Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

principles 2 cardiac anesthesia > Part 2 > Flashcards

Part 2 Flashcards

1
Q

anesthesia considerations for pt coming into surgery with pacer

A
  1. know what kind of pacer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

T/F: AICD can act as a pacer and defibrillator

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

if using a bovie in the OR and pt has a AICD what should you do

A

place magnet on pts chest to shut off cardioverter - still allows pacer to fx but will not pick up interference from bovie, thus will not give un-needed shock to pt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how do you know if a temporary pacer is capturing

A
  1. check pulse
  2. check a line
  3. do not assume activity of the pacer on the monitor is generating a pulse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

with spontaneous breathing LV filling and SV is reduced during ______________; but with mechanical ventilation LV filling and SV is lower during _______________; (this is 2ndary to increase in intrathoracic pressure)

A

inspiration; expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

systolic blood pressure typically fluctuates with spontaneous breathing by about ______________ mmHg

A

5-10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

pulsus paradoxus is when systolic BP fluctuates with breathing by > ___________ mmHg

A

10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

___________________ occurs during controlled mechanical ventilation when arterial pressure rises during inspriation and falls during expiration 2/2 changes in intrathoracic pressure 2/2 PPV

A

reverse pulsus paradoxus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

with pulsus paradoxus (spontaneous breathing) SBP increases during _______________

A

expriation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

with reverse pulsus paradoxus (mechanical ventilation) SBP increases during __________________

A

inspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

formula for SVV

A

(SVmax - SVmin)/ SVmean over a respiratory cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

SVV > _______% suggests that the pt is fluid responsive as it indicates the SV is sensitive to fluctuations in preload 2/2 respiratory cycle

A

10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

formula for pulse pressure

A

SV / arterial compliance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

causes of increased SVV

A
  1. hypovolemia
  2. tamponade
  3. constrictive pericarditis
  4. LV dysfx
  5. massive PE
  6. bronchospasm
  7. dynamic hyperinflation
  8. pneumothorax
  9. raised intrathoracic pressure &/or intraabdominal pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

SVV > 10-13% what should you do?

A

fluid challenge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

SVV < 10% but SV is normal, what should your intervention be

A

pressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

SVV < 10%, but SV is low, what is your intervention

A

inodilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

SVV < 10% but SV is high what is your intervention

A

diuretic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

T/F: Swan and CVP monitors have been proven to improve outcomes

A

FALSE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

limitations to arterial based monitoring (flotrac, vigelio)

A
  1. pt must be intubated, sedated, paralyzed
  2. severe arrhythmias (do not get adequate information)
  3. have to have a pulse rate (IABP, ventricular assist device)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

cerebral oximetry is based on ____________ technology

A

near infared spectroscopy (NIRS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

NIRS should be kept at least ____________% of baseline saturation

A

70-75

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

NIRS should be placed ________________ forehead

A

midline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is rSO2

A

regional oxygen saturation; what the NIRS will typically be set to monitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

if doing a “body” NIRS in peds, what type of O2 monitoring will you set the monitor to

A

regional cerebral tissue oxygen saturation (SctO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

healthy rSO2 on NIRS

A

58-82%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

intervention threshold for rSO2 number with NIRS monitoring

A

~20% from baselin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Critical threshold for rSO2 number with NIRS monitoring

A

~25% from baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

interventions to improve Cerebral rSO2 (NIRS)

A
  1. rule out mechanical cause (head position, cannula position)
  2. increase supply (O2 delivery): increase CO, BP, DO2, PaCO2, Hgb/Hct
  3. decrease demand: increase anesthetic, decrease temperature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

_________________ is the leading cause of death in the US

A

coronary artery disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

risk factors for CAD

A
  1. obese
  2. sedentary life style
  3. smoking
  4. HTN
  5. DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

______________ is the most stressful event for the CV system

A

exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

during exercise CO can be increased by______________x 2/2 increased HR and contractility

A

2.5-7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

at rest the coronary sinus Po2 is __________

A

27%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

ischemia of the myocardium occurs when __________________ exceeds ______________

A

O2 demand; supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

formula for O2 content of blood

A

hgb x 1.34 x SpO2 + (0.003 x PAO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is the normal O2 content of blood

A

20 mL / 100 mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is the primary determinant of O2 content of blood

A

hgb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

coronary perfusion pressure is “autoregulated” btw ____________ - _______ mmHg

A

50-150

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

CPP is completely dependent on ___________, if it is outside of the autoregulation pressure (50-150mmHg)

A

HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

ways to optimize coronary perfusion pressure (CPP)

A
  1. normal to high ADBP
    2.. Low LVEDP
  2. Low HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

formula for Coronary blood flow

A

CBF = coronary perfusion pressure (CPP)/Coronary vascular resistance (CVR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

normal Coronary blood flow value?

