aicu c-10(shock)
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PROPERTIESAllow user to leave interaction: AnytimeShow ‘Next Slide’ Button: Show alwaysCompletion Button Label: View Presentation
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Section of Critical Care MedicineSection of Infectious Diseases
University of Manitoba, Winnipeg, CanadaUMDNJ-Robert Wood Johnson Medical School
Cooper Hospital, NJ
Anand Kumar, MD
SHOCKClassification and Approach
to Management
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Slide 3
Shock
• Cardiogenic Shock -a major component of the mortality associated with cardiovascular disease
• Hypovolemic Shock -the major contributor to early mortality from trauma
• Septic Shock -most common cause of death in American ICUs
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Slide 4
Definition
• Kumar and Parrillo (1995): “the state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then if prolonged, to irreversible cellular injury”
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Shock: Classification
• Hypovolemic Shock -due to decreased circulating blood volume
• Cardiogenic Shock -due to cardiac pump failure related to loss of myocardial contractility/functional myocardium or structural/mechanical failure
• Extra-cardiac Obstructive Shock -due to obstruction to flow in the cardiovascular circuit
• Distributive Shock -caused by loss of vasomotor control
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Shock Hemodynamics
CO SVR PWP EDV
hypovolemic
cardiogenic
obstructive
afterloadpreload
distributive
pre-resuscpost-resusc
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Classification of ShockHypovolemic Cardiogenic Extracardiac Obstructive Distributive
(e.g. Hemorrhage)
Preload
Diastolic filling
(e.g. Myocardial infarction)
Myocardial damage
Systolic and diastolicfunction
Diastolic filling(e.g. tension
pneumothoraxor pericardial tamponade)
Diastolic function Systolic function
Ventricular afterload(e.g. massive pulmonary
embolus) Preload
( Diastolic filling)
( Systolic andDiastolic function)
(e.g. septic)
Myocardialdepression
CO( SVR)
MAP
Shock
MODS
Maldistributionof flow
SVR( CO)
CO = cardiac output; SVR = systemic vascular resistance; MAP = mean arterial blood pressure; MODS = multiple organ dysfunction syndrome.
Kumar and Parrillo, 2001
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Hypovolemic Shock
• degree of volume loss response
– 10% well tolerated (tachycardia)
– 20-25% failure of compensatory mechanisms (hypotension, orthostasis, decreased CO)
– >40% loss associated with overt shock (marked hypotension, decreased CO, lactic acidemia)
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Hypovolemic Shock
• rate of volume loss and pre-existing cardiac reserve response
• acute 1 L blood loss results in mild to moderate hypotension with decreased CVP and PWP
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Cardiogenic Shock
• #1 cause of in-hospital mortality from Q-wave MI
• requires at least 40% loss of functional myocardium
• usually involves left main or left anterior descending obstruction
• historically, incidence of cardiogenic shock post-Q wave MI has run 8-20%with mortality 70-90%
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Cardiogenic Shock
• mortality substantially better for cardiogenic shock due to surgically remediable lesions
– aortic valve failure
– papillary muscle rupture • ischemic form seen 3-7 days post-LAD territory infarct • v wave of > 10 mm often seen in PWP trace
– VSD (post-infarct, rarely traumatic)• post-infarct seen 3-7 days post-LAD occlusion• 5-10% oxygen saturation step-up
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Slide 12
Obstructive Shock
• rate of development of obstruction to blood flow response
– acute, massive PE involving 2 or more lobar arteries and 40-50% pulmonary bed can cause shock
– acute cardiac tamponade can occur with 150 mL fluid but over 2L can be well tolerated if slow accumulation
• similar variability based on presence of pre-existing cardiopulmonary disease
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Slide 13
Distributive Shock
• defining feature: loss of peripheral resistance
• dominantly septic shock, anaphylactic and neurogenic shock less common
• clinical form of shock with greatest contribution of other shock elements i.e., hypovolemia, cardiac failure
