Shock Flashcards
Evidence of cardiovascular organ compromise
Cardiac index < 2.2
SBP < 90
MAP < 65
Signs of hypoperfusion
Cold, clammy, mottled skin
lactate > 2
Scvo2 < 65%
Svo2 < 60%
signs of organ dysfunction
encephalopathy
lethargy
confusion
urine output < 0.5 mL/kg/hr
Blood pressure
CO x SVR
Cardiac output
HR x SV
Stroke volume
preload
intrinsic contractility
afterload
Mean arterial pressure
1/3 SBP + 2/3 DBP
Hypovolemic shock
inappropriately low and sudden loss of intravascular volume:
- blood loss
- GI loss
- severe dehydration
- burns
decreased volume -> decreased preload -> decreased CO
Compensation: increase in SVR
Hypovolemic shock management
Replace fluids
- crystalloids
- occasionally albumin
Hemorrhage:
- replace blood (PRBCs)
- anticoagulation reversal
Cardiogenic shock
LV failure (pump failure)
MI
Arrhythmia
Heart failure
Dilated cardiomyopathy
impaired emptying of left ventricle -> decreased CO -> fluid backup in pump -> preload increases
Compensation: increased SVR
Cardiogenic shock management
MI:
- revascularization CABV
Arrhythmia:
- achieve sinus rhythm
Distributive shock
pronounced vasodilation “vasodilatory shock”
Sepsis
anaphylaxis
neurogenic
myxedema coma (thyroid deficiency)
adrenal insufficiency
hepatic insufficiency
vasodilation -> reduced SVR -> decreased vol returning to heart -> decreased preload
Compensation: HR increase
Obstructive shock
obstruction in LV preventing pushing blood out
- pulmonary embolism
- severe pulmonary hypertension
- tension pneumothorax
- pericardial tamponade
decreased LV stroke volume -> decrease in CO and tissue perfusion
preload will appear high due to obstruction
Compensation: increased SVR
Goal MAP in shock treatment
> 65
Fluid therapy
Crystalloids 30 mL/kg over 15-30 min then 10 mL/kg boluses
Cardiogenic shock : 100-200 mL boluses
increase SV, CO, DO2
initiate vasoactive agent when MAP remains < 65 despite fluid admin
Vasopressors
Norepinephrine
Epinephrine
Dopamine
Phenylephrine
Vasopressin
Norepinephrine
Alpha adrenergic agonist - increases MAP via peripheral vasoconstriction
preferred over dopamine in septic shock
- less risk of arrhythmias
- improves renal blood flow
ADE
- significant vasoconstriction
Epinephrine
potent alpha and beta adrenergic agonist
Low dose -> beta effects -> inc HR, SV, and b2 vasodilation
High dose -> alpha effects
useful for anaphylactic shock
in septic shock, 2nd line after norepinephrine
ADE
- tachycardia
- arrhythmias
- cardiac ischemia
- peripheral vasodilation
- reduced renal blood flow
- hyperglycemia
- hypokalemia
Dopamine
Most effective in hypotensive pts with decreased cardiac function
useful in pts with bradycardia
low dose: dopaminergic
- vasodilation of renal, mesenteric, and coronary
- increases renal blood flow, GFR, and sodium excretion
Med dose: beta adrenergic
- increase cardiac contractility and HR
- increase norepi release form nerve terminals
High dose: alpha adrenergic
- arterial vasoconstriction
ADE:
- tachycardia
- arrythmias
- peripheral vasoconstriction
Phenylephrine
Alpha 1 adrenergic agonist
not recommended in septic shock unless:
- NE produces significant tachyarrhythmias
- cardiac output is high and BP is persistently low
- salvage therapy when standard therapies are ineffective
ADE
- severe vasoconstriction
- bradycardia
- myocardial ischemia
Dobutamine
Inotrope - increased cardiac contractility
added to treatment of shock when cardiac output of SVO2 / SCVO2 goals have not been achieved with vasopressor therapy
often used for cardiogenic shock
Vasopressin
ADH
Relative deficiency in septic shock
Dose: 0.3 U/min
should not be used as the sole vasopressor in sepsis
ADE
- cardiac and mesenteric ischemia
