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APEX > Unit 3 - CV Patho > Flashcards

Unit 3 - CV Patho Flashcards

1
Q

what is the risk of perioperative MI if the patient had an MI < 3 months ago?

A

30%

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2
Q

what is the risk of perioperative MI in the general population?

A

0.3%

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3
Q

when should a patient be referred to a cardiologist before surgery?

A

a pt with an NYHA classification of 3 or 4 who is scheduled for a high- or intermediate-risk surgery

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4
Q

risk of perioperative MI if MI > 6 months

A

6%

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5
Q

risk of perioperative MI if previous MI within 3-6 months

A

15%

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6
Q

highest risk of reinfarction

A

within 30 days of acute MI

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7
Q

ACC/AHA minimum recommended time before considering elective surgery in a patient with recent MI

A

4-6 weeks

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8
Q

6 risk factors for perioperative cardiac morbidity & mortality for non-cardiac surgery

A
  1. high risk surgery
  2. history of IHD (greatest risk with unstable angina)
  3. history CHF
  4. history cerebrovascular disease
  5. DM
  6. serum Cr > 2 mg/dL
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9
Q

what factor confers the greatest risk of perioperative MI

A

unstable angina

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10
Q

3 important biomarkers released by infarcted myocardium

what’s more sensitive of MI diagnosis?

A
  1. creatine kinase-MB
  2. troponin I
  3. troponin T

troponins are more sensitive

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11
Q

when do biomarkers released by infarcted myocardium initially elevate

A

3-12 hours

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12
Q

peak elevation with infarcted myocardium:

CK-MB
Troponin I
Troponin T

A
  • CK-MB: 24 hours
  • Troponin I: 24 hours
  • Troponin T: 12-48 hours
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13
Q

when does CK-MB return to baseline after MI?

A

2-3 days

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14
Q

when do troponin I levels return to normal after infarction?

A

5-10 days

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15
Q

when do troponin T levels return to normal after infarction

A

5-14 days

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16
Q

EKG lead that aids in identification of inferior wall ischemia & monitors for dysrhythmias

A

lead II

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17
Q

best leads for detecting intraoperative LV ischemia

A

V3, V4, V5

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18
Q

which lead may be best for detecting ischemia & why

A

V4

closest to isoelectric level on baseline EKG

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19
Q

combination of what 3 leads has an ischemic detection rate of up to 96%

A

leads II, V4, V5

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20
Q

intraop EKG monitoring in CAD pt

A

RA, RL, LA, LL, and a V lead to monitor for LV ischemia

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21
Q

goal of myocardial ischemia interventions

A

make the heart smaller, slower, and better perfused

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22
Q

how to treat intraop increased myocardial O2 demand caused by increased PAOP

A

nitroglycerin

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23
Q

what is diastolic compliance

A

describes filling pressure that results from a given EDV

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24
Q

what happens to the diastolic pressure-volume curve with decreased compliance

A

curve shifts up and left

higher EDP for given EDV

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25
Q

what happens to diastolic pressure-volume curve with increased compliance

A

shifts down and right

lower EDP for given EDV

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26
Q

5 conditions that make the heart “stiffer” and decrease compliance

(things that affect the diastolic pressure-volume relationship)

A
  1. age > 60
  2. ischemia
  3. pressure overload hypertrophy (aortic stenosis or HTN)
  4. HOCM
  5. pericardial pressure (increased external pressure)
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27
Q

what happens to filling pressures in a poorly compliant ventricle

A

higher filling pressures required to prime poorly compliant ventricle

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28
Q

CVP and PAOP with reduced ventricular compliance

A

may overestimate LVEDV

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29
Q

why is there a risk of pulmonary edema in a poorly compliant ventricles

A

higher filling pressures required

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30
Q

2 conditions that dilate the heart and increase compliance

A
  1. chronic aortic regurg
  2. dilated cardiomyopathy
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31
Q

what type of heart failure is associated with a pumping problem

A

HF with reduced ejection fraction
aka systolic failure

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32
Q

what type of heart failure is assoc. with a filling problem

A

HF with preserved EF
aka diastolic failure

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33
Q

3 etiologies of systolic heart failure (HFrEF)

A
  1. myocardial ischemia
  2. valve insufficiency
  3. dilated cardiomyopathy
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34
Q

7 etiologies of diastolic failure (HFpEF)

A
  1. myocardial ischemia
  2. valve stenosis
  3. HTN
  4. hypertrophic cardiomyopathy
  5. cor pulmonale
  6. obesity
  7. aging
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35
Q

what is HF with reduced EF?

A

heart can’t pump enough blood to satisfy body’s metabolic requirements

volume overload

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36
Q

what is HF with preserved EF

A

heart can’t relax and accept incoming volume d/t decreased ventricular compliance

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37
Q

contractility with HFpEF

A

generally preserved unti late in disease

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38
Q

compensation for HFrEF

A
  • increased SNS
  • increased RAAS
  • increased preload
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39
Q

EDV, EDP, ESV, SV, LV mass, and LV geometry in chronic HFrEF (systolic failure)

A
  • increased EDV
  • increased EDP
  • increased ESV
  • decreased/normal SV
  • increased LV mass
  • eccentric hypertrophy
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40
Q

EDV, EDP, ESV, SV, LV mass, and LV geometry in chronic HFpEF (diastolic failure)

A
  • normal EDV
  • increased EDP
  • normal ESV
  • normal or decreased SV
  • increased LV mass
  • concentric hypertrophy
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41
Q

defining characteristic of HFpEF (diastolic failure)

A

symptomatic heart failure with normal EF

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42
Q

5 ways the body adapts to heart failure & consequences of each

A
  1. SNS activation - increased myocardial work
  2. excessive vasoconstriction - decreased CO
  3. chronic SNS activation - downregulation of beta receptors
  4. fluid retention - ventricular dilation, increased wall stress
  5. myocardial remodeling - decreased myocardial performance
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43
Q

how can myocardial remodeling with heart failure be reversed

A

ACE inhibitors & aldosterone antagonists

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44
Q

3 physiologic functions of BNP

A
  1. natriuresis
  2. diuresis
  3. vasodilation
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45
Q

why does the failing heart release natriuretic peptides into systemic circulation

