Transcript Shock - Cleveland Clinic

Shock
Eric Kaiser M.D.
Rosen’s Chapter 4
9-7-06
Slides by:
Scott Gunderson D.O.
Shock
“Transition between life and death”
Failure to oxygenate & nourish the body
adequately
Mortality > 20%
Pathophysiology
&
Biochemistry
Pathophysiology
Shock affects mitochondria first
Without oxygen mitochondria convert fuels
to lactate → lactic acid
Failure of the krebs cycle

Oxygen is the final electron accepter to form
water
Lactic Acid
Early shock
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
Skeletal muscle and splanchnic organs 1st
affected
Lactic acid production
Resuscitation

Pyruvate delivery from glycolysis can
overwhelm krebs cycle
Systemic Response
Decreased vascular wall tension increases
sympathetic stimulation (blocked in sepsis)


Increased epi, norepi, corticosteroids, renin,
and glucagon
Increased glycogenolysis and lipolysis
Increased glucose and FFA’s to TCA can
overwhelm it
Immune Response
Neutrophil and macrophage activation due
to hypoxia

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Enzymatic organ damage
Capillary plugs causing microischemia
TNF and Interleukins released
Cardiac Physiology
Contraction created by Ca++, ATP/CP, and
troponin C
Calcium inflow determines strength of
contraction
Inotropics increase Ca++ release in the
sarcoplasmic reticulum via β-receptors or
cAMP
Cardiac Physiology
ATP/CP supply almost entirely from
oxidative phosphorylation by mitochondria
Complete turnover of ATP/CP every 5-10
beats
Cardiac Physiology
Gregg Phenomenon

Contractile strength decreases with
decreased coronary perfusion
Decreased coronary perfusion in shock
Decreased workload due to lower SVR
Very minimal cardiac ischemia even in
severe shock
Cardiac Physiology
Inflammatory actions of TNFα,
Interleukins, and NO decrease contractility
Acidosis can decrease contractility but
effect is minimal
Clinical Features &
Management
Clinical Features
Frequently no obvious etiology
Rapid recognition

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H&P, ill appearance, diaphoresis
HR and BP not reliable
HR/SBP ratio better indicator
Normal is less than 0.8

Urine output is great, but takes time
Normal >1.0 ml/kg/hr

Lactic acid or base deficit
Shock
Classification
Rapid, but
detailed H&P
to direct
therapy
Flow diagram

Figure 4-4 in
Rosen’s
Clinical Data
CXR – infection, contusions
EKG – ischemia
Glucose
CBC – anemia, leukocytosis
Electrolytes – dehydration, GI bleed,
acidosis
ABG – base deficit, acidosis
UA – dehydration
Management
IV, O2, monitor
BP readings every 2-5 minutes

Remember BP reading often underestimates
the level of shock until severe
Urine output

>1 cc/kg/min
Management
IV access

Peripheral vs. Central
Most patients OK with one large bore or two
smaller bore peripheral IV’s
CVP pressure may be required for patient with
cardiac failure or renal failure
Indwelling catheters should be used unless
hospital policy states against it in the ED
Volume Replacement
When is the tank full?


Goal CVP slightly elevated of 10-15 cm H2O
Must correlate CVP with SBP, urine output,
and lactate levels to adequately assess
perfusion
Ventilation
Rapid sequence intubation preferred

