Dr Anuj Raj Bijukchhe

SHOCK Dr Anuj Raj Bijukchhe

Introduction Definition of shock Types of shock Causes of shock Signs and symptoms of shock Body’s response to shock Treatment of shock

Definition of Shock In 1852, shock was defined as “a rude unhinging of the machinery of life.” Probably no better definition exists to describe the devastating effects of this process on a patient, but a more recent definition calls shock “the collapse and progressive failure of the cardiovascular system.”

• Shock left untreated may be fatal. It must be recognized and treated immediately, or the patient may die • The definition of shock does not involve low blood pressure, rapid pulse or cool clammy skin - these are merely the signs. • Simply stated, shock results from inadequate perfusion of the body’s cells with oxygenated blood.

• Circulatory shock, commonly known as just shock, is a serious, life-threatening medical condition characterized by a decrease in tissue perfusion to a point at which it is inadequate to meet cellular metabolic needs. • As the blood carries oxygen and nutrients around the body, reduced flow hinders the delivery of these components to the tissues, and can stop the tissues from functioning properly. The process of blood entering the tissues is called perfusion , so when perfusion is not occurring properly this is called a hypoperfusional (hypo = below) state.

Circulatory shock should not be confused with the emotional state of shock , as the two are not related. Medical shock is a lifethreatening medical emergency and one of the most common causes of death for critically-ill people. Shock can have a variety of effects, all with similar outcomes, but all relate to a problem with the body's circulatory system. For example, shock may lead to hypoxemia  (a lack of oxygen in arterial blood)

4 Stages of Shock

• • • •

1. 2. 3. 4.

Initial Compensatory. Progressive Refractory

• An initial non progressive stage- during which reflex compensatory mechanisms are activated and perfusion of vital organ is maintained. • A progressive stage - characterized by tissue hypo perfusion and onset of worsening circulatory and metabolic imbalance. • An irreversible stage - that sets in after the body has incurred cellular & tissue injury so severe that even if the hemodynamic defect are corrected , survival is not possible.

Mechanism of microcirculatory disorder of shock

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The stages and mechanisms of microcirculatory disorder of shock Ischemic hypoxia stage

Stagnant hypoxia stage

Microcirculation failure stage 10

Ischemic hypoxia stage

• Compensatory mechanism Blood pressure

Pulse pressure

Baroreceptors

Blood flow

Blood volume angiotensinogen

chemoreceptors

Adrenal cortex Vasomotor centre

Adrenal medulla Angiotensin ı

Sympathetic noradrenaline nervous adrenaline activity Venous capacitance

Heart rate Myocardial contractility

Maintain cardiac output

aldosterone Angiotensin Ⅱ

Circulating Volume

systemic resistance

Maintain venous return

Maintain blood pressure

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Stagnant hypoxic stage Ischemic hypoxia Of microcirculation Anaerobic metabolism lactate

Dilation of precapillary sphincter

constriction of postcapillary sphincter

In>out

Stagnation of blood

Capillary pressure

Capilary leak

Effctive circulatory blood volume

Blood pressure

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microcirculation Arteriolar and precapillary sphincter

constrict

Microcirculatio n perfusion

Ischemic hypoxia Of microcirculation

Precapillary sphincter constrict

Pressure of capillary

Fluid from outer to vascular compartment

Arteriovenous shunt

Ischemic hypoxia Of microcirculation

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DIC and MODS Stagnation of blood

Ischemic hypoxia of microcirculatio n Injury of endothelium

Release of cytokine

Microembolism

DIC

SIRS

MODS 14

Classification by causes • • • • • • •

Hypovolemic shock Traumatic shock Burn shock septic shock Cardiogenic shock Anaphylactic shock Neurogenic shock

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Classification by pathophysiological changes • • • •

Hypovolemic shock Cardiogenic shock Obstructive shock Distributive shock

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Hypovolemic shock • • • • •

Hemorrhage Burns Diarrhea Vomiting Peritonitis

Cardiogenic • • • • • • •

Pulmonary Embolism Cardiomyopathy Heart Disease Cardiac Contusion Cardiac Tamponade Myocardial Infarction Arrhythmia Aortic Aneurys

Vasogenic • Psychogenic • Anaphylactic • Septic

Hypovolemic Shock Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate perfusion. Trauma Hemorrhage Vomiting / diarrhea Burns

The human body responds to acute hemorrhage by activating 4 major physiologic systems: the hematologic system, the cardiovascular system, the renal system, and the neuroendocrine system.