A

improve Na+ and fluid balance

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46
Q

useful biomarker for assessing risk in pt with heart failure

A

BNP

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47
Q

MOA of neprilysin inhibitors

A

neprilysin degrades natriuretic peptides

inhibition can be used to treat heart failure by increasing concentration of natriuretic peptides in blood

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48
Q

goals of HFrEF (systolic failure)

(preload, afterload, contractility, HR)

A
  • diuretics if preload too high
  • decrease afterload to reduce myocardial work, maintain CPP (SNP)
  • augment contractility with inotropes PRN (dobutamine)
  • HR usually high; may need to stay high to preserve CO with low EF
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49
Q

HD goals of HFpEF (diastolic failure)

(afterload, contractility, HR)

A
  • keep afterload elevated to perfuse thick myocardium (neo)
  • contractility usually normal
  • slow/normal HR to increase diastolic time and CPP
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50
Q

most common cause of right heart failure

A

left heart failure

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51
Q

6 conditions that increase PVR and right heart work

A
  • hypoxia
  • hypercarbia
  • acidosis
  • hypothermia
  • high PEEP
  • N2O
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52
Q

4 surgical procedures with high cardiac risk (risk > 5%)

A
  1. emergency surgery (especially in elderly)
  2. open aortic surgery
  3. peripheral vascular surgery
  4. long surgical procedures with significant volume shifts/blood loss
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53
Q

5 surgical procedures assoc. with intermediate cardiac risk (risk = 1-5%)

A
  1. CEA
  2. head/neck surgery
  3. intrathoracic or intraperitoneal surgery
  4. orthopedic surgery
  5. prostate surgery
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54
Q

5 surgical procedures assoc. with low cardiac risk (risk < %)

A
  1. endoscopic procedures
  2. cataract surgery
  3. superficial procedures
  4. breast surgery
  5. ambulatory procedures
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55
Q

what is the modified NY association functional classification of heart failure

A 
class 1: asymptomatic
class 2: symptomatic with moderate activity
class 3: symptomatic with mild activity
class 4: symptomatic at rest
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56
Q

how is coronary perfusion pressure calculated

A

aortic diastolic pressure - LVEDP

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57
Q

what’s the difference in primary and secondary HTN

A

primary: no identifiable cause (95%)
secondary: identifiable cause (5%)

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58
Q

treatment of RV failure

A
  • inotropes (milrinone, dobutamine)
  • pulmonary vasodilators (iNO, sildenafil)
  • reverse causes of increased PVR
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59
Q

how does HTN cause organ damage

A

increased BP increases myocardial work

higher arterial driving pressure damages nearly every organ in the body

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60
Q

6 complications of HTN

A
  • concentric LVH
  • IHD
  • CHF
  • arterial aneurysm (aorta, cerebral)
  • stroke
  • ESRD
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61
Q

how does LVH contribute to infarction

A
  • leads to CHF
  • increased MvO2 results in coronary insufficiency
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62
Q

diagnosis of HTN

A

BP measured on 2 separate occasions at least 1-2 weeks apart to confirm

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63
Q

normal, elevated, and HTN stages 1-3

A
  • normal: SBP < 120 & DBP < 80
  • elevated: SBP 120-139 & DBP < 80
  • stage 1 HTN: SBP 130-139 or DBP 80-89
  • stage 2 HTN: SBP > 140 or DBP > 90
  • stage 3 HTN (crisis): SBP > 180 and/or DBP > 120
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64
Q

cause of primary HTN

A

increased CO, SVR, or both (SVR almost always the cause)

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65
Q

what plays an integral role in increasing SVR

A

vascular smooth muscle tone (increased intracellular Ca2+ concentration)

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66
Q

what leads to increased SVR in primary HTN

A

SNS overactivity, chronic vasoconstriction

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67
Q

how does chronic vasoconstriction assoc. with primary HTN lead to water and Na+ retention

A
  • results in increased renin release
  • increases AT1, AT2 and aldosterone
  • increases Na+/water retention
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68
Q

why do pts with primary HTN have a vasodilator deficiency

A

decreased NO and prostaglandins

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69
Q

how do patients with primary HTN develop increased vascular stiffness

A

collagen and metalloproteinase depositition in arterial intima

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70
Q

cerebral perfusion pressure remains constant with BP of:

A

50-150 mmHg

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71
Q

BP beyond the limits of autoregulation is dependent on:

A

pressure

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72
Q

cerebral autoregulation curve in pts with chronic HTN

A

shifted to right, narrower

difficult to predict on individual basis

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73
Q

how does HTN contribute to CHF?

A
  • increased myocardial wall tension
  • LVH
  • increased MvO2
  • coronary insufficiency
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74
Q

what is the cerebral autoregulation curve

A

describes the range of BPs where cerebral perfusion pressure remains constant

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75
Q

why does the cerebral autoregulation curve shift to the right in pts with chronic HTN

A

helps the patient’s brain tolerate a higher range of BPs

comes at the expense of not tolerating a lower BP

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76
Q

6 causes of secondary HTN

A
  1. coarctation of aorta
  2. renovascular disease
  3. hyperadrenocorticism (Cushing’s syndrome)
  4. hyperaldosteronism (Conn’s disease)
  5. pheochromocytoma
  6. pregnancy-induced HTN
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77
Q

anticipated HD response to anesthesia in pts with HTN

A
  • exaggerated hypotensive response to induction
  • exaggerated hypertensive response to intubation & extubation
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78
Q

risk of using myocardial depressants and vasodilators with anesthesia in pts with HTN

A

hypertensive pts are volume contracted

agents that cause myocardial depression & vasodilation unmask volume contracted state

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79
Q

how to promote HD stability in patients with HTN

A

adequate hydration before induction

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80
Q

perioperative beta blocker use in hypertensive pts

A
  • continue throughout periop period if already on
  • starting DOS increases risk of hypotension, bradycardia, stroke, death
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81
Q

should ACE inhibitors and ARBs be taken DOS?

A

decision made on case-by-case basis

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82
Q

effects of ACE inhibitors and ARBs with GA

A

can produce vasoplegia and cause a state of hypotension unresponsive to vasopressors and fluids

may need to treat with vasopressin, terlipressin, methylene blue

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83
Q

surgery should be delayed for optimization when BP is what?

