → prioritize correcting the electrolyte imbalance and monitoring for worsening dysrhythmias.

---

Premature Atrial Contractions (PACs) Definition/Pathophysiology

• Early beat originating from an irritable atrial focus.

• An atrial impulse fires before the next expected SA node impulse.

• Usually considered benign.

ECG Findings

• Underlying rhythm is usually normal.

• Premature/early P wave may be:

  • Hidden

  • Difficult to identify

  • Different in shape from normal P waves

• PR interval may be:

  • Shortened (<0.12 sec)

  • Unmeasurable

Causes/Risk Factors

• Often unknown

• MI

• Hypertension

• Diabetes mellitus

• Heart failure

• Certain medications:

  • Digoxin

  • Beta blockers

  • Chemotherapy medications

  • Some antidepressants

• Stress/anxiety

• Fatigue with excessive exercise

• Smoking

• Alcohol use

Clinical Manifestations

• Often asymptomatic

• Palpitations

• Fluttering sensation in chest

• Shortness of breath with activity

Diagnostics

• ECG

• Echocardiogram if cardiac abnormalities are suspected

• Electrolyte testing may be helpful

Nursing Priorities

• Identify triggers.

• Obtain history of:

  • Chronic conditions

  • Medications

  • Stress

  • Smoking

  • Alcohol use

• Assess pulse and heart sounds.

• Reassure the client that PACs are usually benign.

Treatment

• Usually no treatment for infrequent PACs.

• Reduce or eliminate triggering factors.

• Frequent PACs may be treated with low-dose beta blockers.

Client Education

• Reduce stress.

• Avoid smoking and alcohol.

• Monitor exercise-related fatigue.

• Contact the provider if palpitations or dyspnea interfere with ADLs.

NCLEX Key Point

PAC = premature beat from the ATRIA; usually benign and treated by identifying/reducing triggers.

---

First-Degree AV (Heart) Block Definition/Pathophysiology

• Delay in conduction through the AV node.

• The impulse is slowed but not blocked.

• Every atrial impulse is eventually conducted to the ventricles.

Key ECG Finding

• PR interval >0.20 seconds

• PR interval is consistently prolonged.

• Other conduction is generally normal.

Easy Memory Tip

First-degree block = “First, the PR is long.”

Causes/Risk Factors

• Increased age

• MI/coronary artery disease

• Hypokalemia

• Hypomagnesemia

• Increased vagal tone

• Certain infections

• Autoimmune disorders

• Athletes with high vagal tone

• Medications that slow AV conduction

Medications That Can Prolong AV Conduction

• Sodium channel blockers

• Beta blockers

• Calcium channel blockers

• Amiodarone

• Digoxin

• Magnesium

Clinical Manifestations

• Usually asymptomatic

• Possible:

  • Dizziness

  • Shortness of breath with activity

  • Fatigue

Diagnostics

• ECG:

  • PR interval >0.20 sec

  • PR interval remains consistent

• Electrolyte testing may help identify the cause.

• Drug/toxicology testing may be indicated.

Nursing Priorities

• Review medication list.

• Monitor ECG for:

  • Worsening PR prolongation

  • Progression to higher-degree heart block

• Assess for decreased cardiac output.

• Hold medications that prolong the PR interval if indicated by the provider/clinical orders.

• Implement fall precautions if symptomatic.

Treatment

• Asymptomatic: Usually observation and follow-up.

• Treat the underlying cause.

• If significant bradycardia or progression occurs, treatment may include:

  • Atropine

  • Isoproterenol

  • Pacemaker, if necessary

NCLEX Key Point

First-degree AV block = PR interval >0.20 sec and consistent; usually asymptomatic.

---

Quick Comparison Chart

Rhythm	Rate	Rhythm	Main ECG Clue
Normal Sinus Rhythm	60–100	Regular	Normal P-QRS relationship
Sinus Bradycardia	<60	Regular	Normal rhythm, slow rate
Sinus Tachycardia	>100 to <150	Regular	Normal rhythm, fast rate
PVC	Variable	May be irregular	Early, wide QRS >0.12 sec
PAC	Usually normal	May be irregular	Early/abnormal P wave
1st-Degree AV Block	Usually normal	Regular	PR >0.20 sec, consistent

High-Yield Memory Tricks

• P wave = Atria depolarize

• QRS = Ventricles depolarize

• T wave = Ventricles repolarize

• PR >0.20 = First-degree AV block

• Wide premature QRS = PVC

• Early abnormal P wave = PAC

• Slow but otherwise normal = Sinus bradycardia

• Fast but otherwise normal = Sinus tachycardia

• Sinus rhythms originate in the SA node

​

Atrial Fibrillation (A-fib) Pathophysiology

• A-fib is a common cardiac dysrhythmia.

• Occurs when the SA node is not firing appropriately.

• Multiple areas in the atria send electrical impulses.

• Electrical activity becomes:

  • Rapid

  • Chaotic

  • Irregular

• The atria cannot effectively contract.

• Blood is not effectively moved from the atria into the ventricles.

• Results in:

  • Decreased cardiac output

  • Ineffective cardiac contractions

  • Irregular blood flow

• Blood can pool and form blood clots.

• Embolized clots can cause damage to:

  • Brain → stroke

  • Lungs

  • Kidneys

  • Other organs

---

Etiology & Risk Factors

• Diabetes

• Hyperthyroidism

• Obstructive sleep apnea

• Smoking

• Excessive alcohol intake

• Sedentary lifestyle/minimal exercise

• Comorbidities associated with A-fib

• Recovery from cardiac surgery

---

Common Comorbidities

• Hypertension

• Heart failure

• Diabetes mellitus

• Overweight/obesity

• COPD

• Thyroid disease

• Kidney disease

• History of stroke

Major Complications

• Stroke

• Heart failure

• Increased morbidity and mortality

---

Epidemiology

• Most common type of treated cardiac dysrhythmia.

• More common in:

  • Adults older than 65 years

  • Individuals who are overweight or obese

• Causes a significant number of hospitalizations.

---

Impact on Daily Life

• May decrease ability to perform usual activities.

• Possible problems include:

  • Dizziness

  • Palpitations

  • Exercise intolerance

  • Fatigue

• Can decrease overall quality of life.

---

Safety Considerations

• Increased risk for:

  • Stroke

  • Systemic emboli

  • Heart failure

  • Falls due to dizziness/lightheadedness

• Long-term anticoagulant therapy increases the risk for:

  • Spontaneous bleeding

  • Excessive bleeding after injury

---

Clinical Presentation A-fib May Be Asymptomatic

• May only be identified by an irregular pulse.

Symptomatic Findings

• Irregular apical pulse

• Increased heart rate

• Hypotension

• Palpitations

• Chest discomfort

• Shortness of breath:

  • At rest

  • With activity

• Exertional fatigue

• Anxiety

• Dizziness

• Lightheadedness

• Syncope

• Weight gain

• Increased urination

---

Laboratory & Diagnostic Testing Blood Tests

• TSH and thyroxine (T4)

  • Assess for hyperthyroidism.

• Other possible tests:

  • CBC

  • Creatinine

  • Glucose

• Clients taking certain oral anticoagulants, such as warfarin, may require PT/INR monitoring.

---

A-fib ECG Findings ⭐

• Rhythm: Irregular

• P waves:

  • Absent

  • Replaced by indiscernible/chaotic atrial activity

• Ventricular rate may be:

  • 60-100/min: controlled ventricular response

  • 100-200/min: increased ventricular rate

• Rapid ventricular response (RVR): ventricular rate > 100/min

Quick Memory Tip

A-fib = “Irregularly irregular” + no identifiable P waves.

---

Echocardiogram & TEE

• Echocardiogram evaluates:

  • Size of the atria and ventricles

  • Heart valve function

• Transesophageal echocardiogram (TEE):

  • Detects blood clots, especially in the left atrium.

  • May be performed before cardioversion.

---

Nursing Assessment: A-fib Recognize Cues

• Obtain a thorough medical history.

• Ask about:

  • Palpitations

  • Difficulty breathing

  • Dizziness/lightheadedness

  • Ability to complete usual ADLs

• Auscultate the apical pulse for a full 60 seconds.

• Obtain a manual blood pressure when indicated.

• Palpate pulses for a full 60 seconds because the rhythm is irregular.

• Assess for a pulse deficit.

Pulse Deficit

• Compare:

  • Apical pulse

  • Radial pulse

• A-fib may cause the two pulse rates to differ.

• Pulse deficit = apical pulse − radial pulse

• A result of 0 = no pulse deficit.

• A pulse deficit greater than 0 indicates:

  • Inadequate cardiac output

  • Potentially decreased organ perfusion

---

Analyze Cues

• Identify:

  • Irregular ECG rhythm

  • Clinical manifestations of decreased cardiac output

• Assess for signs of embolized clots:

  • Changes in level of consciousness

  • Extremity pain

  • Stroke symptoms

  • Shortness of breath

---

Priority Nursing Goals

• Improve cardiac perfusion.

• Control heart rate.

• Control or restore heart rhythm.

• Prevent:

  • Blood clots

  • Stroke

  • Other embolic complications

---

Treatments for A-fib Major Goals

• Restore and maintain normal sinus rhythm (NSR) when appropriate.

• Control ventricular rate.

• Prevent thromboembolic complications, especially stroke.

---

Medications Antiarrhythmics

• Used to help restore and maintain NSR.

• Monitor for:

  • Bradycardia

  • Prolonged QT interval

Rate-Control Medications

• Beta blockers

• Calcium channel blockers

• Amiodarone

• Digoxin

Effects

• Slow the ventricular rate.

• Decrease conduction through the AV node.

Nursing Consideration

• Assess the apical heart rate before administration.

---

Amiodarone

• Often used when A-fib is more difficult to control.

• Important adverse effects:

  • Pulmonary fibrosis

  • Liver damage

• Obtain baseline:

  • Pulmonary function tests (PFTs)

  • Liver enzyme testing

---

Anticoagulation Therapy Purpose

• Prevent:

  • Blood clot formation

  • Systemic emboli

  • Stroke

Major Nursing Concern

• Bleeding

Bleeding Precautions

• Use a soft-bristled toothbrush.

• Use an electric razor or safety razor.

• Avoid contact sports.

• Avoid high-risk activities that could cause injury.

• Monitor for spontaneous or excessive bleeding.

---

Warfarin (Coumadin) Monitoring

• Requires PT/INR monitoring.

• Frequent monitoring is required initially.

• Once stable, monitoring may occur less frequently.

Important Teaching

• Maintain a consistent intake of vitamin K.

• Do not suddenly increase or decrease vitamin K intake.

• Vitamin K changes can alter warfarin's effectiveness.

High Vitamin K Foods

• Brussels sprouts

• Leafy greens:

  • Beet greens

  • Collard greens

  • Mustard greens

  • Turnip greens

• Kale

• Spinach

Moderate Vitamin K Foods

• Asparagus

• Broccoli

• Cabbage

• Carrots

• Cauliflower

• Celery

• Green beans

• Lettuce

• Mixed vegetables

• Okra

• Peas

• Pickles

Low Vitamin K Foods

• Avocados

• Bananas

• Corn

• Fruit

• Garbanzo beans

• Green/red peppers

• Potatoes

• Tomatoes

Reversal of Warfarin

• Vitamin K

• Fresh frozen plasma (FFP) may also be used depending on the clinical situation.

