Symposium on Shock
Cardiogenic Shock
Phillip Ogburn, D.V.M., Ph.D.*
Numerous clinical and research studies have attempted to define the complex events appearing in patients suffering from shock. Although considerable debate currently exists regarding several aspects of shock, there is nearly universal agreement that shock may be defined as a critical fall in capillary perfusion which reduces oxygen delivery to levels below the tissues' nutritional requirement for maintenance of cellular integrity. 3 The fundamental mechanisms involved in the reduction of capillary perfusion are: (l) a fall in venous return to the heart; (2) an intrinsic inability of the heart to maintain cardiac output; or (3) an abnormality in the peripheral circulation which deprives the capillary bed of its blood flow. Shock resulting from an intrinsic disorder of the heart is a syndrome marked by a reduction of blood flow and is accompanied by progressive impairment of organ function which can occur immediately with or within days after acute cardiac insufficiency. Through this definition, the syndrome of cardiogenic shock cannot be considered separate from the physiologic abnormalities that may and do accompany heart failure. It is especially important that the veterinarian recognize this and treat circulatory abnormalities which generally occur prior to the development of shock in an effort to prevent its development or to improve its prognosis. This section has been written in an effort to illustrate how the heart can contribute to the development of shock as a primary mechanism, The leading cause of cardiogenic shock in man is myocardial infarction brought on by acute coronary arterial occlusion. 4 The loss of myocardial contractility secondary to the interruption of myocardial blood supply results in primary "pump failure," i.e., the affected myocardium cannot generate enough force to expell sufficient blood from the ventricle to meet peripheral circulatory demands. In animal *Assistant Professor, University of Minnesota College of Veterinary Medicine, St. Paul, Minnesota Veterinary Clinics ofNorth America- Vol. 6, No.2, May 1976
181
182
PHILLIP OGBURN
species other than man, acute major coronary vessel occlusion rarely occurs and thus this mechanism of acute cardiac insufficiency is not an important factor in cardiogenic shock. The infrequency of reported cardiac-induced shock syndromes has prompted most veterinary clinicians to dismiss the heart's role in shock as minor and to view cardiogenic shock as a rare phenomenon in animals. 1• 2 Consider, however, the numerous occurrences of "sudden death" in dogs especially· without organic evide~ce of disease in other organ systems. What is your reaction to a diagnosis of "heart attack" as the cause of death which is often suspected or described by an owner when his animal dies or suddenly collapses? Do rapid forms of cardiac failure exist and are they clinically significant? Are these conditions truly cardiogenic shock states? The diagnosis of cardiogenic shock has met with much resistance by veterinarians-and with a great deal of justification. However, even the most skeptical clinician must be willing to recognize that acute declines in cardiac performance may be observed under the following circumstances: (1) cardiac trauma and end-stage myocardial failure, (2) acute cardiac tamponade, (3) arrhythmias, and (4) pharmacologic depression. Generally, left ventricular failure and shock have been-considered as separate complications of acute cardiac insufficiency. The clinical syndromes of each are dissimilar to a point: the prominent signs of left heart failure are pulmonary congestion, dyspnea, and cough, whereas shock presents with signs of abrupt decline of peripheral perfusion as determined by weak thready pulses, pallor, collapse or syncope, reduced urinary output, and so forth. Both represent different manifestations of the same problem- reduced performance of the left ventricle. In left ventricular failure the symptoms are related to a "back up" of blood into the pulmonary veins and capillaries ("backward failure"). However, in cardiogenic shock, inadequate blood is supplied forward, i.e., pumped to the systemic arteries and capillaries to maintain tissue perfusion and cellular integrity ("forward failure"). The development of high left ventricular end diastolic or filling pressure characterizes the backward failure concept and is dependent in part on the gradual expansion of total blood volume characteristic of chronic congestive heart failure. Animals with acute cardiac insufficiency resulting from most common causes have little previous au"gmentation of circulatory volume and may exhibit no elevation in intraventricular pressure or volume. Of course these differences depend upon the mechanism involved in precipitating the shock syndrome. Alteration in regional blood flow, a phenomenon of shock in general, is manifested as a demonstrable inadequacy of tissue perfusion or organ function. Because early recognition of organ changes secondary to shock is important in determining therapy, a comprehensive evaluation of the adequacy of peripheral flow is of vital and continuing con-
