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Episode Notes (High-Yield for NCLEX)Three major cardiac buckets:
Acute coronary syndromes (ACS) – blocked arteries and myocardial infarction
Pump failure – heart failure and cardiogenic shock
Infection and inflammation – pericarditis and infective endocarditis
Constant NCLEX theme:
Assessment before action
Time is muscle in ACS
Fluid status is king in heart failure and shock
Acute Coronary Syndromes and Myocardial Infarction
Core pathophysiology
Coronary artery becomes blocked.
Downstream heart muscle becomes ischemic and, if prolonged, becomes necrotic.
NCLEX hallmark MI features
Chest pain > 20 minutes, not relieved by rest or nitroglycerin.
Pain plus systemic signs: sweating, nausea, shortness of breath, “impending doom.”
Troponin I or T elevated – most specific cardiac biomarker.
ST elevation on ECG = STEMI → true emergency.
MONA (bedside actions while waiting for reperfusion)
M – Morphine: relieves pain and decreases preload, lowering workload on the heart.
O – Oxygen: maintain oxygen saturation ideally above 94.
N – Nitroglycerin: vasodilates coronary arteries; check blood pressure first and avoid if hypotensive.
A – Aspirin: 162–325, chewed for faster absorption; prevents platelet clumping and clot growth.
Reperfusion priorities
PCI (percutaneous coronary intervention): goal is door-to-balloon time within 90 minutes.
If PCI is not possible within about 120 minutes, use fibrinolytics (clot busters).
Post-MI complications to watch
Ventricular dysrhythmias: premature ventricular contractions, runs of V-tack, or ventricular fibrillation needing immediate defibrillation.
Cardiogenic shock.
Papillary muscle rupture leading to acute severe mitral regurgitation.
Angina Pectoris: Stable, Unstable, and Prinzmetal
Shared concept
Chest pain occurs when oxygen demand exceeds oxygen supply, usually due to coronary artery disease.
Stable angina
Trigger: predictable exertion or emotional stress.
Duration: less than 20 minutes.
Relief: rest or nitroglycerin.
Pattern matters: “I walk upstairs, get pain, sit, and it goes away.”
Unstable angina (NCLEX favorite)
Represents a change:
Occurs at rest or with increasing frequency, duration, or intensity.
NCLEX rule:
Treat unstable angina as acute coronary syndrome.
Start MONA, continuous monitoring, and assume MI until proven otherwise.
Prinzmetal (variant) angina
Caused by coronary artery spasm, not always a fixed blockage.
Often occurs at rest or at night.
Typically responds to calcium channel blockers like diltiazem; nitroglycerin can also help.
Heart Failure: Left-Sided vs Right-Sided
Core concept
Heart cannot pump effectively → fluid backs up in the lungs or in the body.
Left-sided heart failure – “Think lungs”
Fluid backs up into the pulmonary circulation.
Key findings:
Shortness of breath.
Crackles on auscultation.
Orthopnea – difficulty breathing when lying flat.
Paroxysmal nocturnal dyspnea – waking suddenly gasping for air.
Right-sided heart failure – “Think body”
Fluid backs up into systemic circulation.
Key findings:
Jugular vein distension.
Peripheral edema – swelling in legs and ankles.
Hepatomegaly – enlarged liver.
Ascites – fluid in the abdomen.
Best noninvasive fluid status monitor
Daily weights:
Same time, same scale, same clothing.
Report gain of about 2–3 pounds in one day or 5 pounds in one week.
Common heart failure medications
ACE inhibitors (example: lisinopril) – decrease afterload.
Beta-blockers (example: carvedilol, metoprolol) – reduce heart rate and workload, protect the heart long term.
Digoxin – increases contractility; watch closely for digoxin toxicity (nausea, visual changes like halos, slow heart rate).
Diuretics:
Loop diuretics such as furosemide remove excess fluid.
Spironolactone is potassium-sparing and also helps with fluid.
Key lab
BNP (brain natriuretic peptide):
Elevated BNP indicates worsening heart failure and increased cardiac stretch.
Patient teaching
Low-sodium diet, typically less than 2 grams a day.
