1. ANESTHETIC MANAGEMENT OF SHOCKED PATIENTS Dr. Haitham Osman, MD

2. Overview: Shock represents a clinical state in which blood flow to the tissues is inadequate to sustain normal metabolic function. Whereas, an overt shock state may be obvious in the presence of tachycardia and hypotension, the clinical presentation may be much more subtle, reflecting end organ dysfunction secondary to hypo perfusion. Furthermore, because individual organs may be variably affected, a patient with an apparently normal blood pressure and pulse rate may manifest shock by such signs as oliguria, skin pallor, coldness of extremities and mental confusion.

3. Abnormalities of tissue perfusion may result from: 1- pump failure, 2- mechanical obstruction, 3- loss of circulating volume, 4- abnormalities of peripheral circulation 5- or combination of these factors. Continuous monitoring of shocked patient allow rapid recognition of changes in patient’s condition and an accurate assessment of progress and response to therapy.

4. CONTINUE Shock is a critical emergency state, so it should be diagnosed and managed as early as possible. The initial management of shock is done by well-established priorities (the ABC f resuscitation).

5. ANESTHETIC MANAGEMENT OF SHOCKED PATIENTS Definition : Shock is defined as acute circulatory failure with inadequate tissue perfusion resulting in generalized cellular hypoxia, hyperlactemia and dysoxia ( SvO2< 65 %).

6. Classification : Shock is classified into 4 main types : 1- hypovolaemic shock. 2- cardiogenic shock. 3- abstructive shock. 4- distributive shock.

7. HYPOVOLAEMIC SHOCK : IT IS DUE TO : 1- Blood loss : as in * Trauma & gastrointestinal bleeding. * Haemothorax & haemoperitoneum. 2-Plasma loss : as in * Burns, TEN syndrome & exfoliative dermatitis. 3- Fluid & electrolyte loss : as in * Vomiting diarrhea & excessive sweating. * Hyperosmolar states (DKA). * Pancreatitis, Ascites & bowel obestruction.

8. CARDIOGENIC SHOCK : DUE TO : Dysrhythmia as tachy or Brady arrhythmia. Dysrhythmia as tachy or Brady arrhythmia. Pump failure secondary to myocardial infarction or cardiomyopathy. Pump failure secondary to myocardial infarction or cardiomyopathy.

9. OBSTRUCTIVE SHOCK : DUE TO : 1- Tension pneumothorax. 2- Pericardial disease (Tamponad or restrictive pericarditis). 3- Massive pulmonary embolism or acute pulmonary hypertension. 4- Cardiac tumor (atrial myxoma). 5- Left atrial mural thrombus. 6- Obstructive valvular disease (Aortic & mitral stenosis).

10. DISTRIBUTIVE SHOCK : DUE TO : 1- Septic shock. 2- Anaphylactic shock. 3- Neurogenic shock. 4- Vasodilator drugs overdose. 5- Acute adrenal insufficiency.

11. PATHOPHYSIOLOGY OF SHOCK : I.Neuro endocrine response to shock : Hypotension stimulate baroreceptors in carotid bulb leading to stimulation of pituitary-adrenal axis this leadsto release of catecholeamines from the adrenal medulla which result in vasoconstriction help to restore blood pressure & cardiac output.

12. II- RENIN-ANGIOTENSIN SYSTEM STIMULATION : Diminished renal perfusion pressure > 55 mmHg leads to hypoxia of the renal cortex which stimulate the juxta glomerular apparatus to release Renin that converts angiotensinogen to angiotensin I which is converted in the lungs by the angiotensin converting enzymes to angiotensin II produces widespread vasoconstriction & release of aldosterone from the adrenal cortex that increase Na reabsorption and subsequent water retention which help to restore the circulating volume.

13. III- GLUCOCORTICOID SECRETION : Plasma cortisol level increases in shock. The extent & duration of the rise is generally related to the severity of the illness.

14. IV- PITUITARY HORMONES SECRETION : Pituitary hormones are released during shock so that, circulatory levels of ACTH, growth hormone (GH) vasopressin are elevated.

15. V- INSULIN LEVEL IN SHOCK : Insulin deficiency occurs in shock due to inhibition of its release and high level of insulin antagonists (e.g. epinephrine, glucagon & cortisol). Insulin begins to increase in the recovering patients.