CARDIOGENIC SHOCK
183
cern to the clinician. This evaluation should include the following assessments. Differential Skin Temperature. Warm extremities usually indicate adequate perfusion of the body. In shock states cutaneous and muscular blood supply is diminished because of enhanced reflex sympathoadrenal discharge that causes vascular constriction and redistribution of blood supply to vital internal organs such as the heart and brain. Not all animals show pronounced redistribution of blood flow and in many it is difficult to assess extremity perfu~ion because of pigmentation of the nails or density of hair coat. Peripheral Pulses and Capillary Refill Time. Thready, tapping, excessive compressibility or absence of the femoral pulses may indicate hypotension or cessation of blood flow due to vascular occlusion- an important consideration in cats. When the skin is warm, weak pulses usually are indicative of arterial hypotension. Femoral arterial pulses which are bounding may indicate intense peripheral vasoconstriction but with maintenance of central arterial pressure. Pulses distal to that area should then be palpated and capillary refill checked for full evaluation. Capillary refill will be prolonged because of vasoconstriction or poor perfusion. The usual refill time is less than two seconds. Central Nervous System. Restlessness, excitement, shivering unresponsiveness, syncope, and seizures are signs of inadequate cerebral blood flow and are usually noted in conjunction with severe hypotension or with cessation of blood flow. Urine Output. Urine flow less than 1.0 ml per kg per hour without prior evidence of urinary tract dysfunction or oliguria is suggestive of inadequate renal blood flow which can contribute to the development of tubular necrosis. Blood Pressure. Recently noninvasive ultrasound techniques have been developed to assess levels of arterial blood pressure. Peak arterial pressures below 80 mmHg or pressures with low pulse difference (20 to 30 mmHg) systolic/diastolic, suggest the presence of shock. In the early phases of shock, blood pressure may be only slightly reduced or normal, whereas other signs of reduced perfusion are present. Central venous pressure reflects the level of venous return as well as the degree of emptying of the right heart. The central nervous pressure is of particular value in assessing the hemodynamic state subsequent to fluid therapy. Normal mean right atrial pressures range from 0 to 15 em water. Acid Base Balance. Subsequent to diminished tissue perfusion and a decline in cellular oxygenation, metabolic acidosis develops with eleYated blood lactate levels. Arterial pH begins to fall with increasing seYerity of hypoperfusion; this therefore makes the determination of arterial gases and pH extremely valuable in evaluating the patient and in monitoring the response to therapy. Cardiac Signs. Persistent arrhythmias, poorly audible heart
184
PHILLIP OGBURN
sounds, diastolic gallops, and so forth, occurring in animals with low arterial pressures, or elevated central venous pressures, must be viewed as presumptive evidence of functional impairment of cardiac performance.
CLINICAL SYNDROMES OF CARDIOGENIC SHOCK The clinical signs of certain forms of cardiogenic shock may vary widely. The recognition of these varying syndromes enables the initiation of management and thereby prognosis of the condition.
ARRHYTHMOGENIC SHOCK
Bradycardias Severe deficiencies in cardiac output may occur in dogs when the ventricular rate drops below 60 beats per minute. Slow heart rates have been recognized in dogs with metabolic disorders such as hypothyroidism and adrenal insufficiency. Atrioventricular dissociation, complete heart block, high grade (3: l and 4: l) second degree atrioventricular block, and sinoatrial block associated with intrinsic cardiac disease, increasingly are being recognized as diagnostic factors in veterinary medicine. An abrupt onset of a bradycardia will reduce cardiac output sufficiently to cause collapse, seizures, and generalized weakness. However, perfusion may be additionally affected when intrinsic myocardial disease is present, such as when serious cardiac arrhythmias exist. Dissociative rhythms embarrass cardiac output by altering the sequence of atrial and ventricular excitation. When the atria and ventricles are not excited in a sequential fashion, the atrial contribution to ventricular filling suffers. Alteration of the normal pathways of ventricular conduction in dissociation may result in asynergy of ventricular contraction causing incomplete emptying of blood from the chamber. Tachycardias Deterioration of arterial pulse and peripheral perfusion is associated with supraventricular or ventricular tachyrhytl}ms in dogs when rates exceed approximately 200 beats per minute. Tissue perfusion may be restored when the rhythm is corrected but occasionally poor How persists even after sinus rhythm has been reestablished. It is important to differentiate these abnormal rhythms from ordinary sinus tachycardia which often accompany the hypovolemic or vasodilatory forms of shock. Tachycardia limits cardiac output by reducing the ventricular