A

225-250

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what influences Coronary vascular resistance (CVR)

A
  1. metabolic factors
  2. ANS
  3. hormonal
  4. endothelial factors
  5. anatomic factors
  6. blood viscosity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

how does ANS influence coronary vascular resistance

A
  1. alpha-1 constriction, mainly epicardial arteries
  2. beta-1 dilation, mainly intramuscular arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what metabolic factors influence coronary vascular resistance

A
  1. pH
  2. CO2
  3. lactate
  4. O2
  5. adenosine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what hormones influence coronary vascular resistance

A
  1. vasopressin
  2. angiotensin
  3. prostacyclin
  4. TXA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what anatomic factors influence coronary vascular resistance

A
  1. capillary recruitment
  2. collateral artery development.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what increases Coronary vascular resistance

A
  1. increased O2
  2. decreased CO2
  3. increased pH
  4. increased alpha-adrenergic tone
  5. increased cholinergic tone
  6. increased vasopressin
  7. increased angiotensni
  8. increased TXA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what decreases coronary vascular resistance

A
  1. decreased O2
  2. increased CO2
  3. decreased pH
  4. lactate
  5. adenosine
  6. increased Beta-adrenergic tone
  7. increased prostacyclin
  8. increased nitric oxide
  9. increased endothelium derived hyperpolarizing factor
  10. increased prostaglandin I2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

___________________ vessesl are already maximally dilated; therefore they cannot respond to increase in demand (and are most susceptible to ischemia)

A

subendocardial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

_______________ is the MOST susceptible to ischemia

A

subendocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

coronary stenosis ___________ CVR and __________ CBF

A

increase; decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

T/F: sequential lesions/plaques in the coronaries are additive

A

true; LAD + circ occlusion is a left main equivalency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

coronary blood flow is reduced with coronary stenosis based on ______________ law

A

poiseuilles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

if you have a 50% decrease in coronary diameter 2/2 stenotic lesion, that area of the heart is now only receiving _______________ of flow

A

1/16

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

why do young individuals with an MI have worse outcomes than older individuals with MI

A

younger individuals have not developed collateral flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what are the 3 main determinants of myocardial oxygen consumption (MVO2)

A
  1. HR
  2. contractility
  3. wall stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

formula for myocardial oxygen consumption (MVO2)

A

MVO2 = CBF - (CaO2 - CvO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what is the MOST important determinant of myocardial oxygen demand

A

HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

doubling the heart rate ___________________ the myocardial oxygen demand

A

more than doubles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

increased contractility causes ______________ myocardial oxygen demand

A

increased (d/t needing more energy and more O2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

clinical measurement of contractility

A
  1. visually during open heart
  2. briskness of upstroke on arterial waveform tracing
  3. echocardiogram (*most accurate)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

cardiac wall stress is dependent on ________________, ________________, and ________________

A

afterload; chamber size (preload), and thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what law helps explain wall stress

A

law of laplace: tension(wall stress) = (P x radius)/(2x wall thickness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

MAP = _______________

A

MVO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

doubling MAP, ________________ myocardial oxygen demand (MVO2)

A

doubles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

clinically to decrease myocardial O2 demand, what do you want to decrease?

A

SVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

MVO2 is increased by an increase in…

A
  1. HR
  2. preload
  3. contractility
  4. afterload
  5. temperature
  6. hgb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

T/F: ECG is the least sensitive method for monitoring for myocardial ischmeia

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

ST depression = ______________, elevation = _________________

A

ischemia; infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

flattening or inversions of T waves indicate __________________

A

ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

ST changes will occur on ECG ____________ after ischemia occurs

A

1-2 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what leads are the most sensitive for ischemia monitoring?

A

an inferior lead (II, III, or aVF) + V5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

_____________% of ischemic events are captured if an inferior lead (II, III, aVF) + V5 are used to monitor

A

90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Sudden increase in PAP indicates what

A

decrease in cardiac function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

if there is a new onset of prominent V wave on PCWP waveform, this indicates what

A

papillary muscle dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

____________________ precedes ECG and PAP changes with myocardial ischemia

A

regional wall motion abnormalitiy (detected with TEE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

gold standard for myocardial ischemia montioring

A

TEE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

_________________ monitoring assess preload, contractility, Reigonal wall motion abnormality, valvular fx, antatomy, and presence of pericardial effusion

A

TEE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

on TEE you see lack of movement of wall, this is called _________________

A

akinesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

on TEE you see decreased regional wall movement, this is called _______________

A

hypokinesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

on TEE you see paradoxical movement during systole this is called ____________________

