SHOCK!!
Justin Bright, M.D.
Emergency Physicians of NW Ohio
February 20, 2013
The Plan For Today
• Define shock
– What it means physiologically
– The different types of shock
• Discuss treatment modalities
• Discuss ways we handle shock in our ED
• Make this fun and interesting
• Reward you with chocolate
What is Shock?
• Circulatory insufficiency that creates
imbalance between oxygen supply and
demand
• Global tissue hypoperfusion
• Causes metabolic acidosis
• Left untreated, progresses to end organ
failure
Why Is Shock A Big Deal?
• People in shock are the most critically ill
patients in our ED
– Shock = “actively trying to die”
• 30-45% of septic shock patients, and 6090% of cardiogenic shock patients die
within 1 month of presentation
• Quick decision making and adequate
treatment can prolong life
Pathophysiology
• Systemic oxygen delivery is a result of
arterial O2 content (CaO2) and cardiac
output (CO)
• A normal Hgb molecule contains 4 O2
molecules
– Tissue takes one O2 (25%), leaving 75% O2
content returning to the heart in venous
circulation
Hemoglobin Molecule
Compensation
• When there is a
supply/demand
imbalance, the body
attempts to compensate
– Pumps out more blood
(increased CO)
– Extracts more O2
(decreases SVO2)
• When compensation fails,
the body switches over to
anaerobic metabolism
– Increases lactate levels in
the blood
More Compensation
• Arteriolar vasoconstriction to redistribute
blood flow
• Constriction of venous capacitance vessels
to increase VR
• Release of catacholamines
• Release of ADH and activation of reninangiotensin system
What’s Happening At
The Cellular Level?
• ATP gets depleted
– Na/K ATPase can no longer function
– Pump dysfunction causes cellular edema
• Cells become less responsive to stress hormones
• Lyosymes get released
• Cellular integrity is lost and cells rupture
– Hemoconcentration, hyperkalemia, hyponatremia,
prerenal azotemia, loss of glycemic control, lactic
acidosis
General Management Plan
• The ABCDE’s of shock
– A: airway management
– B: reduce work of breathing
– C: insure adequate circulation
– D: adequate oxygen delivery
– E: achieving endpoints of resuscitation
What Are The Types of Shock?
• Septic Shock
• Cardiogenic Shock
• Hypovolemic Shock
• Distributive Shock
– Anaphylaxis
– Neurogenic shock
What Is Septic Shock?
• Sepsis is a systemic inflammatory
response to infection
• This major inflammatory response leads to
– Depression of cardiac activity
– Large scale vasodilation
– Increased metabolic consumption
Septic Shock
• Where are the most common sites of
infection?
– Chest
– Abdomen
– Urinary Tract
Clinical Features of Septic Shock
• Constitutional
– Hyperthermia or
hypothermia
– Tachycardia
– Wide pulse pressure
– MS changes
– tachypnea
• Cardiovascular
– Hypotension that does
not respond well to
fluids
– Cardiac depression
• Due to coronary
hypoperfusion with
resultant cardiac
ischemia
Clinical Features of Septic Shock
• Renal
– Acute renal failure
• Pulmonary
– SS is the most common
cause of ARDS
– Significant, non-cardiogenic
pulmonary edema
• Hematologic
– Neutropenia,
thrombocytopenia, DIC
• Endocrine
– Hyperglycemia, even in the
non-diabetic
– Poor glycemic control in
critical patients is
correlated with a much
poorer outcome
Septic Shock
• Back in the olden days
– Patients in septic shock would sit in the ER for
hours waiting for a bed
– They’d get some fluids
– Maybe some antibiotics
– Then they’d go the ICU and die
Take A Moment….
• …To Bow Down To The ER God
The Gist of EGDT
• While the patient is sitting in the ED, you
optimize treatment early
• There are well defined optimization end
points
• Patient goes to the ICU….
• ….and they live!
• Most of the time
Why EGDT is a Big Deal
• It has received the most buzz, and
produced the most significant change in
EM practice in the 21st century
• Clinical data shows it significantly
improves patient outcomes
• Two of our attendings trained under Dr.
Rivers
• We are good, but not great at EGDT
What Does EGDT entail?
• Filling up the tank
• Insuring adequate MAP
• Insuring adequate SVO2
• Reducing work of breathing, which
reduces metabolic demand
• Giving pressure support as needed
• Giving antibiotics
EGDT
• How do we reduce
work of breathing?
– Oxygenation by NRB
– Very low threshold for
intubation
Filling Up The Tank
• Septic shock causes major vasodilation
• Typically will give fluid bolus with minimal
BP response
• How do we know we’ve given enough
fluids?
• Central venous pressures (CVP)
– Done off a central line
– Goal is between 8-12 mmHg
What About The SVO2
and the MAP?
• To increase the SVO2, blood transfusion is
often necessary
– A goal is SVO2 of 70%
• To increase the MAP, pressure support
medications are often needed
– Goal is a MAP between 65 and 90
Pressors in Septic Shock
• Dopamine
– Increases heart rate and blood pressure
• Levophed (norepinephrine)
– Increases blood pressure without affecting HR
• Dobutamine
– Increases HR without really affecting BP
Antibiotics
• Blood cultures obtained before antibiotics
if possible
• Antibiotics given empirically
– Will depend on patient comorbidities and
history
– Ideally will cover against both gram+ and
gram- bacteria
So How Will It All Go Down?
• Labs ordered
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–
–
–
–
–
–
–
CBC
Lytes
Blood culture
UA
Coaggs
ABG
Lactate
Blood type and cross
• Studies
– CXR or AAS
• Procedures
–
–
–
–
Central line
A-line
Foley
Intubation
What Do These Pictures Have In
Common?
