Shock

Definition

SHOCK: inadequate organ

perfusion to meet the tissue’s
oxygenation demand.
 Three major types of shock
 Hypovolemic shock
» Decreased intravascular volume resulting
form loss of blood, plasma, or fluids and
electrolytes
 Cardiogenic shock
» Pump failure due to myocardial damage or
massive obstruction of outflow tracts
 Distributive shock
» Reduction of vascular resistance form
 Sepsis
 Anaphylaxis
 Systemic inflammatory response
syndrome (SIRS)
Cardiogenic Shock
 Cardiogenic Shock

Diminished cardiac output

leading to impaired tissue
perfusion

Most extreme form of pump

failure
 Cardiogenic Shock
Occurs in about 15% of acute MI
patients
Usually occurs when 40% or more
of the left ventricular muscle mass
infarcts
Mortality is 85% or more with
treatment
 Etiologies
 Other conditions complicating
 Acute myocardial large MIs
infarction/ischemia
 LV failure
 Papillary
muscle/chordal
rupture- severe MR
 Ventricular free wall
rupture with subacute
tamponade
» Hemorrhage
» Infection
» Excess negative inotropic or
vasodilator medications
» Prior valvular heart
disease
» Hyperglycemia/ketoacidosis
» Post-cardiac arrest
» Post-cardiotomy
» Refractory sustained
tachyarrhythmias
» Acute fulminant
myocarditis
» End-stage
cardiomyopathyHypertroph
ic cardiomyopathy with
severe outflow obstruction
» Aortic dissection with aortic
insufficiency or tamponade
» Pulmonary embolu
» Severe valvular heart
disease -Critical aortic or
mitral stenosis, Acute
severe aortic or MR
Pathophysiology
 Characteristics of Cardiogenic Shock
 Low cardiac output

 Peripheral vasoconstriction

 Left
sided heart failure leads to pulmonary
venous congestion and pulmonary edema

 Right
sided heart failure leads to systemic
venous congestion and peripheral edema
It is essential to distinguish a cardiogenic from a hypovolemic
shock!
Both forms are associated with reduced cardiac out put, and increased peripheral
vascular resistance, however:

Cardiogenic shock:
jugular venous distention (high
CVP)

Hypovolemic shock: collapsed

capacitance veins (low CVP)
 Signs/Symptoms
Confusion, restlessness,
anxiety, stupor, coma
Cool, clammy skin
Pallor
Weak or absent extremity
pulses
Tachycardia
Slow or absent capillary refill
 Signs/Symptoms
BP< 90 systolic or > 30mmHg
below normal
» BP is NOT the same as perfusion
» Shock can be present with a
“normal” BP
» Evaluate signs of peripheral
perfusion in addition to BP
 Cardiogenic Shock
Treatment Priorities:
» Rate
» Rhythm
» BP (Volume, Pump/Vascular tone)
Correct major disorders of
rate, rhythm before directly
treating BP
 Goals of Management
Improve oxygenation and
peripheral perfusion
Avoid increasing cardiac
workload
» myocardial oxygen demand
 Management
Primary assessment & Focused
Hx
Identify source of problem
» Acute pulmonary edema
» Volume problem
» Pump problem
» Rate problem
 Acute Pulmonary Edema
First line interventions
» IV/O2/ECG Monitor
» If BP > 90-100 mm Hg:
 furosemide 0.5 – 1.0 mg/kg slow IV
(or twice patient’s single daily dose
up to 120 mg)
 Morphine 2 – 10 mg slow IV
 Nitroglycerin 0.4 mg SL