---

Medications/Substances That Affect Warfarin Can Increase INR → ↑ Bleeding Risk

• Acetaminophen

• Allopurinol

• Many antibiotics

• Cephalosporins

• Doxycycline

• Fluoroquinolones

• Macrolides

• Metronidazole

• Penicillins

• Antifungals

• Some chemotherapy medications

• Testosterone

Can Decrease INR → ↑ Clotting Risk

• Dicloxacillin

• Nafcillin

• Rifampin

• Some antiseizure medications:

  • Carbamazepine

  • Phenobarbital

  • Phenytoin

• Azathioprine

• Ritonavir

• Sucralfate

• St. John's wort

• Vitamin K

---

Direct Oral Anticoagulants (DOACs) Examples

• Apixaban (Eliquis)

• Dabigatran (Pradaxa)

• Rivaroxaban (Xarelto)

Advantages

• Generally do not require routine PT/INR testing.

• Usually do not require frequent dose adjustments.

Important Teaching

• Take exactly as prescribed.

• Do not miss doses.

• Missed doses increase the risk for:

  • Systemic emboli

  • Stroke

Reversal Agents

• Dabigatran → Idarucizumab (Praxbind)

• Apixaban & rivaroxaban → Andexanet alfa

---

Herbal Supplements & Anticoagulants Decrease Anticoagulant Effect → ↑ Clotting Risk

• Coenzyme Q-10

• Ginseng

• Licorice

• St. John's wort

Increase Anticoagulant Effect → ↑ Bleeding Risk

• Danshen

• Evening primrose

• Ginkgo biloba

• Saw palmetto

---

Synchronized Electrical Cardioversion Purpose

• Delivers an electrical shock to reset the heart rhythm to NSR.

Key Points

• Shock is synchronized with the QRS complex/R wave.

• Energy typically ranges from 50-200 joules.

• If unsuccessful:

  • Another attempt may be made at a higher energy level.

• Conscious sedation is used.

Nursing Priorities

• Maintain an open airway.

• Monitor:

  • Respiratory status

  • Vital signs

  • Cardiac rhythm

• Anticoagulation may be used before and continued after cardioversion to reduce clot risk.

---

Catheter Ablation

• May be considered if medications or cardioversion are ineffective.

• An electrophysiology (EP) study is performed to:

  • Map the heart's electrical system

  • Identify abnormal conduction pathways

• A catheter delivers:

  • Radiofrequency energy (heat) OR

  • Cryotherapy (cold)

• Creates scar tissue that blocks abnormal electrical conduction.

---

A-fib Client Education Report Immediately

• Palpitations

• Chest pain

• Irregular heart rate

• Dizziness

• Increased fatigue

• Shortness of breath

Lifestyle Modifications

• Maintain a healthy weight.

• Limit alcohol.

• Stop smoking.

• Manage:

  • Sleep apnea

  • Blood glucose

  • Blood pressure

  • Weight

• Avoid unapproved stimulants:

  • Excess caffeine

  • OTC decongestants

  • Illicit stimulants

  • Herbal supplements

---

---

❤ Atrial Flutter Pathophysiology

• A supraventricular dysrhythmia.

• Less common than A-fib.

• Atria beat at a:

  • Regular

  • Very rapid rate

• Atrial rate: approximately 240-400 bpm.

• Multiple rapid electrical impulses occur in the atria.

• Impulses occur too rapidly for the AV node to process normally.

---

Risk Factors

• Recent MI

• Postoperative cardiac surgery

• Diabetes

• Hyperthyroidism

• Obstructive sleep apnea

• Obesity

• Alcohol use

• Smoking

• Cardiomyopathy

• Pericarditis

---

Common Comorbidities

• Similar to A-fib:

  • Hypertension

  • Heart failure

  • Diabetes

  • Obesity

  • COPD

  • Thyroid disease

  • Kidney disease

  • Stroke

---

Clinical Presentation

• Similar to A-fib:

  • Hypotension

  • Lightheadedness

  • Dizziness

  • Palpitations

  • Chest discomfort

  • Shortness of breath

  • Fatigue

  • Syncope

---

Atrial Flutter ECG Findings ⭐

• Rhythm: Usually regular

• P waves:

  • Absent

  • Replaced by characteristic sawtooth/flutter waves

• Ventricular rate: typically 60-100/min

• Atrial rate: approximately 240-340/min

Quick Memory Tip

Atrial flutter = “Sawtooth waves.”

---

Diagnostic Tests

• Blood tests may evaluate for:

  • Electrolyte abnormalities

  • Diabetes

  • Thyroid disease

  • Kidney disease

  • Liver dysfunction

• Echocardiogram:

  • Evaluates chamber size and function.

• TEE:

  • Detects left atrial blood clots before cardioversion.

---

Nursing Priorities for Atrial Flutter Assessment

• Obtain medical history and determine onset of symptoms.

• Monitor:

  • ECG

  • Vital signs

  • Oxygen saturation

  • Signs of decreased cardiac output

Signs the Client May Not Be Tolerating the Rhythm

• Hypotension

• Decreased cardiac output

• Ventricular rate > 150/min

Priority Goals

• Improve cardiac perfusion.

• Restore normal rhythm.

• Prevent:

  • Blood clots

  • Hypotension

  • Bradycardia

  • Tachycardia-related complications

---

Treatment of Atrial Flutter

• Similar to A-fib:

  • Anticoagulants

  • Antiarrhythmics

  • Beta blockers

  • Calcium channel blockers

  • Amiodarone

  • Digoxin

  • Synchronized cardioversion

  • Catheter ablation

• Client education and lifestyle modifications are similar to A-fib.

---

---

❤ Supraventricular Tachycardia (SVT) Pathophysiology

• SVT is a category of narrow-complex tachycardias.

• Electrical impulses originate above the ventricles/AV node.

• Increased atrial excitability causes a rapid heart rate.

PSVT

• Paroxysmal SVT (PSVT) is also called AV nodal reentrant tachycardia (AVNRT).

• Usually:

  • Starts abruptly

  • Stops suddenly

  • May occur without warning

---

Etiology & Triggers

• Stress

• Smoking

• Alcohol

• Caffeine

• Other stimulants

• Heart disease

• Heart failure

• Wolff-Parkinson-White syndrome

• Pregnancy

• Chronic lung disease

---

Associated Conditions

• Coronary artery disease

• Hypertension

• Diabetes

• A-fib

• Heart failure

• Cardiomyopathy

• Hyperthyroidism

• Renal disease

---

Clinical Presentation Common Manifestations

• Sudden onset of:

  • Palpitations

  • Chest discomfort

  • Dizziness

  • Lightheadedness

  • Shortness of breath

• Possible:

  • Hypotension

  • Syncope

  • Diaphoresis

  • Fatigue

  • Anxiety

Safety Concern

• Dizziness and syncope increase the risk for falls and injury.

---

SVT/PSVT Diagnostic Testing Blood Tests

• No blood test confirms SVT or PSVT.

• Blood work may identify underlying causes:

  • Electrolytes

  • CBC

  • Thyroid function

  • Other chronic medical conditions

---

SVT ECG Findings ⭐

• Rhythm: Regular

• Heart rate: approximately 100-220 bpm

• QRS: Narrow, < 0.12 seconds

• P waves:

  • Often difficult or impossible to identify

• PSVT:

  • Similar narrow QRS

  • Heart rate often around 160 bpm

Quick Memory Tip

SVT = Sudden, Very fast, Thin (narrow) QRS.

---

Nursing Process: SVT/PSVT Recognize Cues

• Obtain a thorough medical history.

• Assess ability to complete usual activities.

• Monitor:

  • ECG

  • Heart rate

  • Blood pressure

  • Peripheral pulses

• Assess for:

  • Diaphoresis

  • Fatigue

  • Syncope

  • Anxiety

  • Hypotension

Priority

• Maintain hemodynamic stability.

• Convert the rhythm back to a normal rhythm when indicated.

• Prevent complications from:

  • Hypoxia

  • Dyspnea

  • Hypotension

---

SVT Treatment 1. Vagal Maneuvers

• May slow conduction through the AV node.

• Can help terminate certain SVTs or reveal the underlying rhythm.

Examples

• Valsalva maneuver

• Forceful coughing

• Gagging

• Carotid massage performed by an appropriate provider

Valsalva Maneuver

• Hold breath for approximately 15 seconds.

• Bear down as if having a bowel movement.

Nursing Care

• Monitor:

  • Vital signs

  • Cardiac rhythm

• Assess before, during, and after the maneuver.

---

2. Adenosine Used When

• Vagal maneuvers are ineffective.

Key Points

• Has a very short duration of action.

• Must be administered rapidly.

• Continuous cardiac monitoring is required.

• Keep:

  • Defibrillator

  • Resuscitation equipment

  • Emergency supplies readily available.

Common Administration

• First dose: 6 mg rapid IV push over 1-3 seconds

• Follow immediately with a rapid normal saline flush.

• If ineffective:

  • 12 mg may be given, followed by a rapid saline flush.

Purpose

• Temporarily slows AV nodal conduction.

• May allow identification of the underlying rhythm.

---

3. Additional Medications

If vagal maneuvers and adenosine are ineffective, medications may include:

• Diltiazem

• Esmolol

• Metoprolol

Goal

• Slow the heart rate.

• Improve cardiac perfusion and hemodynamic stability.

---

⭐ Quick Comparison: A-fib vs. Atrial Flutter vs. SVT

Feature	A-fib	Atrial Flutter	SVT/PSVT
Rhythm	Irregularly irregular	Usually regular	Regular
P waves	Absent/chaotic	Sawtooth flutter waves	Often not visible
Atrial activity	Chaotic	Rapid and organized	Rapid electrical activity
Rate	Ventricular rate variable	Atrial rate 240-340+	Usually 100-220 bpm
QRS	Usually normal/narrow	Usually normal/narrow	Narrow <0.12 sec
Major concern	Stroke/clot formation	Clots & decreased cardiac output	Hemodynamic instability
Key treatment	Rate/rhythm control + anticoagulation	Similar to A-fib	Vagal maneuvers → adenosine

NCLEX High-Yield Takeaways ⭐

• A-fib = irregularly irregular + no distinct P waves + stroke risk.

• A-fib with HR >100 = rapid ventricular response (RVR).

• Atrial flutter = sawtooth waves.

• SVT = regular, rapid, narrow QRS tachycardia.

• For SVT, vagal maneuvers are often attempted first if appropriate.

• If vagal maneuvers are ineffective, adenosine may be used.

• Clients with A-fib/flutter often require anticoagulation to prevent thromboembolic stroke.

• Always monitor for bleeding in clients receiving anticoagulants.

• Warfarin requires consistent vitamin K intake and PT/INR monitoring.

• Adenosine is administered rapidly with continuous cardiac monitoring.

​

HTN

Overview

• Hypertension (HTN) = persistently elevated blood pressure (BP).

• One of the most important modifiable risk factors for cardiovascular disease (CVD).

• As BP increases, risk increases for:

  • Myocardial infarction (MI)

  • Heart failure (HF)

  • Stroke

  • Renal disease

  • Vision loss

• Often requires a combination of:

  • Lifestyle modifications

  • Antihypertensive medications

• Patient education is essential for long-term BP control.

• Social determinants of health can significantly affect BP control:

  • Limited access to health care

  • Poverty

  • Chronic stress

  • Limited resources/support

---

Normal Regulation of Blood Pressure Blood Pressure Basics

• BP = force exerted by blood against vessel walls.

• BP must be adequate to maintain tissue perfusion at rest and during activity.

