SHOCK
Dr. Jovelyn Tan, M.D. Chong Hua Hospital Department of Surgery
GENERAL OBJECTIVE
To understand the pathophysiology and diagnosis of shock as well as the priorities for their management
SPECIFIC OBJECTIVES
To understand the pathophysiology of shock and ischemiareperfusion injury
To know the different patterns of shock and the principles and priorities of resuscitation
To know the appropriate monitoring and endpoints of resuscitation
OUTLINE
I. Definition of Terms II. Pathophysiology of shock III. Ischemiareperfusion injury IV. Classification of Shock V. Natural History of Shock VI. Management Principles VII.Monitoring Endpoints VIII.Management Issues
Shock:
A momentary pause in the act of death.
-John Collins Warren, 1800s
DEFINITION
SHOCK:
inadequate organ perfusion to meet the tissues oxygenation demand inadequate removal of cellular waste products
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
ISCHEMIAREPERFUSION 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
DIAGNOSTIC CRITERIA FOR SIGNIFICANT ORGAN DYSFUNCTION
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
CLINICAL CLASSIFICATION
Hypovolemic Shock Distributive (Vasodilatory) Shock
Septic Neurogenic Anaphylactic Adrenergic Intrinsic Compressive
Cardiogenic Shock
Obstructive Shock Traumatic Shock
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
VICIOUS CYCLE OF SHOCK
THE TRIAD OF DEATH
CLINICAL FEATURES
Compensated Lactic Acidosis Urine Output Level of Consciousness Respiratory Rate Pulse Rate Blood Pressure + Normal Normal Normal Mildly Increased Normal Mild ++ Normal Mild Anxiety Increased Increased Normal Moderate ++ Reduced Drowsy Increased Increased Mild Hypotension Severe +++ Anuric Comatose Laboured Increased Severe Hypotension
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)
HYPOVOLEMIC SHOCK
Acute blood loss
Decreased baroreceptor stimulation Decreased inhibition of vasoconstrictor centers Diminished output (Atrial Stretch Receptors) Increase vasoconstriction & Peripheral arterial resistance
Hypovolemia
Sympathetic stimulation
HYPOVOLEMIC SHOCK
HYPOVOLEMIC SHOCK
Treatment:
1. 2. 3. Secure the airway Control the source of blood loss Intravenous volume resuscitation
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
CARDIOGENIC SHOCK
Circulatory pump failure
diminished forward flow and subsequent tissue hypoxia Hemodynamic criteria:
sustained hypotension reduced cardiac index elevated pulmonary artery wedge pressure
50-80% mortality Myocardial Infarction most common cause
Myocardial ischemia myocardial dysfunction myocardial ischemia
CARDIOGENIC SHOCK
Diagnosis:
Signs: hypotension, cool and mottled skin, depressed mental status, tachycardia, diminished pulses Diagnostics: ECG Echocardiography CXR ABG Electrolytes CBC Cardiac enzymes
Invasive Cardiac Monitoring excludes right ventricular
infarction, hypovolemia, & possible mechanical complications
CARDIOGENIC SHOCK
Treatment: 1. Maintenance of adequate oxygen 2. Fluid administration
Correct electrolyte imbalance Pain management Anti-arrhythmic drugs, pacing or cardioversion Inotropic Support Intra-Aortic Balloon Pump
improve cardiac contractility & cardiac output
Increases cardiac output & improves coronary blood flow treatment of choice (cardiogenic shock from AMI)
Percutaneous Transluminal Coronary Angiography
VASODILATORY SHOCK
Systemic response to infection Noninfectious systemic inflammation
Pancreatitis Burns
Prolonged, severe hypotension
Hemorrhagic shock Cardiogenic shock Cardiopulmonary bypass
Metabolic
Hypoxic lactic acidosis Carbon monoxide poisoning
Anaphylaxis Acute adrenal insufficiency
VASODILATORY SHOCK
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
SEPTIC SHOCK
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)
REVISED DIAGNOSTIC CRITERIA FOR SEPSIS
General Variables
Fever [core temp >38.3C (100.9F)]
Hypothermia [core temp <36C (96.8F)]
Heart rate >90 bpm or > 2 SD above the normal value for age Tachypnea
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
REVISED DIAGNOSTIC CRITERIA FOR SEPSIS
Inflammatory variables
Leukocytosis (WBC >12,000 cells/L) Leukopenia (WBC <4000 cells/L) Bandemia (>10% immature band forms)
Plasma C-reactive protein > 2 SD above normal value
Plasma procalcitonin >2 SD above normal value
