MANAGEMENT OF SHOCK

Definition, types, investigation and management of shock

1. PRINCIPLES OF MANAGEMENT OF SHOCK Dr.Bipul Borthakur Prof and head Orthopaedics,smc

2. CONTENTS • Definition • Classification of shock • Pathophysiology of shock • Stages of shock • Management of shock

3. DEFINITION Shock is a systemic state of low tissue perfusion that is inadequate for normal cellular respiration. With insufficient delivery of oxygen and glucose, cells switch from aerobic to anaerobic metabolism. If perfusion is not restored in a timely fashion, cell death ensues. The end result is hypotensio n and cellular hypoxia and, if uncompensated, may lead to impaired cellular metabolism and death.

4. Shock is the most common and therefore the most important cause of death of surgical patients. Death may occur rapidly due to profound state of shock, or be delayed due to consequences of organ ischaemia and reperfusion injury.

5. CLASSIFICATION OF SHOCK Classification of shock on the basis of initiating mechanism: Hypovolaemic shock Cardiogenic shock Obstructive shock Distributive shock Endocrine shock

6. 1 HYPOVOLAEMIC SHOCK Hypovolaemic shock is due to a reduced circulating volume. Hypovolaemia may be due to haemorrhagic or non-haemorrhagic causes. Haemorrhagic causes : Trauma Surgery Non-haemorrhagic causes: poor fluid intake (dehydration) excessive fluid loss due to vomiting, diarrhoea, urinary loss ‘third-spacing’ where fluid is lost into the gastrointestinal tract and interstitial spaces

7. PATHOPHYSIOLOGY OF HYPOVOLAEMIC SHOCK

8. CLASSIFICATION OF HYPOVOLAEMIC SHOCK

9. CARDIOGENIC SHOCK Cardiogenic shock is due to primary failure of the heart to pump blood to the tissues. Causes of Cardiogenic shock include: - Myocardial infarction - Cardiac arrhythmia - Valvular heart disease - Myocardial injury - Cardiomyopathy

10. OBSTRUCTIVE SHOCK: In obstructive shock there is a reduction in preload due to mechanical obstruction of cardiac filling. Common causes of obstructive shock include; - Cardiac tamponade - Tension pneumothorax - Massive pulmonary embolus or Air embolus In each case, there is reduced filling of the left and/or right sides of the heart leading to reduced preload and a fall in cardiac output.

11. DISTRIBUTIVE SHOCK Distributive shock describes the pattern of cardiovascular responses characterising a variety of conditions including; A) Septic shock B) Anaphylactic shock C) Spinal cord injury (Neurogenic shock).

12. A) SEPTIC SHOCK It is related to the release of bacterial products ( endotoxin) and the activation of cellular and humoral components of the immune system. There is maldistribution of blood flow at a microvascular level Arteriovenous shunting Dysfunction of cellular utilization of oxygen. In the later phases of septic shock there is hypovolaemia from fluid loss into interstitial spaces and there may be concomitant myocardial depression.

13. SEPTIC SHOCK

14. PATHOPHYSIOLOGY OF SEPTIC SHOCK

15. B) ANAPHYLACTIC SHOCK It is a type of severe hypersensitivity or allergic reaction. Causes include allergy to insect stings, medicines or foods (Nuts, Berries, Sea foods) etc. It is caused by a severe reaction to an allergen, leading to the release of histamine that causes widespread vasodilation and hypotension.

16. C) NEUROGENIC SHOCK It is caused by spinal cord injury usually as a result of a traumatic injury or accident. There is failure of sympathetic outflow and adequate vascular tone. Damage to CNS impairs cardiac function by reducing heart rate and loosening the blood vessel tone resulting in severe hypotension.

17. PATHOPHYSIOLOGY OF SHOCK Pathophysiology of shock : A) Cellular level B) Microvascular level C) Systemic level

18. A) CELLULAR LEVEL As perfusion to the tissues is reduced, cells are deprived of oxygen and must switch from aerobic to anaerobic metabolism. The product OF anaerobic metabolism lactic acid . the accumulation of lactic acid in the blood produces systemic metabolic acidosis . There is failure of the sodium/potassium pumps . Intracellular lysosomes release autodigestive enzymes and cell lysis ensues. Intracellular contents, including potassium, are released into the bloodstream.

19. B) MICROVASCULAR LEVEL Activation of the immune and coagulation systems. Generation of oxygen free radicals and cytokine release. These mechanisms lead to injury of the capillary endothelial cells. These, in turn, further activate the immune and coagulation system.

20. C) SYSTEMIC LEVEL 1) CARDIOVASCULAR : As preload and afterload decrease, there is a compensatory baroreceptor response resulting in increased sympathetic activity and release of catecholamines into the circulation. This results in tachycardia and systemic vasoconstriction

21. 2) RESPIRATORY SYSTEM: Metabolic acidosis and sympathetic response result in an increased respiratory rate Increased minute ventilation lead to increase the excretion of carbon dioxide. It produce a compensatory respiratory alkalosis .