A

dyskinesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

dyskinesis is typically d/t __________________, and this is an emergency situation

A

ventricular aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

ideal induction agent for cardiac patients

A

etomidate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

ketamine effects on CV

A
  1. increase SVR
  2. increase preload
  3. increase contractility
  4. increase HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what is the perfect induction agent for a pt with cardiac tamponade

A

ketamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

__________________ is not an ideal induction agent for pts with cardiac ischemia

A

ketamine; d/t increased MVO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

propofol CV effects

A
  1. decrease BP
    2.. Decrease SVR
  2. decrease contractility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

BZ effect on CV

A

minimal HD effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

opioids effect on CV

A

decrease myocardial demand, without decreasing contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

CV effects of precedex

A

hypotension and bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

volatile anesthetics effects on MVO2

A
  1. all decrease contracility
  2. all decrease afterload
  3. minimal change in preload
  4. HR increase (esp with des)
  5. vasodilation of normal coronary vasculature decrease perfusion to ischemic areas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

which anesthetic gas is a very poor choice for pts in RV failure or pts with pulmonary HTN

A

nitrous oxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

effects of nitrous oxide on MVO2

A

decreases contractility and increases PVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

___________ HR, _______________ contractility, ________________ SVR, ______________Preload, & _____________ SNS stimulation

A

decrease; minimal effect, decrease, decrease, decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

succinylcholine effect on MVO2

A

bradycardia especially with repeated doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

pancuronium effect on MVO2

A

increases HR by 20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

how can you attenuate the increased HR (and thus increased MVO2) with pancuronium administration

A

high dose narcotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

vecuronium and rocuronium effect on MVO2

A

minimal CV effect (thus minimal MVO2 effect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

cisatracurium effect on MVO2

A

no CV effect (thus no MVO2 effect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

what muscle relaxants are the best choice for cardiac cases

A

vec, roc, or nimbex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

treatments for CAD (surgical)

A
  1. angioplasty
  2. stents
  3. CABG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

what is “fast track” cardiac anesthesia

A
  1. driven by desire to reduce cost
  2. accomplished by better drug selection/dose, new surgical techniques, warmer bypass temps
  3. early extubation and hemostatic control = essential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

anesthetic approach for myocardial revascularization procedures

A
  1. fast track anesthesia
  2. ERAS cardiac
  3. off bypass revascularization
  4. MIDCAB, port access, redo CABG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

which heart failure is more common (systolic or diastolic)?

A

systolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

systolic HF is more common in _____________________, where diastolic HF is more common in ________________

A

middle aged men (2/2 CAD); elderly women (2/2 obesity, htn, DM postmenopause)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

T/F: heart failure is primarily a disease of the elderly

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

T/F: HF spends more healthcare dollars than any other dz

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

most common cause of RV failure?

A

LV failure

111
Q

causes of systolic HF

A
  1. CAD
  2. Dilated CM
  3. chronic pressure overload (AS, HTN)
  4. chronic volume overload (valve insuff, high output failure)
112
Q

sx of systolic HF

A
  1. decreased EF
  2. ventricular dysrhythmias are common (risk of sudden death)
  3. S3 heart sound
113
Q

s/sx of diastolic HF

A
  1. normal EF, but sx of failure
  2. S4 heart sound
  3. increased LVEDP (classic sign)
114
Q

hallmark sign of systolic HF

A

decreased EF

115
Q

classic sign of diastolic HF

A

increased LVEDP

116
Q

which HF is age dependent? increased incidence in 50+; > 50% in those > 70 years of age

A

diastolic

117
Q

______________ HF is an inability to pump; where ______________ HF is an inability to fill

A

systolic; diastolic

118
Q

causes of diastolic HF

A
  1. ischemic heart disease
  2. chronic HTN
  3. progressive aortic stenosis
  4. age
119
Q

T/F: diastolic HF may coexist with Systolic HF

A

TRUE

120
Q

inotropes effect on PV loops

A

shift loop left
1. increase SV
2. decrease ESV

121
Q

diuretics and vasodilators effect on PV loops

A

decrease LVEDP

122
Q

vasopressors effect on the PV loop

A

*shift loop up
increases SBP

123
Q

_________________ = acute or worsening imbalance of myocardial oxygen supply to demand

A

acute coronary syndrome

124
Q

most common cause of ACS

A

focal disruption of atheromatous plaque –> partial/complete occlusion of coronary

125
Q

3 categories of ACS

A
  1. STEMI
  2. NSTEMI
  3. Unstable angina
126
Q

ST segment depression/nonspecific ECG changes with elevated cardiac biomarkers = _______________

