SECTION 111 THE CARDIONASCULAR SYSTEM Cardiac Failure A 70-year-old mn was adnitted to the hospital with shortness of breath,severe fatigue and weakness,abdominal distension.and swelling of ankles.At night he requires four pillows and often wakes up because of acute air hunger.His history revealed episodes of angina pectoris and a progressive shortness of hreath with exertion for several years.On examination the chief abnormalities were slight cyanosis (bluish cast to the skin),distension of the neck veins.rapid respirations (20/nin),rales (crackling sounds)at the lung bases bilaterally,an enlarged heart with slight tachycardia (110 beats/min)and a diastolic gallop rhythm (sounds like galloping horse).enlarged liver.excess fluid in the abdomen.and edema at the ankles and over the lower tibias.His blood pressure was 115/80.The chest x-ray examination showed an emlarged heart and diffuse density (indicative of fluid in the lungs)at both lung bases.An electrocardiogran (ECG)showed normal sinus rhythn. Q waves,and left axis deviation.Treatnent included bed rest and administration of digitalis and a diuretic. 1.Yould you expect cardiac output and stroke volune to be nornal,high,or low? Thy? 2.What do the distension of the neck veins and enlargement of the liver indicate? hat is the mechanis? 3.Is the efficiency of the heart altered?If so,why? 4.What do you expect to find on measurement of ejection fraction and residual olune？Explain, 5.Digitalis significantly inhibits the Na/K purp.Why would this be helpful? 6.Would a calciun channel antagonist be advantageous?Why? 7.Would norepinephrine he helpful?Why? 8.Tould a phlebotomy (removal of blood)or a transfusion be helpful?Why?
SECTION III THE CARDIOVASCULAR SYSTEM Cardiac Failure A 70-year-old man was admitted to the hospital with shortness of breath, severe fatigue and weakness, abdominal distension, and swelling of ankles. At night he requires four pillows and often wakes up because of acute air hunger. His history revealed episodes of angina pectoris and a progressive shortness of breath with exertion for several years. On examination the chief abnormalities were slight cyanosis (bluish cast to the skin), distension of the neck veins, rapid respirations (20/min), rales (crackling sounds) at the lung bases bilaterally, an enlarged heart with slight tachycardia (110 beats/min) and a diastolic gallop rhythm (sounds like galloping horse), enlarged liver, excess fluid in the abdomen, and edema at the ankles and over the lower tibias. His blood pressure was 115/80. The chest x-ray examination showed an enlarged heart and diffuse density (indicative of fluid in the lungs) at both lung bases. An electrocardiogram (ECG) showed normal sinus rhythm, Q waves, and left axis deviation. Treatment included bed rest and administration of digitalis and a diuretic. 1. Would you expect cardiac output and stroke volume to be normal, high, or low? Why? 2. What do the distension of the neck veins and enlargement of the liver indicate? What is the mechanism? 3. Is the efficiency of the heart altered? If so, why? 4. What do you expect to find on measurement of ejection fraction and residual volume? Explain. 5. Digitalis significantly inhibits the Na/K pump. Why would this be helpful? 6. Would a calcium channel antagonist be advantageous? Why? 7. Would norepinephrine be helpful? Why? 8. Would a phlebotomy (removal of blood) or a transfusion be helpful? Why?
