PCCN (Progressive Care)

Acute coronary syndromes (ACS) include unstable angina, non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). All share the same pathophysiology: atherosclerotic plaque rupture, platelet aggregation, and thrombus formation causing partial or complete coronary occlusion.

Typical symptoms are substernal pressure radiating to the arm, neck, or jaw with diaphoresis, nausea, dyspnea, and anxiety. Atypical presentations (fatigue, weakness, dyspnea, epigastric discomfort) are more common in women, older adults, and patients with diabetes.

Additional therapy includes a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor), anticoagulation with unfractionated heparin or enoxaparin, a beta-blocker to reduce myocardial oxygen demand (avoid in heart failure, shock, or bradycardia), an ACE inhibitor within 24 hours in stable patients, and a high-intensity statin.

Primary percutaneous coronary intervention (PCI) is preferred when first medical contact-to-device time can be achieved within 90 minutes. Fibrinolytic therapy is used when timely PCI is unavailable, with a door-to-needle goal of 30 minutes. Absolute contraindications include any prior intracranial hemorrhage, ischemic stroke within 3 months, active bleeding, suspected aortic dissection, and significant recent head trauma.

Complications include cardiogenic shock, dysrhythmias, papillary muscle rupture with acute mitral regurgitation (new holosystolic murmur and flash pulmonary edema), ventricular septal rupture, free wall rupture with tamponade, and pericarditis. Right ventricular infarction presents with hypotension, elevated jugular venous pressure, and clear lung fields; it requires volume and avoidance of nitrates and diuretics.

Heart failure occurs when the heart cannot meet metabolic demands, or can do so only at elevated filling pressures. It is classified by ejection fraction: HFrEF (EF 40% or less), HFmrEF (EF 41–49%), and HFpEF (EF 50% or greater).

Assessment includes vital signs, oxygen saturation, daily weight, intake and output, and BNP or NT-proBNP (levels may be falsely low in obesity and are elevated by renal dysfunction). Treatment optimizes preload, afterload, and contractility:

• Preload reduction: IV loop diuretic (furosemide) first line; nitroglycerin for congestion with adequate blood pressure.
• Afterload reduction: nitroglycerin, nitroprusside, or nicardipine in hypertensive decompensation.
• Contractility: dobutamine or milrinone for low-output states with hypoperfusion; milrinone causes more vasodilation and hypotension and accumulates in renal failure.
• Ventilatory support: CPAP or BiPAP reduces preload and work of breathing in cardiogenic pulmonary edema.

Four drug classes reduce mortality and hospitalization: an ARNI (sacubitril-valsartan) or ACE inhibitor/ARB, an evidence-based beta-blocker (carvedilol, metoprolol succinate, bisoprolol), a mineralocorticoid receptor antagonist (spironolactone, eplerenone), and an SGLT2 inhibitor (dapagliflozin, empagliflozin). Monitor potassium and creatinine with ACE inhibitors, ARNIs, and MRAs; an ARNI must not be started within 36 hours of the last ACE inhibitor dose.

Device therapy includes an implantable cardioverter-defibrillator for primary prevention when EF remains 35% or less despite optimal therapy, and cardiac resynchronization therapy for patients with LBBB and prolonged QRS duration.