Exam #2

What is blood pressure?

The force exerted by the blood against the walls of the blood vessel. This maintains perfusion during activity and rest.

Describe the mechanisms that maintain BP

Maintenance of BP and tissue perfusion requires both systemic factors and local peripheral vascular effects. Primarily a function of CO and SVR!

What is HTN?

Increased BP beyond what may be considered “normal” (healthy, safe, non-problematic)

What is a normal BP?

120/80 or less

Systolic BP

Heart contracting - blood exerting pressure on vessels

Diastolic BP

Heart relaxing - How much pressure in the system during relaxation

What is considered elevated BP?

Systolic 120-129

Diastolic: more than 80

What BP is considered HTN?

Systolic: 130 or higher 

Diastolic: 80 or higher 

Blood pressure formula

BP = CO x systemic vascular resistance

What is cardiac output (CO)? What affects it?

CO = SV x HR
Total blood flow through the systemic or pulmonary circulation (out of the heart) per minute

Effects:

Cardiac system

• heart rate, contractility, conductivity

Renal fluid volume control

• RAAS

  • Renin (angiotensin-aldosterone system)

    • retains water, increases fluid volume (ultimately increases BP)

    • Converts angiotensin 1 to angiotensin 2

    • A 2 increases BP (vasoconstrictor and stimulates adrenal cortex to secrete aldosterone)

• Natriuretic peptides

• Controls sodium excretion and extracellular fluid volume

What is systemic vascular resistance?

The pressure of veins and arteries. The force opposing the movement of blood within the blood within the blood vessels. Think of cholesterol and how that gunk will turn from mushy to hardened. Greater resistance equals increased BP.

What affects the systemic vascular resistance? (SVR)

• sympathetic nervous system

  • alpha 1 and alpha 2 adrenergic receptors (vasoconstrictors)

    • Increased SNS increases HR and contractility producing the vasoconstriction and promotes the release of renin (increase BP)

  • beta 2 adrenergic receptors (vasodilator)

    • Baroreceptors in carotid arteries and aorta sense BP changes and send signals to brainstem that then sends signals to brainstem that then sends message through neurons to excite or inhibit efferent nerves that innervate cardiac and smooth muscle cells

• neurohormonal

  • vasoconstrictors (angiotensin & norepinephrine)

Increased BP: Inhibition of the SNS results in decreased HR, force of contraction, and vasodilation in peripheral arterioles to decrease BP

Decreased BP: Activation of the SNS results in constriction of the peripheral arterioles, increased HR and contractility to increase BP

Causes of secondary HTN

• Cirrhosis

• Coarctation or congenital narrowing of the aorta

• Drug related (estrogen replacement therapy, oral contraceptives, corticosteroids, non steroidal anti-inflammatory drugs, sympathetic stimulants such as cocaine)

• Endocrine disorders

  • Cushing syndrome, thyroid disease

• Neurologic disorders

  • Brain tumors

• Pregnancy

• Renal disease

• Sleep apnea

Risk factors of HTN

Age, alcohol consumption, tobacco use, diabetes mellitus, elevated serum lipids, excess dietary sodium, gender, family hx, obesity, ethnicity, sedentary lifestyle, socioeconomic status, stress

Manifestations of HTN

Fatigue, reduced activity tolerance, dizziness, palpitations/angina, dyspnea

Complications of HTN

Target organ diseases occur most frequently in:

Heart - CAD, LVH, HF
Brain - cerebrovascular disease, increased risk of CVA
Kidney - CKD
Eyes - retinal damage

Treatment of HTN

Overall goals

• Control BP

• Reduce

Primary (essential or idiopathic) HTN

Elevated BP without an identified cause

Most common! 90-95% of HTN cases

Secondary HTN

Elevated BP with a specific cause! 5-10% of adult cases. Clinical findings will relate to an underlying cause.

HTN diagnostic studies

• Bilateral BP measurement (remember, highest in morning and lowest at night) Use arm with highest reading!

• UA, creatinine clearance

• Serum electrolytes, glucose (uncontrolled diabetes)

• BUN and serum creatinine

• Serum lipid profile

• EKG

• Echocardiogram

Effects of HTN on the heart

HTN increases the workload on the heart inducing structural and functional changes in the myocardium. These changes include hypertrophy of the left ventricle which can lead to HF. Heart attacks, chest pain, and arrhythmias can occur because of changes to blood vessels.

