Cardiac Critical care

SCAPE — Sympathetic Crashing Acute Pulmonary Edema What is SCAPE? SCAPE = Sympathetic Crashing Acute Pulmonary Edema It represents the extreme end of the acute heart-failure/pulmonary-edema spectrum, characterized by: abrupt onset severe dyspnea severe respiratory distress marked sympathetic activation usually severe hypertension tachycardia diaphoresis agitation/anxiety hypoxemia diffuse pulmonary edema very rapid clinical deterioration The patient […]

PERICARDITIS  Definition Pericarditis = inflammation of the pericardium, usually involving the visceral and parietal pericardial layers. Clinically, pericardial inflammation may occur with or without pericardial effusion. Anatomy relevant to pericarditis The pericardium consists of: Fibrous pericardium Tough outer layer Limits acute cardiac dilatation Anchors heart to diaphragm, sternum and great vessels Serous pericardium Parietal layer

MYOCARDITIS  DEFINITION Myocarditis = inflammatory disease of the myocardium, diagnosed clinically and/or histologically, with myocardial injury that may produce: myocardial necrosis ventricular dysfunction heart failure arrhythmias conduction abnormalities cardiogenic shock sudden cardiac death. MYOCARDITIS vs MYOPERICARDITIS vs PERIMYOCARDITIS Term Predominant disease LV function Pericarditis Pericardium Usually preserved Myocarditis Myocardium May be impaired Myopericarditis Predominantly pericarditis

Heart Failure with Preserved Ejection Fraction (HFpEF) 1. Definition  Symptoms ± signs of heart failure LVEF ≥50% Evidence of cardiac structural and/or functional abnormality Elevated natriuretic peptides Feature HFpEF HFrEF EF ≥50% ≤50% Dysfunction Diastolic Systolic LV Geometry Concentric Eccentric Main cause HTN CAD 2.  Pathophysiology  A. Central Concept It is  systemic disease with multi-organ

 Acute Decompensated Heart Failure (ADHF) What is ADHF? Acute Decompensated Heart Failure (ADHF) is the rapid onset or worsening of signs and symptoms of heart failure requiring urgent therapy and often hospitalization. It may occur as: De novo HF (newly diagnosed) Acute decompensation of chronic HF Progression to cardiogenic shock Major guidelines: American Heart Association

SHOCK Definition Shock is acute circulatory failure resulting in inadequate oxygen delivery (DO₂) relative to tissue oxygen demand (VO₂), leading to cellular dysoxia, organ dysfunction, and, if untreated, death. The key concept is inadequate tissue perfusion, not simply low blood pressure. Why Shock Is Difficult to Define Historically, shock was equated with hypotension. But hypotension

Hypertensive Crisis Hypertensive crisis is a spectrum of severe blood pressure elevation associated with actual or potential acute target-organ damage. It is broadly classified into: Hypertensive Emergency Hypertensive Urgency (The 2024 AHA Scientific Statement and 2025 AHA/ACC Hypertension Guideline recommend abandoning the term “hypertensive urgency.” Instead, patients are classified as:severe asymptomatic hypertension) Hypertensive Emergency Severe

ATRIAL FIBRILLATION  Atrial fibrillation is a supraventricular tachyarrhythmia characterized by: Irregularly irregular rhythm(One exception to these criteria is that if AF is combined with heart block, then the ventricular response may be regular.) No distinct P waves(If it is unclear whether there are P waves or fibrillation waves, consider obtaining a Lewis Lead ECG) Fibrillatory

Septic Cardiomyopathy (Sepsis-Induced Myocardial Dysfunction, SIMD)  Septic cardiomyopathy (SCM) is an acute, reversible myocardial dysfunction occurring during sepsis or septic shock(20–60% of septic shock patients), characterized by: Reduced myocardial contractility Ventricular dilatation Impaired response to fluid and catecholamines Usually recovers within 7–10 days in survivors SCM occurs without acute coronary artery occlusion and is caused

NON ST ELEVATION ACUTE CORONARY SYNDROME (NSTE-ACS)  Definition NSTE-ACS includes: NSTEMI (Non-ST Elevation Myocardial Infarction) → myocardial necrosis + ↑ troponin Unstable Angina (UA) → ischemia(ECG CHANGES) without necrosis (normal troponin)  PATHOPHYSIOLOGY  Plaque rupture/erosion → platelet activation → thrombus formation Partial or intermittent occlusion (NOT complete like STEMI) Leads to subendocardial ischemia Feature NSTE-ACS STEMI