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

a. Cardiac abnormalities that decrease the ability of the heart to pump blood

b. Factors that decrease venous return

• Circulatory Shock That Occurs Without DiminishedCO

a. Excessive metabolic rate

b. Abnormal tissue perfusion pattterns

Physiologic Causes of Shock

• Tissue Deterioration is the End Result of CirculatoryShock

• Stages of Shock

a. Nonprogressive (compenstated) stage-normal compensatory mechanisms result in full recovery

b. Progressive stage-without theapy, the shock eventuallyresults 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 Reflexesin 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 ownprogression, the person eventually recovers. Factorsthat allow recovery are the negative feedbackmechanisms that attempt to restore CO and arterialpressure

Progressive and Non-progressive Hemorrhagic Shock

a. Baroreceptor reflexes

b. CNS ischemic response

c. Reverse stress-relaxation of the circulatory system

d. Increased secretion of renin and the formation of angiotensin II

e. Increased secretion of vasopressin (ADH)

f. Increased secretion of epinephrine and norepinephrine

g. Compensatory mechanisms that return the blood volume back toward normal

Progressive and Non-progressive Hemorrhagic Shock

• Progressive Shock-Viscous Circle of CardiovascularDeterioration

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 EnergyPhosphate 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

a. Intestinal obstruction

b. Severe burns

Progressive and Non-progressive Hemorrhagic Shock (cont.)

• Hypovolemic Shock Caused by Dehydration

a. Excessive sweatingb. Fluid loss in severe diarrhea or vomitingc. Excess loss of fluid by the kidneysd. Inadequate intake of fluids and electrolytese. 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

a. Deep general anesthesia

b. Spinal anesthesia

c. Brain damage

Progressive and Non-progressive Hemorrhagic Shock (cont.)

• Anaphylactic Shock and Histamine Shock

a. Release of histamine in immune type reactions, causing

1. Venous dilation2. Arteriole dilation3. Increased capillary permeability

Progressive and Non-progressive Hemorrhagic Shock (cont.)

• Septic Shock (bacterial infection)

a. Peritonitis caused by infection from the uterus andfallopian tubes

b. Peritonitis resulting from rupture of the GI tractc. Generalized body infection resulting from the

spread of a skin infection (Staph or Strep)d. Generalized gangrenous infectione. Infection spreading into the blood from the kidney

or urinary tract

Progressive and Non-progressive Hemorrhagic Shock (cont.)

• Special Features of Septic Shock

a. High feverb. Marked vasodilation, especially in infected areasc. High cardiac outputd. Sludging of the blood caused by rbc agglutinatione. Development of micro-blood clots (disseminated

intravascular coagulation)

Progressive and Non-progressive Hemorrhagic Shock (cont.)

• Physiology of Treatment in Shock

a. Replacement therapy with blood and plasma transfusion

b. Dextran solution as a plasma substitutec. Sympathomimetic drugs (simulate sympathetic

stimulation)d. Head down positione. Oxygen therpayf. Glucocorticoids

Progressive and Non-progressive Hemorrhagic Shock (cont.)

• Circulatory Arrest-all blood flow stops

a. Usually as a result of cardiac arrest or ventricular fibrillation

b. Effect on the brain