SECTION III THE CARDIOVASCULAR SYSTEM Hemorrhage and Shock Two soldiers received similar wounds during a battle,and they each lost a substantial amount of blood.Neither was able to receive any treatment other than medication for pain.Each soldier was noted to have a mean arterial blood pressure of about 50 mm Hg shortly after being wounded.Their blood pressures gradually increased for the first 2 hours.Thereafter,soldier A's blood pressure continued to improve,and within 4 or 5 hours,his blood pressure was almost normal.He ultimately survived.However,soldier B's blood pressure reached a peak value of only about 65 mm Hg a few hours after he had been wounded.His blood pressure then gradually declined,and he died about 10 hours after being wounded. 1.Cite the various compensatory mechanisms that may have contributed to the recovery of soldier A. 2.Cite the various decompensatory mechanisms that may have contributed to the demise of soldier B. 3.Assume that a specific,potent positive inotropic drug was available;that is,the drug could improve myocardial contractility substantially,but it would have no appreciable effects on the vasculature.Discuss the potential efficacy of such a drug if it were given to either soldier during the first hour after the injury. ANSWER 1.The body is able to mobilize a number of mechanisms to compensate for the loss of blood.The baroreceptor reflexes are probably the most important of these mechanisms.In response to blood loss,the carotid sinus and aortic arch baroreceptors signal any reduction in arterial pressure to the nucleus tractus solitarius in the medulla oblongata.This nucleus,in turn,initiates an increase in sympathetic activity to the heart and vasculature and a decrease in
SECTION III THE CARDIOVASCULAR SYSTEM Hemorrhage and Shock Two soldiers received similar wounds during a battle, and they each lost a substantial amount of blood. Neither was able to receive any treatment other than medication for pain. Each soldier was noted to have a mean arterial blood pressure of about 50 mm Hg shortly after being wounded. Their blood pressures gradually increased for the first 2 hours. Thereafter, soldier A's blood pressure continued to improve, and within 4 or 5 hours, his blood pressure was almost normal. He ultimately survived. However, soldier B's blood pressure reached a peak value of only about 65 mm Hg a few hours after he had been wounded. His blood pressure then gradually declined, and he died about 10 hours after being wounded. 1. Cite the various compensatory mechanisms that may have contributed to the recovery of soldier A. 2. Cite the various decompensatory mechanisms that may have contributed to the demise of soldier B. 3. Assume that a specific, potent positive inotropic drug was available; that is, the drug could improve myocardial contractility substantially, but it would have no appreciable effects on the vasculature. Discuss the potential efficacy of such a drug if it were given to either soldier during the first hour after the injury. ANSWER 1. The body is able to mobilize a number of mechanisms to compensate for the loss of blood. The baroreceptor reflexes are probably the most important of these mechanisms. In response to blood loss, the carotid sinus and aortic arch baroreceptors signal any reduction in arterial pressure to the nucleus tractus solitarius in the medulla oblongata. This nucleus, in turn, initiates an increase in sympathetic activity to the heart and vasculature and a decrease in
parasympathetic activity to the heart.These actions tend to increase cardiac output and mean arterial blood pressure.The arterial chemoreceptor and cerebral ischemia reflexes also serve to increase sympathetic neural activity to the cardiovascular system.The release of endogenous vasoconstrictor substances,notably epinephrine, vasopressin,and angiotensin,also tends to restore arterial blood pressure toward normal levels.The reduction in peripheral capillary pressure leads to a reabsorption of interstitial fluid into the vascular compartment,thereby tending to augment the total blood volume.Finally,the kidneys act to conserve fluid in response to renal vasoconstriction and to increased blood levels of vasopressin and aldosterone. 2.Hemorrhage also sets into motion various decompensatory mechanisms that tend to aggravate the tenuous state of the cardiovascular system.The low arterial pressure induced by the blood loss serves to diminish the coronary blood flow.This curtailment of myocardial perfusion in turn may diminish cardiac output and thereby further reduce the arterial blood pressure.Other vicious cycles that may be invoked are severe depression of the central nervous system,generalized acidosis, blood-clotting aberrations,and depression of the reticuloendothelial system.All of these reactions tend to diminish the efficacy of the various compensatory mechanisms.If the decompenstory mechanisms predominate over the compensatory mechanisms,cardiovascular function will deteriorate and death will ensue. 3.Fig.32-1 shows hypothetical cardiac and vascular function curves for the effects of a specific,positive inotropic drug on cardiac output and central venous pressure during normovolemia,hypovolemia,and generalized vasoconstriction. Point A represents the intersection between the cardiac and vascular function curves of either soldier under normal conditions (before the injury).In such a normal individual,administration of the positive inotropic drug would increase the cardiac output and decrease the central venous pressure substantially,as reflected by the shift in intersecting points from A to B in the figure.Pure hypovolemia (in the absence of compensatory vascular reactions)would cause a parallel downward shift of the vascular function curve,as shown in the figure
