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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-

END