11/11 Shock - Corbett Flashcards
shock
physiological state characterized by insufficient oxygen delivery to tissues
over time…
- accumulation of cellular energy deficit: low ATP levels
- 40-60% mortality regardless of cause
consequences of low ATP levels
- no protein or RNA synthesis
- failure of membrane ion pumps → loss of membrane potential
- reduced DNA repair
- cytosolic proton burden increases
clinical shock and hypotension
clinical shock often accompanied by hypotension
MAP < 60mmHg in a previously normotensive person
- recall: MAP = [2diastolic + 1systolic]/3
patients can maintain bp in normal range despite profound tissue hypoperfusion through compensatory mechs (ESP YOUNGER PTS)
compensatory mechs for hypotension
1. baroreceptor response
- baroreceptors are tonically active
- decr arterial pressure → decr baroreceptor firing in carotid sinus and aortic arch
- in turn: leads to decr firing of inhibitory neurons → disinhibition of vasomotor center…
- incr SNS tone
- incr vasoconstriction
- incr inotropy, chronotropy
2. renin-angiotensin system
- vasoconstriction
- Na reabsorption
when compensation fails, irreversible shock state is imminent
classifying shock
determinants of bp
compensation and presentation
consider: components of bp
- cardiac output
- systemic vascular resistance
both compensate for the other
ex. when CO drops, vascular resistance will increase to compensate
- clinically, low CO shock:
- cool, clammy skin w/ pale or gray color: vasoconstriction shunts blood from periphery to vital organs →→→ LOOK AT THE SKIN!
- mental status changes: agitation/anx, confusion, obtundation
metabolic acidosis
- induces tachypnea (compensatory respiratory alkalosis)
- lactic acid production exceeds liver’s ability to clear lactate
- anaerobic metabolism leads to rapid worsening acidemia
low cardiac output shock
determinants of CO
types of shock associated with each
cardiac output:
- stroke volume
- myocardial contractility
- cardiogenic shock (ex. MI)
- preload (volume)
- hypovolemic shock (ex. hemorrhage)
- obstructive shock (ex. tension pneumothorax, pericardial tamponade)
- afterload
- ex. pulmonary embolism
- myocardial contractility
- heart rate
classification of shock:
types of low CO shock
- cardiogenic
- hypovolemic
- obstructive
- pericardial tamponade
- tension pneumothorax
cardiogenic shock
basics
pathophys
low CO shock
- leading cause of death for pt with acute MI
- occurs 5-7hr postMI
- STEMI > NSTEMI
- almost 80% mortality
- 50% of deaths in first 48h
- most common reason: primary pump failure
- MI
- cardiomyopathy (fulminant myocarditis, dilated cardiomyopathy)
- rhythm disturbance
- valvular HD
pathophysiology
- coronary occlusion → MI
- profound depression of myocardial contractility
- reduced CO
- low bp
- worsening coronary insufficiency
clinical findings of cardiogenic shock
- hypotension and low CO
- tachycardia, faint pulses, distant heart sounds, displaced apical impulse
- hypoperfusion
- agitation, disorientation, lethargy
- cool, clammy, cyanotic extremities
- oliguria
- congestion
- elevation of jugular venous pressure or pulmonary rales, 3rd heart sounds
cardiogenic shock
- filling pressure
- periph varc resistance
- cardiac output
- cardiac contractility
hypovolemic shock
intravascular volume depletion
- loss of blood cell mass
- trauma, GI bleed, post operative issue
- loss of plasma volume
- extravascular volume fluid sequestration
- GI, GU, or insensible loss
- burn injury
loss of blood and loss of plasma show same symptoms!
- cold/clammy skin; gray/pase/mottled skin
- weak, thready pulse
- narrow pulse pressure
- tachycardia
- altered mental status
- oliguria
Class 1-4 determined by how much blood has been lost (and the degree of compensatory mechanisms seen)
what should we look at to determine if a pt is in hypovolemic shock
systolic bp takes a while/a lot of blood loss to register
diastolic bp can be used to tell a little sooner!
- PVR will increase with blood loss and actually RAISE diastolic bp early on → narrow pulse pressure is a good first sign of hemmorhagic shock
hypovolemic shock
- filling pressure
- periph varc resistance
- cardiac output
- cardiac compliance
obstructive shock
impaired venous return to R or L ventricle
- pericardial tamponade
- tension pneumothorax
- also massive PE
pericardial tamponade
compression of heart due to flud accumulation within pericardium
clinical features
- hypotension
- tachycardia
- muffled heart sounds
- jugular vein distension
- pulsus paradoxus → sensitive (82%)
Beck’s Triad
respiratory variations with inspiration
(normal)
RV volume/filling mechanism
valve?
LV volume/filling mech
valve?
net effect of INSPIRATION: physiologic splitting! (A2 closes sooner, P2 closes later)
- A2 occurs earlier bc pulmo arteries and veins are a little distended and hold more blood, so left side of heart less full
- P2 occurs later bc venous return is increased and right side of the heart of more full
mechanism: pulsus paradoxus
- normally, when you breathe in, incr return to R side of heart BUT no change to L side of heart bc heart is compliant
- in pericardial tamponade, fluid pools all around heart → decr compliance, leading to decr ability to adapt to volume increase
- most compliant region left is the septum, which will be pushed into the LV → worsens ability of L heart to fill
overall: lower volume and lower pressure
→→→ big inspiratory drop in bp in cardiac tamponade!
pericardial tamponade: eletrical alternans
variable electrical signal seen within the same rhythm strip on EKG
→→→ heart is moving within pericardium! floating in the fluid
pericardial tamponade
- filling pressure
- periph varc resistance
- cardiac output
- cardiac contractility
tension pneumothorax
- clinical features
filling pressures
PVR
CO
cardiac contractility
clinical features
- absent breath sounds
- jugular venous distension
- tracheal deviation
shock due to decr in systemic vascular resistance
distributive shock
- septic
- anaphylactic
- neurogenic
compensation: incr in CO
distributive shock
- septic shock: decr in peripheral vascular resistance (despite incr vasopressors)
- neurogenic shock: loss of SNS tone secondary to spinal cord injury
- anaphylactic shock: histamine, leukotriene C4, prostaglandin D2 release → profound vasodilation
septic shock
basics
pathophysiology
source: chest abdomen, urinary tract, primary ploodstream
- Gram- : 25-30%
- Gram+/mixed : 30-50%
initiated by “danger signals” (pathogen-associated molecular patterns: LPS, flagellin, fimbria, DNA, etc) that are picked up by pattern recognition receptors (ex. Toll receptors, Nod receptors)
pathophysiological changes in sepsis
- distributive shock (vasoplegic shock) : failure of vasc smooth muscle constriction
- diffuse endothelial injury
- microvascular leak → hypovolemia, tissue/organ edema
- altered microvascular flow
overall: vasodilation, incr permeability, decr perfusion
sepsis: clinical features
filing pressures
PVR
CO
cardiac contractility
- marked decrease in peripheral vascular resistance
- NO, platelet activating factor, prostacyclin, beta-endorphin
- CO increased
- peripheral bloodflow increased
- impaired peripheral oxygen utilization
- diminished vasoconstrictor response to catecholamines
comparison of types of shock