Effects of HTN on the blood vessels

Thickens the walls of blood vessels and makes them less elastic. Alongside cholesterol deposits in the blood vessels, the risk of a heart attack is increased because there is trouble supplying blood to the heart. Chest pain (angina) and arrhythmias can occur as well. Blood flow is limited throughout the body in general! Kidneys are damaged and unable to work! Kidney failure can occur.

Effects of HTN on the kidneys

HBP can damage the blood vessels leading to the kidneys. Kidney scarring can occur because the tiny blood vessels within the kidneys become scarred and are unable to effectively filter fluid and waste from the blood. Glomerulosclerosis can lead to kidney failure! Damaged blood vessels prevent the kidneys from effectively filtering waste from the blood, allowing dangerous levels of fluid and waste to collect. Treatment may include dialysis or transplant.

List the major classes of antihypertensives

• B-adrenergic blockers (beta blockers)

• Angiotensin Converting Enzyme (ACE) inhibitors

• Angiotensin II receptor blockers (ARBs)

• Calcium channel blockers

• Diuretics

• Direct vasodilator

Mechanism of action, side effects, nursing considerations: B-adrenergic blockers (beta blockers)

-sins & -lols

Action

• decrease peripheral resistance of blood vessels by unknown mechanism

• heart: block beta 1 receptors which decreases HR and contractility, decreases CO, and suppresses reflex tachycardia

• kidney: block renal beta receptors which decreased angiotensin I related vasoconstriction as well as aldosterone related fluid retention

Side effects

• Bradycardia

• SOB

• Edema

Nursing considerations

• monitor HR (report if less than 60bpm)

• monitor for signs of HF (SOB, peripheral edema of extremities, night cough) and report

• Tapering if discontinued

Examples

• Metoprolol (take with food at same time every day)

• Atenolol (before meals - AC, or bedtime)

• Propanolol

Mechanism of action, side effects, nursing considerations: Angiotensin Converting Enzyme (ACE) inhibitors

-ils

Action

• Blocks production of angiotensin II (from angiotensin I) causing vasodilation as well as urinary excretion of sodium/water and retention of potassium

Side effects

• Dry, non-productive cough due to increase in bradykinin

• hypotension

• rash

• metallic taste in mouth

• hyperkalemia, neutropenia (decrease WBC, increased risk of infection)

Nursing considerations

• Start at low dose and gradually increase

• Diuretics may be temporarily stopped

• Monitor BP

• Monitor and report dry cough

• Monitor and report for angioedema

• monitor potassium levels

• monitor WBC count

Examples

• lisinopril, fosinopril

Mechanism of action, side effects, nursing considerations: Angiotensin II receptor blockers (ARBs)

-ans

Action

• Blocks angiotensin II receptors which causes angiotensin II to be unable to bind to those receptor sites, resulting in: arteriolar vasodilation, urinary excretion of sodium and water, and retention of potassium

• Less able to protect patients from acute cardiovascular events (myocardial infarction) making them 2nd choice after ACE inhibitors for treatment of hypertension

Side effects

• angioedema

• dizziness

• hypotension

• headache and insomnia

Nursing considerations

• Monitor BP

• prepare to treat angioedema with IV epi

• monitor and report CNS effects

• Oral only

• With or without food

Examples

• Losartan

• valsartan (Diovan)

• irbesartan (Avapro)

• candesartan (Atacand)

Mechanism of action, side effects, nursing considerations: Calcium channel blockers

-ines

Action

• Bock calcium channels in vascular smooth muscle cells of peripheral arterioles and minimally block calcium channels in cardiac arteries 

• This results in vasodilation (then lowered BP)

Side effects

• Reflex tachycardia

  • Can cause increased anginal pain in clients with angina 

  • Mainly with fast-acting tabs 

• Headache, lightheadedness, dizziness, facial flushing, perception of heat, peripheral edema, arrhythmias 

• Not common: Gingival hyperplasia (overgowth of gum tissue and easy-bleeding gums) 

