Cardiac conditons

Question 1

What is the pathophysiology of Stable Angina?

Answer 1

Stable angina arises from a transient imbalance between myocardial oxygen supply and demand, typically due to coronary artery stenosis caused by atherosclerosis. Atherosclerotic plaques narrow the arterial lumen, impairing blood flow during increased oxygen demand from physical exertion, stress, or other triggers. Endothelial dysfunction, driven by risk factors like hypertension and hypercholesterolemia, promotes plaque formation by disrupting vascular tone and triggering inflammatory responses. During ischemia, chemoreceptors and mechanoreceptors in the heart activate sympathetic pathways, leading to characteristic chest pain or pressure

Question 2

What is the pathophysiology of Unstable Angina?

Answer 2

Unstable angina arises from a dynamic interplay of factors that disrupt myocardial oxygen supply-demand balance, primarily driven by atherosclerotic plaque disruption and intracoronary thrombus formation. When a vulnerable plaque ruptures or erodes, it exposes thrombogenic material, triggering platelet aggregation and partial thrombosis. This thrombus reduces blood flow and releases vasoconstrictive mediators like thromboxane A2, exacerbating ischemia. Concurrent inflammation weakens plaque stability through macrophage-induced matrix metalloproteinases and tissue factor expression, promoting further thrombosis. Endothelial dysfunction impairs vasodilation, while vasospasm or increased myocardial demand (e.g., hypertension, tachycardia) worsens supply-demand mismatch

Question 3

What is the Pathophysiology of Cardiogenic
Shock?

Answer 3

Cardiogenic shock arises from a self-perpetuating cycle of cardiac dysfunction and systemic collapse. It typically begins with myocardial injury (e.g., acute infarction, myocarditis) that severely reduces cardiac output, impairing oxygen delivery to tissues. This triggers compensatory mechanisms:

1. Neurohormonal Activation

The sympathetic nervous system increases heart rate and vasoconstriction to maintain blood pressure, but this raises myocardial oxygen demand, exacerbating ischemia.

Renin-angiotensin-aldosterone system (RAAS) activation increases fluid retention, elevating ventricular filling pressures and causing pulmonary/systemic congestion.

2. Inflammatory Cascade

Hypoperfusion activates systemic inflammation, releasing cytokines (e.g., TNF-α, IL-6) and nitric oxide, which induce pathological vasodilation and myocardial depression.

This inflammation worsens hypotension and reduces coronary perfusion, further impairing contractility.

3. Vicious Cycle of Ischemia

Low cardiac output → hypotension → reduced coronary blood flow → worsening myocardial ischemia → further contractility decline.

Right ventricular failure exacerbates systemic hypoperfusion by limiting left ventricular filling via septal displacement

Question 4

What is the pathophysiology of Cardiogenic
Pulmonary Oedema?

Answer 4

Cardiogenic pulmonary oedema occurs when the heart, most commonly the left ventricle, fails to effectively pump blood, leading to increased pressure in the left atrium and pulmonary veins. This elevated pressure is transmitted backward into the pulmonary capillaries, raising the hydrostatic pressure within these vessels. When this hydrostatic pressure exceeds the plasma oncotic pressure, fluid is forced out of the capillaries and accumulates first in the lung interstitium and then in the alveoli, resulting in pulmonary oedema.

The underlying mechanism is an imbalance in Starling forces-primarily increased capillary hydrostatic pressure-caused by left ventricular systolic or diastolic dysfunction, acute myocardial infarction, valvular disease, or arrhythmias. This process leads to impaired gas exchange, hypoxemia, and respiratory distress