• Main determinants of BP:

  • Cardiac output (CO)

  • Systemic vascular resistance (SVR)

Cardiac Output

• CO = Stroke Volume (SV) × Heart Rate (HR)

• Stroke volume = amount of blood ejected from the left ventricle with each beat.

• ↑ HR and/or ↑ SV → ↑ CO → ↑ BP.

Systemic Vascular Resistance

• SVR = resistance opposing blood flow through blood vessels.

• Mainly determined by the radius of small arteries and arterioles.

• Vasoconstriction → ↑ SVR → ↑ BP.

• Vasodilation → ↓ SVR → ↓ BP.

• Even a small change in arteriole diameter can cause a major change in SVR.

---

Mechanisms of BP Regulation

• BP regulation involves:

  • Short-term mechanisms: seconds to hours

  • Long-term mechanisms: days to weeks

Short-Term Regulation

• Sympathetic nervous system (SNS)

• Baroreceptors

• Vascular endothelium

Long-Term Regulation

• Kidneys

• Hormones

• Renin-angiotensin-aldosterone system (RAAS)

• Control of blood volume and sodium

---

Sympathetic Nervous System (SNS)

• Responds within seconds to changes in BP.

• SNS activation causes:

  • ↑ HR

  • ↑ Cardiac contractility

  • Peripheral vasoconstriction

  • ↑ Renin release

• Overall result: ↑ CO + ↑ SVR = ↑ BP

Parasympathetic Nervous System (PNS)

• Mainly decreases BP by:

  • Decreasing HR through the vagus nerve

  • ↓ HR → ↓ CO → ↓ BP

---

Baroreceptors

• Located in:

  • Carotid arteries

  • Aortic arch

• Sensitive to stretch caused by BP changes.

When BP Increases

• Baroreceptors send inhibitory signals to the SNS.

• Results:

  • ↓ HR

  • ↓ Contractility

  • Peripheral vasodilation

  • ↓ BP

When BP Decreases

• SNS is activated.

• Results:

  • Vasoconstriction

  • ↑ HR

  • ↑ Contractility

  • ↑ BP

Important

• In long-standing hypertension, baroreceptors adapt to the higher BP.

• The elevated BP becomes the patient's new “normal.”

---

SNS Receptors Affecting BP α1 Receptors

• Location:

  • Vascular smooth muscle

  • Heart

• Activation causes:

  • Vasoconstriction

  • ↑ Contractility

α2 Receptors

• Activation:

  • Inhibits norepinephrine release

  • Can cause vasoconstriction in vascular smooth muscle

β1 Receptors

• Location:

  • Heart

  • Juxtaglomerular cells of kidneys

• Activation causes:

  • ↑ HR (positive chronotropic effect)

  • ↑ Contractility (positive inotropic effect)

  • ↑ Conduction speed (positive dromotropic effect)

  • ↑ Renin secretion

β2 Receptors

• Located in smooth muscle of:

  • Coronary arteries

  • Lungs/bronchi

  • Skeletal muscle blood vessels

• Activation causes vasodilation.

Dopamine Receptors

• Primarily located in renal blood vessels.

• Activation causes vasodilation.

---

Vascular Endothelium

• Single-cell layer lining blood vessels.

• Important functions:

  • Regulates platelet adhesion

  • Regulates coagulation

  • Immune function

  • Fluid balance

  • Vascular tone

Endothelial Substances

• Nitric oxide (NO) → vasodilation

• Prostacyclin → vasodilation

• Endothelin (ET) → potent vasoconstriction

Endothelial Dysfunction

• Smoking and diabetes can damage endothelial function.

• Can lead to:

  • Excessive vasoconstriction or dilation

  • Early CVD changes

  • Hypertension

---

Renal System and BP Sodium and Water

• Kidneys regulate BP by controlling:

  • Sodium excretion

  • Extracellular fluid (ECF) volume

• Sodium retention → water retention.

• Water retention → ↑ blood volume.

• ↑ Blood volume → ↑ venous return → ↑ SV → ↑ CO → ↑ BP.

---

Renin-Angiotensin-Aldosterone System (RAAS) Renin Release

• Kidneys release renin in response to:

  • SNS stimulation

  • ↓ Renal blood flow

  • ↓ Serum sodium

RAAS Sequence

• Renin converts angiotensinogen → angiotensin I

• ACE converts angiotensin I → angiotensin II (A-II)

Effects of Angiotensin II

• Potent vasoconstrictor → ↑ SVR → immediate ↑ BP.

• Stimulates adrenal cortex to release aldosterone.

• Causes vascular remodeling and tissue growth.

• Contributes to:

  • Primary hypertension

  • Atherosclerosis

  • Renal disease

  • Cardiac hypertrophy

Aldosterone

• Causes sodium and water retention.

• ↑ Blood volume → ↑ CO → ↑ BP.

---

Natriuretic Peptides

• ANP and BNP are released by heart cells.

• Oppose ADH and aldosterone.

• Cause:

  • Natriuresis = sodium excretion

  • Diuresis = water excretion

• Result:

  • ↓ Blood volume

  • ↓ BP

---

Antidiuretic Hormone (ADH)

• Released from the posterior pituitary.

• Triggered by:

  • ↑ Blood sodium

  • ↑ Osmolarity

• Promotes water reabsorption by the kidneys.

• ↑ Blood volume → ↑ CO → ↑ BP.

---

Epinephrine and BP

• Released by the adrenal medulla during SNS stimulation.

• Causes:

  • ↑ HR

  • ↑ Myocardial contractility

  • ↑ CO

• Effects vary by receptor:

  • β2 receptors → vasodilation

  • α1 receptors → vasoconstriction

---

BP Classification

Category	Systolic BP	Diastolic BP
Normal	<120	<80
Elevated	120–129	<80
Stage 1 HTN	130–139	or 80–89
Stage 2 HTN	≥140	or ≥90

Key Points

• If SBP and DBP fall into different categories, use the higher category.

• Example: 115/86 = Stage 1 hypertension.

• Diagnosis should be based on:

  • 2 or more readings

  • Both arms

  • 2 separate occasions

• SBP tends to increase with age.

• DBP usually rises until about age 55, then declines.

---

Etiology of Hypertension Primary Hypertension

• Also called:

  • Essential hypertension

  • Idiopathic hypertension

• No identifiable cause

• Accounts for 90%–95% of cases.

Contributing Factors

• Endothelial dysfunction

• ↑ SNS activity

• Sodium-retaining hormones

• High sodium intake

• Overweight/obesity

• Age

• Family history/genetics

• Diabetes

• Tobacco use

• Excess alcohol use

Secondary Hypertension

• Hypertension with a specific identifiable cause.

• Accounts for 5%–10% of cases.

• Often suspected when hypertension:

  • Develops suddenly

  • Is severe

  • Is difficult to control

Common Causes

• Renal disease/renal artery stenosis

• Sleep apnea

• Endocrine disorders:

  • Pheochromocytoma

  • Cushing syndrome

  • Thyroid disease

• Pregnancy-induced hypertension

• Coarctation of the aorta

• Neurologic disorders:

  • Brain tumors

  • Stroke

  • TBI

• Cirrhosis

• Drugs:

  • Oral contraceptives

  • Estrogen therapy

  • Corticosteroids

  • NSAIDs

  • Sympathetic stimulants

---

Pathophysiology of Primary Hypertension

• BP increases when CO or SVR increases.

• Early hypertension:

  • ↑ Blood volume

  • ↑ CO

• As hypertension progresses:

  • SVR progressively increases

  • CO may return to normal

• Hemodynamic hallmark of chronic hypertension = persistently increased SVR.

---

Major Risk Factors for Primary Hypertension Nonmodifiable

• Increasing age

• Family history

• Genetics

• Ethnicity

Modifiable

• Excess sodium intake

• Obesity/central obesity

• Sedentary lifestyle

• Excess alcohol use

• Tobacco use

• Stress

• Diabetes/insulin resistance

• Increased serum lipids

---

Sodium and Hypertension

• High sodium intake contributes to hypertension, especially in salt-sensitive individuals.

• Sodium retention → water retention → ↑ blood volume → ↑ BP.

• Sodium sensitivity has a strong genetic component.

• Effects may be more significant in:

  • Black individuals

  • Middle-aged adults

  • Older adults

---

Stress and SNS Activity

• Stressors include:

  • Anger

  • Fear

  • Pain

• Persistent stress can cause prolonged SNS activation.

• Results:

  • Vasoconstriction

  • ↑ HR

  • ↑ Renin release

  • RAAS activation

  • ↑ BP

---

Insulin Resistance and Hyperinsulinemia

• Common in primary hypertension.

• High insulin levels can:

  • ↑ SNS activity

  • Impair NO-mediated vasodilation

  • Promote vascular hypertrophy

  • ↑ Renal sodium reabsorption

• Contributes to hypertension and CVD.

---

Clinical Manifestations “Silent Killer”

• Hypertension is often asymptomatic until severe or target-organ damage develops.

Possible Symptoms of Severe Hypertension

• Fatigue

• Dizziness

• Palpitations

• Angina

• Dyspnea

Important

• Headaches and nosebleeds are not reliable routine symptoms of hypertension.

• In a hypertensive crisis, patients may experience:

  • Severe headache

  • Dyspnea

  • Nosebleeds

---

Target Organ Damage / Complications Heart

• Coronary artery disease (CAD)

• Angina

• MI

• Left ventricular hypertrophy (LVH)

• Heart failure

Brain

• TIA

• Stroke

• Hypertensive encephalopathy

Kidneys

• Nephrosclerosis

• CKD

• Renal failure

Eyes

• Retinal damage

• Blurred vision

• Retinal hemorrhages

• Vision loss

Peripheral Vessels

• Peripheral vascular disease (PVD)

• Aortic aneurysm

• Aortic dissection

• Intermittent claudication

Other

• Erectile dysfunction

---

Hypertensive Heart Disease Coronary Artery Disease

• Hypertension damages coronary endothelium.

• Promotes atherosclerosis.

• Can lead to:

  • Angina

  • MI

  • CAD

Left Ventricular Hypertrophy

• Sustained high BP → increased cardiac workload.

• Left ventricle thickens to compensate.

• Eventually:

  • ↑ Myocardial oxygen demand

  • Progressive cardiac dysfunction

  • Increased risk for HF

Heart Failure

• Occurs when compensatory mechanisms fail.

• ↓ Contractility → ↓ SV and CO.

• Symptoms:

  • Dyspnea on exertion

  • Paroxysmal nocturnal dyspnea

  • Fatigue

---

Cerebrovascular Complications

• Hypertension is a major risk factor for:

  • Cerebral atherosclerosis

  • TIA

  • Stroke

• Even mild hypertension significantly increases stroke risk.

• Adequate BP control decreases stroke risk.

Hypertensive Encephalopathy

• Occurs with a marked rise in BP.

• Cerebral autoregulation fails.

• Results:

  • Cerebral vasodilation

  • Increased capillary permeability

  • Cerebral edema

  • ↑ Intracranial pressure

• Can rapidly cause severe brain damage or death.

---

Nephrosclerosis

• Hypertension is a leading cause of CKD.

• Narrowed renal blood vessels cause:

  • Ischemia

  • Tubular atrophy

  • Glomerular destruction

  • Nephron loss

  • Renal failure

Signs of Renal Damage

• Albuminuria

• Proteinuria

• Microscopic hematuria

• ↑ Creatinine

• ↑ BUN

• Nocturia may be an early symptom

---

Diagnostic Assessment Basic Studies

• History and physical examination

• Ophthalmic examination

• Fasting blood glucose

• Urinalysis

• Basic metabolic panel

• eGFR

• CBC

• Lipid profile

• Uric acid

• Calcium and magnesium

• 12-lead ECG

Possible Additional Tests

• 24-hour creatinine clearance

• Echocardiography

• Liver function tests

• TSH

Purpose of Testing

• Identify secondary causes.

