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Cardiothoracic Pharmacology > Midterm > Flashcards

Midterm Flashcards

1
Q

Aortic annulus is attached to pulmonic annulus by

A

Tendon of conus

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2
Q

Aortic annulus connected to AV valves by

A

Central fibrous body

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3
Q

Compare thickness to LV to RV

A

RV 4-5mm

LV 8-15mm

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4
Q

Location of coronary sinus

A

Between AV orifice and valve of IVC (between LA/LV on posterior surface of the heart

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5
Q

Compare upper 1/3 of septum to lower 2/3

A

Upper 1/3 smooth endocardium

Lower 2/3 is trabeculae

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6
Q

Provides flow to anterior 2/3 of IVS, R and L bundle branches, papillary muscles of MV, anterolateral-lateral and apical LV

A

LAD

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7
Q

Provides flow to LA and posterior-lateral LV

A

circ

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8
Q

Provides flow to SA/AV nodes, RA, RV, posterior 1/3 of IVS

A

RCA

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9
Q

Coronary perfusion pressure and its components

A

CPP = DBP - LVEDP

Neo to raise DBP

Nitro to lower LVEDP

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10
Q

Portion of myocardium most affected by extravascular compression and higher LVEDP

A

Subendocardium

Highest O2 extraction

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11
Q

Key responses to CAD in coronary circulation

A

Collateral flow

Remodeling

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12
Q

Determinants of myocardial O2 supply

A

HR

PCWP

DBP

O2 sat, Hct

CAD

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13
Q

Determinants of myocardial O2 demand

A

HR

PCWP

SBP

CO

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14
Q

2 determinants of myocardial oxygen balance that decrease supply and increase demand

A

HR

PCWP

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15
Q

Distribution of SNS responsible for increasing chronotropy and inotropy

A

Increased SNS (T1-T4)

Cardiac accelerator fibers

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16
Q

Effect of increased PNS activation on chronotropy

A

SNS competes with PNSin medulla which decreases chronotropy and inotropy

PNS only has modest effect on inotropy (30%)

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17
Q

Abnormal accessory pathways between the atria and the ventricles may bypass the AV node and cause

A

Re-entry dysrhythmias

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18
Q

__________ assure rapid distribution of depolarization

A

Purkinje network of fibers

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19
Q

Basic contractile unit of myocardial

A

Sarcomere

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20
Q

Ion permeability of cardiac muscle

A

Relatively permeable to K+

Impermeable to Na and Ca

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21
Q

Effect of increasing preload on PV loop

A

Shift to right

SV increased

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22
Q

Effect of increasing afterload on PV loop

A

Narrow and taller

Lower SV, higher pressure

Higher EDV

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23
Q

Effect of decreasing contractility on PV loop

A

Shift to right

SV maintained at cost of pulmonary congestion

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24
Q

3 ways body compensates for heart failure

A

Salt and water retention

Vasoconstriction

SNS stimulation

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25
Q

CV and respiratory effects of valsalva maneuver

A

Decreased HR

Decreased contractility

Vasodilation

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26
Q

CV and respiratory effects of baroreceptor reflex

A

Decreased HR

Decreased contractility

Vasodilation

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27
Q

CV and respiratory effects of oculocardiac reflex

A

Bradycardia

Asystole

Dysrhythmias

Hypotension

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28
Q

CV and respiratory effects of celiac reflex

A

Bradycardia

Hypotension

APNEA

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29
Q

CV and respiratory effects of bainbridge refles

A

Increased HR

Decreased BP

Decreased SVR

Diuresis

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30
Q

CV and respiratory effects of Cushing reflex

A

SNS stimulation = HTN

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31
Q

CV and respiratory effects of chemoreceptor reflex

A

Increased respiratory drive

Increased BP

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32
Q

Determinants of BP

A

BP = CO X SVR

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33
Q

Determinants of CO

A

CO = HR X SV

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34
Q

SV dependent on

A

Preload

Contractility

Afterload

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35
Q

HR determined by (3)

