Cardiac

NUR 211 Cardiac/Perfusion Exam ReviewMain concept: perfusion

Perfusion is the delivery of oxygenated blood to the tissues.

Signs of decreased perfusion can include:

• Chest pain

• Altered mental status

• Hypotension

• Tachycardia

• Cool, pale or clammy skin

• Weak peripheral pulses

• Delayed capillary refill

• Decreased urine output

• Fatigue or activity intolerance

• Dizziness or syncope

Cardiac output equals:

Cardiac output = heart rate × stroke volume

When cardiac output falls, the brain, kidneys, skin and other organs receive less blood.

Important assessment areas:

• Vital signs

• Oxygen saturation

• Level of consciousness

• Skin color, temperature and moisture

• Peripheral pulses and capillary refill

• Urine output

• Edema and JVD

• Lung sounds

• Heart sounds

• Chest-pain assessment

• ECG or telemetry findings

Important heart sounds:

• S3: commonly associated with volume overload and heart failure

• S4: associated with a stiff or noncompliant ventricle

• Murmur: turbulent blood flow, often from valve disease

• Pericardial friction rub: inflammation of the pericardium

Chapter 24: Coronary Vascular DisordersAtherosclerosis versus arteriosclerosisAtherosclerosis

Abnormal accumulation of lipids and fibrous tissue inside an arterial wall and lumen.

The plaque narrows the coronary artery and reduces blood flow to the myocardium.

If a plaque ruptures:

1. The plaque contents are exposed.

2. Platelets become activated.

3. A thrombus forms.

4. Coronary blood flow decreases or stops.

5. The patient can develop unstable angina, NSTEMI or STEMI.

Arteriosclerosis

Thickening and loss of elasticity of the arteries.

Atherosclerosis is a particular type of arteriosclerosis involving plaque formation.

CAD risk factorsModifiable risk factors

• Smoking or tobacco use

• Hypertension

• Hyperlipidemia

• Diabetes

• Obesity

• Sedentary lifestyle

• Poor diet

• Uncontrolled stress

Nonmodifiable risk factors

• Age

• Family history

• Genetics

• Sex-related risk patterns

Metabolic syndrome

Metabolic syndrome is a cluster of conditions that increases cardiovascular risk:

• Hypertension

• Hyperglycemia

• Excess abdominal fat

• Abnormal cholesterol or triglycerides

Angina Pectoris

Angina occurs when myocardial oxygen demand exceeds the available oxygen supply.

Typical descriptions include:

• Pressure

• Tightness

• Heaviness

• Choking

• Squeezing

The discomfort is frequently retrosternal and may radiate to:

• Neck

• Jaw

• Shoulders

• Back

• One or both arms, usually the left

• Epigastric region

Associated symptoms can include:

• Dyspnea

• Diaphoresis

• Dizziness

• Nausea or vomiting

• Anxiety

• Weakness

• Fatigue

Older adults, women and patients with diabetes may have atypical manifestations:

• Unexplained dyspnea

• Fatigue

• Weakness

• Indigestion

• Nausea

• Confusion

• Little or no chest pain

Stable angina

Stable angina is:

• Predictable

• Usually caused by exertion or emotional stress

• Relieved by rest or nitroglycerin

• Not associated with myocardial necrosis

• Associated with a normal troponin

Teaching includes:

• Stop activity when discomfort begins.

• Sit down and rest.

• Use nitroglycerin as prescribed.

• Keep nitroglycerin available.

• Follow the prescribed emergency plan if pain is not relieved.

Unstable angina

Unstable angina is:

• New chest pain

• Increasingly frequent chest pain

• More severe or prolonged pain

• Pain occurring at rest

• Pain less responsive to rest or nitroglycerin

• Considered acute coronary syndrome

There is ischemia but no measurable myocardial necrosis.