• Detect target-organ damage.

• Assess cardiovascular risk.

• Obtain baseline values before therapy.

ECG Can Detect

• LVH

• Cardiac ischemia

• Previous MI

---

Ambulatory Blood Pressure Monitoring (ABPM) White Coat Hypertension

• BP is high in the clinical setting but normal outside the clinic.

ABPM

• Automated BP monitoring over 12–24 hours.

• Patient wears:

  • BP cuff

  • Small monitoring device

• Patient should:

  • Keep arm still during readings

  • Keep a diary of activities affecting BP

Other Uses

• Suspected medication resistance

• Symptoms of hypotension during therapy

• Episodic hypertension

• Suspected SNS dysfunction

Normal Diurnal Pattern

• BP is usually:

  • Highest in early morning

  • Lower during the day

  • Lowest during sleep

• Normal nighttime BP usually decreases by 10% or more.

Nondippers

• No normal nighttime BP decrease.

• Increased CVD risk.

Reverse Dippers

• Nighttime SBP increases.

• Highest cardiovascular risk.

---

Lifestyle Modifications Main Goals

• Lower BP.

• Reduce overall CVD risk.

• Lifestyle changes are recommended for all patients with elevated BP or hypertension.

Key Health Behaviors

• Manage BP

• Control cholesterol

• Control glucose

• Be physically active

• Eat a healthy diet

• Lose weight if needed

• Stop smoking

---

Weight Loss

• Excess weight increases risk for hypertension and CVD.

• Even moderate weight loss can lower BP.

• Rule of thumb:

  • 1 kg of weight loss ≈ 1 mm Hg BP reduction

• Recommended approach:

  • Calorie restriction

  • Moderate physical activity

---

Nutrition Recommended Diet Patterns

• DASH diet

• Mediterranean diet

• Plant-based dietary patterns

Emphasize

• Fruits

• Vegetables

• Nuts

• Legumes

• Lean proteins

• Fish

---

Sodium Restriction

• General goal: ≤2300 mg/day.

• Intake <1500 mg/day may lower BP even further.

“Salty Six”

Major high-sodium food groups:

• Bread products

• Lunch/cured meats

• Pizza

• Soup

• Sandwiches

• Poultry

Teaching

• Do not add extra salt.

• Read labels on:

  • Packaged foods

  • Prepared foods

  • OTC medications

  • Health products with hidden sodium

Benefits

• May control BP without medication in some patients.

• May allow lower medication doses.

• Can decrease risk of diuretic-related hypokalemia.

---

Potassium and Calcium

• Adequate dietary potassium and calcium are associated with lower BP.

• Encourage obtaining these nutrients from food sources.

• Calcium supplements are not recommended solely to lower BP.

---

Alcohol

• Excess alcohol use increases BP and CVD/stroke risk.

• Limit intake to:

  • Men: no more than 2 drinks/day

  • Women and lighter-weight men: no more than 1 drink/day

---

Physical Activity

• Recommended:

  • 150 minutes/week moderate exercise, OR

  • 75 minutes/week vigorous exercise

• Even some activity is better than none.

• Muscle-strengthening exercises:

  • At least 2 days/week

• Older adults should also perform:

  • Flexibility exercises

  • Balance exercises

Benefits

• Can reduce SBP by approximately 4–9 mm Hg.

• Helps with:

  • Weight control

  • Relaxation

  • Overall cardiovascular health

Nursing Teaching

• Increase activity gradually.

• Choose activity that is:

  • Safe

  • Enjoyable

  • Affordable

  • Easy to fit into daily life

• Patients with serious CVD may need evaluation before starting an exercise program.

---

Tobacco Use

• Nicotine causes:

  • Vasoconstriction

  • ↑ BP

• Smoking greatly increases CVD risk.

• Hypertension + smoking = especially high CVD risk.

• Strongly encourage smoking/tobacco cessation.

---

Social and Psychosocial Risk Factors

• Consider:

  • Socioeconomic status

  • Food access

  • Housing

  • Education

  • Health care access

  • Work/family stress

  • Support systems

  • Exposure to violence

• These factors can affect the cardiovascular system through:

  • SNS activation

  • Stress hormones

  • Poor access to healthy lifestyle resources

• Possible referrals:

  • Counseling

  • Social work

  • Community support

  • Stress-management programs

  • Exercise programs

---

Drug Therapy General BP Goals

• Many adults with hypertension and CVD/risk factors have a treatment goal of 130/80 mm Hg.

• Treatment goals should be individualized based on:

  • Age

  • Comorbidities

  • Functional status

  • Patient preferences

Older Adults

• For many ambulatory adults ≥65:

  • Goal SBP is <130 mm Hg

• More individualized treatment is needed for those with:

  • Multiple comorbidities

  • Limited life expectancy

  • Residence in skilled care settings

---

Main Actions of Antihypertensive Drugs

Antihypertensive medications generally work by:

1. Decreasing circulating blood volume

2. Decreasing systemic vascular resistance

---

First-Line Medications

For Stage 1 hypertension:

• Nonpharmacologic treatment + usually 1 medication.

Preferred First-Line Classes

• Thiazide diuretic

• Calcium channel blocker (CCB)

• ACE inhibitor

• ARB

For Stage 2 hypertension:

• Nonpharmacologic treatment + 2 medications from different classes.

---

Adrenergic-Inhibiting Drugs Central-Acting α-Agonists

Examples:

• Clonidine

• Guanfacine

• Methyldopa

Effects

• ↓ Sympathetic outflow

• ↓ Peripheral sympathetic tone

• Vasodilation

• ↓ SVR

• ↓ BP

Nursing Considerations

• Do not stop clonidine suddenly.

• Sudden discontinuation can cause:

  • Rebound hypertension

  • Tachycardia

  • Headache

  • Tremors

• Can cause dry mouth.

• Alcohol/sedatives increase sedation.

• Methyldopa may cause daytime sedation.

---

α1-Adrenergic Blockers

Examples:

• Doxazosin

• Prazosin

• Terazosin

Effects

• Peripheral vasodilation

• ↓ SVR

• ↓ BP

Nursing Consideration

• Give at bedtime, especially the first dose.

• Major risk: orthostatic hypotension and syncope.

Doxazosin Alert

• First dose can cause a significant BP drop.

• Syncope may occur 30–90 minutes after the first dose.

• Severe hypotension can occur with PDE-5 inhibitors.

---

β-Blockers Cardioselective β1-Blockers

Examples:

• Atenolol

• Metoprolol

• Esmolol

• Bisoprolol

Effects

• ↓ HR

• ↓ Contractility

• ↓ CO

• ↓ Renin secretion

• ↓ BP

Nursing Considerations

• Monitor:

  • HR

  • BP

• Use caution in diabetes:

  • May mask tachycardia associated with hypoglycemia.

• Often beneficial for patients with:

  • Previous MI

  • HF

• Esmolol is IV only.

Nonselective β-Blockers

Examples:

• Propranolol

• Nadolol

• Pindolol

Important

• Block β1 and β2 receptors.

• Can cause bronchospasm.

• Use caution in patients with asthma.

Mixed α- and β-Blockers

Examples:

• Carvedilol

• Labetalol

Effects

• ↓ HR

• ↓ CO

• Peripheral vasodilation

• ↓ SVR

• ↓ BP

Nursing Considerations

• IV forms may be used during hypertensive crisis.

• Monitor for severe orthostatic hypotension.

---

ACE Inhibitors

Examples:

• Lisinopril

• Enalapril

• Benazepril

• Captopril

• Ramipril

Mechanism

• Inhibit ACE.

• ↓ Conversion of angiotensin I → angiotensin II.

• ↓ Vasoconstriction.

• ↓ Sodium and water retention.

Key Nursing Considerations

• Monitor serum creatinine.

• Can cause dry, hacking cough due to bradykinin.

• Aspirin and NSAIDs may decrease effectiveness.

• Adding a diuretic can enhance the effect.

• Avoid combining with potassium-sparing diuretics due to hyperkalemia risk.

• Captopril may be used orally for hypertensive crisis.

---

ARBs

Examples:

• Losartan

• Valsartan

• Candesartan

• Irbesartan

Mechanism

• Block angiotensin II from binding to its receptors.

• Cause:

  • Vasodilation

  • ↑ Sodium and water excretion

Key Points

• Full effect may take 3–6 weeks.

• Do not increase bradykinin.

• Can be used as an alternative for patients who develop an ACE inhibitor cough.

• Do not combine ACE inhibitors and ARBs in patients with kidney disease because of adverse renal effects.

---

Calcium Channel Blockers (CCBs) Non-Dihydropyridines

Examples:

• Diltiazem

• Verapamil

Effects

• Vasodilation

• ↓ HR

• Slows AV conduction

Nursing Considerations

• Use cautiously in HF.

• Avoid with:

  • 2nd-degree AV block

  • 3rd-degree AV block

  • Left ventricular systolic dysfunction

• Avoid grapefruit juice with certain CCBs.

Dihydropyridines

Examples:

• Amlodipine

• Nicardipine

• Nifedipine

• Clevidipine

Effects

• Strong peripheral vasodilation

• ↓ SVR

• ↓ BP

Important

• Short-acting sublingual nifedipine is unsafe and ineffective in hypertensive emergencies.

• IV nicardipine/clevidipine may be used for hypertensive crisis.

---

Direct Vasodilators Hydralazine

• Direct arterial vasodilator.

• ↓ SVR and BP.

• May be IV for hypertensive crisis.

• Not typically used alone.

• Contraindicated in CAD.

Minoxidil

• Powerful arterial vasodilator.

• Reserved for severe/resistant hypertension, especially with renal failure.

Fenoldopam

• Activates dopamine receptors.

• Causes systemic and renal vasodilation.

• IV only for hypertensive crisis.

Nitroglycerin

• Relaxes arterial and venous smooth muscle.

• Low dose → mainly venodilation.

• Higher dose → arterial dilation.

• IV may be used in hypertensive crisis with myocardial ischemia.

Sodium Nitroprusside

• Direct arterial vasodilator.

• IV infusion for hypertensive crisis.

• Requires close BP monitoring.

• Protect solution from light.

• Prolonged use can lead to cyanide/thiocyanate toxicity.

---

Diuretics Main Effects

• Promote sodium and water excretion.

• ↓ Plasma volume.

• ↓ BP.

Thiazide Diuretics

Examples:

• Hydrochlorothiazide

• Chlorthalidone

• Indapamide

• Metolazone

Effects

• ↑ Sodium and chloride excretion

• Initially ↓ ECF volume

• Long-term ↓ SVR

Nursing Considerations

• Monitor for:

  • Orthostatic hypotension

  • Hypokalemia

  • Metabolic alkalosis

• Hypokalemia can increase digoxin toxicity.

• Teach about potassium-rich foods.

• NSAIDs can decrease the diuretic/antihypertensive effect.

Loop Diuretics

Examples:

• Furosemide

• Bumetanide

• Torsemide

Key Points

• More potent than thiazides.

• Effective despite renal insufficiency.

• Monitor:

  • Electrolytes

  • Orthostatic hypotension

Potassium-Sparing Diuretics

Examples:

• Amiloride

• Triamterene

Nursing Considerations

• Monitor for hyperkalemia.

• Avoid potassium supplements.

• Contraindicated in renal failure.