A

SBP > 180
DBP > 110

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84
Q

most common cause of intraoperative HTN

A

surgical stimulation

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85
Q

what is a hypertensive crisis

A

BP > 180/120

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86
Q

when is a hypertensive emergency declared

A

evidence of end-organ injury

  • CNS: encephalopathy, stroke, papilledema
  • cardiac: CHF
  • renal: HTN-induced acute renal dysfunction
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87
Q

treatment of hypertensive crisis

A

depends on cause

beta blockers, CCBs, vasodilators (Nipride)

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88
Q

clinical findings with coarctation of aorta

A
  • upper limb BP > lower limb BP
  • weak femoral pulse
  • systolic bruit
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89
Q

clinical findings with renovascular disease

A
  • bruit (epigastric or abdominal)
  • severe HTN in young pt
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90
Q

clinical findings with Conn’s disease

A
  • HTN
  • hypokalemia
  • alkalosis
  • weakness/fatigue
  • paresthesia
  • nocturnal polyuria & polydipsia
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91
Q

clinical findings of pheo

A
  • headache
  • palpitations
  • diaphoresis
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92
Q

clinical findings of pregnancy-induced HTN

A
  • peripheral and pulmonary edema
  • headache
  • sz
  • RUQ pain
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93
Q

2 major classes of CCBs

A
  • dihydropyridines: nifedipine, nicardipine, amlodipine, clevidipine
  • non-dihydropyridines
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94
Q

example of CCB in phenylalkylamine class

A

verapamil

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95
Q

example of CCB in benzothiazepine class

A

diltiazem

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96
Q

how do alpha 1 antagonists reduce BP

A
  • decreased vascular calcium causes vasodilation
  • decreased SVR
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97
Q

how do beta 1 antagonists decrease BP

A

decreased: inotropy, chronotropy, dromotropy, renin release

vasoconstriction in muscle

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98
Q

beta 1 selective beta blockers

A
  • acebutolol
  • atenolol
  • bisoprolol
  • esmolol
  • metoprolol
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99
Q

alpha:beta anagonistic properties in labetolol

A 
IV = 1:7
PO = 1:3
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100
Q

how do alpha 2 agonists decrease BP

A

decreased SNS outflow

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101
Q

how do CCBs decrease BP

A
  • decreased vascular calcium (vasodilation)
  • decreased SVR
  • decreased inotropy, chronotropy, dromotropy
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102
Q

class of CCBs that target vasculature

A

dihydropyridines

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103
Q

class of CCBs that target myocardium > vessels

A

non-dihydropyridines

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104
Q

how do arteriodilators and venous dilators decrease BP

A

increased NO

venodilators decrease venous return

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105
Q

how do ACE inhibitors decrease BP

A
  • inhibits vasoconstriction d/t AT2
  • inhibits aldosterone release
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106
Q

how do AT2 receptor blockers decrease BP

A
  • inhibits vasoconstriction r/t AT2
  • inhibits aldosterone release
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107
Q

how do loop diuretics decrease BP

A

inhibits Na-K-Cl transporter in thick portion of ascending loop of Henle

diuresis = decreased VR

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108
Q

how do thiazide diuretics decrease BP

A

inhibits Na-Cl transported in distal convoluted tubule

decreased VR

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109
Q

how do K+ sparing diuretics decrease BP

A

inhibit K+ excretion and Na+ reabsorption by principal cells of collecting ducts

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110
Q

MOA of CCBs

A

bind to alpha-1 subunit of L-type calcium channel & prevent calcium from entering cardiac and vascular smooth muscle cells

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111
Q

which cardiac marker is the least sensitive for MI?

A

CK-MB

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112
Q

what are the 3 best EKG leads to monitor intraoperative ST changes?

A

V3
V4
V5

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113
Q

how does a decrease in ventricular compliance affect PAOP

A

PAOP may overestimate LVEDV

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114
Q

how do patients with CHF maintain BP?

A

rely on elevated levels of circulating catecholamines (increased SNS tone)

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115
Q

why can a standard 2 mg/kg propofol induction cause CV collapse in pts with CHF

A

CHF patients rely on increased SNS tone to maintain BP

2 mg/kg propofol reduces SNS tone while simultaneously reducing contractility (instead, slow titration of lower dose)

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116
Q

primary mechanism of CHF that activates RAAS

A

CHF reduces renal blood flow

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117
Q

why do CHF patients release natriuretic peptides

A

atrial dilation increases release of ANP & BNP

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118
Q

how does CHF affect beta receptors

A

causes down-regulation

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119
Q

most common cause of secondary HTN

A

renal artery stenosis

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120
Q

how does renal artery stenosis cause secondary HTN

A
  • narrowed renal artery reduces renal blood flow
  • kidneys activate RAAS in attempt to increase GFR
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121
Q

why are ACE inhibitors contraindicated in a pt with bilateral renal artery stenosis

A

can significantly reduce GFR and precipitate renal failure

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122
Q

examples of arteriodilators

A
  • hydralazine
  • Nipride
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123
Q

examples of venodilators

A
  • NTG
  • Nipride
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124
Q

examples of loop diuretics

A
  • furosemide
  • bumetanide
  • ethacrynic acid
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125
Q

examples of thiazide diuretics

A
  • HCTZ
  • metolazone
  • indapamide
  • chlorthalidone
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126
Q

potassium sparing diuretics

A

triamterene
amiloride

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127
Q

CCB that is a useful coronary antispasmodic

A

nicardipine

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128
Q

only CCB proven to decrease M&M from cerebral vasospasm

A

nimodipine

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129
Q

CCBs that reduce HR in pts with tachycardia, A-fib, or A-flutter

A

verapamil
diltiazem

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130
Q

CCB contractility impairment from greatest to least

A

verapamil > nifedipine > diltiazem > nicardipine

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131
Q

best CCBs for HTN r/t increased SVR

A

nifedipine, amlodipine, nicardipine (vasodilators)

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132
Q

MOA of clevidipine

A

arterial vasodilation decreases SVR without affecting preload

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133
Q

contraindications of clevidipine

A
  • egg allergy
  • soybean allergy
  • impaired lipid metabolism (pathologic HLD, lipid nephrosis, acute pancreatitis with HLD)
  • severe aortic stenosis
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134
Q

