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

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ShockShock

Stephanie N. Sudikoff, MDPediatric Critical CareYale School of Medicine

Learning ObjectivesLearning Objectives

• Understand the pathophysiology of shock

• Understand the principles of treatment of shock

• Examine septic shock as one example

• 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

“The reason you get up in the

morning is to deliver oxygen to

the cells.”

Mark Mercurio, MD

Oxygen Consumption vs. DeliveryOxygen Consumption vs. Delivery

• Oxygen consumption (DEMAND)

– VO2 = CO x (CaO2-CvO2)

• Oxygen delivery (SUPPLY)

– DO2 = CO x CaO2

• Oxygen consumption (DEMAND)

– VO2 = CO x (CaO2-CvO2)

• Oxygen delivery (SUPPLY)

– DO2 = CO x CaO2

What are PRELOAD and

AFTERLOAD?

What are PRELOAD and

AFTERLOAD?

PreloadPreload

• 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

• PreloadLV = (EDPLV)(EDrLV)/2tLV

ED = end diastole

• Represents all the factors that contribute to

passive ventricular wall stress at the end of

diastole

Venous return and COVenous return and CO

Factors affecting venous returnFactors affecting venous return

1. Decrease in intravascular volume

2. Increase in venous capacitance

3. Increase in right atrial pressure

4. Increase in venous resistance

1. Decrease in intravascular volume

2. Increase in venous capacitance

3. Increase in right atrial pressure

4. Increase in venous resistance

AfterloadAfterload

• AfterloadLV = (SPLV)(SrLV)/2tLV

S = systole

• Represents all the factors that contribute to total

myocardial wall stress during systolic ejection

• AfterloadLV = (SPLV)(SrLV)/2tLV

S = systole

• Represents all the factors that contribute to total

myocardial wall stress during systolic ejection

Myocardial contractilityMyocardial contractility

Positive Inotropic Agents

Negative Inotropic Agents

1. Adrenergic agonists

2. Cardiac glycosides3. High extracellular

[Ca++]

1. Ca++-channel blockers

2. Low extracellular

[Ca++]

Heart rateHeart rate

• HR CO

• At high HR, diastolic filling is impaired

• Atrial contraction accounts for up to 30% of Stroke

Volume

• HR CO

• At high HR, diastolic filling is impaired

• Atrial contraction accounts for up to 30% of Stroke

Volume

SHOCKSHOCKSHOCKSHOCK

ShockShock

Classification of ShockClassification of Shock

Decreased preload (hypovolemic) HemorrhageDehydrationCardiac tamponadePneumothorax

Decreased myocardial contractility (cardiogenic)

MyocarditisCardiopulmonary bypassCongestive heart failureMyocardial infarctionDrug intoxicationSepsis

Heart rate abnormalities (cardiogenic) Dysrhythmias

Increased afterload (obstructive) Massive pulmonary embolusCritical aortic and pulmonic stenosis

Decreased afterload (distributive) AnaphylaxisNeurogenic shockSepsis

Abnormalities in Hb affinity (dissociative)

MethemoglobinemiaCarbon monoxide poisoning

Systemic response to low perfusionSystemic response to low perfusion

• Increase CO

– Increase preload• Aldosterone

• Na reabsorption

• Interstitial fluid

reabsorption

• ADH secretion

• Venoconstriction

• Increase CO

– Increase preload• Aldosterone

• Na reabsorption

• Interstitial fluid

reabsorption

• ADH secretion

• Venoconstriction

• Increase CO

– Increase contractility• Sympathetics

– Increase afterload• Vasoconstriction

– Increase HR• Sympathetics

• Increase CO

– Increase afterload• Vasoconstriction

• Increase CO

• Increase SVR

– Vasoconstriction

– Increase blood

volume

• Increase CO

• Increase SVR

– Vasoconstriction

– Increase blood

volume

Local response to low perfusionLocal response to low perfusion

• Increase O2ER

– Opening of

previously closed

capillaries

– Increased surface

area for diffusion

– Shortened diffusion

distance

– Increased transit time

• Increase O2ER

– Opening of

previously closed

capillaries

– Increased surface

area for diffusion

– Shortened diffusion

distance

– Increased transit time

Physical Signs of low COPhysical 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