22. 3) RENAL Increased afferent arteriolar resistance accounts for diminished glomerular filtration rate (GFR) Increased aldosterone and vasopressin, is responsible for reduced urine formation . Reduced filtration at the glomerulus and a decreased urine output. The stimulated renin–angiotensin–aldosterone system resulting in further vasoconstriction and increased sodium and water reabsorption by the kidney .

23. 4) ENDOCRINE Vasopressin (antidiuretic hormone) is released from the hypothalamus in response to decreased preload and results in vasoconstriction. Cortisol is released from the adrenal cortex, contributing to the sodium and water resorption and sensitising cells to catecholamines .

24. 5) METABOLIC There is disruption of the normal cycles of carbohydrate, lipid, and protein metabolism. Aalanine in conjunction with lactate enhances the hepatic production of glucose. With reduced availability of oxygen, the breakdown of glucose to pyruvate, and ultimately lactate, represents an inefficient cycling with minimal net energy production.

25. SEQUENTIAL EVENTS IN THE MECHANISM OF SHOCK: Decreased effective circulating blood volume. Decreased venous return to the heart. Decreased cardiac output. Decreased blood flow. Decreased supply of oxygen. Anoxia. Shock.

26. CLINICAL FEATURES:

27. CAPILLARY REFILL: Most patients in hypovolemic shock will have cool, pale peripheries, with prolonged capillary refill times. This is not a specific marker of whether a patient is in shock. In septic shock, the periphery will be warm and capillary refill will be brisk, despite profound shock.

28. TACHYCARDIA: Tachycardia may not always accompany shock. Patients who are on beta-blockers or who have implanted pacemakers are unable to mount a tachycardia. In young patients, with penetrating trauma where there is hemorrhage but little tissue damage, there may be a paradoxical bradycardia rather than tachycardia.

29. BLOOD PRESSURE : Hypotension is one of the last signs of shock Children and young adults are able to maintain BP until the final stages of shock by increasing stroke volume and peripheral vasoconstriction. These patients can be in profound shock with a normal blood pressure.

30. STAGES OF SHOCK: Divided into 3 stages: 1. Non-progressive (initial, compensated, reversible) shock 2. Progressive decompensated shock 3. Decompensated (Irreversible) shock

31. 1NON-PROGRESSIVE STAGE OF SHOCK: In the early stage of shock, an attempt is made to maintain adequate cerebral and coronary blood supply by redistribution of blood. If the cause are adequately treated, the compensatory mechanism may be able to bring about recovery & re-establish the normal circulation; this is called compensated or reversible shock . These Compensatory mechanisms are: i ) Wide spread vasoconstriction ii) Fluid conservation by the kidney iii) Vascular autoregulation

32. PROGRESSIVE DECOMPENSATED SHOCK: This is a stage when the patient suffers from Risk factors (e.g. Pre-existing cardiovascular and lung disease) besides persistence of the shock so that there is a progressive deterioration. The effects of progressive decompensated shock are: a) Pulmonary hypo perfusion with resultant tachypnoea and ARDS. b) Anaerobic glycolysis resulting in Metabolic acidosis.

33. DECOMPENSATED (IRREVERSIBLE) SHOCK: When the shock is so severe that inspite of compensatory mechanisms, no recovery takes place, it is called decompensated or irreversible shock. Effects due to widespread cell injury include: a) Deterioration in cardiac output. b) Severe metabolic acidosis c) Pulmonary oedema, tachypnoea and ARDS d) Ischemic cell death of brain, heart and kidneys due to reduced blood supply to these organs. Clinically the patient has features of coma , worsened heart function and progressive renal failure.

34. MANAGEMENT OF SHOCK: General principles of shock management: 1. The overall goal of shock management is to improve oxygen delivery/utilisation in order to prevent cellular and organ injury. 2. Effective therapy requires treatment of underlying etiology . 3. Restoration of adequate perfusion, monitoring and comprehensive supportive care. 4. Interventions to restore perfusion centre, increasing cardiac output and optimising oxygen content. 5. Oxygen demand should also be reduced.

35. PHYSICAL EXAMINATION: Increased HR Tachypnea Mean arterial pressure less than 60 mmHg (not always present) Confusion and encephalopathy Oliguria Decreased capillary refill and cold skin.

36. PHYSICAL EXAMINATION: Site of an untreated infection GI Hemorrhage on rectal examination. Pulsus paradox and elevated JVP seen in cardiac tamponade Paucity of breath sounds, deviation of trachea away from the affected side, subcutaneous emphysema seen in tension pneumothorax

37. DIAGNOSTIC TESTING: The laboratory evaluation is directed toward the dual aim of assessing the extent of end organ dysfunction and of gaining insight into the possible etiology of shock.

