Shock Flashcards
when O2 supply< O2 demand and leads to organ dysfunction
shock
OER (O2 extraction)=
VO2/DO2
VO2=
CO(CaO2-CvO2)
DO2=
COxCaO2
what happens if cardiac output (CO) decreases
DO2 and VO2 decrease
total O2 content in arterial blood
CaO2
CaO2=
(Hbx1.34xSaO2/100)+(0.003xPaO2)
depends on pulmonary gas exchange
PaO2
the supply of O2 depends on
CaO2
systemic O2 demand increases in what situations
stress, pain, fever, exercise
shock that has decrease in blood volume and CO
Hypovolemic shock
2 types of hypovolemic shock
hemorrhagic and fluid loss
2 types of hemorrhagic hypovolemic shock
traumatic: spleen rupture
non-traumatic: bleeding ulcer
types of fluid loss hypovolemic shock
diarrhea, vomiting
burn
ascites
polyuria
type of shock dealing w/ heart not functioning properly
cardiogenic shock
main ways cardiogenic shock can happen
MI
myocarditis
arrythmia
aortic and mitral regurgitation
shock due to blood not flowing (venodilation)
distributive shock
most common form of shock and fatal form
septic shock
3 main types of distributive shock
septic
anaphylactic
neurogenic
shock due to diastolic filling not happening due to restriction
obstructive shock
tension pneumothorax
cardiac tamponade
restrictive pericarditis
pulmonary embolism
aortic dissection
all lead to what shock
obstructive shock
best example of obstructive shock due to fluid in pericardial sac
cardiac tamponade
leads to obstructive shock due to L ventricle basically empty due to oxygenated blood unable to come back from lungs
pulmonary embolism
shock due to O2 not being able to be utilized/consumed
Dissociative shock
2 main things that can lead to dissociative shock
CO poisoning
Cyanide poisoning
contractility (inotropy) of heart depends on what
Ca2+ sensitivity and binding to troponin C
sarcomere length based on diastolic filling (preload)
Starling effect
preload is measured by what
pulmonary artery catheter
end diastolic sarcomere length=
preload
how to measure pulmonary capillary wedge pressure
catheter goes from SVC all the way to pulmonary a. and is measured based on end diastolic sarcomere length
decrease in SVR (primary); CO increases (secondary)
distributive shock
decrease in CO (primary); SVR increases (secondary)
cardiogenic shock
obstructive shock
hypovolemic shock
difference b/t cardiogenic LV and cardiogenic RV shock
cardiogenic LV has increased PCWP (wedge pressure)
cardiogenic RV has decreased PCWP (wedge pressure)
ultimately what happens to compensate in shock
baroreceptor reflex and chemosensors respond (sympathetic activation)
one of the earliest and very important signs of shock (most sensitive indicator of shock)
tachycardia
what happens to HbO2 curve to compensate for shock
shifts to the R (O2 unloading)
when DO2 decreases in shock, what compensates
increase in OER (O2 extraction)
what happens if increasing OER doesn’t meet systemic O2 demands
switch metabolism to anaerobic (lactic acidosis)
critical lab to order and diagnose shock
lactate
stage of shock that is reversible; tissue hypoperfusion
compensated
stage of shock where there is vital organ failure
progressive
stage of shock that is irreversible and has multisystem organ failure
decompensated
could be the only sign to diagnose shock
compensatory tachycardia (>100 BPM)
MAP when diagnosing shock
<65 mmHg
levels of lactic acidosis that would diagnose shock
> 2 mmol/L
2 main organ dysfunctions due to hypoperfusion
brain (anxiety/confusion) and kidneys (oliguria)
sign of heart failure
S3 gallop
shock index=
HR / SBP (systolic bp)
shock index of 1.5 means what
patient in shock
most common type of shock
distributive (vasodilatory) shock
main vasodilator in distributive shock
NO
NO binds what receptor
B2 (Gs signaling)
low dose effect of histamine
H1 (Gq) —> NO release
high dose effect of histamine
H2 (Gs) VSMC relaxation
