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Shock Stephanie N. Sudikoff, MD Pediatric Critical Care
Yale School of Medicine
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Learning Objectives Understand the pathophysiology of shock
Understand the principles of treatment of shock Examine septic shock as one example
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“The reason you get up in the morning is to deliver oxygen to the cells.”
Mark Mercurio, MD
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Demand O2 consumption Supply O2 delivery
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Oxygen Consumption vs. Delivery
Oxygen consumption (DEMAND) VO2 = CO x (CaO2-CvO2) Oxygen delivery (SUPPLY) DO2 = CO x CaO2
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Myocardial contractility Hb content and affinity
DO2 CO SV Preload Myocardial contractility Afterload HR CaO2 Hb content and affinity
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What are PRELOAD and AFTERLOAD?
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Preload PreloadLV = (EDPLV)(EDrLV)/2tLV where, LV = left ventricle
ED = end diastole Represents all the factors that contribute to passive ventricular wall stress at the end of diastole
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Venous return and CO
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Factors affecting venous return
Decrease in intravascular volume Increase in venous capacitance Increase in right atrial pressure Increase in venous resistance
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Afterload AfterloadLV = (SPLV)(SrLV)/2tLV where, LV = left ventricle
S = systole Represents all the factors that contribute to total myocardial wall stress during systolic ejection
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Myocardial contractility
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Myocardial contractility
Positive Inotropic Agents Negative Inotropic Agents Adrenergic agonists Cardiac glycosides High extracellular [Ca++] Ca++-channel blockers Low extracellular [Ca++]
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Heart rate HR CO At high HR, diastolic filling is impaired
Atrial contraction accounts for up to 30% of Stroke Volume
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SHOCK
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Demand O2 consumption Supply O2 delivery Shock
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Classification of Shock
Decreased preload (hypovolemic) Hemorrhage Dehydration Cardiac tamponade Pneumothorax Decreased myocardial contractility (cardiogenic) Myocarditis Cardiopulmonary bypass Congestive heart failure Myocardial infarction Drug intoxication Sepsis Heart rate abnormalities (cardiogenic) Dysrhythmias Increased afterload (obstructive) Massive pulmonary embolus Critical aortic and pulmonic stenosis Decreased afterload (distributive) Anaphylaxis Neurogenic shock Abnormalities in Hb affinity (dissociative) Methemoglobinemia Carbon monoxide poisoning
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Systemic response to low perfusion
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Systemic response to low perfusion
Increase CO Increase preload Aldosterone Na reabsorption Interstitial fluid reabsorption ADH secretion Venoconstriction
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Systemic response to low perfusion
Increase CO Increase contractility Sympathetics Increase afterload Vasoconstriction Increase HR
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Systemic response to low perfusion
Increase CO Increase contractility Sympathetics Increase HR Increase SVR Vasoconstriction Increase blood volume
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Local response to low perfusion
Increase O2ER Opening of previously closed capillaries Increased surface area for diffusion Shortened diffusion distance Increased transit time
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Physical Signs of low CO
Organ System ↓ Cardiac Output ↓↓ Cardiac Output (Compensated) ↓↓ Cardiac Output (Uncompensated) CNS — Restless, apathetic Agitated-confused, stuporous Respiration ↑ Ventilation ↑↑ Ventilation Metabolism Compensated metabolic acidemia Uncomensated metabolic acidemia Gut ↓ Motility Ileus Kidney ↑ Specific gravity, ↓ volume Oliguria Oliguria-anuria Skin Delayed capillary refill Cool extremities Mottled, cyanotic, cold extremities CVS ↑ Heart rate ↑↑ Heart rate, ↓ peripheral pulses ↓ blood pressure, central pulses only
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Objective monitors Systemic perfusion base deficit lactate
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Objective monitors Systemic perfusion CO Preload
ABG lactate CO PA catheter Arterio-venous oxygen difference Preload CVP Echo Myocardial contractility Echo Afterload PA catheter Invasive or noninvasive BP HR EKG CaO2 Hb ABG
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TREATMENT OF SHOCK
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Goals of therapy Treat underlying cause ↓ Demand O2 consumption