CCB prepared as a lipid emulsion

A

clevidipine

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135
Q

clevidipine dosing

A

1-2 mg/hr, max 16 mg/hr

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136
Q

PK of clevidipine

A
  • onset 2-4 min
  • half life 1 min (full recovery 5-15 min after gtt off)
  • tissue and plasma esterase metabolism
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137
Q

function of pericardium

A

surrounds heart and provides minimal friction environment

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138
Q

where do the visceral and parietal layers of the pericardium attach

A

visceral - attached to myocardium
parietal - anchored to mediastinum

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139
Q

3 conditions that affect the pericardium

A
  1. acute pericarditis
  2. constrictive pericarditis
  3. cardiac tamponade
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140
Q

what causes constrictive pericarditis

A

fibrosis or any condition that causes pericardium to be thicker

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141
Q

effects of constrictive pericarditis

A
  1. ventricles can’t fully relax during diastole (decreased compliance and diastolic filling)
  2. increased ventricular pressure creates back pressure on peripheral circulation
  3. ventricles increase myocardial mass (impairs systolic function over time)
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142
Q

cause of acute pericarditis

A

usually inflammation
(most commonly viral)

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143
Q

does acute pericarditis affect diastolic filling

A

not usually unless inflammation leads to constrictive pericarditis or tamponade

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144
Q

anesthetic management of constrictive pericarditis

A
  • avoid bradycardia (CO dependent on HR)
  • preserve contractility
  • maintain afterload
145
Q

causes of constrictive pericarditis

A
  • cancer (radiation)
  • cardiac surgery
  • RA
  • TB
  • uremia
146
Q

causes of acute pericarditis

A
  • viral infection
  • Dressler’s syndrome
  • lupus
  • scleroderma
  • trauma
  • cancer (radiation)
147
Q

what is Dressler’s syndrome

A

pericardial inflammation from necrotic myocardium s/o MI

148
Q

s/s constrictive pericarditis

A
  • Kussmaul’s sign (JVD during inspiration)
  • pulsus paradoxus
  • pericardial knock
149
Q

what is pulsus paradoxus

A
  • SBP decreased > 10 mmHg during inspiration
  • indicates impaired diastolic filling

may be seen with constrictive pericarditis

150
Q

treatment of constrictive vs. acute pericarditis

A

pericardiotomy

151
Q

risks & mortality assoc. with pericardiotomy

A

risk hemorrhage and dysrhythmias

mortality 6-19%

152
Q

s/s acute pericarditis

A

acute chest pain with pleural discomfort

  • increased pain with inspiration, postural changes
  • pain relieved when leaning forward or supine

pericardial friction rub

ST elevation with normal enzymes

fever

153
Q

which type of pericarditis usually resolves spontaneously

154
Q

drugs to relieve acute pericarditis pain

A
  • salicylates
  • oral analgesics
  • corticosteroids
155
Q

drugs to use in anesthetic management of constrictive pericarditis

A
  • ketamine
  • pancuronium
  • volatiles with caution
  • opioids, benzos, etomidate OK
156
Q

what is Kussmaul’s sign

A

paradoxical rise in CVP and JVD during inspiration

result of RV filling defect (impaired RV compliance)

157
Q

what separates pericardial tamponade from effusion

A

excess fluid excerts external pressure on the heart, limiting ability to fill and act as a pump

158
Q

CVP in pericardial tamponade

A

rises in tandem with pericardial pressure

159
Q

CVP and PAOP in pericardial tamponade

A

as ventricular compliance deteriorates, left and right diastolic pressure (CVP and PAOP) begin to equalize

160
Q

best method of pericardial tamponade diagnosis

161
Q

best treatment of pericardial tamponade

A
  • pericardiocentesis
  • pericardiostomy
162
Q

effects of increased pericardial pressure

A
  • increased LV pressure
  • decreased coronary perfusion
  • decreased ventricular filling
  • decreased LV volume
  • decreased SV
  • decreased CO
  • increased contractility
  • increased HR
  • increased renal fluid retention
163
Q

2 conditions commonly associated with Kussmaul’s sign

A
  1. constrictive pericarditis
  2. pericardial tamponade

(can occur with any condition limiting RV filling)

164
Q

2 conditions assoc. with pulsus paradoxus

A
  1. constrictive pericarditis
  2. pericardial tamponade
165
Q

treatment for pericardial effusion

A

seldom requires treatment

166
Q

pressure volume loop in pericardial tamponade

A
  • loop shifts to left (decreased LVEDV)
  • narrower (decreased SV)
  • higher slope during ventricular filling (decreased ventricular compliance)
167
Q

beck’s triad

A
  • hypotension
  • JVD
  • muffled heart sounds
168
Q

causes of the symptoms in becks triad

A
  • hypotension: decreased SV
  • JVD: impaired VR to right heart
  • muffled heart tones: fluid accumulation in pericardial space attenuates sound waves
169
Q

preferred anesthetic technique for acute pericardial tamponade undergoing pericardiocentesis

A

local anesthesia

170
Q

primary goal if GA is required for pericardiocentesis

A

preserve myocardial function

171
Q

drugs to avoid with pericardiocentesis

A
  • volatiles
  • propofol
  • thiopental
  • high dose opioids
  • neuraxial anesthesia
172
Q

safer drugs to use in pericardiocentesis

A
  • ketamine (best choice d/t SNS activation)
  • N2O
  • benzos
  • opioids
173
Q

why should spontaneous ventilation be maintained until pericardial tamponade relieved

A

PPV can impair venous return and CO (CV collapse)

174
Q

what happens to SNS tone, HR, inotropy, LVEDP, LVEDV, coronary perfusion pressure, CO, and SV with pericardial tamponade

A
  • SNS increased
  • HR increased
  • inotropy increased
  • LVEDP increased
  • LVEDV decreased
  • CPP decreased
  • CO decreased
  • SV decreased
175
Q

why do patients with pericardial tamponade have decreased EKG voltage

A

excess fluid around the heart attenuates the electrical signal recorded by electrodes