histamine release causes bronchoconstriction how
H1 (Gq) BSMC contraction
Rhoa and ROCK activation can lead to what
blood leaking through cells
why Epi over NE for anaphylactic shock
Epi binds B2 and bronchodilates (taking care of dyspnea)
primary cause of septic shock
massive vasodilation due to NO production
caused by infection + SOFA >/= to 2 points (acute organ dysfunction)
Sepsis
sepsis + circulatory failure (need vasopressors) + tissue hypoxia
septic shock
worst case SOFA for each individual organ
4
maximum total SOFA score
24 (worst case)
main pathogens that cause septic shock
S. aureus
S. pneumo
E. coli
why does uncomplicated infection become sepsis
damage by pathogen
host’s immune response
coagulation abnormalities
hypoxia
clinical features of septic shock (5 things)
warm initially
acute lung inflammation
heart failure
acute kidney injury
CNS
quick test to see whether patient will respond to fluids (fluid responsiveness in shock)
passive leg raise
broad spectrum Ab therapy
VANCOMYCIN (IV)
2 main things to monitor with shock
lactate and MAP
example of distributive shock that deals with spinal cord trauma due to someone falling from a height; disruption of sympathetic outflow
neurogenic shock
triad of bradycardia, hypotension, and peripheral vasodilation
neurogenic shock
HR 50/min; BP 80/40 mmHg after patient fell from height
neurogenic shock
2 main things to do to help w/ cardiogenic shock
- increase BP
- ventilation
in RV failure, LV CO low and PCWP low means what for the lungs
clear lungs b/c no pulmonary congestion
what would make RV failure cardiogenic shock worse
VASODILATORS
B1 and B2 agonist and a1 agonist
dobutamine
“renal dose” does not improve renal function; used in bradycardia and hypotension
dopamine
used in septic shock
vasopressin
vasodilatory shock; best for supraventricular tachycardia
phenylephrine
1st line vasopressor for septic shock
NE
used for anaphylactic shock
Epi
used for cardiogenic shock and septic shock
dobutamine
used in cardiogenic shock and CHF
milrinone
blood loss of 750-1500 mL
tachycardia
class II hemorrhagic shock
sweating
pale and cold
thirsty
hypovolemic shock
3 things to do to Rx hemorrhagic shock
control source
give fluids
take to OR
used to check for free fluid in abdomen
FAST exam
used to replenish volume in hemorrhagic shock
crystalloids
no parasympathetic input to VSMC; but how does Ach cause vasodilation
sodium nitroprusside (used for HTN emergency) produces what 2 things
NO and cyanide
has high affinity for complex IV (holds O2)
cyanide
what can happen from administering sodium nitroprusside that causes O2 not to be able to bind complex IV (leading to dissociative shock)
cyanide poisoning
drug that blocks cyanide from binding complex IV
hydroxocobalamin
patient will have cherry red hue to them from what
cyanide bound to complex IV
what has higher affinity for complex IV than cyanide; and how to treat effect of it
MetHb; methylene blue to treat Methemoglobinemia
how to stop CN- from binding complex IV; and allows O2 to bind
sodium nitrite (will produce CN-Hb(Fe3+)
hepatic enzyme that will take off CN- from MetHb and convert to sodium thiosulfate
Rhodanase
kit to give patient in emergency room with cyanide poisoning
cyanide kit
4 main things you can treat cyanide poisoning with after administering fluids
cyanide kit
hydroxocobalamin
sodium nitrite
sodium thiosulfate (has sulfur)
in neurogenic shock, what drug to administer to increase HR (due to bradycardia)
M-antagonist (ATROPINE)
sympathomimetic agent used in anaphylactic shock
Epi
B1 agonist(Gs—cAMP) that is used in cardiogenic shock
Dobutamine
how would propranolol affect SVR and CO when patient is in rebound HTN
blocking B2 (SVR increases)
blocking B1 (CO decreases)
what will reverse effects of sodium nitroprusside overdose (cyanide poisoning)
sulfur