Nursing considerations

• Monitor HR, lightheadedness/dizziness, assist with ambulation 

• Monitor for development of peripheral edema (report, diuretic may be needed) 

• Monitor BP 

• Regular dental checkups 

Examples

• Nifedipine, amlodipine

Mechanism of action, side effects, nursing considerations: Diuretics

Action

• remove water and electrolytes from the body by increasing urination

Side effects

• headaches

• dizziness, lightheadedness

• increased sensitivity to light

• muscle weakness or cramping

• electrolyte abnormalities

• severe dehydration

• irregular heart rate

Nursing considerations

• Monitor weight, intake, output, serum electrolyte levels

Examples

• spironolactone/ hydrochlorothiazide

• triamterene/ hydrochlorothiazide

Where do thiazide diuretics affect?

Distal tube of henle 

Mechanism of action, side effects, nursing considerations: Direct vasodilator

Action

• Open/dilate blood vessels and prevent the muscles of arteries and veins from tightening and the walls from narrowing

Side effects

• tachycardia

• palpitations

• Edema

• Nausea/vomiting

• headache

• excessive hair growth

• joint pain

• chest pain

Nursing considerations

• Remain flat for 1 hour after admin

examples

• Hydralazine

• Minoxidil

• nitroglycerin

What is coronary artery disease (CAD)?

A type of blood vessel disorder in the general category of atherosclerosis. Soft deposits of fat accumulate in the arteries and harden with age. This can occur in ANY artery in the body.

What are atheromas?

Fatty deposits

Pathophysiology of CAD

• Atherosclerosis (major cause)

  • Characterized by a focal deposit of cholesterol and lipid, primarily within the intimal wall of the artery

  • Endothelial lining becomes altered as a result of inflammation and injury \

• Collateral circulation

  • Normally, some arterial anastomoses exist within the coronary circulation

Risk factors of CAD

• Non-modifiable 

  • Age 

  • Sex

  • Ethnicity 

  • Family Hx 

  • Genetic predisposition 

• Modifiable 

  • Elevated serum lipids 

  • Hypertension 

  • Tobacco/substance use 

  • Physical inactivity 

  • Obesity 

  • Diabetes

  • Metabolic syndrome (r/t insulin resistance) 

  • Psychological states 

  • Homocysteine level 

Manifestations of CAD

• dizziness/lightheadedness

• fatigue

• SOB

• chest discomfort

• chest pain

• Chronic stable angina (nitroglycerin is the treatment)

• acute coronary syndrome

CAD diagnostics

• ECG

• Blood pressure

• Cardiac catheterization

  • Shows presence of atherosclerotic lesions

Nursing management/Collaborative care/Treatment of CAD

• BP meds

• Nitrates

• Lipid lowering

• Oxygen

Complications of CAD

• Chest pain (angina)

• Heart attack

• Heart failure

• Arrhythmias

Clinical manifestations of CAD: Chronic Stable Angina 

• Reversible! The O2 demain is greater than the O2 supply. This can be caused by increase in demand (ex - exertion) or decrease in supply (ex - hematologic or respiratory pathways)

• Chest pain, usually lasts 3-5 min and will. subside when the precipitating factor is relieved. ECG reveals ST-segment depression and/or T wave inversion

• Silent ischemia! Can occur in the absence of any subjective symptoms. Associated with diabetic neuropathy and is confirmed by the ECG

Treatment of Chronic Stable Angina

A - antiplatelet/anticoagulant therapy

B - Beta blocker, BP control

C - Cigarette smoking cessation, cholesterol (lipid) management, calcium channel blockers, cardiac rehabilitation

D - diet (weight management), Diabetes management, Depression screening

E - Education, Exercise

F - flu vaccine

NITRO

Clinical manifestations of CAD: Acute Coronary Syndrome 

• Unstable angina (UA)

• Non-ST segmenet elevation myocardial infarction (NSTEMI)

• ST-segment elevation MI (STEMI)

Signs and symptoms of unstable angina - why is it a medical emergnecy?

Chest discomfort or pain caused by an insufficient flow of blood and oxygen to the heart!

