TYPES OF SHOCK Dr Farzana Salman

SHOCK Generalized inadequate blood flow throughout the body causing tissue damage

CIRCULATORY SHOCK Depression of body functions due to reduced blood flow to the tissues because of some disorder of the cardiovascular system

STAGES OF CIRCULATORY SHOCK Non progressive stage Progressive stage Irreversible stage

Causes/Classification of Circulatory Shock

Causes of shock Reduced blood volume (Hypovolumic shock) Hemorrhage Trauma Surgery Burns Dehydration Increased vascular capacity Neurogenic shock Anaphylactic shock Septic shock ↓ Venous return

Causes of shock Obstruction to blood flow ↓ Venous return Cardiac tamponade Tumors in myocardium Thromboembolism Cardiac diseases ↓ Pumping ability Myocardial ischemia Congestive heart failure Arrhythmia Severe heart valvular dysfunctions

Manifestations ↓BP Tachycardia Vasoconstriction ↓ systolic pressure due reduced filling and reduced stroke volume ↓ diastolic Pressure ↓ pulse pressure Stagnant hypoxia Pale ,cold , clammy skin

Manifestations Sweating Cyanosis ↓Urinary out put Acidosis ↓ Blood flow to the vital organs affected ↓ Blood flow to brain → fainting Death due to brain ischemia or cardiac arrest

Compensatory mechanisms BP maintained Baroreceptor flex Chemoreceptor flex CNS ischemic response Sympathetic stimulation All of the above leads to Vasoconstriction → ↑PR →↑BP Venoconstriction →↑VR →↑COP →↑BP Force and rate of heart contraction More effective in BP maintenance Less effective in COP maintenance

Compensatory mechanisms Reverse stress relaxation phenomenon Rennin angiotensin system Vasopressin Epinephrine and norepinephrine by adrenal medulla. Mechanisms that return the blood volume back to normal

Progressive Shock Cardiac depression. Vasomotor failure Blockage of very small vessels by sludged blood Increased capillary permeability Release of toxins by ischemic tissues Cardiac depression caused by endotoxin Generalized cellular deterioration.

Progressive Shock Tissue necrosis Acidosis in shock

P R O G R E S S I V E Shock

Arterial pressure at different degrees of hemorrhage Nonprogressive shock Progressive shock

Progressive shock Increasing cardiac depression

Irreversible shock

Increased vascular capacity Neurogenic shock General anesthesia Spinal anesthesia Ischemia of brain causing vasodilatation Vasovagal syncope Postural syncope Carotid sinus syncope Vasodilatation

Increased vascular capacity Anaphylaxis Exaggerated allergic reaction Antigen-antibody reaction→ release of histamine, some other vasodilators Vasodilatation ↑permeability Exudation of fluid → further reduction in blood volume Blood volume to total vascular capacity reduced

Increased vascular capacity Septic shock Severe infection anywhere in the body Bacteria produce toxins Generalized Vasodilatation Weakening of myocardium ↑ capillary permeability Exudation of fluid → further reduction in blood volume Blood volume to total vascular capacity reduced

Cardiogenic shock Many IHD patients die of sudden ventricular fibrillation More chances in large infarction Can develop even in small infarctions Sometimes even after many days of infarction (but less likely)

Cardiogenic shock Infarction After a few days degeneration of infarcted muscle Thinning of the site Systolic stretch with each contraction Worsening of the systolic stretch with the passage of time Rupture of the heart Collection of blood in the pericardial cavity Cardiac tamponade Quick death

High COP shock Excessive metabolism Abnormal tissue perfusion pattern Thyrotoxicosis Abnormal tissue perfusion pattern Shunts Inability of tissue to utilize O2 & nutrients Electron transport chain poisoning

Treatment of shock Postural change Blood transfusion Plasma transfusion Transfusion of plasma substitutes Plasma expanders- dextran Concentrated human albumin serum Hypertonic solutions Sympathomimetc drugs Glucocorticoids Oxygen therapy