176
Q

why do pts with pericardial tamponade have increased contractility and afterload

A

increased SNS tone

177
Q

complications of pericardial tamponade treatment

A
  • PTX
  • re-accumulation of fluid
  • puncture of coronary vessels or myocardium
178
Q

goals for HR and rhythm in pts with pericardial tamponade

A
  • maintain HR (CO is HR dependent since SV is reduced)
  • maintain NSR (properly timed atrial kick required to prime less compliant ventricles)
179
Q

preload, inotropy, and afterload goals in pts with pericardial tamponade

A
  • maintain or increase preload; avoid decrease (PPV, hypovolemia, venous pooling)
  • maintain or increase inotropy
  • maintain afterload (essential to compensate for decreased SV and CO)
180
Q

ACC/AHA guidelines for infective endocarditis antibiotic prophylaxis

A

only if pt is at high risk of developing and more likely to suffer adverse outcomes

181
Q

6 patients at highest risk of infective endocarditis (need preop antibiotic prophylaxis)

A
  1. previous infective endocarditis
  2. prosthetic heart valve
  3. unrepaired cyanotic CHD
  4. repaired CHD < 6 months
  5. repaired CHD with residual defects that have impaired endothelialization at graft site
  6. heart transplant with valvuloplasty
182
Q

is antibiotic prophylaxis required for unrepaired cardiac valve disease, CABG, or coronary stent placement?

183
Q

3 surgical procedures that warrant antibiotic prophylaxis against infective endocarditis

A
  1. dental procedures involving gingival manipulation and/or damage to mucosal lining
  2. respiratory procedures that perforate mucosal lining (incision/biopsy)
  3. biopsy of infective lesions on skin or muscle
184
Q

2 definitive procedures for treatment of cardiac tamponade

A
  1. pericardiocentesis
  2. pericardiostomy
185
Q

most common autosomal dominant CV disease

A

hypertrophic obstructive cardiomyopathy (HCOM)

186
Q

most common cause of sudden cardiac death in young athletes

A

obstructive hypertrophic cardiomyopathy

187
Q

what causes LVOT obstruction in HCOM

A
  1. congenital hypertrophy of interventricular septum
  2. systolic anterior motion of anterior leaflet of mitral valve
188
Q

3 key determinants of flow through LVOT

A
  1. systolic LV volume
  2. force of LV contraction
  3. transmural pressure gradient
189
Q

what factors reduce CO in pts with HCOM?

A

things that narrow the LVOT:

  • decreased systolic volume (preload or inc. HR)
  • increased contractility
  • decreased aortic pressure
190
Q

conditions that distend LVOT and decrease obstruction

A
  • increased systolic volume (inc. preload or dec. HR)
  • decreased contractility
  • increased aortic pressure
191
Q

what is systolic anterior motion (SAM)?

A

systolic anterior motion of anterior leaflet of mitral valve

produces mechanical obstruction to flow through LVOT

192
Q

venturi effect in SAM

A

blood rapidly flows across LVOT

velocity increases through stricture

193
Q

how is hypertrophic obstructive cardiomyopathy diagnosed

194
Q

SAM can be a postop complication after which surgery

A

mitral valve repair (not replacement)

195
Q

what happens if some of LV stroke volume can’t pass into aorta

A
  • takes retrograde path actoss mitral valve
  • leads to mitral regurg
196
Q

sign of turbulent flow through LVOT obstruction or mitral regurg

A

systolic murmur

197
Q

what leads to diastolic dysfunction in HCOM

198
Q

why is it v important to promptly treat A-fib or junctional rhythms in pt with hypertrophic obstructive cardiomyopathy

A

preserving LA contraction is very important

199
Q

why is nitroglycerin not a good choice for a pt with hypertrophic obstructive cardiomyopathy

A

reduces preload - reduces systolic LV volume - narrows LVOT - worsens obstruction

200
Q

is esmolol good or bad for HCOM pt?

A

good - slower HR extends LV filling time, so esmolol increases systolic LV volume

also decreases contractility, which improves LVOT obstruction

201
Q

is phenylephrine a good or bad choice for HCOM pt

A

good - increases aortic pressure, which increases transmural pressure and opens LVOT

202
Q

3 surgical options to correct LVOTO

A
  1. septal myomectomy
  2. alcohol injection into septal perforator arteries
  3. mitral valve replacement
203
Q

how long should elective surgery be delayed after PCI angioplasty without stent

204
Q

how long should elective surgery be delayed in pt after PCI with bare metal stent?

A

30 days (3 months preferred)

205
Q

how long should elective surgery be delayed in pt after PCI with drug eluding metal stent in stable ischemic heart disease?

A

first generation DES = 12 months minimum
current generation DES = 6 months minimum

206
Q

how long should elective surgery be delayed in pt after PCI with drug-eluding metal stent in pt with acute coronary syndrome?

A

12 months minimum

207
Q

how long should elective surgery be delayed in pt after a CABG?

A

6 weeks (3 months preferred)

208
Q

what meds are involved in dual antiplatelet therapy (DAPT)

A
  • aspirin
  • thienopyridine (ADP receptor antagonist, usually clopidogrel or ticlopidine)
209
Q

when should a pt on DAPT stop taking aspirin before surgery

A

continue unless absolutely contraindicated

if contraindicated stop 3 days preop

210
Q

when should a pt on DAPT stop taking clopidogrel before surgery

A

7 days preop

211
Q

when should a pt on ticlodopine for DAPT stop taking preop?

A

14 days before surgery

212
Q

what can be given to reverse platelet inhibition in emergency surgery on a pt taking DAPT

213
Q

should UFH/Lovenox be used to “bridge” patients off antiplatelet therapy?

