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OBJECTIVES S hock definitions T ypes of shock, mainly hypovolemia , septic, obstructive

Learn about hypovolemic, septic, cardiogenic, obstructive shocks, their pathophysiology, clinical manifestations, diagnosis, and management strategies in this comprehensive guide.

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OBJECTIVES S hock definitions T ypes of shock, mainly hypovolemia , septic, obstructive

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  1. Shock OBJECTIVES • Shock definitions • Types of shock, mainly hypovolemia, septic, obstructive • Diagnosis • Management

  2. Shock Definition an imbalance between oxygen delivery and oxygen demand Result Cell dysfunction and ultimately cell death and multi organ failure Fact Tissue oxygen delivery may be inadequate and the blood pressure and other vital signs are normal.

  3. Shock Types Hypovolaemic shock • The commonest • Result from a reduction in intravascular volume secondary to loss of blood • trauma • gastrointestinal

  4. Septic shock Results from complex disturbances in oxygen delivery and oxygen consumption. Etiology: • Gram-negative (38%) • Gram-positive (52%) Common sites: • lungs (50-70%) • abdomen (20-25%) • urinary tract (7-10%) • skin

  5. Septic shock Pathophysiology Infection triggers a cytokine-mediated pro-inflammatory response Results in: • peripheral vasodilatation • redistribution of blood flow • endothelial cell activation • increased vascular permeability • formation of microthrombi

  6. Septic shock Pathophysiology Cardiac output typically increases to compensate for the peripheral vasodilation. Despite a global increase in oxygen delivery, microcirculatory dysfunction impairs oxygen delivery to the cells.

  7. Cardiogenic shock A cardiac output insufficient to meet the metabolic requirements of the body (pump failure) Caused by • myocardial infarction • arrhythmias • valve dysfunction • cardiac tamponade • massive pulmonary embolism • tension pneumothorax Obstructive Shock

  8. Anaphylactic shock Systemic hypersensitivity reaction following exposure to an agent (allergen) Triggering release of vasoactive mediators from basophils and mast cells: • Histamine • Kinins • Prostaglandins • Vasodilation • Intravascular volume redistribution • Capillary leak • Reduction in cardiac output.

  9. Neurogenic shock Caused by a loss of sympathetic tone to vascular smooth muscle. Typically occurs following injury to the (thoracic or cervical) spinal cord Results in • profound vasodilation • fall in systemic vascular resistance • hypotension. It can also occur in 'high' spinal anaesthesia.

  10. Pathophysiology In clinical practice there is often significant overlap between the causes of shock for example, patients with septic shock are frequently also hypovolaemic

  11. Pathophysiology Most shock (exception neurogenic) is associated with increased sympathetic activity All share common pathophysiological features at the cellular level.

  12. Macrocirculation Shock can occur in the context of a low, normal or high cardiac output. In hypovolaemicshock: • Catecholamine release from the adrenal medulla and sympathetic nerve endings, • Generation of Angiotesin-II from the renin-angiotensin system

  13. Macrocirculation The resulting tachycardia and increased myocardial contractility act to preserve cardiac output Vasoconstriction acts to maintain arterial blood pressure and divert the available blood to vital organs (brain, heart and muscle) and away from non-vital organs (skin and gut).

  14. Macrocirculation Clinically this manifests as pale, clammy skin with collapsed peripheral veins and a prolonged capillary refill time. The resulting splanchnichypoperfusion is implicated in many of the complications associated with prolonged or untreated shock.

  15. Macrocirculation In septic shock, circulating pro-inflammatory cytokines (notably TNF-interferon and IL) induce endothelial expression of the enzyme nitric oxide synthetasewhich leads to: • Smooth muscle relaxation • Vasodilation • Fall in systemic vascular resistance

  16. Macrocirculation The initial cardiovascular response is a reflex tachycardia and an increase in stroke volume resulting in an increased cardiac output. Clinically this manifests as warm, well-perfused peripheries, a low diastolic blood pressure and raised pulse pressure. As septic shock progresses endothelial dysfunction results in significant extravasation of fluid and a loss of intravascular volume.

