schwartz: shock
DESCRIPTION
surgeryschwartzshockTRANSCRIPT
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SHOCKDr. Jovelyn Tan, M.D.Chong Hua Hospital
Department of Surgery
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GENERAL OBJECTIVE
To understand the pathophysiology and diagnosis of shock as well as the priorities for their management
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SPECIFIC OBJECTIVES
To understand the pathophysiology of shock and ischemia–reperfusion injury
To know the different patterns of shock and the principles and priorities of resuscitation
To know the appropriate monitoring and endpoints of resuscitation
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OUTLINE
I. Definition of TermsII. Pathophysiology of shockIII. Ischemia–reperfusion injuryIV. Classification of ShockV. Natural History of ShockVI. Management PrinciplesVII.Monitoring EndpointsVIII.Management Issues
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Shock:“A momentary pause in the act of
death.”
-John Collins Warren, 1800s
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DEFINITION
SHOCK:
inadequate organ perfusion to meet the tissue’s oxygenation demand
inadequate removal of cellular waste products
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PATHOPHYSIOLOGY
ATP + H2O ADP + Pi + H+ + Energy
Acidosis results from the accumulation of acid when during anaerobic metabolism the creation of ATP
from ADP is slowed.
H+ shift extracellularly and metabolic acidosis develops
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ISCHEMIA–REPERFUSION SYNDROME
• Direct effects of tissue hypoxia and local activation of inflammation
• Acid and potassium load lead to direct myocardial depression, vascular dilatation and further hypotension
• Cellular and humoral elements flushed back into the circulation cause further endothelial injury
• Attenuated by reducing the extent and duration of tissue hypoperfusion
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DIAGNOSTIC CRITERIA FOR SIGNIFICANT ORGAN DYSFUNCTION
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BLALOCK CLASSIFICATION
• Hypovolemic Shock– loss of circulating blood volume
• Vasogenic Shock– ↓ resistance w/in capacitance vessels
• Neurogenic Shock– acute loss of sympathetic vascular tone
• Cardiogenic Shock– failure of the heart as a pump
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CLINICAL CLASSIFICATION• Hypovolemic Shock• Distributive (Vasodilatory) Shock
– Septic – Neurogenic– Anaphylactic– Adrenergic
• Cardiogenic Shock– Intrinsic– Compressive
• Obstructive Shock• Traumatic Shock
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STAGES/SPECTRUM OF SHOCK
• “Preshock” aka compensated/warm shock– Up to ~10% reduction in blood volume– Tachycardia
• “Shock”– Compensatory mechanisms overwhelmed– ~20-25% reduction in blood volume
• “End-organ dysfunction”– Leads to irreversible organ damage/death
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VICIOUS CYCLE OF SHOCK
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THE TRIAD OF DEATH
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CLINICAL FEATURES
Compensated Mild Moderate SevereLactic Acidosis + ++ ++ +++Urine Output Normal Normal Reduced AnuricLevel of Consciousness
Normal Mild Anxiety Drowsy Comatose
Respiratory Rate
Normal Increased Increased Laboured
Pulse Rate Mildly Increased
Increased Increased Increased
Blood Pressure
Normal Normal Mild Hypotension
Severe Hypotension
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HYPOVOLEMIC SHOCK
With total body fluid depletion
Hemorrhage Gastrointestinal tract
losses Renal losses Skin losses Open wound losses Burns
Without total body fluid depletion
Redistribution of the intravascular fluid to the interstitial or intracellular space
Decreased preload due to increased intravascular capacity (Distributive shock)
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Acute blood loss⇓
Decreased baroreceptor stimulation⇓
Decreased inhibition of vasoconstrictor centersDiminished output (Atrial Stretch Receptors)
⇓Increase vasoconstriction & Peripheral arterial resistance
Hypovolemia ⇨ Sympathetic stimulation
HYPOVOLEMIC SHOCK
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HYPOVOLEMIC SHOCK
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HYPOVOLEMIC SHOCK
Treatment:1. Secure the airway2. Control the source of blood loss3. Intravenous volume resuscitation
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CARDIOGENIC SHOCK
Acute MI Pump failure Mechanical complications
• Acute mitral regurgitation from papillary muscle rupture
• Ventricular septal defect• Free-wall rupture• Pericardial tamponade• Right ventricular
infarction
Other causes End-stage cardiomyopathy Myocarditis Severe myocardial
contusion Prolonged cardiopulmonary
bypass Septic shock with severe
myocardial depression Left ventricular outflow
obstruction Obstruction to left
ventricular filling Acute mitral regurgitation Acute aortic insufficiency