16. VI- GLUCAGON LEVEL IN SHOCK : Glucagon hormone is released in response to any type of shock. its main action is glycolysis that increase the release of glucose by the liver. Glucagon also has mild inotropic effect on the heart & potent splanchnic vasodilator effect.

17. VII- RESPIRATORY PATHOPHYSIOLOGICAL CHANGES IN SHOCK :  Pulmonary function changes : which is markedly impaired in shock due to injury of the alveolar membrane & damage of the capillary endothelium.  Adult respiratory distress syndrome (ARDS).  Oxygen utilization changes.

18. VIII- CARDIOVASCULAR CHANGES IN SHOCK :  Cardiac changes : decrease of cardiac output which may be due to decrease in the stroke volume due to decreased blood volume, decreased contractility or too much afterload.  Vascular changes : widespread vasodilatation occurs in distributive shock, and widespread vasoconstriction occurs in the other types of shock, it is usually controlled by local autoregulation mechanisms, neurogenic and hormonal factors.

19. IX- CENTRAL NERVOUS SYSTEM CHANGES IN SHOCK : Patients with shock are liable to develop acute disturbances of cerebral function. This may present as restlessness, irritability, agitation, disorientation, confusion, stupor & even coma. This may be due to : 1- Inadequate cerebral perfusion. 2- Metabolic disturbances, electrolyte imbalance, acid base disorder & hypoxemia. 3- Meningoencephalitis.

20. X- RENAL AFFECTION IN SHOCK : Oliguria is due to increased levels of ADH & aldosterone, oliguria may be due to pre renal, renal or post renal causes.

21. XI- GIT CHANGES IN SHOCK : In hypovolemic & cardiogenic shock there is vasoconstriction in the splanchnic bed which increase the circulating blood volume.

22. XII- HEPATIC AFFECTION IN SHOCK : Hepatic blood flow is decreased due to splanchnic vasoconstriction as an effect of the endogenous catecholeamines, Hyperbilirubinaemia & impaired reticuloendothelial function of the liver. hepatic hypoxia, lactate production, ammonia production and finally shocked liver and hepatic failure.

23. ASSESSMENT & MONITORING OF THE CARDIOVASCULAR SYSTEM : This include : 1- Heart rate (HR). 2- Arterial blood pressure (ABP) preferably invasive. 3- Central venous pressure (CVP). 4- Pulmonary artery pressure (PAP). 5- Cardiac output & myocardial function assessment, using PiCCO or equivalent monitors. 6- Tissue perfusion & oxygenation(SvO2)assessment. 7- Urinary output.

24. PREOPERATIVE MANAGEMENT OF SHOCKED PATIENTS : I.Hypovolemic shock : Fluid resuscitation either with crystalloid or colloid solutions. One disadvantage of crystalloid solutions is their rapid distribution into the extravascular space with edema formation. In contrast, colloid fluid because of their high molecular weight remain in the vascular space & increase the plasma volume.

25. The following are common endpoints of volume resuscitation : 1- CVP = 10 – 15 cm H2O. 2- Stroke volume variation > 20%. 3- Cardiac index > 2.5 L/min/m2. 4- Oxygen venous saturation > 70%. 5- Blood lactate level <4 mmoL/L. 6- Base deficit -3 to +3 mmoL/L. 7- Urine output < 0.5 ml/kg/min.

26. BLOOD COMPONENT THERAPY IN SHOCK : Transfusion targets: 1- Hb. > 7 gm/l. 2- INR > 1.5, 3- PLT > 50,000/mm3, 4- Fibrinogen > 200 mg/l.

27. N.B. I.Packed RBCs : each unit of packed RBCs increase the recipient Hb by about 1gm/dl or HCT by 3%. II.Platelets : each unit of platelets increase the patients platelet count by 7000 to 10000/mm3 III.Cryoprecipitate : it is a collection of thawed coagulation factors & contains factor VIII, IX, von willebrand factor, fibrinogen & anti thrombin II. Cryoprecipitate may be pooled from multiple donors thus increasing the risk of infection transmission. IV.Fresh frozen plasma (FFP) : FFP contains all plasma proteins & all clotting factors. The initial therapeutic dose is usually 10 – 15 ml/Kg.

28. Massive blood transfusion defined as: I.Replacement of total blood volume, with stored homologous bank blood, within 24 hours. II.Acute administration of more than 1.5 times the patient’s blood volume III.A transfusion of half the blood volume per hour IV.A transfusion greater than the total blood volume (10–20 units) V.6 units.

