Shock - Yale medStation

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Transcript Shock - Yale medStation

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
Supply
Oxygen Consumption vs. Delivery
• Oxygen consumption (DEMAND)
– VO2 = CO x (CaO2-CvO2)
• Oxygen delivery (SUPPLY)
– DO2 = CO x CaO2
DO2
CO
Preload
CaO2
SV
HR
Myocardial
contractility
Afterload
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
1. Decrease in intravascular volume
2. Increase in venous capacitance
3. Increase in right atrial pressure
4. 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
Negative
Inotropic Agents Inotropic Agents
1. Adrenergic
agonists
2. Cardiac
glycosides
3. High
extracellular
[Ca++]
1. Ca++-channel
blockers
2. 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
 Supply
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
Sepsis
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
• Sympathetics
Systemic response to low perfusion
• Increase CO
– Increase contractility
• Sympathetics
– Increase HR
• Sympathetics
• 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
Uncomensated
metabolic acidemia 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 monitors
• Systemic perfusion
– base deficit
– lactate
Objective monitors
• 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
TREATMENT OF SHOCK
Goals of therapy
↓ Demand
↑ Supply
O2
consumption
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
DO2
CO
Preload
CaO2
SV
HR
Myocardial
contractility
Afterload
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
• HR
– Fluid resuscitation
– Anti-arrhythmics
– Colloids vs. crystalloids
– Pacer
• Myocardial contractility
– Inotropic support
– ECMO
– Other mechanical
support
• Afterload
– Vasopressors
– Vasodilators
Increase supply:
Restoration of perfusion
• Preload
• HR
– Fluid resuscitation
– Anti-arrhythmics
– Colloids vs. crystalloids
– Pacer
• Myocardial contractility
– Inotropic support
– ECMO
– Other mechanical
support
• Afterload
– Vasopressors
– Vasodilators
– 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
 Supply
Shock
Goals of therapy
↓ Demand
↑ Supply
O2
consumption
O2 delivery
• Treat underlying cause
DO2
CO
Preload
CaO2
SV
HR
Myocardial
contractility
Afterload
Hb content
and affinity
Special thanks to Vince Faustino, MD
for use of his slides