100714 shock Flashcards
shock definition
inadequate tissue perfusion marked by decreased delivery of required metabolic substrates and inadquate removal of cell waste
classification of shock
hypovolemic cardiogenic septic neurogenic traumatic obstructive
ex of obstructive shock
cardiac tamponade, pulmonary embolus
MAP is reduced
stages of shock
initial
compensatory
progressive
refractory
what stage is hyperventilation?
compensatory stage of shock
refractory stage of shock
irreversible organ damage, cell death, degradation of ATP to adenosine
physiological response to shock
progressive vasoconstriction (NE, epinephrine) increased blood flow to vital organs (shunting away from skin, acral regions, splanchnic system)
increase in respiratory rate and tidal volume
reduced urine production
reduced GI activity
pathophysiology of cardiogenic shock
inadequate myocardial perfusion (decreased duration of diastole due to compensatory tachycardia)
excessive increase in myocardial oxygen consumption (tachycardia and increased myocardial wall tension)
metabolic derangement (lactic acidosis, leading to cardiac dysfxn)
in cardiogenic shock, compensatory mechanisms result in
increased pre and afterload (lead to further increase in myocardial oxygen consumption and progression of shock). worsening of cardiac fxn
management of cardiogenic shock
optimize ventricular filling
improve coronary perfusion pressure with vasopressors (ne, phenyepinephrine), inotropics (dobutamine, epinephrine, milrinone), IABP/mechanical circulatory support (LVAD, RVAD)
if acute MI-coronary agiography and immediate revascularization
what adrenergic receptor causes vasoconstriction?
alpha 1
SIRS
at least 2 of the following criteria:
tachypnea
WBC 12000 cells/mm3
HR>90
fever >38 (100.4 F) or hypothermia <36 (96.8 F)
sepsis
SIRS with an infec
on top of SIRS, at least 1 of the following showing inadequate organ perfusion is included:
- altered mental state
- hypoxemia
- elevated plasma lactate
- oliguria
severe sepsis
sepsis induced hypoperfusion or organ dysnfxn
septic shock
has all of the findings of SIRS, sepsis, and severe sepsis BUT has also persistent arterial hypotension in severe sepsis DESPITE ADEQUATE FLUID RESUSCITATION or by tissue hypoperfusion not explained by other causes
culture positive bacteremia exists in only 30-50 % of cases
multi organ dysfxn syndrome
beyond severe sepsis
there’s primary and secondary MODS
primary: direct result of insult
secondary: consequences of host response (ex is cytokine release). inflam response to toxins and other components of microorganisms, leading to clinical manifestations of sepsis
causes of septic and vasodilatory shock
infec noninfec systemic inflam pancreatitis burns anaphylaxis acute adrenal insuff prolonged, severe hypoten hemorrhagic shock cardiogenic shock cardiopulmonary bypass metabolic-hypoxia, lactic acidosis carbond monoxide posioning
recommendations in sepsis
initial resuscitation screening of at risk pts diagnosis antimicrobial therapy (empiric started within 1 hr) source control-draining abscesses, etc infec prevention
initial fluid resuscitation
crystalloids or albumin (if require excessive amts)
therapy for hemorrhagic shock
volume therapy
neurogenic shock
profound vasodilation of arterial and venous blood vessels
causes are injury of brain stem, sp cord, or traumatic brain injury
in higher doses, epinephrine is a
alpha mimetic, leading to vasoconstriction
intraarterial balloon pump
inflates during diastole-use to increase diastolic perfusion pressure to coronary arteries
what do you want to do for shock pts?
optimize milieu control rate and rhythm optimize preload enhance contractility decrease or increase SVR
what to consider when giving beta adrenergic agents
heart rate
systemic vascular resistance
for hypotension that does not respond to initial fluid resuscitation, what will you do?
vasopressors
measure CVP, central venous oxygen saturation
diaphoresis can be seen in
shock
also MI
loss of bladder control could indicate
anaphylactic shock
