SECTION III THE CARDIOVASCULAR SYSTEM Coronary Artery Disease and Bypass Surgery-Familial Dysbetalipoproteinemia A 42-year-old man entered the hospital because of multiple complaints.His family history reveals that his father and his two older brothers died of coromary artery disease in their midforties.For several years the patient has had increasing bouts of angina pectoris (which was relieved by nitroglycerin),pain in the calves of his legs when he climbs stairs,and two episodes of transient cerebral ischeaia within the past month.Physical examination was not remarkable,except for xanthoma (yellow-orange fatty deposits)on his palns and around his knees and elbows and absence of pulses in the feet.Angiograms showed extensive atheromatous disease in the abdominal aorta and in the carot id,coronary,mesenteric,femoral,and popliteal arteries with alnost complete blockage of blood flow in two coroeary arteries. Because of his leg probleas,he was given a cardiac stress test with an intravenous infusion of adenosine,instead of exercise on a treadmill.The test elfeited angina and ST segment changes indicative of mocardial ischemia.Blood cholesterol level and triglycerides were elevated,and genetic analysis revealed that he had fanilial dysbetalipoproteinemia. After a thoracotomy for coronary bypass surgery.he was heparinized.placed on a pump-oxygenator,and had potassium chloride injeeted into his coronary arteries and ice-cold saline applied to his heart.After coapletion of the coronary bypass surgery,he was hypotensive when taken off the pump-oxygenator and was treated with a vasoconstrictor to maintain a normal blood pressure.Were it not for the extensive atherosclerosis in his femoral arteries and abdominal aorta.he would have had a counterpulsation device placed in his abdominal aorta via a femoral artery.This device consists of a long inflatable balloon.Inflation and deflatfon are synchronized with the heartbeat:the balloon is inflated during diastole and deflated during systole
SECTION III THE CARDIOVASCULAR SYSTEM Coronary Artery Disease and Bypass Surgery—Familial Dysbetalipoproteinemia A 42-year-old man entered the hospital because of multiple complaints. His family history reveals that his father and his two older brothers died of coronary artery disease in their midforties. For several years the patient has had increasing bouts of angina pectoris (which was relieved by nitroglycerin), pain in the calves of his legs when he climbs stairs, and two episodes of transient cerebral ischemia within the past month. Physical examination was not remarkable, except for xanthoma (yellow-orange fatty deposits) on his palms and around his knees and elbows and absence of pulses in the feet. Angiograms showed extensive atheromatous disease in the abdominal aorta and in the carotid, coronary, mesenteric, femoral, and popliteal arteries with almost complete blockage of blood flow in two coronary arteries. Because of his leg problems, he was given a cardiac stress test with an intravenous infusion of adenosine, instead of exercise on a treadmill. The test elicited angina and ST segment changes indicative of myocardial ischemia. Blood cholesterol level and triglycerides were elevated, and genetic analysis revealed that he had familial dysbetalipoproteinemia. After a thoracotomy for coronary bypass surgery, he was heparinized, placed on a pump-oxygenator, and had potassium chloride injected into his coronary arteries and ice-cold saline applied to his heart. After completion of the coronary bypass surgery, he was hypotensive when taken off the pump-oxygenator and was treated with a vasoconstrictor to maintain a normal blood pressure. Were it not for the extensive atherosclerosis in his femoral arteries and abdominal aorta, he would have had a counterpulsation device placed in his abdominal aorta via a femoral artery. This device consists of a long inflatable balloon. Inflation and deflation are synchronized with the heartbeat; the balloon is inflated during diastole and deflated during systole
A week after the bypass surgery.his coroeary blood flow,as neasured by the thernodilution technique,vas found to be improved. 1.What is the rationale of the adenosine stress test? 2.Why was potassium chloride injected,and why was ice-cold saline applied to the heart when the patient was placed on the pump-oxygenator? 3.Why would a counterpulsation device have been beneficial during the postoperative recovery period? 4.How is thernodilution used to neasure coronary blood flow? 5.What are the physical factors that affect coronary blood flow in this patient? 6.What role do the sympathetic nerves play in the regulation of his coronary blood f1ow？ 7.What are the chenical factors that influence his coronary blood flow? 8.Would epicardial and endocardfal blood flos be affected equally? 9.Bow does nitroglycerin relieve the patient's angina pectoris?What effect does this drug have on blood pressure and skin blood flow? 10.What causes the developrent of collateral vessels in this patient's heart? 11.With central activation of the sympathetic nervous systen how do vascular beds in heart,skeletal muascle.skin,gastrointestinal tract,kidney,and hrain differ? 12.What effect would elevation of emvironmental temperature have on this patient? 13.What effect would exposure to cold have on this patient? 14.What role do the venous valves play in the different vascular beds of this patient? 15.The patient experienced pain in the right leg when climbing stairs.What effect might this have on regional cerebral blood flow? 16.What happens to gastrointestinal and liver blood flow and digestive activity when the patient exercises (runs)? 17.What effect would CO.inhalation have on his cerebral blood flow?
