Author Question: Leon is an African American, 55-year-old male. He is a non-smoker, is a nondrinker, and has a ... (Read 47 times)

piesebel · **on:** Jun 25, 2018

Leon is an African American, 55-year-old male. He is a non-smoker, is a nondrinker, and has a healthy weight for his height.

On weekends, he coaches a youth baseball team in his community and loves to eat hot dogs and nachos with the children after they play. Leon attends a community health clinic to have a routine urinalysis and blood pressure monitored. At his last visit, his blood pressure was 168/92 mm Hg. Although Leon was pleased that the lower number dropped from 96 to 92, his physician was still concerned. He warned Leon about the dietary choices he was making and reminded him to limit his salt intake. He also renewed Leon's prescription for diuretics and added an ACE inhibitor to Leon's treatment regime.

Speculate how Leon's ethnicity contributes to his hypertension. What other determinants of health contribute to the prevalence of hypertensive disease in this population?

What is the significance of an elevated systolic pressure, even in the absence of diastolic hypertension?

What is the mechanism of action of the two classes of drugs Leon was prescribed for the management of his hypertension?

Question 2

Martha had just finished dinner with her husband, and they had just sat down to watch television. She is 72 years old and has had a history of angina.

Shortly after they sat down, Martha said she had indigestion and went to take some antacid tablets. An hour later, she began to feel warm, restless, and anxious. Her husband noticed she was looking pale and said he would take her to a nearby walk-in clinic. By the time they arrived, Martha said her left arm and shoulder were sore. Suspecting Martha was having a heart attack, her husband turned the car around and rushed her to the hospital. Three hours after the onset of her symptoms, Martha was receiving oxygen, fibrinolytic therapy, and nitroglycerin in the emergency ward. Afterward, she was moved to the cardiac unit for STEMI.

An ECG of Martha's heart demonstrated an elevated ST segment. What are the physiological effects of myocardial ischemia that produce this finding? What variables affect the ECG tracing of a patient with ACS?

What are the benefits of administering fibrinolytic therapy, nitroglycerin, and oxygen in the early management of STEMI?

What is the inflammatory response in the postinfarction recovery period? Why will Martha's heart function be compromised after her STEMI?

gstein359 · **Reply #1 on:** Jun 25, 2018

Answer to Question 1

The reason for the high incidence of hypertension among African Americans is not entirely clear. Salt sensitivity, or the increase of blood pressure in response to a high-sodium diet, has been speculated. This condition is thought to involve an impaired renal sodium transport mechanism. Increased vasomotor tone and abnormal endothelium-dependent vasodilation are other possibilities for the prevalence of hypertension among African Americans.
Barriers to care are noteworthy in this population. There are frequently financial considerations, difficulties in accessing health care, or long wait times for treatment. Furthermore, health education materials may not be culturally sensitive and fail to address the high rate of salt sensitivity, smoking, and obesity among African Americans.

An elevated systolic pressure, even in the absence of diastolic hypertension, carries with it a high risk for cardiovascular disease. Increased systole is associated with left ventricular hypertrophy, increased myocardial demand for oxygen, and subsequent heart failure. An absolute or relative decrease in diastolic pressure limits coronary perfusion. Finally, a widened pulse pressure damages arterial tissues and predisposes an individual to atherosclerosis and aneurysm formation.

Diuretics reduce blood pressure by increasing renal secretion of sodium and water. They reduce cardiac output and with prolonged use, decrease peripheral vascular resistance. ACE inhibitors limit the activity of ACE in converting angiotensin I to angiotensin II. As a result, less circulating angiotensin II is available to trigger aldosterone secretion and vasoconstriction. ACE inhibitors also inhibit bradykinin degradation and stimulate the production of prostaglandins that have a vasodilating effect.

Answer to Question 2

An elevated ST segment is indicative of acute, transmural ischemia. The result is a decreased resting membrane potential and shortened action potential in damaged myocardial fibers. The current of injury is what appears on the electrocardiogram. Variables affecting the ECG produced include the duration of the ischemic event, the extent of myocardial damage, and the location of the injury in the cardiac tissue.

Myocardial ischemia triggers anaerobic metabolism and subsequent inability for the heart to produce enough energy to function adequately. Fibrinolytic therapy dissolves clot formations so that reperfusion can occur and prevent, or limit, necrosis and microvascular damage. Nitroglycerin mimics endogenous nitric oxide from endothelial tissue and acts as a vasodilator to increase blood flow to cardiac tissue. Vasodilation reduces preload and afterload, therefore reducing demands on the heart. Because nitroglycerin relieves the pain associated with MI, it may assist in the reduction of the sympathetic response. This also contributes to decrease metabolic demand on the heart. The administration of oxygen increases hemoglobin saturation levels to ensure well-oxygenated blood is present in the coronary circulation.

Myocardial damage typically involves a necrotic zone, an area of injury, and an ischemic region. The inner necrotic zone is incapable of recovery or repair. The inflammatory response involves the migration of macrophages to this area to remove the necrotic tissue and cellular debris. Following this process is the lay down of granulation tissue and subsequent deposition of fibrin. Scar tissue finally replaces the area of ischemic insult and has the effect of decreasing extensibility and contractility of the cardiac wall. The initiation and conduction of action potentials are also compromised in the noncontractile area.