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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 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 Terms II. Pathophysiology of shock III. Ischemia–reperfusion 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 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 .

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 .ISCHEMIA–REPERFUSION SYNDROME • • • • Direct effects of tissue hypoxia and local activation of inflammation Acid and potassium load lead to direct myocardial depression.

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 .

3.HYPOVOLEMIC SHOCK  Treatment: 1. Secure the airway Control the source of blood loss Intravenous volume resuscitation . 2.

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 .

diminished pulses  Diagnostics: ECG Echocardiography CXR ABG Electrolytes CBC Cardiac enzymes Invasive Cardiac Monitoring – excludes right ventricular infarction. cool and mottled skin.CARDIOGENIC SHOCK  Diagnosis:  Signs: hypotension. depressed mental status. & possible mechanical complications . hypovolemia. tachycardia.

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 .CARDIOGENIC SHOCK  Treatment: 1. Maintenance of adequate oxygen 2.

severe hypotension • Hemorrhagic shock • Cardiogenic shock • Cardiopulmonary bypass  Metabolic • Hypoxic lactic acidosis • Carbon monoxide poisoning  Anaphylaxis  Acute adrenal insufficiency .VASODILATORY SHOCK  Systemic response to infection  Noninfectious systemic inflammation • Pancreatitis • Burns  Prolonged.

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 .

Oliguria.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. Hypotension) . Malaise.

REVISED DIAGNOSTIC CRITERIA FOR SEPSIS  General Variables  Fever [core temp >38.3°C (100.8°F)]  Heart rate >90 bpm or > 2 SD above the normal value for age  Tachypnea .9°F)]  Hypothermia [core temp <36°C (96.

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 .

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 .REVISED DIAGNOSTIC CRITERIA FOR SEPSIS  Inflammatory variables  Leukocytosis (WBC >12.

5 L/min per square meter . or SBP decrease >40 mmHg in adults or <2 SD below normal for age)  Mixed venous saturation (SVO2) >70% in adults  Cardiac index >3. MAP <70 mmHg.REVISED DIAGNOSTIC CRITERIA FOR SEPSIS  Hemodynamic variables  Arterial hypotension (SBP <90 mmHg.

5 or aPTT > 60 s) .5 mg/dL  Coagulation abnormalities (INR > 1.5 mL/kg per hour or 45 mmol/L for at least 2 hours)  Creatinine increase > 0.REVISED DIAGNOSTIC CRITERIA FOR SEPSIS  Organ dysfunction variables  Arterial hypoxemia (PaO2/FiO2 < 300  Acute oliguria (urine output < 0.

000 cells/µL)  Hyperbilirubinemia (plasma total bilirubin > 4 mg/dL or 70 mmol/L) .REVISED DIAGNOSTIC CRITERIA FOR SEPSIS  Organ dysfunction variables  Ileus  Thrombocytopenia (platelet count < 100.

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 *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 Decompression Immediate Tube Thoracostomy Echocardiography Pericardiocentesis Diagnostic Pericardial Window .

TRAUMATIC SHOCK  Systemic response after trauma (soft tissue injury. & blood loss)  Treatment : • • • • • Control of hemorrhage Adequate volume resuscitation Debridement Stabilization of bony injuries Appropriate treatment of soft tissue injuries . long bone fractures.

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 .

carbon dioxide levels • Near infrared spectroscopy  Cellular • Membrane potential • Adenosine triphosphate (ATP) . oxygen.ASSESSMENT OF ENDPOINTS  Systemic/global • • • • Lactate Base deficit Cardiac output Oxygen delivery and consumption  Tissue-specific • Gastric tonometry • Tissue pH.

ASSESSMENT OF ENDPOINTS  Oxygen Transport Supranormal O2 transport variables o O2 delivery >600mL/min per sq. meter Inability to repay O2 debt – predictor of mortality & organ failure O2 debt correlate with serum lactate and base deficit . meter o Cardiac index >4. meter o O2 consumption index >170mL/min per sq.5L/min per sq.

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 .

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  Base deficit (ABG) amount of base in millimoles that is required to titrate 1L of whole blood to a pH of 7.

≥7.ASSESSMENT OF ENDPOINTS  Gastric Tonometry Used to assess perfusion of the GIT pHi .a3 .3. ↓ in decreased O2 delivery .good prognostic indicator  Near Infrared (NIR) Spectroscopy Measure tissue oxygenation & redox state of cytochcrome a.

O2.ASSESSMENT OF ENDPOINTS  Tissue pH. & 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 .

5 percent sodium chloride) .Immunomodulatory . length of stay. or incidence of pulmonary edema Marginal benefit with the infusion of hypertonic saline (7.CONTROVERSIES ON FLUID RESUSCITATION  Crystalloid / Colloid solutions No difference in overall mortallity.

0-9.BLOOD TRANSFUSION  Inherent • • • risks: Transfusion reactions Infection Immunosuppression (7.appropriate in the treatment of critically-ill patients .0 g/dL) & Hct levels (>30%)  Hgb .

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  Conclusions: Any delay in surgery for control of hemorrhage increases mortality With uncontrolled hemorrhage attempting to achieve normal BP may increase mortality .

Shock: “rude unhinging of the machinery of life.” -Samuel D..Don’t‫‏‬forget.. Gross. 1872- .

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