A CLINICAL PRESENTATION ON-SHOCK,TYPES,ASSOCIATED PATHOPHSYIOLOY AND MANAGEMENT

PRESENTATION ON-SHOCK,TYPES,ASSOCIATED PATHOPHSYIOLOY AND MANAGEMENT

1. SHOCK BY-DR.RUCHIK ARUN JADHAO

2. 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.

3. PATHOPHYSIOLOGY

4. METABOLIC ACIDOSIS INCREASE SYMPATHETIC ACTIVITY INCREASE RESPIRATORY RATE INCREASE MINUTE VENTILATION INCREASE CO2 EXCRETION COMPENSATORY RESPIRATORY ALKALOSIS

5. STAGES OF SHOCK

6. SEVERITY OF SHOCK TACHYCARDIA TACHYPNIA BP MAINATAINED BUT DECREASE PULSE PRESSURE MILD ANXIETY COLD AND SWEATY PERIPHERIES(except in distributive shock) URINE OUTPUT MILDLY DECREASED PATIENT DROWSY AND CONFUSED RENAL COMPENSATORY MECHANISM FAILS RENAL PERFUSION FAILS AND URINE OUTPUT <0.5ML/KG/HR PATIENT UNCONCIOUS WITH LABOURED BREATHING PROFOUND TACHYCARDIA BP FALLS PROUFOUND DECREASED URINE OUTPUT

7. EFFECTS OF SHOCK CVS : Low perfusion → low venous return → decreased cardiac output → hypotension → tachycardia. Persistent shock causes hypoxia and release of myocardial depressants leading to further cardiac damage

8. RS : : Interstitial oedema → decreased gaseous exchange → pulmonary arteriovenous shunting → tachypnoea → Adult/Acute respiratory distress syndrome (ARDS) and pulmonary oedema

9. RENAL : GFR decreases and tubular reabsorption of salt and water increases for compensatory response. But in severe cases tubular necrosis sets in leading into irreversible damage.

10. CNS : Brain perfusion, when decreases the patient becomes drowsy. Brain is the last organ to get under perfused in shock.

11. METABOLIC : Shock leads to hypoxia, which activates anaerobic metabolism leading to lactic acidosis. Antidiuretic hormone (ADH) is released which increases the reabsorption of water from renal tubules. Other hormones released are ACTH, prostaglandins, histamine, bradykinin, and serotonin to compensate the effects of shock to increase the perfusion of vital organs like heart, brain and lungs

12. CLASSIFICATION OF SHOCK ● Hypovolaemic shock ● Cardiogenic shock ● Obstructive shock ● Distributive shock ● Endocrine shock

13. HYPOVOLUMIC SHOCK MOST COMMON TYPE CAUSES- Haemorrhage, may be due to injury to the liver, spleen, bone fractures, haemothorax, vascular injury, severe bleeding on table during surgeries of thyroid, liver, portal vein or major vessels. Vomiting, diarrhoea due to any cause. Burn

14. CARDIOGENIC SHOCK Cardiogenic shock is defined as circulatory failure causing diminished forward flow leading into tissue hypoxia in the setting of adequate intravascular volume with systolic blood pressure <90 mmHg for 30 minutes; cardiac index <2.2 L/minute/ sq metre; raised PCWP (pulmonary capillary wedge pressure) >15 mmHg. Commonly seen in acute MI with a mortality >50%.

15. Cardiogenic shock develops within 24 hours of MI, it occurs when 50% of left ventricular wall is damaged by infarction. It leads to pulmonary oedema and severe hypoxia. Ischaemic necrosis of left ventricular wall causes failure of pump thereby decreasing stroke volume.

16. CAUSES- a. Acute myocardial infarction, acute carditis b. Drug induced c. Toxaemia of any causes d. Cardiac surgical conditions like valvular diseases, congenital heart diseases

17. Diagnosis is established by ECG, echocardiography, arterial blood gas analysis, cardiac enzymes, PCWP and electrolyte estimation (hypokalaemia and hypomagnesaemia are common) are the essential investigations

18. 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 .

19. 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 Distributive shock describes the pattern of cardiovascular responses characterising a variety of conditions, including – septic shock anaphylaxis spinal cord injury .