A

no - paradoxically increases platelet aggregation in the stent

214
Q

whats the best treatment for stent thrombosis

A

PCI

best outcome if blood flow restored < 90 min

215
Q

purpose of roller pump in CPB

A

compresses blood tubing, creates occlusion point as it mechanically propels blood forward

216
Q

CPB pump flow with afterload changes

A

remains constant d/t roller pump

217
Q

how can roller clamp cause tubing rupture

A

if arterial inflow line is clamped, pump continues pushing forward and can rupture inflow tubing

218
Q

complication with roller pump on CPB if venous reservoir runs dry

A

air embolism

219
Q

what type of CPB is less traumatic to blood cells

A

centrifugal pump

220
Q

which CPB tends to not entrain air

A

centrifugal pump - can’t produce excessive negative pressure, tends to not entrain air

221
Q

disadvantage of centrifugal CPB pump

A

lack of an occlusion point

if afterload is excessively high, blood backs up towards venous circulation and decreases circulating blood volume

222
Q

component of CPB where gas exchange occurs

A

oxygenator

223
Q

which CPB oxygenator is safer

A

membrane oxygenator (uses blood-membrane-gas interface)

224
Q

which CPB oxygenator carries risk of cerebral air embolism

A

bubble oxygenator (uses a blood-gas interface)

225
Q

what is the CPB circuit primed with

A
  • mannitol
  • albumin
  • heparin
  • bicarb
226
Q

when is awareness most common with CPB

A

during sternotomy

227
Q

ACT goal for CPB

A

> 400 seconds

228
Q

what should be used for anticoagulation for CPB if pt has heparin allergy

A
  • bivalirudin
  • hirudin
  • another factor 10 inhibitor
229
Q

SBP goal before aortic cannulation

A

< 100 mmHg (HTN can cause dissection)

230
Q

best way to reduce myocardial O2 consumption during CBP

A

cardioplegia (K+ containing solution that arrests heart in diastole)

231
Q

where is antegrade cardioplegia introduced

A

into aortic root
solution enters coronaries

232
Q

required for antegrade cardioplegia to work

A

competent aortic valve & clamped aorta

233
Q

where is retrograde cardioplegia introduced

A

through a cannula into coronary sinus

234
Q

alpha-stat ABG

A
  • doesn’t correct for pt’s temp
  • aims to keep constant pH across all temps
235
Q

which blood gas measurement in CPB is assoc. with better outcomes in adults

A

alpha-stat

236
Q

which blood gas measurement in CPB is assoc. with better outcomes in peds

237
Q

pH-stat ABG

A
  • corrects for pt’s temp
  • aims to keep constant pH across all temperatures
238
Q

dose of protamine after off bypass

A

~1 mg for each 100 units heparin given

239
Q

radial artery pressure immediately after CPB

A

may be artificially low

240
Q

common post-bypass AEs

A
  • myocardial depression
  • heart block

(may need vasoactives and pacing)

241
Q

why is MAP not a good surrogate for organ perfusion during CPB

A

blood flow is non-pulsatile

242
Q

what is the difference in full bypass and partial bypass

A
  • full: all venous return drained in venous reservoir
  • partial: heart receives and pumps a fraction of venous return
243
Q

why is an LV vent used during CABG surgery?

A
  • removes blood from LV
  • this blood usually comes from Thesbian veins and bronchial circulation (anatomic shunt)
244
Q

how does protamine reverse heparin

A

neutralization reaction (forms acid/base complex)

245
Q

how should post-bypass protamine dose be calculated

A

account for amount of heparin predicted to remain in circulation after bypass

if based on initial heparin dose, may contribute to protamine overdose

246
Q

administration of protamine

A

over 10-15 min to reduce systemic vasodulation and pulmonary vasoconstriction

247
Q

indications for IABP

A
  • cardiogenic shock
  • MI
  • intractible angina
  • difficult CPB separation
248
Q

contraindications for IABP

A
  • aortic insufficiency
  • descending aortic disease (aneurysm)
  • severe PVD
  • sepsis
249
Q

where is IABP inserted

A

through femoral artery and advanced along descending aorta

250
Q

what is an IABP?

A

a counterpulsation device that improves myocardial o2 supply while reducing O2 demand

251
Q

how does IABP function in diastole?

A

pump inflation augments coronary perfusion

252
Q

how does IABP function in systole?

A

pump deflation reduces afterload and improves CO

253
Q

what do IABP inflation and deflation correlate with on monitoring waveforms?

A
  • inflation correlates with dicrotic notch and T wave
  • deflation correlates with R wave
254
Q

where should the IABP distal tip be and why

A
  • 2cm distal to left subclavian
  • more proximal can occlude left common carotid and brachiocephalic arteries
255
Q

how is proper IABP position confirmed

A
  • CXR
  • TEE
  • fluoro
256
Q

effects of priming the CPB circuit with anything other than blood

A

hemodilution:

  • decreased Hct
  • decreased plasma concentration of drugs and plasma proteins
  • decreased O2 carrying capacity
  • decreased blood viscosity
  • increased microvascular flow
257
Q

what can happen if air enters the venous line of CPB circuit

258
Q

MOA of potassium based cardioplegia

A
  • arrests heart in diastole
  • K+ increases RMP, which locks voltage-gated Na+ channels in closed-inactive state
259
Q

contraindication to antegrade cardioplegia

A

incompetent aortic valve

260
Q

when does the IABP inflate and deflate

A
  • inflates during diastole (increases coronary perfusion pressure/O2 supply)
  • deflates during systole (reduces afterload, decreases O2 demand)
261
Q

when is aortic pressure higher with IABP

A

higher in diastole than during unassisted systole

262
Q

most common IABP complications

A
  • vascular injury
  • infection at insertion site
  • thrombocytopenia
263
Q

purpose of an LVAD

A

mechanical device that unloads failing heart by pumping blood from LV to aorta

264
Q

where is the inflow cannula of LVAD inserted

A

in apex of LV

265
Q

conditions that require surgical correction before LVAD can be used

A
  • PFO
  • AI
  • tricuspid regurg
266
Q

purpose of LVAD

A
  • bridge to recovery
  • bridge to transplant
  • destination therapy
267
Q

why might SpO2 and NIBP be ineffective with LVAD

A

flow may be non-pulsatile depending on native function

consider AL and cerebral ox

268
Q

most common cause of death with LVAD

269
Q

common long-term complication with LVAD

A

GI bleeding (requires anticoagulation)

