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CV pathophysiology Flashcards

1
Q

high risk procedures for a patient with CAD include (4)

A

emergency surgery (esp in elderly)
open aortic surgery
peripheral vascular surgery
long surgical procedures with volume shifts and/or blood loss

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2
Q

general risk factors for cardiac risk patients include (6)

A

high risk surgery
hx of ischemic heart disease (unstable angina confers greatest risk of perioperative MI)
CHF
CVD
DM
serum creatinine >2

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3
Q

risk of reinfarction after MI is:
>6 mo:
3-6 mo:
<3 mo:

A

> 6 mo: 6%
3-6 mo: 15%
<3 mo: 30%

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4
Q

intermediate risk surgeries include (5)

A

CEA
head and neck surgery
intrathoracic or inter peritoneal surgery
ortho surgery
prostate surgery

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5
Q

low risk surgeries include (5)

A

endoscopic procedures
cataract surgery
superficial procedures
breast surgery
ambulatory procedures

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6
Q

NYHA classification, level of impairment, and functional limitation (4 classes)

A
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7
Q

which classes of NYHA patients should be referred to a cardiologist before surgery

A

class 3 or 4
unless its a minor procedure under MAC

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8
Q

PAOP is a surrogate for

A

LVEDP
ex) CPP=DBP-LVEDP but only have PAOP

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9
Q

CKMB initial elevation, peak elevation, return to baseline after MI

A

initial: 3-12h (same as Troponin I and T)
peak elevation: 24h
return to baseline: 2-3d

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10
Q

Troponin I initial elevation, peak elevation, return to baseline after MI

A

initial: 3-12h (same as CKMB and troponin T)
peak elevation: 24h
return to baseline: 5-10d

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11
Q

Troponin T initial elevation, peak elevation, return to baseline after MI

A

initial: 3-12h (same as CKMB and Troponin I)
peak elevation: 12-48h
return to baseline: 5-14d

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12
Q

best leads to use to detect an MI and WHY

A

leads II, V5.
lead II: aids in ID of inferior wall ischemia. also monitors for dysrhythmias where QRS is narrow and P wave is crucial for dx
V5: classic teaching says this is best for LV ischemia but new data says maybe V3/4 is best,
CHOOSE V4 on NCBRNA***

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13
Q

CVP and PAOP may over estimate LVEDV for any condition that does what?

A

reduces ventricular compliance

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14
Q

name examples that would shift the compliance curve to the red (highest) (5)

A

age >60y
ischemia
pressure overload hypertrophy (aortic stenosis or HTN)
hypertrophic obstructive cardiomyopathy
pericardial pressure (increased external pressure)

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15
Q

etiology of HFrEF (systolic failure)

A

pumping problem
MI
valve insufficiency
dilated cardiomyopathy

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16
Q

etiology of HF with preserved EF (diastolic failure) (7)

A

filling problem
MI
valve stenosis
HTN
hypertrophic cardiomyopathy
cor pulmonale **
obesity*

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17
Q

compare systolic HF and diastolic HF in terms of
EDV
EDP
ESV
SV
LV mass
LV geometry

A
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18
Q

which drugs can reverse cardiac remodeling

A

ACEI’s and spironolactone (aldosterone antagonists)

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19
Q

compare anesthetic management of systolic HF and diastolic HF in terms of
preload
afterload
contractility
HR

A
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20
Q

most common cause of RV failure

A

LV failure

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21
Q

tx for RV failure includes

A

inotropes (milrinone, dobut)
pulmonary vasodilators (inhaled NO or sildenafil, PDE5)
reverse cause of increased PVR

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22
Q

conditions that increase PVR (5)

A

increased PEEP
N2O
Hothermia
acidosis
hypercarbia

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23
Q

list 4 physiologic adaptations of HF

A
  1. SNS activation
  2. excessive vasoconstriction
  3. fluid retention
  4. myocardial remodeling
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24
Q

3 physiologic functions of BNP

A
  1. natriuresis
  2. diuresis
  3. vasodilation
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25
Q

how does CHF effect beta receptors?

A

causes down regulation of beta receptors

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26
Q

most common cause of constrictive pericarditis

A

cardiac surgery

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27
Q

the patient has an aortic balloon pump. which part of this arterial BP waveform corresponds with diastolic augmentation and improvement of coronary BF?