21. SEPTIC SHOCK -Septic shock may be due to gram-positive organisms, gram negative organisms, fungi, viruses or protozoal origin Common causes are biliary, urinary, GIT sepsis (peritonitis, strangulation), respiratory (pneumonia) Common bacteria are E. coli, Klebsiella, Pseudomonas Common pathophysiologies are release of toxins, neutrophil activation, cytokine release, and sick cell syndrome, SIRS, MODS Clinical stages are hyperdynamic and hypodynamic

22. Find out the source of the infection by USG, CT scan Do pus/blood/urine culture Start antibiotics of high generations like ceftazidime, amikacin, cefoperazone ,Dopamine/dobutamine infusion (slow) Monitoring by pulse, BP, respiration, urine output, level of consciousness Ventilator support, ICU management Treat the underlying cause

23. ANAPHYLACTIC SHOCK- Sudden onset , type 1 hypersensitivity reaction Distributive shock Bronchospasm, laryngeal oedema Generalised rashes and oedema Hypotension ,feeble pulse Mortality 10% To start Oxygen with foot end elevation, , IV fluids, adrenaline 100 ug IV, steroids,Ventilator in severe cases Cardiac massage, defibrillation

24. NEUROGENIC SHOCK- It is usually due to spinal cord injury, which causes dilatation of splanchnic vessels. This type can safely be treated with vasoconstrictor drugs to bring up the blood pressure. There will be bradycardia, hypotension, arrhythmias, and decreased cardiac output. Blood pressure control, oxygen delivery, maintenance of haemodynamics , airway, fluid therapy, intravenous methylprednisolone therapy should be done. Dopamine and or phenylephrine (α agonist) can be used.

25. ENDOCRINE SHOCK Endocrine shock may present as a combination of hypovolaemic, cardiogenic or distributive shock. Causes of endocrine shock include hypo- and hyperthyroidism and adrenal insufficiency.

26. Hypothyroidism causes a shock state similar to that of neurogenic shock due to disordered vascular and cardiac responsiveness to circulating catecholamines. Cardiac output falls due to low inotropy and bradycardia. There may also be an associated cardiomyopathy. Thyrotoxicosis may cause a high-output cardiac failure. Adrenal insufficiency leads to shock due to hypovolaemia

27. CONSEQUENCES OF SHOCK UNRESUSCITATABLE SHOCK There is myocardial depression and loss of responsiveness to fluid or inotropic therapy. Peripherally there is loss of the ability to maintain systemic vascular resistance and further hypotension ensues Death is the inevitable result. MULTI ORGAN FAILURE Multiple organ failure is defined as two or more failed organ systems. Multiple organ failure currently carries a mortality of 60%; thus, prevention is vital by early aggressive identification and reversal of shock.

28. MONITORING

29. CENTRAL VENOUS PRESSURE CVP measurements should be assessed dynamically as response to a fluid challenge .A fluid bolus (250–500 mL) is infused rapidly over 5–10 minutes. The normal CVP response is a rise of 2–5 cmH2O which gradually drifts back to the original level over 10–20 minutes. Patients with no change in their CVP are empty and require further fluid resuscitation. Patients with a large, sustained rise in CVP have high preload and an element of cardiac insufficiency or volume overload.

30. CARDIAC OUTPUT Cardiac output monitoring allows assessment of the systemic vascular resistance and, depending on the technique used, end diastolic volume (preload) and blood volume. Can help distinguish the types of shock present (hypovolaemia, distributive, cardiogenic), especially when they coexist. Measurement desirable in patients who do not respond as expected to first-line therapy, or have evidence of cardiogenic shock or myocardial dysfunction.

31. Early consideration should be given to instituting cardiac output monitoring for patients who require vasopressor or inotropic support.

32. BASE DEFECIT AND LACTATE Lactic acid is generated by cells undergoing anaerobic respiration. The degree of lactic acidosis, as measured by serum lactate level and/or the base deficit, is sensitive for both diagnosis of shock and monitoring the response to therapy. Base deficit over 6 mmol/L have a much higher morbidity and mortality than those with no metabolic acidosis. These parameters are measured from arterial blood gas analyses,

33. MIXED VENOUS OXYGEN SATURATION The percentage saturation of oxygen returning to the heart from the body is a measure of the oxygen delivery and extraction by the tissues Normal mixed venous oxygen saturation levels are 50–70%.

34. Levels below 50% indicate inadequate oxygen delivery and increased oxygen extraction by the cells. This is consistent with hypovolaemic or cardiogenic shock. High mixed venous saturations (>70%) are seen in sepsis and some other forms of distributive shock. In sepsis, there is disordered utilisation of oxygen at the cellular level, and arteriovenous shunting of blood at the microvascular level.

35. RESUSCITATION

36. CONDUCT OF RESUSCITATION Resuscitation should not be delayed in order to definitively diagnose the source of the shocked state. However, the timing and nature of resuscitation will depend on the type of shock and the timing and severity of the insult.

37. In patients who are actively bleeding (major trauma, aortic aneurysm rupture, gastrointestinal haemorrhage), it is counterproductive to institute high-volume fluid therapy without controlling the site of haemorrhage. Increasing blood pressure merely increases bleeding from the site while fluid therapy cools the patient and dilutes available coagulation factors. Thus operative haemorrhage control should not be delayed and resuscitation should proceed in parallel with surgery.

