SECTION III THE CARDIOVASCULAR SYSTEM Acute Myocardial Infarction A 68-year-old woman was adnitted to the coronary intensive care unit with the diagnosis of acute myocardial infarction.Soon after admission.she was resting comfortably.and seemed to be doing well,except for occasional prerature ventricular contractions.Her arterial blood pressure,central venous pressure,and other vital signs were pormal.except that her heart rate was moderately increased. On the second hospital day,the cardiac monitor showed that the patient suddenly developed ventricular fibrillation.her arterial blood pressure dropped precipitously to about 8 m lg.and her central venous pressure,which had heen about 3 mm Hg,rapidly rose to about 8 m Hg. 1.Why did the development of ventricular fibrillation lead to a rise in the patient's central venous pressure? 2 Why was the fall in arterial blood pressure so mch greater than the rise in central venous pressure? This patient was successfully resuscitated,and her condition improved rapidly. She was discharged from the hospital 10 days after admission.However,4 months later she noticed that she frequently becane short of breath on mild exertion.Her physician made the diagosis of congestive heart failure and recomrended that she be treated with a new,experimental drug that improved myocardial contractility. The patient's cardiac output before treatrent was 4.3 L/min,and her central venous pressure was 12 m Hg.One hour after she bad received the new drug.her cardiac output had increased to 5.2 L/min,and her central venous pressure had diminished to 6 m Hg. 3.Explain bow a drug that acts specifically to enhance myocardial contractility can increase cardiac output and decrease central venous pressure
SECTION III THE CARDIOVASCULAR SYSTEM Acute Myocardial Infarction A 68-year-old woman was admitted to the coronary intensive care unit with the diagnosis of acute myocardial infarction. Soon after admission, she was resting comfortably, and seemed to be doing well, except for occasional premature ventricular contractions. Her arterial blood pressure, central venous pressure, and other vital signs were normal, except that her heart rate was moderately increased. On the second hospital day, the cardiac monitor showed that the patient suddenly developed ventricular fibrillation, her arterial blood pressure dropped precipitously to about 8 mm Hg, and her central venous pressure, which had been about 3 mm Hg, rapidly rose to about 8 mm Hg. l. Why did the development of ventricular fibrillation lead to a rise in the patient's central venous pressure? 2. Why was the fall in arterial blood pressure so much greater than the rise in central venous pressure? This patient was successfully resuscitated, and her condition improved rapidly. She was discharged from the hospital 10 days after admission. However, 4 months later she noticed that she frequently became short of breath on mild exertion. Her physician made the diagnosis of congestive heart failure and recommended that she be treated with a new, experimental drug that improved myocardial contractility. The patient's cardiac output before treatment was 4.3 L/min, and her central venous pressure was 12 mm Hg. One hour after she had received the new drug, her cardiac output had increased to 5.2 L/min, and her central venous pressure had diminished to 6 mm Hg. 3. Explain how a drug that acts specifically to enhance myocardial contractility can increase cardiac output and decrease central venous pressure
4.Is an increase in cardiac output in the presence of a redoction in the ventricular filling pressure (central venous pressure)incompatible with the Frank-Starling nechanisn? The experinental drug given to improve myocardial contractility did not prove to be sufficiently efficacious.Therefore her physician decided to use a more conventional treatment,nanely an after/oad reducimg agent.This type of drug acts mainly to relax arteriolar snooth musele cells.This treatment effectively relieved her shortness of breath on exertion.However,she frequently noticed that on arising fron the recurbent position,she felt very light-headed and sonetines had difficulty remaining upright.Her physician found that the patient's arterial blood pressure was normal while she was recubent,but that when she stood up,her blood pressure decreased substantially:this phenomenon is called orthostatic hypotension. 5.In healthy individuals receiving no drug therapy.what changes in cardiac output and arterial blood pressure occur when they assume the upright posture? 6.What compensatory mechanisss are called into play mormally? 7.What effect does the vascular smooth muscle relaxant drug have on these overall henodynanic reactions in the patient who developed orthostatic hypotension when she assumed the upright posture? Two years later,this patient developed serious problems with her AV conduction systen,and she had an artificial pacemaker installed.When her heart was paced at a rate of 60 beats/min,her stroke volune was 80 al:but when her heart was paced at 100 beats/min,her stroke volume was only 48 ml. 8.What was the cardiac output when the heart was paced artificially at each frequency? 9.Bow do stroke volume and cardiac output vary as a functfon of the frequency of cardiac contraction (heart rate)? ANSVER
