CIRCULATORY SHOCK 2-Feb-19 shock

Circulatory shock Circulatory shock means Generalized inadequacy of blood flow throughout the body including Heart, brain, liver, kidneys, GIT to the extend that the body tissues are damaged. Tissue damage occur because of too little flow, especially because of too little delivery of oxygen and other nutrients to the tissue cells. 2-Feb-19 shock

Circulatory Shock Symptoms Initially are agitation and restlessness which later progress to lethargy, confusion and coma. 2-Feb-19 shock

Stages of shock. Non progressive stage Progressive stage Irreversible stage 2-Feb-19 shock

Non progressive stage Also known as compensated stage Normal circulatory compensatory mechanisms eventually cause full recovery without help form outside therapy. 2-Feb-19 shock

Progressive stage Shock become steadily worse until death If no therapy 2-Feb-19 shock

Irreversible stage The shock has progressed to such an extent that all forms of known therapy are inadequate to save life Even though the moment, the person is still alive. 2-Feb-19 shock

Irreversible shock Even in this stage, therapy can on rare occasions, still return the arterial pressure and even the CO to normal or near normal for short period But the circulatory system nevertheless continue to deteriorate and death ensues in another few minutes to few hours. 2-Feb-19 shock

Irreversible shock Hemorrhage 100 – -- CO (% of normal) 25 -- Progressive stage CO (% of normal) Transfusion Irreversible shock 30 60 90 120 150 minutes 2-Feb-19 shock

Irreversible shock There is depletion of cellular high Energy Phosphate reserves Creatine Phosphate, ATP 2-Feb-19 shock

Pathophysiology of shock Shock usually results from inadequate CO. Therefore any condition that reduces CO will probably lead to circulatory shock. These include diminished cardiac pumping ability Factors decreasing venous return 2-Feb-19 shock

Diminished cardiac pumping ability Cardiac abnormalities that decrease the pumping ability of the heart. include: Myocardial infarction Severe heart valve dysfunction Cardiac arrhythmias Other cardiac diseases Circulatory shock resulting from diminished cardiac pumping ability cardiogenic shock. 2-Feb-19 shock

Cardiogenic shock Results from markedly decreased CO Inadequate cardiac function eg from MI,mechanical disorders Abnormally slow or fast ventricular rate. 2-Feb-19 shock

Factors that decrease the venous return Decreased vascular tone esp. of the venous reservoirs Low resistance shock Diminished blood volume Hypovolemic shock The most common type. Obstruction to blood flow at some point in the circulation esp. in the venous return pathway to the heart. obstructive shock 2-Feb-19 shock

Low resistance shock Occurs when neural reflexes or toxic substances cause excessive vasodilatation Leading to Reduced venous return Low CO Diminished venous return caused by vascular dilatation venous pooling of blood. 2-Feb-19 shock

Low resistance shock This includes Primary shock/neurogenic shock Anaphylactic shock 2-Feb-19 shock

Primary /neurogenic shock Also called syncope, fainting Leads to loss of consciousness Due to increased vascular capacity Caused by a reflex that produce arteriolar and venous dilatation causing peripheral pooling of blood. 2-Feb-19 shock

Primary /neurogenic shock Increased vascular capacity reduces the mean systemic filling pressure Which in turn reduces venous return Without an adequate venous return the cardiac output declines, arterial blood pressure decreases, and blood flow to the brain decreases. 2-Feb-19 shock

Primary /neurogenic shock One of the major causes, is sudden loss of vasomotor tone throughout the body Causing esp. massive dilatation of the veins Some of the factors that can cause loss of vasomotor tone include Deep general anesthesia often depresses the vasomotor center Spinal anesthesia, can block the sympathetic nervous system. Brain damage 2-Feb-19 shock

Primary/neurogenic shock provoked by pain, stress, fright or heat. 2-Feb-19 shock

Vasovagal Syncope Emotional fainting Not caused by vasomotor failure Results from strong emotional activation of parasympathetic signals to slow the heart and also activation of inverse sympathetic signals to dilate the peripheral vasculature thereby reducing CO and arterial pressure 2-Feb-19 shock

Vasovagal Syncope Called Vasovagal Syncope to differentiate it from other fainting that result from other neurogenic causes of reducing CO 2-Feb-19 shock

Anaphylactic shock Antigen antibody reaction Histamine causes: cause the basophils and mast cells to release histamine or a histamine like substance Histamine causes: An increased vascular capacity because of venous dilatation Dilatation of the arterioles reduce TPR Increased capillary permeability The net effect is a great reduction in venous return and often such serious shock that the person dies within minutes. 2-Feb-19 shock

Other causes of low resistance shock Severe hypoxia, drugs overdose, trauma to the nervous system. 2-Feb-19 shock

Hypovolemic shock. Caused by low blood volume Includes Hemorrhagic shock Plasma loss Dehydration shock Septic shock 2-Feb-19 shock

