Unit Four: The Circulation Chapter 24: Circulatory Shock and Its Treatment Guyton and Hall, Textbook of Medical Physiology, 12 edition

Physiologic Causes of Shock Circulatory Shock Caused by Decreased CO Cardiac abnormalities that decrease the ability of the heart to pump blood Factors that decrease venous return Circulatory Shock That Occurs Without Diminished CO Excessive metabolic rate Abnormal tissue perfusion pattterns

Physiologic Causes of Shock Tissue Deterioration is the End Result of Circulatory Shock Stages of Shock Nonprogressive (compenstated) stage-normal compensatory mechanisms result in full recovery Progressive stage-without theapy, the shock eventually results in death c. Irreversible stage-all forms of therapy are inadequate

Shock Caused by Hypovolemia-Hemorrhagic Shock Relationship of Bleeding Volume to CO and Arterial Pressure Fig. 24.1 Effect of hemorrhage on CO and arterial pressure

Shock Caused by Hypovolemia-Hemorrhagic Shock Sympathetic Reflex Compensations Value of Sympathetic Nervous Reflexes Greater Effect of the Sympathetic Nervous Reflexes in Maintaining Arterial Pressure than in Maintaining CO Protection of Coronary and Cerebral Blood Flow

Progressive and Non-progressive Hemorrhagic Shock Non-progressive (Compensated) Shock If the shock is not severe enough to cause its own progression, the person eventually recovers. Factors that allow recovery are the negative feedback mechanisms that attempt to restore CO and arterial pressure

Progressive and Non-progressive Hemorrhagic Shock Baroreceptor reflexes CNS ischemic response Reverse stress-relaxation of the circulatory system Increased secretion of renin and the formation of angiotensin II Increased secretion of vasopressin (ADH) Increased secretion of epinephrine and norepinephrine Compensatory mechanisms that return the blood volume back toward normal

Progressive and Non-progressive Hemorrhagic Shock Progressive Shock-Viscous Circle of Cardiovascular Deterioration Fig. 24.3 Different types of “positive feedback” that can lead to progression of shock

Progressive and Non-progressive Hemorrhagic Shock (cont.) Cardiac Depression Fig. 24.4 CO curves of the heart at different times after hemorrhagic shock begins

Progressive and Non-progressive Hemorrhagic Shock (cont.) Vasomotor Failure Blockage of Small Vessels Increased Capillary Permeability Release of Toxins by Ischemic Tissue Cardiac Depression Caused by Endotoxin Generalized Cellular Deterioration Tissue Necrosis in Severe Shock and Acidosis

Progressive and Non-progressive Hemorrhagic Shock (cont.) Irreversible Shock –Depletion of Cellular Hight Energy Phosphate Reserves Fig. 24.6 Failure of transfusion to prevent death in irreversible shock

Progressive and Non-progressive Hemorrhagic Shock (cont.) Hypovolemic Shock Caused by Plasma Loss Intestinal obstruction Severe burns

Progressive and Non-progressive Hemorrhagic Shock (cont.) Hypovolemic Shock Caused by Dehydration Excessive sweating Fluid loss in severe diarrhea or vomiting Excess loss of fluid by the kidneys Inadequate intake of fluids and electrolytes Destruction of the adrenal cortices, with the loss of aldosterone Hypovolemic Shock Caused by Trauma

Progressive and Non-progressive Hemorrhagic Shock (cont.) Neurogenic Shock-sudden loss of vasomotor tone Deep general anesthesia Spinal anesthesia Brain damage

Progressive and Non-progressive Hemorrhagic Shock (cont.) Anaphylactic Shock and Histamine Shock Release of histamine in immune type reactions, causing Venous dilation Arteriole dilation Increased capillary permeability

Progressive and Non-progressive Hemorrhagic Shock (cont.) Septic Shock (bacterial infection) Peritonitis caused by infection from the uterus and fallopian tubes Peritonitis resulting from rupture of the GI tract Generalized body infection resulting from the spread of a skin infection (Staph or Strep) Generalized gangrenous infection Infection spreading into the blood from the kidney or urinary tract

Progressive and Non-progressive Hemorrhagic Shock (cont.) Special Features of Septic Shock High fever Marked vasodilation, especially in infected areas High cardiac output Sludging of the blood caused by rbc agglutination Development of micro-blood clots (disseminated intravascular coagulation)

Progressive and Non-progressive Hemorrhagic Shock (cont.) Physiology of Treatment in Shock Replacement therapy with blood and plasma transfusion Dextran solution as a plasma substitute Sympathomimetic drugs (simulate sympathetic stimulation) Head down position Oxygen therpay Glucocorticoids

Progressive and Non-progressive Hemorrhagic Shock (cont.) Circulatory Arrest-all blood flow stops Usually as a result of cardiac arrest or ventricular fibrillation b. Effect on the brain