schwartz: shock

SHOCKDr. 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 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

OUTLINE

I. Definition of TermsII. Pathophysiology of shockIII. Ischemia–reperfusion injuryIV. Classification of ShockV. Natural History of ShockVI. Management PrinciplesVII.Monitoring EndpointsVIII.Management Issues

Shock:“A momentary pause in the act of

death.”

-John Collins Warren, 1800s

DEFINITION

SHOCK:

inadequate organ perfusion to meet the tissue’s 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

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

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

• Cardiogenic Shock– Intrinsic– Compressive

• 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 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

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)

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

HYPOVOLEMIC SHOCK

HYPOVOLEMIC SHOCK

Treatment:1. Secure the airway2. Control the source of blood loss3. 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

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

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

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

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

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

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

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


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


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


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


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)


Organ dysfunction variables

Ileus

Thrombocytopenia (platelet count < 100,000 cells/µL)

Hyperbilirubinemia (plasma total bilirubin > 4 mg/dL or 70 mmol/L)


Tissue perfusion variables

Hyperlactatemia (> 1 mmol/L)

Decreased capillary filling or mottling

Treatment:Fluid resuscitation & restoration of circulatory

volumeAntibioticsVasopressorsIntensive Insulin Therapy Activated Protein CCorticosteroids

SEPTIC 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

NEUROGENIC SHOCK

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

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

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

Diagnosis & Treatment:Pleural/ Pericardial DecompressionImmediate Tube ThoracostomyEchocardiographyPericardiocentesisDiagnostic Pericardial Window

OBSTRUCTIVE 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

TRAUMATIC SHOCK

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)

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


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


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)


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


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


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

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

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

Don’t forget...

-Samuel D. Gross, 1872-

Shock: “rude unhinging of the machinery of life.”

END…

schwartz: shock

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