Cardiac Care: Practice Questions & Explanations

ST-elevation myocardial infarction (STEMI) is a medical emergency where coronary occlusion is causing actively-progressing myocardial damage. 'Time is muscle' — delays in reperfusion increase infarct size and worsen outcomes. Standard initial management (often remembered as MONA-BASH or similar mnemonics, though MONA is no longer routine): (1) Oxygen if SpO2 below 90% (no longer routine for everyone — supplemental O2 may worsen outcomes in non-hypoxic patients); (2) Aspirin 325 mg chewed (decreases platelet aggregation, reduces mortality); (3) Nitroglycerin sublingual (vasodilation, reduces preload and afterload, relieves ischemia — contraindicated in inferior MI with right ventricular involvement, sildenafil use in 24 hrs, severe hypotension); (4) Morphine for pain not relieved by nitrates (use cautiously); (5) IV access and continuous monitoring; (6) Reperfusion: PCI (percutaneous coronary intervention) within 90 minutes from first medical contact is gold standard; thrombolytics if PCI unavailable within timeframe. Other meds: beta-blocker, statin, ACE inhibitor.

Women, elderly clients, and people with diabetes may present with atypical MI symptoms that delay diagnosis. Classic 'textbook' MI: crushing substernal chest pain radiating to left arm or jaw, diaphoresis, nausea, sense of impending doom. Atypical presentations more common in women, elderly, diabetic clients: unusual fatigue (often weeks before the event); shortness of breath as the primary or only symptom; indigestion or epigastric pain often mistaken for GI issues; nausea and vomiting; back, jaw, or neck pain; lightheadedness or syncope; pain in shoulders or arms; sleep disturbances. Women frequently delay seeking care because their symptoms are dismissed or attributed to anxiety. Nurses must maintain high index of suspicion for cardiac etiology when women, elderly, or diabetic clients present with vague or atypical symptoms. Diabetes can blunt typical pain because of neuropathy — silent MI is common in diabetic clients.

Furosemide (Lasix) is a loop diuretic — the most potent class of diuretic. Mechanism: inhibits the sodium-potassium-chloride co-transporter in the ascending loop of Henle, causing large amounts of sodium, chloride, potassium, and water to be excreted. Used for: heart failure, edema, hypertension, ascites. Adverse effects: (1) Hypokalemia — can cause weakness, arrhythmias; monitor K+ and supplement as needed; (2) Hyponatremia and other electrolyte imbalances; (3) Dehydration and hypotension — monitor weight (best indicator of fluid status), blood pressure, orthostatic changes; (4) Ototoxicity — especially with rapid IV administration of high doses, or combined with other ototoxic drugs (aminoglycosides); give IV slowly; (5) Hyperglycemia, hyperuricemia (can trigger gout); (6) Photosensitivity. Teaching: take in morning to avoid nocturia; rise slowly to prevent orthostatic hypotension; eat potassium-rich foods (bananas, oranges, leafy greens) unless on potassium-sparing diuretic. Daily weight monitoring (same time, same scale, same clothing) — report gain over 2 lbs in a day or 5 lbs in a week.

This presentation describes acute pulmonary edema — fluid in the alveoli — a life-threatening complication of acute heart failure. The priority diagnosis is impaired gas exchange because oxygen cannot diffuse across fluid-filled alveoli. Other features: orthopnea (unable to lie flat), paroxysmal nocturnal dyspnea, S3 gallop, jugular venous distention, peripheral edema, decreased urine output. Immediate management (LMNOP or Lasix-Morphine-Nitrates-Oxygen-Position): (1) High-Fowler's position to ease breathing; (2) High-flow oxygen — non-rebreather mask or BiPAP/CPAP, possibly intubation if severe; (3) IV diuretics (furosemide) — rapid diuresis to reduce preload; (4) IV nitroglycerin — vasodilator, reduces preload and afterload; (5) Morphine — reduces anxiety, decreases preload through venodilation (controversial in some recent guidelines because of associations with worse outcomes); (6) Continuous monitoring of vital signs, oxygen saturation, urine output, cardiac rhythm; (7) Address the underlying cause (ischemia, hypertensive emergency, valvular disease, atrial fibrillation, medication noncompliance, dietary indiscretion). Once stabilized: optimize chronic heart failure medications (ACE inhibitor/ARB, beta-blocker, mineralocorticoid receptor antagonist, SGLT2 inhibitor).

DIGOXIN (a cardiac glycoside) has a narrow therapeutic index and specific assessment requirements before administration.

Priority assessment: APICAL PULSE — measure for a full 60 seconds; HOLD and notify provider if: below 60 bpm in adults; below 70 bpm in children; below 90 bpm in infants; POTASSIUM (K+) — hypokalemia sensitises the myocardium to digoxin toxicity; even therapeutic digoxin levels can cause toxicity when potassium is low; target K+ 3.5-5.0 mEq/L; DIGOXIN LEVEL — therapeutic range 0.5-2.0 ng/mL (though lower end preferred for heart failure); DIGOXIN TOXICITY SIGNS — early: nausea, vomiting, anorexia, visual disturbances (yellow-green halos around lights, blurred vision); cardiac: bradycardia, heart block, any new dysrhythmia.

Management of toxicity: hold digoxin; check serum level and electrolytes; provide potassium supplementation if hypokalemic; severe toxicity: Digoxin Immune Fab (DigiFab/Digibind) — specific antidote; MEDICATIONS THAT INCREASE DIGOXIN TOXICITY: hypokalemia-causing agents (loop diuretics, thiazides); antiarrhythmics (amiodarone, quinidine increase digoxin levels); verapamil.