Hypovolemic Shock:Hematologic System Activating the coagulation cascade and contracting the bleeding vessels (via local thromboxane A2 release). Platelets are activated which form an immature clot on the bleeding source. The damaged vessel exposes collagen, which subsequently causes fibrin deposition and stabilization of the clot.

Hypovolemic Shock: Cardiovascular System Increases the heart rate, increasing

myocardial contractility, and constricting peripheral blood vessels. This response occurs secondary to an increase in release of nor epinephrine and a decrease in baseline vagal tone (regulated by the baroreceptors in the carotid arch, aortic arch, left atrium, and pulmonary vessels). The cardiovascular system also responds by redistributing blood to the brain, heart, and kidneys and away from skin, muscle, and GI tract.

Renal System The kidneys respond to hemorrhagic shock by stimulating an increase in renin secretion from the juxta glomerular apparatus.

Angiotensin II has 2 main effects, both of which help reverse hypovolemic shock, vasoconstriction of arteriolar smooth muscle and stimulation of aldosterone secretion by the adrenal cortex.

Hypovolemic Shock: Neuro endocrine System • Causes an increase in circulating antidiuretic hormone (ADH). • ADH is released from the posterior pituitary gland in response to a decrease in blood pressure (as detected by baroreceptors) and a decrease in sodium concentration. • ADH indirectly leads to an increase in reabsorption of water and salt (NaCl) by the distal tubule, the collecting ducts, and the loop of Henle.

Signs and symptoms Hypovolemic shock • • • • • • • • • •

Anxiety, restlessness, altered mental state  due to decreased cerebral perfusion and subsequent hypoxia. Hypotension due to decrease in circulatory volume. A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia. Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction. Rapid and shallow respirations due to sympathetic nervous system stimulation and acidosis. Hypothermia due to decreased perfusion and evaporation of sweat. Thirst and dry mouth, due to fluid depletion. Fatigue due to inadequate oxygenation. Cold and mottled skin , especially extremities, due to insufficient perfusion of the skin. Distracted look in the eyes or staring into space, often with pupils dilated.

Cardiogenic Shock • Cardiogenic shock is characterized by a decreased pumping ability of the heart causing a shock-like state with inadequate perfusion to the tissues. • It occurs most commonly in association with, and as a direct result of, acute ischemic damage to the myocardium.

Cause Intrinsic Myocardial injury Tachycardia Bradycardia Valvular defect Extrinsic Pericardial tamponade Tension pneumothorax Large pulmonary emblous

Cardiogenic Shock: History Most patients presenting with cardiogenic shock do so in conjunction with an AMI and therefore, present with the constellation of symptoms of acute cardiac ischemia (e.g. Chest pain, shortness of breath, diaphoresis, nausea and vomiting). Patients experiencing cardiogenic shock may also present with pulmonary edema and presyncopal or syncopal symptoms.

Cardiogenic Shock: Physical Physical examination will often reveal a patient in the middle of an AMI. Patients appear in frank extremis, profoundly diaphoretic and complaining of severe shortness of breath and chest pain. Clinical assessment begins with attention to the ABCs and vital signs.

Neck examination may reveal jugular venous distention. This is evidence of right ventricular failure and may be prominent. With increasing degrees of ventricular dysfunction, pulmonary edema and severe hypotension may develop. Auscultation of the chest may reveal varying degrees of congestive heart failure (CHF).

• Cardiogenic shock, similar to hypovolemic shock but in addition : Distended jugular veins due to increased jugular venous pressure • Weak or absent pulse • Arrhythmia, often tachycardia

Vasogenic Shock • Septic Shock Hyperdynamic Hypodynamic • Toxic Shock • Neurogenic Shock • Psychogenic Shock

Septic Shock vs. SIRS Systemic Inflammatory Response Syndrome (SIRS) Physiologic alternations and organ dysfunction seen with bacterial infections. 2 or more changes in these 4 factors, as follows: body temperature, heart rate, respiratory function, and peripheral leukocyte count.

