Case Study for Chapter

Coronary Artery Disease

A 57-year-old man experienced several months of vague pains in his left chest and shoulder when climbing stairs. During a touch football game at a family picnic, he had much more intense pain and had to rest. After about 45 minutes of intermittent pain, his family brought him to the emergency department.

His heart rate is 105 beats/min, his blood pressure is 105/85 mm Hg, and his hands and feet are cool to touch and somewhat bluish. He is sweating and is short of breath. An electrocardiogram indicates an elevated ST segment, which was most noticeable in leads V4 to V6. The attending cardiologist administers streptokinase intravenously.

One hour later, the ST segment abnormality is less noticeable. The heart rate is 87 beats/min, the arterial blood pressure is 120/85 mm Hg, and the patient's hands and feet are pink and warm. The patient is alert, not sweating, and does not complain of chest pain or shortness of breath.

During a 4-day stay in the hospital, percutaneous angioplasty was performed to open several partially blocked coronary arteries. The patient is told to take half of an adult aspirin pill every day and is given a prescription of a statin drug to lower blood lipids. In addition, he is assigned to a cardiac rehabilitation program designed to teach proper dietary habits and improve exercise performance and, together, to lower gradually body fat.

Questions

1. How did the left chest and shoulder pain during stair climbing predict some abnormality of coronary artery function?

2. Why was a 45-minute delay before going for medical intervention after intense pain started inappropriate for the man's health?

3. How does the lower than normal arterial pressure, smaller than normal arterial pulse pressure, and decreased blood flow to the hands and feet indicate impairment of the contractile function of the heart?

4. How did the streptokinase improve performance of the heart?

5. How is aspirin useful to protect the coronary vasculature from occlusions by blood clots?

6. How might lowering the low-density lipoproteins and raising the high-density lipoproteins with a combination of diet, exercise, and statin therapy lessen the chance of a second heart attack?

Answers to Case Study Questions for Chapter 17

1. The exercise of stair climbing imposed a substantial demand on the heart to pump blood, thereby, requiring more oxygen for the heart cells. Partially occluded arteries did not provide sufficient blood flow to provide the needed oxygen and hypoxia resulted. Coronary artery problems leading to mild hypoxia of the heart muscle typically cause a referred pain to the left chest and shoulder area. In some persons, the pain extends into the left arm and hand, as well as neck and jaw.

2. There is a major risk that cardiac hypoxia will initiate abnormal electrical activity in the heart. The results can range from mild disturbances of conduction to rapidly lethal ventricular fibrillation. In addition, the longer cardiac cells are without adequate blood flow, the more damage is done to the cells. The sooner oxygenation is restored, the less repair is needed in the heart tissue.

3. When the contractile ability of the heart is compromised, the typical result is a reduced stroke volume, which would explain the decreased pulse pressure. If cardiac output decreases, in spite of an increased heart rate, then arterial pressure tends to fall. The decreased blood flow to the hands and feet indicates that the sympathetic nervous system has been activated to constrict peripheral blood vessels, preserving the arterial pressure as much as possible in the presence of reduced cardiac function.

4. Streptokinase is a bacterial product that activates plasminogen, which leads to clot dissolution. Blood flow and oxygen supply to the downstream muscle will then be restored. If the muscle cells are not seriously injured, they will show prompt recovery of contractile function to restore the stroke volume and cardiac output.

5. Aspirin blocks the cyclooxygenase enzymes in all cells. With aspirin present, platelets are far less likely to be activated, limiting clot formation in areas of vessels with damaged endothelial cells. The production of prostaglandins by platelets is part of the clotting process. Also, thromboxane released by activated platelets will cause constriction of coronary arteries and arterioles, lowering blood flow in an already flow-deprived state.

6. Although regression of plaques is not dramatic when low-density lipoproteins are reduced, continued growth of the plaque is decreased and, in some cases, virtually stopped. This lowers the probability of a plaque rupturing and starting the formation of a new clot that will occlude the artery. In addition, lowering the LDL concentration will limit the formation of new plaques and, thereby, reduces the risk of vessel occlusion.

Reference

Lilly LS. Pathophysiology of Heart Disease. Baltimore: Williams

& Wilkins, 1998.

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