Predisposing Factors

Precipitating Factors

Age: 55 years old

Genetic Factor:

Sedentary Lifestyle
(+) heart disease - paternal side

Obesity: 171 lbs.

(+) stroke - maternal uncle side

High Blood Pressure: 160/ 84 mmHg

(+) hypertension - first line of

History of hypercholesterolemia

blood in the family

Personality features: Type A Personality

Diet
Caffeine Consumption: 3 cups/ day

Increases in the content of lipoproteins within regions of the intima.

Bind to constituents of the extracellular matrix

Lipoproteins that accumulate in the extracellular space of the intima of arteries

Lipoproteins undergo oxidative modifications

Oxidative modification of sequestered lipoproteins

Rise of hydroperoxides, lysophospholipids, oxysterols, and aldehydic breakdown products of fatty acids and phospholipids

Breakdown of peptide backbone as well as derivatization of certain amino acid residues

Activation of pro-inflammatory lipids

Activation of the monocyte, macrophages, lymphocytes

Monocytes attach to the endothelium and migrate to intima

Build up made of fat, cholesterol, calcium, and other cellular waste in the inner lining of the coronary artery

Plaque formation

Disruption or rupture of a vulnerable plaque

Platelets initiate thrombosis at the site of a ruptured plaque

A mural thrombus forms at the site of plaque disruption / site of vascular injury

Thrombotic occlusion of the coronary artery

Acute coronary syndrome

Decreased blood flow in the blood vessel

Decreased oxygen supply, increased demand for oxygen -- tachycardia

Cells are deprived from oxygen

Shortness of breath
Restlessness

Myocardial ischemia

Anaerobic metabolism

Lactic acid formation

Cells send pain signals to the brain

Prolonged oxygen deprivation

inability to produce ATP aerobically.

nausea & heartburn/ feeling of indigestion

Cells fail to meet their metabolic needs

Progressive occlusion of the plaque in the artery

Increased myocardial contraction

The brain is overloaded with escalating pain signals coming from the heart

Tachycardia

chest pain

Sodium-potassium pump suspends where the sodium ions and water begin to fill in eventually causing them to lyse.

With lysis, cells release of intracellular potassium store and intracellular enzymes which injure neighboring cells.

Intracellular proteins gain access to general circulation and interstitial space resulting to interstitial edema and swelling around
myocardial cells

Initiation of inflammatory reactions where platelets accumulate, release of clotting factors.

Degranulation of mast cell begins resulting to the release of histamine

pain radiating to shoulders
and various prostaglandins. Some may have vasoconstrictive
properties and may stimulate clotting.

Cell death.

ACUTE MYOCARDIAL INFARCTION

Necrosis of the heart muscle

Alters conduction, increases

automaticity and promotes triggered
activity related to
after-depolarizations.

Massive muscle loss.

Presence of sinus tachycardia,
premature ventricular
contraction (PVC),

Reference: Harrisons principle of Medicine

Left ventricular failure and cardiogenic shock

Presence of s4, fine

crackles on the lungs,
shortness of breath