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Circulatory pump failure ⇒ diminished forward flow and subsequent tissue hypoxia
Hemodynamic criteria: sustained hypotensionreduced cardiac indexelevated pulmonary artery wedge pressure
50-80% mortality Myocardial Infarction – most common cause
Myocardial ischemia ⇒ myocardial dysfunction ⇒ ↑myocardial ischemia
CARDIOGENIC SHOCK
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Diagnosis:Signs: hypotension, cool and mottled skin, depressed
mental status, tachycardia, diminished pulsesDiagnostics:
ECG Echocardiography CXR ABG Electrolytes CBC Cardiac enzymes
Invasive Cardiac Monitoring – excludes right ventricular infarction, hypovolemia, & possible mechanical
complications
CARDIOGENIC SHOCK
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Treatment: 1. Maintenance of adequate oxygen 2. Fluid administration
Correct electrolyte imbalancePain managementAnti-arrhythmic drugs, pacing or cardioversion Inotropic Support
• improve cardiac contractility & cardiac output Intra-Aortic Balloon Pump
• Increases cardiac output & improves coronary blood flowPercutaneous Transluminal Coronary Angiography
• treatment of choice (cardiogenic shock from AMI)
CARDIOGENIC SHOCK
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VASODILATORY SHOCK
Systemic response to infection
Noninfectious systemic inflammation • Pancreatitis • Burns
Anaphylaxis Acute adrenal
insufficiency
Prolonged, severe hypotension• Hemorrhagic shock• Cardiogenic shock• Cardiopulmonary bypass
Metabolic• Hypoxic lactic acidosis • Carbon monoxide
poisoning
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Failure of the vascular smooth muscle to constrict Characterized by:
• Peripheral vasodilatation with resultant hypotension• Resistance to treatment with vasopressors
Final common pathway for profound and prolonged shock 30- 50% mortality Findings: Enhanced cardiac output
Peripheral vasodilation Fever Leukocytosis Hyperglycemia Tachycardia
iNOS ⇒ vasodilatory effects
VASODILATORY SHOCK
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Diagnosis:• Sepsis – evidence of an infection & systemic signs of
inflammation• Severe Sepsis – hypoperfusion with signs of organ
dysfunction• Septic Shock – severe sepsis with more significant
evidence of tissue hypoperfusion & systemic hypotension
Manifestations: • Fever• Tachycardia & Tachypnea• Signs of Hypoperfusion (Confusion, Malaise, Oliguria, Hypotension)
SEPTIC SHOCK
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REVISED DIAGNOSTIC CRITERIA FOR SEPSIS
General Variables
Fever [core temp >38.3°C (100.9°F)]
Hypothermia [core temp <36°C (96.8°F)]
Heart rate >90 bpm or > 2 SD above the normal value for age
Tachypnea
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REVISED DIAGNOSTIC CRITERIA FOR SEPSIS
General Variables
Altered mental status
Significant edema or positive fluid balance (>20 mL/kg over 24 h)
Hyperglycemia (plasma glucose > 120 mg/dL or 7.7 mmol/L) in the absence of diabetes
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REVISED DIAGNOSTIC CRITERIA FOR SEPSIS
Inflammatory variables Leukocytosis (WBC >12,000 cells/µL)
Leukopenia (WBC <4000 cells/µL)
Bandemia (>10% immature band forms)
Plasma C-reactive protein > 2 SD above normal value
Plasma procalcitonin >2 SD above normal value
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REVISED DIAGNOSTIC CRITERIA FOR SEPSIS
Hemodynamic variables
Arterial hypotension (SBP <90 mmHg, MAP <70 mmHg, or SBP decrease >40 mmHg in adults or <2 SD below normal for age)
Mixed venous saturation (SVO2) >70% in adults
Cardiac index >3.5 L/min per square meter
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REVISED DIAGNOSTIC CRITERIA FOR SEPSIS
Organ dysfunction variables
Arterial hypoxemia (PaO2/FiO2 < 300
Acute oliguria (urine output < 0.5 mL/kg per hour or 45 mmol/L for at least 2 hours)
Creatinine increase > 0.5 mg/dL
Coagulation abnormalities (INR > 1.5 or aPTT > 60 s)
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REVISED DIAGNOSTIC CRITERIA FOR SEPSIS
Organ dysfunction variables
Ileus
Thrombocytopenia (platelet count < 100,000 cells/µL)
Hyperbilirubinemia (plasma total bilirubin > 4 mg/dL or 70 mmol/L)
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REVISED DIAGNOSTIC CRITERIA FOR SEPSIS
Tissue perfusion variables
Hyperlactatemia (> 1 mmol/L)
Decreased capillary filling or mottling
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Treatment:Fluid resuscitation & restoration of circulatory
volumeAntibioticsVasopressorsIntensive Insulin Therapy Activated Protein CCorticosteroids
SEPTIC SHOCK
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Diminished tissue perfusion from loss of vasomotor tone to peripheral arterial beds
Etiology: Spinal cord injuries Spinal cord neoplasms Spinal epidural/anesthetic
NEUROGENIC SHOCK
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Classic Description: • Decreased blood pressure• Warm extremities• Motor & Sensory deficits• Radiographic evidence of a vertebral column fracture
Management: • BP Control• Oxygenation• Hemodynamics