4. Is an increase in cardiac output in the presence of a reduction in the ventricular filling pressure (central venous pressure) incompatible with the Frank-Starling mechanism? The experimental drug given to improve myocardial contractility did not prove to be sufficiently efficacious. Therefore her physician decided to use a more conventional treatment, namely an afterload reducing agent. This type of drug acts mainly to relax arteriolar smooth muscle cells. This treatment effectively relieved her shortness of breath on exertion. However, she frequently noticed that on arising from the recumbent position, she felt very light-headed and sometimes had difficulty remaining upright. Her physician found that the patient's arterial blood pressure was normal while she was recumbent, but that when she stood up, her blood pressure decreased substantially; this phenomenon is called orthostatic hypotension. 5. In healthy individuals receiving no drug therapy, what changes in cardiac output and arterial blood pressure occur when they assume the upright posture? 6. What compensatory mechanisms are called into play normally? 7. What effect does the vascular smooth muscle relaxant drug have on these overall hemodynamic reactions in the patient who developed orthostatic hypotension when she assumed the upright posture? Two years later, this patient developed serious problems with her AV conduction system, and she had an artificial pacemaker installed. When her heart was paced at a rate of 60 beats/min, her stroke volume was 80 ml; but when her heart was paced at 100 beats/min, her stroke volume was only 48 ml. 8. What was the cardiac output when the heart was paced artificially at each frequency? 9. How do stroke volume and cardiac output vary as a function of the frequency of cardiac contraction (heart rate)? ANSWER
1.Ventricular fibrillation is a grave rhyth disturbance in shich many reentry circuits proceed haphazardly throughout the ventricles.Because the myriad myocardial cells that comprise the ventricles are contracting and relaxing so asynchronously,the beart pumps no blood.In this patient,the arterial and central venous pressures were normal just before the onset of fibrillation.Therefore at the very beginning of the arrhythmia,the flow from the systemic arteries to the systenic veins through the capillaries was normal initially.even though cardiac output suddenly becane xero.However.the flow through the capillaries from arteries to veins caused the arterial pressure to fall rapidly and the venous pressure to rise.This process contimed until pressures equilibrated throughout the systemic vascular hed. 2 When cardiac output suddenly became zero,blood continued to flow from arteries to veins until the pressures equilibrated.The volune of blood lost from the arteries was virtually equal to the volume of blood gained by the veins (i.e., AV.AV.).If the arterial and venous compliances were equal,then the decline in arterial pressure would have been equal to the rise in venous pressure. Fron the definition of compliance.we can predict the changes in arterial and venous pressure that take place when a given volume of blood is translocated from the arteries to the veins.By rearranging the definitions of C.and C.: △P,·△v./C △P.=△v./C Bowever,.because△y。"-△.，it follows that: C.△P.=-C.△P Therefore AP./△P.=-C/C That is,the ratio of the increment in P.to the decrement in P.is inversely proportional to their respective complfances.Thus if their compliances were equal
1. Ventricular fibrillation is a grave rhythm disturbance in which many reentry circuits proceed haphazardly throughout the ventricles. Because the myriad myocardial cells that comprise the ventricles are contracting and relaxing so asynchronously, the heart pumps no blood. In this patient, the arterial and central venous pressures were normal just before the onset of fibrillation. Therefore at the very beginning of the arrhythmia, the flow from the systemic arteries to the systemic veins through the capillaries was normal initially, even though cardiac output suddenly became zero. However, the flow through the capillaries from arteries to veins caused the arterial pressure to fall rapidly and the venous pressure to rise. This process continued until pressures equilibrated throughout the systemic vascular bed. 2. When cardiac output suddenly became zero, blood continued to flow from arteries to veins until the pressures equilibrated. The volume of blood lost from the arteries was virtually equal to the volume of blood gained by the veins (i.e., ∆Va ∆Vv). If the arterial and venous compliances were equal, then the decline in arterial pressure would have been equal to the rise in venous pressure. From the definition of compliance, we can predict the changes in arterial and venous pressure that take place when a given volume of blood is translocated from the arteries to the veins. By rearranging the definitions of Ca and Cv: ∆Pa = ∆Va/Ca ∆Pv = ∆Vv/Cv However, because ∆Va = - ∆Vv , it follows that: Ca * ∆Pa = - Cv * ∆Pv Therefore ∆Pv/∆Pa = - Ca/Cv That is, the ratio of the increment in Pv to the decrement in Pa is inversely proportional to their respective compliances. Thus if their compliances were equal
