Shock

Principle and classification of shock with management

1. MARMAGHAT (SHOCK) Dr. Alok Kumar PhD Shalya Tantra NEIAH, Shillong

2. Samanya lakshana of marmaghata देहप्रसुप्तिर्गुरुता सम्मोहः शीतकामिता| स्वेदो मूर्च्छा वमिः श्वासो मर्मविद्धस्य लक्षणम् || A.S. Sa. 7/47 Numbness , spasm/heaviness, confusion/ nervousness, thirst, sweating, unconsciousness, vomiting, dyspnea are the common features of marmaghata.

3. भ्रमः प्रलापः पतनं प्रमोहो विचेष्टनं संलयनोष्णते च | स्रस्ताङ्गता मूर्च्छनमूर्ध्ववातस्तीव्रा रुजो वातकृताश्च तास्ताः ||३४|| मांसोदकाभं रुधिरं च गच्छेत् सर्वेन्द्रियार्थोपरमस्तथैव | दशार्धसङ्ख्येष्वपि विक्षतेषु सामान्यतो मर्मसु लिङ्गमुक्तम् ||३५ || Su.Su 25/34-35 देहस्य रुधिरं मूलं रुधिरेणैव धार्यते | तस्माद्यत्नेन संरक्ष्यं रक्तं जीव इति स्थितिः ||४४|| Su.Su 14/44

4. DEFINITION Shock is a systemic state of low tissue perfusion , which 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 .

5. Pathophysiological Events All theses event happens simultaneously…. Cellular Micro-vascular Systemic

6. Cellular Cells run-down with oxygen and glucose Aerobic respiration turns to Anaerobic Collection of lactic acid lead to metabolic acidosis As glucose exhausted respiration ceases Sodium potassium pump stop Intracellular lysosomes release autodigestive enzymes and cell lysis ensues Intracellular contents, including potassium, are released into the bloodstream.

7. Micro-vascular As tissue ischemia progresses, changes in the local environment activation of the immune and coagulation systems generation of oxygen free radicals and cytokine release injury of the capillary endothelial cells . Damaged endothelium loses its integrity and becomes ‘leaky ’ Spaces between endothelial cells allow fluid to leak out and tissue oedema ensues, worsening cellular hypoxia

8. Systemic These system take active participation in shock Cardiovascular Respiratory Renal Endocrine

9. Cardiovascular As preload and afterload decrease Compensatory baroreceptor response resulting in increased sympathetic activity and release of catecholamines into the circulation . This results in tachycardia and systemic vasoconstriction (except in sepsis).

10. Respiratory The metabolic acidosis and increased sympathetic response Increased respiratory rate and tiny ventilation Leads to increase the excretion of carbon dioxide ( and so produce a compensatory respiratory alkalosis).

11. Renal Decreased perfusion pressure in the kidney L eads to reduced filtration at the glomerulus Resulting decreased urine output . The renin–angiotensin–aldosterone axis is stimulated R esulting in further vasoconstriction and increased sodium and water reabsorption by the kidney

12. Endocrine As well as activation of the adrenal and renin–angiotensin systems Vasopressin (antidiuretic hormone) is released from the hypothalamus in response to decreased preload and results in vasoconstriction and reabsorption of water in the renal collecting system. Cortisol is also released from the adrenal cortex, contributing to the sodium and water reabsorption and sensitizing the cells to catecholamines

13. Ischaemia–reperfusion syndrome Tissue damage due to Hypoxia & local inflammation Normal circulation is restored The acid and potassium recirculate in body C an lead to direct myocardial depression, vascular dilatation and further hypotension

14. The cellular and humoral elements activated by the hypoxia (complement, neutrophils, micro-vascular thrombi) are flushed back into the circulation They causes further endothelial injury to organs such as the lungs and kidneys This leads to acute lung injury, acute renal injury, multiple organ failure and death.

15. How to avoid ???? Reducing the extent and duration of tissue hypo-perfusion.

16. Classification of shock (HODEC) There are various classification of shock but most clinical approachable is on the basis of initiating mechanism Hypovolemic Obstructive Distributive Endocrine Cardiogenic

17. Hypovolemic Caused by a reduced circulating volume May be: Hemorrhagic Non-hemorrhagic (dehydration, excessive fluid loss by diarrheoa , vomiting, urinary or fluid in third space i.e. exudation) Hypovolemia is probably the most common form of shock and is to some degree a component of all other forms of shock. Absolute or relative hypovolemia must be excluded or treated in the management of the shocked state, regardless of cause.

18. Cardiogenic shock Failure of the heart to pump blood to the tissues. Causes Myocardial infarction, cardiac dysrhythmias, valvular heart disease, blunt myocardial injury and cardiomyopathy . Cardiac insufficiency may also be caused by myocardial depression resulting from endogenous factor like (e.g. bacterial and humoral agents released in sepsis) or exogenous factors, such as pharmaceutical agents or drug abuse. Evidence of venous hypertension with pulmonary or systemic oedema may coexist with the classic signs of shock.

19. Obstructive shock In obstructive shock there is a reduction in preload because of mechanical obstruction of cardiac filling. Cardiac tamponade , tension pneumothorax , massive pulmonary embolus and 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

20. Distributive shock Inadequate organ perfusion is complemented by vascular dilatation with hypotension, low systemic vascular resistance , inadequate afterload and a resulting abnormally high cardiac output . Present in Anaphylaxis Septicemia ( septic shock) Spinal cord injury

21. Endocrine shock Endocrine shock may present as a combination of hypovolaemic , cardiogenic and distributive shock. Causes of endocrine shock include hypo- and hyperthyroidism and adrenal insufficiency . Hypothyroidism causes a shock result of disordered vascular and cardiac responsiveness to circulating catecholamines . Cardiac output falls because of low inotropy and bradycardia. There may also be an associated cardiomyopathy. Thyrotoxicosis may cause a high-output cardiac failure .

