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*1ABA Applied Exam1 > Cardiac > Flashcards

Cardiac Flashcards

1
Q

What determines the “dominance” of coronary blood flow?

A

The blood supply to the AV node:

RCA in 85-90% of people

LCx in 10-15% of people

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2
Q

When in PCI contraindicated?

A

left main disease where distal vessels are not protected by collaterals

diffuse/multivessel disease

no discrete lesion

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3
Q

What is the normal LVEDP (or PA occlusion pressure)?

A

6-15 mmHg

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4
Q

How is LV wall motion characterized by echocardiography?

A

normal: thickening > 30%
hypokinetic: thickening 10-30%
akinetic: thickening < 10%
dyskinetic: outward motion during systole

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5
Q

What are the determinants of myocardial oxygen consumption?

A

wall tension

contractility

heart rate

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6
Q

What is the equation of wall tension?

A

The Law of LaPlace:

T = P x R /2Th

T-tension, P-pressure, R-radius, Th-thickness

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7
Q

What are the determinants of myocardial oxygen supply?

A

coronary perfusion pressure (aortic diastolic pressure - LVEDP)

coronary vascular tone

coronary patency

arterial oxygen content

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8
Q

Is digoxin continue through heart surgery?

A

No, it is stopped 2 days (one half life) in advance to prevent toxicity after bypass

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9
Q

Do ß-blockers have more effect on heart rate or contractility?

A

reductions in HR occur with lower serum levels that depression of contractility

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10
Q

What is a normal Allen’s test?

A

Palmar flush occurs in < 7 seconds, indicating adequate collateral ulnar flow

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11
Q

Where is core temperature measured? Peripheral temperature?

A

Core temperature: esophageal, nasopharyngeal, bladder, tympanic

Peripheral: axiallary, rectal

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12
Q

How can you tell when the PA catheter advances from the RV into the PA?

A

1) Diastolic pressure is higher in the PA than in the RV

Normal RV: 20-25/0-5

Normal PA: 20-25/5-10

2) PA pressure tracing has a dichrotic notch from pulmonic valve closure

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13
Q

What is the normal PA occlusion pressure?

A

4-12 mmHg

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14
Q

What are the complications specific to PA catheter insertion?

A

arrhythmias

PA or RA perforation

tricuspid injury

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15
Q

What is the earliest and most sensitive sign of myocardial ischemia?

A

RWMA on echocardiography

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16
Q

What is the sensitivity, specificity, and predictive values of PAOP for myocardial ischemia?

A

Bad (40-60%)

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17
Q

What combination of ECG leads has the best sensitivity for detecting myocardial ischemia?

A

II and V5: 80%

V4 and V5: 90%

II, V4, and V5: 96%

*V5 has the best sensitivity of any single lead*

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18
Q

Is IV or inhaled anesthesia preferable for cardiac cases?

A

There is no consensus.

There is some data that inhaled anesthetics protect myocardium against ischemia-reperfusion injury.

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19
Q

Should isoflurane be used for patients with CAD?

A

There is no consensus.

Some data suggests coronary vasodilatation with isoflurance that decreases blood flow and causes coronary steal

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20
Q

Why should nitrous oxide be avoided after cardiopulmonary bypass?

A

It could expand remaining air bubbles in the coronary and cerebral circulation.

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21
Q

Why is pancuronium nice for cardiac surgery?

A

long-lasting

vagolytic effects usually counteracted by the presence of ß-blockers

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22
Q

How do you treat intra-opertive ST depressions?

A

increase oxygen supply: correct hypotension, hypoxemia and anemia

decrease oxygen demand: correct hypertension and tachycardia

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23
Q

Should you give prophylactic nitroglycerin to patients undergoing CABG?

A

No, it does not prevent myocardial ischemia

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24
Q

Should PA occlusion pressure be monitored continuously?

A

No, the gradient between PAOP and PA diastolic pressure should be noted on insertion, then PA diastolic pressure can be followed

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25
Q

What are the strategies for blood conservation during cardiac surgery?