A

NSTEMI

127
Q

ST depression/nonspecific ECG changes with normal cardiac biomarkers = __________________

A

unstable angina

128
Q

________________ occurs when coronary blood flow decreases abruptly

A

STEMI

129
Q

5 common pathophysiologic process that causes NSTEMI

A
  1. rupture/erosion of coronary plaque that leads to non-occlusive thrombosis
  2. dynamic obstruction d/t VC
  3. worsening coronary luminal narrowing due to progressive atherosclerosis, instent restenosis, or narrowing of CABG
  4. inflammation
  5. myocardial ischemia due to demand increase
130
Q

Basic set up for CABG

A
  1. std monitors + ABP/PAP/CVP, cerebral oximetry, BIS, TEE
  2. emergency meds: inotrope (epi), vasopressor (neo), vasodilator (cardene)
  3. routine induction meds: etomidate, paralytic, narcotics, heparin
  4. at least 2 units blood ready
  5. temporary pacer checked, and battery is working
  6. infusions are set up and ready
131
Q

what is the purpose of giving versed and fentanyl prior to CABG

A

decrease unwanted SNS response 2/2 anxiety

132
Q

pt coming in for CABG who should you caution premedication of versed and fentanyl with ?

A

CHF, low CO, and pulmonary HTN pts

133
Q

pre-bypass goals

A
  1. keep pt at baseline
  2. do not start correcting numbers until surgical correction has been made
  3. do no harm
134
Q

periods of increased stimulation (pre-bypass CABG)

A
  1. incision
  2. sternotomy & retraction
  3. sympathetic nerve dissection (at LIMA)
  4. pericardiotomy
  5. aortic cannulation
135
Q

inadequate anesthesia during times of increased stimulation with CABG (prebypass) can result in…

A

increased circulating catecholamines –>
1. HTN
2. dyrhythmias
3. tachycardia
4. ischemia
5. HF

136
Q

pre-bypass CABG, periods of decreased stimulation (“slump”)

A
  1. preincision
  2. peripheral graft harvest (from leg)
  3. IMA dissection
  4. venous cannulation
137
Q

periods of decreased stimulation (“slump”) with prebypass CABG - what are the risks?

A
  1. Hotn
  2. bradycardia
  3. dysrhythmias
  4. ischemia
138
Q

what is teh most stimulating part of the induction period for CABG pt?

A

laryngoscopy

139
Q

what is your first line tx for hypotension for the pt on pump

A

neosynephrine (not fluids, need to avoid hemodilution)

140
Q

autologous blood removal for CABG

A

taking 1 unit of blood prior induction via gravity.

141
Q

risks with autologous blood removal

A
  1. Hotn 2/2 hovolemia
  2. decreased O2 carrying capacity (will be reflected through mixed venous sat)
  3. infection
142
Q

autologous blood is stored in a bag with _________________ (similarly to banked blood)

A

citrate phosphate dextrose solution

143
Q

relative c/i to autologous blood removal

A
  1. left main dz
  2. LV dysfx (cannot handle hovol with losing 1 unit blood
  3. anemia with hgb < 12
  4. emergent surgery
144
Q

when would you expect there to be a high risk of major structure accidently being cut during CABG?

A

redo sternotomy 2/2 adhesions and scar tissue

145
Q

if a major structure is accidently cut during CABG (specifically with sternotomy) what do you do

A
  1. put on bypass immediately
  2. have blood products checked and ready for administration
146
Q

prolonged sternotomy dissection for CABG increases the risk of _______________ redo surgery

A

dysrhythmias

147
Q

what are the vessels that could be used for coronary bypass

A
  1. LIMA/RIMA
  2. saphenous vein
  3. radial artery
148
Q

endoscopic vein harvest for CABG is typically done if which vein is used

A

saphenous

149
Q

what is the preferred agent for anticoagulation with CPB

A

unfractionized heparin

150
Q

initial dose of unfractionized heparin for anticoagulation prior to CPB

A

300 units/kg

151
Q

retrograde autologous priming

A

draining blood out of pt through aortic cannula to prime CPB circuit

152
Q

what is the most common arterial access site for aortic cannulation

A

distal ascending aorta

153
Q

before aortic cannulation, ACT must be greater than ___________

A

400 s

154
Q

if the distal ascending aorta is not an arterial access option for aortic cannulation, what are the other arterial access sites that can be used?

