Hemodynamic Instability Flashcards
1
Q
what is an aortic aneurysm
A
permanet localized dilation of the aorta that is 50% greater than the normal diameter
2
Q
what are the three classifications of aortic aneurysms
A
ascending
descending
abdominal
3
Q
what is the most common location
A
infarenal
4
Q
what are the 3 layres of blood vessel
A
tunica intima (inner thin) tunica media (smooth muscle, middle) tunica adventitia (outer
5
Q
what causes aneurysms
A
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
6
Q
risk factors for AAA
A
tobacco use advanced age male etOh family hx atherlerclerosis
7
Q
what are the 4 main arteries coming off the abdominal aorta
A
celiac superior mesenteric renal inferior mesenteric iliac
8
Q
what do the celiac arteries supply
A
foregut
stomach, speleen, liver, esophagus and parts of the pancreas and duodenum
9
Q
what do the superior mesenteric arteries supply
A
midgut
jejunum, ilieum, appendix, cecum, ascending colon, 2/3 transverse colon
10
Q
what do the renal arteries supply
A
kidneys
11
Q
what do the inferior mesenteric arteries supply
A
hindgut
distal 1/3 of transverse colon, descending colon, sigmoid and rectum
12
Q
what do the iliac arteries supply
A
the legs
13
Q
T or F 2/3s of AAA are asymptomatic and found on routine exam
A
T
14
Q
symptoms of AAA include
A
abdominal pain low back pain flank pain N/V ischemia to lower limbs
15
Q
what is the triad of symptoms associated with AAA rupture
A
severe abdominal pain
hypotension
pulsatile mass
16
Q
if AAA is ruptured is sx required
A
yes
17
Q
if AAA is not ruptured what are your two options
A
open surgical repair
insertion of endovascular stent (high risk)
18
Q
how is heparin reversed post AAA sx
A
protamine
19
Q
what is the most common postop complication for EVAR
A
endoleak - leak around stent
20
Q
what can prolonged cross-clamp time cause
A
spinal ischemia and neuro deficits
21
Q
what are the 5 Ps of ischemia
A
pain pallor pulselessness paralysis paresthesia
22
Q
what do you need to have good control of post AAA sx
A
hypertension
23
Q
what can cause ischemia in lower limbs post AAA sx
A
embolization of thrombus/debris to lower limbs, gut or kidney
24
Q
what are 3 common drugs given for HTN
A
hydralazine
labetalol
nitroglycerin
25
how does hydralazine work
arterial vasodilator
| decreases afterload
26
how does labetalol work
beta 1 and 2 and alpha antagonist
| decreases HR and afterload
27
if a pts hr is 59 should you give labetalol
no
28
how does nitro work
venous vasodilation
arterial vasodilation at higher doses
decreases preload and afterload
dilates coronary arteries
29
what is shock
acute widespread impaired tissue perfusion resulting in cellular, metabolic and hemodynamic alterations
30
what does shock result from
any determinants in CO (preload, afterload, contractility)
31
what receptors sense a decrease in stretch of the vessel wall? what do they activate
baroreceptors
| SNS
32
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
33
what do B1 receptors do when the SNS is activated
increase HR and contractility
34
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
35
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
36
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
37
what are the 4 types of shock
hypovolemic
distributive
cardiogenic
obstrcutive
38
what is the primary problem with hypovolemic shock
decreased preload
39
what is the primary problemw ith distributive shock
decreased afterload
40
what is the priamry problem with cardiogenic shock
decreased contractility
41
what is the primary problemw ith obstructive shock
high afterload and decreased preload
| outflow is obstructed
42
what are the 4 stages of shock
initial stage
compensatory stage
progressive stage
refractory stage
43
what occurs in the inital stage of shock
decreased CO threatens tissue perfusion
44
what occurs in compensatory stage of shock
homeostsatic mechanism kick in
45
what occurs are neural compensatory mechanisms
increased HR/contractility, vasoconstriction, shunting to vital organs
46
what are chemical compensatory mechanisms
chemoreceptor mediated resp changes triggrered by hypoxemia and hypercapnia