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
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)
REVISED DIAGNOSTIC CRITERIA FOR SEPSIS
Organ dysfunction variables
Ileus
Thrombocytopenia (platelet count < 100,000 cells/L) Hyperbilirubinemia (plasma total bilirubin > 4 mg/dL or 70 mmol/L)
REVISED DIAGNOSTIC CRITERIA FOR SEPSIS
Tissue perfusion variables
Hyperlactatemia (> 1 mmol/L)
Decreased capillary filling or mottling
SEPTIC SHOCK
Treatment:
Fluid resuscitation & restoration of circulatory volume Antibiotics Vasopressors Intensive Insulin Therapy Activated Protein C Corticosteroids
NEUROGENIC SHOCK
Diminished tissue perfusion from loss of vasomotor tone to peripheral arterial beds
Etiology: Spinal cord injuries Spinal cord neoplasms Spinal epidural/anesthetic
NEUROGENIC SHOCK
Classic Description:
Decreased blood pressure Warm extremities Motor & Sensory deficits Radiographic evidence of a vertebral column fracture
Management:
BP Control Oxygenation Hemodynamics
OBSTRUCTIVE SHOCK
Pericardial tamponade Pulmonary embolus Tension pneumothorax IVC obstruction
Deep venous thrombosis Gravid uterus on IVC Neoplasm Excess positive end-expiratory pressure Neoplasm
Increased intrathoracic pressure
OBSTRUCTIVE SHOCK
Tension Pneumothorax / Cardiac Tamponade
( Intrapleural Pressure) ( Intrapericardial Pressure)
Reduced filling of the Right side of the Heart
Decreased cardiac output with pressure
central venous
OBSTRUCTIVE SHOCK
Diagnosis
& Treatment:
Classic Findings:
Respiratory distress Diminished breath sounds Hyperresonance
*Becks Triad: Hypotension + Muffled heart tones + Neck vein distention
Cardiac tamponade
Elevated central venous pressure Pulsus paradoxus
right atrial & right ventricular pressure
OBSTRUCTIVE SHOCK
Diagnosis
& Treatment:
Pleural/ Pericardial Decompression Immediate Tube Thoracostomy Echocardiography Pericardiocentesis Diagnostic Pericardial Window
TRAUMATIC SHOCK
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
CARDIOVASCULAR AND METABOLIC CHARACTERISTICS OF SHOCK
Hypovolemia Cardiogenic Obstructive Distributive Cardiac Output Vascular Resistance Venous Pressure Mixed Venous Saturation Base Deficit
CORE PRINCIPLES IN MANAGEMENT
Secure Airway Prompt control of active hemorrhage Volume resuscitation
Goal of Treatment: Restoration of adequate organ perfusion & tissue oxygenation
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)
ASSESSMENT OF ENDPOINTS
Oxygen
Transport
Supranormal O2 transport variables o O2 delivery >600mL/min per sq. meter o Cardiac index >4.5L/min per sq. meter o O2 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
Lactate
Conversion of pyruvate (lactate dehydrogenase) in the setting of insufficient oxygen Metabolized by the liver (50%) and kidneys (30%) Indirect measure of oxygen debt *Base deficit and volume of blood transfusion requiredbetter predictors of mortality
ASSESSMENT OF ENDPOINTS
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 37C and PaCO2 of 40mm Hg Mild (3-5) Moderate (6-14) Severe (15)
ASSESSMENT OF ENDPOINTS
Gastric
Tonometry
Used to assess perfusion of the GIT pHi - 7.3; in decreased O2 delivery - good prognostic indicator
Near
Infrared (NIR) Spectroscopy
Measure tissue oxygenation & redox state of cytochcrome a,a3
ASSESSMENT OF ENDPOINTS
Tissue
pH, O2, & CO2 Concentration
Tissue probes with optical sensors
Right
Ventricular End-Diastolic Volume Index (RVEDVI)
Correlate with preload-related increases in cardiac output LVP >320mm Hg L/min per sq meter
CONTROVERSIES ON FLUID RESUSCITATION
Crystalloid
/ Colloid solutions
No difference in overall mortallity, length of stay, or incidence of pulmonary edema Marginal benefit with the infusion of hypertonic saline (7.5 percent sodium chloride)
- Immunomodulatory
BLOOD TRANSFUSION
Inherent
risks: Transfusion reactions Infection Immunosuppression (7.0-9.0 g/dL) & Hct levels (>30%)
Hgb
- appropriate in the treatment of critically-ill patients
HYPOTENSIVE RESUSCITATION
Conclusions:
Any delay in surgery for control of hemorrhage increases mortality With 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
Dontforget...
Shock: rude unhinging of the machinery of life.
-Samuel D. Gross, 1872-
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