A

femoral artery

155
Q

what is the number one complication from aortic cannulation (CABG)

A

embolic phenomena 2/2 air or atherosclerotic plaque dislodgement

156
Q

aortic cannulation complications (CABG)

A
  1. emboli
  2. Hotn
  3. dysrhythmias
  4. aortic dissection with cannula misplacement
  5. bleeding
  6. air entrainment from around cannula with systemic embolization
157
Q

CPB venous cannulation

A
  1. incision into right atrium –> cannula placed into atrium and down into IVC
  2. accompanied by significant dysrythias and hypotension
158
Q

bicaval venous cannulation (CPB)

A

SVC cannula added through RA (in addition to the IVC cannula)

159
Q

alternative venous cannulation site from RA –> IVC

A

femoral vein

160
Q

complications with CPB venous cannulation

A
  1. Hotn
  2. Bleeding (if RA or SVC/IVC torn)
  3. dysrhythmias
  4. air entrainment
161
Q

what is cardioplegia

A

Cold K+ solution that stops the heart before a CABG procedure

162
Q

aortic root vent on the cardioplegia (anterograde) line

A

used for de-airing the heart at end of CPB

163
Q

blood pressure goals when cannulating your cardioplegia lines

A

SBP 90-100 (same as aortic cannulation)

164
Q

what is the basic sequence of CPB (starting with going on by pass)

A
  1. go on bypass
  2. cool pt (32-36)
  3. Ao cross clamp
  4. cardioplegia infused either anterograde or retrograde to arrest the heart
  5. operation: SVG placed on most severely dz’d coronary first; IMA constructed last
  6. rewarming when final distal anatamosis is begun
  7. Ao unclamped
  8. pacing wires placed
  9. come off bypass
165
Q

anterograde cardioplegia is achieved by administering the solution into the ________________

A

aortic root (btwn Ao valve and XC)

166
Q

why is the time btwn cross clamping of Ao and administration of cardioplegia kept to a minimum?

A

to prevent any warm ischemia

167
Q

cardioplegia is a solution high in __________, which arrests the heart in _______________

A

potassium; diastole

168
Q

retrograde cardioplegia is administered through the _______________

A

coronary sinus

169
Q

hypothermia for CPB will ____________ anesthetic requirements

A

decrease

170
Q

what monitoring should be used to monitor depth of anesthesia during CPB?

A
  1. HD cues
  2. check pt for pupil dilation and/or sweating (*sign of awareness)
  3. monitor BIS
171
Q

what is the best drug for induction with heart failure

A

etomidate

172
Q

what is the most common genetic CV disease

A

hypertrophic cardiomyopathy

173
Q

hypertrophic cardiomyopathy is a _______________ genetic d/o

A

autosomal dominant

174
Q

hypertrophic cardiomyopathy is aka

A

idiopathic hypertrophic subaortic stenosis (IHSS)

175
Q

_____________ is LV hypertrophy in the absence of any other cardiac dz

A

hypertrophic cardiomyopathy

176
Q

pathophysiology of hypertrophic cardiomyopathy

A

myocardial hypertrophy –> dynamic LVOT obstruction –> systolic anterior movement of the mitral valve –> diastolic dysfunction

177
Q

s/sx of hypertrophic cardiomyopathy

A

wide range: asymptomatic - sudden death

  1. angina
  2. fatigue
  3. syncope
  4. tachydysrythmias
  5. HF
  6. murmur present with gallop
178
Q

sudden death 2/2 hypertrophic cardiomyopathy is most common in thosed aged _____________

A

10-30

179
Q

with hypertrophic cardiomyopathy, _____________ will relieve the sx, but _____________ aggravates them

A

lying down; valsalva

180
Q

Dx of hypertrophic cardiomyopathy

A
  1. ECG
  2. echo
  3. histology via endomyocardial biopsy
181
Q

what is the most common and best way to dx hypertrophic cardiomyopathy? what is the only way to definitively dx hypertrophic cardiomyopathy

A

echo; histological endomyocardial biopsy (reserved for pts where dx cannot be established otherwise)

182
Q

Tx goals with hypertrophic cardiomyopathy

A
  1. improve diastolic filling
  2. reduce LVOT obstruction
  3. decrease myocardial ischemia
183
Q

what are the three most common responses to pericardial injury

A
  1. acute pericarditis
  2. pericardial effusions
  3. constrictive pericarditis
184
Q

tamponade presents with….

A

fluid under pressure

185
Q

acute pericarditis is most commonly caused by ___________

A

viral infection

186
Q

what is acute pericarditis that presents 2 weeks - months after a myocardial event ?