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Ketamine or etomidate are good choices due
to minimal cardiovascular depression
Intubation protects aspiration, decreases
breathing workload, and initial treatment for
acidemia
High negative pressures in bronchospasm or
ARDS can decrease LVEF and positive
pressure removes this
Acidosis
Acidosis is a negative inotrope
No evidence supports using bicarbonate
for treatment
Treat with improved ventilation and mild
hyperventilation
THAM (tris[hydroxymethl]-aminomethane)
may be used IV for acidosis reversal
Optimal Hemoglobin
Hemoglobin carries oxygen
High hematocrits increase viscosity and
cardiac workload
Optimal balance is a hemoglobin of 10-12
gm%
Goal-Directed Therapy
Goal directed therapy is the practice of
resuscitating to a defined physiologic endpoint
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Wedge pressures – measures left ventricular filling
pressures – controversial risk/benefit
Lactate clearing index – decrease in arterial lactate by
50% in 1 hour and continued efforts until lactate < 2
mM
GI tonography – permeable balloon in stomach or
rectum measuring pH to estimate perfusion
Questionable data supporting
Specific Causes &
Treatment
Hemorrhagic Shock
Rapid reduction in blood volume
Heart rate and blood pressure responses
can be variable
No firm conclusion can be made by simply
HR and BP readings
Hemorrhagic Shock
General Progression
Increased heart rate
Narrowed pulse pressure
Shunting from noncritical organs
Decreased cardiac filling
leading to decreased CO
Decreased SBP
Hemorrhagic Shock
Decreased perfusion to splanchnic organs
precedes lower BP


Lactic acid production
Base deficit
Normal base deficit is greater than -2 mEq/L
After 1/3 of blood volume lost hypotension
occurs
Acidemia occurs about then as patient
cannot create enough respiratory
compensation for the lactic acid
Hemorrhagic Shock
Organ injury in resuscitation

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Release of activated neutrophils &
inflammatory cytokines
Distorted balance of vasodilatation vs.
vasoconstriction
May lead to ARDS, acute tubular necrosis, &
centrilobular ischemic liver damage
Consensus Definition
Hemorrhagic Shock – 3 classifications

Simple hemorrhage
Bleeding with normal vital signs and base deficit
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Hemorrhage with hypoperfusion
Bleeding with base deficit < -5 mmol or persistent HR >100

Hemorrhagic shock
Bleeding with 4 or more of below
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Ill appearance or mental status
HR >100
RR >22 or PaCO2 <32
Base deficit < -5 or lactate > 4
Urine output < 0.5 cc/kg/hr
Hypotension > 20 minutes
Hemorrhagic Shock Treatment
Several liters of crystalloids in adults
Three 20 cc/kg boluses in children
If still in shock after bolus start PRBC’s at
5-10 cc/kg
Blood substitutes possibly in future but not
currently advantageous
Hemorrhagic Shock Treatment
Controlling hemorrhage is still always the
cornerstone of treatment
Immediate surgery if hemorrhage cannot
be controlled
In very rare cases inotropics may be
beneficial
Septic Shock
Any microbe may cause, but gram
negative most common
Lipopolysaccharide is a key mediator
1/3 of cases no organism is identified
Higher causes recently of gram positive
due to
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Hospitalized patients
Immunocompromised
Indwelling catheters
Increasing drug resistance
Septic Shock
3 major effects

Hypovolemia
Relative due to increased venous capacitance
Absolute due to GI loss, diaphoresis, tachypnea

Cardiovascular depression
Depression due to inflammatory mediators

Systemic inflammation
Capillary leak causing ARDS in up to 40%
Consensus Definition
SIRS

Two or more of the following
Temperature > 38 C or <36 C
Heart rate > 90
Respiratory rate > 20 resp/min or PaCO2 <32
WBC > 12,000, < 4,000, or >10% bands
Septic Shock

Severe sepsis with hypotension unresponsive to fluid
resuscitation and perfusion abnormalities
Septic Shock Treatment
Ventilatory support

Decrease respiratory workload and correct
hypoxia
Fluids

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Increase ventricular filing
20-25 cc/kg crystalloids followed by 5-10
cc/kg colloids
Blood