Follow fluid restriction if prescribed.
Understand warning signs: rapid weight gain, increasing shortness of breath, swelling.
Cardiogenic Shock: Extreme Pump Failure
When it happens
Frequently a complication of a large MI.
Heart muscle is so damaged it cannot maintain adequate cardiac output.
Key assessment features
Profound hypotension – very low systolic blood pressure.
Decreased urine output – typically less than 30 per hour, showing poor kidney perfusion.
Cool, clammy skin.
Weak, thready pulses.
Altered mental status – confusion, lethargy.
Medications used
Dopamine – increases blood pressure and cardiac output at certain doses.
Dobutamine – increases contractility.
Norepinephrine – go-to vasopressor for severe hypotension.
Mechanical support
Intra-aortic balloon pump (IABP):
Inflates and deflates in sync with the heart.
Decreases workload on the left ventricle and improves coronary perfusion.
Primary goal
Maintain vital organ perfusion.
Target: mean arterial pressure (MAP) above 65 to protect organs like brain and kidneys.
Pericarditis: Inflammation of the Heart Sac
Pathophysiology
Inflammation of the pericardium, often after viral illness, kidney failure, or MI.
Pain pattern (NCLEX gold)
Sharp, pleuritic chest pain:
Worse with deep breathing, coughing, or lying flat.
Improves when the patient sits up and leans forward – classic positional relief.
Assessment findings
Pericardial friction rub – scratchy, leather-like sound.
ECG: diffuse ST elevation across many leads, sometimes with PR depression.
Treatment
High-dose NSAIDs (example: ibuprofen).
Colchicine often added to reduce recurrence.
Critical NCLEX “do not”
Do NOT give anticoagulants (no heparin, no warfarin) in pericarditis.
Risk: bleeding into the pericardial sac → cardiac tamponade.
Cardiac tamponade – life-threatening complication
Beck’s triad:
Low blood pressure.
Muffled or distant heart sounds.
Jugular vein distension.
Pulsus paradoxus:
Significant drop in systolic blood pressure with inspiration.
Requires immediate pericardiocentesis to drain fluid and relieve pressure.
Infective Endocarditis: Infection on Heart Valves
Pathophysiology
Infection of the endocardium and valves, usually bacterial (strep or staph).
Vegetations can break off and cause emboli.
NCLEX hallmark signs
Persistent fever.
New or changing heart murmur – suggests valve damage.
Embolic phenomena (high-yield “weird” signs)
Janeway lesions – small, painless spots on palms and soles.
Osler nodes – small, painful nodules on fingers or toes.
Roth spots – retinal hemorrhages.
Splinter hemorrhages – thin, dark lines under fingernails.
Management
Prolonged IV antibiotics, often 4–6 weeks or longer (examples: vancomycin, gentamicin, depending on organism).
Critical first step:
Obtain blood cultures before starting antibiotics (usually three sets from different sites).
Use echocardiography:
Start with transthoracic, escalate to transesophageal if needed.
Nursing priorities
Monitor for new embolic events – stroke symptoms, splenic pain.
Watch for worsening heart failure from valve destruction.
Educate high-risk patients about prophylactic antibiotics before dental procedures.
Cross-Cutting NCLEX Priorities and “Nursing Pearls”
Assessment Before Action
Always gather data first: vital signs, pain description, lung sounds, ECG changes, urine output, mental status.
Use SBAR to communicate: Situation, Background, Assessment, Recommendation.
Fluid Status Is King
Especially critical in heart failure and shock.
Daily weights are your best noninvasive monitor:
About 2–3 pounds gain in a day or 5 pounds in a week = red flag.
Know Your Critical Medication Rules
MONA is for acute coronary syndrome, not stable angina.
Never give anticoagulants in pericarditis because of tamponade risk.
Treat unstable angina like an MI until ruled out.
Watch for digoxin toxicity and be intentional with vasopressors and inotropes.
Connect the Dots
One cardiac problem often leads to another:
Large MI → cardiogenic shock.
MI → later pericarditis.
Valve infection → heart failure or stroke.
Thinking like a nurse means seeing relationships between conditions, not just memorizing lists.
