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NSCC 7320 - Critical Care Theory 3 > Hemodynamic Instability > Flashcards

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

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2
Q

what are the three classifications of aortic aneurysms

A

ascending
descending
abdominal

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3
Q

what is the most common location

A

infarenal

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4
Q

what are the 3 layres of blood vessel

A 
tunica intima (inner thin)
tunica media (smooth muscle, middle)
tunica adventitia (outer
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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

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6
Q

risk factors for AAA

A 
tobacco use 
advanced age 
male
etOh 
family hx 
atherlerclerosis
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7
Q

what are the 4 main arteries coming off the abdominal aorta

A 
celiac
superior mesenteric
renal 
inferior mesenteric
iliac
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8
Q

what do the celiac arteries supply

A

foregut

stomach, speleen, liver, esophagus and parts of the pancreas and duodenum

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9
Q

what do the superior mesenteric arteries supply

A

midgut

jejunum, ilieum, appendix, cecum, ascending colon, 2/3 transverse colon

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10
Q

what do the renal arteries supply

A

kidneys

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11
Q

what do the inferior mesenteric arteries supply

A

hindgut

distal 1/3 of transverse colon, descending colon, sigmoid and rectum

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12
Q

what do the iliac arteries supply

A

the legs

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13
Q

T or F 2/3s of AAA are asymptomatic and found on routine exam

A

T

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14
Q

symptoms of AAA include

A 
abdominal pain
low back pain
flank pain
N/V
ischemia to lower limbs
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15
Q

what is the triad of symptoms associated with AAA rupture

A

severe abdominal pain
hypotension
pulsatile mass

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16
Q

if AAA is ruptured is sx required

A

yes

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17
Q

if AAA is not ruptured what are your two options

A

open surgical repair

insertion of endovascular stent (high risk)

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18
Q

how is heparin reversed post AAA sx

A

protamine

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19
Q

what is the most common postop complication for EVAR

A

endoleak - leak around stent

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20
Q

what can prolonged cross-clamp time cause

A

spinal ischemia and neuro deficits

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21
Q

what are the 5 Ps of ischemia

A 
pain
pallor
pulselessness
paralysis 
paresthesia
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22
Q

what do you need to have good control of post AAA sx

A

hypertension

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23
Q

what can cause ischemia in lower limbs post AAA sx

A

embolization of thrombus/debris to lower limbs, gut or kidney

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24
Q

what are 3 common drugs given for HTN

A

hydralazine
labetalol
nitroglycerin

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25
Q

how does hydralazine work

A

arterial vasodilator

decreases afterload

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26
Q

how does labetalol work

A

beta 1 and 2 and alpha antagonist

decreases HR and afterload

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27
Q

if a pts hr is 59 should you give labetalol

A

no

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28
Q

how does nitro work

A

venous vasodilation
arterial vasodilation at higher doses
decreases preload and afterload
dilates coronary arteries

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29
Q

what is shock

A

acute widespread impaired tissue perfusion resulting in cellular, metabolic and hemodynamic alterations

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30
Q

what does shock result from

A

any determinants in CO (preload, afterload, contractility)

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31
Q

what receptors sense a decrease in stretch of the vessel wall? what do they activate

A

baroreceptors

SNS

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32
Q

what do alpha receptors do when the SNS is activated where are they located

A

vasoconstriction
skin, GI, peripheral vessels
increases afterload
shunts blood to important areas

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33
Q

what do B1 receptors do when the SNS is activated

A

increase HR and contractility

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34
Q

where are B2 receptors found and what do they do when SNS stimulated

A

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

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35
Q

describe the steps in RAAS

A

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

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36
Q

How does RAAS affect preload and afterload

A

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

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37
Q

what are the 4 types of shock

A

hypovolemic
distributive
cardiogenic
obstrcutive

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38
Q

what is the primary problem with hypovolemic shock

A

decreased preload

39
Q

what is the primary problemw ith distributive shock

A

decreased afterload

40
Q

what is the priamry problem with cardiogenic shock

A

decreased contractility

41
Q

what is the primary problemw ith obstructive shock

A

high afterload and decreased preload

outflow is obstructed

42
Q

what are the 4 stages of shock

A

initial stage
compensatory stage
progressive stage
refractory stage

43
Q

what occurs in the inital stage of shock

A

decreased CO threatens tissue perfusion

44
Q

what occurs in compensatory stage of shock

A

homeostsatic mechanism kick in

45
Q

what occurs are neural compensatory mechanisms

A

increased HR/contractility, vasoconstriction, shunting to vital organs

46
Q

what are chemical compensatory mechanisms

A

chemoreceptor mediated resp changes triggrered by hypoxemia and hypercapnia

47
Q

what are hormonal compensatory changes

A

activation of RAAS

48
Q

what happens in the progresive stage of shock

A

failing compensatory mechanisms
swtich to anaerobic metabolism
vasodilation and permeability
SIRS