38. Conversely, a patient with bowel obstruction and hypovolaemic shock must be adequately resuscitated before undergoing surgery otherwise the additional surgical injury and hypovolaemia induced during the procedure will exacerbate the inflammatory activation and increase the incidence and severity of end-organ insult.

39. ISCHEMIA-REPURSION SYNDROME DAMAGE CAUSED AT CELLULAR AND ORGAN LEVEL DUE TO HYPOXIA AND LOCAL ACTIVATION OF INFLAMATION  LACTIC ACID AND POTASSIUM BUILT UP  TISSUE PERFUSION DONECELLULAR AND HUMORAL ELEMENTS ACTIVATED BY HYPOXIA FLUSHED INTO CIRCULATION  CAUSING MORE ENDOTHLIAL INJURY AND EVEN MORE MYOCARDIAL DEPRESSION AND VASODILATION

40. FLUID THERAPY Plasma, normal saline, Ringer’s lactate, plasma expander ( haemaccel ) (maximum 1 litre can be given in 24 hours). Initially crystalloids then colloids are given. Blood transfusion is done whenever required. Fluid therapy is ideally done with crystalloids like normal saline, Ringer’s lactate, Hartmann’s solution.

41. Blood loss should be corrected by blood transfusion only. Crystalloids and colloids do not have O2 carrying capacity. Hypotonic solutions like dextrose are poor volume expanders and so should not be used in shock.

42. DYNAMIC FLUID RESPONSE The shock status can be determined dynamically by the cardiovascular response to the rapid administration of a fluid bolus. In total, 250–500 mL of fluid is rapidly given (over 5–10 minutes) and the cardiovascular responses in terms of heart rate, blood pressure and central venous pressure are observed. Patients can be divided into ‘responders’, ‘transient responders’ and ‘non-responders’.

43. Responders have an improvement in their cardiovascular status that is sustained. These patients are not actively losing fluid but require filling to a normal volume status. Transient responders have an improvement, but this then reverts to the previous state over the next 10–20 minutes. These patients have moderate ongoing fluid losses (either overt haemorrhage or further fluid shifts reducing intravascular volume). Non-responders are severely volume depleted and are likely to have major ongoing loss of intravascular volume, usually through persistent uncontrolled haemorrhage.

44. ONGOING VOLUME LOSS RESPONDERS TRANSIENT/ NON-RESPONDERS PRIORITISE COAGULATION PRIORITISE PERFUSION PERFUSION TARGETED RESUSCITATION DAMAGE CONTROL RESUSCITATION

45. VASOPRESSORS AND IONOTROPIC SUPPORT Vasopressor agents ( phenylephrine, noradrenaline ) are indicated in distributive shock states (sepsis, neurogenic shock) where there is peripheral vasodilatation, and a low systemic vascular resistance, leading to hypotension despite a high cardiac output. Where the vasodilatation is resistant to catecholamines (e.g. absolute or relative steroid deficiency) vasopressin may be used as an alternative vasopressor.

46. In cardiogenic shock , or where myocardial depression has complicated 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.

47. x Catheterisation to measure urine output (30–50 ml/hour or >0.5 ml/kg/hour should be maintained). x Nasal oxygen to improve oxygenation or ventilator support with intensive care unit monitoring has to be done. x Correction of acid-base balance: Acidosis is corrected by using 8.4% sodium bicarbonate intravenously. x Steroid is often life-saving. 500–1000 mg of hydrocortisone can be given. It improves the perfusion, reduces the capillary leakage and systemic inflammatory effects. x Antibiotics in patients with sepsis; proper control of blood sugar and ketosis in diabetic patients. x CVP line to perfuse adequately and to monitor fluid balance. TPN is given when required. x PCWP to monitor very critical patient.

48. x MAST (military antishock trouser) : Provides circumferential external pressure of 40 mmHg. It is wrapped around lower limbs and abdomen, and inflated with required pressure. It redistributes the existing blood and fluid towards centre. It should be deflated carefully and gradually.

49. END POINTS OF RESUSCITATON A patient therefore may be resuscitated to restore central perfusion to the brain, lungs and kidneys and yet continue to underperfuse the gut and muscle beds. Activation of inflammation and coagulation may be ongoing and lead to reperfusion injury when these organs are finally perfused, and ultimately multiple organ failure. This state of normal vital signs and continued underperfusion is termed ‘occult hypoperfusion’.

50. With current monitoring techniques, it is manifested only by a persistent lactic acidosis and low mixed venous oxygen saturation. Patients with occult hypoperfusion for more than 12 hours have two to three times the mortality of patients with a limited duration of shock Resuscitation algorithms directed at correcting global perfusion end points (base deficit, lactate, mixed venous oxygen saturation) rather than traditional end points have been shown to improve mortality and morbidity in high-risk surgical patients

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