29. COMPLICATIONS OF MASSIVE BLOOD TRANSFUSION : Immediate: 1- Hypothermia. 2- Electrolyte imbalance : as hypokalemia, hyperkalemia, hypocalcaemia & hypercalcemia. 3- Acid base disorders : as acidosis or alkalosis. Late: 1- Coagulopathy and DIC: due to - dilutional thrombocytopenia. - factors V & VIII depression. 2- TRALI: transfusion Related Acute Lung Injury. 3- Infections : as - Hepatitis B & C. - Cytomegalovirus. - Human immunodeficiency virus (HIV). - Malaria.

30. II- MANAGEMENT OF SEPTIC SHOCK : Early Goal Directed Therapy (EGDT): 1- CVP 8-12 cmH2o. 2- SvO2 > 70%, 3- MAP > 65 mmHg, 4- Urine output > 1 ml/kg/min.

31. EGDT ALGORITHM:

32. This is achieved through: 1- Respiratory management : by assurance of oxygenation, ventilation & airway stability. 2- Hemodynamic management : by rapid infusion of intravenous solutions and Norepinephrine aiming at restoration of perfusion pressure & Oxygen delivery (Do2). 3- Management of infection : using broad spectrum antimicrobial therapy as early as possible. The immunosuppressed patients should receive anti-pseudomonal, antifungal & antiviral agents usually 1 gm Tienam+1 gm Vancomycein. anti-pseudomonal, antifungal & antiviral agents usually 1 gm Tienam+1 gm Vancomycein. 4- Correction of coagulation abnormalities : using vit k for vit k deficiency. Fresh frozen plasma is recommended to correct the microvascular bleeding with elevation of PT or PTT >1.5 times normal (10-15 ml/kg)

33. III- MANAGEMENT OF CARDIOGENIC SHOCK : 1- Decrease the preload and afterload via Vasodilators : Nitroglycerin : it has a dose dependent vasodilator effect on veins & arteries & is active in systemic & pulmonary circulations. Continuous infusion of low dose 200 mcg/min. produce arterial dilator effect. Nitroprusside : it produces cyanide & thiocyanate intoxication. Used only when there is no alternative drug.

34. 2- Inotropic drugs : Dobutamine : it is a synthetic catecholamine which is predominant B1 agonist. it causes a dose dependent increase in the stroke volume accompanied by a partial decrease in systemic vascular resistance thus, MAP remains unchanged. The usual dose range is 5-15 mcg/kg/min. usually used in combination with vaso active agents. Dopamine : it produces a dose dependent activation of several types of adrenergic & dopaminergic receptors : - Low dose (0.5-3 mcg/kg/min) activates dopaminergic receptors in the renal, mesenteric & cerebral circulation increasing the blood flow to these organs. - Intermediate dose (3-7.5 mcg/kg/min) stimulates B- receptors in the heart cardiac output. - High dose (>7.5 mcg/kg/min) produces dose dependent activation of  -receptors in the systemic & pulmonary circulations resulting in progressive vasoconstriction increasing the blood pressure.

35. 3- Levosimendan: is a calcium sensitizer it increases the sensitivity of the heart to calcium, thus increasing cardiac contractility without a rise in intracellular calcium. Levosimendan exerts its positive inotropic effect by increasing calcium sensitivity of myocytes by binding to cardiac troponin C in a calcium- dependent manner. It also has a vasodilatory effect, by opening adenosine triphosphate (ATP)-sensitive potassium channels in vascular smooth muscle to cause smooth muscle relaxation. The combined inotropic and vasodilatory actions result in an increased force of contraction, decreased preload and decreased afterload. Moreover, by opening also the mitochondrial (ATP)-sensitive potassium channels in cardio myocytes, the drug exerts a cardio protective effect. is a calcium sensitizer it increases the sensitivity of the heart to calcium, thus increasing cardiac contractility without a rise in intracellular calcium. Levosimendan exerts its positive inotropic effect by increasing calcium sensitivity of myocytes by binding to cardiac troponin C in a calcium- dependent manner. It also has a vasodilatory effect, by opening adenosine triphosphate (ATP)-sensitive potassium channels in vascular smooth muscle to cause smooth muscle relaxation. The combined inotropic and vasodilatory actions result in an increased force of contraction, decreased preload and decreased afterload. Moreover, by opening also the mitochondrial (ATP)-sensitive potassium channels in cardio myocytes, the drug exerts a cardio protective effect.

