Cardiac Pathophysiology Flashcards

Vocabulary flashcards focusing on cardiac pathophysiology, including angina types, myocardial infarction, free radical actions, and valvular disorders.

Angina Pectoris

Severe pain originating from the heart that occurs in response to an inadequate oxygen supply to myocardial cells compared to demand, considered reversible myocardial ischemia.

Stable Angina

Angina occurring with exertion or increased workload by the myocardium at a predictable level of activity, typically lasting $3\text{-}5\,\text{minutes}$ and relieved by rest.

Prinzmetal's (Variant) Angina

Angina occurring at rest with no obvious increase in workload, caused by severe coronary artery spasm, and usually disappearing in about $5\,\text{minutes}$.

Unstable Angina

Angina occurring with exertion or at rest, caused by transient clot formation and coronary spasm, lasting $10\text{-}20\,\text{minutes}$, and unrelieved by immediate rest.

Anginal Pain Pathway

Afferent sympathetic nerve fibers that transmit cardiac pain signals entering the spinal cord at levels $C3$ to $T4$ ($\text{Cervical } 3$ to $\text{Thoracic } 4$).

Acute Myocardial Infarction (AMI)

The death of myocardial cells resulting from prolonged oxygen deprivation.

Epicardium

The outermost layer of the heart wall lying beneath the pericardial sac.

Myocardium

The middle muscular layer of the heart wall that is primarily responsible for cardiac contraction.

Endocardium

The innermost layer of the heart wall that lines the cardiac chambers and protects against friction.

Subendocardial Infarction

Infarction occurring at the distal ends of capillaries involving only the innermost layer of cardiac tissue, clinically manifesting as a Non-STEMI.

Transmural Infarction

Infarction extending all the way through the full thickness of the myocardium wall, clinically manifesting as a STEMI.

Reactive Oxygen Species (ROS)

Free radicals formed as byproducts of normal oxygen metabolism in mitochondria that act as mediators of vascular wall changes.

Physiologic Actions of Free Radicals

Normal beneficial ROS actions including promoting smooth muscle relaxation, killing bacteria and tumor cells, inhibiting platelet aggregation, and promoting collateral circulation.

Pathologic Actions of Oxidized Free Radicals

Damaging effects of excess oxidized ROS including promoting vascular permeability, cellular toxicity, white cell plugging, worsening reperfusion injuries, and decreasing $\text{Ca}^{++}$ release.

Collateral Circulation

Alternative blood flow pathways formed by small anastomoses between arterioles that dilate during occlusion to provide compensatory perfusion.

Troponin I (Cardiac)

The most sensitive cardiac biomarker protein released secondary to myocardial cell lysis during cardiac injury.

Heart Fatty Acid-Binding Protein (H-FABP)

A cardiac marker released by damaged myocardial cells within $30\,\text{minutes}$ of ischemic injury.

Pericarditis

Inflammation of the fluid-filled pericardial sac surrounding the heart, which typically resolves on its own in $2\text{-}4\,\text{weeks}$.

Pericardial Tamponade

A life-threatening complication where excess fluid accumulation in the pericardial space or myocardial rupture compresses the heart chambers.

Myocarditis

Inflammation of the myocardium unrelated to CAD or AMI, most commonly caused by viral infection, leading to a flabby, dilated heart muscle.

Cardiomyopathies

Any disease or injury of the heart muscle not related to coronary artery disease, hypertension, or congenital malformations.

Rheumatic Fever

A preventable inflammatory disease occurring $1\text{-}4\,\text{weeks}$ post untreated Group A beta-hemolytic streptococcus throat infection that can permanently affect cardiac valves.

Stenosis

The narrowing of any vessel, valve, or opening, which forces the upstream chamber to pump more forcefully to propel blood.

Mitral Valve Stenosis

Narrowing of the mitral valve opening that causes left atrial hypertrophy, pulmonary congestion, fatigue, and right-sided heart failure.

Aortic Valve Stenosis

Narrowing of the aortic valve opening causing left ventricular hypertrophy, reduced cardiac output, pulmonary congestion, dizziness, and fatigue.