Aldosterone Receptor Blockers

Examples:

• Spironolactone

• Eplerenone

Effects

• Block aldosterone.

• Decrease sodium retention.

• Spare potassium.

Nursing Considerations

• Monitor for:

  • Hyperkalemia

  • Orthostatic hypotension

• Use caution with ACE inhibitors and ARBs.

---

Renin Inhibitor Aliskiren

• Directly inhibits renin.

• Reduces formation of angiotensin I.

• Can cause angioedema.

• Do not use during pregnancy.

---

Resistant Hypertension

• Failure to reach goal BP despite full doses of an appropriate 3-drug regimen that includes a diuretic.

• Associated with a significantly increased risk of:

  • MI

  • Stroke

  • Other complications

Management

• Assess:

  • Medication adherence

  • Contributing risk factors

  • Secondary causes

  • Drug interactions

• Alternative medications may be needed.

• Renal denervation may be considered in some patients.

---

Nursing Management Priority Clinical Problems

• Altered BP

• Body weight problems

• Difficulty coping

• Health maintenance alteration

• Impaired cardiac function

• Impaired sexual function

• Inadequate tissue perfusion

• Nutritional problems

Overall Goals

The patient should:

• Achieve and maintain goal BP.

• Experience minimal treatment side effects.

• Understand and manage their condition.

• Reduce risk of target-organ damage.

---

Nursing Assessment Assess

• BP trends

• Age and sex considerations

• Diet:

  • Sodium intake

  • Alcohol intake

• Weight patterns

• Tobacco use

• Physical activity

• Stress

• Family history of:

  • Hypertension

  • CVD

  • Stroke

  • Renal disease

  • Diabetes

• All medications:

  • Prescription

  • OTC

  • Recreational drugs

• Previous history of high BP and treatment

---

Accurate BP Measurement Proper Technique

• Use the correct cuff size.

• Place cuff on the bare upper arm.

• Align cuff bladder with the brachial artery.

• Keep the arm at heart level.

• Support the arm during measurement.

Cuff Size

• Too small → falsely high BP

• Too large → falsely low BP

Both Arms

• Measure BP in both arms initially.

• If readings differ:

  • Document the difference.

  • Use the arm with the higher BP for future measurements.

If Using the Forearm

• Document the site.

• Forearm and upper-arm BP readings are not interchangeable.

---

Orthostatic BP Assessment Assess In

• Older adults

• Patients taking antihypertensive medications

• Patients with:

  • Lightheadedness

  • Dizziness

  • Syncope

Procedure

1. Rest supine for 3 minutes.

2. Measure BP and pulse.

3. Have patient sit; repeat measurements.

4. Have patient stand; measure BP and pulse.

5. Repeat after standing for 3 minutes.

Orthostatic Hypotension

• Drop in SBP ≥20 mm Hg, OR

• Drop in DBP ≥10 mm Hg, AND/OR

• HR increase of ≥20 beats/min

• Symptoms such as dizziness or lightheadedness are abnormal.

Common Causes

• Dehydration

• Disease-related impaired vasoconstriction

• Antihypertensive medications

---

Auscultatory Gap

• A temporary disappearance of Korotkoff sounds between the first sound and later beats.

• If the cuff is not inflated high enough:

  • SBP may be underestimated.

• Important for accurate BP measurement.

​

Resistant Hypertension Causes of Pseudoresistant Hypertension

• Improper BP measurement

  • Wrong BP cuff size

  • Incorrect technique

• Inadequate medication doses

• Inappropriate drug therapy

• Poor medication adherence

  • Side effects

  • Financial concerns

• White coat syndrome

Causes Related to Volume Overload

• Drug-induced

  • Corticosteroids

  • Cyclosporine

  • Tacrolimus (Prograf)

  • Erythropoietin

  • NSAIDs

  • Oral contraceptives

  • Sympathomimetics

    • Decongestants

    • Diet pills

• Excess sodium intake

• Herbal supplements

  • Ma huang

  • Bitter orange

• Inadequate diuretic therapy

• Illegal drugs

  • Cocaine

  • Amphetamines

• Licorice

• Kidney disease causing fluid/volume retention

Associated Conditions

• Excessive alcohol use

• Increasing obesity

• Obstructive sleep apnea (OSA)

---

Home Blood Pressure Monitoring

• Verify the home BP machine is validated for accuracy.

• Encourage measurements at the same time each day for consistency.

• Compare home and office BP readings to determine average BP.

• Home readings may be:

  • Lower than office readings

  • Better predictors of cardiovascular disease (CVD) risk

• Patients should understand:

  • Their target/goal BP

  • When to contact their health care provider (HCP)

  • Why regular monitoring is important

Patient Teaching for Home BP Monitoring

• Use an automatic/oscillometric BP monitor with an upper-arm or wrist cuff.

• Bring the monitor to the office to verify:

  • Correct cuff size

  • Device accuracy

  • Correct patient technique

• Measure BP:

  • In the nondominant arm, OR

  • In the arm with the higher BP if there is a known difference

• Check BP:

  • First thing in the morning, preferably before medications

  • At night before bed

• Record all readings and bring the record to office visits.

• For medication changes or clinical decisions:

  • Take readings as instructed for 1 week

• Stable patients with normal BP:

  • Check morning and evening readings for at least 1 week every 3 months

---

Community Hypertension Screening

• Used to identify people with elevated BP.

• Give each person:

  • A written, numeric BP reading

  • An explanation of what the reading means

  • Information about the need for further evaluation if indicated

---

Nursing Assessment: Hypertension Subjective Data Health History

Assess for:

• Duration and previous evaluation of hypertension

• Cardiovascular disease

• Cerebrovascular disease

• Renal disease

• Thyroid disease

• Diabetes

• Pituitary disorders

• Obesity

• Dyslipidemia

• Menopause or hormone replacement therapy

Medications

Ask about:

• Prescription medications

• OTC medications

• Recreational drugs

• Herbal products

• Current antihypertensive medications

Health Management

Assess for:

• Family history of hypertension or CVD

• Tobacco use

• Alcohol use

• Sedentary lifestyle

• Health literacy

• Readiness to make lifestyle changes

Nutrition

Assess:

• Sodium intake

• Fat intake

• Weight gain or loss

Elimination

• Nocturia

Activity/Exercise

Assess for:

• Fatigue

• Dyspnea on exertion

• Palpitations

• Exertional chest pain

• Intermittent claudication

• Muscle cramps

• Usual exercise pattern

Neurologic/Perceptual

Assess for:

• Dizziness

• Blurred vision

• Paresthesias

Sexual Health

Assess for:

• Erectile dysfunction

• Decreased libido

Stress

• Identify stressful life events.

---

Objective Assessment Findings Cardiovascular

• Consistently elevated BP

• Orthostatic changes in BP and HR

• Significant BP difference between arms

• Abnormal heart sounds

• Laterally displaced apical pulse

• Decreased or absent peripheral pulses

• Carotid, renal, or femoral bruits

• Peripheral edema

Gastrointestinal/Body Habitus

• Obesity

  • BMI ≥ 30 kg/m²

• Abnormal waist-to-hip ratio

Neurologic

• Mental status changes

Possible Diagnostic Findings

• Abnormal electrolytes, especially potassium

• Increased:

  • BUN

  • Creatinine

  • Glucose

  • Cholesterol

  • Triglycerides

• Proteinuria

• Albuminuria

• Microscopic hematuria

• ECG findings:

  • Ischemic heart disease

  • Left ventricular hypertrophy (LVH)

• Echocardiogram:

  • Structural heart disease

  • LVH

• Funduscopic examination:

  • Arteriovenous nicking

  • Retinal hemorrhages

  • Papilledema

---

Accurate Blood Pressure Measurement Before Measurement

• No:

  • Smoking

  • Exercise

  • Caffeine

• Avoid these for 30 minutes before BP measurement.

Proper Technique

1. Seat patient with:

   • Legs uncrossed

   • Feet flat on floor

   • Back supported

2. Bare the arm and support it at heart level.

3. Allow the patient to rest quietly for 5 minutes.

4. Patient should:

   • Relax

   • Not talk during measurement

5. Use the correct cuff size.

6. Initially measure BP in both arms.

7. Use the arm with the higher BP for future measurements.

Do Not Use an Extremity With

• Deep venous thrombosis (DVT)

• Arteriovenous fistula or graft

• PICC line

• Lymphedema

• Limb ischemia

Oscillometric/Automatic Devices

• Preferred for routine BP measurement.

• Accuracy may be limited in patients with:

  • Severe hypertension

  • Hypotension

  • Dysrhythmias such as atrial fibrillation

Atrial Fibrillation

• HR variations can cause BP variations.

• Take 3 separate measurements over several minutes to confirm BP.

Manual/Auscultatory Measurement

• Palpate radial pulse and inflate cuff until the pulse disappears.

• Inflate an additional 20–30 mm Hg above that point.

• Deflate at 2–3 mm Hg/second.

• SBP: first of 2 or more Korotkoff sounds.

• DBP: point when Korotkoff sounds disappear.

• Document:

  • BP reading

  • Patient's BP goal

  • Follow-up recommendations

---

Antihypertensive Medication Teaching Common Reasons for Nonadherence

• Unpleasant side effects

• Side effects may improve with time.

• Severity of side effects may depend on the dose.

• The medication or dose may need to be changed.

• Teach patients to report side effects to the HCP.

Important Medication Instructions

• Know:

  • Medication names

  • Actions

  • Dosages

  • Side effects

• Take medications at regular, convenient times.

• Do NOT stop antihypertensive medications abruptly.

  • Can cause severe rebound hypertension.

• Do NOT double doses after a missed dose.

• Do not change the dose based on BP readings without consulting the HCP.

• Do not take someone else's medication.

Diuretics

• May cause:

  • Dry mouth

  • Frequent urination

• Helpful interventions:

  • Sugarless gum or hard candy for dry mouth

  • Take earlier in the day to reduce nighttime urination

---

Orthostatic Hypotension Causes

• Common side effect of antihypertensive medications.

• Results from altered autonomic regulation of BP during position changes.

Symptoms

• Dizziness

• Lightheadedness

• Faintness when standing

Teaching

• Rise slowly.

• Sit on the side of the bed for several minutes before standing.

• Stand slowly.

• Begin walking only if no dizziness occurs.

• Avoid standing still for prolonged periods.

• Perform leg exercises to increase venous return.

• Sleep with the head of the bed elevated if instructed.

• If dizziness occurs:

  • Sit or lie down immediately.

---

Sexual Side Effects

• Many antihypertensive medications can cause:

  • Decreased libido

  • Erectile dysfunction

• Sexual side effects may lead patients to stop medications.

• Nurses should:

  • Address the topic sensitively

  • Encourage discussion with the HCP

  • Explain that the medication may be causing the problem

• Changing the medication or dose may improve symptoms.

---

Patient Adherence Common Causes of Nonadherence

• Inadequate patient education

• Low health literacy

• Unpleasant side effects

• BP returns to normal, so patient thinks medication is no longer needed

• High medication costs

• Lack of insurance

• Lack of social support

• Lifestyle or cultural barriers

Nursing Interventions

• Determine the reason for nonadherence.

• Assess:

  • Diet

  • Activity

  • Lifestyle

  • Social support

• Develop a plan with the patient and caregiver.

• Make the plan compatible with:

  • Patient habits

  • Cultural beliefs

  • Lifestyle

• Encourage active patient participation.

• Consider:

  • More affordable medications

  • Involving caregivers

  • Combination medications to reduce pill burden and cost

Key Point

• Primary hypertension is chronic and cannot be cured.