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Slide 14
Compensatory Responses to Shock
• Maintain mean circulatory pressure
• Volume
– Fluid redistribution to vascular space
– Decrease Renal losses
• Pressure
– Decreased venous capacitance
Kumar and Parrillo, 2001
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Compensatory Responses to Shock
• Maximize cardiac performance
• Increase contractility
• Redistribute perfusion
• Optimize oxygen unloading
Kumar and Parrillo, 2001
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Slide 16
hypovolemia
intravascularvolume
sepsis
venouscapacitance
venous pressure
myocardial dysfunction (e.g. MI)cardiovascular obstruction (e.g. massive PE)
renal perfusion
stretch receptorsright atrialpulmonary artery
renal juxtaglomerular apparatus
cardiac contractility vasoconstriction flow redistribution
sympathetic responsehormonal
epinepherinenorepinephrinerenin/angiotensinaldosterone
Na/H2O retention cardiac contractility vasoconstriction flow redistribution
cardiovascular stresscirculatory shock ( MAP)
baroreceptorsaortic arch, carotid body
vascular chemoreceptorscarotid, aortamedullary
chemoreceptorCNS pituitary response
neural ACTH/ADH
cortisolaldosterone
Na retentionmaintain cardiovascular catecholamine responsiveness
Kumar and Parrillo, 2001
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ORGAN SYSTEM DYSFUNCTION
CNS Encephalopathy (ischemic or septic)Cortical necrosis
Heart Tachycardia, bradycardiaSupraventricular tachycardiaVentricular ectopyMyocardial ischemiaMyocardial depression
Pulmonary Acute respiratory failureAdult respiratory distress syndrome (ARDS)
Kidney Prerenal failureAcute tubular necrosis
GI IleusErosive gastritisPancreatitisAcalculous cholecystitisColonic submucosal hemorrhageTransluminal translocation of acteria/endotoxin
ORGAN SYSTEM MANIFESTATIONS
Kumar and Parrillo, 2001
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Organ System Dysfunction
Liver Ischemic hepatitis“Shock” liverIntrahepatic cholestasis
Hematologic Disseminated intravascular coagulationDilutional thrombocytopenia
Metabolic HyperglycemiaGlycogenolysisGluconeogenesisHypoglycemia (late)Hypertriglyceridemia
Immune System Gut barrier function depressionCellular immune depressionHumoral immune depression
ORGAN SYSTEM MANIFESTATIONS
Kumar and Parrillo, 2001
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Slide 19
Shock Suspected
• Hypotension• Tachycardia• Peripheral hypoperfusion• Oliguria• Encephalopathy
DIAGNOSTICTHERAPEUTIC
Clinical Approach to Diagnosis and Management
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Slide 20
Diagnosis and Evaluation
• Clinical Signs
– primary diagnosis
– differential Dx
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Slide 21
Diagnosis and Evaluation
• Laboratory
– Hgb, WBC, platelets
– PT/PTT
– Electrolytes, arterial blood gases
– BUN, Cr
– Ca, Mg
– serum lactate
– ECG
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Clinical Approach to Diagnosis and Management
• Initial Diagnostic Steps
• CXR
• abdominal views*
• CT scan abdomen or chest*
• echocardiogram*
• pulmonary perfusion scan*
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Slide 23
Diagnosis and Evaluation
• Invasive Monitoring
– arterial pressure catheter
– CVP monitoring
– ScvO2
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Clinical Approach to Diagnosis and Management
• Admit to Intensive Care Unit (ICU)
• Venous access
• Central venous catheter
• Arterial catheter
• EKG monitoring
• Pulse oximetry
• Hemodynamic support (MAP <60 mmHg)
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Clinical Approach to Diagnosis and Management
• Diagnosis Remains Undefined or Hemodynamic Status Requires Repeated Fluid Challenges of Vasopressors
• Pulmonary Artery Catheterization
• Echocardiography
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Diagnosis Using Pulmonary Artery Catheterization
Pulmonary Artery Cardiac Miscellaneous Diagnosis Occlusion Pressure Output Comments Cardiogenic Shock
Cardiogenic shock Usually occurs with due to myocardial evidence of extensive dysfunction myocardial infarction (40% of LV infarcted),
severe cardiomyopathy, or myocarditis.
Cardiogenic shock due to a mechanical defect
Acute VSD LVCO Predominant shunt is and RVCO left to right, pulmonary
>LVCO blood flow is greaterthan systemic bloodflow: oxygen “step-up”occurs at RV level.