A

remember balloons inflates during diastole. pressure is higher than unassisted systole. balloon deflates during systole to decrease after load.

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28
Q

which region of the pressure volume loop corresponds to S3 heart sound?

A

best heard during the middle 1/3 of diastole after S2 (aortic valve closure)
gallop, suggestive of HF but can be a normal finding in children and teens.

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29
Q

with a patient who has an LVAD, CO is highly dependent on

A

preload

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30
Q

mnemonic for debakey classification of aneurysm: BAD

A

B: both (type 1)
A: ascending (type 2)
D: descending (type 3)

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31
Q

stage 1 HTN

A

130-139 SBP OR 80-89 DBP

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32
Q

stage 2 HTN

A

SBP >140 OR DBP >90

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33
Q

stage 3 HTN (hypertensive crisis)

A

SBP >180 and/or DBP >120

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34
Q

cerebral auto regulation happens between a CPP of

A

50-150mmHg

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35
Q

what does chronic HTN do to cerebral auto regulation

A
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36
Q

SBP and DBP that permit anesthesia delay

A

SBP >180 and DBP >110

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37
Q

when does a HTN crisis turn into a HTN emergency

A

evidence of end organ damage ex) encephalopathy, stroke, papilledema, CHF, renal dysfunction

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38
Q

coarctation of aorta clinical findings and diagnostic tests

A

clinical findings: upper limb BP > lower limb BP, weak femoral pulse, systolic bruit, HTN
dx tests: aortography, echo, CT/MRI

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39
Q

renovascular disease clinical findings (3) and diagnostic tests (4)

A

clinical findings: HTN, bruit, severe HTN in young patient
dx tests: CT angiography, MRA, aortography, duplex ultrasonography

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40
Q

hyperadrenocorticism (cushings disease) clinical findings and diagnostic tests

A

clinical findings: HTN*, weight gain (truncal obesity), hyperglycemia, muscle and bone weakness, weakened immunity, hirsutism, moon face
dx: dexamethasone suppression test, glucose tolerance test, urinary cortisol, adrenal CT/MRI

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41
Q

hyperaldosteronism (conns disease) clinical findings and diagnostic tests

A

clinical findings: HTN*, hypokalemia, alkalosis, fatigue/weakness, parasthesia, nocturnal polyuria/polydipsia
dx: Cp aldosterone, Cp renin, Cp K, urinary potassium

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42
Q

pheochromocytoma clinical findings and diagnostic tests

A

clinical findings: HA, palpitations, diaphoresis
dx: plasma metanephrines, urinary catecholamines, urinary vanillylmandelic acid (VMA)

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43
Q

pregnancy induced HTN clinical findings (4) and diagnostic tests (4)

A

clinical findings: peripheral and pulmonary edema, HA, sz, RUQ pain
dx: urinary protein, platelet count, uric acid, CO

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44
Q

how alpha 1 antagonists decrease BP

A

decrease iCa2+ and decrease SVR

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45
Q

how B1 antagonists decrease BP

A

decrease inotropy, chronotropy, HR, dromotropy, and renin release from juxtaglomerular apparatus

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46
Q

selective B1 antagonists

A

acebutolol
atenolol
bisoprolol
esmolol
metoprolol

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47
Q

non selective b1 and b2 antagonists

A

nadolol
pindolol
propanolol
sotalol
timolol

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48
Q

mixed a1/b1/b2 antagonists

A

bucindolol, carvedilol, labetalol

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49
Q

how a2 agonists decrease BP

A

decrease SNS outflow

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50
Q

how CCB’s (dihydropiridines) decrease BP

A

decrease intravascular calcium and decrease SVR

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51
Q

how CCB’s (non dihydropiridines including verapamil and diltiazem) decrease BP

A

targets myocardium more than vessels

deceased inotropy, chronotropy, dromotropy, svr

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52
Q

what hydralazine dilates primarily and how it decreases BP

A

arteriodilator that increases NO and decreases SVR (after load)

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53
Q

what SNP dilates primarily and how it decreases BP

A

equal arterial and venodilator and increases NO, decreases SVR (after load) and decreases venous return (preload)

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54
Q

what NTG primarily dilates and how it decreases BP

A

primarily venules, increases NO, decreases venous return (pre load)

