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SHOCK (Renjatan)

Dr.Yung Chee Tien Master Of Emergency Medicine


is Shock? Types of Shock. Features of Shock. How the human body handles shock. How to manage Shock.

What is Shock?
generalized inadequacy of blow flow throughout the body. tissues are damaged - too little delivery of 02 & nutrients to the tissue cells. Even the cardiovascular system itself - begins to deteriorate, so that the shock becomes progressively worse.

Types Of Shock

HYPOVOLAEMIC (e.g Bleeding)

- loss of whole blood, plasma or extracellular fluid CARDIOGENIC (e.g Myocardial Infarction) - failure of the pump, severe alterations in rhythm or
mechanical defect

OBSTRUCTIVE (e.g Tension Pneumothorax)

outflow from the heart

- inability of the heart to fill properly or obstruction to

DISTRIBUTIVE (e.g Anaphylactic Shock)

- loss of sympathetic vasomotor tone

- presence of vasodilating substance in the blood - shunting of vascular fluid to the interstitial space


Shock due to loss of intravascular fluid volume Possible causes Internal or external hemorrhage Traumatic hemorrhage Long bone or open fractures Severe dehydration from GI losses Plasma losses from burns Diabetic ketoacidosis Excessive sweating


an allergic condition in which the cardiac output and the arterial pressure often fall drastically. Results primarily from antigen-antibody reaction that takes place immediately after an antigen to which the person is sensitive has entered the circulation. Principal effects is to cause the basophils in the blood and the mast cells in the pericapillary tissues to release histamine or histamine-like substance.

Histamine causes : 1. Increase in vascular capacity because of venous dilatation 2. Dilatation of the arterioles causing greatly reduced arterial pressure 3. Greatly increase capillary permeability with rapid loss of fluid and protein into tissue space The net effect is a great reduction on venous return and often serious shock cause patient death within minutes

Formerly known as blood poisoning Simply means widely disseminated infection to many areas of the body, with the infection being borne through blood from one tissue to another and cause extensive damage


Special features of septic shock : 1. High fever 2. Marked vasodilatation throughout the body, especially in the effected tissue. 3. High cardiac output in perhaps half of the patient, cause by vasodilatation in the infected tissue and also by high metabolic rate and vasodilatation elsewhere in the body resulting from bacterial toxin stimulation of cellular metabolism and from the high body temperature.

4. Sludging of the blood cause by red cell agglutination in response to degenerating tissue 5. Development of microclots in widespread areas in the body, a condition called disseminated intravascular coagulation causes the clotting factor to be used up so that hemorrhages occur in many tissue, esp into the gut wall and into the intestinal tract



This happens when theres increase of vascular capacity => normal amount of blood becomes incapable to filling the circulatory system adequately. One major cause is sudden loss of vasomotor tone leading to venous pooling of blood. Causes of Neurogenic Shock: Spinal injury Brain damage

Failure of the heart to pump blood adequately. Differs from haemorrhagic shock in that CO falls despite normal or elevated blood volume and cardiac pressures. Occurs: - Damage to the heart -> MI - Ineffective pumping -> Cardiac Dysrhythmias - Mechanical defects -> Complication of MI (ventricular aneurysm, acute dysruption of valvular function) Most common cause is MI (15%-20%)


Features of Shock

Victim becomes pale & grey in colour Skin is cold and moist with sweat Giddiness Pulse becomes weak and rapid Breathing is shallow and fast Victim maybe become anxious or restless Thirst Unconscious

Body Response To Shock


Mechanisms involved are: Baroreceptor reflexes which elicits powerful sympathetic stimulation of the circulation. -Increase in HR and contractility. -Constriction of venous capacitance vessel. -Release of vasoactive hormones adrenaline, noradrenaline, dopamine and cortisol to maintain arteriolar and venoconstriction. -Release of ADH and activation .of reninangiotensin axis. -Arteriolar vasoconstriction overcome local autoregulation and redistribute blood volume.


Central nervous system ischaemic response even more powerful sympathetic stimulation throughout the body when arterial pressure falls below 50 mmHg. 3. . Formation of Angiotensin constricts the peripheral arteries and causes increased conservation of H20 and salt by kidneys.

4. Formation of Vasopressin (ADH) constricts peripheral arteries and veins. Also increases H20 retention by the kidneys. 5. Compensation mechanisms that return

the blood volume back to normal

absorption of large quantities of fluids from GIT & interstitial spaces, conservation of H20 & salt and increased thirst.

What to do?

1. 2. 3. 4.

Aim improve blood supply to the brain, heart and lungs, and arrange urgent removal to the hospital. DO NOT move the casualty unnecessarily.
Treat any cause you can remedy e.g external bleeding. Lay him down, keeping his head low and to one side (reduce risk of aspiration of vomit). Raise his legs and rest them on folded clothes or other suitable props. Loosen tight clothing at his neck, chest and waist.

5. Shelter him from extremes of temperature. 6. Check breathing rate, pulse and level of responsiveness at 10 mins intervals. 7. If breathing becomes difficult or vomiting likely, place him in the Recovery Position. 8. If casualty becomes unconscious, start ABC if resuscitation. 9. Arrange urgent removal to hospital.