Acute Coronary Syndromes & Ischemic Cardiac Lesions

Question-and-answer flashcards covering definitions, causes, pathophysiology, conduction disturbances, arrhythmias, and clinical consequences of acute coronary syndromes and ischemic heart disease.

What vascular structures supply oxygenated blood directly to the heart muscle itself?

The coronary arteries and veins, collectively known as the coronary vasculature.

What is myocardial ischemia?

A decrease in oxygen-rich blood flow to the heart muscle.

What symptom is classically produced by transient myocardial ischemia?

Angina—chest pain caused by reduced oxygen delivery to heart tissue.

What is a myocardial infarction?

Irreversible myocardial tissue death (necrosis) caused by prolonged ischemia.

List the typical progression from oxygen deprivation to tissue death in the heart.

Ischemia → Angina → Infarction.

Name six common mechanisms that narrow or obstruct coronary arteries and cause ischemia.

Plaque formation, thrombus formation, inflammation, arterial constriction, decreased nitric oxide levels, and allergic reactions.

Which cardiac structures can sustain permanent damage during ischemia?

Cardiac muscle, pacemakers/high-speed conduction pathways, coronary vasculature, intrinsic cardiac nervous system, papillary muscles, and AV valves.

After myocardial infarction, what replaces dead myocardium and how does it influence conduction?

Scar tissue (cardiac fibrosis) replaces dead myocardium; it is poorly conductive and predisposes to abnormal electrical activity.

Define atrioventricular (AV) block.

Impaired conduction of action potentials from the atria to the ventricles.

What ECG change characterizes a first-degree AV block?

Prolongation of the PR interval without missed ventricular beats.

How does a second-degree Mobitz I (Wenckebach) AV block present?

Progressive PR prolongation followed by a dropped ventricular beat.

Describe a second-degree Mobitz II AV block.

Intermittent failure to trigger a ventricular action potential without PR prolongation.

What is a 2:1 AV block?

Every other atrial impulse fails to conduct to the ventricles (one conducted beat followed by one blocked).

What defines a third-degree (complete) AV block?

No atrial impulses reach the ventricles, resulting in complete atrioventricular dissociation.

Give three potential clinical consequences of significant AV block.

Decreased cardiac output, heart failure, and possible death (with reduced quality of life).

What electrophysiologic mechanism can ischemia trigger in high-speed pathways that leads to arrhythmia?

Reentry, caused by unidirectional block and recovery of excitability around an ischemic zone.

Which life-threatening rhythm can result from ventricular reentry circuits?

Ventricular fibrillation.

Why does ventricular fibrillation drastically decrease cardiac output?

Chaotic, non-coordinated ventricular contractions prevent effective blood ejection.

What specialized conduction fibers rapidly distribute impulses through the ventricles?

Purkinje fibers (components of the high-speed conduction pathways).

How does scar-induced conduction slowing favor reentry?

Scar tissue lengthens the effective refractory period and creates areas of unidirectional block, allowing circulating impulses to re-excite tissue.

What are two major endpoints of untreated severe ischemia highlighted in the lecture?

Heart failure and death.

Summarize the "big picture" consequences of cardiac ischemia outlined on slide 18.

Ischemia leads to angina and infarction, causing myocardial cell death/fibrosis, AV block, reentry or ectopic action potentials, arrhythmias, heart failure, and potentially death.