• Change in usual pattern of stable angina 

• New in onset 

• Occurs at rest 

• Has a worsening pattern 

• UA is unpredictable and represents a medical emergency because the unstable plaque can rupture into thrombus (can be dislodged and lead to STEMI or NSTEMI)

Signs and symptoms of chronic stable angina

Stable angina (angina pectoris) is a type of chest pain that happens when your heart muscle needs more oxygen. It occurs intermittently, over a long period of time, with a similar pattern of onset, duration, and intensity of symptoms

Can happen when you are exercising or when it is cold outside

Temporary chest pain BUT can lead to acute coronary syndrome

• Chest pain that feels like pressure or indigestion.

• Pain that radiates to your left shoulder or down your left arm

• SOB

• Dizziness.

• Nausea.

• Exhaustion

Relieved with nitroglycerin

What is acute coronary syndrome (ACS)?

a term for a group of conditions that suddenly stop or severely reduce blood from flowing to the heart muscle. When blood cannot flow to the heart muscle, the heart muscle can become damaged

Non-ST-elevation myocardial infarction (NSTEMI), ST-elevation MI (STEMI), and unstable angina are the three traditional types of ACS.

Pathophysiology of ACS

develops when ischemia is prolonged and not immediately reversible!

Deterioration of once stable plague —> rupture —> platelet aggregation —> thrombus

Results in partial occlusion of coronary artery: UA or NSTEMI
Total occlusion of coronary artery: STEMI

Manifestations of ACS

Unstable angina

Myocardial infarction

Nursing/collaborative care/Treatment/interventions for ACS

• ECG monitoring

• IV access

• O2 therapy

• Medications (MONA)

  • Morphine sulfate

    • Vasodilator and pain relief

    • Reduces anxiety

    • Decreases contractility, BP, HR

  • Oxygen

  • Nitroglycerin

    • Reduces pain

    • Improves coronary blood flow

  • Aspirin

    • anti-platelet

  • Antidysrhythmics

    • Prevent them

  • Lipid lowering drugs

    • Statins

• Rest and comfort to balance rest and activity while beginning cardiac rehab

• ambulatory and home care

  • Patient and caregiver teaching

  • Physical exercise

Diagnostic studies for ACS

• cardiac biomarkers

• EKG

• Coronary angiography

  • Opens up occluded artery and limit infarction size

What is a myocardial infarction?

The result of sustained ischemia! Causes irreversible myocardial cell death and eventual necrosis of myocardium. The degree of altered function depends on area of the heart and size. Most involve the LV.

Signs/symptoms of MI

• Cardiovascular

  • Increased HR, BP (then BP lowers secondary to decreased CO)

  • Crackles as a result of LV dysfunction

  • JVD as result of RV

  • Abnormal heart sounds (S3 or S4), new onset murmurs

• Nausea and vomiting

• Fever

  • systemic inflammatory process caused by cell death

Myocardial infarction (MI) - healing process

Within 24 hours, leukocytes infiltrate the area of cell death.

Enzymes are released from the dead cardiac cells (important indicators of MI).

Proteolytic enzymes of neutrophils and macrophages remove all necrotic tissue by the second or third day.

Development of collateral circulation improves areas of poor perfusion.

Necrotic zone identifiable by ECG changes and nuclear scanning

10 to 14 days after MI, scar tissue is still weak and vulnerable to stress.

By 6 weeks after MI, scar tissue has replaced necrotic tissue.

Area is said to be healed, but less compliant.

Ventricular remodeling

Normal myocardium will hypertrophy and dilate in an attempt to compensate for the infarcted muscle.

Complications of MI

• Dysrhythmias

• Heart failure

• Cardiogenic shock

• Acute pericarditis

What is the treatment of choice for a confirmed MI?

Emergent PCI - non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup, a condition known as atherosclerosis.

STEMI - What is it? Causes? Signs and symptoms?

ST-elevated MI - FULLY occluded artery

• Caused by chest pain, pallor, SNS stimulation, N/V, fever, SOB

• ST elevation on EKG

• Cell death

• Emergent and must be treated within 90 minutes with PCI or thrombolytic therapy

NSTEMI - What is it? Causes?Signs and symptoms>?

