Cardiovascular

Rupture of an unstable atherosclerotic plaque triggers thrombus formation that partially or completely occludes a coronary artery, and the resulting ECG and troponin pattern (STEMI, NSTEMI, or unstable angina) dictates exactly how urgently the vessel must be reopened.

Diffuse inflammation of the pericardial sac roughens its two layers so they rub together with every heartbeat, producing sharp pain that worsens lying flat and eases leaning forward, with widespread ECG changes because the injury current spreads across the whole heart rather than one coronary territory.

A tear in the aortic intima lets high-pressure blood force its way into the vessel wall, splitting it along its length to create a false lumen that can obstruct branch arteries, rupture, or compromise the aortic valve, so the priority is same-hour imaging and blood pressure control, not analgesia alone.

Progressive narrowing of the aortic valve forces the left ventricle to generate ever-higher pressures to maintain forward flow, and the compensatory hypertrophy this produces keeps patients symptom-free for years until the ventricle finally fails, giving the classic late triad of angina, syncope and heart failure.

Chaotic re-entrant electrical activity replaces organised atrial contraction, so the atria quiver rather than pump, producing an irregularly irregular pulse and blood stasis that drives thromboembolic risk independent of how the rhythm is managed.

Failure or delay of impulse generation or conduction anywhere from the sinus node to the ventricles slows or interrupts the heart's electrical cascade, so the exact pattern of block on the ECG predicts how much of the atrial rhythm still reaches the ventricles, and therefore how dangerous it is.

A state in which the heart cannot deliver enough output for the body's needs at normal filling pressures, triggering neurohormonal compensations that relieve symptoms short-term but drive progression, which the key drugs are designed to block.

Stasis, vessel wall injury and hypercoagulability tip the normal balance of coagulation towards clot formation in a deep vein, obstructing venous return and provoking local inflammation, and the real danger is that a fragment of that clot breaks off and embolises to the lungs.

A sustained rise in systemic arterial pressure that is usually clinically silent because vessels adapt gradually with no acute pain signal, so screening and end-organ assessment (not symptoms) drive both diagnosis and the urgency of treatment.

Bloodstream bacteria seed a damaged or abnormal endocardial surface and become trapped in a platelet-fibrin vegetation that shields them from the immune system, so the disease is driven simultaneously by local valve destruction, embolisation of vegetation fragments, and immune complex deposition at distant sites.

A fixed atherosclerotic narrowing limits how much extra blood flow a coronary artery can deliver, so it cannot meet the higher oxygen demand of exertion, producing predictable, reproducible chest pain that resolves once demand falls back within the fixed supply ceiling.