A

pre-operative autologous donation

pre-operative erythropoietin

intraoperative normovolemic hemodilution

TXA

cell saver

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26
Q

What are the considerations for intraoperative normovolemic hemodilution?

A

blood, platelets, and clotting factors are spared the stress of bypass, improving coagulation

not recommended if Hct < 33

not recommended with left main disease or severe aortic stenosis

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27
Q

What is the dose of heparin before bypass? ACT goal?

A

300 (200-400) units per kg

ACT goal > 400

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28
Q

Why does the LV need to be vented on bypass?

A

To prevent distention of the LV with blood from:

bronchial veins

pleural veins

Thebesian veins

aortic insufficiency

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29
Q

What kind of oxygenator is used on the CPB machine?

A

membrane oxygenator (more economical and efficient, less traumatic to blood)

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30
Q

What is the CBP machine primed with (500-1000mL)?

A

a balanced salt solution, albumin, and mannitol

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31
Q

What should MAP be during cardiopulmonary bypass?

A

50-70 in patients at low risk for cerebral embolization

80-100 in patients at high risk for cerebral embolization

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32
Q

If using cerebral oximetry to monitor cerebral blood flow during CPB, what is the goal?

A

70% of baseline or >40% saturation, whichever is higher

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33
Q

How is hypertension treated during CPB?

A

increasing the depth of anesthesia

**pump flow rate should NOT be reduced**

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34
Q

What is the normal pump flow rate on CPB

A

2-3 L/min/m2 (for both adults and children)

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35
Q

Why is muscle relaxant given during CPB?

A

prevent diaphragmatic movement

prevent shivering

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36
Q

How do you assess adequate perfusion during CPB?

A

urine output

no metabolic acidosis

PmvO2 40-45 mmHg

cerebral oximetry

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37
Q

What is the V/Q ratio of the CBP machine?

A

2L of gas for every 1L pump flow

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38
Q

Why should hypocapnea be avoided on CPB?

A

decreased cerebral blood flow

decreased O2 delivery (left shift in curve)

hypokalemia

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39
Q

What is the difference between alpha-stat and pH stat strategies?

A

alpha stat maintains a constant ratio of OH-/H+

pH stat maintains a constant pH

40
Q

When is alpha stat used? pH stat?

A

alpha stat for adult CPB

pH stat for pediatric deep hypothermic circulatory arrest

41
Q

What is the goal hematocrit during CPB?

A

18-20%

42
Q

What are cardioprotective strategies during CPB?

A

When crossclamp is off:

avoid tachycardia

prevent and treat V-fib

vent the left ventricle

maintain coronary perfusion pressure

When crossclamp is on:

cardioplegia

hypothermia

43
Q

When should retrograde cardioplegia be used?

A

severe obstructive coronary lesions (to avoid poor distribution of cardioplegia)

significant aortic insufficiency

44
Q

How long can the aorta be crossclamped?

A

60-120 minutes (the shorter the better)

45
Q

Why would the urine become pink on CPB?

A

massive hemolysis

46
Q

How warm should the patient be before coming off pump?

A

core temperature: 37oC

peripheral temperature: 35oC

47
Q

What energy is used for internal defibrillation?

A

5-10 J

48
Q

Why do blood glucose levels rise during CPB?

A

NPO starvation state

sympathetic activaiton

hypothermia reduces insulin production

cardioplegia contains dextrose

49
Q

Is is platelet dysfunction or decreased clotting factors that causes most non-surgical bleeding after CPB and heparin reversal?

A

platelet dysfunction

50
Q

What is the checklist for coming off CPB?

A

ABG normalized

patient warm

adequate ventilation

rate/rhythm/contractility treated

afterload treated

preload visualized on TEE

51
Q

What considerations go into starting an inotrope to come off CPB?

A

patient age

pre-op ventricular function

duration of cross clamp

success of surgical repair

**IABP should be considered if predicted EF < 25%**

52
Q

What is the dose of protamine?

A

1 mg per 100 units of the initial heparin bolus

53
Q

How does protamine reverse heparin?

A

Heparin is highly negatively charged.