270
Q

what 3 things are CO dependent on in a pt with LVAD

A
  1. LV preload
  2. pump speed
  3. pressure gradient across pump (afterload)
271
Q

what is LV suck down with LVAD & how is it treated

A
  • low preload + relatively high pump speed produces suction
  • part of LV sucked into LV cavity, occludes inflow cannula
  • treated with IVF to increase preload, decrease pump speed
272
Q

consequences of suction with LVAD

A
  • hypotension
  • ventricular dysrhythmias
  • L shift of interventricular septum
  • decreased RV contractility
  • decreased compliance
273
Q

consequences of mechanical shear stress with LVAD

A
  • coagulopathy
  • platelet dysfunction
274
Q

Crawford aneurysm classification: type 1

A

involves all or most of descending thoracic aorta and upper abdominal aorta

275
Q

Crawford aneurysm classification: type 2

A

involves all or most of descending thoracic aorta, most of abdominal aorta

276
Q

Crawford aneurysm classification: type 3

A

involves lower descending thoracic aorta and most of abdominal aorta

277
Q

Crawford aneurysm classification: type 4

A

involves most of abdominal aorta only

278
Q

DeBakey aneurysm classification: type 1

A

tear in ascending aorta + dissection along entire aorta

279
Q

DeBakey aneurysm classification: type 2

A

tear + dissection only in ascending aorta

280
Q

DeBakey aneurysm classification: type 3a

A

tear in proximal descending aorta with dissection limited to thoracic aorta

281
Q

DeBakey aneurysm classification: type 3b

A

tear in proximal descending aorta with dissection along thoracic & abdominal aorta

282
Q

Crawford vs. Debakey aneurysm classification

A
  • Crawford: classifies aortic aneurysms into 4 types based on involvement in thoracic/abdominal aorta
  • DeBakey: classified according to location of dissection
283
Q

Stanford Aneurysm classification

A
  • type A: involves ascending aorta
  • type B: doesn’t involve ascending aorta
284
Q

in which types of dissection should you be worried about aortic insufficiency

A

DeBakey 1/2 or Stanford A (involve ascending aorta)

285
Q

which type of aortic aneurysms are most difficult to repair

A

crawford types 2 & 3

286
Q

which type of aortic aneurysm has the most significant perioperative risks & why

A

crawford type 2

  • paraplegia
  • renal failure

mandatory period for stopping blood flow to renal arteries and some radicular arteries that perfuse anterior spinal cord

287
Q

aortic aneurysms that are surgical emergencies

A

acute dissection of ascending aorta

(Debakey 1/2, Stanford A)

288
Q

type of aortic aneurysm that is often managed medically

A

dissection of descending aorta (meds for HR, BP, pain)

289
Q

incidence of AAA in pts > 50

290
Q

independent risk factors for AAA

A
  • cigarette smoking
  • male
  • advanced age
291
Q

how is AAA most commonly detected

A
  • pulsatile abdominal mass
  • generally asymptomatic
292
Q

primary mechanism of AAA

A

destruction of elastin and collagen that form matrix of vessel wall

293
Q

pathologic changes that cause abdominal aorta to weaken/dilate

A
  • atherosclerosis
  • inflammation
  • endothelial dysfunction
  • platelet activation
294
Q

what AAA measurements correlates with risk of rupture

A

diameter (increased radius = increased transmural pressure = increased wall stress)

295
Q

when is surgical correction of AAA recommended

A

when > 5.5cm or if it grows > 0.6-0.8 cm/year

296
Q

risk of AAA rupture when > 8 cm diameter

297
Q

classic triad of symptoms in AAA rupture

A
  • hypotension
  • back pain
  • pulsatile abdominal mass

**only in ~50% of patients**

298
Q

where do most AAA rupture

A

left retroperitoneum

299
Q

most common cause of AAA postop death

300
Q

how does aortic cross clamp contribute to risk of anterior spinal artery syndrome?

A
  • clamp above artery of Adamkiewicz may cause ischemia to lower anterior spinal cord
  • can result in anterior spinal artery syndrome (Beck’s syndrome)
301
Q

how does anterior spinal artery syndrome present

A
  • flaccid paralysis of lower extremities
  • bowel and bladder dysfunction
  • loss of temp and pain sensation
  • preserved touch and proprioception
302
Q

why dont most AAA rupture pts immediately exsanguinate

A

most aneurysms rupture in left retroperitoneum, allowing for tamponade and clot formation

303
Q

effects of aortic cross clamp:

  • venous return
  • CO
  • MAP
  • SVR
  • PAOP
A
  • VR increased (blood shift proximal to clamp)
  • CO decreases or doesn’t change (depends on reserve)
  • MAP increased (inc. preload & SVR)
  • SVR increases (mechanical effect, catecholamine release, RAAS activation)
  • PAOP increased/unchanged (inc venous return)
304
Q

physiologic effects of removing aortic cross clamp

  • LV wall stress
  • MVO2
  • coronary blood Q
  • renal blood Q
  • total body VO2
  • SvO2
A
  • LV wall stress increased (inc preload/afterload)
  • MVO2 increased
  • coronary blood Q increased
  • renal blood Q decreased
  • total body VO2 decreased (aerobic metabolism distal to clamp)
  • SvO2 increased (decreased total body VO2)
305
Q

infrarenal clamp time associated with increased risk ARF

306
Q

effects of aortic cross clamp removal:

  • venous return
  • CO
  • MAP
  • SVR
  • PAOP
A
  • VR decreased (central hypovolemia, capillary leak)
  • CO decreased (dec. preload & contractility)
  • MAP decreased (dec. preload & SVR)
  • SVR decreased (anaerobic metabolites, vasodilation)
  • PAOP increased (increased PVR)
307
Q

effects of aortic cross clamp release:

  • LV wall stress
  • MVo2
  • coronary blood Q
  • renal blood Q
  • total body VO2
  • SvO2
A
  • LV wall stress decreased
  • MVo2 decreased (increased if PAOP increased)
  • coronary blood Q decreased
  • renal blood Q decreased/unchanged (depends on MAP)
  • total body VO2 increased (cells distal to clamp receive O2)
  • SvO2 decreased (increased total body VO2)
308
Q

advantages of EVAR over open repair

A
  • decreased operative time
  • decreased transfusion rate
  • shorter LOS
  • decreased morbidity
  • no need for aortic cross clamp
  • avoid resp risks assoc. with midline abdominal incision
309
Q

complications of EVAR

A
  • baroreceptor reflex activation
  • massive hemorrhage
  • aortic rupture
  • cerebral embolism
  • endoleak
310
Q

what is an endoleak

A

EVAR complication - original graft fails to prevent blood from entering aortic sac

311
Q

endoleak treatment

A

sometimes resolve spontaneously (especially early), may require placement of 2nd graft or open repair