Non-ST elevated MI - PARTIALLY occluded artery

• Caused from deterioration of stable plaque that ruptures and forms a thrombi —> MI

• Elevated troponin

• St depression on ECG or T wave inversion

• Cell death

• Not emergent but must go to cath lab within 12-72 hours

What is sudden cardiac death?

Unexpected death from cardiac causes! Rapid CPR, defibrillation with AED, and early advanced cardiac life support increase survival. There is abrupt disruption in electrical function of cardiac muscle, resulting in acute loss of CO and cerebral blood flow. Death is usually within one hour of onset of acute symptoms (angina, palpitations)

Sudden cardiac death - etiology and pathophysiology + causes + risk factors

• Most SCD caused by ventricular dysrhythmias (e.g.,ventricular tachycardia), i.e., an electrical problem

• SCD occurs less commonly as a result of LV outflow obstruction (e.g., aortic stenosis).

• Primary risk factors

  • Left ventricular dysfunction (EF 30%)

  • Ventricular dysrhythmias following MI

Depolarization of the cardiac muscle causes a contraction. Immediately following depolarization, the heart enters a(n) ___________ during which it cannot be stimulated, prior to a(n) ___________ during which a significantly strong impulse may excite it. With repolarization, the heart muscle enters a period of ___________.

• absolute refractory phase (it can't beat again)

• relative refractory period (can be if the stimulus is great enough)

• full excitability 

List the 3 muscular layers

• endocardium (inner)

• Myocardium (muscle layer)

• Epicardium (outer layer)

Pericardium

sac that surrounds the heart

The left ventricular wall is 2-3x thicker than the right ventricular wall - why?

This is because the left ventricle pumps oxygenated blood round the entire body while the right ventricle only pumps blood to the lungs which is a much shorter distance.

Explain the circulation of blood throughout the heart

• Deoxygenated blood enters RA (from SVC and IVC)

• Tricuspid valve (AV valve)

• Right ventricle

• Pulmonary semilunar valve

• pulmonary artery

• lungs (gas exchange in the capillaries)

• Pulmonary veins

• left atrium (oxygenated blood from lungs)

• Bicuspid (mitral) valve (AV valve)

• Left ventricle

• aortic semilunar valve

• aorta

What does lub and dub stand for?

Lub - associated with closure of the tricuspid and mitral valves

Dub - associated with the closure of the aortic and semilunar valves

What is mean arterial pressure? How do you calculate it?

Average pressure within the arterial system that is felt by the organs in the body

SBP + 2DBP / 3

Discuss electrical conduction in the normal heart (pathway of the action potential)

• SA node

• Internodal pathways

• AV node

• Bundle of His

• Left and right bundle branches

• Purkinje fibers

What are the three natriuretic peptides?

1. atrial natriuretic peptide (ANP) from the atrium

2. B-type natriuretic peptide (BNP) from the ventricles

   1. BNP is the marker of choice for distinguishing a cardiac or respiratory cause of dyspnea

3. C-type natriuretic peptide from the endothelial and renal epithelial cells

Automaticity

Ability to initiate an impulse spontaneously and continuously

Excitability

ability to be electrical stimulated

Conductivity

Ability to transmit an impulse along a membrane in an orderly manner

Contractility

Ability to respond mechanically to an impulse

P wave

• Atrial depolarization (contraction)

• Firing of the SA nod

• Should be upright

• Normal duration: 0.06-0.12 seconds

PR interval

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

• Represents time taken for impulse to spread through the atria, AV node and bundle of His , bundle branches, and purkinje fibers, to a point immediately before ventricular contraction

• Normal duration: 0.12-0.20 sec

• Duration could vary due to disturbance in conduction usually in AV node, bundle of His, or bundle branches but can be in atria as well

QRS interval

• Measured from beginning to end of QRS complex

• Represents time taken for depolarization of ventricles (systole)

• Duration: <0.12 sec

• Variation could be due to disturbance in conduction in bundle branches or in ventricles

Q wave

• First negative (downward) deflection after the P wave, short and narrow, not present in several leads

• Duration: <0.03 seconds

• MI may result in development of a pathologic Q wave that is wide (greater than or equal to 0.03 seconds) and deep (greater than or equal to 25% of the height of the R wave)