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55
Q

MOA of ACEI’s

A

inhibits ATII mediated vasoconstriction and inhibits aldosterone release

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56
Q

MOA of AT2 receptor blockers

A

inhibits ATII mediated vasoconstriction and inhibits aldosterone release

57
Q

MOA of loop diuretics and examples

A

Inhibits Na/K/2Cl transporter in thick portion of ascending loop of henle. increased diuresis and decreased venous return
ex) furosemide, bumetanide, ethacrynic acid

58
Q

MOA of thiazide diuretics and examples

A

inhibits Na/Cl transporter in distal convoluted tubule
diuresis- decreased venous return
ex) HCTZ, metolazone, indapamide, chlorthalidone

59
Q

MOA of K sparing diuretics and examples

A

inhibits K excretion and Na reabsorption by principal cells in collecting ducts.
acts independently of aldosterone
ex) triamterene, amiloride

60
Q

MOA of aldosterone antagonists and examples

A

inhibits K excretion and Na reabsorption by principal cells in collecting ducts.
blocks aldosterone at mineralocorticoid receptors
ex) spironolactone

61
Q

compare and contrast dihydropiridines and non dihydropiridines in terms of
target
clinical effects
examples

A
62
Q

which CCB impairs contractility the most

A

verapamil

63
Q

only CCB shown to reduce M&M from cerebral vasospasm

A

nimodipine

64
Q

clevidipine MOA

A

arterial vasodilator that reduces SVR without affecting preload

65
Q

contraindications to clevidipine (3)

A

allergy to eggs, soy, egg products, soy products, severe AS***, impaired lipid metabolism

66
Q

compare and contrast constrictive and acute pericarditis in terms of
cause
s/sx
tx
anesthetic management

A
67
Q

becks triad

A

JVD (decreased venous return to right heart)
HoTN (decreased SV)
muffled heart tones (fluid accumulation around sac)

68
Q

does pericardial effusion affect diastolic filling time or ventricular compliance

A

no because it doesn’t increase pericardial pressure

69
Q

best method of dx for cardiac tamponade

A

TEE

70
Q

what pathophysiological issue is outlined by this pressure volume loop (green part)

A

cardiac tamponade. decreased LVEDV (loop shifts to left), decreased SV (loop is narrower), decreased ventricular compliance (notice higher slope during ventricular filling)

71
Q

presentation of cardiac tamponade

A

becks triad (muffled heart tones, HTN, JVD), pulsus paradoxus, kussmauls sign (increased CVP and JDV during inspiration), reduced EKG voltage, compression of heart, lungs, trachea, esophagus

72
Q

drugs to avoid and drugs that are safe to use during cardiac tamponade as well as other anesthetic management techniques

A

maintain SNS since SV is severely decreased and this helps with compensation
maintain spontaneous ventilation- PPV can impair venous return and CO
-local anesthesia is preferred for pericardiocentesis with spontaneous ventilation

73
Q

hemodynamic goals for cardiac tamponade:
HR
preload
contractility
afterload

A

HR: maintain. since SV is reduced, CO is dependent on HR
preload: maintain or increase.
contractility: maintain or increase (inotropes)
afterload: maintain. essential to decrease SV and CO

74
Q

patients at high risk for infective endocarditis that need prophylactic abx (6)

A

previous infective endocarditis
prosthetic heart valve
unprepared cyanotic congenital heart disease
repaired congenital heart defect if repair is less than 6 months old
repaired congenital heart defect that have residual effects and impaired endothelialization at the graft site
heart transplant with valvuloplasty

75
Q

abx prophylaxis is not required for patients with a hx of (3)

A

unrepaired cardiac valve disease including mitral valve prolapse
CABG
coronary stent placement

76
Q

procedures where abx prophylaxis to protect against endocarditis include

A

dental procedures with gingival manipulation and/or damage to mucosal lining
resp procedures that perforate mucosal lining with incision or biopsy
biopsy of infective lesions in skin or muscle

77
Q

IV abx of choice if PCN allergic

A

clinda 600mg or for peds 20mg/kg

78
Q

three things that determine BF through LVOT

A
  1. systolic LV volume
  2. force of LV contraction (decreasing contractility decreases obstruction and increases CO)
  3. transmural pressure
79
Q

LVOT is caused by

A

congenital hypertrophy of intraventricular septum
systolic anterior motion of anterior leaflet of mitral valve. occurs during systole!