Protamins is highly positively charged.

They form a stable, inactive salt.

54
Q

What is wrong with giving too much protamine?

A

It is an anticoagulant due to its inhibition of platelet aggregation and direct thrombin inhibition.

55
Q

What are the effects of protamine on cardiovascular function (i.e., why do we give it slowly)?

A

1) systemic hypotension due to histamine release (side effect)
2) anaphylactic or anaphylactoid reactions (decreased SVR and PVR, patient on NPH isulin at risk)
3) catastrophic pulmonary hypertension and bronchoconstriction (mediated by C5a anaphylotoxins and thromboxane, steroids and antihistamines ineffective)

56
Q

What is the principle of IABP?

A

increased myocardial oxygen supply during diastole

decrease myocardial oxygen consumption during systole

57
Q

Is PAOP a surrogate for LVEDV after CABG?

A

no, they are poorly correlated, likely due to changes in ventricular compliance

58
Q

Where is the optimal position of an IABP?

A

between take-off of the left subclavian artery and the take-off of the renal arteries

59
Q

What are the contraindications for IABP?

A

significant aortic insufficiency

aortic pathology (aneurysm, dissection, severe plaque)

sepsis

coagulopathy

60
Q

What factors decrease VAD output?

A

hypovolemia

increased afterload (SVR or PVR)

61
Q

How is ACLS different in a patient with a VAD?

A

external chest compressions are contraindicated as they may dislodge the catheters

62
Q

What is the primary concern in a patient undergoing LVAD placement?

A

RV failure (hypoxia, hypercarbia, and acidosis must be avoided)

63
Q

What equation describes a pressure gradient across a valve?

A

Gorlin’s equation

pressure gradient = {flow rate/(K x valve area)}2

64
Q

What symptoms are associated with aortis stenosis?

A

angina

syncope

congestive heart failure

65
Q

How should you think about pre-medication with valvular lesions?

A

AS: good, prevents tachycardia

AI: good, prevents increased SVR

MS: be careful, hypercapnea can worsen PVR and RV failure

MR: maybe, hypercapnea can worsen PVR, but decreased SVR can improve forward flow

66
Q

What are the hemodynamic goals for aortic stenosis?

A

HR: 60-70 and sinus (dependent on atrial kick)

preload: full (maximize LV filling)
afterload: maintain (coronary perfusion)
contractility: maintain

67
Q

What are the hemodynamic goals for AI?

A

HR: 80-90 (minimize time in diastole)

preload: maintain
afterload: reduce (SVR is driving force for regurgitant flow)
contractility: support (dilated LV ineffective)

68
Q

What are the hemodynamic goals for MS?

A

HR: 60-70 (need time to fill LV)

preload: full (maximize LV filling)
afterload: maintain
contractility: support (disuse atrophy of LV)

69
Q

What are the hemodynamic goals of MR?

A

HR: 80-90 (avoid overfilling of LV and annular dilatation)

preload: maintain
afterload: reduce (encourage forward flow)
contractility: support (dilated LV ineffective)

70
Q

What are the anesthetic consideration for valve replacement with AS?

A

avoid hypotension and hypoxia

maintain sinus rhythm (particularly during atrial cannulation)

hypertophied LV may be poorly protected by cardioplegia

LV still poorly compliant after valve replaced

71
Q

What are the anesthetic considerations for valve replacement with AI?

A

increased SVR must be combined with increased inotropy (e.g., ephedrine and epinehrine are better than phenylephrine)

retrograde cardioplegia is often necessary

inotropic support is often necessary

72
Q

What are the anesthetic considerations for valve replacement with MR?

A

decreased SVR promotes forward flow

may need inotropic support for chronically dilated LV after valve is fixed

73
Q

Should patient with bifascicular or trifascicular block get a PPM prior to anesthesia?

A

No, they rarely progress to CHB intraoperatively

74
Q

What is the three-letter code that describes pacemaker modes?

A

1st letter: the chamber(s) paced (A, V, or D)

2nd letter: the chamber(s) sensed (A, V, or D)

3rd letter: response when intrinsic activity is sensed (Triggered, Inhibited, or D)

75
Q

What are the three pacing modes of modern pacemakers?