A

(+) or (-) chronotropic effects from SNS, PNS, SA node

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36
Q

Determinants of SVR

A

SVR = Tone X Viscocity

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37
Q

Tone dependent on

A

Radius

Pressure gradient

Vessel length

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38
Q

Viscosity dependent on

A

COP and Hg

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39
Q

Hemodynamic effects of Alpha 1 receptors

A

Vasoconstricts

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40
Q

Hemodynamic effects of Alpha 2 receptors

A

Blocks output (vasodilation)

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41
Q

Hemodynamic effects of Beta 1 receptors

A

Increased HR and contractility

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42
Q

Hemodynamic effects of Beta 2 receptors

A

Vasodilates

Bronchodilation

Increased gluconeogenesis

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43
Q

Hemodynamic effects of dopamine receptors

A

Vary depending on dose

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44
Q

Hemodynamic effects of muscarinic receptors

A

Decrease HR

Activates salivary and sweat glands

Decrease vascular tone (much lesser degree)

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45
Q

How is NE removed from nerve ending

A

Diffusion out of cleft into circulation

Metabolized by COMT in cleft

Reuptake into neuron, broken down by MAO

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46
Q

Receptor and hemodynamic effect of dexmedetomidine

A

Alpha 2 agonist

Decrease BP and HR

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47
Q

Receptor and hemodynamic effect of carvedilol

A

Mixed alpha/beta antagonist

Decrease HR and BP

48
Q

Receptor and hemodynamic effect of NE

A

Alpha 1 and 2 agonist

Beta 1 agonist

Increase HR, contractility, PVR
Vasoconstriction

49
Q

Receptor and hemodynamic effect of epi

A

All Alpha and Beta agonist

Increase HR, contractility

Vasoconstriction

Gluconeogenesis

Bronchodilation

50
Q

Receptor and hemodynamic effect of labetalol

A

Mixed Alpha 1, Beta1, Beta 2 antagonist

Ratio 6:1 alpha:beta

Vasodilation

Bradycardia

Bronchoconstriction

51
Q

Receptor and hemodynamic effect of esmolol

A

Beta 1 antagonist

Bradycardia

52
Q

4 mechanisms of adrenergic receptor activation

A

Direct binding

Promotion of NE release

Blockade of NE reuptake

Inhibition of NE inactivation

53
Q

Catecholamines adrenergic agonists

A

Epi

NE

Isoproterenol

Dopamine

Dobutamine

54
Q

Noncatecholamine adrenergic agonists

A

Ephedrine

Phenylephrine

Terbutaline

55
Q

CV effects of beta 1 receptor activation

A

Increased HR, contractility, automaticity, conduction, renin release

56
Q

cardiopulmonary and vascular effects of PDE-3 inhibitors

A

Inhibition of enzyme prevents cAMP breakdown and increasing intracellular concentration

Increased inotropy, chronotropy, dromotropic

57
Q

Dopamine 1-5 mcg/kg/min

A

Induces natriuresis

58
Q

Dopamine 5-10 mcg/kg/min

A

Beta 1 activation

Increased contractility and HR

59
Q

Dopamine >10mcg/kg/min

A

Alpha 1

60
Q

Increased density of receptors

Seen with chronic decrease in receptor stimulation

A

Up regulation

61
Q

Decreased density of receptors

Caused by chronic increase in receptor stimulation

A

Down regulation

62
Q

Mechanisms responsible for BP effects seen with propofol

A

Decreased SNS outflow

Direct vasodilation

63
Q

Mechanisms responsible for BP effects seen with thiopental

A

Decrease in BP due to venous pooling

Decreased contractility due to decrease Ca availability

If absent or impaired baroreflex CO and BP fall dramatically due to uncompensated pooling and myocardial depression