9.What does the diastolic zallop rhytha mean? 10.What effect does the patient's condition have on cardiac contractility?On dP/dt? 11.Bow inportant is atrial contraction for ventricular filling in this patient? 12.Is peripheral resistance changed?If so,why? 13.Why is the heart rate slightly elevated? 14.What effect would changing preload have? 15.What effect would changing afterload have? 16.Would you expect the arteriovenous oxygen difference to be normal?Why? 17.Are the force and velocity of cardiac contraction normal in this patient? How are these two variables related? 18.Is valve function normal in this patient? 19.Are the heart sounds louder,softer,or of normal intensity in this patient? 20.Why is the heart enlarged? 21.Why do the ventricles contract as a single unit? 22.How would you measure cardiac output in this patient? 23.Why is the patient short of breath? 24.Why does the patient have edena of the legs? 25.Why was a diuretic given?How does it work? 26.Should there be any dietary restrictions?If so.what? ANSVER 1.Cardiac output would be slow as a result of a decreased stroke volune.The reason for the reduced stroke volune is a weakened myocardiun.resulting froa ischenic danage from an inadequate coronary blood supply (severe narrowing of the coronary arteries).The curve of developed pressure versus diastolie filling pressure (Starling curve)would be shifted to the right and would be flatter than the normal curve
9. What does the diastolic gallop rhythm mean? 10. What effect does the patient's condition have on cardiac contractility? On dP/dt? 11. How important is atrial contraction for ventricular filling in this patient? 12. Is peripheral resistance changed? If so, why? 13. Why is the heart rate slightly elevated? 14. What effect would changing preload have? 15. What effect would changing afterload have? 16. Would you expect the arteriovenous oxygen difference to be normal? Why? 17. Are the force and velocity of cardiac contraction normal in this patient? How are these two variables related? 18. Is valve function normal in this patient? 19. Are the heart sounds louder, softer, or of normal intensity in this patient? 20. Why is the heart enlarged? 21. Why do the ventricles contract as a single unit? 22. How would you measure cardiac output in this patient? 23. Why is the patient short of breath? 24. Why does the patient have edema of the legs? 25. Why was a diuretic given? How does it work? 26. Should there be any dietary restrictions? If so, what? ANSWER 1. Cardiac output would be slow as a result of a decreased stroke volume. The reason for the reduced stroke volume is a weakened myocardium, resulting from ischemic damage from an inadequate coronary blood supply (severe narrowing of the coronary arteries). The curve of developed pressure versus diastolic filling pressure (Starling curve) would be shifted to the right and would be flatter than the normal curve
2.The neck vein distension and the liver enlargement indicate that the right ventricle is umable to pump out the large volume of blood present on the venous side of the circulation.This large volune of venous blood is caused by a shift of blood fron the arterial to the venous side secondary to the reduced cardiac output and by an increase in total blood volume,resulting from the reduced cardiac output- decreased renal hlood flow increased aldosterone secretion-sodiun retention water retention.This hack pressure in the venous system leads to swelling of the liver. 3.The efficiency of the heart is reduced in this patient with heart failure. The heart is greatly dilated,and more energy is required to eject the same volume of blood per beat than is required in the mormal beart.This can be explained by the Laplace equation: "Pxr/程 where o (stress)is the force per unit area of cross-section of the ventricular wall.P is the pressure in the left ventricle,r is the radius of the left vemtricle. and w is the thickness of the left ventricular wall.In this patient,the left ventricle is greatly dilated.Therefore the r value is large and results in an increase in o,that is,in the force that each unit area of myocardial fibers must generate.P and w are within normal linits. 4.The ejection fraction.the fraction of the end-diastolie volune ejected with each beat (stroke volume)is low,and the residual volume (amount of blood remaining in the ventricle at the end of ejection)is high.When the heart is dilated and its contractility is reduced,as in this patient with heart failure,the weak ventricular contractions eject less than the normal stroke volume.This,coupled with a large volune of blood in the ventricle during diastole and systole,greatly decreases the ejection fraction. 5.Digitalis was given to increase the contractility of the heart;that is, at a constant preload and afterload,the force of comtraction is enhanced.By poisoning the Nat.K+-ATPase,less Na+is pumped out of the myocardial cells.As
