CIRCULATORY SHOCK AND BASIC PRINCIPLES OF MANAGEMENT LEARNING OBJECTIVES: At the end of the lecture, the student should

be able to: Define Circulatory Shock. Explain the physiologic causes of circulatory shock. Describe the stages of circulatory shock. Describe Hemorrhagic Shock. Give details of Neurogenic Shock. Characterize Anaphylactic Shock. Give details of Septic Shock. Explain Physiology of Treatment in Shock. CIRCULATORY SHOCK: . Definition: Inadequate perfusion of the bodys cells with oxygenated blood, resulting in: Organ dysfunction 2 .Cellular and organ damage, and if not quickly corrected 3 .Death.

PHYSIOLOGIC CAUSES OF SHOCK:

A .Due to diminished Cardiac Output: Cardiac abnormalities . Myocardial infarction, Toxic states of the heart, Severe heart valve dysfunction 2 .Dec venous return. Diminished blood volume. Dec vascular tone Obstruction to blood flow.

PHYSIOLOGIC CAUSES OF SHOCK: B. Without Diminished Cardiac Output: Excessive metabolism of the body, so that even a normal cardiac output is inadequate. (2) Abnormal tissue perfusion patterns, so that most of the cardiac output is passing through blood vessels besides those that supply the local tissues with nutrition.

CLASSIFICATION

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CLASSIFICATION Low Output Circulatory Failure: Hypovolemic shock (too little volume) Cardiogenic shock (pump failure) Obstructive shock Distributive shock: Venous pooling High Output Circulatory Failure: Distributive Shock: Sepsis, toxic shock, anaphylaxis. STAGES OF SHOCK: STAGE 1:

Compensated or Nonprogressive Shock. (PHYSIOLOGICAL MECHANISMS ONLY). STAGE 2: Decompensated or Progressive Shock. (PHYSIOLOGICAL MECHANISMS + THERAPY). STAGE 3: Irreversible Shock. (THERAPY BECOME INADEQUATE). STAGE 1: COMPENSATED NONPROGRESSIVE SHOCK: Non-Progressive shock Cerebral and Coronary blood flow is maintained by auto regulation. Sympathetic reflexes (30 min). Arterial pressure is maintained near normal level in the hemorrhaging person longer than is the CO . 35% to 45% removal of blood volume can be sustained ,in the presence of sympathetic response. STAGE 2: DECOMPENSATED PROGRESSIVE SHOCK:

A.Cardiac depression: BP < 60 mmHg leads to dec blood flow myocardial ischemia, dec C.O further decrease of BP ( positive feedback loop)

Progressive shock Vasomotor failure. Intravascular clotting. Increased Capillary Permeability. Release of toxins. Cardiac depression by endotoxin. Generalized cellular deterioration. Acidosis in shock. STAGE 3: IRREVERSIBLE SHOCK:

Heart deteriorates until it can no longer pump and death occurs. Depletion of Adenosine phosphate system. Cardiac and other tissue irreversibly damaged. Characterized by: Decreasing cardiac function Progressive blood vessel dilation Progressive increase in vessel permeability Depletion of Adenosine phosphate system

Symptoms Low Cardiac output. Low urine output Cool extremities, ashen and cyanotic Systemic hypotension ultimately develops Exertional dyspnea or dyspnea at rest, palpitations and generalized anxiety

HYPOVOLEMIC SHOCK SUBDIVIDED INTO: Hemorrhagic Shock. Traumatic Shock.

Loss of plasma Burn Shock. HEMORRHAGIC SHOCK: Most common cause of hypovolemic shock. Decrease in filling pressure of the circulation and, as a consequence, decreases venous return. The cardiac output falls below normal and shock may ensue.

Cardiogenic shock
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NEUROGENIC SHOCKINCREASED VASCULAR CAPACITY: Loss of vasomotor tone. Causes pooling of blood and there is generally no actual blood loss. Cardiac output may be normal or increased. Classic signs of shock may not be present. CAUSES:

General anesthesia. Brain damage.

Neurogenic Shock
Sympathetic Tone Or Parasympathetic Tone Vascular Tone

Tissue perfusion

Massive Vasodilation

Cardiac Output

SVR & Preload

ANAPHYLACTIC SHOCK AND HISTAMINE SHOCK:

Anaphylaxis is an allergic condition in which the cardiac output and arterial pressure often decrease drastically. One of the principal effects is to cause the basophils in the blood and mast cells in the pericapillary tissues to release histamine or a histamine-like substance. THE HISTAMINE CAUSES: An increase in vascular capacity because of venous dilation, thus causing a marked decrease in venous return; (2) Dilation of the arterioles, resulting in greatly reduced arterial pressure; and (3) Greatly increased capillary permeability, with rapid loss of fluid and protein into the tissue spaces. The net effect is a great reduction in venous return and sometimes such serious shock that the person dies within minutes. Anaphylaxis

SEPTIC SHOCK: ENDOTOXIC SHOCK Results from widespread, overwhelming infections. CAUSES OF SEPTIC SHOCK

Peritonitis Generalized bodily infection 3. Generalized gangrenous infection 4. Infection spreading into the blood from the kidney or urinary tract.

C linical S pectrumof Infection

Infection Bacteremia Sepsis Severe Sepsis Septic Shock PHYSIOLOGY OF TREATMENT IN SHOCK REPLACEMENT THERAPY: BLOOD AND PLASMA TRANSFUSION: Treat the cause. Transfusion of whole blood.

Administration of plasma. Plasma substitutes. REPLACEMENT THERAPY: DEXTRAN SOLUTION AS A PLASMA SUBSTITUTE: Principal requirement of a truly effective plasma substitute: remain in the circulatory system. nontoxic and must contain appropriate electrolytes. large enough molecular size to exert colloid osmotic pressure. TREATMENT OF SHOCK WITH SYMPATHOMIMETIC DRUGS: A sympathomimetic drug is a drug that mimics sympathetic stimulation. Drugs Include nor epinephrine and epinephrine. Especially beneficial in: A. Neurogenic shock, a sympathomimetic drug takes the place of the diminished sympathetic actions and can often restore full circulatory function. B. Anaphylactic shock, opposes the vasodilation effect of histamine. TREATMENT BY THE HEAD-DOWN POSITION. Especially in hemorrhagic and neurogenic shock

First essential step in the treatment of many types of shock. Placing the patient with the head at least 12 inches lower than the feet helps tremendously in promoting venous return, thereby also increasing cardiac output. OXYGEN THERAPY: Giving the patient oxygen to breathe can be of benefit in many instances. Because the major deleterious effect of most types of shock is too little delivery of oxygen to the tissues. This is far less beneficial because the problem in most types of shock is not inadequate oxygenation of the blood by the lungs but inadequate transport of the blood after it is oxygenated. TREATMENT WITH GLUCOCORTICOIDS: (1) Glucocorticoids frequently increase the strength of the heart in the late stages of shock. (2) Glucocorticoids stabilize lysosomes in tissue cells. (3) Glucocorticoids might aid in the metabolism of glucose by the severely damaged cells.

REFERENCES: TEXT BOOK OF MEDICAL PHYSIOLOGY TWELFTH EDITION GUYTON & HALL.

REVIEW OF MEDICAL PHYSIOLOGY WLLIUM F.GANONG - TWENTY SECOND EDITION.

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