then the fall in P.would equal the rise in P.-However,the veins are much more compliant than the arteries,and the compliance ratio is about 20 to 1.Therefore the decline in systemie arterial pressure is about 20 times greater than the rise in systemic venous pressure when the beart stops beating. 3.One manifestation of an enhancement of myocardial contractility is that for a given ventricular filling pressure (which,for the right vemtricle,is equivalent to the central venous pressure),the heart will pump a greater cardiac output.If this new drug has no direct effect on the resistance blood vessels,an increase in cardiac output will tend to redistribute the blood volune such that a greater fraction will reside in the arteries and a smaller fraction will reside in the veins. This will be reflected by a rise in arterial blood pressure and a fall in central venous pressure. 4.According to the Frank-Starling sechanisn cardiac performance (including cardiac output)varies as a function of the initial length of the myocardial fibers (as determined hy the filling pressure).For a given level of contractility,the Frank-Starling mechanism can be represented by a curve of cardiac output (Y axis) as a function of the ventricular filling pressure (axis).When contractility is enhanced,bowever,the characteristic curve is shifted to the left:thus the Frank-Starling mechanism is actually represented by a family of curves,rather than by a single curve.A pure increase in myocardial contractility will cause the coordinates of the operating point to shift upward and to the left from the control contractility curve to the enhanced contractility curve.This diagonal shift will reflect the Increse in cardiac output and the deerewse in central venous pressure. The precise diagonal path from one curve to the other is dictated by the specific "vascular function curve"that defines the state of the vascular system-that is. the curve depends on the total blood volune,the total peripheral resistance,and the arterial and venous complfances. 5.When a recurbent person assumes the upright posture,gravity tends to redistribute the blood volune toward those vessels that lie below the heart.The pressure in the blood vessels below the heart (the dependent"vessels)tends to
then the fall in Pa would equal the rise in Pv. However, the veins are much more compliant than the arteries, and the compliance ratio is about 20 to 1. Therefore the decline in systemic arterial pressure is about 20 times greater than the rise in systemic venous pressure when the heart stops beating. 3. One manifestation of an enhancement of myocardial contractility is that for a given ventricular filling pressure (which, for the right ventricle, is equivalent to the central venous pressure), the heart will pump a greater cardiac output. If this new drug has no direct effect on the resistance blood vessels, an increase in cardiac output will tend to redistribute the blood volume such that a greater fraction will reside in the arteries and a smaller fraction will reside in the veins. This will be reflected by a rise in arterial blood pressure and a fall in central venous pressure. 4. According to the Frank-Starling mechanism, cardiac performance (including cardiac output) varies as a function of the initial length of the myocardial fibers (as determined by the filling pressure). For a given level of contractility, the Frank-Starling mechanism can be represented by a curve of cardiac output (Y axis) as a function of the ventricular filling pressure (X axis). When contractility is enhanced, however, the characteristic curve is shifted to the left; thus the Frank-Starling mechanism is actually represented by a family of curves, rather than by a single curve. A pure increase in myocardial contractility will cause the coordinates of the operating point to shift upward and to the left from the control contractility curve to the enhanced contractility curve. This diagonal shift will reflect the increase in cardiac output and the decrease in central venous pressure. The precise diagonal path from one curve to the other is dictated by the specific "vascular function curve" that defines the state of the vascular system—that is, the curve depends on the total blood volume, the total peripheral resistance, and the arterial and venous compliances. 5. When a recumbent person assumes the upright posture, gravity tends to redistribute the blood volume toward those vessels that lie below the heart. The pressure in the blood vessels below the heart (the "dependent" vessels) tends to
rise as a function of the distance (h)below the beart:the increase in pressure (AP)equals hpg.where p is the density of blood,and is the acceleration of gravity.Because the veins are more compliant than the arteries,most of the increased blood volume resides in the dependent veins.With respect to the magnitude of the cardiae filling pressure,this sequestration of blood volume in the dependent veins has an influence on cardiac output and nean arterial pressure sinilar to that exerted by blood loss froa the body. 6.The tendency for gravity to reduce cardiac output and arterial blood pressure when an individual shifts fron the recurbent to the upright position quickly invokes the baroreceptor reflexes.As the pressure decreases in the carotid sinuses and aortic arch,the changes in baroreceptor activity in these regions bring about increases in total peripberal resistance,in heart rate.and in myocardial contractility.These respoeses tend to ninimize the reductions in arterial blood pressure and in cerebral blood flow (which accounts for the light-beadedness). Another compensatory reaction involves an increase in skeletal muscle activity:as a person hecomes light-beaded.he or she tends to nove pore.Contraction of the muscles in the legs (acting in conjunction with the valves in the leg veins)tends to massage blood (an auxiliary pump)in the leg veins back toward the heart. 