80
Q

if the patient has bare metal stent, delay surgery for

A

30 days

81
Q

how long to wait for surgery if patient got angioplasty without stent

A

2-4 weeks

82
Q

for stable ischemic heart disease, first generation drug eluding stents you should wait ______ months and current generation you can wait ______ months

A

12 months minimum for first gen
6 months minimum for current gen

83
Q

for acute coronary syndrome, wait for surgery after insertion of drug eluding stent for

A

12 months minimum

84
Q

after a CABG, wait how long until surgery

A

6 weeks
3 months preferred

85
Q

stop ASA how many days before surgery if not absolutely contraindicated?

A

3 days

86
Q

stop clopidogrel how many days before surgery

A

7 days

87
Q

stop ticlodipine how many days before surgery

A

14 days

88
Q

best outcome for stent occlusion is if intervention happens in

A

<90m

89
Q

key facts of roller pump for CPB

A

compresses blood tubing that mechanically pumps blood forward
pump flow remains constant regardless of afterload
roller pump is more likely to entrain air if venous reservoir runs dry, which can lead to air embolism

90
Q

key facts of centrifugal pump for CPB

A

non occlusive, uses gravity and spins blood through a cone.
less traumatic to blood cells
reduces pressure if increased after load is detected and has less chance of VAE
does have lack of an occlusion point. therefore if theres an excessively high after load, blood backs up towards venous circulation which reduces patients circulating BV.

91
Q

oxygenator in CPB

A

point in CPB where gas exchange occurs.
membrane oxygenator uses blood membrane gas interface. safer.

92
Q

you can prime CPB with

A

blood or balanced salt solution (mannitol, albumin, heparin, HCO3-)

93
Q

ACT for CPB

A

> 400 seconds

94
Q

where is anterograde cardioplegia introduced

A

aortic root (where circulation gets to coronary arteries). aortic valve must be competent and the aorta must be clamped.

95
Q

where is retrograde cardioplegia introduced

A

coronary sinus

96
Q

the tip of an aortic balloon pump should be positioned

A

2cm distal to the left SCA

97
Q

indications for IABP (4)

A

cardiogenic shock
MI
intractable angina
difficult separation from CPB

98
Q

contraindications for IABP (4)

A

severe AI
descending aortic disease (aneurysm)
severe PVD
sepsis

99
Q

how to confirm position of IABP (3 tests)

A

CXR, fluoro, TEE

100
Q

outline arterial waveform and IABP

A

inflation correlates with dichrotic notch on aortic pressure wave form

101
Q

deflation of IABP during systole correlates with what on EKG

A

R wave

102
Q

when a patient has an LVAD, CO is dependent upon (3)

A
  1. LV preload
  2. Pump speed
  3. pressure gradient across the pump (after load)
103
Q

how LVAD works

A

pumps blood from LV to aorta
inflow of cannula is inserted into apex of LV. blood is returned to aorta through outflow cannula

104
Q

with an LVAD, what are some issues the patient cannot have in order to receive it (4)

A

PFO, AI, tricuspid regurgitation, competent aortic valve

105
Q

if a patient has an LVAD and the flow is non pulsatile how can you measure SpO2/NIBP (3)

A

aline, serial ABG’s, cerebral oximetry

106
Q

describe LV suck down when patient has LVAD

A

LV preload low, pump speed high. part of LV is sucked into LV cavity-occludes inflow cannula

five IVF and reduce pump speed

107
Q

outline the crawford classification of aortic aneurysms

A

Type 1: outlines all or most of descending aorta and only upper part of abdominal aorta
Type 2: outlines all or most of descending aorta and most of of abdominal aorta
Type 3: only lower part of descending thoracic aorta and most of abdominal aorta
Type 4: none of descending thoracic aorta and most of abdominal aorta

108
Q

classification of aortic dissection: stanford

A

type A: involves ascending aorta
type B: does not involve ascending aorta

109
Q

classification of aortic dissection: debakey

A

BAD mnemonic
type 1: tear in ascending aorta and dissection along entire aorta
type 2: tear in ascending aorta and dissection only in ascending aorta
type 3: tear in proximal descending aorta with
3a: dissection limited to thoracic aorta
3b: dissection along thoracic and abdominal aorta