64
Q

Mechanisms responsible for BP effects seen with midazolam

A

Profound decrease in SVR when used with opioid

Less profound with diazepam

65
Q

Mechanisms responsible for BP effects seen with etomidate

A

10-15% decrease in SVR will increase BP 19%

66
Q

Mechanisms responsible for BP effects seen with ketamine

A

Increased PVR and SVR

67
Q

3 benefits of using N20 in addition to other inhaled anesthetics

A

Hasten onset

Ultrashort duration

Decrease dose of other inhaled agent

68
Q

Cardiac anesthesia dose of propofol

A

Hypnotic

0.2-1.5mg/kg

69
Q

Cardiac anesthesia dose of thiopental

A

Hypnotic

0.5-4mg/kg

70
Q

Cardiac anesthesia dose of etomidate

A

Hypnotic

0.1-0.3mg/kg

71
Q

Cardiac anesthesia dose of fentanyl

A

Opioid

3-25mcg/kg

72
Q

Cardiac anesthesia dose of Sufentanil

A

Opioid

0.5-2mcg/kg

73
Q

Cardiac anesthesia dose of Remifentanil

A

Opioid

0.1-0.75 mcg/kg/min

74
Q

Cardiac anesthesia dose of cisatracurium , Vecuronium, pancuronium

A

70-100mcg/kg

75
Q

Cardiac anesthesia dose of succinylcholine

A

1-2 mg/kg

76
Q

Primary mechanism thought to be responsible for CV effects of volatile anesthetics

A

Reduction in calcium influx through sarcolemma dm depression of Ca release from SR

77
Q

Relationship between dose of volatiles on BP, SVR, HR, and CI

A

All decrease BP in dose dependent fashion

Due to decrease in SVR

CV decrease due to vasodilation and preload reduction

HR increase and compensatory so CI maintained

78
Q

Volatile most associated with increased HR

A

Desflurane

Sevo can at > 1 MAC

79
Q

Effects of modern volatile agents on conduction, contractility, dysrhythmia potential, baroreflexes, and ischemic heart

A

Depress contractility and BP

Prolong AV conduction and QT interval

Predispose to catecholamine induced dysrhythmia

Attenuate baroreflexes in dose dependent fashion

80
Q

Effect of volatile on coronary blood flow

A

Decreased coronary vascular resistance but coronary blood flow also decreased due to effects on DBP

81
Q

Volatile considered to be agent of choice for pt with cerebrovascular disease undergoing cardiac surgery

A

Isoflurane

82
Q

Non anesthetic drugs considered to have a synergistic relationship with volatiles on hemodynamics

A

Synergistic with ACE

Less with beta blockers

Limitations interaction with CBD

83
Q

How does N20 interact with volatiles to impact hemodynamics

A

Decreased CO and SV

Also decreased MAC requirements

84
Q

How does fentanyl interact with volatiles to impact hemodynamics

A

Decreases MAC, SVR, HR

85
Q

How does propofol interact with volatiles to impact hemodynamics

A

Dose related circulatory depression

Decreased CO and BP

86
Q

How does dexmedetomidine interact with volatiles to impact hemodynamics

A

Modestly affects circulatory effects

Decreased HR and SVR

87
Q

Circulatory effects of N20 and how affected by other anesthetic agents

A

Activates SNS = increased SVR

Increased CVP and arterial pressure

SNS response intact w/ other volatiles

When given with opioids augments cardiac depression

88
Q

Effect of moderate to high dose opioids on hemodynamics

A

More disinfectant bradycardia and vasodilation

89
Q

Possible mechanisms for hemodynamic effect of opioids

A

Influence of SNS outflow from SNS

Bradycardia due to direct stimulant effect on central vagal nuclei

90
Q

Opioid considered to have most favorable effect on HR and BP for intubation and intraop BP control