Used to keep Hct at 30-35% if needed
Septic Shock Treatment
Antibiotics

If focus identified
Use clinical experience

If no focus identified
Semisynthetic PCN with β-lactamase inhibitor with
an aminoglycoside and vancomycin
Imipenem-cilastatin good monotherapy choice
Antifungal in immunocompromised
Septic Shock Treatment
Vasopressors
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Dopamine
Most common first line agent and a bad idea
Remove from you armamentarium
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Norepinephrine
Start 0.5-1 µg/min and titrate to response
Excellent first choice; well studied
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Dobutamine
Start 5 µg/kg/min
Hypotension unresponsive to vasopressors and
IVF.
Cardiogenic Shock
Pump failure
Results when more than 40% of
myocardium damaged
Similar circulatory and metabolic changes
to hemorrhagic shock
May also be due to a PE
Consensus Definitions
Cardiogenic

Cardiac failure
Evidence of impaired cardiac outflow including
dyspnea, tachycardia, rales, edema, or cyanosis

Cardiogenic shock
Cardiac failure plus four of below criteria
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Ill appearance or mental status
HR >100
RR >22 or PaCO2 <32
Base deficit < -5 or lactate > 4
Urine output < 0.5 cc/kg/hr
Hypotension > 20 minutes
Cardiogenic Shock Treatment
Ventilatory support

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Often needed in pulmonary edema or if
respiratory failure imminent
Avoid barbiturates, morphine, propofol and
benzodiazepines
Negative inotropic effects
Fentanyl, ketamine and etomidate much better
choices
Cardiogenic Shock Treatment
Ionotropics/vasopressors
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Dobutamine and Milrinone are agents of
choice
Amrinone (Replaced by Milrinone)
Milrinone
Similar to amrinone
Load at 50 µg/kg (Consider half loading dose)
Infuse at 0.375 - 0.75 µg/kg/min
Be prepared for hypotension
Cardiogenic Shock Treatment
Intraaortic balloon pump
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When all pharmacologic therapy is failing
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Requires appropriate facility and ICU/CCU
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Improves cardiac output by 30%
Cardiogenic Shock Treatment
Myocardial infarction causing cardiogenic
shock

Management not significantly different than
another MI accept additional management
Ventilatory support as needed
Treat dysrhythmias
Inotropic support
Aspirin
Heparin
PTCA vs. thrombolytics
Cardiogenic Shock Treatment
Pulmonary Embolism
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Ventilatory support
IV fluids
Norepinephrine
Thrombolytics (systemic vs. intra-arterial)
Possis catheter
Surgical embolectomy at few centers
Anaphylactic Shock
IgE mediated response to an allergen
Mast cells release histamine
Histamine causes
Smooth muscle relaxation
Bronchial contraction
Capillary leak
Anaphylactic Shock Treatment
Epinephrine
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1 cc of 1:10,000 IV infused slowly and watch
response
5 mg in 500 cc NS at 10 cc/hr thereafter
May titrate to response

Use even with coronary artery disease if
hypotensive
Anaphylactic Shock Treatment
Corticosteroids
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Decrease immune response
Methylprednisolone 125mg IV
Hydrocortisone 5-10 mg/kg IV
Antihistamines
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Diphenhydramine 0.5 mg/kg IV
Cimetidine 2-5 mg/kg IV
Famotidine
Intubation if needed
Neurogenic Shock
CNS cord lesions above T1

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Heart gets unopposed vagal simulation
Bradycardia and hypotension
Atropine

First line therapy
Neurogenic Shock Treatment
Volume expansion

Confirm by CVP and BP
Vasopressors

Ephedrine
10 mg IV bolus good for 3-4 hours

Phenylephrine
100-180 µg/min IV until stable
Summary
Early recognition of shock and early
treatment is key
Do not rely solely on a HR and BP to
determine their status
Aggressive and goal directed therapy have
proven to decrease mortality
References
Jones, Alan E., & Kline, Jeffrey A. (2006). “Shock.” In Marx,
John A., Hockberger, Robert S., & Walls, Ron M. (Eds.). Rosen's
Emergency Medicine: Concepts and Clinical Practice, 6th ed.,
Pg. 41-56. Mosby.