» If BP < 90 mm Hg:
 Vasopressors based on SBP
 Volume Problem
IV/O2/ECG Monitor
Fluid challenge until rales or if
evidence of anterior wall AMI
Vasopressors based on SBP
 Pump Problem
IV/O2/ECGMonitor
SBP <70 mmHg:
» norepinephrine 0.5 – 30 mcg/min IV
inf
SBP 70 – 100 mm Hg & shock
» dopamine 5 – 15 mcg/kg/min IV inf
SBP > 100 mm Hg w/o shock
» dobutamine 2 – 20 mcg/kg/min IV inf
 Management
If
rate/rhythm adequate, treat
BP
» Consider fluid challenge of 250cc
LR over 10-15 minutes if relative
or absolute hypovolemia possible,
including RVF and NO
pulmonary edema
» Avoid use of vasopressors until
volume deficits corrected or
pulmonary edema presents
 BP Treatment Review
Ifrate, rhythm, volume
adequate, treat BP with
vasopressors:
» Norepinephrine, or
» Dopamine
 Norepinephrine
 0.5 - 30 mcg/min
 Inotropic and vasoconstrictive
properties
 Can be used if systolic BP < 70
 If systolic BP > 70, use dopamine
instead
 DO NOT use until hypovolemia
corrected
 DO NOT allow infiltration
 Dopamine
2 - 20 mcg/kg/min
» Place 200 mg/250cc of D5W
» Begin at 5 mcg/kg/min
» In 2 - 10 mcg/kg/min range,  effects
dominate
» > 20 mcg/kg/min  effects dominate
» Use lowest dose that produces good
perfusion
 Useas initial vasopressor if BP 70-100
systolic
» If dopamine infusion rate is > 20
mcg/kg/min use norepinephrine
 Dopamine
May cause tachycardia, ectopy,
nausea
DO NOT use until hypovolemia
is corrected
Distributive Shock
 Distributive Shock
Reduced peripheral vascular tone
leads to pooling of blood in
extremities  poor venous return
Physical exam depends on stage
» Early: Warm extremities, wide pulse
pressure, low diastolic pressure
» Late: perfusion pressure falls and acidosis
develops
 Distributive Shock
 Sepsis
» Due to gram negative or gram positive
bacteria
 Anaphylaxis
» Due to previous sensitization to an
allergen
 Neurogenic
» Due to traumatic spinal cord injury
» Effects of epidural or spinal
anesthetics
» Reflex parasymapthetic stimulation
 Bacteremia, SIRS, Sepsis
 Bacteremia: an identifiable organism
cultured from the blood
 Systemic Inflammatory Response Syndrome
(SIRS): sepsis without organism identified.
Meet at least 2 of criteria:
» Hypo or hyperthermia
» Tachycardia or bradycardia
» Tachypnea
» Leukocytosis or leukopenia
 Sepsis:SIRS from a systemic illness
(bacterial, viral, protozoal)
 Pathogenesis of Septic Shock
(vasodilatory shock)
 Sepsis is defined as a systemic inflammatory
response to a bacterial infection with bacteriemia
(though blood cultures can be negative)

 Severe sepsis is defined by additional end-organ

dysfunction (mortality rate: 25-30%)

 Septic shock is defined as sepsis with

hypotension despite fluid resuscitation and
evidence of inadequate tissue perfusion (40-70%)
NEJM 2004, Vol. 351;2 pp 159-169
 The syndrome of septic shock is
characterized by
 Systemic vasodilation (hypotension)

 Diminished myocardial contractility

 Widespread endothelial injury and

activation leading to fluid leakage
(capillary leak) resulting in acute
respiratory distress syndrome (ARDS)

 Activation of the coagulation cascade

(DIC)
 Septic Shock
 Early “Warm Shock”  Late “Cold Shock”
 ↑ CO and ↓ SVR and  Uncompensated shock
wide pulse pressure with drop in CO
 Signs: warm  Signs: cyanosis, cold,
extremities, flushing, clammy skin, thready
bounding pulses, ↑ HR, pulse, shallow
confusion respiration
 Hypocarbia, elevated  Metabolic acidosis,
lactate, hyperglycemia hypoxia,
coagulopathy,
hypoglycemia
 S/S of Septic Shock
Increased to low blood
pressure
High fever, no fever,
hypothermic
Skin flushed, Pale, Cyanotic
Difficulty breathing and
altered lung sounds
 TX of Septic Shock
Airway control
Administer oxygen
IV of crystalloid solution
Dopamine for blood pressure
support
Monitor other vitals
 Anaphylatic Shock
Severe immune response to
foreign substance
S/S most often occur within
minutes but can take up to
hours to occur
The faster the reaction
develops the more severe it is
likely to be
Death will occur if not treated
promptly
 S/S of Anaphylactic Shock
 Skin
- Flushing
- Itching
- Hives
-Swelling
-Cyanosis
 S/S of Anaphylactic Shock
Respiratory System
- Breathing difficulty
- Sneezing, Coughing
- Wheezing, Stridor
- Laryngeal edema
- Laryngospasm
 S/S of Anaphylactic Shock
Cardiovascular System
- Vasodilation
- Increased heart rate
- Decreased blood pressure
 S/S of Anaphylactic Shock
Gastrointestinal System
- Nausea, vomiting
- Abdominal cramping
- Diarrhea
 TX for Anaphylactic Shock

 Airway protection which may include

Endotracheal Intubation
 Establish IV with crystalloid solution
 Pharmacological interventions:
Epinephrine, Antihistamines(Benadryl),
Corticosteroids(dexamethasone),
Vasopressors(dopamine, Epinephrine), and
inhaled beta agonist(albuterol)