A

Sufentanil

91
Q

Effects of fentanyl sufentanil on epi and NE levels

A

NE level lower with sufentanil

Lower epi intraop with Demerol

92
Q

Effect of CPB on drug absorption

A

Reduced oral or IM absorption

93
Q

Effect of CPB on drug distribution

A

Decreased volume of distribution

Decreased pulmonary drug distribution- increased systemic drug levels

94
Q

Effects of CPB on drug elimination

A

Decreased drug clearance

Decreased renal function

95
Q

3 drug classes commonly used as anti-ischemic therapy in pt with CAD

A

Nitrates

Beta blockers

Calcium channel blockers

96
Q

MOA of NTG causing vasodilation

A

Converted to nitric oxide in smooth muscle

Vasodilation

Enhances myocardial oxygen delivery and reduces demand

97
Q

Start to see decrease in SVR with NTG at what dose

A

> 50 mcg/min

98
Q

4 beneficial effects of NTG in pt with CAD

A

Decreased PCWP/LVEDP

Decreased wall tension

Decreased myocardial O2 demand

Decreased ischemia

99
Q

Dose dependent effects of NTG on venous and arterial blood vessels

A

Larger doses = arterial vasodilation

100
Q

How NTG better suited for pulmonary HTN than other more potent arterial vasodilators

A

Vasodilation of pulmonary arteries and veins more than systemic

Decreased RAP

Decreased PCWP

Decreased PAP

101
Q

Unique effects of NTG on coronary artery flow

A

Potent coronary vasodilators

Smaller coronaries dilate more

Reverses or prevents vasospasm

102
Q

How use of NTG improves CPP

A

CBP improves as PCWP decreases

Reduces subendocardial pressure

Improves collateral flow

103
Q

In pt with CHF NTG effect on cardiac performance

A

Decreased mitral regurg and afterload

Increased CO

104
Q

Effect of NTG on cardiac performance in pt with normal LV

A

Inadequate preload = decreased CO

105
Q

Effect of NTG on cardiac performance in pt with ischemic heart disease

A

Decreased wall tension, O2 demand, ischemia

Improved cardiac function

106
Q

Benefits of beta blockade in pt with ischemic heart disease

A
  • decreased cardiac O2 consumption
  • improved coronary flow and collateral flow
  • prolonged diastole
  • increased flow to ischemic area
  • reduced mortality after MI
  • improved oxygen dissociation
107
Q

Dose of esmolol

A

5-20 mg

Half life 9.5 minutes

108
Q

Dose of metoprolol

A

Bolus 1-5 mg

Half-life 3-6 minutes

109
Q

Dose of labetalol

A

Bolus 2.5-5mg

Half-life 2-6 hours

110
Q

3 mechanisms by which calcium blocking drugs reduce myocardial oxygen demand

A

Depress contractility

Decreased HR

Decreased afterload (SBP)

111
Q

2 drugs with primary action on heart CBD

A

Diltiazem

Verapamil

112
Q

Primary action on arterioles (2) CBD

A

Nicardipine

Nifedipine

113
Q

First line anti-hypertensive drug for heart failure pt with HTN

A

ACE inhibitor

Angiotensin converting enzyme inhibitors

114
Q

4 advantages of ACEI over conventional anti-hypertensives

A

Free of CNS effects

Free of myocardial depressant effects

Metabolic changes not seen

Rebound HTN not seen

115
Q

2 hemodynamic concerns associated with ACEI and ARBs during general anesthesia

A

Renin response impaired

Diuretics worsen hypotension

Normal response to surgical stimulation may be attenuated

May cause LVH to regress (impair remodeling)

Hypotension upon induction

116
Q

Dose of hydralazine

A

2.5-10 mg IV or IM

Slow onset - 10 minutes

Offset 4 hours

117
Q

Why thiosulfate used with nitroprusside

A

Reacts with sulfur do now

Effectively detoxifies cyanide

Cardiothoracic Pharmacology (3 decks)

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