• It can be controlled with:

  • Medication

  • Diet changes

  • Physical activity

  • Lifestyle modifications

  • Regular follow-up

---

Nursing Management of Hypertension Nurse Responsibilities

• Develop hypertension screening programs.

• Assess risk factors.

• Develop risk-modification plans.

• Teach about:

  • Lifestyle changes

  • Medications

  • Home BP monitoring

• Monitor for adverse medication effects.

• Evaluate treatment effectiveness.

• Ensure accurate BP measurements.

• Monitor for complications:

  • Coronary artery disease (CAD)

  • Heart failure (HF)

  • Cerebrovascular disease/stroke

  • Peripheral vascular disease (PVD)

  • Renal disease

• Assess hypertensive crisis for target-organ damage.

• Manage hypertensive urgency/emergency as ordered.

• Supervise assistive personnel measuring BP.

• Report significantly high or low BP promptly.

• Obtain postural BP measurements as directed.

• Refer to:

  • Dietitian

  • Exercise programs/physical therapy

  • Stress management programs

Expected Outcomes

The patient should:

• Achieve and maintain their individualized goal BP.

• Understand and follow the treatment plan.

• Have minimal medication side effects.

---

General Patient Teaching

• Know and understand BP readings and goals.

• Monitor BP at home.

• Contact the HCP if BP exceeds prescribed high or low limits.

• Hypertension is often asymptomatic.

  • Symptoms such as nosebleeds do not reliably indicate BP level.

• Long-term treatment is necessary.

• Lifestyle modifications include:

  • Weight management

  • Sodium reduction

  • Smoking cessation

  • Regular physical activity

• Controlled hypertension usually has a good prognosis.

• Untreated hypertension can lead to:

  • Stroke

  • MI/heart attack

  • Other target-organ damage

High-Risk OTC Medications/Substances

Use caution with:

• High-sodium antacids

• NSAIDs

• Appetite suppressants

• Cold and sinus medications

---

Older Adult Considerations Why Hypertension Is Common

Age-related changes include:

• Loss of arterial elasticity/atherosclerosis

• Increased myocardial stiffness

• Increased peripheral vascular resistance

• Decreased adrenergic receptor sensitivity

• Blunted baroreceptor reflexes

• Decreased renal function

• Decreased renin response

Nursing Considerations

• Older adults are more likely to experience:

  • White coat hypertension

  • Orthostatic hypotension

  • Acute kidney injury

• Measure BP and HR:

  • Supine

  • Sitting

  • Standing

• Start medications at low doses.

• Increase doses slowly.

• Assess closely for:

  • Falls

  • Dizziness

  • Orthostatic hypotension

  • Renal dysfunction

Postprandial Hypotension

• BP may drop after meals.

• Greatest decrease is often about 1 hour after eating.

• BP usually returns toward baseline within 3–4 hours.

NSAID Warning

NSAIDs may:

• Cause loss of BP control.

• Worsen heart failure.

• Increase renal adverse effects.

• Increase risk of hyperkalemia when combined with:

  • ACE inhibitors

  • ARBs

  • Aldosterone antagonists

---

Hypertensive Crisis Definition

• SBP >180 mm Hg and/or DBP >120 mm Hg

• BP may be as high as >220/140 mm Hg.

Two Types Hypertensive Urgency

• Severe BP elevation

• NO acute target-organ damage

• Usually managed with:

  • Oral medications

  • Outpatient follow-up, often within 24 hours

Hypertensive Emergency

• Severe BP elevation WITH acute or progressive target-organ damage

• Requires:

  • Hospitalization

  • IV antihypertensive medications

  • Intensive monitoring

Possible Target-Organ Damage

• Encephalopathy

• Intracranial or subarachnoid hemorrhage

• Heart failure

• MI

• Renal failure

• Aortic dissection

• Retinopathy

---

Causes of Hypertensive Crisis

• Acute aortic dissection

• Cocaine use

• Amphetamine use

• Exacerbation of chronic hypertension

• Head injury

• MAOIs combined with tyramine-containing foods

• Pheochromocytoma

• Preeclampsia/eclampsia

• Abrupt withdrawal of antihypertensive medications:

  • Clonidine

  • Beta-blockers

---

Clinical Manifestations of Hypertensive Crisis Neurologic

• Severe headache

• Confusion

• Seizures

• Altered level of consciousness

• Coma

• Blurred vision

• Nausea/vomiting

Cardiac/Respiratory

• Chest pain

• Dyspnea

• Unstable angina

• MI

• Pulmonary edema

Other

• Nosebleeds

• Renal insufficiency or renal failure

• Sudden severe chest and back pain with decreased/absent pulses may indicate aortic dissection.

---

Hypertensive Encephalopathy

• Caused by a sudden severe increase in BP.

• May cause:

  • Severe headache

  • Nausea

  • Vomiting

  • Seizures

  • Confusion

  • Coma

• Results from increased cerebral capillary permeability.

• Can cause:

  • Cerebral edema

  • Impaired cerebral function

• Retinal findings may include:

  • Exudates

  • Hemorrhages

  • Papilledema

---

Emergency Management Immediate Interventions

• Obtain baseline:

  • Vital signs

  • O₂ saturation

• Begin:

  • Continuous BP monitoring

  • ECG monitoring

• Auscultate:

  • Heart sounds

  • Breath sounds

• Insert IV access.

• Obtain baseline blood work.

• Administer O₂ as indicated.

• Administer IV antihypertensives as prescribed.

Ongoing Monitoring

• Monitor:

  • BP

  • HR

  • Level of consciousness

  • Neurologic status

  • Heart and breath sounds

  • ECG/rhythm

  • O₂ saturation

• Titrate medication according to ordered:

  • MAP

  • SBP

• Assess response to treatment.

• Measure urine output hourly.

• Maintain bed rest as indicated.

• Provide reassurance and emotional support.

• Explain procedures and interventions to the patient and caregiver.

---

MAP and BP Reduction MAP Formula

• MAP = (SBP + 2 × DBP) ÷ 3

Treatment Goal

• Initially decrease MAP by no more than 20%–25%, OR

• Lower MAP to approximately 110–115 mm Hg as ordered.

Critical Safety Point

• Do NOT lower BP too quickly.

• Rapid BP reduction can decrease:

  • Cerebral perfusion

  • Coronary perfusion

  • Renal perfusion

• This can cause:

  • Stroke

  • MI

  • Renal failure

---

Special Situations Aortic Dissection

• SBP may need to be lowered rapidly to <100–120 mm Hg, if tolerated.

Acute Ischemic Stroke

• BP management differs depending on:

  • Thrombolytic eligibility

  • Need to maintain cerebral perfusion

• Elevated BP immediately after a stroke may be a compensatory response.

---

IV Medications for Hypertensive Emergency Vasodilators

• Sodium nitroprusside

• Fenoldopam

• Nicardipine

Adrenergic Inhibitors

• Phentolamine

• Labetalol

• Esmolol

Calcium Channel Blocker

• Clevidipine (Cleviprex)

Sodium Nitroprusside

• Highly effective IV medication for hypertensive emergencies.

---

IV Antihypertensive Monitoring

• IV drugs act within seconds to minutes.

• Initially assess BP and HR every 2–3 minutes.

• Use:

  • Arterial line, OR

  • Automated noninvasive BP monitoring

• Titrate medications according to ordered MAP or SBP.

• Monitor ECG for:

  • Dysrhythmias

  • Ischemia

  • MI

• Use extreme caution with:

  • CAD

  • Cerebrovascular disease

• Measure urine output hourly to assess renal perfusion.

• Bed rest may be required.

  • Standing or getting up may cause cerebral ischemia or syncope.

---

Hypertensive Urgency Management

• Usually does not require hospitalization.

• Often treated with oral antihypertensive medications.

• Common oral medications:

  • Captopril

  • Labetalol

  • Clonidine (Catapres)

  • Amlodipine (Norvasc)

• Follow-up is typically needed within 24 hours.

• Determine and address the underlying cause to prevent recurrence.

Nonpharmacologic Measures

• Allow patient to sit quietly for 20–30 minutes.

• Reduce environmental stimuli:

  • Noise

  • Stress

• Encourage the patient to discuss fears and concerns.

• Answer questions and provide reassurance.

• BP may decrease significantly with rest and a calm environment.

---

Drug Alerts Labetalol

• Do NOT stop abruptly.

• Abrupt withdrawal can cause:

  • Angina

  • Heart failure

Clonidine (Catapres)

• Change positions slowly.

• May cause:

  • Orthostatic hypotension

  • Drowsiness

• Avoid hazardous activities if drowsy.

• Do NOT stop abruptly.

  • Can cause rebound hypertension.

heart rhythms

Atrial Fibrillation (A-fib) Pathophysiology

• A-fib is a common cardiac dysrhythmia.

• Occurs when the SA node is not firing appropriately.

• Multiple areas in the atria send electrical impulses.

• Electrical activity becomes:

  • Rapid

  • Chaotic

  • Irregular

• The atria cannot effectively contract.

• Blood is not effectively moved from the atria into the ventricles.

• Results in:

  • Decreased cardiac output

  • Ineffective cardiac contractions

  • Irregular blood flow

• Blood can pool and form blood clots.

• Embolized clots can cause damage to:

  • Brain → stroke

  • Lungs

  • Kidneys

  • Other organs

---

Etiology & Risk Factors

• Diabetes

• Hyperthyroidism

• Obstructive sleep apnea

• Smoking

• Excessive alcohol intake

• Sedentary lifestyle/minimal exercise

• Comorbidities associated with A-fib

• Recovery from cardiac surgery

---

Common Comorbidities

• Hypertension

• Heart failure

• Diabetes mellitus

• Overweight/obesity

• COPD

• Thyroid disease

• Kidney disease

• History of stroke

Major Complications

• Stroke

• Heart failure

• Increased morbidity and mortality

---

Epidemiology

• Most common type of treated cardiac dysrhythmia.

• More common in:

  • Adults older than 65 years

  • Individuals who are overweight or obese

• Causes a significant number of hospitalizations.

---

Impact on Daily Life

• May decrease ability to perform usual activities.

• Possible problems include:

  • Dizziness

  • Palpitations

  • Exercise intolerance

  • Fatigue

• Can decrease overall quality of life.

---

Safety Considerations

• Increased risk for:

  • Stroke

  • Systemic emboli

  • Heart failure

  • Falls due to dizziness/lightheadedness

• Long-term anticoagulant therapy increases the risk for:

  • Spontaneous bleeding

  • Excessive bleeding after injury

---

Clinical Presentation A-fib May Be Asymptomatic

• May only be identified by an irregular pulse.

Symptomatic Findings

• Irregular apical pulse

• Increased heart rate

• Hypotension

• Palpitations

• Chest discomfort

• Shortness of breath:

  • At rest

  • With activity

• Exertional fatigue

• Anxiety

• Dizziness

• Lightheadedness

• Syncope

• Weight gain

• Increased urination

---

Laboratory & Diagnostic Testing Blood Tests

• TSH and thyroxine (T4)

  • Assess for hyperthyroidism.

• Other possible tests:

  • CBC

  • Creatinine

  • Glucose

• Clients taking certain oral anticoagulants, such as warfarin, may require PT/INR monitoring.

---

A-fib ECG Findings ⭐

• Rhythm: Irregular

• P waves:

  • Absent

  • Replaced by indiscernible/chaotic atrial activity

• Ventricular rate may be:

  • 60-100/min: controlled ventricular response

  • 100-200/min: increased ventricular rate

• Rapid ventricular response (RVR): ventricular rate > 100/min

Quick Memory Tip

A-fib = “Irregularly irregular” + no identifiable P waves.