  17. Macrocirculation Ventricular dysfunction also impairs the com­pensatory increase in cardiac output. As a result, peripheral perfusion falls and the clinical signs may become indistinguishable from those associated with the low-output state.

  18. Macrocirculation In neurogenic shock, traumatic disruption of sympathetic efferent nerve fibres results in • loss of vasomotor tone • peripheral vasodilation • fall in systemic vascular resistance.

  19. Cellular function Under normal (aerobic) conditions, • glycolysis converts glucose to pyruvate • pyruvate is converted to acetyl-coenzyme­ A (acetyl-CoA) and enters the Krebs cycle.

  20. Cellular function 0xidation of acetyl-CoA in the TCA cycle generates nicotin amide adenine di nucleotide ( ADH) and flanine adenine dinucleo­tide (FADH, which enter the electron transport chain and a re oxidized to ADP oxidative phosphorylation of adenosine diphosphate (ADP) to ATP.

  21. Cellular function Oxidative metabolism of glucose is energy efficient, yielding up to 38 moles of ATP for each mole of glucose, but requires a continuous supply of oxygen to the cell. Hypoxaemia blocks mitochondrial oxidative phosphorylation, inhibiting ATP synthesis. and an accumulation of pyruvate that is unable to enter the TCA cycle.

  22. Cellular function Cytosolic conversion of pyruvate to lactate allows the regeneration of some ADP, enabling the limited production of ATP by anaerobic glycolysis. However, anaerobic glycolysis is significantly less efficient, generating only 2 moles of ATP per mole of glucose and predisposing cells to ATP depletion. Anaerobic metabolism leads to a rise in lactic acid in thesystemic circulation.

  23. Cellular function Under normal conditions, the tissues globally extract about 25% of the oxygen delivered to them, with the normal oxygen saturation of mixed venous blood being 70-75%.

  24. Cellular function In absence of significant renal or liver disease, serum lactate concentration may is a useful marker of global cellular hypoxia. Similarly, a fall in mixed venous oxygen saturations may reflect increased oxygen extraction by the tissues and an imbalance between oxygen delivery and oxygen demand.

  25. Cellular function, Cell Necrosis In sepsis • Mitochondrial dysfunction Disruption of protein synthesis Damage lysosomal & mitochondrial membranes + Failure of ATP-dependent cell functions + Reduction of intracellular pH associated with high lactic acid cell necrosis

  26. Shock & Organ Systems: compensatory mechanisms Shock leads to increased sympathetic activity. leads to • Rise CO, SVR and MAP. • Preservation and redistribution of cardiac output, coupled. organ autoregulation, helps to maintain adequate perfusion and oxygen delivery to vital organs (brain, heart, skeletal muscle).

  27. Shock & Organ Systems: These compensatory mechanisms have limits. In case of severe, pro­longed and / or uncorrected shock ('decompensated' shock), the clinical manifestations of organ hypoperfusion become apparent. Shock also leads to the up-regulation of pro-inflammatory cytokines (TNF-a, IL-lP and IL-6)

  28. Shock & Organ Systems: Cardiovascular • Cardiogenic shock leads to a fall in CO • Neurogenic shock leads to vasodilation and reduced SVR. • Significant myocardial and vascular dys­ function frequently occur in other causes of shock.

  29. Shock & Organ Systems: Cardiovascular • Severe (diastolic)hypotension results in animbalance between myocardial oxygen supply and demand and ischaemia result in endocardium. • This impairs myocardial contraction • Hypoxaemia and acidosis deplete myocardial storesand diminish the cardiac response to both endogenous and exogenous catecholmines. • Acid-base and electrolyte abnormalities predispose to both atrial and ventricular dysrhythmias.