A week after the bypass surgery, his coronary blood flow, as measured by the thermodilution technique, was found to be improved. 1. What is the rationale of the adenosine stress test? 2. Why was potassium chloride injected, and why was ice-cold saline applied to the heart when the patient was placed on the pump-oxygenator? 3. Why would a counterpulsation device have been beneficial during the postoperative recovery period? 4. How is thermodilution used to measure coronary blood flow? 5. What are the physical factors that affect coronary blood flow in this patient? 6. What role do the sympathetic nerves play in the regulation of his coronary blood flow? 7. What are the chemical factors that influence his coronary blood flow? 8. Would epicardial and endocardial blood flow be affected equally? 9. How does nitroglycerin relieve the patient's angina pectoris? What effect does this drug have on blood pressure and skin blood flow? 10. What causes the development of collateral vessels in this patient's heart? 11. With central activation of the sympathetic nervous system, how do vascular beds in heart, skeletal muscle, skin, gastrointestinal tract, kidney, and brain differ? 12. What effect would elevation of environmental temperature have on this patient? 13. What effect would exposure to cold have on this patient? 14. What role do the venous valves play in the different vascular beds of this patient? 15. The patient experienced pain in the right leg when climbing stairs. What effect might this have on regional cerebral blood flow? 16. What happens to gastrointestinal and liver blood flow and digestive activity when the patient exercises (runs)? 17. What effect would CO2 inhalation have on his cerebral blood flow?
18.What effeect would hypoxia have on his cerebral blood flow? 19.What effect does the patient's atherosclerosis have on cerebral blood flow and arteriolar resistance? 20.If this patient had a patent ductus arteriosus,what kind of murmur would he have and why? ANSVER 1.An intravemous infusion of adenosine dilates arterioles,particularly in the heart.In cases where coronary artery obstruction exists and hence blood flow is linited,the arterioles distal to the obstructed vessels become maximally dilated by the release of local metabolites (e.g.,adenosine)and cannot be dilated further by the adninistered adenosine.However,the cogmate arterioles of the patent arteries dilate.As a result,the pressure in these patent arteries decreases.and flow froa these arteries via collateral vessels to the ischeaic myocardium is reduced.This produces greater myocardial ischemia with precordial pain and/or electrocardfographie evidence of ischeaia.With this type of stress test,the heart is stressed by reducing its oxygen supply rather than by increasing the cardiac workload with exereise. 2.Potassiun chloride was given to arrest the heart in diastole in order to nake the operation technically easier and to reduce the oxygen need of the mocardium during the time when blood flow to the heart muscle and lumgs is stopped.The cold saline also reduces the cardiac oxygen needs by lowering cardiac metabolic activity and thereby prevents ischenic damage to the myocardium. 3.The increased aortic resistance during diastole raises blood pressure proximal to the balloon and thereby improves coronary perfusion at a tine when extravascular compression by the myocardiun is absemt.During systole the deflation of the halloon reduces resistance to ejection by the left ventricle and thereby decreases cardiac work and the oxygen needs of the myocardiun
18. What effect would hypoxia have on his cerebral blood flow? 19. What effect does the patient's atherosclerosis have on cerebral blood flow and arteriolar resistance? 20. If this patient had a patent ductus arteriosus, what kind of murmur would he have and why? ANSWER 1. An intravenous infusion of adenosine dilates arterioles, particularly in the heart. In cases where coronary artery obstruction exists and hence blood flow is limited, the arterioles distal to the obstructed vessels become maximally dilated by the release of local metabolites (e.g., adenosine) and cannot be dilated further by the administered adenosine. However, the cognate arterioles of the patent arteries dilate. As a result, the pressure in these patent arteries decreases, and flow from these arteries via collateral vessels to the ischemic myocardium is reduced. This produces greater myocardial ischemia with precordial pain and/or electrocardiographic evidence of ischemia. With this type of stress test, the heart is stressed by reducing its oxygen supply rather than by increasing the cardiac workload with exercise. 2. Potassium chloride was given to arrest the heart in diastole in order to make the operation technically easier and to reduce the oxygen need of the myocardium during the time when blood flow to the heart muscle and lungs is stopped. The cold saline also reduces the cardiac oxygen needs by lowering cardiac metabolic activity and thereby prevents ischemic damage to the myocardium. 3. The increased aortic resistance during diastole raises blood pressure proximal to the balloon and thereby improves coronary perfusion at a time when extravascular compression by the myocardium is absent. During systole the deflation of the balloon reduces resistance to ejection by the left ventricle and thereby decreases cardiac work and the oxygen needs of the myocardium
