Cardiac Critical care

approach to shock

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 […]

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Hypertensive Crisis

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

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ATRIAL FIBRILLATION

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

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Septic Cardiomyopathy

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

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NON ST ELEVATION ACUTE CORONARY SYNDROME

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

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