T wave

• Represents time for ventricular repolarization

• Should be upright

• Duration: 0.16 sec

• Disturbances (ex - tall, peaked, inverted) usually caused by electrolyte imbalances, ischemia, or infarction

ST segment

• Measured from the S wave of the QRS complex to the beginning of the T wave

• Represents the time between ventricular depolarization and repolarization (diastole)

• Should be isoelectric (flat)

• Duration: 0.12 seconds

• Disturbances (like elevation, depression) usually caused by ischemia, injury, or infarction

QT interval

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

• Represents time taken for entire electrical depolarization and repolarization of the ventricles

• normal adult women have slightly longer QT intervals than men

• Duration: 0.34-0.43 seconds

• Disturbances usually affecting repolarization more than depolarization and caused by drugs, electrolyte imbalances, and changes in heart rate

How to determine HR from a 6 second strip

• 1500 method (most accurate)

  • 1500/# of small boxes between R waves

• 300 method

  • 300/# of large boxes between R waves

• Lazy way

  • Count the number of QRS complexes in a strip and multiply by 10

Identify the rhythm! Discuss nursing and collaborative care

Normal sinus rhythm

• Heart rate is 60-100 bpm 

• P wave appears normal and precedes each QRS (1:1 ratio)

• PR interval is 0.12-0.20 seconds 

• QRS complex is 0.06-0.10 seconds 

• P waves and QRS complexes are evenly spaced

Identify the rhythm! Discuss nursing and collaborative care

Sinus bradycardia

• 50 bpm

• P wave, PR interval, and QRS complex are same as NSR

• May or may not represent a problem

  • Clinical assessment

  • Cap refill

  • Hypotension

  • Decreased perfusion

  • Altered LOS

Identify the rhythm! Discuss nursing and collaborative care

Sinus tachycardia

• 130 bpm

• Heart rate >100 bpm 

• P wave is normal but may merge with T wave at very fast rates 

• PR interval and QRS complex are same as NSR 

• QT interval narrows with increasing heart rate 

• May or may not present a problem 

• During exercise, tachycardia may be benign 

• Ominous sign - decreased cardiac output and hypotension due to blood loss, or conditions such as sepsis

• If we decided it was a problem:

  • Depends on the problem!

  • Fever: antipyretic (ibuprofen, tylenol)

  • Chest pain: Nitro, oxygen, aspirin 

  • Blood loss: Blood transfusion, stop the bleeding

Identify the rhythm! Discuss nursing and collaborative care

Ventricular tachycardia (VT)

• Heart rate is usually 100-250 bpm 

• P wave is absent, PR interval is not measurable, and QRS complex is typically wide > 0.10 seconds and unusual in appearance 

• Life threatening and can develop into VF

• Stable (pulse) unstable (pulseless)

• if pulseless: CPR and rapid defibrillation

• If unconscious and pulse is present, maximize oxygenation and prepare for cardioversion with synchronized defibrillation.

Identify the rhythm! Discuss nursing and collaborative care

Atrial fibrillation (AF or Afib)

• Rhythm appears irregular 

• Atrial rate is variable and may be very fast (> 350 bom), but ventricular rate may be slow, normal, or fast 

• P wave features are absent - erratic waves are present 

• PR interval is absent 

• QRS complex is normal or may be widened due to conduction delays 

• May represent a problem with the SA node and/or conduction across the atria and/or the presence of multiple pacemaker cells. Asynchronous contraction of the atria decreased “atrial kick” by inhibiting complete contraction and by stimulating rapid ventricular repolarization (“rapid ventricular response” or RVR) which decreases passive filling time. Inadequate ventricular filling results in decreased cardiac output

• Patients should be assessed for hypotension, perfusion, and use of anticoagulant medication. New onset Afib may be converted chemically or electrically once anticoagulation is established or maintained for 24 hours 

• What do you do?