49
Q

what occurs in the refractory stage

A

shock unresponsive to therapy, irreversible MODS and death

50
Q

what is the effect of hypovolemic shcok on O2 S&D

A

decreased preload
decreased contractility
decreased CO

51
Q

what are 5 ways to evaluate volume status

A 
POCUS
CVP
Passive leg raise
hx 
physical assesment
52
Q

what are 4 physical assesment findings that indicate depleted volume status

A

dry skin/mucous membranes
tachycardia (compensatory)
decreased EOP (decreased UO, cool extremeites)
increased afterload d/t compesnatory mechanisms

53
Q

what are crystalloid fluids that are isotonic

A

NS
RL
plasmalyte

54
Q

what is a hypertonic crystalloid

A

3% NS

55
Q

what are examples of colloids

A

albumin
PRBC
FFP
Platelets

56
Q

T or F D5W is isotonic but becomes hypotonic

A

T glucose gets used up by brain

57
Q

what are the three types of distributive shock

A

anaphylaxis
neurogenic
sepsis

58
Q

what is distributive shock

A

decreased afterload from profound arterial dilation

decreased preload as a result of decreased venous return

59
Q

what type of pulse pressure would you see in sepsis

A

wide/low diastolic

60
Q

what is cardiogenic shock

A

impaired ability of heart to pump
poor contractility
impaired ability of LV emptying –> increased preload and pulmonary edema

61
Q

what effects does norepinephrine have

A

sympathomimetic
strong alpha but does have some beta
increases afterload

62
Q

what part of CO does levo effect

A

afterload

63
Q

what receptors does epinephrine work on

A

beta 1, 2 and alpha receptors
primarily beta @ low doses results in inc HR and contractility
more alpha @ high doses increasing afterload

64
Q

what is vasopressin and what part of CO does it work on

A

antiduretic hormone

increases afterload and preload

65
Q

T or F vasopressin is typically ran at a fixed rate

A

true

66
Q

what receptors does vasopressin work on

A

V1 increasing afterload and smooth muscle contraction of GI tract
V2 influencing preload as it works on the kidney producing antidiuretic effects

67
Q

What receptors does phenylephrine work on and what part of CO does it affect

A

alpha receptors to increase afterload

68
Q

what happens to stroke volume nad CO in cardiogenic shock

A

decreased stroke volume

decreased CO

69
Q

what type of pulse pressure would you see in cardiogenic shock

A

narrow

70
Q

what are 4 caues of cardiogenic shock

A

damaged myocardial msucle
mechnical impairment
cardiomyopathies
sepsis

71
Q

what are some examples of mecahnical impairment causing cardiogenic shock

A

large PE, cardiac tamponade, vavlular disease

72
Q

why does sepsis cause cadiogenic shock

A

release of MDF

73
Q

4 clinical findings in a pt with cardiogenic shock

A

pulmonary edema and generalized edema
frothy sputum
cool, cyanotic extremeites, delayed cap refill
decreased EOP

74
Q

what types of meds would we want to give to help with cardiogenic shock

A

inotropes!

75
Q

what are inotropes often titrated to

A

ScVO2 or lactate

76
Q

what receptors does dobutamine work on

A

beta 1 primarily but some beta 2

77
Q

what does dobutamine do

A

increased contraclitly with some potential decreased afterload
fast onset 10-20 mins

78
Q

T or F dobutamine is more likely to cause tachycardia then dopamine

A

False it is less likely

79
Q

what type of drug is milrinone and how does it work

A

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
Q

does milrinone have a long half life

A

yes dose change q6h

81
Q

what inotrope is used to treat pulmoanary HTN and rt ventricular afterload

A

milrinone

82
Q

what type of drug is dopamine

A

sympathomimetic agent acting on B1 restuling in inc Hr and contractility
effects are dose dependent

83
Q

what does dopamine do at low doses

A

inc renal perfusion

84
Q

what does dopamine do at medium doses

A

increased contracility

85
Q

what does dopamine do at high doses

A

increased afterload

86
Q

does dopamine cause tachycardia

A

is a common finding

87
Q

what is obstructive shock caused by

A

obstruction of the great vessels or the heart itself

88
Q

what type of shock is there a rapid massive drop in CO and b[

A

obstructive

89
Q

what are some examples of obstructive shock

A 
tamponade
tension pneumo
high PEEP
PE
SAM 
heart tumor
90
Q

Describe what happens with preload, afterload, contarctility, HR and CO in hypovolemic shock

A 
preload decreased
afterload increased
contracility decreased
HR up
CO down b/c reduced stretch
91
Q

Describe what happens with preload, afterload, contarctility, HR and CO in cardiogenic shock

A 
preload increased
afterload increased
contractility decreased
HR up
CO decreased d/t poor LV emptying
92
Q

Describe what happens with preload, afterload, contarctility, HR and CO in distributive shock

A 
preload decreased
afterload decreased
contractility normal 
HR inc
CO decreased d/t vasodilation and decreased afterload
93
Q

Describe what happens with preload, afterload, contarctility, HR and CO in obstructive shock

A 
preload decreased
afterload increased
contractility normal
HR increased
CO sudden decrease

NSCC 7320 - Critical Care Theory 3 (5 decks)

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