185
CARDIOGENIC SHOCK
diastolic filling period which decreases the amount of blood the ventricle has to pump. Additionally, tachycardia is expensive in terms of myocardial oxygen demand; with increases in the rate of contraction, the myocardial oxygen consumption rises but the efficiency of cardiac work declines. This condition may further aggravate a hypoxic or ischemic myocardium. PHARMACOLOGIC SHOCK
Shock may be precipitated by administration of negative inotropic drugs such as anesthetics (halothane, methoxyflurane) and antiarrhythmic compounds (propranolol, quinidine, procainamide). In addition to chemotherapeutic agents, a myocardial depressant factor has been liberated from organ systems during shock and this factor may compound the effect on an otherwise equilibrated heart. Current knowledge regarding the myocardial depressant factor reveals that it is likely to influence cardiac output only in later stages of shock when tissue hypoxia has led to a breakdown of lysosomal enzymes. Anesthetics or other cardiodepressive agents used in shock therapy may have a prolonged pharmacologic effect. This fact must be considered when use of this type of medication is anticipated. PowER FAILURE SHOCK (CARDIAC TRAUMA AND END-STAGE MYOCARDIAL FAILURE)
Symptoms associated with progressively falling cardiac output are typical of severe myocardial damage in injuries to the thorax resulting from automobile accidents, falls, and so forth, or from intrinsic myocardial disease. Early signs of this form of cardiac insufficiency are weakening of the femoral pulse, pallor, increasing unresponsiveness to stimuli, tachycardia, and so forth. With further diminishment of cardiac output, peripheral vasoconstriction increases, urinary output falls, pallor becomes more evident, the femoral pulse becomes weak and thready, and stupor ensues. When the arterial pressure falls rapidly as with severe myocardial trauma, the course may be so short and signs of deterioration so abbreviated that death may occur before recognition of the problem. Signs of pulmonary congestion, fulminating edema, and hemorrhage may accompany this syndrome. In patients with a less severely damaged myocardium, as with myocardial disease, the signs of falling cardiac output and increasing peripheral vasoconstriction become evident more gradually. The condition may actually stabilize for a period during which the insufficiency of blood flow is not evident enough to provide the typical picture of shock. Animals with this form of shock show progressive decline in condition. When perfusion does reach a critical point, how-
186
PHILLIP OGBURN
ever, the course may be telescoped into a short period of rapidly deteriorating circulatory function and death.
AcuTE CARDIAC TAMPONADE
Acute cardiac tamponade is characterized by a rapid rise in venous pressure with a coincident decline in arterial pressure. The heart sounds are often diminished or muffled but may be normal. Pallor, collapse, and rapidly progressing dyspnea are frequently obvious. Acute tamponade is usually brought on by hemorrhage into the pericardia! sac. Hemorrhage may be induced by a variety of events, (usually traumatic). Causes include direct trauma from various accidents, iatrogenic insult from cardiac punctures during resuscitative maneuvers, and catheter penetration during cardiac catheterization. Rapid cardiac hemorrhage can occur from left atrial rupture in severe forms of mitral valve insufficiency and by rupture of tumors such as hemangiosarcomas. The manifestation of this syndrome occurs through a rapid rise in intrapericardial pressure. Once the pressure rises to a level sufficient to interfere with diastolic expansion of the ventricles, a decrease in ventricular filling occurs. With a decrease in ventricular filling, the cardiac output falls. Compensatory mechanisms are activated to maintain output: (1) an increase in peripheral resistance by vasoconstriction helps to maintain arterial pressure; (2) tachycardia helps to maintain cardiac output in view of lower stroke volume; and (3) systemic and pulmonary venous pressure rise tends to augment cardiac filling. These venous pressures rise in concert with increased intrapericardial pressure and thus may provide a guide to the severity of the situation. With an unchecked rise in intrapericardial pressure, the compensating mechanisms can no longer sustain cardiac output and death results through an inability of the heart to receive blood.