  • Ask if they have had it 

  • Ask if they are on a blood thinner (they should be) 

• Usually occurs because of poor cardiac health (typically seen in older patients)

• Treatment: calcium channel blockers, beta blockers and digoxin, amiodarone and ibutilide, electrical cardioversion, anticoagulants

Identify the rhythm! Discuss nursing and collaborative care

Atrial flutter (A-flutter)

• Atrial rate is rapid (250-350 bpm) but ventricular rate is slower

• Rhythm appears more regular than A-fib 

• P wave and PR interval are not observable 

• “Sawtooth” flutter waves are present 

• QRS complex is typically normal (0.06-0.10 seconds)

• Can be asymptomatic or symptomatic (decreased exercise, tolerance, palpitations, lightheadedness, fatigue, SOB) 

• Can lead to cardiomyopathy and heart failure because of high ventricular rates and loss of atrial kick (P wave) decrease CO

• Treatment: electrical cardioversion, beta blockers, calcium channel blockers, and anticoagulants  

Identify the rhythm! Discuss nursing and collaborative care

Supraventricular tachycardia (SVT)

• Heart rate is fast (150-250)

• P wave is often merged with T wave 

• PR interval is normal (0.12) but can be difficult to measure 

• QRS complex will typically be normal (0.10 sec) 

• SVT may be asymptomatic but may also present with anxiety, palpitations, chest pain, lightheadedness, syncope, SOB upon exertion and/or exercise intolerance. Intermittent SVT without provoking factors (medications, caffeine, alcohol, nicotine, or stress) referred to as pSVT, is more common among women 

• Cardioversion of SVT can be achieved biomechanically (ex - carotid massage, vagal or valsalva maneuver), chemically (adenosine), or electrically (synchronized defibrillation). Hemodynamic instability (hypotension, hypoxia, SOB, chest pain, shock, evidence of poor end-organ perfusion, or altered mental status) should be treated quickly without synchronized cardioversion. Like defibrillation, adenosine disrupts myocardial conduction but has a short half life (less than 6 seconds) so must be administered rapidly. Vagal maneuvers may be accompanied by encouraging an alert patient to increase intrathoracic pressure against a closed glottis (ex - bear down) 

Valsalva maneuver

• Used for supraventricular tachycardia (SVT)

• Exhale against obstruction 

• Hold breath and “bear down”

• Produce emotional shock 

• Peds

  • Infants - ice water to face 

  • Blow through a 5cc syringe 

Adenosine function

• SVT

• Slows conduction through AV node 

• Rapid IV push followed by 20 cc saline flush 

• Pre administration procedure 

  • Oxygenate patient (NC, etc), have RT present 

  • Ensure continuous cardiac monitoring 

  • Attach defibrillator pads or have paddles at ready 

  • Patient teaching - explain that the drug may slow or stop the heart and can produce anxiety/panic and may lead to loss of consciousness 

  • Half life is 10 seconds - this means the heart will start up (hopefully)

Identify the rhythm! Discuss nursing and collaborative care

ventricular fibrillation

• Doesn’t really have any characteristic waveforms

  • Heart rhythm is irregularly irregular and heart rate is not measurable 

  • P wave is absent, PR interval is not measurable, and QRS complexes are absent 

  • VF is incompatible with a palpable pulse because the ventricles are quivering, not contracting. 

  • Assess patient for LOC, if unconscious initiate CPR and prepare for immediate unsynchronized defibrillation. If conscious check your monitor 

Identify the rhythm! Discuss nursing and collaborative care

asystole

• No discernable wave forms 

• Change monitor leads to confirm in a second lead

• Assess LOC and pulse, if either exists check monitor 

• Beware of agonal heart beats (erratic, non-sustainable electrical impulses that are residual to life. Also note that implanted pacemakers can produce electrical waveforms despite death of patient) 

• Many think to defibrillate the patient but NO! Why stop a heart when its already stopped? You want to start compressions to mimic the heart

Identify! what precipitates them, and their medical and nursing management and treatment

Torsades de pointe

• Rhythm appears to undulate (big and then small) and heart rate is not measurable 

• Cause: Low magnesium 

• P waves are absent, PR interval is not measurable, and QRS complexes appear abnormal 

• Indicates irritability of the myocardium

• Assess patient for LOC and pulse. If no pulse is present, initiate CPR and prepare for unsynchronized defibrillation. If unconscious with pulse, prepare for cardioversion with synchronized defibrillation and assess serum magnesium. If conscious with pulse, maximize oxygenation and, administer iV magnesium, and prepare for cardioversion with synchronized defibrillation with conscious sedation and/or pain management 