Expected findings:

• Troponin remains normal

• ECG may be normal

• ECG may show ST depression

• ECG may show T-wave inversion

Acute Coronary Syndrome

ACS includes:

• Unstable angina

• NSTEMI

• STEMI

Unstable angina versus NSTEMI versus STEMIUnstable angina

• Coronary ischemia without myocardial necrosis

• Troponin remains normal

• ECG may show ST depression or T-wave inversion

• Symptoms may be new, worsening or occurring at rest

NSTEMI

• Usually caused by partial or severe coronary obstruction

• Myocardial necrosis occurs

• Troponin is elevated

• ECG commonly shows ST depression or T-wave inversion

• Does not produce the diagnostic ST elevation of a STEMI

STEMI

• Usually caused by complete coronary occlusion

• Myocardial necrosis occurs

• Troponin is elevated

• ECG shows ST-segment elevation

Kim’s slide specifies:

At least 1 mm of ST elevation in two anatomically contiguous leads supports STEMI.

High-yield comparison

The major difference between unstable angina and NSTEMI is the troponin:

• NSTEMI = elevated troponin

• Unstable angina = normal troponin

Cardiac Diagnostics and NumbersTwelve-lead ECG

The ECG should be obtained rapidly for suspected ACS.

It is used to identify:

• Ischemia

• Injury

• ST elevation

• ST depression

• T-wave inversion

• Dysrhythmias

• Area of the myocardium affected

A normal or nondiagnostic initial ECG does not automatically rule out ACS.

Troponin

Troponin is the primary laboratory marker of myocardial injury.

Know Kim’s numbers:

• Begins to rise approximately 2–3 hours after chest-pain onset

• Generally peaks between 12–48 hours

• Falls toward normal over approximately 4–10 days

An early normal troponin may require repeat or serial testing.

CK-MB

CK-MB is another cardiac isoenzyme associated with myocardial injury.

Troponin is the more important marker in the provided material, but CK-MB may help evaluate possible reinfarction because it returns to baseline sooner.

BNP

BNP is secreted by the ventricles in response to excessive ventricular stretching.

Kim’s NSTEMI handout states:

BNP greater than 100 may indicate heart failure.

Always interpret BNP with the patient’s assessment and the facility’s reference range.

Other labs

• CBC

• Chemistry panel

• BUN and creatinine

• Potassium

• Magnesium

• Glucose

• Lipid panel

• PT/INR

• aPTT

• Hemoglobin and hematocrit

These help identify:

• Anemia

• Electrolyte disturbances

• Kidney dysfunction

• Bleeding risk

• Diabetes

• Lipid abnormalities

Echocardiogram

Evaluates:

• Heart chambers

• Valve structure

• Valve function

• Wall motion

• Ejection performance

• Pericardial effusion

Stress testing

Used to identify inducible ischemia in an appropriate, stable patient.

Stress testing is not the first action for a patient experiencing active, unstable ACS symptoms.

Initial Nursing Care for Chest Pain

For new chest pain:

1. Stop the patient’s activity.

2. Position the patient at rest.

3. Perform a rapid ABC assessment.

4. Obtain vital signs and oxygen saturation.

5. Complete a focused chest-pain assessment.

6. Obtain or prepare for a 12-lead ECG.

7. Establish IV access.

8. Draw ordered laboratory tests.

9. Administer ordered or protocol-directed medications.

10. Continually reassess pain, vital signs and ECG findings.

11. Prepare for reperfusion or a higher level of care when indicated.

Kim’s PowerPoint specifically says:

• Place the patient in semi-Fowler’s position

• Administer oxygen at 2 L/min by nasal cannula

• Give nitroglycerin and reassess

• Nitroglycerin may be given for up to three doses

For clinical safety, oxygen is generally guided by:

• Oxygen saturation

• Respiratory distress

• Hypoxemia

• Provider orders

• Facility protocol

Know Kim’s specific slide directions for the exam.

Important Cardiac MedicationsAspirin

Used early in suspected ACS because it inhibits platelet aggregation.

Nursing considerations:

• Check for allergy

• Check for active bleeding

• Usually given in chewable form during ACS

• Monitor for GI or other bleeding

Nitroglycerin

Nitroglycerin causes vasodilation and reduces myocardial workload and oxygen demand.

Before giving it:

• Check blood pressure.

• Assess the chest pain.

• Ask about recent PDE-5 inhibitor use.

• Check the medication order or protocol.

Examples of PDE-5 inhibitors include sildenafil and tadalafil.

Combining these drugs with nitroglycerin can cause profound hypotension.