NEUROGENIC SHOCK
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OBSTRUCTIVE SHOCK Pericardial tamponade Pulmonary embolus Tension pneumothorax IVC obstruction
• Deep venous thrombosis• Gravid uterus on IVC• Neoplasm
Increased intrathoracic pressure• Excess positive end-expiratory pressure• Neoplasm
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Tension Pneumothorax / Cardiac Tamponade
(↑ Intrapleural Pressure) ⇓ (↑ Intrapericardial Pressure)
Reduced filling of the Right side of the Heart
⇓Decreased cardiac output with ↑ central venous
pressure
OBSTRUCTIVE SHOCK
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Diagnosis & Treatment:Classic Findings:
Respiratory distress Diminished breath sounds Hyperresonance
*Beck’s Triad: Hypotension + Muffled heart tones + Neck vein distention
Cardiac tamponade ⇒ Elevated central venous pressure Pulsus paradoxus ↑ right atrial & right ventricular
pressure
OBSTRUCTIVE SHOCK
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Diagnosis & Treatment:Pleural/ Pericardial DecompressionImmediate Tube ThoracostomyEchocardiographyPericardiocentesisDiagnostic Pericardial Window
OBSTRUCTIVE SHOCK
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Systemic response after trauma (soft tissue injury, long bone fractures, & blood loss)
Treatment : • Control of hemorrhage• Adequate volume resuscitation• Debridement• Stabilization of bony injuries• Appropriate treatment of soft tissue injuries
TRAUMATIC SHOCK
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CARDIOVASCULAR AND METABOLIC CHARACTERISTICS OF SHOCK
Hypovolemia Cardiogenic Obstructive Distributive
Cardiac Output ↓ ↓ ↓ ↑
Vascular Resistance ↑ ↑ ↑ ↓
Venous Pressure ↓ ↑ ↑ ↓
Mixed Venous Saturation
↓ ↓ ↓ ↑
Base Deficit ↑ ↑ ↑ ↑
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CORE PRINCIPLES IN MANAGEMENT
Secure Airway Prompt control of active hemorrhage Volume resuscitation
Goal of Treatment: Restoration of adequate organ perfusion & tissue oxygenation
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ASSESSMENT OF ENDPOINTS
Systemic/global• Lactate• Base deficit• Cardiac output• Oxygen delivery and consumption
Tissue-specific• Gastric tonometry• Tissue pH, oxygen, carbon dioxide levels• Near infrared spectroscopy
Cellular• Membrane potential• Adenosine triphosphate (ATP)
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Oxygen TransportSupranormal O2 transport variables
oO2 delivery >600mL/min per sq. meteroCardiac index >4.5L/min per sq. meteroO2 consumption index >170mL/min per sq. meter
Inability to repay O2 debt – predictor of mortality & organ failure
O2 debt correlate with serum lactate and base deficit
ASSESSMENT OF ENDPOINTS
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LactateConversion of pyruvate (lactate dehydrogenase) in the
setting of insufficient oxygenMetabolized by the liver (50%) and kidneys (30%)Indirect measure of oxygen debt
*Base deficit and volume of blood transfusion required- better predictors of mortality
ASSESSMENT OF ENDPOINTS
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Base deficit(ABG) amount of base in millimoles that is required to
titrate 1L of whole blood to a pH of 7.40 with the sample fully saturated with O2 at 37˚C and PaCO2 of 40mm Hg
Mild (3-5)Moderate (6-14)Severe (≥15)
ASSESSMENT OF ENDPOINTS
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Gastric TonometryUsed to assess perfusion of the GITpHi - ≥7.3; ↓ in decreased O2 delivery
- good prognostic indicator
Near Infrared (NIR) SpectroscopyMeasure tissue oxygenation & redox state of
cytochcrome a,a3
ASSESSMENT OF ENDPOINTS
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Tissue pH, O2, & CO2 ConcentrationTissue probes with optical sensors
Right Ventricular End-Diastolic Volume Index (RVEDVI)Correlate with preload-related increases in cardiac outputLVP >320mm Hg L/min per sq meter
ASSESSMENT OF ENDPOINTS
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Crystalloid / Colloid solutionsNo difference in overall mortallity, length of stay, or
incidence of pulmonary edemaMarginal benefit with the infusion of hypertonic
saline (7.5 percent sodium chloride)- Immunomodulatory
CONTROVERSIES ON FLUID RESUSCITATION
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Inherent risks: • Transfusion reactions• Infection• Immunosuppression
Hgb (7.0-9.0 g/dL) & Hct levels (>30%)- appropriate in the treatment of critically-ill patients
BLOOD TRANSFUSION
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Conclusions: Any delay in surgery for control of hemorrhage increases
mortalityWith uncontrolled hemorrhage attempting to achieve
normal BP may increase mortality- SBP goals:
• Penetrating injury: 80- 90 mm Hg• Blunt injury: 110 mm Hg
Profound hemodilution should be avoided by early transfusion of RBC
HYPOTENSIVE RESUSCITATION
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Don’t forget...
-Samuel D. Gross, 1872-
Shock: “rude unhinging of the machinery of life.”
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END…