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

2. 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

3. 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

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

5. 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

6. 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

7. 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

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

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

10. 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

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

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

13. 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

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

15. 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

16. 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

17. 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)

18. 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

19. 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