↑ Supply O2 delivery Treat underlying cause
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Reduction of demands for CO
Treat hyperthermia aggressively
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Reduction of demands for CO
Treat hyperthermia Reduce work of breathing As much as 20% of CO goes to respiratory muscles
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PPV and CO Advantages Decreases work of breathing Improves acidosis
Decreases PVR Decreases LV afterload Improves oxygenation
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Reduction of demands for CO
Treat hyperthermia Reduce work of breathing Sedation Seizure control Paralysis
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Myocardial contractility Hb content and affinity
DO2 CO SV Preload Myocardial contractility Afterload HR CaO2 Hb content and affinity
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Increase supply: Restoration of perfusion
Preload Fluid resuscitation Colloids vs. crystalloids
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Increase supply: Restoration of perfusion
Preload Fluid resuscitation Colloids vs. crystalloids Myocardial contractility Inotropic support ECMO Other mechanical support
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Increase supply: Restoration of perfusion
Preload Fluid resuscitation Colloids vs. crystalloids Myocardial contractility Inotropic support ECMO Other mechanical support Afterload Vasopressors Vasodilators
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Increase supply: Restoration of perfusion
Preload Fluid resuscitation Colloids vs. crystalloids Myocardial contractility Inotropic support ECMO Other mechanical support Afterload Vasopressors Vasodilators HR Anti-arrhythmics Pacer
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Increase supply: Restoration of perfusion
Preload Fluid resuscitation Colloids vs. crystalloids Myocardial contractility Inotropic support ECMO Other mechanical support Afterload Vasopressors Vasodilators HR Anti-arrhythmics Pacer Beta-blockers? CaO2 Blood transfusion Oxygen support
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SEPTIC SHOCK
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Types of septic shock Cold shock ↓ CO, ↑ SVR (60% pediatric)
Narrow pulse pressure, thready pulses, delayed capillary refill
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Phases of septic shock Warm shock (“early”) ↑ CO, ↓ SVR ↓ CO, ↓ SVR
Wide pulse pressure, bounding pulses, brisk capillary refill Cold shock (“late”) ↓ CO, ↑ SVR Narrow pulse pressure, weak pulses, delayed capillary refill
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Early recognition!
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Early recognition!
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Increase preload Aggressive fluid resuscitation
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Increase preload Aggressive fluid resuscitation
Usually requires mL/kg but can be as much as 200 mL/kg 20 mL/kg IV push titrated to clinical monitors
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Monitor improvement in CO
Cardiac output Heart rate Urine output Capillary refill Level of consciousness Blood pressure NOT reliable endpoint
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Increase preload Aggressive fluid resuscitation with crystalloids or colloids Usually requires mL/kg but can be as much as 200 mL/kg 20 mL/kg IV push titrated to clinical monitors Maintain hemoglobin within normal for age (≥10 g/dL)
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Antibiotic therapy IV antibiotics within 1 hr of recognition of severe sepsis Cultures before antibiotics Cover appropriate pathogens Penetrate presumed source of infection
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Improve myocardial contractility and titrate afterload
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Cold Shock, Adequate BP: Decrease afterload
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Adequacy of resuscitation
Capillary refill < 2 sec Adequate pulses Warm limbs Normal mental status Urine output > 1 mL/kg/hr Adequate blood pressure Improved base deficit Decreased lactate ScvO2 > 70%
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Early shock reversal improves outcome
† † † † Carcillo JA et al. Pediatrics 2009;124:
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SUMMARY
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Demand O2 consumption Supply O2 delivery Shock
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Goals of therapy Treat underlying cause ↓ Demand O2 consumption
↑ Supply O2 delivery Treat underlying cause
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Myocardial contractility Hb content and affinity
DO2 CO SV Preload Myocardial contractility Afterload HR CaO2 Hb content and affinity
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Special thanks to Vince Faustino, MD for use of his slides
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