312
Q

amaurosis fugax

A

blindness in one eye

sign of impending stroke. emobli travel from internal carotid to opthalmic artery & impairs perfusion of optic nerve

causes retinal dysfunction

313
Q

what perfuses the posterior 1/3 spinal cord

A

posterior spinal arteries

314
Q

perfuses anterior 2/3 spinal cord

A

anterior spinal artery (1)

315
Q

where does artery of Adamkiewicz originate

A

on left side between T11-T12

  • 75% of population: originates between T8-T12
  • another 10%: originates L1-L2
316
Q

what are watershed areas

A

some regions of spinal cord only have a single blood supply

317
Q

why does a patient with Beck syndrome present with flaccid paralysis of lower extremities

A

the corticospinal tract is perfused by anterior blood supply

318
Q

why does pt with Beck’s syndrome have bowel & bladder dysfunction

A

ANS fibers perfused by anterior blood supply

319
Q

why does pt with beck syndrome lose pain and temp sensation

A

spinothalamic tract perfused by anterior blood supply

320
Q

why does a pt with beck syndrome have preserved touch & proprioception

A

dorsal column perfused by posterior blood supply

321
Q

thoracic cross clamp time that significantly increases risk of cord ischemia

322
Q

method to reduce spinal cord O2 consumption

A

moderate hypothermia (30-32 deg C)

323
Q

what does spinal cord perfusion pressure depend on

A

pressure gradient between anterior spinal artery and CSF

CSF will drain with decreased pressure and increased gradient

324
Q

BP goals during cross clamp to prevent beck’s syndrome

A

maintain proximal HTN (MAP ~ 100)

325
Q

monitoring that monitors posterior cord

326
Q

spinal cord protecting drugs

A
  • corticoteroids
  • CCBs
  • mannitol
327
Q

incidence of amaurosis fugax

A

in 25% of pts with high grade stenosis

328
Q

regional techniques for CEA

A
  • local infiltration
  • superficial plexus block (C2-C4)
  • deep cervical plexus block (C2-C4)
329
Q

risk of regional anesthesia in CEA pt

A

risk of ipsilateral phrenic nerve block - caution with severe COPD

330
Q

cerebral perfusion pressure =

331
Q

what does cerebral perfusion depend on during carotid artery clamp (CEA)

A

collateral flow from circle of willis (contralateral carotid and vertebral vessels)

332
Q

EEG findings that indicate risk of cerebral hypoperfusion

A
  • loss of amplitude
  • decreased beta wave activity
  • slow wave activity
333
Q

things that increase frequency in EEG

A
  • mild hypercarbia
  • early hypoxemia
  • seizure
  • ketamine
  • N2O
  • light anesthesia
334
Q

things that decrease EEG frequency

A
  • extreme hypercarbia
  • hypoxia
  • cerebral ischemia
  • hypothermia
  • anesthetic OD
  • opioids
335
Q

what is cerebral oximetry

what indicates cerebral perfusion is at risk

A

uses NIRS to monitor cerebral O2 sat (rSO2) in frontal lobe

perfusion at risk when reduced 25%+ from baseline

336
Q

use of transcranial doppler in CEA

A

assess continuous blood flow velocity in middle cerebral artery (where most emboli lodge)

may indicate when shunt should be placed

337
Q

anesthesia considerations for SSEP

A
  • requires light plane of anesthesia
  • monitors sensory pathways only
  • volatiles decrease amplitude and increase latency (mirror ischemia)
338
Q

where is carotid stump pressure measured

A

distal to clamp

339
Q

carotid stump pressure that indicates risk of ipsilateral cerebral hypoperfusion

A

stump pressure < 50m mmHg

340
Q

risk assoc. with carotid shunt placement

A

increased risk embolic stroke

341
Q

BP goal during carotid clamping (CEA)

A

keep BP normal/slightly elevated - brain perfusion is pressure dependent d/t loss of autoregulation

342
Q

what reflex can be activated during CEA or following carotid balloon inflation

A

baroreceptor reflex

343
Q

ETCO2 goal in CEA

A

maintain normocapia or mild hypocapnia

cerbral vessels distal to stenosis may be maximally dilated - hypercarbia dilates cerebral vessels and shunts blood from hypoperfused tissue

344
Q

lab value that increases risk stroke or death in CEA

A

blood sugar > 200 mg/dL DOS

345
Q

5 complications assoc. with CEA

A
  • hematoma
  • RLB injury
  • hemodynamic instability (altered baroreceptor sensitivity)
  • stroke (usually embolic)
  • carotid denervation
346
Q

when is carotid denervation a problem

A

hx bilateral CEA

reduced ventilatory response to hypoxia

347
Q

what is carotid artery angioplasty stenting (CAS)

A

uses percutaneous transvacuolar access to pass stent to carotid

348
Q

ACT goal for CAS

349
Q

most common complication of CAS & how is it treated

A

thromboembolic stroke

treat w recombinant tPA

350
Q

what is subclavian steal syndrome

A

occlusion of subclavian or innominate artery proximal to origin of ipsilateral vertebral artery (usually on left side) causes vertebral blood flow to reverse flow toward ipsilateral subclavian artery

351
Q

BP in subclavian steal

A

much lower in ipsilateral arm

352
Q

treatment of choice for subclavian steal syndrome

A

subclavian endarterectomy

353
Q

s/s subclavian steal

A
  • syncope
  • vertigo
  • ataxia
  • hemiplegia
  • arm ischemia
  • weak pulse in ipsilateral arm
354
Q

why does the RV subendocardium remain well perfused throughout cardiac cycle

A

vs. LV subendocardium - thinner wall

doesn’t generate enough pressure to occlude its own circulation

355
Q

when is LV subendocardium primarily perfused

A

during diastole

356
Q

which region of myocardium receives the least amount of perfusion during systole & why

A

LV subendocardium
tissue compresses its own blood supply as aortic pressure increases

357
Q

why is LV subendocardium predisposed to ischemia

A

high compressive pressures in LV + decreased coronary flow during systole increases coronary vascular resistance

358
Q

2 factors assoc. with highest O2 consumption

A

pressure work
HR

359
Q

MOA of aldosterone antagonists & example

A
  • inhibit K excretion & Na reabsorption by principal cells of collecting ducts
  • block aldosterone at mineralocorticoid receptors

spironalactone

APEX (54 decks)

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