parasympathetic activity to the heart. These actions tend to increase cardiac output and mean arterial blood pressure. The arterial chemoreceptor and cerebral ischemia reflexes also serve to increase sympathetic neural activity to the cardiovascular system. The release of endogenous vasoconstrictor substances, notably epinephrine, vasopressin, and angiotensin, also tends to restore arterial blood pressure toward normal levels. The reduction in peripheral capillary pressure leads to a reabsorption of interstitial fluid into the vascular compartment, thereby tending to augment the total blood volume. Finally, the kidneys act to conserve fluid in response to renal vasoconstriction and to increased blood levels of vasopressin and aldosterone. 2. Hemorrhage also sets into motion various decompensatory mechanisms that tend to aggravate the tenuous state of the cardiovascular system. The low arterial pressure induced by the blood loss serves to diminish the coronary blood flow. This curtailment of myocardial perfusion in turn may diminish cardiac output and thereby further reduce the arterial blood pressure. Other vicious cycles that may be invoked are severe depression of the central nervous system, generalized acidosis, blood-clotting aberrations, and depression of the reticuloendothelial system. All of these reactions tend to diminish the efficacy of the various compensatory mechanisms. If the decompenstory mechanisms predominate over the compensatory mechanisms, cardiovascular function will deteriorate and death will ensue. 3. Fig. 32-1 shows hypothetical cardiac and vascular function curves for the effects of a specific, positive inotropic drug on cardiac output and central venous pressure during normovolemia, hypovolemia, and generalized vasoconstriction. Point A represents the intersection between the cardiac and vascular function curves of either soldier under normal conditions (before the injury). In such a normal individual, administration of the positive inotropic drug would increase the cardiac output and decrease the central venous pressure substantially, as reflected by the shift in intersecting points from A to B in the figure. Pure hypovolemia (in the absence of compensatory vascular reactions) would cause a parallel downward shift of the vascular function curve, as shown in the figure
The same positive inotropic drug would be expected to evoke increases in cardiac output and decreases in central P.similar to those elicited under normovolemic conditions.Hypovolemia rapidly induces reflex vasoconstriction,however,and such vasoconstriction is reflected by a counterclockwise rotation of the vascular function curve.Under such conditions,even a substantial enhancement of myocardial contractility does not elicit a very great increase in cardiac output (as denoted by the small differences in the Y-coordinates of points E and F).The reason for the counterclockwise rotation of this curve is that when peripheral resistance is increased,a given change in cardiac output produces a greater reduction in central P,than it does when resistance is normal.Thus when peripheral resistance is elevated,any agent that tends to increase cardiac output would also tend to lower central P,substantially,and this in turn would minimize the augmentation of cardiac output
The same positive inotropic drug would be expected to evoke increases in cardiac output and decreases in central Pv similar to those elicited under normovolemic conditions. Hypovolemia rapidly induces reflex vasoconstriction, however, and such vasoconstriction is reflected by a counterclockwise rotation of the vascular function curve. Under such conditions, even a substantial enhancement of myocardial contractility does not elicit a very great increase in cardiac output (as denoted by the small differences in the Y-coordinates of points E and F). The reason for the counterclockwise rotation of this curve is that when peripheral resistance is increased, a given change in cardiac output produces a greater reduction in central Pv than it does when resistance is normal. Thus when peripheral resistance is elevated, any agent that tends to increase cardiac output would also tend to lower central Pv substantially, and this in turn would minimize the augmentation of cardiac output