Shock DONE BY AISWARYA THOMAS2ND YEAR PHARMD

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Definition of Shock

• Inadequate oxygen delivery due to reduction of effective circulating blood volume.

• Results in global tissue hypoperfusion and metabolic acidosis.

• If uncompensated it leads to impaired cellular metabolism and death. 2

Is This Patient in Shock?

• Restless• Confused• Skin cool and

mottled or hot and flushed

• Weak or absent peripheral pulses

• Low BP• Tachycardia • Drowsiness,

coma3

Yes! These are all signs and symptoms of shock

PATHOGENESIS

All forms of shock involves following 3 derangement :

•Reduced effective circulating blood volume

•Reduce supply of oxygen to the cells and tissues results

anoxia.

•Inflammatory mediators and toxins released from shock

induced cellular injury.

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1)REDUCED EFFECTIVE CIRCULATORY BLOOD VOLUME• By actual loss of blood volume occurs in hypovolaemic shock •By decreased cardiac output without actual loss of blood occurs in cardiogenic shock and septic shock.

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2) IMPAIRED TISSUE OXYGENATION

Reduction in the effective circulatory blood volume from either above or other etiologic agents, there is a decreased venous return to the heart resulting in decreased cardiac output.

This consequently causes reduced supply of oxygen to the organs and tissues and hence tissue anoxia, which sets in cellular injury.

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3) RELESE OF INFLAMATORY MEDIATORS

•As a response to cell injury inflammatory mediators are released but eventually these agents themselves become the cause of cell injury.•Endotoxins in bacterial wall in septic shock stimulate massive release of pro- inflammatory mediators (cytokines) but a similar process of release of agents takes place in late stages of shock from other causes. 8

• Several pro inflammatory mediators are released from monocytes-macrophages, other leucocytes and other body cells, the most important being the tumour necrosis factor (TNF)-α and interleukin-1 (IL-1) cytokines.

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Types of Shock

• Hypovolaemic• Septic• Cardiogenic • Other types

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Traumatic ShockNeurogenic Shock

Hypoadrenal shock

Hypovolaemic Shock

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Results from inadequate circulatory

blood volumeDue to loss of red cell mass and plasma or from loss of plasma

volume alone

ETIOLOGY

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1. Loss of whole blood Hemorrhage

Trauma Gastrointestinal ulcer Surgery Inadequate clotting2. Loss of other body fluids

Vomiting Diarrhea Diuretic therapy Burns(>10% surface)

Pathogenesis

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Hypovolaemia Decreased circulatory

volume

Decreased venous return to heart

  Decreased stroke volume

  Decreased cardiac output

  Decreased cellular oxygen

supply  Decreased tissue perfusion

  Impaired cellular metabolism

Shock

Clinical features

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Increased heart rate(Tachycardia)

Low BP (hypotension)Low urinary outputPallor , cool and clammy skinAnxiety , confusion , agitationAbsent bowel sounds Diagnostic findings Decreased hematocrit Increased lactate Increased urine specific

gravity Changes in electrolytes

Septic Shock

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Septic shock is the result of bacterial infections or septicemia along with the presence of tissue perfusion abnormalities.Gram positive septicemia(exotoxic shock)Gram negative septicemia(endotoxic shock) – more common

Etiology

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Gram negative septicaemia Example: infection with

E.coli Proteus

Pseudomonas

BacteroidesGram positive septicaemia Example: infection with

Streptococci

Pneumococci

Pathogenesis of Sepsis

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Clinical Features•Hyperthermia or hypothermia

•Tachycardia•Wide pulse pressure•Low blood pressure (SBP<90)•Mental status changes,agitation,coma•Hypoxemia•Urine output•Gastro intestinal bleedingDiagnostic findingsIncrease or decrease of WBCDecrease plateletsIncrease urine specific gravityDecrease urine sodium

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Cardiogenic Shock

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Acute circulatory failure with sudden fall in cardiac output from acute diseases of the heart without actual reduction of the blood volume (normovolaemia)

Etiologies

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• MI• Cardiac arrhythmias• Myocarditis• Pulmonary embolism• Rupture of heart, ventricle or papillary muscles• Acute aortic insufficiency•Tension pneumothorax

Pathogenesis

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Clinical Features• Cool, mottled skin• Tachypnea, Nausea, omitting• Altered mental status , anxiety ,

confusion• Narrowed pulse pressure and

hypotension• Decreased renal blood flow and urine

output• Chest pain may or may not be present• Decreased capillary refill timeDIAGNOSTIC FINDINGS Increase blood glucose Increase cardiac marksECGEchocardiogramChest X ray

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4) OTHER TYPES1.Neurogenic shock:- Arise due to interruption of sympathetic vasomotor supply.

2.Hypoadrenal shock :- Arise from unknown adrenal insufficiency, patients fails to respond normally to stress 0f Trauma, surgery or illness.

3.Traumatic shock :- Shock resulting from trauma is initially due to hypovolemia but even after haemorrhage has been controlled, these patient continue to suffer loss of plasma volume into the interstitial of injured tissue.