A

dresslers syndrome

187
Q

dresslers syndrome is often _____________

A

autoimmune

188
Q

what is acute benign pericarditis

A

acute pericarditis in the absence of pericardial effusion

189
Q

T/F: acute benign pericarditis alters cardiac function

A

FALSE

190
Q

Dx of acute pericarditis

A
  1. based on sx (chest pain, friction rub, EKG changes)
  2. low grade fever with ST
  3. friction rub
  4. EKG changes in 90% of people
191
Q

EKG changes with acute pericarditis? this is caused by what?

A
  1. ST segment elevation, PR segment depression, & T wave inversion
  2. caused by inflammation of the superficial myocardium
192
Q

Primary tx for acute pericarditis

A

asprin or NSAIDs

193
Q

tx for acute pericarditis

A
  1. Asprin or Nsaids
  2. codeine
  3. colchincine
  4. steroid
194
Q

why are steroids typically not a first line tx with acute pericarditis

A

once the steroids are stopped –> pericarditis relapse; only used when other therapies do not work

195
Q

pericarditis presents in _____% of pts after cardiac surgery

A

10-40

196
Q

pericarditis is most common in ____________ patients after cardiac surgery

A

pediatric

197
Q

pericardial space normally contains _________cc of fluid

A

25-50

198
Q

causes of pericardial effusion

A
  1. infection
  2. MI (dresslers syndrome)
  3. trauma or cardiotomy (cardiac surgery)
  4. metastatic dz
  5. drugs
  6. mediastinal radiation
  7. systemic Dz (lupus, RA)
199
Q

with pericardial effusion as pericardial pressure increases ________ increases; –> atrial and ventricular filling being restricted –> SV becoming FIXED, thus CO becoming _____________ dependent

A

RAP; rate (HR)

200
Q

a large pericardial effusion can compress structures –> what sx

A
  1. anorexia & dysphagia (esphogeal compression)
  2. dyspnea, cough, hoarseness (tracheal & lung compression)
201
Q

up to ___________L can be accomodated in the pericardial sac with chronic effusion, but with acute increases of ________mL –> tamponade

A

2; 40-50

202
Q

s/sx of tamponade

A
  1. kussmauls sign (JVD w/ inspiration)
  2. pulsus paradoxus
  3. becks triad (distended neck veins, muffled heart sounds, Hotn)
203
Q

changes with cardiac numbers with tamponade

A
  1. CVP > RAP
  2. tachycardia (CO becomes HR dependent)
  3. good ctx, poor preload
  4. eventual equilibration of pressures
204
Q

causes of cardiac tamponade

A
  1. trauma/iatrogenic injury
  2. infection
  3. neoplastic dz, uremia, connective tissue d/o
  4. acute MI
  5. postop bleeding
  6. Ao dissection
205
Q

Tx of tamponade

A
  1. pericardiocentesis (at bedside)
  2. drainage of fluid through subxiphoid or mini thorocotomy incision (OR)
206
Q

anesthetic management goals with cardiac tamponade

A
  1. FAST (tachycardia)
  2. TIGHT (vasocontriction)
  3. FULL (volume)
207
Q

what is the drug of choice for cardiac tamponade anesthetic management?

A

ketamine
cardiac stimulant, keeps pt spontaneously breathing

208
Q

what drug is avoided with cardiac tamponade

A

BETA blockers
*any drugs that depress that myocardium

209
Q

anesthetic management of cardiac tamponade

A
  1. ketamine for induction
  2. avoid BB
  3. arterial BP prior to induction
  4. correct metabolic acidosis from low CO state
  5. if have to use GA –> fast RR and low TV until relieved
  6. be prepared for post HTN
210
Q

what is “concretio cordis”

A

constrictive pericarditis

211
Q

causes of constrictive pericarditis

A
  1. idiopathic (most common)
  2. previous cardiac surgery
  3. radiation therapy
  4. Tb
212
Q

_____________ is characterized by a fibrous scarring and adhesions that obliterate the pericardial space –> “rigid shell” around the heart

A

constrictive pericarditis

213
Q

S/Sx of constrictive pericarditis

A
  1. progressive dyspnea and fatigue (dec CO)
  2. increased CVP
  3. JVD, edema, ascites
  4. afib (25%)
  5. SV maintained
  6. Square root sign on RVP tracing
  7. kussmauls and pulsus paradoxus
214
Q

how do you dx constrictive pericarditis

A

TEE, CT, or MRI

215
Q

what is the difference btwn tamponade and constrictive pericarditis with ventricular filling

A

with constrictive pericarditis the restriction to ventricular filling only occurs during the last 2/3 fo diastole, and SV is maintained

216
Q

with ________________ you will see a “square root sign” on the RVP tracing

A

constrictive pericarditis

217
Q

anesthetic management with constrictive pericarditis

A
  1. maintain HR, volume, and ctx
  2. use ketamine and pancuronium
  3. note that arrhythmias, hotn, and bleeding is common
218
Q

with blunt injuries to the chest, which part of the heart is most likely to be injured

A

RV

219
Q

with pericardial traumas, they will do a ______________ incision for quick access to the thoracic cavity

A

clamshell

220
Q

what is commotio cordis

A
  1. syndrome caused by blunt trauma to the heart –> ventricular dysrhythmias and death if untx
  2. the mechanical “thud” –> R on T
221
Q

a kid playing baseball gets hit in the chest with baseball, and immediately drops requiring CPR, what has occured?

