Studies in Clinical Shock and Hypotension: IV. Variations in Reflex Vasoconstriction and Cardiac Stimulation

Hemodynamic studies were performed on 44 patients with nonhemorrhagic shock or hypotension in order to assess the degree of vasoconstriction and cardiac stimulation.In 19 patients, reflex adrenergic discharge was characterized by elevated total peripheral vascular resistance, a high ratio of central blood volume to total blood volume, tachycardia, and clinical signs of skin vasoconstriction. Reduced total blood volume in most of these patients at the time of study could be explained as the result of fever, administration of vasopressor drugs, or prolonged reflex vasoconstriction.Eight patients were hypotensive with low peripheral resistance usually associated with tachycardia and hypovolemia. The fact that all died within several hours suggests that this “irreversible” syndrome was related to local accumulation of acid metabolites with terminal failure of vasoconstriction.In 17 patients, absence of reflex vasoconstriction despite hypotension was manifested by low or normal peripheral resistance, low ratios of central blood volume to total blood volume, warm skin, and normal total blood volume. While tachycardia often was absent in this group, heart rate was more closely related to body temperature than to vasoconstriction. Lack of intense adrenergic discharge in these hypotensive patients could be attributed either to the absence of a hypovolemic stimulus or to impairment of normal sympathetic nervous system pathways. The high incidence of alcoholism, cirrhosis, malignancy, pulmonary emphysema, and diabetesin these patients suggests the possibility that adrenergic insufficiency was a factor in the failure of vasoconstriction in at least some of them.The frequency of hypovolemia in the patients with vasoconstriction stresses the need for recognition and correction of occult depletion of blood volume in shock of diverse etiologies.

[1]  J. Cohn Relationship of plasma volume changes to resistance and capacitance vessel effects of sympathomimetic amines and angiotensin in man. , 1966, Clinical science.

[2]  J. Cohn,et al.  Studies in clinical shock and hypotension. 3. Comparative effects of vasopressor drugs and dextran. , 1965, Archives of internal medicine.

[3]  I. Penn,et al.  HEMODYNAMIC ASPECTS OF HEMORRHAGIC AND SEPTIC SHOCK. , 1965, JAMA.

[4]  E. Sharpey-Schafer,et al.  Hypotension from absent circulatory reflexes. Effects of alcohol, barbiturates, psychotherapeutic drugs, and other mechanisms. , 1963, Lancet.

[5]  J. Siemsen,et al.  Bronchogenic carcinoma associated with severe orthostatic hypotension. , 1963, Annals of internal medicine.

[6]  M. Weil,et al.  Hemodynamic studies on clinical shock associated with infection. , 1963, The American journal of medicine.

[7]  S. Albert,et al.  BLOOD VOLUME , 1960, Anesthesiology.

[8]  A. Cobbold,et al.  Nervous and local chemical control of pre-capillary sphincters in skeletal muscle as measured by changes in filtration coefficient. , 1963, Acta physiologica Scandinavica.

[9]  T. Cooper,et al.  Cardiac and peripheral vascular responses to hyperthermia induced by blood stream heating. , 1962, The Journal of thoracic and cardiovascular surgery.

[10]  F. Ashton The physiology of shock. , 1962, Acta chirurgica Belgica.

[11]  B. Zweifach Aspects of comparative physiology of laboratory animals relative to the problem of experimental shock. , 1961, Federation proceedings.

[12]  C HEYMANS,et al.  Reflexogenic Areas of the Cardiovascular System , 2015, Perspectives in biology and medicine.

[13]  B. Folkow,et al.  Role of the Nervous System in the Control of Vascular Tone , 1960, Circulation.

[14]  E. Sharpey-Schafer,et al.  Absent circulatory reflexes in diabetic neuritis. , 1960, Lancet.

[15]  W. Hamilton,et al.  The pressure-volume responses of human forearm veins during epinephrine and norepinephrine infusions. , 1957, The Journal of clinical investigation.

[16]  E. Freis,et al.  Alterations in systemic vascular volume of the dog in response to hexamethonium and norepinephrine. , 1957, The American journal of physiology.

[17]  Gilbert Rp,et al.  Hemodynamics of shock due to infection. , 1955, Stanford medical bulletin.

[18]  R. J. Becker,et al.  Hemodynamics of shock due to infection. , 1955, Stanford medical bulletin.

[19]  A. Fox,et al.  Hemodynamic Studies of Patients with Myocardial Infarction , 1954, Circulation.

[20]  M. Power,et al.  Intercellular plasma of centrifuged human erythrocytes as measured by means of iodo 131 albumin. , 1953, Journal of applied physiology.

[21]  E. Freis,et al.  Hemodynamic alterations in acute myocardial infarction. I. Cardiac output, mean arterial pressure, total peripheral resistance, central and total blood volumes, venous pressure and average circulation time. , 1952, The Journal of clinical investigation.

[22]  Harold D. Green,et al.  BLOOD FLOW, PERIPHERAL RESISTANCE AND VASCULAR TONUS, WITH OBSERVATIONS ON THE RELATIONSHIP BETWEEN BLOOD FLOW AND CUTANEOUS TEMPERATURE , 1944 .

[23]  R. P. Noble,et al.  Studies of the circulation in clinical shock , 1943 .

[24]  N. E. Freeman DECREASE IN BLOOD VOLUME AFTER PROLONGED HYPERACTIVITY OF THE SYMPATHETIC NERVOUS SYSTEM , 1932 .

[25]  E. Landis,et al.  Micro-injection studies of capillary blood pressure in human skin , 1930 .