  30. Shock & Organ Systems: Cardiovascular Inflammatory mediators in sepsis: • Depress myocardial contractility and ventricular function. • Increase indothelial permeability (volume depletion). • Widespread activation of both coagulation and fibrinolysis (DlC).

  31. Shock & Organ Systems: Respiratory Tachypnoea • Driven by pain, pyrexia, local lung patholgy, pulmonary oedema, metabolic acidosis or cytokines • One of the earliest features of shock.

  32. Shock & Organ Systems: Respiratory Increased minute volume results in reduced PC02 andrespiratory alkalosis Initially this is to compensate for the metabolic acidosis of shock but eventually this mechanism is overwhelmed and blood pH falls.

  33. Shock & Organ Systems: Respiratory In hypovolaemic states underperfusion of ventilated alveoli • Reduction in pulmonary blood flow increasing ventilation-perfusion (V /Q) mismatch

  34. Respiratory In cardiogenic shock Left ventricular failure and pulmonary oedema often compromises the ventilation of perfused alveolar units increasing the shunt fraction within the lung.

  35. Shock & Organ Systems: Respiratory Increased V / Q mismatch and shunt fraction also occur in sepsis. Net result is hypoxaemia that may be refractory to increases in inspired oxygen concentration.

  36. Shock & Organ Systems: Respiratory Sepsis and hypovolaemic shock are both recognized causes of acute lung injury and its more severe variant, the acute respiratory distress syndrome (ARDS).

  37. Shock & Organ Systems: Renal Reduced renal blood flow results in: • low urine volume (< O.5ml / kg/ h) • high urine osmolality • low urine sodium content urine. If shock is not reversed, hypoxia leads to acute tubular necrosis (ATN) characterized by oligouria or anurine with a high sodium concentration and an osmolality close to that of plasma.

  38. Shock & Organ Systems: Renal With a fall in glomerular filtration • High blood urea and creatinine • Hyperkalaernia and a metabolic acidosis Renal failure occurs in about 30-50% of patients with septic shock.

  39. Shock & Organ Systems: Nervous system Due to the increased sympathetic activity, patients appear anxious. Cerebral hypoperfusion and hypoxia cause increasing restlessness, confusion, stupor and coma. Unless cerebral hypoxia has been prolonged, effective resuscitation will usually correct the depressed conscious level rapidly.

  40. Shock & Organ Systems: Gastrointestinal Redistribution of cardiac output observed in shock leads to a marked reduction in splanchnic blood flow.

  41. Shock & Organ Systems: Gastrointestinal In the stomach, the resulting mucosal hypo­ perfusion and hypoxia predispose to stress ulceration and haemorrhage. In the intestine, movement (translocation) of bacteria and/or bacterial endotoxin from the lumen to the portal vein and cisterna chili; from here it goes into the systemic circulation.

  42. Shock & Organ Systems: Hepatobiliary Ischaemic hepatic injury is frequently seen following hypovolaemic or cardiogenic shock. Reversible transaminase levels elevation indicates hepatocellular injury & occurs 1-3 days after ischaemic insult. Increases in prothrombin time and/or hypoglycaemia are markers of severe injury.

  43. Shock Management General principles: • Identification and treatment of the underlying cause. • Maintenance of adequate tissue oxygen delivery. • CAB • Treatment and diagnosis should occur simultaneously. • The early recognition and treatment of potentially reversible causes (e.g. bleeding, intra-abdominal sepsis, myocardial ischaemia, pulmonary embolus, cardiac tamponade). • Most patients with shock will require admission to a high dependency (HDU) or intensive care unit (ICU).

  44. Shock Management Airway and breathing Hypoxaemia • Must be prevented • If present, rapidly corrected by maintaining a clear airway (e.g. head tilt if no trauma, chin lift) and high flow oxygen (e.g.10-15 litres/min). The adequacy of this therapy can be estimated continuously using pulse oximetry (SpO2 Severe hypoxaemia need intubation.

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