A

commotio cordis

222
Q

Tx of commotio cordis

A
  1. rapid defibrillation with AED
223
Q

Tx of constrictive pericarditis

A

surgical “stripping”

224
Q

how do you tx mild sx (with sx of HF) of hypertrophic cardiomyopathy

A
  1. beta blockers
  2. CCB
  3. diuretic
225
Q

preoperative anesthetic management of hypertrophic cardiomyopathy

A
  1. minimize LVOT obstruction by decreasing contractility and increasing afterload and preload
  2. cardiac eval, ECg, echo, continue meds, turn off ICP apply pads
  3. anxiolytics to blunt SNS
226
Q

intraoperative anesthetic management of hypertrophic cardiomyopathy

A

SLOW-TIGHT-FULL
1. blunt SNS to DL (consider BB)
2. ABP and TEE
3. use NEOSYNEPHRINE (avoid Beta Agonist)
4. NO vasodilators
5. maintain NSR, treat SVT quickly

227
Q

what vent settings are appropriate for pt with hypertrophic cardiomyopathy

A
  1. avoid PPV (avoid PEEP)
  2. small Tv, increase Rate
228
Q

postop anesthetic management of hypertrophic cardiomyopathy

A
  1. avoid all SNS stimulation (pain, shivering, anxiety, hypoxia, hypercarbia)
  2. maintain euvolemia with prompt tx of Hotn
229
Q

MOST heparin resistance can be managed by _________________

A

giving more heparin

230
Q

if pt is unresponsive to heparin: requires > 600 units/kg and/or cannot get ACT > 450 what should you do

A

give ATIII, FFP or plasma

231
Q

heparin resides physiologically in ____________, but is commerically derived from __________________

A

mast cells; bovine lung or porcine intestine

232
Q

heparin is ____________ charged at physiologic pH

A

negatively

233
Q

MOA of heparin

A

binds to ATIII and potentiates its action 10x; inhibits thrombin, Xa, IXa, XIa, and XIIa

234
Q

inhibition of thrombin requires stimultaneous binding of heparin to __________ & __________

A

thrombin and ATIII

235
Q

s/e heparin

A
  1. bolus will decrease SVR
  2. anaphylaxis
  3. bleeding
  4. HIT
236
Q

what is a normal ACT value

A

110-140 s

237
Q

goal of ACT for bypass (range)

A

400-480 (>450 great!) s

238
Q

ACT is prolonged by

A

hypothermia and hemodilution

239
Q

_______________ is a cation that binds with anionic heparin –> neutralization and elimination of anticoauglation activity

A

protamine

240
Q

_________ mg of protamine neutralizes 1 mg (100 units) of heparin

A

1

241
Q

post protamine ACT should return to ____________ above pts baseline

A

<10%

242
Q

s/e of protamine

A
  1. Hotn with rapid administration (<3 min)
  2. anaphylaxis
  3. pulmonary vasoconstriction –> RV failure
  4. antihemostatic effects
243
Q

protamine is c/i in what pts

A
  1. those with allergy to vertebrate fish
  2. those with allergy to NPH
244
Q

what do you want your blood pressure to be prior to administering protamine? if it < SBP goal, how should you intervene

A

SBP 90-120; fluid

245
Q

what are the antifibrinolytic agents used with cardiac surgery

A

amicar and TXA

246
Q

MOA of amicar and TXA

A

lysine analogues that bind to the lysine binding site of plasminogen –> reversible complex with plasmin inhibiting fibrinolysis

247
Q

which antifibrinolytic agent is 5-10 x more potent w/ higher affinity for plasminogen ? (TXA or amicar)