2. The neck vein distension and the liver enlargement indicate that the right ventricle is unable to pump out the large volume of blood present on the venous side of the circulation. This large volume of venous blood is caused by a shift of blood from the arterial to the venous side secondary to the reduced cardiac output and by an increase in total blood volume, resulting from the reduced cardiac output → decreased renal blood flow → increased aldosterone secretion → sodium retention → water retention. This back pressure in the venous system leads to swelling of the liver. 3. The efficiency of the heart is reduced in this patient with heart failure. The heart is greatly dilated, and more energy is required to eject the same volume of blood per beat than is required in the normal heart. This can be explained by the Laplace equation: σ = P x r / w where σ (stress) is the force per unit area of cross-section of the ventricular wall, P is the pressure in the left ventricle, r is the radius of the left ventricle, and w is the thickness of the left ventricular wall. In this patient, the left ventricle is greatly dilated. Therefore the r value is large and results in an increase in σ, that is, in the force that each unit area of myocardial fibers must generate. P and w are within normal limits. 4. The ejection fraction, the fraction of the end-diastolic volume ejected with each beat (stroke volume) is low, and the residual volume (amount of blood remaining in the ventricle at the end of ejection) is high. When the heart is dilated and its contractility is reduced, as in this patient with heart failure, the weak ventricular contractions eject less than the normal stroke volume. This, coupled with a large volume of blood in the ventricle during diastole and systole, greatly decreases the ejection fraction. 5. Digitalis was given to increase the contractility of the heart; that is, at a constant preload and afterload, the force of contraction is enhanced. By poisoning the Na+, K+-ATPase, less Na+ is pumped out of the myocardial cells. As
a result,the Na+-Ca++exchange is reversed and less Ca++leaves the mrocytes.The greater intracellular Ca++increases the cardiac contractile force. 6.A calciun channel antagomist would not be useful,because a greater intracellular caleium is needed to enhance myocardial contraetility in this patient. However,the calcium antagonist could reduce afterload by relaxing the vascular smooth museles of the arterioles. 7.Norepinephrine would increase myocardial contractility.which would be beneficial.Bowever,it also increases heart rate and peripheral resistance,which would be deleterious.A catecholamine that is sometimes used in heart failure is dobutanine.which has less effect on heart rate and peripheral resistance. Catecholanines act mainly by increasing intracellular caleiun. 8.A phlebotony would relieve the venous distension and ease the large preload on the heart.However.it is only indicated when there is acute,life-threatening pulnonary edena.and even then,tourniquets on the extrenities are pore cormonly used.The best way to ease the preload burden on the heart is by the use of diureties. A transfusion would be contraindicated.because it would increase the already high preload. 9.The diastolic gallop rhythn indicates severe heart disease and is caused by vibrations of the ventricle walls.The vibrations are elicited by abrupt cessation of ventricular distension and the deceleration of the entering blood when the ventricle is stretched to the point that it becomes stiff. 10.Contractility is reduced,and the cardiac fibers are stretched beyond their optinal length so that the actin and myosin filaments do not have sufficient overlap for mximal crosshridge activity.dP/dt serves as an index of contractility.It is the naximal rate of pressure derelopnent during ventricular systole. 11.Atrial contraction is relatively unimportant in ventricular filling in this patient because of the high venous pressure and the large residual volume of blood in the ventricles.The atrial contribution to ventricular filling is more important in normal hearts,especially at fast beart rates
a result, the Na+-Ca++ exchange is reversed and less Ca++ leaves the myocytes. The greater intracellular Ca++ increases the cardiac contractile force. 6. A calcium channel antagonist would not be useful, because a greater intracellular calcium is needed to enhance myocardial contractility in this patient. However, the calcium antagonist could reduce afterload by relaxing the vascular smooth muscles of the arterioles. 7. Norepinephrine would increase myocardial contractility, which would be beneficial. However, it also increases heart rate and peripheral resistance, which would be deleterious. A catecholamine that is sometimes used in heart failure is dobutamine, which has less effect on heart rate and peripheral resistance. Catecholamines act mainly by increasing intracellular calcium. 