REFERENCES l. Brasmer, T. H.: Shock-basic pathophysiology and treatment. VET. CuN. NoRTH AM.,
2:219, 1972. 2. Ettinger, S. J.: Cardiac emergencies. VET. CLIN. NoRTH AM., 2:235, 1972. 3. Jacobson, E. D.: A physiologic approach to shock. New Engf. .J. Med., 278:834, 1968. 4. Kones, R. J.: Cardiogenic Shock: Mechanism and Management. Mount Kisco, New York, Futura Publishing Co., 1974. College of Veterinary Medicine University of Minnesota St. Paul, Minnesota 5510 I
Cardiogenic Shock
Phillip Ogburn, D.V.M., Ph.D.*
Numerous clinical and research studies have attempted to define the complex events appearing in patients suffering from shock. Although considerable debate currently exists regarding several aspects of shock, there is nearly universal agreement that shock may be defined as a critical fall in capillary perfusion which reduces oxygen delivery to levels below the tissues' nutritional requirement for maintenance of cellular integrity. 3 The fundamental mechanisms involved in the reduction of capillary perfusion are: (l) a fall in venous return to the heart; (2) an intrinsic inability of the heart to maintain cardiac output; or (3) an abnormality in the peripheral circulation which deprives the capillary bed of its blood flow. Shock resulting from an intrinsic disorder of the heart is a syndrome marked by a reduction of blood flow and is accompanied by progressive impairment of organ function which can occur immediately with or within days after acute cardiac insufficiency. Through this definition, the syndrome of cardiogenic shock cannot be considered separate from the physiologic abnormalities that may and do accompany heart failure. It is especially important that the veterinarian recognize this and treat circulatory abnormalities which generally occur prior to the development of shock in an effort to prevent its development or to improve its prognosis. This section has been written in an effort to illustrate how the heart can contribute to the development of shock as a primary mechanism, The leading cause of cardiogenic shock in man is myocardial infarction brought on by acute coronary arterial occlusion. 4 The loss of myocardial contractility secondary to the interruption of myocardial blood supply results in primary "pump failure," i.e., the affected myocardium cannot generate enough force to expell sufficient blood from the ventricle to meet peripheral circulatory demands. In animal *Assistant Professor, University of Minnesota College of Veterinary Medicine, St. Paul, Minnesota Veterinary Clinics ofNorth America- Vol. 6, No.2, May 1976
181
182
PHILLIP OGBURN
species other than man, acute major coronary vessel occlusion rarely occurs and thus this mechanism of acute cardiac insufficiency is not an important factor in cardiogenic shock. The infrequency of reported cardiac-induced shock syndromes has prompted most veterinary clinicians to dismiss the heart's role in shock as minor and to view cardiogenic shock as a rare phenomenon in animals. 1• 2 Consider, however, the numerous occurrences of "sudden death" in dogs especially· without organic evide~ce of disease in other organ systems. What is your reaction to a diagnosis of "heart attack" as the cause of death which is often suspected or described by an owner when his animal dies or suddenly collapses? Do rapid forms of cardiac failure exist and are they clinically significant? Are these conditions truly cardiogenic shock states? The diagnosis of cardiogenic shock has met with much resistance by veterinarians-and with a great deal of justification. However, even the most skeptical clinician must be willing to recognize that acute declines in cardiac performance may be observed under the following circumstances: (1) cardiac trauma and end-stage myocardial failure, (2) acute cardiac tamponade, (3) arrhythmias, and (4) pharmacologic depression. Generally, left ventricular failure and shock have been-considered as separate complications of acute cardiac insufficiency. The clinical syndromes of each are dissimilar to a point: the prominent signs of left heart failure are pulmonary congestion, dyspnea, and cough, whereas shock presents with signs of abrupt decline of peripheral perfusion as determined by weak thready pulses, pallor, collapse or syncope, reduced urinary output, and so forth. Both represent different manifestations of the same problem- reduced performance of the left ventricle. In left ventricular failure the symptoms are related to a "back up" of blood into the pulmonary veins and capillaries ("backward failure"). However, in cardiogenic shock, inadequate blood is supplied forward, i.e., pumped to the systemic arteries and capillaries to maintain tissue perfusion and cellular integrity ("forward failure"). The development of high left ventricular end diastolic or filling pressure characterizes the backward failure concept and is dependent in part on the gradual expansion of total blood volume characteristic of chronic congestive heart failure. Animals with acute cardiac insufficiency resulting from most common causes have little previous au"gmentation of circulatory volume and may exhibit no elevation in intraventricular pressure or volume. Of course these differences depend upon the mechanism involved in precipitating the shock syndrome. Alteration in regional blood flow, a phenomenon of shock in general, is manifested as a demonstrable inadequacy of tissue perfusion or organ function. Because early recognition of organ changes secondary to shock is important in determining therapy, a comprehensive evaluation of the adequacy of peripheral flow is of vital and continuing con-