---

Echocardiogram & TEE

• Echocardiogram evaluates:

  • Size of the atria and ventricles

  • Heart valve function

• Transesophageal echocardiogram (TEE):

  • Detects blood clots, especially in the left atrium.

  • May be performed before cardioversion.

---

Nursing Assessment: A-fib Recognize Cues

• Obtain a thorough medical history.

• Ask about:

  • Palpitations

  • Difficulty breathing

  • Dizziness/lightheadedness

  • Ability to complete usual ADLs

• Auscultate the apical pulse for a full 60 seconds.

• Obtain a manual blood pressure when indicated.

• Palpate pulses for a full 60 seconds because the rhythm is irregular.

• Assess for a pulse deficit.

Pulse Deficit

• Compare:

  • Apical pulse

  • Radial pulse

• A-fib may cause the two pulse rates to differ.

• Pulse deficit = apical pulse − radial pulse

• A result of 0 = no pulse deficit.

• A pulse deficit greater than 0 indicates:

  • Inadequate cardiac output

  • Potentially decreased organ perfusion

---

Analyze Cues

• Identify:

  • Irregular ECG rhythm

  • Clinical manifestations of decreased cardiac output

• Assess for signs of embolized clots:

  • Changes in level of consciousness

  • Extremity pain

  • Stroke symptoms

  • Shortness of breath

---

Priority Nursing Goals

• Improve cardiac perfusion.

• Control heart rate.

• Control or restore heart rhythm.

• Prevent:

  • Blood clots

  • Stroke

  • Other embolic complications

---

Treatments for A-fib Major Goals

• Restore and maintain normal sinus rhythm (NSR) when appropriate.

• Control ventricular rate.

• Prevent thromboembolic complications, especially stroke.

---

Medications Antiarrhythmics

• Used to help restore and maintain NSR.

• Monitor for:

  • Bradycardia

  • Prolonged QT interval

Rate-Control Medications

• Beta blockers

• Calcium channel blockers

• Amiodarone

• Digoxin

Effects

• Slow the ventricular rate.

• Decrease conduction through the AV node.

Nursing Consideration

• Assess the apical heart rate before administration.

---

Amiodarone

• Often used when A-fib is more difficult to control.

• Important adverse effects:

  • Pulmonary fibrosis

  • Liver damage

• Obtain baseline:

  • Pulmonary function tests (PFTs)

  • Liver enzyme testing

---

Anticoagulation Therapy Purpose

• Prevent:

  • Blood clot formation

  • Systemic emboli

  • Stroke

Major Nursing Concern

• Bleeding

Bleeding Precautions

• Use a soft-bristled toothbrush.

• Use an electric razor or safety razor.

• Avoid contact sports.

• Avoid high-risk activities that could cause injury.

• Monitor for spontaneous or excessive bleeding.

---

Warfarin (Coumadin) Monitoring

• Requires PT/INR monitoring.

• Frequent monitoring is required initially.

• Once stable, monitoring may occur less frequently.

Important Teaching

• Maintain a consistent intake of vitamin K.

• Do not suddenly increase or decrease vitamin K intake.

• Vitamin K changes can alter warfarin's effectiveness.

High Vitamin K Foods

• Brussels sprouts

• Leafy greens:

  • Beet greens

  • Collard greens

  • Mustard greens

  • Turnip greens

• Kale

• Spinach

Moderate Vitamin K Foods

• Asparagus

• Broccoli

• Cabbage

• Carrots

• Cauliflower

• Celery

• Green beans

• Lettuce

• Mixed vegetables

• Okra

• Peas

• Pickles

Low Vitamin K Foods

• Avocados

• Bananas

• Corn

• Fruit

• Garbanzo beans

• Green/red peppers

• Potatoes

• Tomatoes

Reversal of Warfarin

• Vitamin K

• Fresh frozen plasma (FFP) may also be used depending on the clinical situation.

---

Medications/Substances That Affect Warfarin Can Increase INR → ↑ Bleeding Risk

• Acetaminophen

• Allopurinol

• Many antibiotics

• Cephalosporins

• Doxycycline

• Fluoroquinolones

• Macrolides

• Metronidazole

• Penicillins

• Antifungals

• Some chemotherapy medications

• Testosterone

Can Decrease INR → ↑ Clotting Risk

• Dicloxacillin

• Nafcillin

• Rifampin

• Some antiseizure medications:

  • Carbamazepine

  • Phenobarbital

  • Phenytoin

• Azathioprine

• Ritonavir

• Sucralfate

• St. John's wort

• Vitamin K

---

Direct Oral Anticoagulants (DOACs) Examples

• Apixaban (Eliquis)

• Dabigatran (Pradaxa)

• Rivaroxaban (Xarelto)

Advantages

• Generally do not require routine PT/INR testing.

• Usually do not require frequent dose adjustments.

Important Teaching

• Take exactly as prescribed.

• Do not miss doses.

• Missed doses increase the risk for:

  • Systemic emboli

  • Stroke

Reversal Agents

• Dabigatran → Idarucizumab (Praxbind)

• Apixaban & rivaroxaban → Andexanet alfa

---

Herbal Supplements & Anticoagulants Decrease Anticoagulant Effect → ↑ Clotting Risk

• Coenzyme Q-10

• Ginseng

• Licorice

• St. John's wort

Increase Anticoagulant Effect → ↑ Bleeding Risk

• Danshen

• Evening primrose

• Ginkgo biloba

• Saw palmetto

---

Synchronized Electrical Cardioversion Purpose

• Delivers an electrical shock to reset the heart rhythm to NSR.

Key Points

• Shock is synchronized with the QRS complex/R wave.

• Energy typically ranges from 50-200 joules.

• If unsuccessful:

  • Another attempt may be made at a higher energy level.

• Conscious sedation is used.

Nursing Priorities

• Maintain an open airway.

• Monitor:

  • Respiratory status

  • Vital signs

  • Cardiac rhythm

• Anticoagulation may be used before and continued after cardioversion to reduce clot risk.

---

Catheter Ablation

• May be considered if medications or cardioversion are ineffective.

• An electrophysiology (EP) study is performed to:

  • Map the heart's electrical system

  • Identify abnormal conduction pathways

• A catheter delivers:

  • Radiofrequency energy (heat) OR

  • Cryotherapy (cold)

• Creates scar tissue that blocks abnormal electrical conduction.

---

A-fib Client Education Report Immediately

• Palpitations

• Chest pain

• Irregular heart rate

• Dizziness

• Increased fatigue

• Shortness of breath

Lifestyle Modifications

• Maintain a healthy weight.

• Limit alcohol.

• Stop smoking.

• Manage:

  • Sleep apnea

  • Blood glucose

  • Blood pressure

  • Weight

• Avoid unapproved stimulants:

  • Excess caffeine

  • OTC decongestants

  • Illicit stimulants

  • Herbal supplements

---

---

❤ Atrial Flutter Pathophysiology

• A supraventricular dysrhythmia.

• Less common than A-fib.

• Atria beat at a:

  • Regular

  • Very rapid rate

• Atrial rate: approximately 240-400 bpm.

• Multiple rapid electrical impulses occur in the atria.

• Impulses occur too rapidly for the AV node to process normally.

---

Risk Factors

• Recent MI

• Postoperative cardiac surgery

• Diabetes

• Hyperthyroidism

• Obstructive sleep apnea

• Obesity

• Alcohol use

• Smoking

• Cardiomyopathy

• Pericarditis

---

Common Comorbidities

• Similar to A-fib:

  • Hypertension

  • Heart failure

  • Diabetes

  • Obesity

  • COPD

  • Thyroid disease

  • Kidney disease

  • Stroke

---

Clinical Presentation

• Similar to A-fib:

  • Hypotension

  • Lightheadedness

  • Dizziness

  • Palpitations

  • Chest discomfort

  • Shortness of breath

  • Fatigue

  • Syncope

---

Atrial Flutter ECG Findings ⭐

• Rhythm: Usually regular

• P waves:

  • Absent

  • Replaced by characteristic sawtooth/flutter waves

• Ventricular rate: typically 60-100/min

• Atrial rate: approximately 240-340/min

Quick Memory Tip

Atrial flutter = “Sawtooth waves.”

---

Diagnostic Tests

• Blood tests may evaluate for:

  • Electrolyte abnormalities

  • Diabetes

  • Thyroid disease

  • Kidney disease

  • Liver dysfunction

• Echocardiogram:

  • Evaluates chamber size and function.

• TEE:

  • Detects left atrial blood clots before cardioversion.

---

Nursing Priorities for Atrial Flutter Assessment

• Obtain medical history and determine onset of symptoms.

• Monitor:

  • ECG

  • Vital signs

  • Oxygen saturation

  • Signs of decreased cardiac output

Signs the Client May Not Be Tolerating the Rhythm

• Hypotension

• Decreased cardiac output

• Ventricular rate > 150/min

Priority Goals

• Improve cardiac perfusion.

• Restore normal rhythm.

• Prevent:

  • Blood clots

  • Hypotension

  • Bradycardia

  • Tachycardia-related complications

---

Treatment of Atrial Flutter

• Similar to A-fib:

  • Anticoagulants

  • Antiarrhythmics

  • Beta blockers

  • Calcium channel blockers

  • Amiodarone

  • Digoxin

  • Synchronized cardioversion

  • Catheter ablation

• Client education and lifestyle modifications are similar to A-fib.

---

---

❤ Supraventricular Tachycardia (SVT) Pathophysiology

• SVT is a category of narrow-complex tachycardias.

• Electrical impulses originate above the ventricles/AV node.

• Increased atrial excitability causes a rapid heart rate.

PSVT

• Paroxysmal SVT (PSVT) is also called AV nodal reentrant tachycardia (AVNRT).

• Usually:

  • Starts abruptly

  • Stops suddenly

  • May occur without warning

---

Etiology & Triggers

• Stress

• Smoking

• Alcohol

• Caffeine

• Other stimulants

• Heart disease

• Heart failure

• Wolff-Parkinson-White syndrome

• Pregnancy

• Chronic lung disease

---

Associated Conditions

• Coronary artery disease

• Hypertension

• Diabetes

• A-fib

• Heart failure

• Cardiomyopathy

• Hyperthyroidism

• Renal disease

---

Clinical Presentation Common Manifestations

• Sudden onset of:

  • Palpitations

  • Chest discomfort

  • Dizziness

  • Lightheadedness

  • Shortness of breath

• Possible:

  • Hypotension

  • Syncope

  • Diaphoresis

  • Fatigue

  • Anxiety

Safety Concern

• Dizziness and syncope increase the risk for falls and injury.

---

SVT/PSVT Diagnostic Testing Blood Tests

• No blood test confirms SVT or PSVT.

• Blood work may identify underlying causes:

  • Electrolytes

  • CBC

  • Thyroid function

  • Other chronic medical conditions

---

SVT ECG Findings ⭐

• Rhythm: Regular

• Heart rate: approximately 100-220 bpm

• QRS: Narrow, < 0.12 seconds

• P waves:

  • Often difficult or impossible to identify

• PSVT:

  • Similar narrow QRS

  • Heart rate often around 160 bpm

Quick Memory Tip

SVT = Sudden, Very fast, Thin (narrow) QRS.

---

Nursing Process: SVT/PSVT Recognize Cues

• Obtain a thorough medical history.