22. Adrenal insufficiency leads to shock as a result of hypovolaemia and a poor response to circulating and exogenous catecholamines . Adrenal insufficiency may result from pre-existing Addison’s disease or it may be a relative insufficiency caused by a pathological disease state such as systemic sepsis.

23. Severity of shock Compensated shock De-compensated Mild shock Moderate shock Severe shock

24. Compensated shock Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines ) there may be no other clinical signs of hypovolaemia . This condition is occult tissue perfusion this state will lead to multiple organ failure and death if prolonged because of the ischaemia –reperfusion effect . Patients with occult hypo-perfusion (metabolic acidosis despite normal urine output and cardiorespiratory vital signs) for more than 12 hours have a significantly higher mortality rate, infection rate and incidence of multiple organ failure. In general, loss of around 15% of the circulating blood volume is within normal compensatory mechanisms. Kidneys Lungs Brain Skin Muscle Gastrointestinal tract .

25. De-compensation Further loss of circulating volume overloads the body’s compensatory mechanisms and there is progressive renal , respiratory and cardiovascular de-compensation. Blood pressure is usually well maintained and only falls after 30–40% of the circulating volume has been lost.

26. Mild shock Mild shock Initially there is tachycardia, tachypnoea and a mild reduction in urine output and the patient may exhibit mild anxiety . Blood pressure is maintained although there is a decrease in pulse pressure. The peripheries are cool and sweaty with prolonged capillary refill times (except in septic distributive shock).

27. Moderate shock As shock progresses, renal compensatory mechanisms fail, renal perfusion falls and urine output dips below 0.5mlkg–1h–1. There is further tachycardia and now the blood pressure starts to fall. Patients become drowsy and mildly confused.

28. Severe shock In severe shock there is profound tachycardia and hypotension . Urine output falls to zero and patients are unconscious with laboured respiration .

29. Clinical feature Compensated Mild Moderate Severe Lactic acidosis + ++ ++ +++ Urine output Normal Normal Reduced Anuric Level of consciousness Normal Mild anxiety Drowsy Comatose Respiratory rate Normal Increased Increased Laboured Pulse rate Normal Increased Increased Increased Blood pressure Normal Normal Mild hypotension Severe hypotension Clinical feature of shock

30. Pitfalls The problem is that all these classical sign symptoms are not present in every patient. Patient may have shock despite the absence of these classical sign. Capillary refill Tachycardia Blood pressure

31. Consequences Un- resuscitatable shock Multiple organ failure

32. RESUSCITATION Resuscitation should not be delayed in order to definitively diagnosis… T he timing and nature of resuscitation will depend on the type of shock and the timing and severity of the insult . Rapid clinical examination will provide adequate clues to make an appropriate first determination, even if a source of bleeding or sepsis is not immediately identifiable . If there is initial doubt about the cause of shock it is safer to assume the cause is hypovolaemia and begin with fluid resuscitation, followed by an assessment of the response. If patient is actively loosing blood, operative haemorrhage control should not be delayed and resuscitation should proceed in parallel with surgery. If patient not loosing blood actively then must be resuscitated before underwent surgery. For eg in bowel obstruction leading shock patient must resuscitated before surgery.

33. Fluid therapy In all cases of shock, regardless of classification, hypovolaemia and inadequate preload must be addressed before other therapy is instituted. Therefore, First-line therapy is intravenous access and administration of intravenous fluids. Access should be through short, wide-bore catheters that allow rapid infusion of fluids as necessary .

34. Type of fluids Blood Crystalloid ( Normal saline, R inger’s lactate , Hartmann’s solution) Colloid (albumin or commercially available products)

35. Dynamic fluid response The shock status can be determined dynamically by the cardiovascular response to the rapid administration of a fluid bolus. The 250-500 ml fluid should be given in first 5-10 minute and the response of therapy must be observed in term of- H eart R ate B lood P ressure C entral V enous P ressure (CVP ) Patients can be divided into ‘responders’, ‘transient responders’ and ‘ non-responders ’.

36. R esponders 1. Severely volume depleted and are likely to have major on-going loss of intravascular volume, usually through persistent uncontrolled haemorrhage . 1. Improvement but then revert to their previous state over the next 10–20min. 2. These patients have moderate on-going fluid losses I mprovement in their cardiovascular status, which is sustained. These patients are not actively losing fluid but require filling to a normal volume status Non-responders T ransient responders

37. Vasopressor and inotropic support Not included in first line therapy for shock.. 1. Vasopressor agents ( phenylephrine, noradrenaline ) are indicated in distributive shock states. 2. In cardiogenic shock or when myocardial depression complicates a shock state (e.g. severe septic shock with low cardiac output), inotropic therapy may be required to increase cardiac output and, therefore, oxygen delivery. The inodilator dobutamine is the agent of choice.

38. Monitoring Minimum ■ Electrocardiogram ■ Pulse oximetry ■ Blood pressure ■ Urine output Additional modalities ■ Central venous pressure ■ Invasive blood pressure ■ Cardiac output ■ Base deficit and serum lactate

39. Endpoints of resuscitation Traditionally patients have been resuscitated until they have a normal pulse, blood pressure and urine output. Resuscitation algorithms directed at correcting global perfusion endpoints are base deficit, lactate, mixed venous oxygen saturation.