Identify what type of heart block is shown! Discuss symptoms

1st degree heart block

• Heart rate is unaffected, typically 60-100 

• P wave present, PR interval is prolonged (0.21-0.48 seconds usually - should be less than 0.2 seconds), QRS is normal 

• Typically asymptomatic, assess patient for potential cause

  • Ischemia/myocardial infarction 

  • Medications 

  • Athletic predisposition 

• Typically seen in well conditioned athletes 

• Can or can’t be a problem - ask about symptoms 

Identify what type of heart block is shown! Discuss symptoms

2nd degree heart block - Mobitz type 1 (Wenckebach)

After the 4th, there us a pause 

• PR interval gradually increases until a QRS does not follow a P wave (drops) after which the cycle repeats 

• Typically asymptomatic if heart rate is adequate 

Identify what type of heart block is shown! Discuss symptoms

2nd degree heart block - Mobitz type 2 

• P waves are normal and consistent, PR is constant if QRS is present, but some P waves do not initiate a QRS. QRS may be normal or wide depending upon when conduction is blocked

• More serious than Mobitz type 1, it may progress to 3rd degree block without warning. May be symptomatic (angina, SOB, lethargy) if ventricular rate is slow 

• Anticipate the need for transcutaneous pacing and the placement of an internal pacemaker

Identify what type of heart block is shown! Discuss symptoms

3rd degree heart block

• P waves are present and consistent 

• PR interval is inconsistent 

• QRS is present and consistent 

• No relationship between P and QRS. Atria and ventricles beat independently and at different rates 

• Symptomatic if slow ventricular rate affects cardiac output 

• Anticipate the emergent need for transcutaneous pacing and eventual placement of an internal pacemaker 

What is pacing?

• Turn AED/defibrillator to pacer mode 

• Two controls: rate & amplitude 

  • How fast the pacer stimulates beats (70 bpm ex) 

  • How much energy is needed to achieve ventricular response 

• Two concepts 

  • Electrical capture = pacer spike followed by a QRS 

  • Mechanical capture = pacer spike and QRS and a palpable pulse 

• For transcutaneous pacing 

  • Address pain control and/or LOC

What is pulseless electrical activity (PEA)? What causes it?

• A condition in which an organized rhythm, is seen on the monitor, but the patient is unconscious and has no pulse

• Pulseless VT is a form 

• VF does not represent PEA either because by definition is not an organized rhythm, and the patient is presumed pulseless 

• Used to be called Electrical-mechanical dissociation 

  • A name that aptly describes what is going on 

  • The electrical system of the heart is functioning but is not stimulating the mechanical system to function, they are not associated, and therefore myocardial contraction does not occur 

• Without immediate treatment, it is lethal! 

• Causes: Hs & Ts 

  • Hypovolemia (not enough blood makes it hard for the heart to contract

  • Hypothermia (too cold for too long) or hyperthermia

  • hypo/hyper kalemia 

  • Hydrogen ions (acidotic)

  • Cardiac tamponade (trauma to chest, something is pushing on pericardial sac and it can’t beat or contract because it is being squished)  (bleeding in pericardial sac) 

  • Pneumothorax (collapsed lung) (can be due to broken rib that punctures the lung)

What is heart failure?

• The heart muscle is unable to deliver adequate CO to meet the body’s metabolic needs due to inadequate ventricular filling or ventricular ejection 

• Most common reason for hospitalization of adults >65 years old

Primary risk factors of HF

• CAD

• HTN

• Valvular & congenital disorders 

• Myocarditis 

• Advanced age 

• Diabetes 

• Tobacco use 

• Vascular disease 

Systolic failure (HFrEF) - What is it? What is it caused by?

**heart failure with reduced ejection fraction **

• Impaired ability of left ventricle to pump sufficient volume with each contraction

• Distinguishing Characteristic: Decreased left ventricular ejection fraction (EF) less than 40% (normal is 55–65%)

• Caused by

  • Impaired contractile function (e.g.,MI - ischemic, injured, necrotic)

  • Increased afterload (e.g., hypertension)

  • Cardiomyopathy

  • Mechanical abnormalities (e.g., valve disease)