A

asynchronous (e.g., VOO)

single chamber (e.g., AAI, or VVI)

dual chamber (e.g., DDD)

76
Q

What is the difference between DDD and DDI?

A

In DDD mode, AV sequencial pacing is maintained whether the atrial beat is sensed or paced; in DDI mode AV sequencial pacing only happens when the atrial beat is paced

77
Q

Why does intra-operative hyperventilation increase heart rate in a patient with a PPM?

A

“rate response” pacing increase heart rate in response to motion or changes in minute ventilation

78
Q

What is an AICD measuring? How does it respond?

A

R-R interval

If there is a run of short R-R intervals, it will choose anti-tachycardia pacing or shock dependin on the algorithm

79
Q

What does a magnet do to a PPM? To an AICD?

A

A magnet will put a PPM in a fixed-rate pacing mode.

A magnet will disable the ICD functions of an AICD but will not affect its pacing functions

80
Q

If a patient with an AICD goes into VT or VF intraoperatively, what do you do?

A

stop electrocautery

remove the magnet and wait ~12 sec to charge

if no response, proceed with external defibrillation

81
Q

Is ESWL contraindicated in patients with PPMs?

A

No

AICDs should have a magnet placed

82
Q

Is ECT contraindicated in patients with PPMs?

A

devices should be reprogrammed into an asynchronous mode and tachycardia detection should be disabled

83
Q

How does pacemaker-mediated tachycardia occur?

A

In DDD mode, a PVC is conducted retrograde up the AV node and sensed as an atrial beat, which triggers ventricular pacing.

**most PPMs can detect and terminate this process**

84
Q

What are the risks of asyncrhonous pacing?

A

R-on-T leading to VF

competing nonperfusing rhythms

85
Q

How does a dipyridamole stress test work?

A

it vasodilates normal coronary arteries causing “coronary steal” and revealing at-risk myocardium

86
Q

What is equalization of diastolic pressures classically a sign of?

A

cardiac tamponade: CVP = PADP = PAOP

**often not seen after cardiac surgery because compression is not homogeneous**

87
Q

What is pulsus paradoxus? Kussmaul’s sign?

A

drop in SBP with inspiration of > 10 mmHg

distention of neck veins on inspiration

88
Q

Does the normal heart experience ischemia during tamponade?

A

No, reduced coronary perfusion is offset by reduced oxygen consumption (less preload and afterload)

89
Q

What are the hemodynamic goals in a patient with tamponade?

A

Fast: stroke volume is limited so CO is dependent on HR

Full: to maximize filling with poor compliance

Tight: to maximize end-organ perfusion is setting of reduced CO

90
Q

Describe induction options for cardiac tamponade.

A

Patient prepped and draped and surgeon scrubbed and gloved prior to induction

awake w/ local: usually not possible

inhalational: often too slow

etomidate or ketamine w/ muscle relaxant: minimize PPV until tamponade relieved

91
Q

Why are patient considered “preload-dependent” after heart transplant?

A

Donor heart sinus node is denervated from the vagus nerve and only modulate HR in response to catecholamines

92
Q

Do you need to give glycopyrrolate or atropine with neostigmine in a patient who has had a heart transplant?

A

Yes, slow reinervation is possible and neostigmine can cause bradycaria

93
Q

What is cardiac allograft vasculopathy?

A

accelerated atherosclerosis in the transplanted heart

94
Q

What are the five RCRI predictors of cardiac risk?

A

History of:

ischemic heart disease

CHF

cerebrovascular disease

insulin-dependent diabetes

Cr > 2.0

95
Q

How long does dual anti-platelet therapy need to be continued after stent placement?

A

4-6 weeks after bare metal stent

6-12 month after DES

96
Q

Does clonidine premedication prevent adverse cardiac events?

A

No, nonfatal cardiac arrest and significatn hypotension were higher with clonidine in the POISE-2 trial

*1ABA Applied Exam1 (12 decks)

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