Adverse effects:

• Hypotension

• Headache

• Dizziness

• Flushing

Expected therapeutic response:

• Reduced chest discomfort

Metoprolol and other beta blockers

Beta blockers:

• Decrease heart rate

• Decrease blood pressure

• Decrease myocardial workload

• Decrease myocardial oxygen demand

Before administration:

• Check heart rate

• Check blood pressure

• Evaluate for symptomatic bradycardia or hypotension

• Evaluate for worsening decompensated heart failure

ACE inhibitors and ARBs

These reduce afterload and may help manage:

• Hypertension

• Heart failure

• Ventricular remodeling following MI

Monitor:

• Blood pressure

• Potassium

• BUN and creatinine

• Renal function

ACE-inhibitor complications:

• Dry cough

• Hyperkalemia

• Hypotension

• Angioedema

Facial, tongue or throat swelling is an emergency.

Diuretics

Decrease excess fluid and pulmonary/systemic congestion.

Monitor:

• Daily weight

• Intake and output

• Blood pressure

• Lung sounds

• Edema

• Potassium

• Sodium

• Renal function

Antiplatelet medications

Aspirin and P2Y12 inhibitors help prevent platelet aggregation.

Patients with coronary stents may receive dual antiplatelet therapy.

Important teaching:

• Do not stop antiplatelet medication without speaking to the cardiology team.

• Monitor for bleeding.

• Report black stools, bloody urine, unusual bruising or persistent bleeding.

Anticoagulants

Anticoagulants prevent clot formation or propagation but do not directly dissolve an existing clot.

Nursing considerations:

• Monitor for bleeding.

• Check the ordered coagulation studies.

• Use bleeding precautions.

• Review kidney function when relevant.

• Verify correct dose and indication.

Thrombolytics

Thrombolytics dissolve a thrombus but do not correct the underlying atherosclerotic plaque.

They may be used for an eligible STEMI patient when timely PCI is unavailable.

They are not routinely used for:

• NSTEMI

• Unstable angina

Major contraindications include:

• Active internal bleeding

• Known bleeding disorder

• Previous intracranial hemorrhage

• Recent major surgery or trauma, depending on timing

• Certain severe or uncontrolled hypertension presentations

Kim’s handout emphasizes:

Door-to-needle goal: approximately 30 minutes when thrombolytic therapy is indicated.

PCI, PTCA and Coronary StentsPCI/PTCA

A balloon-tipped catheter is used to open a narrowed or blocked coronary artery.

A stent may be placed to keep the vessel open.

Possible complications:

• Coronary artery dissection

• Coronary perforation

• Abrupt vessel closure

• Acute MI

• Reperfusion dysrhythmias

• Ventricular tachycardia

• Cardiac arrest

• Bleeding

• Hematoma

• Retroperitoneal bleeding

• Embolic complications

• Acute kidney injury from contrast

Post-cardiac catheterization/PCI care

Assess:

• Vital signs

• Cardiac rhythm

• Chest pain

• Insertion site

• Bleeding or hematoma

• Peripheral pulses

• Color and temperature of the affected extremity

• Capillary refill

• Movement and sensation

• BUN and creatinine

• Urine output

Kim’s slide specifies:

Remain flat for a minimum of four hours after femoral sheath removal.

Positioning and activity restrictions may depend on the access site, closure device and facility protocol.

Retroperitoneal bleeding

Watch for:

• Back or flank pain

• Hypotension

• Tachycardia

• Falling hemoglobin or hematocrit

• Restlessness

• Weakness

• Signs of hypovolemia

Do not massage an enlarging hematoma.

CABG

CABG means coronary artery bypass graft.

A blood vessel is grafted around an occluded coronary artery so blood can flow beyond the obstruction.

Possible indications:

• Chest pain not controlled with medication

• CAD not adequately treated with PCI

• Significant coronary anatomy that is better treated surgically

• Prevention or treatment of complications related to ischemia

Post-CABG nursing assessment

Monitor:

• Neurologic status

• Cardiac output and perfusion

• Heart rate and rhythm

• Blood pressure

• Respiratory status

• Oxygenation

• Chest-tube drainage

• Bleeding

• Peripheral circulation

• Urine output

• BUN and creatinine

• Fluid and electrolytes

• Blood glucose

• Temperature

• Pain

Goals include:

• Adequate cardiac output

• Adequate tissue perfusion

• Adequate gas exchange

• Fluid and electrolyte balance

• Glycemic control

• Adequate kidney perfusion

• Pain relief

• Prevention of delirium and complications

Complications of ACS and MIDysrhythmias and cardiac arrest

Dysrhythmias are major early complications of MI.