• Assess ability to complete usual activities.

• Monitor:

  • ECG

  • Heart rate

  • Blood pressure

  • Peripheral pulses

• Assess for:

  • Diaphoresis

  • Fatigue

  • Syncope

  • Anxiety

  • Hypotension

Priority

• Maintain hemodynamic stability.

• Convert the rhythm back to a normal rhythm when indicated.

• Prevent complications from:

  • Hypoxia

  • Dyspnea

  • Hypotension

---

SVT Treatment 1. Vagal Maneuvers

• May slow conduction through the AV node.

• Can help terminate certain SVTs or reveal the underlying rhythm.

Examples

• Valsalva maneuver

• Forceful coughing

• Gagging

• Carotid massage performed by an appropriate provider

Valsalva Maneuver

• Hold breath for approximately 15 seconds.

• Bear down as if having a bowel movement.

Nursing Care

• Monitor:

  • Vital signs

  • Cardiac rhythm

• Assess before, during, and after the maneuver.

---

2. Adenosine Used When

• Vagal maneuvers are ineffective.

Key Points

• Has a very short duration of action.

• Must be administered rapidly.

• Continuous cardiac monitoring is required.

• Keep:

  • Defibrillator

  • Resuscitation equipment

  • Emergency supplies readily available.

Common Administration

• First dose: 6 mg rapid IV push over 1-3 seconds

• Follow immediately with a rapid normal saline flush.

• If ineffective:

  • 12 mg may be given, followed by a rapid saline flush.

Purpose

• Temporarily slows AV nodal conduction.

• May allow identification of the underlying rhythm.

---

3. Additional Medications

If vagal maneuvers and adenosine are ineffective, medications may include:

• Diltiazem

• Esmolol

• Metoprolol

Goal

• Slow the heart rate.

• Improve cardiac perfusion and hemodynamic stability.

---

⭐ Quick Comparison: A-fib vs. Atrial Flutter vs. SVT

Feature	A-fib	Atrial Flutter	SVT/PSVT
Rhythm	Irregularly irregular	Usually regular	Regular
P waves	Absent/chaotic	Sawtooth flutter waves	Often not visible
Atrial activity	Chaotic	Rapid and organized	Rapid electrical activity
Rate	Ventricular rate variable	Atrial rate 240-340+	Usually 100-220 bpm
QRS	Usually normal/narrow	Usually normal/narrow	Narrow <0.12 sec
Major concern	Stroke/clot formation	Clots & decreased cardiac output	Hemodynamic instability
Key treatment	Rate/rhythm control + anticoagulation	Similar to A-fib	Vagal maneuvers → adenosine

NCLEX High-Yield Takeaways ⭐

• A-fib = irregularly irregular + no distinct P waves + stroke risk.

• A-fib with HR >100 = rapid ventricular response (RVR).

• Atrial flutter = sawtooth waves.

• SVT = regular, rapid, narrow QRS tachycardia.

• For SVT, vagal maneuvers are often attempted first if appropriate.

• If vagal maneuvers are ineffective, adenosine may be used.

• Clients with A-fib/flutter often require anticoagulation to prevent thromboembolic stroke.

• Always monitor for bleeding in clients receiving anticoagulants.

• Warfarin requires consistent vitamin K intake and PT/INR monitoring.

• Adenosine is administered rapidly with continuous cardiac monitoring.

electrical conduction of the heart

P: Atrial depolarization

QRS: Ventricular depolarization

T: Ventricular repolarization

Depolarization: contraction

Repolarization: relaxation

P-P: measures Atrial rate and regularity

R-R: Measures ventricular rate and regularity

electrical conduction of heart pt 2

waveforms

normal PR interval?

0.12-0.20 sec

normal QRS complex?

0.06-0.12 sec

why isnt there a standard QT interval range

it changes with heart rates?

sinus rhythm

Rate: 60-100

rhythm: even, P-P even and R-R even

measurement: PR: 0.2 or less sec (less than or equal to 5 boxes), QRS: 0.12 sec or less (less than or equal to 3 boxes), QT varies

sinus bradycardia

Rate: less than 60

rhythm: even, P-P even and R-R even

measurement: PR: 0.2 or less sec (less than or equal to 5 boxes), QRS: 0.12 sec or less (less than or equal to 3 boxes), QT varies

Not an emergency unless symptomatic

• hypotension, delayed cap refill, confusion, weak pulses

• tx: atropine, external pace

No it's still in sinus because it has AP wave before the QRS complex

Sinus Tachycardia

Rate: greater than 100

rhythm: even, P-P even and R-R even

measurement: PR: 0.2 or less sec (less than or equal to 5 boxes), QRS: 0.12 sec or less (less than or equal to 3 boxes), QT varies

Prolonged tachycardia will cause the heart to fail

• drug is a stimulant, poor cardiac output, stress, secondary tachycardia, hypoperfusion, fever are all causes

sinus dysrhythmia

rate: 60-100

rhythm: not even

measurement: PR: 0.2 or less sec (less than or equal to 5 boxes), QRS: 0.12 sec or less (less than or equal to 3 boxes), QT varies

as client breathes in rate speeds up, as breathes out rate slows down

What does it mean to be symptomatic bradycardia

When being Bradycardic becomes an emergency due to poor profusion

What pharmacology might encourage bradycardia

Negative chronotropes because it slows down the heart rate

Beta blockers and digoxin

What symptoms might the nurse notice if the SA node isn't working

The AV node will take over causing bradycardia

How would the nurse respond if a client was demonstrating bradycardia

Not an emergency unless symptomatic

What are some causes of tachycardia

Anxiety, positive chronotropes, exercise

Chronic tachycardia will fail the heart

premature atrial contraction (PAC)

An over excited AV node Causes an extra cardiac cycle

An early ectopic atrial beat that occurs before the next expected sinus beat

It can be caused by an irritable SA node, stimulant, electrolyte imbalance

rate: underlying is normal, rhythm: irregular due to PAC, and measurement: PR: shortened/ abnormal for PAC, QRS: 0.06-0.12 sec, QT: ~0.40 sec

UNDERLYING RHYTHM IS REGULAR

atrial flutter

rate: atria: 250-350. ventricles: half of atria rate

regular rhythm (fixed block)

measurement: PR and QRS not measurable, QT: ~40 sec

Can be due to electrolytes stress or heart failure

each sawtooth pattern is the SA node firing

Atria contract rapidly in a reentry circuit

atrial fibrillation

rate: tachycardic, A lot of times in RVR

irregularly regular

measurements: hard

Most deadly rhythm we're learning this semester

atria shaking so there is no discernible P wave

There is poor cardiac output causing poor perfusion which can lead to clotting problems and stroke

Can be caused by atrial enlargement or structural heart disease, hypertension, valvular disease, ischemia

An atrial kick is the final atrial contraction that contributes to about 20 to 30%

The goal is to control ventricular rate and rhythm, prevent thromboembolism or stroke and treat the underlying cause (heparin→ start 2nd line) (dont draw labs off of central line with heparin)

• monitor PTT every 6 hours

• before cardioversion, check for clots using TEE, if cardioversion doesnt work → ablasion (cauterize)

• atria is not fully contracting

40 mL/hr

an irregular rhythm can allow for blood stasis and clot formation. An embolus can travel to the brain causing an ischemic stroke and deficits

When is bradycardia an emergency

When the patient is symptomatic or it is causing poor perfusion like hypotension ultimate status acute heart failure shock or syncope

normal sinus

HR: 100

Sinus tachycardia

HR: 140

sinus bradycardia

HR: 40

afib w/ RVR

HR: 150

atrial flutter

HR: 80

atrial flutter

HR: 70

normal sinus

HR: 90

Afib

HR: 50

Sinus bradycardia with STEMI

HR: 50

PAC

HR: 70

hemodynamics

Blood Pressure (BP) = Cardiac Output (CO) × Peripheral Vascular Resistance (PVR)

Systolic BP : The pressure when the ventricles contract forcefully and push blood into circulation.

Diastolic BP : The pressure when the ventricles rest and fill with blood from the atria.

S1 : The "LUB" heart sound.

S2 :The "DUB" heart sound.

S3 :Heart sound that occurs early in diastole.

S4 :Heart sound that occurs before systole (pre-systolic).

preload

volume of blood in the ventricles at the end of diastole

afterload

resistance left ventricle must overcome to circulate blood

increased afterload = increased cardiac workload

why should we care (TEST Q)

HTN is a silent killer

leads to peripheral vascular disease affecting:

• heart: leads to HF, affecting coronary arteries (clamped down)

• brain: stroke, aneurisms

• eyes: retina

• kidneys: decreased GFR, poor perfusion

HTN classification (TEST Q)

Hypertension (HTN): A condition of persistently elevated blood pressure that increases the risk for cardiovascular and end-organ complications.

Normal BP: Systolic <120 mmHg AND diastolic <80 mmHg.

Elevated BP: Systolic 120–129 mmHg AND diastolic <80 mmHg.

Stage 1 Hypertension: Systolic 130–139 mmHg OR diastolic 80–89 mmHg.

Stage 2 Hypertension: Systolic ≥140 mmHg OR diastolic ≥90 mmHg.

Hypertensive Crisis: Systolic >180 mmHg AND/OR diastolic >120 mmHg.

primary/essesntial HTN: no underlying rhyme or reason

secondary HTN: from something

needs to be on 3 separate occasions (recheck in 10 minutes if not sypmtomatic (exercise, PAIN, cuff size, positioning can affect BP)

RISK factors for HTH

mechanisms that result in HTN

Increased Sodium Intake: ↑ Sodium causes fluid retention, ↑ stroke volume, and ↑ blood pressure. and increased preload

RAAS: Activation of the renin-angiotensin-aldosterone system contributes to hypertension. Angiotensin II A potent vasoconstrictor that increases blood pressure. Angiotensin II and Aldosterone ↑ Angiotensin II causes ↑ aldosterone release.

Aldosterone: Promotes sodium and fluid retention and increases potassium excretion. Low Potassium and Hypertension Low plasma K+ contributes to increased vasoconstriction.

Sympathetic Nervous System: ↑ Sympathetic activity causes ↑ vasoconstriction and ↑ peripheral vascular resistance.

labs and diagnostic testing (TEST Q)

Renal: UA/BUN/ and or creatinine- Protein in the urine; may indicate renal target-organ damage. Elevated BUN and Creatinine May indicate renal target-organ damage.

Endocrine Testing for Hypertension: Serum sodium, potassium, calcium, and TSH.

Metabolic Testing for Hypertension: Fasting blood glucose and lipid profile. Hypertension Metabolic Findings ↑ fasting blood glucose (>100), ↑ LDL, ↑ triglycerides, and ↓ HDL.

Echocardiogram Finding in Hypertension Left ventricular hypertrophy may indicate cardiac target-organ damage.

management of HTN

Assess underlying cause and implement lifestyle modifications and medications as needed.

Lifestyle Modifications for Hypertension

Weight management, diet modification (DASH -dietary approash to stop HTN, decrease sodium, lean meatsm decrease saturated fats, whole foods, decrease sugars, increase fruits and veggies)

limiting alcohol

exercise

stress management

Hypertension Medications

Diuretics (know these)

calcium channel blockers

beta blockers

ACE inhibitors

ARBs

central alpha agonists

diet considerations

DASH Diet Dietary approach used to help manage blood pressure.

Mediterranean Diet A dietary approach recommended as a consideration for hypertension management. (fruits, veggies,, nuts)

Low-Sodium Diet Dietary approach that limits sodium intake to help manage blood pressure.