Hypovolemic Shock
• Due to deficiency in intravascular volume
• 3 different categories
– Hemorrhage
• Trauma, surgery, GI bleeding
– Intravascular volume loss
• Gastroenteritis, burns, diabetes insipidus, heat stroke
– Interstitial loss
• Burns, sepsis, nephrotic syndrome, bowel obstruction,
ascities
Treatment of Hypovolemic Shock
• ABC’s
• Volume expansion
– Repetitive bolus and re-assessment
– If no hemodynamic improvement after 2-3
boluses, patient should get blood products
Cardiogenic Shock
• Decreased cardiac output producing inadequate
•
tissue perfusion despite adequate or excessive
circulating volume
Causes
– Massive AMI causing LV dysfunction
– Depression of cardiac contractility
• CHF, sepsis, contusion
– Obstruction of forward flow
• Stenosis, myxoma, HCOM
– Regurgitation of LV output
• Valve deficiency
What Will We Order?
• Studies
– EKG
– CXR
– Cardiac echo
• Labs
– Chest-O
– BNP
– lactate
Clinical Findings in
Cardiogenic Shock
• Tachypnea
• Cool, mottled extremities
• Significant peripheral edema
• JVD
• Cardiac murmurs
Treatment of Cardiogenic Shock
• ABC’s
• Central line and a-line
• If due to AMI
– Heparin, ASA, cath lab
Hypotension in Cardiogenic Shock
• Excessive fluid administration is
contraindicated
– Problem is not volume, its that there’s no
means to push the blood around
• Very small fluid challenges (250 cc)
Pressure Support in
Cardiogenic Shock
• Dobutamine and milrinone are your friends
– Increase contractility
– Can’t use if SBP < 90 because have vasodilatory
properties
• Dopamine alone is bad news  increases
cardiac workload too much
– Has been shown to work well when used in
conjunction with dobutamine
Cardiogenic Shock
• What do these patient’s need more than
anything
– Reperfusion with a quickness
• Cath lab is better than thrombolytics
• Intraaortic balloon pump helps by decreasing
afterload and decreases cardiac work
Distributive Shock
• Anaphylaxis
• Neurogenic
Anaphylaxis
• A severe systemic hypersensitivity reaction
• Multisystem involvement
• May include airway compromise and
significant hypotension
• Caused by a massive release of a cascade
of inflammatory mediators from mast cells
and basophils
Risk Factors for Anaphylaxis
• Those with severe asthma or previous history of
•
anaphylaxis are at risk for fatal or near-fatal
anaphylactic episodes
Recurrence risks are not 100%
– 40-60% for insect stings
– 20-40% for radiocontrast
– 10-20% for penicillin
• Atopic individuals are NOT considered to be at
any greater risk
Clinical Features of Anaphylaxis
• Diffuse uticaria and
•
•
•
•
•
angioedema
Nausea/vomiting
Bronchospasm
Conjunctivitis and
rhinorrhea
Hypotension
Symptoms tend to occur
within 60 minutes of
exposure
Anaphylaxis Pathophysiology
• Mast cell and basophil degranulation and
mediator release
• Causes IgE mediated reaction
• Complement activation
• Process requires a previous exposure
So What Do We Do About It?
• ABC’s
• Single most important step is
administration of epinephrine
• Decontamination/removal of offending
agent
Epinephrine
• Research shows epi is underused in
anaphylaxis
• Start by giving epi bolus (0.1mg) IV
– If refractory, then given epi drip at 1-4
mcg/min
• if Sx less severe, can give IM epinephrine
After Epi….
• Fluids for hypotension
• Steroids (Solumedrol 125mg IV)
• Antihistamines
– Benadryl (50mg IV) is a H1 blocker
– Pepcid (20mg IV) is a H2 blocker
• H2 blockers are controversial, but our attendings tend to use
them  won’t harm patient, might help
• Albuterol + Atrovent nebulizers for
bronchospasm
Neurogenic Shock
• Occurs after acute spinal
cord injury
• Causes disruption of
sympathetic chain
– Leaves unopposed vagal
tone (PNS)
– Causes hypotension and
bradycardia
• Neurogenic shock is NOT
the same as spinal shock
– Spinal shock resolves
within 48 hours and is due
to swelling around the
spinal cord
Neurogenic Shock
• Predominantly due to blunt cord injury
• Most common causes
– MVC
– Falls
– Sports injury
• C-spine is most commonly affected area
Primary vs. Secondary Cord Injury
• Primary
– Caused by initial traumatic event
– Compression, laceration, or stretching of the cord
• Secondary
– Occurs over days to weeks
– Cord ischemia
– Importance is that presentation can change
• An initial incomplete cord injury can evolve into a complete
cord injury
Clinical Features of Neurogenic
Shock
• Generally hypotensive
• Warm, dry skin
– Patient has lost ability to redirect blood from
periphery to the core organs
• Bradycardia
• Hypothermia
• The higher the injury, the more severe
– More likely to disrupt sensory and motor tracts
– Injuries C5 and higher are going to impact patient’s
capacity to breathe on his/her own
Treatment of Neurogenic Shock
• ABCDE’s
– A = airway AND c-spine protection
• Neurosurgery gets involved early
• Use of steroids is controversial and
neurosurgeon dependant
The Moral of the Story
Type
Preload
PCWP
Cardiac
Output
Syst Resist
SvO2
Hypovolemic
i
i
h
i
Cardiogenic
h
i
h
i
Distributive
n
h
i
h
We’re Done!
• Any questions or
comments?