8. A phlebotomy would relieve the venous distension and ease the large preload on the heart. However, it is only indicated when there is acute, life-threatening pulmonary edema, and even then, tourniquets on the extremities are more commonly used. The best way to ease the preload burden on the heart is by the use of diuretics. A transfusion would be contraindicated, because it would increase the already high preload. 9. The diastolic gallop rhythm indicates severe heart disease and is caused by vibrations of the ventricle walls. The vibrations are elicited by abrupt cessation of ventricular distension and the deceleration of the entering blood when the ventricle is stretched to the point that it becomes stiff. 10. Contractility is reduced, and the cardiac fibers are stretched beyond their optimal length so that the actin and myosin filaments do not have sufficient overlap for maximal crossbridge activity. dP/dt serves as an index of contractility. It is the maximal rate of pressure development during ventricular systole. 11. Atrial contraction is relatively unimportant in ventricular filling in this patient because of the high venous pressure and the large residual volume of blood in the ventricles. The atrial contribution to ventricular filling is more important in normal hearts, especially at fast heart rates
12.Peripheral resistance is increased.With a low cardiac output,arterial pressure would decrease and activate the baroreceptor reflex.which enhances peripheral resistance and thereby mafntains blood pressure. 13.Increased heart rate is a compensatory mechanisa that is nediated hy the baroreceptor reflex.The increased heart rate and the increased peripheral resistance are both elicited by the reduced blood pressure,which is caused by the decrease in cardiac output. 14.Reducing preload would take some of the stress off the dilated ventricles and allow the heart to move back to a more optimal functioning position on the Starling curve (fron descending linb to ascending limb).of course,if the cardiac muscle fibers were optimally stretched by the large volume of blood in diastole, then a decrease in preload would reduce cardiac output.An increase in preload would push the heart further to the right on the Starling curve (descemding limb)and decrease its purping action. 15.Increasing afterload would place an additional burdem on the left ventricle, and cardiac output would decrease.Decreasing the afterload with the use of vasodilators (decrease peripheral resistance)can he helpful in the treatment of patients with heart failure. 16.The arteriovenous oxygen difference would be expected to be greater than normal because the venous blood oxygen content would be low.With a low cardiac output and hence a low blood flow through the peripheral tissues,more oxygen is extracted fron the blood in the capillaries.Even with greater oxygen extraction the oxygen supply is less than optimal for the muscles.The reduced supply of oxygen can account in part for the feeling of weakness and fatigue. 17.Both force of contraction and velocity of contraction are decreased in this patient's heart as a result of the "heart failure"caused by inadequate blood supply to the myoeardial fibers over a period of many years. 18.Yes,valve function is apparently normal.However.with severe dilation of the ventricles,the valve rings can be overstretched and produce valve insufficiency. causing cardiac mrmurs
12. Peripheral resistance is increased. With a low cardiac output, arterial pressure would decrease and activate the baroreceptor reflex, which enhances peripheral resistance and thereby maintains blood pressure. 13. Increased heart rate is a compensatory mechanism that is mediated by the baroreceptor reflex. The increased heart rate and the increased peripheral resistance are both elicited by the reduced blood pressure, which is caused by the decrease in cardiac output. 14. Reducing preload would take some of the stress off the dilated ventricles and allow the heart to move back to a more optimal functioning position on the Starling curve (from descending limb to ascending limb). Of course, if the cardiac muscle fibers were optimally stretched by the large volume of blood in diastole, then a decrease in preload would reduce cardiac output. An increase in preload would push the heart further to the right on the Starling curve (descending limb) and decrease its pumping action. 15. Increasing afterload would place an additional burden on the left ventricle, and cardiac output would decrease. Decreasing the afterload with the use of vasodilators (decrease peripheral resistance) can be helpful in the treatment of patients with heart failure. 16. The arteriovenous oxygen difference would be expected to be greater than normal because the venous blood oxygen content would be low. With a low cardiac output and hence a low blood flow through the peripheral tissues, more oxygen is extracted from the blood in the capillaries. Even with greater oxygen extraction the oxygen supply is less than optimal for the muscles. The reduced supply of oxygen can account in part for the feeling of weakness and fatigue. 17. Both force of contraction and velocity of contraction are decreased in this patient's heart as a result of the "heart failure" caused by inadequate blood supply to the myocardial fibers over a period of many years. 18. Yes, valve function is apparently normal. However, with severe dilation of the ventricles, the valve rings can be overstretched and produce valve insufficiency, causing cardiac murmurs