Kumar and Parrillo, 2001
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Diagnosis Using Pulmonary Artery Catheterization
Pulmonary Artery Cardiac Miscellaneous Diagnosis Occlusion Pressure Output Comments Cardiogenic Shock Acute mitral Forward V waves in pulmonary
regurgitation CO artery occlusion pressure tracing.
Right ventricular Normal or Elevated RA and RVfilling infarction
pressures with low or normal pulmonary artery occlusion pressures.
Extracardiac obstructive forms of shock
Pericardial or RA mean, RV end- tamponade diastolic, pulmonary artery occlusion mean
pressures are elevated and within 5 mmHg of one another.
Kumar and Parrillo, 2001
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Diagnosis Using Pulmonary Artery Catheterization
Pulmonary Artery Cardiac Miscellaneous
Diagnosis Occlusion Pressure Output Comments Extracardiac obstructive forms of shock
Massive pulmonary Normal or Usual finding is embolism elevated right-sided
pressures.
Hypovolemic shock Distributive forms of shock
Septic shock or normal or normal, Pre-resuscitation rarely cardiac output
isAnaphylactic or normal or normal decreased shock
Kumar and Parrillo, 2001
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Clinical Approach to Diagnosis and ManagementImmediate Goals in Shock
Hemodynamic support MAP >60mmHg PAOP = 12-18 mmHg Cardiac Index >2.2 L/min/m2
Maintain oxygen delivery Hemoglobin >9 g/dL Arterial saturation >92%
Supplemental oxygen and mechanical ventilation
Reversal of oxygen dysfunction Decreasing lactate (<2.2 mM/L) Maintain urine output Reverse encephalopathy Improving renal, liver function tests
MAP = mean arterial pressure; PAOP = pulmonary artery occlusion pressure.
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Clinical Approach to Diagnosis and Management
• Hypovolemic Shock
• Rapid replacement of blood, colloid orcrystalloid
• Identify source of blood or fluid loss
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Slide 31
Clinical Approach to Diagnosis and Management
• Cardiogenic Shock
• RV infarction
– fluid and inotropes with PA catheter monitoring
• Mechanical abnormality
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Slide 32
Results of Current Therapy
Inotropic support 90
+ Thrombolysis 80-90
+ IABP 80
+ CABG 50-60
+ PTCA if successful 50-60
if unsuccessful 80-90
Treatment In-hospital Strategy Mortality Rate (%)
From Klein L. W.: Intra-aortic balloon pumping. In Parrillo J.E., Bone R.C. (eds), Critical Care Medicine: Principles of diagnosis and management, St. Louis, 1995: Mosby.
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Slide 33
Clinical Approach to Diagnosis and Management
• Extracardiac Obstructive Shock
• Pericardial tamponade
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Slide 34
Courtesy of David Hunter, MDUniversity of Minnesota
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Slide 35
Clinical Approach to Diagnosis and Management
• Distributive Shock
• Septic shock - Identify site of infection and drain, if possible
• Goals:
– SV02 >70%
– improving organ function
– decreasing lactate levels
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Slide 36
Fluid Therapy
• Crystalloids
• Colloids
• Packed red blood cells
• Infuse to physiologic endpoints
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Slide 37
Relative Potency: Vasopressors/Inotropes
CARDIAC PERIPHERAL VASCULAR
Agent Dose Heart Contractility Vasoconstriction Vasodilation Dopaminergic Rate Dopamine 1-4 (/k)/min 1+ 1+ 0 1+ 4+
4-20 (g/kg)/min 2+ 2-3+ 2-3+ 0 2+
Norepi 2-20 g/min 1+ 2+ 4+ 0 0
Dobutamine 2-15 (g/kg)/min 1-2+ 3-4+ 0 2+ 0
Isoproterenol 1-5 g/min 4+ 4+ 0 4+ 0
Epinephrine 1-20 g/min 4+ 4+ 4+ 3+ 0
Phenylephrine 20-200 g/min 0 0 3+ 0 0
Vasopressin 0.01-0.04 u/min 0 0 4+ 0 0
Milrinone 37.5-75 g/kg 1+ 3+ 0 2+ 0bolus; then 0.375-0.75 ug/kg/min
Kumar and Parrillo, 2001
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Slide 38
Conclusion
• This concludes the presentation.