Kim’s slide states:

More than 50% of deaths from MI occur within the first 72 hours.

The patient requires continuous rhythm monitoring.

Cardiogenic shock

Cardiogenic shock occurs when the heart cannot pump enough blood to support the organs.

Findings:

• Hypotension

• Tachycardia

• Weak pulses

• Cool, pale or clammy skin

• Altered mental status

• Decreased urine output

• Pulmonary congestion

• Increasing dyspnea

Heart failure

Findings can include:

• Dyspnea

• Orthopnea

• Crackles

• Hypoxemia

• S3

• Edema

• JVD

• Rapid weight gain

• Decreased urine output

• Reduced activity tolerance

Cardiac tamponade

Fluid or blood accumulates in the pericardial sac and compresses the heart.

This prevents adequate ventricular filling and reduces cardiac output.

Findings:

• Hypotension

• Tachycardia

• JVD

• Muffled heart sounds

• Narrow pulse pressure

• Weak pulses

• Restlessness

• Decreased urine output

• Poor perfusion

Beck’s triad

• Hypotension

• JVD

• Muffled heart sounds

Cardiac tamponade is an emergency.

Chapter 25: Structural, Infectious and Inflammatory DisordersInfective Endocarditis

Infective endocarditis is infection and inflammation of the endocardial surface, usually involving the heart valves.

Risk factors:

• Prosthetic heart valve

• Previous endocarditis

• Congenital or structural heart disease

• Rheumatic heart disease

• IV drug use

• Invasive procedures

• Poor oral hygiene

• Bacteremia

• Indwelling vascular catheters

• Prolonged IV therapy

• Immunocompromised state

Assessment findings:

• Fever

• Chills

• Malaise

• Fatigue

• Weight loss

• New or changing murmur

• Petechiae

• Heart-failure manifestations

• Stroke or other embolic manifestations

Important peripheral findings:

• Osler nodes: painful nodules on the fingers or toes

• Janeway lesions: painless red or purple macules on the palms or soles

• Splinter hemorrhages: small hemorrhages under the nails

• Roth spots: retinal hemorrhages

Memory aid:

Osler = ouch = painful

Diagnostics:

• Blood cultures

• CBC

• Echocardiogram

• ECG

• Other tests based on complications

When possible, obtain ordered blood cultures before beginning antimicrobial therapy.

Treatment:

• Prolonged organism-specific antimicrobial therapy

• Management of heart failure

• Management of embolic complications

• Valve repair or replacement if severe damage occurs

Complications:

• Heart failure

• Valve destruction

• Embolic stroke

• Systemic emboli

• Abscess formation

• Sepsis

Rheumatic Fever and Rheumatic Heart Disease

Rheumatic fever is an autoimmune inflammatory reaction that can occur following group A beta-hemolytic streptococcal pharyngitis.

Symptoms commonly begin:

Approximately 1–6 weeks after strep throat

Important manifestations:

• Fever

• Migratory polyarthritis

• Carditis or new murmur

• Chorea

• Erythema marginatum

• Subcutaneous nodules

Prevention:

• Promptly diagnose strep throat.

• Complete the prescribed antibiotic treatment.

• Reinforce long-term preventive therapy when ordered.

Chronic rheumatic heart disease commonly damages the mitral valve and can cause:

• Mitral stenosis

• Mitral regurgitation

Myocarditis

Myocarditis is inflammation of the myocardium.

It is often caused by a viral infection but may result from other infectious, autoimmune or toxic causes.

It can damage:

• Cardiac muscle fibers

• Myocardial contractility

• Electrical conduction system

Manifestations:

• Fatigue

• Dyspnea

• Chest discomfort

• Palpitations

• Dysrhythmias

• Signs of acute heart failure

A major clue is an otherwise healthy patient who rapidly develops:

• Acute decompensated heart failure

• Dysrhythmias

• Decreased cardiac output

Management is primarily supportive and directed at:

• Treating the cause

• Reducing cardiac workload

• Managing heart failure

• Managing dysrhythmias

• Preventing complications

Pericarditis

Pericarditis is inflammation of the pericardial sac.

