Shock

2. Shock ByDR. Ahmad Gaber Mahmoud

3. Introduction • Definition of shock • Types or causes of shock • Pathophysiology of shock • Diagnosis of shock 1.Clinical stages of shock 2. Causes of shock • Treatment of shock

4. A more recent definition calls shock “the collapse and progressive failure of the cardiovascular system.” I.e. Acute circulatory failure. • Shock left untreated may be fatal. It must be recognized and treated immediately, or the patient may die.

5. Shock 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 leading to failure of tissue oxygenation with Generalized cellular hypoxia.

6. Maintaining perfusion requires: • Volume • Pump • Vessels • Failure of one or more of these causes shock

7. Types of Shock

8. Types or causes of shock: • S: Septic shock • H: Hypovolemic shock • O: Obstructive shock • C: Cardiogenic shock • K: Kinetic or Distributive shock

9. Shock • Septic Shock • Mixed Shock • Overwhelming infection • Caused by gram negative bacteria that release endotoxins (endotoxemic shock). • Peritonitis, cholangitis, genitourinary infection & infected CV catheter • Predisposed by immunosuppression • Diabetes, corticosteroids, chemotherapy • Malignancy & HIV/ AIDS

10. Shock • Hypovolemic Shock = Low Volume • True hypovolaemia: • Blood loss • Plasma loss • Extracellular fluid loss • Apparent hypovlaemia • Sepsis • Adrenal insufficiency • Anaphylaxis • Neurogenic

11. Shock • Obstructive Shock = Obstruction to blood flow • Tension pneumothorax or haemothorax • Cardiac tamponade (due to pericardial effusion or hemopericardium) • Aortic stenosis or critical coarctation • Pulmonary embolism

12. Shock • Cardiogenic Shock = Pump Failure • Acute M I • Acute CHF • Bradyarrhythmias • Tachyarrhythmias • Late septic shock (toxic myocarditis) • advanced shock ( myocardial ischemia)

13. Shock • Kinetic or Distributive = venular or arterial dilatation • Anaphylactic shock: due to drugs, foods, insect stings, serums, immunoglobulins. • Neurogenic Shock: • Vasovagal attack • Loss of sympathetic outflow

14. Pathophysiology of Shock

15. Shock Pathophysiology of shock • Hypoperfusion of tissues is serious as it lead to tissue iscaemia ( hypoxia & substrate deficiency) and tissue damage

16. Shock Inadequate oxygenation or perfusion causes: Inadequate cellular oxygenation Shift from aerobic to anaerobic metabolism

17. Inadequate Cellular Oxygen Delivery Lactic Acid Production Inadequate Anaerobic Energy Production Metabolism Metabolic Failure Metabolic Acidosis CELL DEATH Ultimate Effects of Anaerobic Metabolism

18. Shock Pathophysiological stages of shock: • Three phases • Compensated stage • Decompensated stage • Irreversible stage

19. Compensated Shock • During this early stage there is Sympathoadrenal response with excess catecholamine release to prevent the fall in blood pressure.

20. Compensated Shock • Cardiac effects • Increased force of contractions • Increased rate • Increased cardiac output

21. Compensated Shock • Peripheral effects • Arteriolar constriction • Pre-/post-capillary sphincter contraction • Increased peripheral resistance • Shunting of blood to core organs

22. Compensated Shock • Decreased renal blood flow • Renin released from kidney arteriole • Renin & Angiotensinogen combine • Converts to Angiotensin I • Angiotensin I converts to Angiotensin II • Peripheral vasoconstriction • Increased aldosterone release (adrenal cortex) • promotes reabsorption of sodium & water

23. Compensated Shock • Decreased blood flow to hypothalamus • Release of antidiuretic hormone (ADH or Arginine Vasopressin) from posterior pituitary • Retention of salt, water • Peripheral vasoconstriction

24. Compensated Shock • Insulin •  secretion caused by epinephrine • contributes to hyperglycemia • Glucagon •  release caused by epinephrine • promotes liver glycogenolysis & gluconeogenesis • ACTH • stimulates adrenal cortex release of cortisol •  glucose production

25. Compensated Shock • Peripheral capillaries contain minimal blood • Stagnation & sludging • Aerobic metabolism changes to anaerobic • Extracellular potassium shifts begin

26. Decreased Cardiac Output Catecholamine Release Aldosterone, ADH Release Increased Blood Volume Increased PVR Increased Cardiac Output Increased Myocardial Work, O2 Demand Increased Volume Loss Compensated Shock Leading to Decompensation Myocardial Ischemia

27. Decompensated Shock • Compensatory mechanisms fail and hypotension occurs • Cardiac Effects • Decreased RBC oxygenation • Decreased coronary blood flow • Myocardial ischemia • Decreased force of contraction

28. Decompensated Shock • Presentation • Peripheral effects • Relaxation of precapillary sphincters • Continued contraction of postcapillary sphincters • Peripheral pooling of blood • D.I.C. • Plasma leakage into interstitial spaces

29. Decompensated Shock • Presentation • Peripheral effects • Continued anaerobic metabolism • Continued increase in extra cellular potassium

30. Irreversible Shock • Post-capillary sphincter relaxation • Loss of peripheral vascular resistance

31. Irreversible Shock • Washout of accumulated products • Hydrogen ion • Potassium • Carbon dioxide • Systemic metabolic acidosis occurs • Cardiac Output decreases further

32. Irreversible Shock • Permanent cellular damage. • Death occurs due to refractory acidosis, myocardial & brain ischemia.