Hemorrhagic shock Hemorrhage is the most common cause of hypovolemic shock Occurs as a result of internal or external blood loss caused by rupture of vessels. 2-Feb-19 shock

Hemorrhagic shock Hemorrhage As a consequence decreases venous return decreases the filling pressure of the circulation As a consequence decreases venous return As a result the CO falls bellow normal and shock ensues. 2-Feb-19 shock

Hypovolemic shock caused by Plasma loss Plasma loss can be severe enough to reduce the total Blood volume markedly leading to hypovolemic shock similar to that caused by hemorrhage Severe plasma loss occurs in Intestinal obstruction Severe burn 2-Feb-19 shock

Intestinal obstruction Distention of intestines partly blocks venous blood flow in the intestinal circulation Increasing intestinal capillary pressure Fluid leakage into the intestinal walls and into the intestinal lumen. Severe burn Also causes plasma loss 2-Feb-19 shock

Dehydration Dehydration can reduce the blood volume and cause hypovolemic shock similar to that resulting from hemorrhage. Some of the causes of dehydration are: Fluid loss from GIT diarrhea, vomiting Skin burns ,Excessive sweating 2-Feb-19 shock

Dehydration Kidneys Inadequate intake of fluid and electrolytes Diabetes mellitus/insipidius, excessive use of diuretics Nephrotic syndrome Destruction of the adrenal cortex absence of aldosterone Inadequate intake of fluid and electrolytes 2-Feb-19 shock

Septic shock Infections in the blood stream Gram –negative sepsis esp. Gram –negative bacteria or bacterial toxins released from an infected site cause hypotension Gram –negative sepsis increase the permeability of the microvasculature, facilitating the movement of fluid into the tissues and intensifying the hypotension. 2-Feb-19 shock

Obstructive shock CO is reduced as a result of a mechanical impediment to Lt or Rt ventricular filling Massive pulmonary emboli, tension pneumothorax, cardiac tamponade can all lead to obstructive shock. 2-Feb-19 shock

More Causes of shock Occasionally the CO is normal or even greater than normal and yet a person is in circulatory shock. This can result from Excessive metabolism of the body Abnormal tissue perfusion patterns Note: Arterial pressure may be almost normal in severe shock powerful nervous reflexes Arterial pressure can fall to one – half normal but the person still has normal tissue perfusion and is not in shock. 2-Feb-19 shock

Trauma . Trauma is one of the most common cause of circulatory shock Hemorrhage Contusion of the body can damage the capillaries sufficiently to allow Excessive loss of plasma into the tissues Pain of trauma can cause neurogenic shock 2-Feb-19 shock

Circulatory shock Tissue deterioration is the end stage of circulatory shock. Inadequate blood flow causes the tissues to begin deteriorating including the heart and circulatory system itself. This causes even more decrease in CO, And vicious circle ensues with progressive increasing circulatory shock, less adequate tissue perfusion more shock and so forth until death. 2-Feb-19 shock

Compensatory mechanisms The factors that cause a person to recover from moderate degrees of shock are all the negative feedback control mechanisms of the circulation that attempt to return Cardiac output and arterial pressure back to normal levels. They compensate enough to prevent further deterioration of the circulation. 2-Feb-19 shock

Compensatory mechanisms They include Sympathetic reflexes and factors that return blood volume back towards normal 2-Feb-19 shock

Sympathetic reflexes These include Baroreceptor reflexes CNS ischaemic response Chemoreceptor response 2-Feb-19 shock

CO&Arterial pressure (% of normal) Relationship of bleeding volume to CO and BP About 10% of total blood volume can be removed with almost no effect on either arterial pressure or CO Greater blood loss usually diminishes the CO first and later the pressure 100 BP CO&Arterial pressure (% of normal) 50 CO 10 20 30 40 50 % of total blood removed 2-Feb-19 shock

CO&Arterial pressure (% of normal) Relationship of bleeding volume to CO and BP Both of these falling to zero when about 35 – 45% total blood volume has been removed. Sympathetic reflexes maintain BP. 100 BP CO&Arterial pressure (% of normal) 50 CO 10 20 30 40 50 % of total blood removed 2-Feb-19 shock

CO&Arterial pressure (% of normal) Relationship of bleeding volume to CO and BP Powerful sympathetic reflexes initiated mainly by the baroreceptors and by low pressure vascular stretch receptors These reflexes stimulate SNS Vasoconstriction 100 BP CO&Arterial pressure (% of normal) 50 CO 10 20 30 40 50 % of total blood removed 2-Feb-19 shock

CO&Arterial pressure (% of normal) Relationship of bleeding volume to CO and BP constriction of arterioles increases the TPR Constriction of veins helps to maintain adequate venous return 100 BP CO&Arterial pressure (% of normal) 50 CO 10 20 30 40 50 % of total blood removed 2-Feb-19 shock