Terms Sepsis Systemic host response to infection with SIRS plus a documented infection Severe Sepsis Sepsis plus end-organ dysfunction or hypoperfusion Septic Shock Sepsis with hypotension, despite fluid resuscitation with evidence of inadequate tissue perfusion

Septic Shock: Pathophysiology In septic shock due to bacterial infection, circulatory insufficiency occurs when bacterial products interact with host cells and serum proteins to initiate a series of reactions that may ultimately lead to cell injury and death. Not only are these bacterial products harmful themselves, but the widespread and unregulated host response to these substances also results in the elaboration or an extensive array of chemical mediators that lead to further cell damage.

Septic shock develops in less than one half of patients with bacteremia. It occurs in about 40% of those patients with gram negative bacteremia and about 20% of those patients with Staphylococcus aureus bacteremia.

Septic Shock: History • • • •

Fever Chills Sweating Altered mental status Apprehension Anxiety Agitation

• Some localizing symptoms Head and neck infections - earache, sore throat, sinus pain or congestion, nasal congestion or exudate, swollen lymph glands • Chest and pulmonary infections - cough (especially if productive), pleuritic chest pain, dyspnea • Abdominal and GI infections - abdominal pain, nausea, vomiting, diarrhea • Pelvic and genitourinary infections - pelvic or flank pain, vaginal or urethral discharge, dysuria, frequency, urgency • Bone and soft tissue infections - focal pain or tenderness, focal erythema , edema

Septic shock

• • • • • • •

Similar to hypovolaemic shock except in the first stages Pyrexia , due to increased level of cytokines Systemic vasodilation resulting in hypotension Warm and sweaty skin due to vasodilation Systemic leukocyte adhesion to endothelial tissue Reduced contractility of the heart Diffuse capillary damage in the lung Activation of the coagulation pathways, resulting in disseminated intravascular coagulation Increased levels of neutrophils

Neurogenic shock •  Neurogenic shock is the rarest form of shock. It is caused by trauma  to the spinal cord  resulting in the sudden loss of autonomic and motor  reflexes below the injury level. Without stimulation by sympathetic nervous system the vessel walls relax uncontrolled, resulting in a sudden decrease in peripheral vascular resistance , leading to vasodilation  and hypotension .

Neurogenic shock,

• similar to hypovolemic shock except in the skin's characteristics. In neurogenic shock, the skin is warm and dry or a clear sweat line exists, above which the skin is diaphoretic

Anaphylactic shock • Caused by a severe anaphylactic reaction to an allergen , antigen , drug or foreign protein causing the release of histamine  which causes widespread vasodilation, leading to hypotension and increased capillary permeability.

Psychogenic Shock

Also known as “fainting spells” Caused by sudden dilation of blood vessels which temporarily halts blood flow to the brain

Obstructive shock  • In this situation the flow of blood is obstructed which impedes circulation and can result in circulatory arrest . Several conditions result in this form of shock.Cardiac tamponade in which fluid in the pericardium prevents inflow of blood into the heart (venous return). Constrictive pericarditis , in which the pericardium  shrinks and hardens, is similar in presentation. • Tension pneumothorax . Through increased intrathoracic pressure, bloodflow to the heart is prevented (venous return). • Massive pulmonary embolism is the result of a thromboembolic incident in the bloodvessels of the lungs and hinders the return of blood to the heart. • Aortic stenosis hinders circulation by obstructing the ventricular outflow tract .

• Obstructive shock, similar to hypovolaemic shock but in addition:Distended jugular veins due to increased jugular venous pressure • Pulsus paradoxus  in case of tamponade

Clinical manifestations

• The clinical syndrome of shock can develop over the course of a few minutes or several hours, depending on the cause;all systems may be affected.

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Common manifestations

• Tachycardia, oliguria, a clouded •

sensorium, cool mottled extremities indicative of reduced blood flow to the organ. Metabolic acidosis ,often due to elevated blood lactate levels, reflects prolonged inadequate blood flow to tissues. 50

Specific manifestations

• Hypovolemic shock:have a history of • •

gastrointestinal bleeding ,hemorrhage,or diarrhea,vomitting Cardiogenic shock ： have signs of heart disease,gallop rhythms Distributive shock: localized infection as well as fever and chills

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Manifestations Cardiovascular system

Early

Lately

• Blood pressure N or ↓ N or ↑ • Heart rate N or min↑ • Cardiac output

↓↓ ↑↑ ↓↓

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Manifestations Cardiovascular system

 The ECG frequently shows signs of ischemia, ST depression and flattening of the T waves.  The CVP can initially be high in cardiogenic and obstructive shock,low in hypovolemic shock, and normal or low in septic shock.