Possible causes:

• Viral infection

• MI

• Cardiac surgery

• Autoimmune disease

• Certain medications

• Other infections or inflammatory processes

Assessment findings:

• Sharp, stabbing or pleuritic chest pain

• Pain worsens with deep inspiration

• Pain worsens when lying flat

• Pain improves when sitting up and leaning forward

• Fever

• Pericardial friction rub

• Dyspnea

This helps differentiate pericarditis from myocardial ischemia:

• Pericarditis: sharp, pleuritic and positional

• MI/angina: pressure, heaviness or squeezing; generally not relieved by leaning forward

Treatment depends on the cause and may include:

• NSAIDs or other anti-inflammatory therapy

• Colchicine, depending on the prescribed regimen

• Corticosteroids in selected cases

• Antibiotics when caused by bacterial infection

Complications:

• Pericardial effusion

• Cardiac tamponade

• Constrictive pericarditis

Pericardiocentesis

Pericardiocentesis removes fluid from the pericardial space.

Reasons:

• Relieve cardiac tamponade

• Improve cardiac output

• Obtain fluid for diagnostic testing

Before and during:

• Explain the procedure.

• Obtain baseline vital signs.

• Establish IV access.

• Maintain ECG monitoring.

• Monitor blood pressure and respiratory status.

• Position as ordered, commonly semi-Fowler’s.

• Prepare sterile equipment.

Afterward, monitor for:

• Improved blood pressure

• Decreased JVD

• Improved heart sounds

• Improved perfusion

• Improved dyspnea

• Dysrhythmias

• Bleeding

• Pneumothorax

• Infection

• Reaccumulation of fluid

Valve DisordersBasic definitionsStenosis

The valve does not open completely.

This obstructs forward blood flow and increases the workload of the chamber pumping through the valve.

Think:

Stenosis = tight = will not open

Regurgitation

The valve does not close completely.

Blood leaks backward through the valve.

Think:

Regurgitation = floppy or leaky = will not close

Prolapse

A valve leaflet bulges backward into the chamber behind it.

Mitral Valve Prolapse

The mitral leaflets bulge into the left atrium during systole.

Often asymptomatic.

Possible findings:

• Palpitations

• Dizziness

• Fatigue

• Anxiety

• Chest discomfort

• Dyspnea

• Midsystolic click

• Murmur

Management:

• Symptom management

• Follow-up examinations

• Monitoring for progression to mitral regurgitation

• Education about symptoms of endocarditis

Mitral Regurgitation

The mitral valve does not close completely.

Blood flows:

Left ventricle → back into left atrium during systole

Result:

1. Increased left-atrial volume

2. Pulmonary congestion

3. Increased left-ventricular workload

4. Decreased forward cardiac output

5. Possible heart failure

Findings:

• Cough

• Dyspnea

• Orthopnea

• Fatigue

• Palpitations

• Murmur

• Crackles

• S3

• Heart-failure manifestations

Possible causes:

• Mitral valve prolapse

• Rheumatic heart disease

• Infective endocarditis

• Ischemic heart disease

• Left-ventricular enlargement

• Papillary-muscle dysfunction following MI

Mitral Stenosis

The mitral valve is narrowed.

Blood flow is obstructed:

Left atrium → left ventricle

Result:

1. Increased pressure in the left atrium

2. Blood backs into pulmonary circulation

3. Pulmonary congestion develops

4. Pulmonary hypertension may develop

5. Right-sided heart failure may eventually occur

Findings:

• Dyspnea on exertion

• Orthopnea

• Fatigue

• Dizziness

• Palpitations

• Chest discomfort

• Cough

• Hemoptysis

• Murmur

• Atrial fibrillation

• Heart-failure manifestations

Important complication:

Left-atrial enlargement can cause atrial fibrillation and blood stasis, increasing the risk of:

• Atrial thrombus

• Embolic stroke

Rheumatic heart disease is an important cause of mitral stenosis.

Aortic Regurgitation

The aortic valve does not close completely.

Blood flows:

Aorta → back into left ventricle during diastole

Result:

• Left-ventricular volume overload

• Left-ventricular enlargement

• Decreased forward cardiac output

• Eventually heart failure

Findings:

• Forceful heartbeat in the head or neck

• Bounding peripheral pulses

• Wide pulse pressure

• Dyspnea

• Fatigue

• Palpitations

• Chest pain

• Diastolic murmur

• Heart-failure manifestations

Possible causes:

• Congenital bicuspid valve

• Rheumatic endocarditis

• Infective endocarditis

• Aortic dilation

• Aortic dissection

• Degenerative valve changes

Aortic Stenosis

The aortic valve does not open completely.