36. 4- NOREPINEPHRINE: Usually in combination with Dobutamine to maintain MAP > 65 mmHg. A higher mean arterial pressure (MAP) achieved by norepinephrine up-titration may improve organ blood flow in critically ill, whereas norepinephrine-induced afterload rise might worsen myocardial function. Norepinephrine up-titration increased MAP to the predefined values in all patients with concomitant mild increase in filling pressures and heart rate. Systemic vascular resistance increased, whereas cardiac output remained unchanged.

37. ANESTHETIC MANAGEMENT OF SHOCKED PATIENTS : Spinal & epidural anesthesia are contraindicated in shocked patients because they interfere with hemostatic compensation for hypovolemia. Premedication : No premedication is used because it is an urgent operation.

38. Induction of anesthesia : rapid sequence induction with cricoid pressure or an awake intubation is considered for fear of regurgitation and aspiration chemical pneumonitis which produce mortality up to 70% of patients. rapid sequence induction with cricoid pressure or an awake intubation is considered for fear of regurgitation and aspiration chemical pneumonitis which produce mortality up to 70% of patients. Also we can give small defasciculation dose of the non depolarizing muscle relaxant to prevent vigorous fasciculations produced by succinylcholine induced increase of intra gastric pressure. Position of the patient for intubation : Sitting or semi sitting position is the best to decrease the risk of regurgitation & aspiration during intubation.

39. Maintenance of anesthesia : when the patient becomes hemodynamically stable other anesthetic agents can be carefully titrated to prevent hypotension : -Sedatives are given in a small doses when tolerated narcotics should be titrated. -Nitrous oxide must be carefully used because it has the capacity to accumulate in closed spaces as the pleura & bowel. -Inhalational anesthetics are used in low concentrations as not to compromise the patient’s hemodynamics.

40. WHICH INTRAVENOUS ANESTHETIC AGENT? -Ketamine is the drug of choice in hypovolemic shock because it elevates the blood pressure & HR through the release of the indirect action by release of norepinephrine from the sympathetic nerve terminals. Ketamine also provide excellent analgesia & Broncho dilatation. -Thiopental & propofol are better avoided due to their myocardial depressant and vasodilatory effects. -Etomidate has minimal or no cardiac depressant effects.

41. WHICH MUSCLE RELAXANTS ? -Rocuronium is the first non depolarizing relaxant to replace succinylcholine. In contrast to succinylcholine; Rocuronium does not cause hyperkalemia & elevated ICP. -Pipecuronium & Doxacuronium are long acting muscle relaxants with no cardiovascular effects. -Vecuronium, Rocuronium & Cisatracurium are free of cardiovascular side effects and has an intermediate duration of action & so are acceptable choice. -Pancuronium is along acting muscle relaxant with vagolytic action & may be deleterious to the patient.

42. SPECIAL ANESTHETIC CONSIDERATIONS FOR PATIENTS WITH CARDIOGENIC SHOCK : -The basic challenge during induction & maintenance of anesthesia is to achieve the balance between oxygen delivery and oxygen demand by optimizing the heart rate, MAP and COP. -Induction of anesthesia should have minimal hemodynamic effects & provide sufficient depth of anesthesia.

43. CHOICE OF DRUGS : -Barbiturates, Etomidate, Benzodiazepines, Opioids in various combinations usually used as induction agents. -Ketamine is contraindicated because of its indirect sympathomimetic effects that will increase the HR and SVR. -Opioid based anesthesia is advocated for patients with significant ventricular dysfunction (except meperidine) pethidine. -Etomidate has no or minimal cardiac depressant effects, so its administration results in stable or minimally decreased heart rate, blood pressure & systemic vascular resistance.

44. MAINTENANCE AGENTS : -Patients with good ventricular function are managed with volatile agents while those with impaired ventricular function are managed with opioid based anesthesia. -All volatile agents have favorable effect on myocardial oxygen balance reducing demand more than supply. -Isoflurane is the most potent coronary vasodilator but, under certain conditions it can cause coronary steal phenomenon that exacerbate ischemia. Muscle Relaxants : - Rocuronium, Vecuronium, Pipecuronium & doxacuronium are the ideal muscle relaxants for cardiac patients.

45. Post operative care Post operative care -Post operative care in high dependency unit. -Better to continue controlled ventilation, continuous analgesia and good nutrition.