7.The major corponent of the baroreceptor reflexes in buffering the tendency for the arterial blood pressure to fall when an individual assumes the upright posture is the increase in total peripheral resistance.which is achieved by a contraction of the smooth ruscle in arterioles throughout the body.The use of a vascular smooth muscle relaxant,for example,in the treatment of hypertension, would tend to prevent an effective increase in total peripheral resistance and would thereby attenuate substantially the efficacy of the baroreceptor reflexes to buffer a reduction in arterial blood pressure. 8.Cardiac output (Q)equals stroke volume (SV)times heart rate (HR).When the pacing rate was 60 beats/min.Q was 80 x 60.or 4800 ml/min.When the pacing
rise as a function of the distance (h) below the heart; the increase in pressure (∆P) equals hρg, where ρ is the density of blood, and g is the acceleration of gravity. Because the veins are more compliant than the arteries, most of the increased blood volume resides in the dependent veins. With respect to the magnitude of the cardiac filling pressure, this sequestration of blood volume in the dependent veins has an influence on cardiac output and mean arterial pressure similar to that exerted by blood loss from the body. 6. The tendency for gravity to reduce cardiac output and arterial blood pressure when an individual shifts from the recumbent to the upright position quickly invokes the baroreceptor reflexes. As the pressure decreases in the carotid sinuses and aortic arch, the changes in baroreceptor activity in these regions bring about increases in total peripheral resistance, in heart rate, and in myocardial contractility. These responses tend to minimize the reductions in arterial blood pressure and in cerebral blood flow (which accounts for the light-headedness). Another compensatory reaction involves an increase in skeletal muscle activity; as a person becomes light-headed, he or she tends to move more. Contraction of the muscles in the legs (acting in conjunction with the valves in the leg veins) tends to massage blood (an auxiliary pump) in the leg veins back toward the heart. 7. The major component of the baroreceptor reflexes in buffering the tendency for the arterial blood pressure to fall when an individual assumes the upright posture is the increase in total peripheral resistance, which is achieved by a contraction of the smooth muscle in arterioles throughout the body. The use of a vascular smooth muscle relaxant, for example, in the treatment of hypertension, would tend to prevent an effective increase in total peripheral resistance and would thereby attenuate substantially the efficacy of the baroreceptor reflexes to buffer a reduction in arterial blood pressure. 8. Cardiac output (Qh) equals stroke volume (SV) times heart rate (HR). When the pacing rate was 60 beats/min, Qh was 80 x 60, or 4800 ml/min. When the pacing
rate was 100 beats/min,Q was 48 x 100,or 4800 ml/min.Hence Q vas equal at these two pacing rates. 9.An increase in HR tends to increase C.but it also abridges the time available for ventricular filling.Thus over a substantial range of heart rates, SV tends to he inversely proportional to HR Therefore over that range of heart rates,Q is not appreciably affected by changes in HR.At heart rates below this plateau range,further reductions in HR are not attended by proportionate increases in diastolic filling volunes,because the ventricles are approaching their maximal volumes (partly imposed by the pericardium).Hence,Q decreases sharply with further reductions in HR.At the other end of the frequency range. additional increases in HR do not allow sufficient time for adequate ventricular filling.Hence,the curtailed filling volumes are not compensated for by the increased nunber of cardiac contractions per ninute.Therefore,Q decreases sharply with further increases in HR
rate was 100 beats/min, Qh was 48 x 100, or 4800 ml/min. Hence Qh was equal at these two pacing rates. 9. An increase in HR tends to increase Qh, but it also abridges the time available for ventricular filling. Thus over a substantial range of heart rates, SV tends to be inversely proportional to HR. Therefore over that range of heart rates, Qh is not appreciably affected by changes in HR. At heart rates below this plateau range, further reductions in HR are not attended by proportionate increases in diastolic filling volumes, because the ventricles are approaching their maximal volumes (partly imposed by the pericardium). Hence, Qh decreases sharply with further reductions in HR. At the other end of the frequency range, additional increases in HR do not allow sufficient time for adequate ventricular filling. Hence, the curtailed filling volumes are not compensated for by the increased number of cardiac contractions per minute. Therefore, Qh decreases sharply with further increases in HR