Blood flow is obstructed:

Left ventricle → aorta

Result:

1. Left ventricle must generate greater pressure.

2. Left-ventricular hypertrophy develops.

3. Cardiac output decreases.

4. Myocardial oxygen demand increases.

5. Heart failure may eventually occur.

Classic symptoms:

SAD

• S: Syncope

• A: Angina

• D: Dyspnea

Other findings:

• Fatigue

• Palpitations

• S4

• Systolic murmur

• Reduced activity tolerance

• Heart-failure manifestations

Severe aortic stenosis can cause sudden cardiac death.

Valve Management

Medical management can include:

• Diuretics

• ACE inhibitors

• ARBs

• Beta blockers

• Dysrhythmia management

• Anticoagulation when indicated

• Heart-failure management

The patient may eventually require:

• Balloon valvuloplasty

• Commissurotomy

• Annuloplasty

• Valve repair

• Valve replacement

• Transcatheter aortic valve replacement

Balloon valvuloplasty

A catheter with a balloon is used to open a stenotic valve.

It is performed in the catheterization lab.

Monitor for:

• Bleeding

• Hematoma

• Dysrhythmias

• Embolic event

• Heart failure

• Valve damage

• Regurgitation

• Restenosis

Postprocedure care is similar to post-cardiac catheterization care.

Chapter 25 notes:

• The balloon may be inflated for approximately 15–60 seconds

• Aortic balloon valvuloplasty can have a restenosis rate of approximately 50% within the first six months

These textbook numbers may be lower-priority than the PowerPoint information, but they are worth recognizing.

Commissurotomy/valvotomy

Surgical separation or incision of fused valve leaflets to relieve stenosis.

Annuloplasty

A ring or band is placed around the valve annulus to reshape and support it.

Mechanical Versus Tissue ValvesMechanical valve

Advantages:

• Very durable

• Long-lasting

Disadvantages:

• Higher clot risk

• Usually requires lifelong anticoagulation with warfarin

Tissue or bioprosthetic valve

Advantages:

• Lower clot risk

• Often does not require lifelong anticoagulation unless another indication exists

Disadvantages:

• Less durable

Kim’s PowerPoint states:

Bioprosthetic valves may last approximately 7–10 years.

Types mentioned in the chapter/slides:

• Cow tissue

• Pig tissue

• Horse tissue

• Homograft from human donor tissue

• Autograft using the patient’s own pulmonic valve

Warfarin Teaching

The patient should:

• Take warfarin exactly as prescribed.

• Obtain PT/INR testing.

• Keep vitamin K intake consistent.

• Avoid suddenly increasing or decreasing vitamin K-rich foods.

• Use bleeding precautions.

• Report unusual bruising.

• Report bleeding gums.

• Report nosebleeds.

• Report blood in urine or stool.

• Report black, tarry stools.

• Consult the provider before taking NSAIDs, OTC medications or herbal products.

• Never stop warfarin independently.

• Wear medical-alert identification.

Cardiomyopathies

Cardiomyopathy is disease of the heart muscle associated with cardiac dysfunction.

Dilated cardiomyopathy

The ventricles enlarge and contract poorly.

This causes systolic dysfunction and reduced cardiac output.

Findings:

• Dyspnea

• Orthopnea

• Fatigue

• Crackles

• Edema

• S3

• Dysrhythmias

• Heart failure

• Possible thromboembolism from blood stasis

Hypertrophic cardiomyopathy

The myocardium becomes abnormally thick, often involving the septum.

This can:

• Reduce ventricular filling

• Obstruct left-ventricular outflow

• Reduce cardiac output

• Cause dangerous dysrhythmias

Findings:

• Exertional dyspnea

• Angina

• Syncope

• Palpitations

• Sudden cardiac death

Major dehydration or sudden preload reduction can worsen outflow obstruction in susceptible patients.

Restrictive cardiomyopathy

The ventricles become stiff and cannot fill normally.

This produces diastolic dysfunction.