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Manifestations renal system

 Reduction of hourly urinary output to less than 0.5ml/kg occurs early in shock, initially because of prerenal insufficiency.  Without treatment,there may be rapid progression to acute tubular necrosis .

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Manifestations repiratory system

• Early

Lately

• Tachypnoea Tachypnoea Laboured breathing • Central cyanosis •

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Manifestations Gastrointestinal system

• There may be vomiting or diarrhea, hepatic failure ,stress ulcer. Late in shock. bowel sounds are infrequent or absent. • Peritonitis is a common source of septic shock and is accompanied by abdominal pain and board-like rigidity.

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Organ dysfunction • Heart

mechanism

• Blood volume of myocardium • Oxygen consumption of myocardium • Acidosis myocardial contractility • DIC in myocardium • endotoxin 57

Organ dysfunction • Respiratory failure  Acute lung injury and acute respiratory distress syndrome(ARDS) are menifested as non cardiogenic pulmonary edema resulted from diffuse pulmonary capillary endothelial and alveolar epithelial injury,hypoxia,and bilateral diffuse pulmonary infiltrates.

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Organ dysfunction

• Impairment of digestive system  stress ulcer, erosive gastritis, pancreatitis, submucosal hemorrhage  enteric Ischemia-reperfusion injury induced enteric bacteria and endotoxin translocate from gut lumen to the systemic circulation

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Organ dysfunction • Acute renal failure

Renal perfusion

early stage

GFR

oliguria

Acute renal failure (prerenal failure) Functional renal failure GFR- glomerular filtration rate 60

Organ dysfunction • Acute renal failure

late stage

Ischemia and microembolism Acute tubular necrosis of renal

oliguria

Acute renal fuailure Parenchymal renal failure

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Diagonsis of shock • Step 1 look: investigating the patient’s skin and facial expression; • Step 2 inquire: inquiring the history and know if his/her sense is clear; • Step 3 touching: touching the patient’s pulse to know its intensity 、 speed and rhythm, and touching the temperature and humidity of the skin; • Step 4 listen: listening to the heart sound and measuring the blood pressure.

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Diagonsis • Manifestation: Dysfunctional signs of each organ, BP increase ,heart rate increase compensatory stage BP decrease, heart rate increase decompensatory stage

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Diagnostic standard by stages •

Early stage: Mechanism:Activation of sympathetic nerve and release of catecholamine. Symptom: Pale ,cool and damp extremities; normal consciousness with agitation ,decreased urine output ,normal or a little decreased BP, Pulse pressure <20mmHg,SBP decreased more than 40mmHg if the patient has hypertension before.

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Diagnostic standard by stages • Middle stage: Symptom: Normal consciousness but with a slow response, thirsty for water , thready pulse, Trachypnoea ， urine output<20ml/h ， SBP 60~80mmHg.

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Diagnostic standard by stages • End stage: Symptom: Confusion or coma , cool mottled or pale skins or cyanotic extremities, peripheral pulses become thready or may be absent;SBP <60mmHg or can not be measured, anuria ， Tachypnoea, tendency of DIC, manifestation of acidosis.

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Shock monitoring 1. 2. 3. 4.

Normal index Invasive hemodynamic monitoring Function of oxidative metabolism Laboratory monitoring

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Normal index • Mental status: • Vital signs: Temperature, heart rate , breath rate, blood pressure • Colour and temperature of the skin • Shock index: pulse rate/SBP > 1.0-1.5 indicate shock; >2.0 severe shock

• Urine output <25ml/h indicate inadequate tissue perfusion; >30ml/h indicate shock corrected

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Invasive hemodynamic monitoring • MAP: DBP ＋ 1/3pulse pressure • CVP: heart

≥80mmHg good perfusion ≤65mmHg poor perfusion Signs of blood volume ,pressure of right

5 ～ 10cmH2O indicate normal; <5cmH2O indicate hypovolemia; >15cmH2O indicate heart failure or high pressure of pulmonary circulation.

