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PATHOLOGY AND MANAGEMENT OF SHOCK
This document summarizes the key aspects of shock. Shock occurs when there is inadequate oxygen delivery to tissues, which can lead to cellular damage and death if left untreated. The main causes of shock discussed are hypovolaemic, septic, and cardiogenic shock. Signs and symptoms of shock include low blood pressure, fast heart rate, pale skin, confusion, and low urine output. Management involves identifying the type and stage of shock to guide fluid resuscitation and drug therapy aimed at restoring adequate circulation and oxygen delivery to tissues.
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Introduction by Aiswarya Thomas on the topic of shock.
Inadequate oxygen delivery leading to metabolic acidosis and symptoms of shock like low BP.Three main issues in shock: reduced blood volume, impaired oxygenation, and inflammatory mediators.
Overview of different types of shock: hypovolaemic, septic, and cardiogenic shock.
Hypovolaemic shock from reduced circulatory volume due to blood/fluid loss causes.
Pathophysiology showing the cascade from hypovolaemia to impaired metabolism.
Common clinical signs include tachycardia, low BP, and diagnostic findings like increased lactate.
Description of septic shock caused by infections leading to tissue perfusion issues.
Features of septic shock such as temperature changes, hypotension, and mental status changes.
Definition of cardiogenic shock with emphasis on decreased cardiac output without blood volume loss.
Symptoms of cardiogenic shock including mottled skin and altered mental status.
Additional types of shock including neurogenic and traumatic shock.
Stages of shock categorized into non-progressive, progressive, and irreversible.
Compensated shock mechanisms include vasoconstriction and fluid conservation.
Effects of progressive shock include pulmonary hypoperfusion and tissue ischaemia concerns.
Severe shock signs leading to irreversible damage affecting vital organs.
Tissue damage during shock activates coagulation, leading to complications.
Approach to managing shock includes fluid replacement, drug therapy, and nutritional therapy.
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PATHOLOGY AND MANAGEMENT OF SHOCK
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- 2. of Shock • Inadequateoxygen 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
- 3. Shock?• Restless • Confused •Skin cool and mottled or hot and flushed • Weak or absent peripheral pulses • Low BP • Tachycardia • Drowsiness, coma 3 Yes! These are all signs and symptoms of shock
- 4. NESIS All forms ofshock 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. 4
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- 6. 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. 6
- 7. 2) IMPAIRED TISSUEOXYGENATION 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. 7
- 8. 3) RELESE OFINFLAMATORY 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
- 9. • Several proinflammatory 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. 9
- 10. Types of Shock • Hypovolaemic •Septic • Cardiogenic • Other types 10 Traumatic Shock Neurogenic Shock Hypoadrenal shock
- 11. Hypovolae mic Shock 11 Results frominadequate circulatory blood volume Due to loss of red cell mass and plasma or from loss of plasma volume alone
- 12. ETIOLOGY 12 1. Loss ofwhole blood Hemorrhage Trauma Gastrointestinal ulcer Surgery Inadequate clotting 2. Loss of other body fluids Vomiting Diarrhea Diuretic therapy Burns(>10% surface)
- 13. Pathogenes is 13 Hypovolaemia Decreased circulatory volume Decreasedvenous return to heart Decreased stroke volume Decreased cardiac output Decreased cellular oxygen supply Decreased tissue perfusion Impaired cellular metabolism Shock
- 14. Clinical features 14 Increased heart rate(Tachycardia) LowBP (hypotension) Low urinary output Pallor , cool and clammy skin Anxiety , confusion , agitation Absent bowel sounds Diagnostic findings Decreased hematocrit Increased lactate Increased urine specific gravity
- 15. Septic Shock 15 Septic shockis 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
- 16. Etiology 16 Gram negative septicaemia Example:infection with E.coli Proteus Pseudomonas Bacteroides Gram positive septicaemia Example: infection with Streptococci Pneumococci
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- 18. Features• Hyperthermia orhypothermia • Tachycardia • Wide pulse pressure • Low blood pressure (SBP<90) • Mental status changes,agitation,coma • Hypoxemia • Urine output • Gastro intestinal bleeding Diagnostic findings Increase or decrease of WBC Decrease platelets Increase urine specific gravity 18
- 19. ic Shock 19 Acute circulatory failurewith sudden fall in cardiac output from acute diseases of the heart without actual reduction of the blood volume (normovolaemia)
- 20. Etiologies 20 • MI • Cardiacarrhythmias • Myocarditis • Pulmonary embolism • Rupture of heart, ventricle or papillary muscles • Acute aortic insufficiency •Tension pneumothorax
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- 22. 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 time DIAGNOSTIC FINDINGS Increase blood glucose Increase cardiac marks ECG Echocardiogram Chest X ray 22
- 23. 4) OTHER TYPES 1.Neurogenicshock:- 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. 23
- 24. Stages Of Shock Deterioraton ofthe circulation in shock is a progressive phenomenon and can be divided arbitrarily into 3 ways:- Non-Progressive (Initial,compensated,reversible shock) Progressive Decompensated Shock Decompensated (Irreversible) Shock 24
- 25. • 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. 25
- 26. 1)WIDESPREAD CONSTRICTION • The neuraland 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
- 27. 2) FLUID CONSERVATION BYTHE KIDNEY Following 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. 27
- 28. 3) STIMULATION OF ADRENALMEDULA • 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. 28
- 29. PROGRESSIVE DECOMPENSATED SHOCK Patient suffers fromsome other stress or risk factors ( eg:- pre existing cardiovascular & lung disease) The effect of progressive decompensated shock due to tissue hypoperfusion are:- 1)PULMONARY HYPOPERFUSION It increase vascular permeability resulting in tachypnea and adult respiratory distress syndrome. 29
- 30. 2) TISSUE ISCHAEMIA •Itcause 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. 30
- 31. IRREVERSIBLE DECOMPENSATED SHOCK • Shock isso 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. 31
- 32. 2)INCREASED VASCULAR PERMEABILITY • Anoxic damageto tissue release inflammatory mediators which cause increased vascular permeability. • This results in escape of fluid from circulation into the interstitial tissue, thus deteriorating effective circulating32
- 33. 3)MYOCARDIAL DEPRESSANT FACTOR • DecreasedBP 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. 33
- 34. 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. 34
- 35. 6)HYPERCOAGULABILIT Y 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. 35
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- 37. MANAGEMENT • Critical factorsin 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 37
- 38. FLUID REPLACEMENT Thecornerstone 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. 38
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