CARDIOGENIC SHOCK
183
cern to the clinician. This evaluation should include the following assessments. Differential Skin Temperature. Warm extremities usually indicate adequate perfusion of the body. In shock states cutaneous and muscular blood supply is diminished because of enhanced reflex sympathoadrenal discharge that causes vascular constriction and redistribution of blood supply to vital internal organs such as the heart and brain. Not all animals show pronounced redistribution of blood flow and in many it is difficult to assess extremity perfu~ion because of pigmentation of the nails or density of hair coat. Peripheral Pulses and Capillary Refill Time. Thready, tapping, excessive compressibility or absence of the femoral pulses may indicate hypotension or cessation of blood flow due to vascular occlusion- an important consideration in cats. When the skin is warm, weak pulses usually are indicative of arterial hypotension. Femoral arterial pulses which are bounding may indicate intense peripheral vasoconstriction but with maintenance of central arterial pressure. Pulses distal to that area should then be palpated and capillary refill checked for full evaluation. Capillary refill will be prolonged because of vasoconstriction or poor perfusion. The usual refill time is less than two seconds. Central Nervous System. Restlessness, excitement, shivering unresponsiveness, syncope, and seizures are signs of inadequate cerebral blood flow and are usually noted in conjunction with severe hypotension or with cessation of blood flow. Urine Output. Urine flow less than 1.0 ml per kg per hour without prior evidence of urinary tract dysfunction or oliguria is suggestive of inadequate renal blood flow which can contribute to the development of tubular necrosis. Blood Pressure. Recently noninvasive ultrasound techniques have been developed to assess levels of arterial blood pressure. Peak arterial pressures below 80 mmHg or pressures with low pulse difference (20 to 30 mmHg) systolic/diastolic, suggest the presence of shock. In the early phases of shock, blood pressure may be only slightly reduced or normal, whereas other signs of reduced perfusion are present. Central venous pressure reflects the level of venous return as well as the degree of emptying of the right heart. The central nervous pressure is of particular value in assessing the hemodynamic state subsequent to fluid therapy. Normal mean right atrial pressures range from 0 to 15 em water. Acid Base Balance. Subsequent to diminished tissue perfusion and a decline in cellular oxygenation, metabolic acidosis develops with eleYated blood lactate levels. Arterial pH begins to fall with increasing seYerity of hypoperfusion; this therefore makes the determination of arterial gases and pH extremely valuable in evaluating the patient and in monitoring the response to therapy. Cardiac Signs. Persistent arrhythmias, poorly audible heart
184
PHILLIP OGBURN
sounds, diastolic gallops, and so forth, occurring in animals with low arterial pressures, or elevated central venous pressures, must be viewed as presumptive evidence of functional impairment of cardiac performance.
CLINICAL SYNDROMES OF CARDIOGENIC SHOCK The clinical signs of certain forms of cardiogenic shock may vary widely. The recognition of these varying syndromes enables the initiation of management and thereby prognosis of the condition.
ARRHYTHMOGENIC SHOCK
Bradycardias Severe deficiencies in cardiac output may occur in dogs when the ventricular rate drops below 60 beats per minute. Slow heart rates have been recognized in dogs with metabolic disorders such as hypothyroidism and adrenal insufficiency. Atrioventricular dissociation, complete heart block, high grade (3: l and 4: l) second degree atrioventricular block, and sinoatrial block associated with intrinsic cardiac disease, increasingly are being recognized as diagnostic factors in veterinary medicine. An abrupt onset of a bradycardia will reduce cardiac output sufficiently to cause collapse, seizures, and generalized weakness. However, perfusion may be additionally affected when intrinsic myocardial disease is present, such as when serious cardiac arrhythmias exist. Dissociative rhythms embarrass cardiac output by altering the sequence of atrial and ventricular excitation. When the atria and ventricles are not excited in a sequential fashion, the atrial contribution to ventricular filling suffers. Alteration of the normal pathways of ventricular conduction in dissociation may result in asynergy of ventricular contraction causing incomplete emptying of blood from the chamber. Tachycardias Deterioration of arterial pulse and peripheral perfusion is associated with supraventricular or ventricular tachyrhytl}ms in dogs when rates exceed approximately 200 beats per minute. Tissue perfusion may be restored when the rhythm is corrected but occasionally poor How persists even after sinus rhythm has been reestablished. It is important to differentiate these abnormal rhythms from ordinary sinus tachycardia which often accompany the hypovolemic or vasodilatory forms of shock. Tachycardia limits cardiac output by reducing the ventricular