Findings:

• Fatigue

• Exercise intolerance

• JVD

• Edema

• Pulmonary or systemic congestion

• Signs of reduced cardiac output

Cardiomyopathy nursing priorities

• Monitor cardiac rhythm.

• Assess perfusion.

• Monitor respiratory status.

• Assess for heart failure.

• Monitor daily weight.

• Measure intake and output.

• Monitor renal function.

• Administer prescribed medications.

• Teach individualized activity restrictions.

• Teach the patient to report syncope, chest pain, palpitations or worsening dyspnea.

The cardiomyopathy information is in Chapter 25 but is not emphasized as heavily in Kim’s HYBRID PowerPoint as valves, endocarditis, myocarditis and pericarditis.

“Old Bones” Fundamentals Kim Could AddPrioritization

• ABCs come before routine teaching or documentation.

• Acute problems come before chronic problems.

• Unexpected findings come before expected findings.

• Unstable patients come before stable patients.

• Actual problems generally come before potential problems.

• New chest pain, hypotension, altered LOC, active bleeding or a new neurologic deficit requires rapid attention.

Medication administration

Before giving a medication:

• Verify allergies.

• Confirm indication.

• Check relevant vital signs.

• Check relevant laboratory results.

• Check contraindications.

• Confirm the correct patient, medication, dose, route and time.

• Evaluate whether the patient can safely receive it.

After giving a medication:

• Reassess the intended effect.

• Monitor for adverse effects.

• Document the response.

Consent

The procedural provider obtains informed consent.

The nurse:

• Verifies that consent is signed

• Witnesses according to policy

• Confirms the patient is voluntarily consenting

• Reports unanswered questions to the provider

The nurse should not provide the procedural explanation in place of the provider.

Delegation

The RN does not delegate:

• Initial assessment

• Clinical judgment

• Patient teaching

• Evaluation

• Care of an unstable patient

Experienced unlicensed personnel may obtain routine vital signs on a stable patient and report abnormalities.

Patient education

Use teach-back for:

• Nitroglycerin

• Antiplatelet medications

• Warfarin

• Post-cath restrictions

• Surgical incision care

• Symptoms requiring emergency assistance

Numbers and Facts to Know

• Troponin starts rising approximately 2–3 hours after chest-pain onset.

• Troponin generally peaks in 12–48 hours.

• Troponin may fall toward normal over 4–10 days.

• STEMI: at least 1 mm of ST elevation in two contiguous leads according to Kim’s slide.

• Kim’s chest-pain slide lists oxygen at 2 L/min by nasal cannula.

• Kim’s slide allows nitroglycerin for up to three doses, with reassessment.

• Kim’s post-femoral-sheath slide states the patient remains flat for at least four hours.

• When thrombolytics are used, the handout emphasizes a 30-minute door-to-needle goal.

• Kim’s handout associates BNP greater than 100 with heart failure.

• Kim’s slide states more than 50% of MI deaths occur within 72 hours.

• Rheumatic fever manifestations may begin 1–6 weeks after strep throat.

• Kim’s slide states tissue valves may last approximately 7–10 years.

• Chapter 25 states valvuloplasty balloons may be inflated for 15–60 seconds.

• Chapter 25 notes approximately 50% restenosis within six months after aortic balloon valvuloplasty.

Final High-Yield Connections

• Unstable angina: ischemia, normal troponin, no necrosis

• NSTEMI: elevated troponin, necrosis, ST depression/T-wave inversion

• STEMI: elevated troponin, necrosis, ST elevation

• Endocarditis: fever, new murmur, cultures, antibiotics, embolic risk

• Myocarditis: inflamed heart muscle, rapid HF and dysrhythmias

• Pericarditis: sharp positional pain, friction rub, tamponade risk

• Tamponade: hypotension, JVD and muffled heart sounds

• Mitral stenosis: pulmonary backup, A-fib and embolic risk

• Mitral regurgitation: blood leaks from LV to LA during systole

• Aortic stenosis: SAD—syncope, angina and dyspnea

• Aortic regurgitation: bounding pulses and wide pulse pressure

• Mechanical valve: durable but generally requires lifelong anticoagulation

• Post-PCI: bleeding and distal neurovascular assessment

• Cardiogenic shock: hypotension plus evidence of organ hypoperfusion

•