Chapter 24 Understanding Circulatory Shock

• Circulatory shock involves generalized inadequate blood flow, leading to tissue damage due to insufficient oxygen and nutrient delivery.
• The cardiovascular system's deterioration accelerates the progression of shock.

Physiological Causes of Shock

• Shock primarily stems from inadequate cardiac output.
• Cardiac abnormalities impairing the heart's pumping ability and factors reducing venous return can severely diminish cardiac output.
• Cardiogenic shock results from diminished heart pumping ability.
• Decreased venous return, often caused by diminished blood volume or reduced vascular tone, also reduces cardiac output.
• Normal or increased cardiac output can still lead to circulatory shock due to excessive metabolic rate or abnormal tissue perfusion patterns.
• Shock leads to inadequate nutrient delivery and waste removal in critical tissues and organs.

Arterial Pressure in Shock

• Arterial pressure isn't always a reliable indicator of circulatory function.
• Nervous reflexes can maintain arterial pressure despite severe shock.
• Arterial pressure decreases with decreased cardiac output, especially in shock from blood loss, but not always to the same extent.

Tissue Deterioration

• A critical state of circulatory shock initiates a vicious cycle, with tissue deterioration causing further cardiac output decrease and shock progression, until death occurs. Timely treatment can reverse this decline.

Stages of Shock

• Shock is divided into three stages: nonprogressive (compensated), progressive, and irreversible.
• In the nonprogressive stage, compensatory mechanisms allow full recovery without outside help.
• In the progressive stage, shock steadily worsens without therapy until death.
• In the irreversible stage, therapy is inadequate to save the person's life.

Hypovolemic Shock

• Hypovolemia from hemorrhage decreases venous return, causing decreased cardiac output and potential shock.
• Removal of about 10% of blood volume has little effect on arterial pressure or cardiac output without compensation.
• Sympathetic reflexes maintain arterial pressure through arteriolar constriction, venous reservoir constriction, and increased heart activity.
• Reflexes help maintain venous return from falling too much, in addition to maintaining arterial pressure.
• Ischemic response of the central nervous system activates extreme sympathetic stimulation to try and keep the arterial pressure from falling too low.

Protection of Coronary and Cerebral Blood Flow

• Maintaining arterial pressure protects blood flow through the coronary and cerebral circulations.
• Local blood flow autoregulation and lack of sympathetic constriction in these areas maintain blood flow.
• Blood flow to the heart and brain remains normal as long as mean arterial pressure remains above 70 mm Hg.

Hemorrhagic Shock

• The circulatory system can recover as long as the degree of hemorrhage is no greater than a certain amount.
• Crossing a critical threshold of blood loss makes the eventual difference between life and death.
• Hemorrhage beyond a critical level causes shock to become progressive, and the shock itself causes still more shock.

Compensated Shock

• Negative feedback control mechanisms help a person recover from moderate shock.
• The mechanisms include baroreceptor reflexes, central nervous system ischemic response, reverse stress-relaxation of the circulatory system, and increased secretion of renin, vasopressin, epinephrine, and norepinephrine
• The readjustment of blood volume, absorption of fluid, and intake of water and salt help recovery from nonprogressive shock.
• Sympathetic reflexes and increased secretion of catecholamines by the adrenal medullae provide rapid help toward recovery.

Progressive Shock

• Positive feedbacks depress cardiac output in shock, causing the shock to become progressive. These feedbacks include cardiac depression, vasomotor failure, sludged blood, increased capillary permeability, and toxin release from ischemic tissue.
• Impaired coronary blood flow from low arterial pressure weakens the heart muscle.
• Vasomotor center depression in the brain occurs when blood flow is diminished.
• Blockage in small blood vessels occurs from sluggish flow.
• Increased capillary permeability causes fluid to transude into the tissues.
• Ischemic tissues release toxins such as histamine, serotonin, and tissue enzymes.
• Diminished blood flow to the intestines may cause enhanced formation and absorption of endotoxin, causing cardiac depression.
• Generalized cellular deterioration occurs as shock becomes severe.

Generalized Cellular Deterioration

• Active transport through the cell membrane diminishes, and sodium and chloride accumulate in the cells.
• Mitochondrial activity in the liver and other issues becomes depressed.
• Lysosomes in cells break open, and hydrolases are released, causing further deterioration.
• Metabolic derangements occur.
• Not all cells are equally damaged by shock.
• Tissues that have better blood supplies don't get as damaged as other tissues.
• Metabolic derangements leading to acidosis occur in shocked tissue, which diminishes oxidative metabolism.
• A critical cardiac output level exists above which a person in shock recovers and below which death proceeds.

Irreversible Shock

• Transfusion or therapy cannot save the person's life after shock has progressed to a certain stage.

Cellular Depletion

• Cellular depletion of high energy compounds is devastating for the development of the final state of irreversibility.

Hypovolemic Shock with Plasma Loss

• Loss of plasma can cause hypovolemic shock. This can occur with severe burns.
• Intestinal obstruction occurs.
• Dehydration can cause hypovolemic shock as well.
• Aldosterone secretion occurs as well.

Hypovolemic Shock with Trauma

• Shock results from hemorrhage caused by the trauma.

Neurogenic Shock

• The major cause of neurogenic shock is sudden loss of vasomotor tone throughout the body.
• Loss of vasomotor tone is caused by deep general anesthesia, spinal anesthesia, or brain damage.

Anaphylactic and Histamine Shock

• Results from an antigen-antibody reaction that occurs after an antigen has entered the circulation
• Causes histamine release, resulting in decreased venous return, reduced arterial pressure, and increased capillary permeability.
• This causes great reduction in venous return and shock.

Septic Shock

• Septic shock is a bacterial infection widely disseminated causing extensive damage. This is caused by Gram-positive bacteria.
• Typical causes include peritonitis, generalized bodily infection, generalized gangrenous infection, and infection spreading into the blood.
• Septic shock has a high fever, marked vasodilation, and high cardiac output. In addition, sludging of the blood and micro-blood clots occurs.

Treatment for Shock

• For shock caused by hemorrhage, use blood transfusions. For shock caused by plasma loss, use plasma. For shock caused by dehydration, use electrolyte solutions.
• Dextran solution is a plasma substitute.
• Use sympathomimetic drugs for neurogenic shock or anaphylactic shock.
• Use the head-down position to promote venous return.
• Oxygen therapy can be beneficial.
• Use glucocorticoids-adrenal cortex hormones.
• Restore normal cardiac rhythm.
• Prevent Blood Clots
• If blood clots are prevented from occurring with the use of heparin the brain can avoid being effected by circulatory arrest for a while.