Shock Stephanie N. Sudikoff, MD Pediatric Critical Care Yale School of Medicine

Learning Objectives Understand the pathophysiology of shock Understand the principles of treatment of shock Examine septic shock as one example

“The reason you get up in the morning is to deliver oxygen to the cells.” Mark Mercurio, MD

Demand O2 consumption Supply O2 delivery

Oxygen Consumption vs. Delivery Oxygen consumption (DEMAND) VO2 = CO x (CaO2-CvO2) Oxygen delivery (SUPPLY) DO2 = CO x CaO2

Myocardial contractility Hb content and affinity DO2 CO SV Preload Myocardial contractility Afterload HR CaO2 Hb content and affinity

What are PRELOAD and AFTERLOAD?

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

Venous return and CO

Factors affecting venous return Decrease in intravascular volume Increase in venous capacitance Increase in right atrial pressure Increase in venous resistance

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

Myocardial contractility

Myocardial contractility Positive Inotropic Agents Negative Inotropic Agents Adrenergic agonists Cardiac glycosides High extracellular [Ca++] Ca++-channel blockers Low extracellular [Ca++]

Heart rate HR  CO At high HR, diastolic filling is impaired Atrial contraction accounts for up to 30% of Stroke Volume

SHOCK

 Demand O2 consumption  Supply O2 delivery Shock

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

Systemic response to low perfusion

Systemic response to low perfusion Increase CO Increase preload Aldosterone Na reabsorption Interstitial fluid reabsorption ADH secretion Venoconstriction

Systemic response to low perfusion Increase CO Increase contractility Sympathetics Increase afterload Vasoconstriction Increase HR

Systemic response to low perfusion Increase CO Increase contractility Sympathetics Increase HR Increase SVR Vasoconstriction Increase blood volume

Local response to low perfusion Increase O2ER Opening of previously closed capillaries Increased surface area for diffusion Shortened diffusion distance Increased transit time

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

Objective monitors Systemic perfusion base deficit lactate

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

TREATMENT OF SHOCK

Goals of therapy Treat underlying cause ↓ Demand O2 consumption ↑ Supply O2 delivery Treat underlying cause

Reduction of demands for CO Treat hyperthermia aggressively

Reduction of demands for CO Treat hyperthermia Reduce work of breathing As much as 20% of CO goes to respiratory muscles

PPV and CO Advantages Decreases work of breathing Improves acidosis Decreases PVR Decreases LV afterload Improves oxygenation

Reduction of demands for CO Treat hyperthermia Reduce work of breathing Sedation Seizure control Paralysis

Myocardial contractility Hb content and affinity DO2 CO SV Preload Myocardial contractility Afterload HR CaO2 Hb content and affinity

Increase supply: Restoration of perfusion Preload Fluid resuscitation Colloids vs. crystalloids

Increase supply: Restoration of perfusion Preload Fluid resuscitation Colloids vs. crystalloids Myocardial contractility Inotropic support ECMO Other mechanical support

Increase supply: Restoration of perfusion Preload Fluid resuscitation Colloids vs. crystalloids Myocardial contractility Inotropic support ECMO Other mechanical support Afterload Vasopressors Vasodilators

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

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

SEPTIC SHOCK

Types of septic shock Cold shock ↓ CO, ↑ SVR (60% pediatric) Narrow pulse pressure, thready pulses, delayed capillary refill

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

Early recognition!

Early recognition!

Increase preload Aggressive fluid resuscitation

Increase preload Aggressive fluid resuscitation Usually requires 40-60 mL/kg but can be as much as 200 mL/kg 20 mL/kg IV push titrated to clinical monitors

Monitor improvement in CO Cardiac output Heart rate Urine output Capillary refill Level of consciousness Blood pressure NOT reliable endpoint

Increase preload Aggressive fluid resuscitation with crystalloids or colloids Usually requires 40-60 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)

Antibiotic therapy IV antibiotics within 1 hr of recognition of severe sepsis Cultures before antibiotics Cover appropriate pathogens Penetrate presumed source of infection

Improve myocardial contractility and titrate afterload

Cold Shock, Adequate BP: Decrease afterload

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%

Early shock reversal improves outcome † † † † Carcillo JA et al. Pediatrics 2009;124:500-508

SUMMARY

 Demand O2 consumption  Supply O2 delivery Shock

Goals of therapy Treat underlying cause ↓ Demand O2 consumption ↑ Supply O2 delivery Treat underlying cause

Myocardial contractility Hb content and affinity DO2 CO SV Preload Myocardial contractility Afterload HR CaO2 Hb content and affinity

Special thanks to Vince Faustino, MD for use of his slides