Shock Stephanie N. Sudikoff, MD Pediatric Critical Care Yale School of Medicine Stephanie N....
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Transcript of Shock Stephanie N. Sudikoff, MD Pediatric Critical Care Yale School of Medicine Stephanie N....
ShockShock
Stephanie N. Sudikoff, MDPediatric Critical CareYale School of Medicine
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
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 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
where, LV = left ventricle
S = systole
• Represents all the factors that contribute to total
myocardial wall stress during systolic ejection
• 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 contractilityMyocardial contractility
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
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
Systemic response to low perfusionSystemic response to low perfusion
• Increase CO
– Increase contractility• Sympathetics
– Increase afterload• Vasoconstriction
– Increase HR• Sympathetics
• Increase CO
– Increase contractility• Sympathetics
– Increase afterload• Vasoconstriction
– Increase HR• Sympathetics
Systemic response to low perfusionSystemic response to low perfusion
• Increase CO
– Increase contractility• Sympathetics
– Increase HR• Sympathetics
• Increase SVR
– Vasoconstriction
– Increase blood
volume
• Increase CO
– Increase contractility• Sympathetics
– Increase HR• Sympathetics
• 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
Reduction of demands for COReduction of demands for CO
• Treat hyperthermia
• Reduce work of breathing
– As much as 20% of CO goes to respiratory
muscles
• Treat hyperthermia
• Reduce work of breathing
– 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
Reduction of demands for COReduction of demands for CO
• Treat hyperthermia
• Reduce work of breathing
• Sedation
• Seizure control
• Paralysis
• Treat hyperthermia
• Reduce work of breathing
• Sedation
• Seizure control
• Paralysis
Increase supply:Restoration of perfusionIncrease supply:Restoration of perfusion
• Preload
– Fluid resuscitation
– Colloids vs.
crystalloids
• Preload
– Fluid resuscitation
– Colloids vs.
crystalloids
Increase supply:Restoration of perfusionIncrease supply:Restoration of perfusion
• Preload
– Fluid resuscitation
– Colloids vs.
crystalloids
• Myocardial
contractility
– Inotropic support
– ECMO
– Other mechanical
support
• Preload
– Fluid resuscitation
– Colloids vs.
crystalloids
• Myocardial
contractility
– Inotropic support
– ECMO
– Other mechanical
support
Increase supply:Restoration of perfusionIncrease supply:Restoration of perfusion
• Preload
– Fluid resuscitation
– Colloids vs. crystalloids
• Myocardial contractility
– Inotropic support
– ECMO
– Other mechanical
support
• Afterload
– Vasopressors
– Vasodilators
• Preload
– Fluid resuscitation
– Colloids vs. crystalloids
• Myocardial contractility
– Inotropic support
– ECMO
– Other mechanical
support
• Afterload
– Vasopressors
– Vasodilators
Increase supply:Restoration of perfusionIncrease supply:Restoration of perfusion
• Preload
– Fluid resuscitation
– Colloids vs. crystalloids
• Myocardial contractility
– Inotropic support
– ECMO
– Other mechanical
support
• Afterload
– Vasopressors
– Vasodilators
• Preload
– Fluid resuscitation
– Colloids vs. crystalloids
• Myocardial contractility
– Inotropic support
– ECMO
– Other mechanical
support
• Afterload
– Vasopressors
– Vasodilators
• HR
– Anti-arrhythmics
– Pacer
• HR
– Anti-arrhythmics
– Pacer
Increase supply:Restoration of perfusionIncrease supply:Restoration of perfusion
• Preload
– Fluid resuscitation
– Colloids vs. crystalloids
• Myocardial contractility
– Inotropic support
– ECMO
– Other mechanical
support
• Afterload
– Vasopressors
– Vasodilators
• 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
• HR
– Anti-arrhythmics
– 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!
Early recognition!Early recognition!
Increase preloadIncrease preload
• Aggressive fluid resuscitation• Aggressive fluid resuscitation
Increase preloadIncrease 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
• 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
• Cardiac output– Heart rate– Urine output– Capillary refill– Level of consciousness– Blood pressure NOT reliable endpoint
Increase preloadIncrease 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)
• 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%
• 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
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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