17. Shock & IHD

Passive process where blood outflow is impaired, either systemically or locally, leading to blood accumulation in tissues.

Dusky or reddish-blue discoloration of tissues due to accumulated deoxygenated blood.

Area of tissue death due to lack of blood flow (ischemia).

Pale, well-defined area of necrosis in organs with a single blood supply, caused by arterial occlusion.

Venous congestion leads to ulcers by increasing venous pressure, causing fluid accumulation, decreased blood flow, and tissue breakdown.

Excess fluid in interstitial spaces, causing swelling.

Fluid with low protein and cellular content, caused by pressure imbalances.

Fluid with high protein and cellular content, caused by inflammation/vessel damage.

Forces regulating fluid exchange across capillary walls.

Pressure drawing fluid into blood vessels, mainly due to proteins.

Pressure pushing fluid out of blood vessels.

Edema caused by increased hydrostatic pressure.

Edema caused by blocked lymphatic drainage.

Shock's initial stage where the body maintains blood pressure despite decreased cardiac output or blood volume.

Shock's advanced stage where the body's compensatory mechanisms fail, leading to hypotension and diminished organ perfusion.

Insufficient blood supply to the heart muscle (myocardium), often due to atherosclerosis.

A heart attack caused by the sudden blockage of blood flow to the heart muscle.

A disease causing the hardening and narrowing of arteries due to plaque buildup.

Atherosclerosis causing gradual narrowing of coronary arteries leading to heart failure.

A sudden blockage of blood flow to the heart muscle due to a blood clot.

An abnormally fast heart rate, a compensatory mechanism in shock where the body tries to increase blood flow.

Chest pain caused by temporary coronary artery spasms.

Chronic lack of blood causes heart muscle cells to grow larger, affecting contraction.

New blood vessels grow to supply blood to heart muscle with blocked arteries.

Inner heart muscle walls are at greatest risk during heartbeats due to pressure.

Heart attack affecting the entire heart wall thickness.

Heart attack affecting only the inner layer of the heart wall.

Stable narrowing of coronary arteries that limits blood flow during exertion.

Unstable plaque can burst, forming clots that block blood flow.

Initial cellular changes in myocardial infarct, including swelling, glycogen loss, and reversibility; cells can't contract yet.

Injury that occurs 30-60 minutes after ischemia, marked by mitochondrial swelling, membrane disruption, and intracellular substance release leading to necrosis.

Pathway in MI where ATP depletion and ROS damage lead to mitochondrial dysfunction and cell injury to necrosis

Pathway in MI where membrane damage leads to enzyme leakage, function impairment, and ultimately necrosis.

Increased intracellular calcium in MI, disrupting mitochondrial function and activating enzymes, promoting necrosis.

Neutrophils enter the infarct area, marking the start of the inflammatory response within a few days after myocardial injury.

Macrophages replace neutrophils, followed by collagen deposition for scar tissue formation. A weakened heart wall is a risk at this stage.

Collagen continues to accumulate, completely replaces the infarcted area while the tissue heals and stabilizes.

Damage to heart muscle after blood flow is restored following a blockage.

Heart muscle cell death due to hypercontraction and disorganization after blood flow returns.

Heart attack affecting the entire thickness of the heart wall.

Heart attack affecting only part of the heart wall thickness.

Coronary artery frequently associated with anterior heart attack.

Predictable chest pain related to exertion, relieved by rest or medication.

Severe chest pain, changing or new, not relieved by rest or meds.

Death of heart muscle tissue due to lack of blood flow.