CO&Arterial pressure (% of normal) Relationship of bleeding volume to CO and BP Sympathetic stimulation increases heart activity increasing HR to as high as 160 – 180 beats/min Also force of contraction 100 BP CO&Arterial pressure (% of normal) 50 CO 10 20 30 40 50 % of total blood removed 2-Feb-19 shock

CO&Arterial pressure (% of normal) Relationship of bleeding volume to CO and BP Without sympathetic reflexes only 15 – 20% of blood can be removed over a period of 30min before a person dies. Cf. 30 – 40% blood volume loss that a person can sustain when the reflexes are intact. 100 BP CO&Arterial pressure (% of normal) 50 CO 10 20 30 40 50 % of total blood removed 2-Feb-19 shock

CO&Arterial pressure (% of normal) Relationship of bleeding volume to CO and BP Sympathetic reflexes are geared more for maintaining arterial pressure than for maintaining cardiac output. TPR. 100 BP CO&Arterial pressure (% of normal) 50 CO 10 20 30 40 50 % of total blood removed 2-Feb-19 shock

CO&Arterial pressure (% of normal) Relationship of bleeding volume to CO and BP Second plateau at about 50mmHg in the arterial pressure curve is due to activation of CNS ischaemic response. Which causes extreme stimulation of SNS due to brain hypoxia 100 BP CO&Arterial pressure (% of normal) 50 CO 10 20 30 40 50 % of total blood removed 2-Feb-19 shock

Note Sympathetic stimulation does not cause significant constriction of either the cerebral or the cardiac vessels 2-Feb-19 shock

Factors that restore blood volume Rennin Angiotensin system Release of ADH (vasopressin) Compensatory mechanisms that return the blood volume back toward normal may require 1 – 48hrs 2-Feb-19 shock

Decompensatory mechanisms Progressive shock Is caused by a vicious circle of cardiovascular deterioration Caused by decompensatory mechanisms 2-Feb-19 shock

Decompensatory mechanisms These include: Cardiac depression Vasomotor failure Blockage of minute vessels Increased capillary permeability Release of toxins by ischaemic tissues Generalized cellular deterioration 2-Feb-19 shock

Cardiac depression When arterial pressure falls low enough Coronary blood flow decreases below that required for adequate nutrition of myocardium. This weakens the heart muscle and thereby decreases the CO still more. Thus a positive feedback cycle has developed whereby the shock becomes more and more severe. 2-Feb-19 shock

Vasomotor failure. There comes a point in which diminished blood flow to the brain’s vasomotor center so depresses the center that it becomes progressively less active And finally totally inactive Vasomotor center fails only in the late stage of shock 2-Feb-19 shock

Blockage of minute vessels Initiated by sluggish blood flow in the microvessels Metabolic activities lead to accumulation of acids Acidity plus other products from ischaemic tissues cause local blood agglutination, resulting in minute blood clots and leading to minute plugs in the small vessels This causes shock to progress. 2-Feb-19 shock

Increased capillary permeability Occur after many hours of capillary hypoxia and lack of other nutrients Large quantities of fluid transude into the tissues decreasing the blood volume even more with resultant further decrease in CO 2-Feb-19 shock

Release of toxins by Ischaemic tissues Toxic substances such as histamine, serotonin and tissue enzymes cause further deterioration of the circulatory system. Endotoxin causes greatly increased cellular metabolism, despite the inadequate nutrition of the cells It affects cardiac muscle to cause cardiac depression. 2-Feb-19 shock

Generalized cellular deterioration As shock becomes severe, many signs of generalized cellular deterioration occur throughout the body. Among the damaging cellular effects are: diminished active transport of Na+ and K+(greatly) Depressed mitochondria activity (severely) Intracellular release of hydrolases from lysosomes causing further intracellular deterioration Depressed cellular metabolism of nutrients such as glucose. 2-Feb-19 shock

Decompensatory mechanisms Decreased CO Arterial pressure Systemic blood flow Cardiac nutrition Nutrition of tissues Vascular system nutrition Intravascular clotting Brain nutrition Vasomotor activity Tissue ischemia Capillary permeability Release of toxins Vascular dilatation Blood volume Venous pooling of blood Cardiac depression Venous return 2-Feb-19 shock

Treatment of shock Replacement therapy Sympathomimetic drugs Blood and plasma transfusion Plasma substitute Sympathomimetic drugs eg. Epinephrine, norepinephrine Sometimes useful, sometimes not Useful in neurogenic and anaphylactic shock Not proved to be very valuable in hemorrhage shock 2-Feb-19 shock

Treatment of shock Other therapy Glucocorticoids Head down position Oxygen therapy glucocorticoids Glucocorticoids Increases the strength of the heart in the late stage of shock Stabilize the lysosomal membrane Might aid in the metabolism of glucose by the severely damaged cells. 2-Feb-19 shock