185
CARDIOGENIC SHOCK
diastolic filling period which decreases the amount of blood the ventricle has to pump. Additionally, tachycardia is expensive in terms of myocardial oxygen demand; with increases in the rate of contraction, the myocardial oxygen consumption rises but the efficiency of cardiac work declines. This condition may further aggravate a hypoxic or ischemic myocardium. PHARMACOLOGIC SHOCK
Shock may be precipitated by administration of negative inotropic drugs such as anesthetics (halothane, methoxyflurane) and antiarrhythmic compounds (propranolol, quinidine, procainamide). In addition to chemotherapeutic agents, a myocardial depressant factor has been liberated from organ systems during shock and this factor may compound the effect on an otherwise equilibrated heart. Current knowledge regarding the myocardial depressant factor reveals that it is likely to influence cardiac output only in later stages of shock when tissue hypoxia has led to a breakdown of lysosomal enzymes. Anesthetics or other cardiodepressive agents used in shock therapy may have a prolonged pharmacologic effect. This fact must be considered when use of this type of medication is anticipated. PowER FAILURE SHOCK (CARDIAC TRAUMA AND END-STAGE MYOCARDIAL FAILURE)
Symptoms associated with progressively falling cardiac output are typical of severe myocardial damage in injuries to the thorax resulting from automobile accidents, falls, and so forth, or from intrinsic myocardial disease. Early signs of this form of cardiac insufficiency are weakening of the femoral pulse, pallor, increasing unresponsiveness to stimuli, tachycardia, and so forth. With further diminishment of cardiac output, peripheral vasoconstriction increases, urinary output falls, pallor becomes more evident, the femoral pulse becomes weak and thready, and stupor ensues. When the arterial pressure falls rapidly as with severe myocardial trauma, the course may be so short and signs of deterioration so abbreviated that death may occur before recognition of the problem. Signs of pulmonary congestion, fulminating edema, and hemorrhage may accompany this syndrome. In patients with a less severely damaged myocardium, as with myocardial disease, the signs of falling cardiac output and increasing peripheral vasoconstriction become evident more gradually. The condition may actually stabilize for a period during which the insufficiency of blood flow is not evident enough to provide the typical picture of shock. Animals with this form of shock show progressive decline in condition. When perfusion does reach a critical point, how-
186
PHILLIP OGBURN
ever, the course may be telescoped into a short period of rapidly deteriorating circulatory function and death.
AcuTE CARDIAC TAMPONADE
Acute cardiac tamponade is characterized by a rapid rise in venous pressure with a coincident decline in arterial pressure. The heart sounds are often diminished or muffled but may be normal. Pallor, collapse, and rapidly progressing dyspnea are frequently obvious. Acute tamponade is usually brought on by hemorrhage into the pericardia! sac. Hemorrhage may be induced by a variety of events, (usually traumatic). Causes include direct trauma from various accidents, iatrogenic insult from cardiac punctures during resuscitative maneuvers, and catheter penetration during cardiac catheterization. Rapid cardiac hemorrhage can occur from left atrial rupture in severe forms of mitral valve insufficiency and by rupture of tumors such as hemangiosarcomas. The manifestation of this syndrome occurs through a rapid rise in intrapericardial pressure. Once the pressure rises to a level sufficient to interfere with diastolic expansion of the ventricles, a decrease in ventricular filling occurs. With a decrease in ventricular filling, the cardiac output falls. Compensatory mechanisms are activated to maintain output: (1) an increase in peripheral resistance by vasoconstriction helps to maintain arterial pressure; (2) tachycardia helps to maintain cardiac output in view of lower stroke volume; and (3) systemic and pulmonary venous pressure rise tends to augment cardiac filling. These venous pressures rise in concert with increased intrapericardial pressure and thus may provide a guide to the severity of the situation. With an unchecked rise in intrapericardial pressure, the compensating mechanisms can no longer sustain cardiac output and death results through an inability of the heart to receive blood.
REFERENCES l. Brasmer, T. H.: Shock-basic pathophysiology and treatment. VET. CuN. NoRTH AM.,
2:219, 1972. 2. Ettinger, S. J.: Cardiac emergencies. VET. CLIN. NoRTH AM., 2:235, 1972. 3. Jacobson, E. D.: A physiologic approach to shock. New Engf. .J. Med., 278:834, 1968. 4. Kones, R. J.: Cardiogenic Shock: Mechanism and Management. Mount Kisco, New York, Futura Publishing Co., 1974. College of Veterinary Medicine University of Minnesota St. Paul, Minnesota 5510 I
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