Cardiovascular

The "silent killer": years of symptomless pressure quietly damaging heart, brain, kidneys and eyes — until a crisis turns it into an emergency.

Plaque narrows the coronary arteries until oxygen supply can’t meet demand — predictable exertional chest pain that becomes an emergency the moment the pattern changes.

A ruptured plaque, a growing clot, and heart muscle on the clock — one mechanism, three diagnoses, and the tightest time targets in nursing.

The heart can no longer fill with or eject enough blood for the body — and the compensation designed to help makes it worse.

Any rhythm that isn’t normal sinus — from a benign skipped beat to the four rhythms of cardiac arrest — and the decision logic that separates “monitor” from “shock now.”

A clot forms in a deep leg vein — and if it breaks loose, it becomes a pulmonary embolism. The DVT itself rarely kills; the embolus can.

A heart valve that will not open (stenosis) or will not close (regurgitation) overloads a chamber with pressure or volume — the murmur is heard years before the symptoms that mark the prognosis cliff.

Bacteria colonize a damaged heart valve and build a vegetation that destroys the valve, sheds emboli, and hides from antibiotics — which is why cultures come first and the IV course runs 4–6 weeks.

The sac around the heart becomes inflamed — sharp positional chest pain, a friction rub, and diffuse ST elevation that mimics an MI. If fluid fills the sac faster than it can stretch, the heart cannot fill: cardiac tamponade, an obstructive-shock emergency drained by needle.

Atherosclerosis in the leg arteries — pain with walking, then pain at rest, then tissue that dies. The leg is the symptom; the heart and brain are what kill.

The aortic wall loses its structure and balloons — silently, until it ruptures or tears. Rupture kills 80–90%; an untreated type A dissection kills 1–2% per hour.

Diseases of the heart muscle itself — and the drug logic flips between types: what rescues a dilated heart can make a hypertrophic one faint.

Leaky valves let blood fall back down the leg, venous pressure stays high, and over years the skin of the lower leg stains, hardens and finally breaks down into a shallow ulcer above the inner ankle — a problem managed for life with compression, elevation and walking.

Two ways the blood vessels fail. In Raynaud's phenomenon, cold or stress clamps the fingers and toes white, then blue, then red; the secondary form (for example with scleroderma) can ulcerate. In vasculitis the vessel wall itself is inflamed — most testably giant cell arteritis, where a new headache, jaw pain and scalp tenderness in a person over 50 can precede sudden, permanent blindness, so steroids start on suspicion.