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Stages Of Shock

Deterioraton of the circulation in shock is a progressive phenomenon and can be divided arbitrarily into 3 ways:-

Non-Progressive (Initial,compensated,reversible shock)

Progressive Decompensated ShockDecompensated (Irreversible) Shock24

• COMPENSATED (NON-PROGRESSIVE, INITIAL, REVERSIBLE) SHOCK

• In early stages of shock, an attempt is made to maintain adequate cerebral and coronary blood supply by redistribution of blood so that the vital organs(brain and heart) are adequately perfused and oxygenated.

• These is achieved by activation of various neuro hormonal mechanism causing widespread vaso constriction,fluid conservation by the kidney and by stimulation of adrenal medulla.

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1)WIDESPREAD CONSTRICTION

• The neural and humeral factors(baroreceptor,chemoreceptors,catacholamines, renin and angiotensin II) are activated,in turn brings vasoconstriction particular in the vessel in the skin and abdominal viscera

• Wide spread vasoconstriction is a protective mechanism which increase peripheral resistance increased heart rate and increased blood pressure. 26

2) FLUID CONSERVATION BY THE KIDNEYFollowing factors may assist in restoring the blood volume(caused by shock) and improve venous return to the heart. Release of aldosterone from hypoxic kidney by activation of renin-angiotensin- aldosterone mechanism.Release of ADH due to decreased effective circulating blood volume.Reduced GFR due to arteriolar constriction.Shifting of tissue fluids into the plasma due to lowered capillary hydro static pressure.

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3) STIMULATION OF ADRENAL MEDULA

• In response to cardiac out put adrenal medulla is stimulated to release excess of catecholamine's ( epinephrine and non epinephrine) which increase heart rate and try to increase cardiac output.

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PROGRESSIVE DECOMPENSATED SHOCK

Patient suffers from some other stress or risk factors ( eg:- pre existing cardiovascular & lung disease)

The effect of progressive decompensated shock due to tissue hypoperfusion are:-

1)PULMONARY HYPOPERFUSIONIt increase vascular permeability resulting in tachypnea and adult respiratory distress syndrome.

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2) TISSUE ISCHAEMIA•It cause switch from aerobic to anaerobic glycolysis resulting in metabolic lactic acidosis which reduces the tissue pH which makes vasomotor response ineffective.•It cause vasodilation and peripheral pooling of blood.•The patient develops confusion and worsening of renal function.

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IRREVERSIBLE DECOMPENSATED

SHOCK• Shock is so severe that in spite of compensatory

mechanisms and despite therapy and control of etiologic agent no recovery is taking place, it is called Irreversible Decompensated Shock.

1)PROGRESSIVE VASODILATION• Anoxia damages the capillary and venular wall.

Arterioles become unresponsive to vasoconstriction and begin to dilate which results in peripheral pooling of blood which further deteriorate the effective circulating blood volume.

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2)INCREASED VASCULAR PERMEABILITY

•Anoxic damage to tissue release inflammatory mediators which cause increased vascular permeability.

•This results in escape of fluid from circulation into the interstitial tissue, thus deteriorating effective circulating blood volume.

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3)MYOCARDIAL DEPRESSANT FACTOR

• Decreased BP and persistently reduce blood flow to myocardium causes coronary insufficiency and myocardial ischemia due to release of myocardial depressant factor.

• It make depression of cardiac function, reduced cardiac output and decreased blood flow.

4)WORSENING PULMONARY HYPOPERFUSION

• It cause respiratory distress due to pulmonary oedema, tachypnoea and adult respiratory distress syndrome.

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5)ANOXIC DAMAGES TO HEART, KIDNEY, BRAIN

• There is release of inflammatory cytokines and other inflammatory mediators and generation of free radicals.

• There will be ischaemic cell death in the tissue due to aerobic respiration for ATP generation.

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6)HYPERCOAGULABILITY OF BLOOD

• Tissue damages in shock activates coagulation cascade with release of clot promoting factor, thromboplastin and release of platelet aggregator, which slows blood- stream and vascular thrombosis.

• It cause hypercoagulability of blood, impair the blood flow and cause tissue necrosis.

• Clinically, patient features coma, worsened heart function and progressive renal failure due to acute tubular necrosis.

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MANAGEMENT• Critical factors in the successful

management of a patient experiencing shock relate to early recognition of shock more precisely determination the correct stage of shock and it can very well help in the treatment of shock. Management may include:-

• FLUID REPLACEMENT• DRUG THERAPY• NUTRITIONAL THERAPY

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FLUID REPLACEMENT The cornerstone of therapy for shock other

than cardiogenic shock is volume expansion with administration of the appropriate fluid. Both crystalloid (Eg:-Normal saline solution)and colloid (Eg:-Albumin) have a role in fluid resuscitation

Crystalloid such as normal saline are used in the initial shock resuscitation, eventhough approximately 2/3 of the crystalline volume will diffuse out of the vascular space and into the intestinal space.

Colloids are effective volume expanders because the size of their molecules keeps them in vascular space for a longer time.

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DRUG THERAPY

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