Hemodynamic Instability Flashcards
what is an aortic aneurysm
permanet localized dilation of the aorta that is 50% greater than the normal diameter
what are the three classifications of aortic aneurysms
ascending
descending
abdominal
what is the most common location
infarenal
what are the 3 layres of blood vessel
tunica intima (inner thin) tunica media (smooth muscle, middle) tunica adventitia (outer
what causes aneurysms
degenerative processes of elastin/collagen and smooth muscles - thinning of tunica media causing loss of structural integrity and dilation d/t large volumes and pressures in aorta
risk factors for AAA
tobacco use advanced age male etOh family hx atherlerclerosis
what are the 4 main arteries coming off the abdominal aorta
celiac superior mesenteric renal inferior mesenteric iliac
what do the celiac arteries supply
foregut
stomach, speleen, liver, esophagus and parts of the pancreas and duodenum
what do the superior mesenteric arteries supply
midgut
jejunum, ilieum, appendix, cecum, ascending colon, 2/3 transverse colon
what do the renal arteries supply
kidneys
what do the inferior mesenteric arteries supply
hindgut
distal 1/3 of transverse colon, descending colon, sigmoid and rectum
what do the iliac arteries supply
the legs
T or F 2/3s of AAA are asymptomatic and found on routine exam
T
symptoms of AAA include
abdominal pain low back pain flank pain N/V ischemia to lower limbs
what is the triad of symptoms associated with AAA rupture
severe abdominal pain
hypotension
pulsatile mass
if AAA is ruptured is sx required
yes
if AAA is not ruptured what are your two options
open surgical repair
insertion of endovascular stent (high risk)
how is heparin reversed post AAA sx
protamine
what is the most common postop complication for EVAR
endoleak - leak around stent
what can prolonged cross-clamp time cause
spinal ischemia and neuro deficits
what are the 5 Ps of ischemia
pain pallor pulselessness paralysis paresthesia
what do you need to have good control of post AAA sx
hypertension
what can cause ischemia in lower limbs post AAA sx
embolization of thrombus/debris to lower limbs, gut or kidney
what are 3 common drugs given for HTN
hydralazine
labetalol
nitroglycerin
how does hydralazine work
arterial vasodilator
decreases afterload
how does labetalol work
beta 1 and 2 and alpha antagonist
decreases HR and afterload
if a pts hr is 59 should you give labetalol
no
how does nitro work
venous vasodilation
arterial vasodilation at higher doses
decreases preload and afterload
dilates coronary arteries
what is shock
acute widespread impaired tissue perfusion resulting in cellular, metabolic and hemodynamic alterations
what does shock result from
any determinants in CO (preload, afterload, contractility)
what receptors sense a decrease in stretch of the vessel wall? what do they activate
baroreceptors
SNS
what do alpha receptors do when the SNS is activated where are they located
vasoconstriction
skin, GI, peripheral vessels
increases afterload
shunts blood to important areas
what do B1 receptors do when the SNS is activated
increase HR and contractility
where are B2 receptors found and what do they do when SNS stimulated
lungs and skeletal muscle (legs)
dilate bronchi
take faster and deeper breaths to improve ventilation and gas exchange
dilates arteries in skeletal muscle to increase perfusion
describe the steps in RAAS
renin is secreted from the kidney d/t decreased perfusion, renin then converts angiotensinogen from the liver to angiotensin 1 which is converted to angiotensiongen 2 by ACE in the lungs which is a potent vasoconstrictor, stimulates ADH from posterior pituatoary, stimulates aldosterone
How does RAAS affect preload and afterload
angiotensin 2 is a potent arterial vasoconstrictor (inc afterload)
stimulates ADH to be released from the posterior pit which increases preload
stimulates aldosterone which increase preload
what are the 4 types of shock
hypovolemic
distributive
cardiogenic
obstrcutive
what is the primary problem with hypovolemic shock
decreased preload
what is the primary problemw ith distributive shock
decreased afterload
what is the priamry problem with cardiogenic shock
decreased contractility
what is the primary problemw ith obstructive shock
high afterload and decreased preload
outflow is obstructed
what are the 4 stages of shock
initial stage
compensatory stage
progressive stage
refractory stage
what occurs in the inital stage of shock
decreased CO threatens tissue perfusion
what occurs in compensatory stage of shock
homeostsatic mechanism kick in
what occurs are neural compensatory mechanisms
increased HR/contractility, vasoconstriction, shunting to vital organs
what are chemical compensatory mechanisms
chemoreceptor mediated resp changes triggrered by hypoxemia and hypercapnia
what are hormonal compensatory changes
activation of RAAS
what happens in the progresive stage of shock