38. DIAGNOSTIC TESTING: BLOOD TESTS: Blood urea nitrogen (BUN), creatinine, transaminase evaluation show extent of end organ damage Urine electrolytes, FE Na, FE urea indicate hypovolemia status Increased WBCs show infective process Increased cardiac enzymes show primary cardiac problem Blood cultures, urine cultures and sputum cultures should be obtained. Lactate measurement

39. MONITORING:

40. MONITORING: Echocardiography: an echocardiogram should be obtained in patients with suspected cardiogenic shock. Advanced hemodynamic monitoring: recently new central venous catheter systems linked with computer based algorithms provides continuous monitoring of hemodynamic parameters. Cardiac catheterization and coronary angiography indicated in all patients with cardiogenic shock.

41. SYSTEMIC AND ORGAN PERFUSION: The best measure of organ perfusion and the best monitor of adequacy of shock therapy remains the urine output .

42. RESUSCITATION: Resuscitation should not be delayed in order to definitively diagnose the source of the shocked state. If there is initial doubt of cause of shock, it is safer to assume the cause is hypovolemia. And begin fluid resuscitation. Intravenous fluids should be given through short, wide bore catheters. The oxygen carrying capacity of crystalloid and colloids is zero If blood is being lost, the ideal replacement is blood, although crystalloid therapy may be required while awaiting blood products.

43. VASOPRESSOR AND INOTROPIC SUPPORT: Vasopressor agents (phenylephrine, noradrenaline) are indicated in distributive shock. When vasodilation is resistant to catecholamines, vasopressin may be used as an alternative vasopressor. In cardiogenic shock, inotropic therapy required to increase cardiac output, dobutamine is the agent of choice.

44. END POINTS OF RESUSCITATION: Traditionally, patients have been resuscitated until they have a normal pulse, BP, and urine output. Occult hypoperfusion: state of normal vital signs and continued underperfusion . With current monitoring techniques, occult hypoperfusion is manifested only by a persistent lactic acidosis and low mixed venous oxygen saturation. Resuscitation algorithms directed at correcting global perfusion end points ( base deficits, lactate, mixed venous oxygen saturation ) rather than traditional end points have been shown to improve mortality and morbidity in high risk surgical patients .

45. MANAGEMENT OF HYPOVOLAEMIC SHOCK: • Maximise oxygen delivery -completed by ensuring adequacy of ventilation • Control further blood loss. • Fluid resuscitation .

46. MANAGEMENT OF HYPOVOLAEMIC SHOCK:

47. MANAGEMENT OF SEPTIC SHOCK: The most important aspects of therapy for patients with septic shock/sepsis include: Adequate oxygen delivery. Crystalloid fluid administration-normal saline (0.9% NaCl), Ringer lactate. Broad spectrum antibiotics - cefotaxim , clindamycin, ceftriaxone, ciprofloxacin, metronidazole, cefepime, levofloxacin, vancomycin. Alpha and beta adrenergic agonists -nor epinephrine, dopamine, dobutamine, epinephrine, vasopressin, phenylephrine. Corticosteroids like hydrocortisone, dexamethasone.

48. MANAGEMENT OF SEPTIC SHOCK :

49. MANAGEMENT OF SEPTIC SHOCK : General Supportive Care : Patients requiring a vasopressor should have an arterial catheter placed as soon as is practical. Hydrocortisone is not suggested in septic shock. Continuous or intermittent sedation should be minimized in mechanically ventilated sepsis patients. A protocol-based approach to blood glucose management should be used in ICU patients with sepsis, with insulin dosing initiated when two Consecutive blood glucose levels are >180 mg/dL. Continuous or intermittent renal replacement therapy should be used in patients with sepsis and acute kidney injury. Stress ulcer prophylaxis should be given to patients with risk factors for gastrointestinal bleeding.

50. MANAGEMENT OF NEUROGENIC SHOCK: Immobilization: if the patient has a suspected case of spinal cord injury. High dose steroid to reduce inflammation IV fluids : administration of IV fluids is done to stabilize the patient’s blood pressure. Inotropic agents such as dopamine may be infused for fluid resuscitation. Atropine is given intravenously to manage severe bradycardia.

51. MANAGEMENT OF CARDIOGENIC SHOCK: Management of Cardiogenic shock includes supportive measures which includes: Oxygen therapy Judicious use of fluids with careful monitoring of central venous pressure or pulmonary wedge pressure. Other monitoring include continuous ECG, 12 lead ECG, urine output, urea and electrolytes & blood gases. Patient should be preferably managed in coronary care unit. Drugs like morphine 5-10mg IV helps to relieve pain and anxiety associated with myocardial infarction. Inotropic support, vasodilators and mechanical support may be needed.

52. MANAGEMENT OF ANAPHYLACTIC SHOCK: During an anaphylactic attack, cardiopulmonary resuscitation (CPR) may be needed if breathing or heart beat is stopped. Medications in Anaphylactic shock includes: Epinephrine (adrenaline) to reduce body’s allergic response. Oxygen , which helps in breathing. Intravenous anti histaminics and cortisone to reduce inflammation of air passages and improve breathing. Beta agonist (e.g. Albuterol ) to relieve breathing symptoms.

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