Nursing rule: Count the pulse, check the potassium, then give digoxin.

THROMBOLYTIC THERAPY (tPA, alteplase, tenecteplase) for STEMI carries a serious risk of HAEMORRHAGE — including intracranial haemorrhage (ICH), which can be fatal or permanently disabling. ABSOLUTE CONTRAINDICATIONS to thrombolytics: PRIOR HAEMORRHAGIC STROKE at any time — a prior haemorrhagic stroke indicates brain blood vessels that have previously bled; thrombolytics would lyse any existing clots maintaining fragile vessel integrity; ISCHAEMIC STROKE within the past 3 months — recent ischaemic stroke with potential haemorrhagic transformation; INTRACRANIAL NEOPLASM, AVM, or ANEURYSM — these lesions are at high risk of haemorrhage; ACTIVE INTERNAL BLEEDING (excluding menses); SIGNIFICANT CLOSED HEAD TRAUMA or FACIAL TRAUMA within 3 months; SUSPECTED AORTIC DISSECTION — thrombolytics would be catastrophic if the underlying condition is aortic dissection rather than MI; RELATIVE CONTRAINDICATIONS (risk-benefit decision): BP above 180/110 despite treatment; pregnancy; active peptic ulcer; recent surgery (within 2 weeks); prolonged CPR with rib fractures; INR above 2 or heparin use with elevated aPTT.

Nursing role: Know the contraindications; verify history before administration; neurological monitoring every 30 minutes during and after infusion; stop immediately if neurological changes occur; do NOT give IM injections or perform arterial puncture in non-compressible sites within 24 hours; minimise vascular access attempts.

PULSELESS VENTRICULAR TACHYCARDIA or VENTRICULAR FIBRILLATION is a shockable cardiac arrest rhythm requiring immediate CPR and defibrillation.

Recognition: Wide-complex tachycardia (QRS wider than 0.12 seconds) at 180 bpm + unresponsive client = likely PULSELESS VT or VF; do not waste time trying to perfectly identify the rhythm before acting — the patient is in cardiac arrest. ACLS ALGORITHM for pulseless VT/VF: (1) CALL for help immediately / activate Code Blue; (2) Start HIGH-QUALITY CPR — 30 compressions : 2 breaths; compressions at 100-120/min, depth 2-2.4 inches, full chest recoil, minimise interruptions; (3) DEFIBRILLATE AS SOON AS POSSIBLE — biphasic 120-200J (or device-recommended); monophasic 360J; (4) Resume CPR immediately after shock (2 minutes); (5) IV/IO access; (6) EPINEPHRINE 1 mg IV/IO every 3-5 minutes; (7) AMIODARONE 300 mg IV/IO for pulseless VT/VF refractory to defibrillation; (8) Identify and treat REVERSIBLE CAUSES (Hs and Ts: Hypovolemia, Hypoxia, Hydrogen ion/acidosis, Hypo/hyperkalaemia, Hypothermia; Tension pneumothorax, Tamponade, Toxins, Thrombosis — pulmonary/coronary).

Time matters: Every 1-minute delay in defibrillation for VF reduces survival by 7-10%. Chest compressions maintain perfusion until defibrillation is possible.

DIGOXIN TOXICITY signs include: nausea, vomiting, anorexia; VISUAL DISTURBANCES (blurred or yellow-green vision, halos around lights); BRADYCARDIA (slow heart rate) and dysrhythmias; confusion, weakness. NCLEX physiological/pharmacology. Digoxin has a NARROW therapeutic range (0.5-2.0 ng/mL); toxicity is common. HOLD digoxin and notify the provider if the apical pulse is below 60 bpm (assess apical pulse for a full minute before administering). HYPOKALEMIA increases the risk of toxicity (monitor potassium, especially with diuretics). The antidote for severe toxicity is digoxin immune Fab. Recognizing digoxin toxicity (GI symptoms, visual changes, bradycardia) is a heavily tested NCLEX pharmacology concept.

TROPONIN (cardiac troponin I or T) is the MOST SPECIFIC and sensitive lab marker for myocardial infarction (heart attack). NCLEX physiological/cardiac. Troponin is released into the blood when heart muscle is damaged; it rises within a few hours of an MI, peaks, and stays elevated for days — making it valuable for diagnosis. Serial troponins are drawn. OTHER cardiac markers: CK-MB (creatine kinase-MB) and myoglobin (less specific). Troponin's high specificity for cardiac muscle damage makes it the gold-standard biomarker for MI. Combined with the ECG and clinical presentation, troponin confirms the diagnosis. Knowing troponin is the most specific MI marker is a commonly tested NCLEX cardiac concept.

Worsening HEART FAILURE / FLUID OVERLOAD signs include: SUDDEN WEIGHT GAIN (the most sensitive early indicator — fluid retention; a gain of 2-3 lbs in a day or 5 lbs in a week should be reported); increased SHORTNESS OF BREATH (dyspnea, orthopnea, paroxysmal nocturnal dyspnea); EDEMA (swelling, especially legs/ankles); CRACKLES (rales) in the lungs (pulmonary congestion); jugular vein distension; fatigue; cough. NCLEX physiological/cardiac.

Teaching: weigh daily (same time, same scale, same clothing) and report rapid gains; low-sodium diet; take medications (diuretics, etc.); monitor symptoms. Daily weight is the key self-monitoring tool. Recognizing worsening heart failure (especially sudden weight gain) is a commonly tested NCLEX concept.