4.For measurement of coronary blood flow by thermodilution,a double lumen catheter is inserted into the coronary sinus via a peripheral vein.Ice-cold saline is injected from the catheter tip,and a temperature probe a few centimeters proximal (domnstream)to the catheter tip senses the blood temperature.The smaller the terperature change after the cold saline injection,the greater the coronary sinus blood flow. 5.The physical factors that affect coronary blood flow in this patient are the systolic,and especially the diastolic,aortic pressure,the extravascular compression exerted by the beart susele on the coronary vessels.blood viscosity, and of greatest importance,arterial and arteriolar resistances. 6.The sympathetic merves do not play a significant role in the regulation of coronary blood flow in this patient,particularly hecause the arterioles are dilated by local metabolites.Even in normal individuals the local metabolic factors predoninate over neural factors in the regulation of coroeary blood flo. 7.Several agents have been proposed as mediators of the vasodilation that occurs in the coronary circulation when blood flow to the myocardiun is inadequate. Adenosine is involved,and as yet unidentified substances may also contribute to vasodilation secondary to ischemia. 8.No.Endocardial blood flow would be more compromised than epicardial blood flow because of the greater vascular compression by the endocardial myocardium. 9.It is not firmly established how nitroglyeerin relieves angina pectoris,but evidence suggests that (1)it dilates coronary collateral vessels and (2)it decreases preload by relaxing the large veins such as the vena cava.The drug dilates resistance vessels throughout the body and thereby produces a transient reduction in arterial blood pressure. 10.The progressive narrowing of a coronary artery results in the developaent of collateral vessels from patent coronary artery,which supplies some blood to the muscle served by the obstructed artery.The collaterals develop froa preexisting capillaries.and the coobination of ischenia and the high pressure gradient leads to collateral vessel formation
4. For measurement of coronary blood flow by thermodilution, a double lumen catheter is inserted into the coronary sinus via a peripheral vein. Ice-cold saline is injected from the catheter tip, and a temperature probe a few centimeters proximal (downstream) to the catheter tip senses the blood temperature. The smaller the temperature change after the cold saline injection, the greater the coronary sinus blood flow. 5. The physical factors that affect coronary blood flow in this patient are the systolic, and especially the diastolic, aortic pressure, the extravascular compression exerted by the heart muscle on the coronary vessels, blood viscosity, and of greatest importance, arterial and arteriolar resistances. 6. The sympathetic nerves do not play a significant role in the regulation of coronary blood flow in this patient, particularly because the arterioles are dilated by local metabolites. Even in normal individuals the local metabolic factors predominate over neural factors in the regulation of coronary blood flow. 7. Several agents have been proposed as mediators of the vasodilation that occurs in the coronary circulation when blood flow to the myocardium is inadequate. Adenosine is involved, and as yet unidentified substances may also contribute to vasodilation secondary to ischemia. 8. No. Endocardial blood flow would be more compromised than epicardial blood flow because of the greater vascular compression by the endocardial myocardium. 9. It is not firmly established how nitroglycerin relieves angina pectoris, but evidence suggests that (1) it dilates coronary collateral vessels and (2) it decreases preload by relaxing the large veins such as the vena cava. The drug dilates resistance vessels throughout the body and thereby produces a transient reduction in arterial blood pressure. 10. The progressive narrowing of a coronary artery results in the development of collateral vessels from patent coronary artery, which supplies some blood to the muscle served by the obstructed artery. The collaterals develop from preexisting capillaries, and the combination of ischemia and the high pressure gradient leads to collateral vessel formation
11.Relative to other tissues,the vascular beds of the heart and especially the brain are not very responsive to general sympathetic activation.These two vascular beds are primarily under the control of local petabolic factors.Skin, gastrointestinal tract,kidney.and resting skeletal muscle show a high degree of vasoconstriction in response to sympathetic activity.However,in comtracting skeletal muscle sympathetic neural regulation yields to local metabolic factors. 12.An increase in envirommental temperature would dilate skin blood vessels. which facilitates heat loss and tends to maintain a constant core temperature.This dilation would decrease vascular resistance and could decrease arterial blood pressure,especially if body temperature rises and other vascular beds also dilate. If body temperature is increased.an added burden is placed on the heart and circulation by increasing the oxygen demnds of the myocardiun and other body tissues. 13.Cold exposure would comstriet the skin arterioles,thereby preventing heat loss and maintaining body temperature constant.This vasoconstriction is accomplished via a skin reflex and via cooled blood reaching the terperature-regulating center in the hypothalamus.Blood pressure could be reflexly increased by cold exposure.Any reduction in body temperature would reduce the metabolic needs of the body an thereby reduce the heart and body oxygen requirenemts. 14.The venous valves in this patient (and in all sub jeets)serve to aid in the return of blood to the heart.With the patient in the upright position,musele contraction in the leg squeezes the veins and forces blood out of them in the direction of the heart,because the venous valves prevent flow in the opposite direction 15.The pain in the right leg (caused by ischemia)produces vasodilation in the contralateral sensory-motor cortex in the region that serves the leg.This response is prohably mediated by the release of nitric oxide from the endothelium of the vessels in this cortical region and is not associated with adenosine release in the cortex.Adenosine release is associated with either increased metabolic activity or a reduced oxygen supply