110
Q

which crawford type aneurysms are the most difficult to repair

A

crawford type 2 and 3

111
Q

which kind of aortic dissections are a surgical emergency

A

debakey 1 or 2 or stanford a (consider AI as well). this involves acute dissection of ascending aorta

112
Q

dissection of descending aorta management

A

medical

113
Q

how is AAA most commonly detected and what is the triad

A

pulsatile abdominal mass
HoTN, back pain, pulsatile abdominal mass
most aneurysms rupture in left retroperitoneum

114
Q

most common cause of postop death after AAA repair

A

MI

115
Q

which factors increase following cross clamp removal during AAA repair

A

PVR and total body O2 consumption increase

116
Q

applying aortic cross clamp creates central hypervolemia by

A

reducing venous capacity
shifting greater proportion of blood volume to proximal clamp
increasing venous return

117
Q

removing aortic cross clamp creates central hypovolemia by

A

restoring venous capacity
shifting greater proportion of blood to lower body
decreasing venous return
creating capillary leak that contributes to loss of intravascular volume

118
Q

what is an EVAR

A

minimally invasive approach for correcting AAA

119
Q

anesthetic management of EVAR patient

A

continuously monitor BP with aline
patient will receive IV contrast dye
maintain UOP

120
Q

describe endoleak

A

when original graft fails to prevent blood from entering aortic sac. some resolve spontaneously while some need a new graft or open repair

121
Q

2 posterior spinal arteries

A

aorta–> segmental a–> posterior radicular a –>posterior spinal artery
aorta –> SCA –> vertebral artery –>posterior spinal artery

122
Q

what part of SC does posterior spinal arteries perfuse

A

posterior 1/3 of SC (in green)

123
Q

what part of SC does anterior spinal artery perfuse

A

anterior 2/3 of SC (yellow)

124
Q

where does artery of adamkeweisz most commonly originates from

A

T11-12

125
Q

becks syndrome aka anterior spinal artery syndrome sx

A

flaccid paralysis of LE’s
bowel and bladder dysfunction
loss of temperature and pain sensation
touch and proprioception are preserved

126
Q

which spinal tracts are perfused via anterior blood supply

A

corticospinal tract (motor, flaccid paralysis)
autonomic motor fibers (bowel and bladder dysfunction)
spinothalamic (sensory tract, loss of pain and temperature sensation)

127
Q

spinal cord protection strategies during thoracic cross clamp includes

A

moderate hypothermia (30-32c)
CSF drainage
proximal HTN during xclamp (MAP 100)
avoidance of hyperglycemia
SSEP/MEP monitoring
partial CPB (LA to femoral artery)
drugs (corticosteroids, CCB’s, and/or mannitol)

128
Q

what does SSEP monitor

A

only monitors posterior cord

129
Q

sign of impending stroke during CEA

A

amaurosis fugax (blindness in one eye)
emboli travel from ICA to ophthalmic artery

130
Q

ways to monitor neurological integrity and cerebral perfusion

A

keep patient awake
EEG
cerebral oximetry
transcranial doppler
SSEP
carotid stump pressure

131
Q

after aortic cross clamping, reduce aortic BP to <

A

145mmHg systolic

132
Q

postop considerations for CEA

A

hematoma
RLN injury
hemodynamic instability
carotid denervation

133
Q

carotid artery angioplasty stenting (CAS)

A

uses percutaneous trans vascular access to pass stent into carotid artery
maintain ACT >250s
balloon inflation can activate baroreceptor reflex, pretx
filter placed beyond angioplasty balloon
embolic CVA treated with recombinant tissue plasminogen activator

134
Q

in the patient with right subclavian steal syndrome, arterial flow is diverted from the

A

right vertebral artery to right SCA

135
Q

describe subclavian steal syndrome

A

occlusion of sublavian or innominate a. proximal to origin of ipsilateral vertebral artery
-results in reversal of BF where vertebral BF flows toward ipsilateral SCA

136
Q

s/sx subclavian steal syndrome (think brain and ipsilateral arm)

A

syncope, vertigo, ataxia, hemiplegia
arm ischemia, weak pulse

137
Q

3 best EKG leads to monitor for intraop ST changes

A

V3, V4, V5

138
Q

most common cause of secondary HTN

A

renal artery stenosis

139
Q

dresslers syndrome

A

acute pericarditis after MI

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