A

TXA

248
Q

evaluation of hemostasis post CPB

A
  1. ACT to assess heparin neutralization
  2. TEG maximal amplitude for plt fux
  3. PT, aPTT, TEG-R, TEG-K to assess coagulation
  4. TEG-lysis index, fibrin degradation products, D-dimer to assess fibrinolysis
249
Q

s/sx of aortic stenosis

A

Triad:
1. angina
2. syncope
3. dyspnea on exertion

250
Q

murmur with aortic stenosis will be heard in _____________

A

systole

251
Q

once the triad of sx present with aortic stenosis life expectancy is __________

A

<5 years

252
Q

changes with pressure volume loop with aortic stenosis

A
  1. elevated peak SBP
  2. decreased SV
  3. LVEDP increased
  4. EDPVR increased
  5. ESV increased
253
Q

intraop management of aortic stenosis

A

SLOW-TIGHT-FULL
1. adequate preload (volume)
2. lower HR (50-70): gives longer diastole and adequate systolic ejection
3. keep SVR high with neosynephrine (alpha agonist)

254
Q

anesthetic management of Aortic stenosis

A
  1. light premed to avoid drop in SVR
  2. A line
  3. if ischemia develops use NTG cautiously
  4. PCWP may overestimate preload d/t noncompliant LV
  5. TEE
255
Q

pts with aortic stenosis are ___________ dependent

A

preload

256
Q

primary cause of mitral stenosis

A

rheumatic heart disease (2/2 scarring and fibrosis)

257
Q

s/sx of mitral stenosis

A
  1. first associated with exercise/high CO
  2. progressive decline with repeated epsiodes of fatigue, chest pain, palpatations, SOB, paroxysmal nocturnal dyspnea, pulmonary edema, hemoptysis
  3. hoarseness
  4. diastolic murmur (at apex)
  5. broad notched p wave on ECG = p mitrale
  6. afib in 1/3 of pts
258
Q

severe mitral valve stenosis valve area

A

< 1 - 1.5

259
Q

smallest mitral valve area compatible with life

A

0.3-0.4 cm

260
Q

changes to pressure volume loop with mitral stenosis

A
  1. EDV and ESV decreased
  2. SV decreased
  3. LVEDP decreased
261
Q

HD management of mitral stenosis

A

SLOW, TIGHT, FULL
1. preload dependent for forward flow across valve - ensure adequate volume, but be careful LAP already increased
2. slower HR bc blood flows across MV at diastole
3. SVR and PVR will be increased - try to keep them there

262
Q

anesthetic management of pt with mitral stenosis

A
  1. light premed to avoid decrease in preload or oversedation
  2. avoid ketamine
  3. short acting BB (esmolol) to tx tachycardia
  4. PA catheter
  5. TEE
  6. slow muscle relaxant reversal to avoid tachycardia with anticholinergic administration
263
Q

indication for TAVR

A

aortic valve replacement for…
1. high risk or inoperable 2/2 age and comorbidities
2. want to avoid sternotomy
3. want to avoid going on pump

264
Q

what are the different approaches for a TAVR

A
  1. retrograde (percutaneous via femoral artery)
  2. anterograde (aka transapical, through the apex)
  3. transaortic approach (through Ao root)
265
Q

what is the preferred approach for a TAVR

A

retrograde (percutaneous through the femoral artery)

266
Q

complications of TAVR

A
  1. stroke
  2. cognitive dysfunction
  3. Ao dissection
  4. bleeding
  5. mediastinal hematoma
  6. femoral/Iliac artery injury
  7. valve size mismatch
  8. conduction system issues
  9. perivalvular leaks
267
Q

why do we pace with TAVR

A

rapid pacing at 180 bpm keeps the aortic valve open

268
Q

use of BB with heart failure

A
  1. decrease SNS stimulation –> decreased circulating catecholamines
  2. increases EF
  3. decreases remodelling
269
Q

use of natriuretic peptides for HF

A
  1. diuresis
  2. natriueresis
  3. vasodilation
  4. antiinflammatory
  5. inhibits SNS and RAAS
270
Q

use of RAAS medications for HF

A
  1. prevents cardiac remodelling
    2.. prevents vasoconstriction –> no increase in cardiac filling, no decrease in CO
  2. prevents sodium and water retention (no increase in cardiac filling pressures
271
Q

management of diastolic HF

A
  1. if have SHF –> prevent!
  2. caution use of diuretics
  3. maintain normal sinus rhythm and HR control
  4. correct preciptiating factors
272
Q

surgical mangement of heart failure

A
  1. PTCA or CABG
  2. cardiac resynchronization therapy
  3. AICD
  4. cardioMEMS - implanted PAP monitor
  5. VAD bridge therapy
  6. total artifical heart
  7. transplant
273
Q

anesthesia considerations with heart failure

A
  1. optimize pt condition
  2. cardiac resynchronization therapy
  3. AICD
  4. cardioMEMS - implanted PAP monitor
  5. VAD bridge therapy
  6. total artifical heart
  7. transplant

principles 2 cardiac anesthesia (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions