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Moderator : Dr.Vikram Mahajan

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1 Moderator : Dr.Vikram Mahajan
GOOD MORNING Moderator : Dr.Vikram Mahajan

2 Shock “A rude unhinging of the machinery of life”
“A brief pause in the act of dying”

3 Shock Inadequate peripheral perfusion leading to failure of tissue oxygenation  may lead to anaerobic metabolism

4 Clinically Hypotension (ie. SBP < 90mmHg or MAP <60mmHg or reduced by >30% for last 3min) Oliguria (Urine output20ml/hr or 0.3ml/kg/hr for 2 consecutive hours) Poor peripheral perfusion (eg. Skin is cool and clammy; demonstrates poor capillary refill). With cardiogenic/septic, Skin exhibits cyanosis mottling which occurs first over knees.

5 Etiology of shock Cardiogenic
Acute myocardial infarction (implies >40% LV muscle loss)Shock accompanies 6-20% of all acute MI’s ;more common with patients with ant. MI Dilated cardiomyopathy Acute myocarditis

6 Metabolic and pharmacologic myocardial depression Arrhythmias
Mechanical Mitral regurgitation Ventricular septal defect Left ventricular aneurysm Left ventricular outflow obstruction Metabolic and pharmacologic myocardial depression Arrhythmias

7 Extra cardiac obstructive
Massive pulmonary embolism Severe pulmonary hypertension Pericardial obstruction Tension pneumothorax

8 Oligemic: _ Hemorrhagic Distributive Volume depletion
Adrenal insufficiency Distributive Septic Toxic agents including adverse reaction to medications and certain drug overdose Anaphylaxis Neurogenic

9 The Stages Compensated Decompensated
15-25% of fluid loss from the vessels Signs are subtle Patient may show signs of an adrenaline rush Decompensated 25-35% of fluid loss from the vessels The body cells are profoundly hypoxic Classic signs of shock Irreversible > 35% fluid loss from the vessels Body cells die All vital signs bottom out

10 Pathophysiology





15 Compensated Shock Baroreceptors sense a drop in pressure in the arteries Medulla is stimulated Sympathetic NS Response Clammy and pale skin Increased HR Cells receive less oxygen as a result of a loss of RBC by the vomiting of blood Pre-capillary sphincter closes in periphery and Blood shunted to the core

16 Compensated Shock (cont)
Sympathetic NS response continues Adrenal hormones released Chemoreceptors sense changes in CO2 and oxygen concentrations Medulla stimulated again Increase in RR HR continues to rise Cellular Ischemic Phase Cells transition from aerobic to anaerobic metabolism Lactic acid begins to build Blood begins to coagulate behind the closed precapillary sphincter Post-capillary sphincter closes.

17 Decompensated Shock Less blood flow and oxygen delivery impact more of the body Tissues in the core become hypoxic • More shifts to anaerobic metabolism • Organ function slows Capillary Stagnation Phase • Lactic acid build in the cells and leak into the capillaries • Cell function drops dramatically Continued closure of postcapillary sphincters reduce preload Cardiac output drops Blood pressure begins to fall

18 Irreversible Shock The medulla stops working
Sympathetic nervous system stimulation ceases Heart function drops Drop in heart rate and contractility Vessels dilate No more energy to constrict Capillary Washout Phase Cell functions cease and cells die Potassium, acid dumps into the capillaries Large accumulations of acid force the opening of the capillary sphincters Sludge, clots and acid circulates throughout the entire body Other organ systems die off from this wave of destruction

19 General Management Initial Approach to patient in shock ABC Airway
Indications for intubation in patients with shock Severe hypoxemia In appropriately high pCo2 Obtundation (ensure protection of airway) Vital organ Hypoperfusion Resting ventilatory muscles will permit diversion of cardiac output to other hypoperfused organs

20 Breathing oxygen Circulation
a. Immediate determination of relative intravascular volume status is required. Physical Examin- sufficient to distinguish shock with volume overload (ie. Cardiogenic shock) with pulmonary edema from shock with inadequate volume / eg. Septic shock with low cardiac filling pressures. Unless there are signs of intravascular volume overload initial resuscitation with IV fluids is generally indicated. b. Vasopressor medications should be selected based on the cause of shock

21 Management of cardiogenic shock
Definition Clinical Poor cardiac output Tissue hypoxemia 1. Oliguria 2. Cyanosis 3. Altered mentation 4 . Cool extremities Adequate blood volume

22 2. Hemodynamic systolic hypotension (< 90 mm or 30mm below baseline) Increased arterial venous oxygen difference >5.5ml/dl Low cardiac index (<2.2) Elevated PCWP (>18) The LV ejection fraction can be misleading and in one case study of patients with cardiogenic shock the avg LVEF was 31% (circulation 2003/107:279-84)

23 Management (Cardiogenic )
Establish Airway and ensure ventilation if necessary Assessment Identify and correct rhythm disturbances Exchange other frequent mimics of cardiogenic shock (PE, Sepsis, Aortic dissection, Ruputred Aortic Aneurysm pericardial tamponade)

24 Assess Volume Status An adequate pre load is prerequisite to successful resuscitation Clinical assessment is often in accurate CVP, PCWP is many circumstances. Insertion of Swan Ganz catheter is indicated in patient with hypotension unresponsive to fluid administration or if fluids are contraindicated (circulation 2004;110)

25 Replace volume In the absence of clinical evidence of pulmonary edema, an immediate fluid challenge is indicated. Often small volume of fluid can mean the difference between inadequate LV filling pressure and pulmonary edema. Frequent small volume 250cc saline bolus are preferable in cardiogenic shock resuscitation.

26 Vasopressors Dobutamine Dose- 2.5-20g/kg/min
First line drug if shock is mild with relatively pressured blood pressure. Dopamine Dosage g/kg/min In moderate – severe cardiogenic shock dopamine is drug of 1st choice.

27 Norepinephrine Dosage g/kg/min Use is primarily reserved for patients failing to respond to dopamine. Phenylephrine Dose g/kg/min Use is primarily reserved for patients with septic shock with high cardiac output refractory to nor epinephrine,dopamine

28 Vasodilators (Rarely useful in acute cardiogenic shock)
Nitroprusside useful only if cardiogenic shock accompanied by in appropriately high after load acute mitral regurgitation acute aortic regurgitation acute ventricular septal defect Dosage- 10mcg/min (0.6ml/hr) increase by 10mcg/min every 5-10 min to achieve optimal effect b. Nitroglycerin useful only if cardiogenic shock accompanied by in appropriately high preload. Dosage-10mcg/min 6ml/hr increase by 10mcg/min every 5-10 min to achieve optimal effect.


30 Intra Aortic Balloon counter pulsation
Indications Cardiogenic shock not responding promptly to pharmacologic therapy Right ventricular infarction with shock not responding to volume infusion. Refractory post infraction angina for stabilization before and during angiography. Use as bridge to the surgical correction of mechanical complication of acute myocardial infarction. Intractable recurrent tachycardia accompanied by hemodynamic compromise. IABP can enhance diastolic coronary artery blood flow thus reducing ischemia to ‘Stunned’ myocardium

31 Thrombolytics In one small uncontrolled study of 8 patients, if BP could first be raised with vasopressors subsequent in fusion of t-PA was effective (CanJ Cardial 1995;11:30-6) Reasonable to try unless contra- indications exist and if angioplasty is not available.

32 Identify correctable causes of cardiogenic shock Approx 8% of pts
Identify correctable causes of cardiogenic shock Approx 8% of pts. With cardiogenic shock will have surgically correctable cause, usually MR or vs rupture (circulation 1995;91:873-81) Acute mitral regurgitation (J Am loll cardiol 1986;8:558) Ventricular Aneurysm (NEJM 1984;311:1001-6) Acute VSD (Chest 1989; 95:292-98) Ruptured ventricle (Chest 1987; 92: )

33 Role of Interventional Cardiac Catheterization
Coronary angiography should be considered in all patients in cardiogenic shock after myocardial infarction Results of the shock study (should we emergently revascularize Occluded Coronary for cardiogenic shock) indicated that patients who underwent emergent coronary revascularization with either PTCA or CABG had improved 1 – year survival compared to patients who unwent thrombolysis and/or intra-aorticballoon counterpulsation (46.7% surviva versus 33.6% survival) (JAMA 2001;285:190-2)

34 Indications for Emergent Surgical Intervention In patients with cardiogenic shock.
Papillary muscle rupture Acute ventricular septal defect LV aneurysm with pump failure Intractable ventricular tachycardia Pump failure with cardiogenic shock (angioplasty usually attempted first)

35 The special case of right ventricular infarction 1. Pathogenesis:
Usually right coronary artery occlusion More frequent interior infarctions 2. Exam may reveal: Hypotension Clear lungs Elevated jugular venous pressure Kussmaul’s sign (jugular venous distension with inspiration

36 4. Frequent EKG findings:
3. Hemodynamics: Right atrial pressure>10 mm Right atrial pressure within 5 mm of PCWP 4. Frequent EKG findings: RBBB Complete heart block 1 mm ST elevation in lead V4R (very specific)

37 5. Treatment: IV volume loading with saline
Avoid nitrates, morphine, and diuretics Correct arrythmias Dobutamine if shock persists IABP Vasodilators Consider angioplasty (or thrombolysis if angioplasty not immediately available)

38 Management of Extracardiac Obstructive shock
Pulmonary Embolus Thrombolytics Pericardial Tamponade Intravenous fluids Pericardiocentesis Pneumothorax Chest tube Pulmonary hypertension Vasodilators

39 OLIGEMIC SHOCK In a 70kg adult male
Class1: ml(10-15%)BV loss; no cinical features Class2: ml(15-30%)BV loss; postural hypotension Class3: ml(30-40%)BV loss; hypotesion,tachycardia Class4: >2000ml(40%)BV loss;severe shock

40 Managementof oligemic shock
Operative control of blood loss is the major consideration in patients with continuing hemorrhage Passive leg raising to increase central blood volume during resucitation

41 Management of oligemic shock (Crit care 2004; 8:373-81)
Protect/ensure patent airway and provide ventilation if necessary Establish Adequate Venous Access Flow dependent on catheter diameter plus catheter length Flow through a small (2 inch) wide bore (16 gauge) peripheral IV is far better than through a central line port optimally, place 2 wide bore peripheral IVs

42 Volume replacement 1. Solutions: Saline (140 mEq Na, 140 mEq Cl)
Lactated Ringer’s solution (130 nEg Na, 4mEq k, 10g mEq cl, 28mEq lactate) Albumin Dextran Hydorxyethyl starch Packed red blood cell 2. Volume expansion equivalents: 6 liters D5W = 2 liters saline/Ringer’s =1 liter albumin = 1 unit PRBCs

43 SEPSIS Clinical syndrome with infection along with two criteria of systemic inflammatory response markers of inflammation: changes in temperature(>38 ̊c<36̊c),tachycardia(>90 per minute) , tachypnea (>20 per minute) changes in wbc count in peripheral bld (<4000or>12000cells per µL ,or immature forms of granulocytes

44 SEPTIC SHOCK Severe sepsis is diagnosed by presence of tissue hypoperfusion (elevated lactate or altered mental status), arterial hypotension or other organ dysfunction due to systemic manifestations of infection. Once BP remains low, despite adequate fluid resucitation, progression of sepsis to shock

45 Management of septic shock
Pathophysiology of sepsis: 1. Invasive factors Endotoxins (lipopolysaccharide; LPS) Exotoxins Other microbial antigens 2. Host factors Tumor necrosis factor – many pro-inflammatory effects Interleukin-1 – many pro-inflammatory effects Interleukin -8 – neutrophil recruitment Complement – many pro-inflammatory effects Platelet activating factor – many pro-inflammatory effects Endorphins – myocardial depression Nitric oxide (endothelium-derived) – vasodilator Histamine-vasodilation

46 i. Atrial natriuretic factors – vasodilation
Catecholamines – variable Serotonin – vasodilation Prostacyclin – vasodilation Thomboxane A2 – vasoconstriction Angiotensin – vasoconstriction Vasopressin - vasoconstriction Kinins – vasodilation Genetics: TNF2 polymorphism is associated with an increase in the risk of death from septic shock

47 B. Pathophysiology of Multiple Organ Dysfunction Syndrome
Changes in oxygen uptake – oxygen delivery curves Altered blood flow distribution & shunt Endothelial injury Mitochondrial dysfunction

48 C. Clinical Findings Temperature Hemodynamic changes
Early: normal BP, low SVR, increased CO Intermediate: low BP, normal SVR, low Co Late: very low BP, normal SVR, low CO

49 Early : respiratory alkalosis
ABG Changes Early : respiratory alkalosis Intermediate: respiratory alkalosis + metabolic acidosis Late: metabolic acidosis

50 4.Adult respiratory distress syndrome (ARDS)
Vascular “leak” Exudative pulmonary edema Alveolar neutrophil accumulation Microatelectasis Shunt physiology

51 5. Acute tubular necrosis 6. Hematologic mainfestations
WBC vacuolization Eosinopenia Thrombocytopenia DIC 7. Neurologic manifestations

52 8.Gastrointestinal manifestations
Cholestatic jaundice (bilirubin usually<10; mostly direct Stress ulcers 1-2 mm erosions of stomach & sometimes duodenum 9. Cutaneous manifestation 10. Metabolic manifestation Hypocalcemia Lactic acidosis Hyper – or hypo-glycemia

53 Evidence based Surviving sepsis
Definitions: Grades of Evidence 1 Large, randomized trials with clear-cut results; low risk of false-positive (alpha) error or false-negative (beta) error II Small, randomized trials with uncertain results; moderate-to-high risk or false-positive (alpha) and/or false-negative (beta) error III Nonrandomized, contemporaneous controls IV Nonrandomized, historical controls and expert opinion V Case series, uncontrolled studies, and expert opinion

54 Grades of Recommendation
A Supported by at least two level I investigations B Supported by one level I investigation C Supported by level II investigations only D Supported by at least one level III investigation E Supported by level IV or V evidence

55 Sepsis survival campaign 2008
Initial Resuscitation as soon as the syndrome is recognized Central venous pressure: 8-12 mm Hg Mean arterial pressure >65 mm Hg Urine output >0.5 mL/kg/hr Central venous (superior vena cava) or mixed venous oxygen saturation >70%Grade of Recommendation B If not achieved with fluid,transfuse packed red blood cells to achieve a hematocrit of >30% and/or administer a dobutamine infusion (up to a maximum of 20 micrograms/kg/minGrade of Recommendation: B

56 Diagnosis Appropriate cultures at least two blood cultures with at least one drawn percutaneously and one drawn through each vascular access device, unless the device was recently (<48 hrs) inserted. Cultures before antibiotic therapy .Grade of Recommendation: D Diagnostic studies to determine the source of the infection and the causative organism. Imaging studies and sampling of likely sources of infection should be performed. Grade of Recommendation: E

57 Antibiotic Therapy within the first hour of recognition of severe sepsis.Grade of Recommendation: E The choice of drugs- susceptibility patterns of microorganisms in the community and in the hospital.Grade of Recommendation: D reassessed after hrs on the basis of microbiological; prevent the development of resistance, to reduce toxicity, and to reduce costs. Once a causative pathogen is identified, monotherapy for 7-10 days and guided by clinical response.Grade of Recommendation: E Some experts prefer combination therapy for patients with Pseudomonas infection and neutropenic patients

58 Vasopressors When an appropriate fluid challenge fails to restore adequate blood pressure and organ perfusion.Grade of Recommendation: E Either norepinephrine or dopamine first-choice Grade of Recommendation: D Low-dose dopamine should not be used for renal protection as part of the treatment of severe sepsis.Grade of Recommendation: B All patients requiring vasopressors should have an arterial catheter placed as soon as practical.Grade of Recommendation: E Vasopressin use may be considered in patients with refractory shock despite adequate fluid resuscitation and high-dose conventional vasopressors. If used in adults, it should be administered at infusion rates of units/min.Grade of Recommendation: E

59 Inotropic Therapy In patients with low cardiac output despite adequate fluid resuscitation, dobutamine to increase cardiac output. If used in the presence of low blood pressure, it should be combined with vasopressor therapy.Grade of Recommendation: E A strategy of increasing cardiac index to achieve an arbitrarily predefined elevated level is not recommended.Grade of Recommendation: A

60 Steroids IVcorticosteroids (hydrocortisone mg/day, for 7 days in three or four divided doses or by continuous infusion) who, despite adequate fluid replacement, require vasopressor therapy to maintain adequate blood pressure.Grade of Recommendation: C Some experts 250-microgram ACTH stimulation test to identify responders (>9 micrograms/dL increase in cortisol mins post-ACTH administration) and discontinue therapy in these patients. Clinicians should not wait for ACTH stimulation results to administer corticosteroids.Grade of Recommendation: E Some experts decrease dosage of steroids after resolution of septic shock.Grade of Recommendation: E Some experts consider tapering the dose of corticosteroids at the end of therapy.Grade of Recommendation: E Some experts add fludrocortisone (50 micrograms orally four times per day) to this regimen.Grade of Recommendation: E

61 Doses of corticosteroids >300 mg hydrocortisone not to be used
Doses of corticosteroids >300 mg hydrocortisone not to be used.Grade of Recommendation: A In the absence of shock, corticosteroids should not be administered for the treatment of sepsis. There is, however, no contraindication to continuing maintenance steroid therapy or to using stress dose steroids if the patient’s history of corticosteroid administration or the patient’s endocrine history warrants.Grade of Recommendation: E

62 Recombinant Human Activated Protein C (rhAPC)
rhAPC is recommended in patients at high risk of death (Acute Physiology and Chronic Health Evaluation II >25, sepsis-induced multiple organ failure, septic shock, or sepsis-induced acute respiratory distress syndrome [ARDS]) no absolute contraindication related to bleeding risk or relative contraindication that outweighs the potential benefit of rhAPC.Grade of Recommendation: B

63 Blood Product Administration
RBC transfusion if Hb <7.0 g/dL (<70 g/L) ; target g/dL.Grade of Recommendation: B Erythropoietin only accepted reasons for administration of erythropoietin such as renal failure induced anemiaGrade of Recommendation: B No Routine use of fresh frozen plasma to correct laboratory clotting abnormalities.Grade of Recommendation: E Antithrombin administration not recommended.Grade of Recommendation: B Platelets administered <5,000/mm3 (5 x 109/L) regardless of apparent bleeding. Platelet transfusion when counts are 5,000-30,000/mm3 (5-30 x 109/L) if there is a significant risk of bleeding. Higher platelet counts (>50,000/mm3 [50 x 109/L])for surgery or invasive procedures.Grade of Recommendation: E

64 Mechanical Ventilation of Sepsis-Induced Acute Lung Injury (ALI)/ARDS
High tidal volumes with high plateau pressures avoided in ALI/ARDS. reduction in tidal volumes over 1-2 hrs to a "low" tidal volume (6 mL per kilogram of predicted body weight) as a goal in conjunction with the goal of maintaining end-inspiratory plateau pressures <30 cm H2O.Grade of Recommendation: B Hypercapnia (allowing PaCO2 to increase above normal, so-called permissive hypercapnia) if required to minimize plateau pressures and tidal volumes.Grade of Recommendation: C

65 positive end-expiratory pressure to prevent lung collapse at end-expiration.Grade of Recommendation: E In facilities with experience, prone position for ARDS requiring potentially injurious levels of FIO2.Grade of Recommendation: E Unless contraindicated, mechanically ventilated patients should be maintained semirecumbent, with the head of the bed raised to 45 degrees to prevent the development of ventilator-associated pneumonia.Grade of Recommendation: C

66 A weaning protocol mechanically ventilated patients should undergo a spontaneous breathing trial when a) arousable; b) hemodynamically stable (without vasopressor agents); c) no new potentially serious conditions; d) low ventilatory and end-expiratory pressure requirements; and e) requiring levels of FIO2 that could be safely delivered with a face mask or nasal cannula. If the spontaneous breathing trial is successful, consider extubation. Spontaneous breathing trial options include a low level of pressure support with continuous positive airway pressure 5 cm H2O or a T-piece.

67 Sedation, Analgesia, and Neuromuscular Blockade in Sepsis
Protocols should be used when sedation of critically ill mechanically ventilated patients is required.Grade of Recommendation: B Either intermittent bolus sedation or continuous infusion sedation to predetermined end points (e.g., sedation scales) with daily interruption/lightening of continuous infusion sedation with awakening and retitration.Grade of Recommendation: B Neuromuscular blockers should be avoided ( risk of prolonged neuromuscular blockade following discontinuation).Grade of Recommendation: E

68 Renal Replacement Bicarbonate Therapy
In acute renal failure, and in the absence of hemodynamic instability, continuous venovenous hemofiltration and intermittent hemodialysis are considered equivalent.Grade of Recommendation: B Bicarbonate Therapy Bicarbonate therapy is not recommended for treatment of hypoperfusion-induced lactic acidemia with pH >7.15.Grade of Recommendation: C

69 Deep Vein Thrombosis Prophylaxis
: A low-dose unfractionated heparin or low-molecular weight heparin. mechanical prophylactic device (graduated compression stockings or intermittent compression device) contraindication for heparin use (i.e., thrombocytopenia, severe coagulopathy, active bleeding, recent intracerebral hemorrhage), the use of a of peripheral vascular disease). In very high-risk patients such as those who have severe sepsis and history of deep vein thrombosis, a combination of both.Grade of Recommendation Stress Ulcer Prophylaxis H2 receptor inhibitors more efficacious than sucralfate and are the preferred agents. Proton pump inhibitors have not been assessed in a direct comparison with H2 receptor antagonists.Grade of Recommendation: A

70 Management of anaphylactic shock
Generally a clinical diagnosis The offending agent can often be difficult to identify (eg. Latex, metabisulfites, food allergy, etc) and sometimes seemingly benign drugs can be responsible (diphenhydramine, steroid creams, oral steroids, lidocaine, etc.) Seurm tryptase may be useful in difficult diagnostic cases but is not immediately available in many laboratories - this may be primarily useful in autopsy cases and when serum can be saved for later determination of the cause of shock (J Clin Immunol 1994;14: )

71 Initial Therapy Maintain Adequate Ventilation Stop absorption
Oxygen Establish an airway if needed Stop absorption Epinephrine This remains the most important pharmacological management of anaphylaxis (J All Clin Innunol, 1994; 94:666-8) 0.3 – 0.5 mg IV or SQ Use 0.3 – 0.5 ml of 1:1,000 dilution SQ Use 3 – 5 ml of 1:10,000 dilution IV Inhaled beta-agonists Establish Adequate Venous Access

72 Secondary Therapy Antihistamines (H1 & H2 blockers)
25-50mg hydroxyzine or diphenhydramine Q6 hours Cimetidine 300mg every 8-12 hours Corticosteroids (may shorten protracted reactions but do not provide immediate benefit) 250 mg hydrocortisone Q6 hours IV Aminophylline (probably not as useful as inhaled b-agonists) Load with 6 mg/kg/hr IV Maintain with 0.3 – 0.6 mg/kg/hr IV Observation in the hospital for at least 24 hours (for relapse) Glucagon (1 mg IV) can be useful in patients which anaphylactic shock on beta-blockers as these patients may be resistent to epinephrine

73 Shock in Children Small blood volume Increased hypovolemia risk
Very efficient compensatory mechanisms Failure may cause “sudden” shock Pallor, altered LOC, cool skin = shock UPO Avoid massive fluid infusion Use 20 cc/kg boluses High surface to volume ratio Increased hypothermia risk

74 Severity of Hemorrhage
Comparison of Adult vs Child

75 Shock in the Elderly Poor cardiovascular condition
Rapid decompensation Sepsis more likely Hypoperfusion can cause: CVA AMI Seizures Bowel Infarctions Renal failure

76 Shock in the Elderly Assessment more difficult
Peripheral vascular disease Weak pulses Altered sensorium Hypertension masking hypoperfusion Beta-blockers masking hypoperfusion Fluid infusion may produce volume overload/CHF

77 Shock in OB Patients Pulse increases 10 to 15 bpm
BP lower than in non-pregnant patient Blood volume increased by 45% Slower onset of shock signs/ symptoms Fluid resuscitation requires greater volume

78 Shock in OB Patients Oxygen requirement increased 10 to 20%
Pregnant uterus may compress vena cava, decreasing venous return to heart Place women in late-term pregnancy on left-side Fetus can be in trouble even though mother looks well-perfused

79 Thank you

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