33. Diagnosis of Shock

34. Diagnosis of Shock • Should includes: 1- Clinical stages of shock 2- Cause of shock

35. Clinical stages of Shock • Grade I (Early shock= peripheral hypoperfusion) • Grade II (Established shock = Arterial hypotension) • Grade III (Advanced shock = Vital organ hypoperfusion) • Grade IV (Irreversible shock = irreversible cellular damage)

36. 1- Early Shock • Clinical manifestations: • Restlessness, anxiety • Earliest sign of shock • Tachycardia • ?Bradycardia in cardiogenic, neurogenic • Peripheral hypoperfusion: • Cold extremities • Slow capillary refill over fingernails • Skin mottling & peripheral cyanosis • In septic shock, peripheral vasoconstriction is absent (Warm shock)

37. 2- Established Shock • The clinical triad of tachycardia, hypotension & poor peripheral perfusion becomes evident. • Early manifestations of vital organ hypoperfusion start to appear: • Deep rapid respiration ( metabolic acidosis) • Oliguria (renal hypoperfusion) • Irritability followed by drowsiness & confusion

38. 3- Advanced Shock • Multiple organ system failure (MOSF). • Reperfusion injury due to release of harmful mediators from endothelium, endotoxins & different cells • Manifestations of MOSF: • Kidneys: Acute renal failure • Lungs: ARDS • GIT: stress ulcers, bacterial translocation • Liver: Acute hepatic failure • Metabolic: acidosis & electrolyte disturbance • Blood: DIC, thrmbocytopenia • Brain: Hypoxic ischemic encephalopathy • Heart: myocardial ischaemia

39. 4- Irreversible (refractory) Shock • Terminal stage with irreversible cellular damage: • Serious arrhythmias (myocardial ischemia) • Deep coma (brain ischemia) • Metabolic acidosis refractory to therapy (pH is below 7.0 in spite of vigorous correction with sodium bicarbonate) • Other MOSF becomes evident

40. Detection of the cause of Shock • Etiologically shock is classified into the known 5 types • It is important to realize the following: • Mixed shock • Changing shock

41. Detection of Cause of Shock • 1- Septic Shock: clinical manifestations of sepsis & shock can be divided into 5 stages with increasing severity: • Sepsis and systemic inflammatory response syndrome (SIRS). • Sever sepsis. • Early septic shock. • Late or refractory septic shock. • Multiple organ system failure (MOSF)

42. I. Sepsis &SIRS • Clinical manifestation of infection • Fever or Hypothermia • Tachycardia and tachypnea • Bandemia( above 10%), leukocytosis or leukopenia, elevated ESR &CRP

43. II. Severe Sepsis • Clinical manifestation of sepsis plus one or more of the following: - acute mental changes. - oliguria. - lactic acidosis. - hypoxaemia

44. III. Early septic shock • Clinical manifestation of sever sepsis. • Hypotension or poor peripheral perfusion that respond to I.V. fluids. • Peripheral hypoperfusion is usually absent during this stage (warm shock).

45. IV. Late or refractory septic shock • Clinical manifestation of sever sepsis. • Hypotension or poor peripheral perfusion refractory to I.V. fluids. • Peripheral hypoperfusion is marked during this stage (cold shock). • Inotropic drug support is necessary to improve myocardial contractility.

46. V. Multiple organ system failure • More than one of the following 5: • DIC • ARDS • ARF • AHF • Acute CNS dysfunction • Mortality rate is very high during this stage ( 50 %).

47. Detection of Cause of Shock • 2- Hypovolemic Shock: • Clinical diagnosis is not difficult as the manifestation of causative disease are well evident ( hemorrhage, burn, dehydration). • It usually respond dramatically to volume expansion and specific replacement therapy.

48. Detection of Cause of Shock • 3- Obstructive Shock: • Occurs due to either obstruction of venous return or obstruction to arterial out flow. • The condition suspected in any shock state not responding to volume expansion. • Chest x- ray (pneumothorax) and echocardiography ( cardiac tamponade) are essential for diagnosis.

49. Detection of Cause of Shock • 4- Cardiogenic Shock: Clinical situations suggesting cardiogenic shock: • Shock following cardiopulmonary resuscitation (due to myocardial ischemia). • Shock in patients with known congenital or acquired heart disease. • Shock in patients without history of cardiac disease but with cardiomegally. • Septic shock not responding to I.V. fluid expansion (for more than 1 hour)

50. Detection of Cause of Shock • 5- Distributive Shock: • It occurs due to vascular dilatation which leads to relative hypovolaemia & decreased venous retune. • Early septic shock, anaphylactic shock and neurogenic shock are classical examples. • All these types respond to volume expansion and specific therapy (antibiotic in septic shock and antihistaminic & steroids in anaphylactic shock).