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Invasive hemodynamic monitoring • By Swan-Ganz catheter • PCWP :(pulmonary capillary wedge pressure) PCWP is similar to the pressure of left atria PCWP<12mmHg indicate hypovolemia, 12 － 15mmHg indicate normal, >15mmHg indicate hypervolemia or left heart failure

• CO and CI :CO 4 ～ 6L/min, CI 2.5~3.5L/ (min.m2) CO=heart rate ×stroke volume ,CI=CO/body area 70

Function of oxidative metabolism • Sp02 ＞ 90% simple and noninvasive • Arterial blood gas analysis 80 ～ 100mmHg; • PaO2  PaCO2 35 ～ 45mmHg ；  PH 7.35 ～ 7.45;  HCO322-27mmol/L ●

Lactic acid monitoring lactic acid >2mmol/L

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Laboratory monitoring • Blood routine :Red blood cell count, hemoglobin, and Hematocrit • Electrolyte and renal function :K ,Na,Ca, Serum creatinine • DIC:  Tendency of bleeding clinically  APTT>normal index +3 seconds  Number of platelet < 80×109/L or decline gradually  Fg<1.5g/L or gradually decreased APTT --activated partial thromboplastin time 72

Differential diagnose  Cardiogenic shock:History,ECG, cardiac enzymes,cTnT,cTnI  Gastrointestinal bleeding: Shock with hematemesis and melena.  Hemorrhage in abdomen: Rupture of spleen ,liver, kidney ， tumor,and other kinds of hemorrhage.  Hemorrhage of fracture:The volume of bleeding amount to 1000-2000ml

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Treatment The aim of therapy is to improve the supply of oxygenated blood to the tissues.

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Principle of treatment 1. 2. 3. 4. 5. 6. 7. 8. 9.

Normal treatment Aetiology treatment Restore normal blood volume Provision of adequate oxygenation vasoactive drugs Correct acidosis, electrolyte disturbance Glucocorticoids therapy Prevention of DIC Protect function of organs,prevention of MODS

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Normal treatment • Body posture: lay flat or the legs are elevated by 30 。 Keep body calm and warm • Keep the respiratory tract smoothly ， clear away respiratory secretions in time. supply oxygen by nasal catheter, mask, mechanical ventilation or endotracheal intubation. oxygen flow • Set up Venous access as early as possible. subclavian vein, Jugular vein, Femoral vein catheterization for the purpose of fluid infusion .CVP • conscious-sedation ， alleviate pain ： if the patient is agitated. proper treatment. • Shock monitoring.

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Restore normal blood volume • Restoration of optimal circulating blood volume • Fluid infusion is a most important therapeutic measure in the treatment of shock, whether it is the initial cause of shock ,or a complication of cardiogenic , distributive or obstructive shock. the velocity of liquid can be very fast , the kind of liquid can be colloids or crystalloids .But The volume and speed of administration depends on the patient’s cardiac competence and must be considered carefully if acute left ventricular failure and the resultant pulmonary edema are to be avoided.

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Treatment • Shock requires immediate interventions to preserve life. Therefore, the early recognition and treatment is essential even before a specific diagnosis is made. Most forms of shock seen in trauma or sepsis respond initially to aggressive intravenous fluids (ie. 1 liter normal saline bolus over 10 minutes). Therefore this treatment is usually instituted as the person is being further evaluated. • Re-establishing perfusion to the organs is the primary goal through restoring and maintaining the blood circulating volume ensuring oxygenation and blood pressure are adequate, achieving and maintaining effective cardiac function, and preventing complications .

Hypovolemic shock • In hypovolemic shock, usually hemorrhagic shock caused by traumatic injury , it is necessary to immediately control the bleeding and restore the casualty's blood volume by giving infusions of isotonic crystalloid solutions.  • Blood transfusions , packed red blood cells (RBCs ),Albumin  (or other colloid solutions), or freshfrozen plasma are necessary for loss of large amounts of blood , but can be avoided in smaller and slower losses.  • Hypovolemia due to burns, diarrhea, vomiting, etc. is treated with infusions of electrolyte solutions that balance the nature of the fluid lost.

Type of fluid used in shock. • •

• • •

Crystalloids – Such as sodium chloride (0.9%), or Lactated Ringer's solution  (Hartmann's solution). Dextrose solutions which contain free water are less effective at re-establishing circulating volume, and promote hyperglycaemia. Colloids – For example, polysaccharide (Dextran), polygeline (Haemaccel), succinylated gelatin (Gelofusine) and hetastarch (Hespan). Colloids are, in general, much more expensive than crystalloid solutions and have not conclusively been shown to be of any benefit in the initial treatment of shock. Combination – Some clinicians argue that individually, colloids and crystalloids can further exacerbate the problem and suggest the combination of crystalloid and colloid solutions. Blood – Essential in severe hemorrhagic shock, often pre-warmed and rapidly infused. It is to be noted that NO plain water should be given to the patient at any point, as the patient's low electrolyte levels would easily cause water intoxication , leading to premature death.

