Normal Cardiac Physiology
The heart has 4 chambers, 2 on the left (left atrium and ventricle), 2 on the right (right atrium and ventricle). Deoxygenated blood enters the right side of the heart into the right atrium and is pumped into the lungs from the right ventricle through the pulmonic valve to be oxygenated (Berkowitz, A., 2007, p. 1). Once the blood is oxygenated in the lungs, it is then returned to the left atrium, then left ventricle to be distributed out to the body through the aortic valve and into circulation.
Figure 4. Normal Heart (CEUFast, 2019)
There are 4 valves (tricuspid, pulmonic, mitral, and aortic) in the heart. These valves prevent the blood from back flowing into the previous area the blood was pumped out of. The tricuspid and pulmonic valves are on the right side of the heart. The mitral and aortic are on the left side of the heart (Berkowitz, A., 2007, p. 1).
The heart also has a conduction system that generates electrical currents to contract the atria and ventricles. The contractions are what pumps the blood into different areas of the heart. The Sinoatrial node starts the impulse in the right atrium and causes the atria to contract. The impulse then continues on to the atrioventricular node, Bundle of His, and Purkinje fibers. The electrical impulse is spread through the ventricles by the Purkinje fibers and cause the ventricles to contract simultaneously (Berkowitz, A., 2007, p. 14-15).
The heart’s blood supply is provided by the coronary arteries. There are two main arteries that supply the heart with oxygen- rich blood and carry away the deoxygenated blood away. These arteries are called the left main coronary artery and right coronary artery. These arteries wrap around the heart muscle and have smaller branches that go down into the muscle to ensure adequate blood flow throughout the whole heart muscle (McCance and Huether, 2019, p.1024).
Altered Cardiac Pathophysiology
The heart’s blood supply comes from the coronary arteries. If the blood supply is decreased for any reason, then the heart has to work harder and thus increases the chance of complications damaging the heart muscle. Blood supply can be decreased by the build-up of plaque in the arteries supplying blood flow to the heart. Over time, the blood vessels can narrow from plaque buildup. These plaques can rupture and form a blood clot. If the clot is large enough, it can block all blood flow from that artery to the heart and deprive the heart of oxygen and nutrients.
Significant predisposing risk factors for alterations in the pathophysiology of blood flow to the heart are dyslipidemia, hypertension, smoking, diabetes mellitus, obesity, atherosclerosis, and poor diet (McCance and Huether, 2019, p. 1074-78).
Hypertension is a risk factor for myocardial infarction because it contributes to endothelial injury, causing myocardial hypertrophy, which increases myocardial demand for coronary flow (McCance and Huether, 2019, pg.1077) Diet high in salt, fats, trans fats, and carbohydrates contribute not only to the development of hypertension but also myocardial infarction (McCance and Huether, 2019, p. 1078).
Smoking is another major contributor to developing a myocardial infarction because nicotine stimulates the release of catecholamines, which increase the heart rate and cause peripheral vascular constriction therefore increasing cardiac workload and oxygen demand (McCance and Huether, 2019, p. 1077). Cigarette smoking is associated with an increase in LDL and contributes to vessel inflammation and thrombosis (McCance and Huether, 2019, p. 1077).
The effects of diabetes include: endothelial damage, thickening of the vessel wall, increased inflammation and leukocyte adhesion, increased thrombosis, and decreased production of vasodilators (McCance and Huether, 2019, p. 1077).
Obesity has a very strong link with coronary artery disease because its related to insulin resistance, decreased HDL levels, increased blood pressure, and inflammation (McCance and Huether, 2019, p. 1077). Obesity is also associated with deposition of perivascular adipose tissue that contributes to atherogenesis (McCance and Huether, 2019, p. 1077).
Dyslipidemia plays a major role in the development of atherosclerosis because elevated low-density lipoproteins are needed to begin the cascade of events leading to atherosclerosis (McCance and Huether, 2019, p. 1075). Atherosclerosis is the thickening and hardening of the arteries that occurs from lipid -laden macrophages within the arterial wall, leading to the formation of plaque (McCance and Huether, 2019, p. 1072).
All of these risk factors lead to an unstable environment within the coronary vasculature. When coronary blood flow is interrupted for an extended period, myocyte necrosis occurs resulting in myocardial infarction (McCance and Huether, 2019, p. 1083). The events leading up to a myocardial infarction are as follows: an unstable athlersclerotic plaque ruptures due to shear forces, inflammation, apoptosis, and production of vasoconstrictors (McCance and Huether, 2019, p.1083). The clotting cascade is activated and a thrombus forms. This thrombus occludes the vessel for a long period initially causing myocardial ischemia, but then progresses to myocyte necrosis and death (McCance and Huether, 2019, p. 1082-84). After 8-10 seconds of decreased blood flow, the affected myocardium becomes cyanotic and cooler (McCance and Huether, 2019, p. 1084). Glycogen stores decrease as anaerobic metabolism begins (McCance and Huether, 2019, p. 1084). However, glycolysis can only supply 65-70% of the total myocardial energy requirement (McCance and Huether, 2019, p. 1084). Hydrogen ions and lactic acid accumulates, and acidosis can lead to a suppressed impulse conduction and contractile function leading to heart failure (McCance and Huether, 2019, p. 1084). Loss of contractility and pumping ability is also due to electrolyte disturbances caused by oxygen deprivation (McCance and Huether, 2019, p. 1084). Ischemic myocardial cells release epinephrine and norepinephrine putting the patient at risk for sympathetic and parasympathetic dysfunction, dysrhythmias, and heart failure (McCance and Huether, 2019, p. 1084). The most common and dangerous complication of an acute MI is dysrhythmias (McCance and Huether 2019, p. 1087).
Correct Diagnosis
Myocardial Infarction
Figure 5. Myocardial Infarction (Medbullets, 2019)
The first symptom of acute MI is sudden, severe chest pain, which is Mr. Smith’s first complaint (McCance and Huether, 2019, p. 1085). His EKG shows ST-segment changes in specific leads (II, III, AVf) helping pinpoint the exact area of infarct (McCance and Huether, 2019, p. 1086). Mr. Smith is experiencing nausea, tachycardia, and elevated blood pressure, caused by stimulation of vomiting centers by pain fibers, and activation of the sympathetic nervous system (McCance and Huether, 2019. p. 1086). The patient’s troponin was elevated at the 2 hour and 6 hour mark, helping to further estimate infarct size and likelihood of complications (McCance and Huether, 2019, p. 1086). His clinical presentation, personal, family, and social history, along with predisposing risk factors lead to the conclusion Mr. Smith is experiencing a myocardial infarction.