11. Relative to other tissues, the vascular beds of the heart and especially the brain are not very responsive to general sympathetic activation. These two vascular beds are primarily under the control of local metabolic factors. Skin, gastrointestinal tract, kidney, and resting skeletal muscle show a high degree of vasoconstriction in response to sympathetic activity. However, in contracting skeletal muscle sympathetic neural regulation yields to local metabolic factors. 12. An increase in environmental temperature would dilate skin blood vessels, which facilitates heat loss and tends to maintain a constant core temperature. This dilation would decrease vascular resistance and could decrease arterial blood pressure, especially if body temperature rises and other vascular beds also dilate. If body temperature is increased, an added burden is placed on the heart and circulation by increasing the oxygen demands of the myocardium and other body tissues. 13. Cold exposure would constrict the skin arterioles, thereby preventing heat loss and maintaining body temperature constant. This vasoconstriction is accomplished via a skin reflex and via cooled blood reaching the temperature-regulating center in the hypothalamus. Blood pressure could be reflexly increased by cold exposure. Any reduction in body temperature would reduce the metabolic needs of the body an thereby reduce the heart and body oxygen requirements. 14. The venous valves in this patient (and in all subjects) serve to aid in the return of blood to the heart. With the patient in the upright position, muscle contraction in the leg squeezes the veins and forces blood out of them in the direction of the heart, because the venous valves prevent flow in the opposite direction. 15. The pain in the right leg (caused by ischemia) produces vasodilation in the contralateral sensory-motor cortex in the region that serves the leg. This response is probably mediated by the release of nitric oxide from the endothelium of the vessels in this cortical region and is not associated with adenosine release in the cortex. Adenosine release is associated with either increased metabolic activity or a reduced oxygen supply
16.With physical exereise,blood flow is increased to the active muscles by the action of local metabolites,and it is decreased to the gastrointestinal tract and liver by arteriolar constriction mediated by the sympathetic nerves. 17.Cerebral blood flow in this patient and in normal individuals is increased by CD.inhalation.Because the cerebral arterioles are probably someshat dilated as a result of the carotid artery atherosclerosis and the comsequent increase in resistance to blood flow,CD,would have less effect in this patient than in a normal person. 18.Hypoxia would increase cerebral blood flow by enhancing the formation and release of adenosine and other vasodilator metabolites in the brain tissue. 19.The atheroselerosis reduces blood flow to the brain and can cause brief reversible 'strokes"called transient ischemic attacks (TIAs).Arteriolar resistance would be reduced because of the release of vasodilator metabolites from the inadequately perfused brain tissue. 20.A patent ductus arteriosus causes a continuous murmur over the precordium because of blood flow from the aorta (higher pressure)to the pulmonary artery (lower pressure).The murmur is loudest during systole,when the pressure gradient between the aorta and pulmonary artery is greatest
16. With physical exercise, blood flow is increased to the active muscles by the action of local metabolites, and it is decreased to the gastrointestinal tract and liver by arteriolar constriction mediated by the sympathetic nerves. 17. Cerebral blood flow in this patient and in normal individuals is increased by CO2 inhalation. Because the cerebral arterioles are probably somewhat dilated as a result of the carotid artery atherosclerosis and the consequent increase in resistance to blood flow, CO2 would have less effect in this patient than in a normal person. 18. Hypoxia would increase cerebral blood flow by enhancing the formation and release of adenosine and other vasodilator metabolites in the brain tissue. 19. The atherosclerosis reduces blood flow to the brain and can cause brief reversible "strokes" called transient ischemic attacks (TIAs). Arteriolar resistance would be reduced because of the release of vasodilator metabolites from the inadequately perfused brain tissue. 20. A patent ductus arteriosus causes a continuous murmur over the precordium because of blood flow from the aorta (higher pressure) to the pulmonary artery (lower pressure). The murmur is loudest during systole, when the pressure gradient between the aorta and pulmonary artery is greatest