Cardiogenic shock • In cardiogenic shock, depending on the type of myocardal infarction, one can infuse fluids such as or in shock refractory to infusing fluids, normal saline would be an example of said fluids . • Inotropic agents, which enhance the heart's pumping capabilities, are used to improve the contractility and correct the hypotension.

• The main goals of the treatment of cardiogenic shock are the re-establishment of circulation to the myocardium, menimising heart muscle damage and improving the heart's effectiveness as a pump. This is most often performed by percutaneous coronary intervention and insertion of a stent in the culprit coronary lesion or sometimes by cardiac bypass.

Blood transfusion • Packed red cells ： Haematoglobin concertration ≤ 70g ／ L 。 patient with no active bleeding ,1 unit infusion can increase heamatoglobin concertration 10g/L,hematocrit increase 3%. • Platelet: <50×109 ／ L or hypofunction • Fresh frozen plasma: Increase colloid osmotic pressure , supply blood coagulation factor ， massive haemorrhage 。 • the whole blood and plasma are better than colloids in order to increase blood volume.

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Provision of adequate oxygenation • All patients who are clinically shocked should be given supplementary oxygen. • Lung is an organ injured most easily in shock,manifested as respiratory failure ,or with shock goes on ,patient lay in coma. we can take endotracheal intubation to maintain the respiratory function by mechanical ventilation.

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Provision of adequate oxygenation • Mechanical ventilation is required if oxygenation remains inadequate,i.e.a PaO2 ＜ 60mmHg or if respiratory acidosis develops,i.e. a PaCO2 ＞ 60mmHg.

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To prevent the risks of oxygen toxicity , the inspired oxygen concentration should be limited to 60% or less.The PaO2 should be kept at about 100mmHg and PaCO2 about 40mmHg. The addition of positive end expiratory pressure(peep),up to 15 cmH2O,should be used if higher concentrations of oxygen appear to be necessary 。

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vasoactive drugs • vasoconstrictor :High-output and low-resistance  Dopamine  Dobutamine  Noradrenaline  Adrenaline  Cardiac stimulant • Vasodilatator :Low-output and high-resistance  Nitroprusside sodium  Phentolamine  Glycerol trinitrate

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Correct acidosis,electrolyte disturbance • lactic acidosis is most common in metabolic acidosis .metabolic acidosis decrease the myocardial contractility,increase the resistance of pulmonary and renal circulation,decrease the affinity of Hb for O2 • cardiogenic shock and hypovolemic acidosis :deal with etiological factor and volume resuscitation; 5%sodium bicarbonate ivgtt by ABGA pH<7 ． 20 。 • Septic shock:deal with acidosis actively. 89

Glucocorticocids therapy Glucocorticocids :  Mechanism ：  Anti-shock ,anti-toxin ,antiinflammatory response, antianaphylaxis,stabilize cell membrane . Inhibit release of inflammatory mediators.It can be used in all kinds of shock. 90

Prevention of DIC give heparin in early stage.

Protect function of organs, prevention of MODS.especially acute renal failure.

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Distributive shock • In distributive shock  caused by sepsis the infection is treated with antibiotics  and supportive care is given (i.e. inotropica , mechanical ventilation , renal function replacement ).  • Anaphylaxis is treated with adrenaline  to stimulate cardiac performance and corticosteroids to reduce the inflammatory response . • In neurogenic shock because of vasodilation in the legs, one of the most suggested treatments is placing the patient in the Trendelenburg position, thereby elevating the legs and shunting blood back from the periphery to the body's core.

Obstructive shock • In obstructive shock , the only therapy consists of removing the obstruction.  • Pneumothorax  or hemothorax  is treated by inserting a chest tube , pulmonary embolism requires thrombolysis (to reduce the size of the clot), or embolectomy(removal of the thrombus ). • Tamponade is treated by draining fluid from the pericardial space through pericardiocentesis .

Prognosis • The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. • Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. • Septic shock however, is a grave condition and with a mortality rate between 30% and 50%. • The prognosis of cardiogenic shock is even worse.

Conclusion • The ultimate outcome in the treatment of shock depends on the reversibility of the underlying cause,the early recognition and aggressive treatment of complications. 95