failing compensatory mechanisms
swtich to anaerobic metabolism
vasodilation and permeability
SIRS
what occurs in the refractory stage
shock unresponsive to therapy, irreversible MODS and death
what is the effect of hypovolemic shcok on O2 S&D
decreased preload
decreased contractility
decreased CO
what are 5 ways to evaluate volume status
POCUS CVP Passive leg raise hx physical assesment
what are 4 physical assesment findings that indicate depleted volume status
dry skin/mucous membranes
tachycardia (compensatory)
decreased EOP (decreased UO, cool extremeites)
increased afterload d/t compesnatory mechanisms
what are crystalloid fluids that are isotonic
NS
RL
plasmalyte
what is a hypertonic crystalloid
3% NS
what are examples of colloids
albumin
PRBC
FFP
Platelets
T or F D5W is isotonic but becomes hypotonic
T glucose gets used up by brain
what are the three types of distributive shock
anaphylaxis
neurogenic
sepsis
what is distributive shock
decreased afterload from profound arterial dilation
decreased preload as a result of decreased venous return
what type of pulse pressure would you see in sepsis
wide/low diastolic
what is cardiogenic shock
impaired ability of heart to pump
poor contractility
impaired ability of LV emptying –> increased preload and pulmonary edema
what effects does norepinephrine have
sympathomimetic
strong alpha but does have some beta
increases afterload
what part of CO does levo effect
afterload
what receptors does epinephrine work on
beta 1, 2 and alpha receptors
primarily beta @ low doses results in inc HR and contractility
more alpha @ high doses increasing afterload
what is vasopressin and what part of CO does it work on
antiduretic hormone
increases afterload and preload
T or F vasopressin is typically ran at a fixed rate
true
what receptors does vasopressin work on
V1 increasing afterload and smooth muscle contraction of GI tract
V2 influencing preload as it works on the kidney producing antidiuretic effects
What receptors does phenylephrine work on and what part of CO does it affect
alpha receptors to increase afterload
what happens to stroke volume nad CO in cardiogenic shock
decreased stroke volume
decreased CO
what type of pulse pressure would you see in cardiogenic shock
narrow
what are 4 caues of cardiogenic shock
damaged myocardial msucle
mechnical impairment
cardiomyopathies
sepsis
what are some examples of mecahnical impairment causing cardiogenic shock
large PE, cardiac tamponade, vavlular disease
why does sepsis cause cadiogenic shock
release of MDF
4 clinical findings in a pt with cardiogenic shock
pulmonary edema and generalized edema
frothy sputum
cool, cyanotic extremeites, delayed cap refill
decreased EOP
what types of meds would we want to give to help with cardiogenic shock
inotropes!
what are inotropes often titrated to
ScVO2 or lactate
what receptors does dobutamine work on
beta 1 primarily but some beta 2
what does dobutamine do
increased contraclitly with some potential decreased afterload
fast onset 10-20 mins
T or F dobutamine is more likely to cause tachycardia then dopamine
False it is less likely
what type of drug is milrinone and how does it work
phosphodiesterase 3 inhibitor
leads to increase in available calcium and causes increased contractility
also causes vasodilation including pulmonary arteries redicing rt and lt afterload
does milrinone have a long half life
yes dose change q6h
what inotrope is used to treat pulmoanary HTN and rt ventricular afterload
milrinone
what type of drug is dopamine
sympathomimetic agent acting on B1 restuling in inc Hr and contractility
effects are dose dependent
what does dopamine do at low doses
inc renal perfusion
what does dopamine do at medium doses
increased contracility
what does dopamine do at high doses
increased afterload
does dopamine cause tachycardia
is a common finding
what is obstructive shock caused by
obstruction of the great vessels or the heart itself
what type of shock is there a rapid massive drop in CO and b[
obstructive
what are some examples of obstructive shock
tamponade tension pneumo high PEEP PE SAM heart tumor
Describe what happens with preload, afterload, contarctility, HR and CO in hypovolemic shock
preload decreased afterload increased contracility decreased HR up CO down b/c reduced stretch
Describe what happens with preload, afterload, contarctility, HR and CO in cardiogenic shock
preload increased afterload increased contractility decreased HR up CO decreased d/t poor LV emptying
Describe what happens with preload, afterload, contarctility, HR and CO in distributive shock
preload decreased afterload decreased contractility normal HR inc CO decreased d/t vasodilation and decreased afterload
Describe what happens with preload, afterload, contarctility, HR and CO in obstructive shock
preload decreased afterload increased contractility normal HR increased CO sudden decrease