↑↑ Heart rate, ↓ blood pressure, central pulses only

Objective monitorsObjective monitors

• Systemic perfusion

– base deficit

– lactate

• Systemic perfusion

– base deficit

– lactate

Objective monitorsObjective monitors

• Systemic perfusion– ABG

– lactate

• CO– PA catheter

– Arterio-venous oxygen difference

• Preload– CVP

– Echo

• Systemic perfusion– 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

• Myocardial contractility– Echo

• Afterload– PA catheter

– Invasive or noninvasive BP

• HR– EKG

• CaO2

– Hb

– ABG

TREATMENT OF SHOCKTREATMENT OF SHOCKTREATMENT OF SHOCKTREATMENT OF SHOCK

Goals of therapyGoals of therapy

• Treat underlying cause• Treat underlying cause

Reduction of demands for COReduction of demands for CO

• Treat hyperthermia aggressively• Treat hyperthermia aggressively

• Treat hyperthermia

• Reduce work of breathing

– As much as 20% of CO goes to respiratory

muscles

– As much as 20% of CO goes to respiratory

muscles

PPV and COPPV and CO

Advantages

• Decreases work of breathing

• Improves acidosis

• Decreases PVR

• Decreases LV afterload

• Improves oxygenation

Advantages

• Decreases work of breathing

• Improves acidosis

• Decreases PVR

• Decreases LV afterload

• Improves oxygenation

• Sedation

• Seizure control

• Paralysis

• Sedation

• Seizure control

• Paralysis

Increase supply:Restoration of perfusionIncrease supply:Restoration of perfusion

• Preload

– Fluid resuscitation

– Colloids vs.

crystalloids

• Preload

– Colloids vs.

crystalloids

• Preload

– Colloids vs.

crystalloids

• Myocardial

contractility

– Inotropic support

– ECMO

– Other mechanical

support

• Preload

– Colloids vs.

crystalloids

• Myocardial

contractility

– ECMO

support

• Preload

– Colloids vs. crystalloids

• Myocardial contractility

– ECMO

support

• Afterload

– Vasopressors

– Vasodilators

• Preload

– ECMO

support

• Afterload

– Vasopressors

– Vasodilators

• Preload

– ECMO

support

• Afterload

– Vasopressors

– Vasodilators

• Preload

– ECMO

support

• Afterload

– Vasopressors

– Vasodilators

• HR

– Anti-arrhythmics

– Pacer

• HR

– Pacer

• Preload

– ECMO

support

• Afterload

– Vasopressors

– Vasodilators

• Preload

– ECMO

support

• Afterload

– Vasopressors

– Vasodilators

• HR

– Pacer

– Beta-blockers?

• CaO2

– Blood transfusion

– Oxygen support

• HR

– Pacer

– Beta-blockers?

• CaO2

– Blood transfusion

– Oxygen support

SEPTIC SHOCKSEPTIC SHOCKSEPTIC SHOCKSEPTIC SHOCK

Types of septic shockTypes of septic shock

• Cold shock

– ↓ CO, ↑ SVR (60% pediatric)

– Narrow pulse pressure, thready pulses, delayed

capillary refill

• Cold shock

– ↓ CO, ↑ SVR (60% pediatric)

– Narrow pulse pressure, thready pulses, delayed

capillary refill

Phases of septic shockPhases 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

• 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 preloadIncrease preload

• Aggressive fluid resuscitation• Aggressive fluid resuscitation

• 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

• 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 COMonitor improvement in CO

• Cardiac output– Heart rate– Urine output– Capillary refill– Level of consciousness– Blood pressure NOT reliable endpoint

• 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)

• 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 therapyAntibiotic therapy

• IV antibiotics within 1 hr of recognition of severe

sepsis

• Cultures before antibiotics

• Cover appropriate pathogens

• Penetrate presumed source of infection

• 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 afterloadImprove myocardial contractility and titrate afterload

Cold Shock, Adequate BP:Decrease afterloadCold Shock, Adequate BP:Decrease afterload

Adequacy of resuscitationAdequacy 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 outcomeEarly shock reversal improves outcome

Carcillo JA et al. Pediatrics 2009;124:500-508

††††

††

SUMMARYSUMMARYSUMMARYSUMMARY

ShockShock

Goals of therapyGoals of therapy

• Treat underlying cause• Treat underlying cause

Special thanks to Vince Faustino, MD

for use of his slides

Special thanks to Vince Faustino, MD

for use of his slides

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

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