47
what are hormonal compensatory changes
activation of RAAS
48
what happens in the progresive stage of shock
failing compensatory mechanisms
swtich to anaerobic metabolism
vasodilation and permeability
SIRS
49
what occurs in the refractory stage
shock unresponsive to therapy, irreversible MODS and death
50
what is the effect of hypovolemic shcok on O2 S&D
decreased preload
decreased contractility
decreased CO
51
what are 5 ways to evaluate volume status
```
POCUS
CVP
Passive leg raise
hx
physical assesment
```
52
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
53
what are crystalloid fluids that are isotonic
NS
RL
plasmalyte
54
what is a hypertonic crystalloid
3% NS
55
what are examples of colloids
albumin
PRBC
FFP
Platelets
56
T or F D5W is isotonic but becomes hypotonic
T glucose gets used up by brain
57
what are the three types of distributive shock
anaphylaxis
neurogenic
sepsis
58
what is distributive shock
decreased afterload from profound arterial dilation
| decreased preload as a result of decreased venous return
59
what type of pulse pressure would you see in sepsis
wide/low diastolic
60
what is cardiogenic shock
impaired ability of heart to pump
poor contractility
impaired ability of LV emptying --> increased preload and pulmonary edema
61
what effects does norepinephrine have
sympathomimetic
strong alpha but does have some beta
increases afterload
62
what part of CO does levo effect
afterload
63
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
64
what is vasopressin and what part of CO does it work on
antiduretic hormone
| increases afterload and preload
65
T or F vasopressin is typically ran at a fixed rate
true
66
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
67
What receptors does phenylephrine work on and what part of CO does it affect
alpha receptors to increase afterload
68
what happens to stroke volume nad CO in cardiogenic shock
decreased stroke volume
| decreased CO
69
what type of pulse pressure would you see in cardiogenic shock
narrow
70
what are 4 caues of cardiogenic shock
damaged myocardial msucle
mechnical impairment
cardiomyopathies
sepsis
71
what are some examples of mecahnical impairment causing cardiogenic shock
large PE, cardiac tamponade, vavlular disease
72
why does sepsis cause cadiogenic shock
release of MDF
73
4 clinical findings in a pt with cardiogenic shock
pulmonary edema and generalized edema
frothy sputum
cool, cyanotic extremeites, delayed cap refill
decreased EOP
74
what types of meds would we want to give to help with cardiogenic shock
inotropes!
75
what are inotropes often titrated to
ScVO2 or lactate
76
what receptors does dobutamine work on
beta 1 primarily but some beta 2
77
what does dobutamine do
increased contraclitly with some potential decreased afterload
fast onset 10-20 mins
78
T or F dobutamine is more likely to cause tachycardia then dopamine
False it is less likely
79
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
80
does milrinone have a long half life
yes dose change q6h
81
what inotrope is used to treat pulmoanary HTN and rt ventricular afterload
milrinone
82
what type of drug is dopamine
sympathomimetic agent acting on B1 restuling in inc Hr and contractility
effects are dose dependent
83
what does dopamine do at low doses
inc renal perfusion
84
what does dopamine do at medium doses
increased contracility
85
what does dopamine do at high doses
increased afterload
86
does dopamine cause tachycardia
is a common finding
87
what is obstructive shock caused by
obstruction of the great vessels or the heart itself
88
what type of shock is there a rapid massive drop in CO and b[
obstructive
89
what are some examples of obstructive shock
```
tamponade
tension pneumo
high PEEP
PE
SAM
heart tumor
```
90
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
```
91
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
```
92
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
```
93
Describe what happens with preload, afterload, contarctility, HR and CO in obstructive shock
```
preload decreased
afterload increased
contractility normal
HR increased
CO sudden decrease
```