19.The heart sounds are probably normal,although they may be slightly diminished because of the relatively weak cardiac contractions. 20.Because of prolonged inadequate blood supply.the mrocardial fibers contract less effectively.In addition,an increase in blood volume caused by salt and water retention by the kidneys,in response to a low cardiac output,contributes to the dilation of the heart. 21.Although the beart is mde up of millions of individual muscle fibers,the ventricular fibers contract together as do the atrial fibers because the heart functions as a syncytium.That is,the electrical inpulse spreads rapidly fron cell to cell through very low-resistance pathways called gap junctions. 22.The Fick principle could be used to measure cardiac output.This method would require measurenents of oxygen consurption and oxygen content of mixed venous (pulnonary artery)blood and of arterial blood.A simpler and more widely used nethod is thermodilution. 23.The patient is short of breath because (1)excess fluid in the lung interstitiun makes the lungs stiff,which in turn requires a greater effort to expand then:and (2)fluid in the alveoli of the lung bases (rales and x-ray density) interferes with gas exchange,especially the diffusion of oxygen from alveoli to pulnonary capillaries. 24.The leg edema is caused by the increased hydrostatic pressure in the capillaries and venules in the legs.The large blood volume and high venous pressure cause the hydrostatie pressure to exceed the omcotic pressure,particularly in the dependent parts of the body.This results in movenent of fluid fron the vascular compartment to the interstitial compartment.When the patient is bedridden,the hydrostatie pressure is greatest over the sacral region (most dependent part of the body),and sacral edema occurs. 25.A diuretic was given to increase sodium excretion in the urine.The diuretic reduces the reabsorption of sodium in the remal tubules and thereby increases the loss of sodiu and accompanying vater
19. The heart sounds are probably normal, although they may be slightly diminished because of the relatively weak cardiac contractions. 20. Because of prolonged inadequate blood supply, the myocardial fibers contract less effectively. In addition, an increase in blood volume caused by salt and water retention by the kidneys, in response to a low cardiac output, contributes to the dilation of the heart. 21. Although the heart is made up of millions of individual muscle fibers, the ventricular fibers contract together as do the atrial fibers because the heart functions as a syncytium. That is, the electrical impulse spreads rapidly from cell to cell through very low-resistance pathways called gap junctions. 22. The Fick principle could be used to measure cardiac output. This method would require measurements of oxygen consumption and oxygen content of mixed venous (pulmonary artery) blood and of arterial blood. A simpler and more widely used method is thermodilution. 23. The patient is short of breath because (1) excess fluid in the lung interstitium makes the lungs stiff, which in turn requires a greater effort to expand them; and (2) fluid in the alveoli of the lung bases (rales and x-ray density) interferes with gas exchange, especially the diffusion of oxygen from alveoli to pulmonary capillaries. 24. The leg edema is caused by the increased hydrostatic pressure in the capillaries and venules in the legs. The large blood volume and high venous pressure cause the hydrostatic pressure to exceed the oncotic pressure, particularly in the dependent parts of the body. This results in movement of fluid from the vascular compartment to the interstitial compartment. When the patient is bedridden, the hydrostatic pressure is greatest over the sacral region (most dependent part of the body), and sacral edema occurs. 25. A diuretic was given to increase sodium excretion in the urine. The diuretic reduces the reabsorption of sodium in the renal tubules and thereby increases the loss of sodium and accompanying water
26.The intake of salt would be restricted to prevent edena (peripheral and ulmonary）and ascites
26. The intake of salt would be restricted to prevent edema (peripheral and pulmonary) and ascites