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Cardiothoracic Pharmacology > Test 1 > Flashcards

Test 1 Flashcards

1
Q

Aortic annulus is attracted to pulmonic annulus by

A

Tendon of conus

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2
Q

Aortic annulus also connected to AV valves by

A

Ventral fibrous body

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3
Q

What constitutes the fibrous cardiac skeleton

A

Four valve annuli

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4
Q

4 components of skeletal base of heart

A

Valve annuli

Aortic and pulmonary roots

Central fibrous body

Fibrous trigones

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5
Q

Location of coronary sinus

A

Between AV orifice and valve of IVC

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6
Q

Compare thickness of RV and LV

A

RV 4-5mm

LV 8-15mm

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7
Q

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

A

Upper 1/3 is smooth endocardium

Lower 2/3 is trabeculae

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8
Q

Myocardium is ____ layers. Middle is _____

A

3

Middle is muscular which runs in spiral fashion

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9
Q

Normal size of aortic, tricuspid, and mitral valve

A

Aortic. 2.5-3.5 cm2

Mitral. 4-6 cm2

Tricuspid. 7 cm2

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10
Q

Coronary artery which typically provides flow to bundle branches

A

LAD

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11
Q

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

A

LAD

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12
Q

Provides flor to LA and posterior-lateral LV

A

Circumflex

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13
Q

Provides flow to SA/AV nodes

A

RCA

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14
Q

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

A

RCA

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15
Q

Dominance is determined by

A

Whether the circumflex of RCA provides flow to PDA

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16
Q

Effect of CAD of coronary vascular smooth muscle tone and anitcoagluation

A

Thickening of endothelium resulting in clot- vasospasm

Adversely effects autoregulatory fx of vascular endothelial cells expressing anticoagulant substances and myocardial blood flow

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17
Q

Define coronary perfusion pressure and its component/formula

A

CPP = DBP - LVEDP

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18
Q

Compare LV and RV perfusion in systole and diastole

A

RV fills throughout cycle

LV fills during diastole

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19
Q

Area of myocardium most affected by extravascular compression and higher LVEDP

A

Subendocardium

Lower heart rate minimizes compression

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20
Q

Key responses to CAD in coronary circulation

A

Collateral flow and remodeling

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21
Q

4 determinants of coronary blood flow

A

Perfusion pressure

Myocardial extravascular compression

Myocardial Metabolism

Neurohumoral control

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22
Q

Determinants of myocardial oxygen supply

A 
Heart rate **
PCWP/LVEDP**
DBP
O2 sat
Hct
CAD
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23
Q

Components of myocardial oxygen demand

A

Heart rate **
PCWP/LVEDP **
SBP
CO

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24
Q

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

A

Increased HR and PCWP/LVEDP

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25
Q

Increased SNS from what segments increase chronotropy and inotrope

A

T1-T4

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26
Q

Effect of increased PNS activation on chronotropy

A

SNS competes with PNS in medulla

PNS has only modest effect on inotropy 30%

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27
Q

Role of accessory pathways in dysrhythmia

A

Abnormal accessory pathways bw atria and ventricles may bypass the AV node and cause re-entrant dysrhythmias

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28
Q

Basic contractile unit of monocytes

A

Sarcomere

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29
Q

Effect of actin-myosin configuration on contractility based on frank starling law

A

If hypovolemia don’t have same wall tension and suboptimal interaction

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30
Q

Wall stress is typically greatest where

A

Subendocardium

Blood supply lowest and demand highest

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31
Q

normal size of aortic valve

A

> 2cm

2.5-3.5cm2

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32
Q

Normal mitral valve area

A

> 2cm

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33
Q

role of accessory pathways in dysrhythmias

A

Bypass AV node causing re-entrant dysrhythmias

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34
Q

LaPlace’s law. ______ and ______ vary directly with _________. Inversely with _____

A

Wall stress and MVO2 diaries directly with internal pressure.

Inversely with wall thickness

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35
Q

Wall stress is typically greatest in ______

Why

A

Subendocardium

Blood supply lowest due to LVEDP

Demand highest

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36
Q

Myocardial sarcomere are relatively permeable to _______ and impermeable to_____

A

Permeable to K+

Impermeable to Na and Ca

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37
Q

Phase 0 ion movment

A

Fast Na channels open

Then slow Ca channels

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38
Q

Phase 1 ion movement

A

K+ channels open

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39
Q

Phase 2 ion movement

A

Ca channels more open

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40
Q

Phase 3 ion movment

A

K+ channels open more

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41
Q

Phase 4 ion movement

A

RMP

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42
Q

SA node AP has no phase _____

A

1 and 2

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43
Q

Pint 1 on pressure volume loop

A

MV closes

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44
Q

Point 2 on pressure volume loop

A

AV valve opens

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45
Q

Point 3 on pressure volume loop

A

AV closes

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46
Q

Point 4 on pressure volume loop

A

MV opens

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47
Q

Increased preload effect on pressure volume loop

A

Shifts to right

Increased SV

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48
Q

EDPVR is directly related to

A

LV compliance

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49
Q

Effect of increased afterload on pressure volume loop

A

Narrow and taller

Lower SV and higher pressures

Higher EDV

ESPVR reduced

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50
Q

ESPVR related to

A

Myocardial contractility

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51
Q

ESPVR is heart rate sensitive index of

A

Contractility

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52
Q

Heart failure shifts LV volume loop

A

To right

Compensates for decreased contractility

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53
Q

Aortic stenosis effect on PV loop

A

Higher pressure for given volume

Taller

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54
Q

Diastolic heart failure PV loop changes

A

Flat frank starling curve

55
Q

Ways body compensates for heart failure

A

Salt and water retention

Vasoconstriction

Sympathetic stimulation

56
Q

CV effects of valsalva maneuver

A

Decreased HR, contractility, vasodilation

57
Q

CV effects of baroreceptors reflex

A

Decreased HR, contractility, vasodilation

58
Q

CV effects of Oculocardiac reflex

A

Bradycardia
asystole
dysrhythmia
hypotension

59
Q

CV effects of celiac reflex

A

Bradycardia
Hypotension
Apnea

60
Q

CV effects of Bainbridge reflex

A

Increased HR

Decreased BP

Decreased SVR

Diuretics

61
Q

CV effects Cushing reflex

A

SNS = hypertension

62
Q

CV effects Chemoreceptors reflex

A

Increased respiratory drive

Increased BP

63
Q

Determinants of BP

A

Cardiac Output

  • HR
  • SV

SVR

64
Q

CO components

65
Q

Components of SVR

A

Tone X Viscosity

66
Q

Effect of alpha 1 receptors

A

Vasoconstriction

67
Q

Effect of alpha 2 receptors

A

Blocks output- vasodilation

68
Q

Effect of beta1 receptors

A

Increase heart rate and contractility

69
Q

Effect of beta 2 receptors

A

Vasodilates

Increases glyco neo genesis

70
Q

Effect of Muscarinic receptors

A

Decrease heart rate

Activates salivary/sweat glands

Limited decreased vascular tone

71
Q

Epinephrine activates which receptors

A

Alpha and beta

72
Q

NE activates

A

Alpha 1, alpha 2, and beta 1 receptors

NO beta 2

73
Q

Dopamine activates which receptors

A

Alpha 1, beta 1, and dopamine receptors

NO alpha 2 or beta 2

74
Q

Only catecholamines that activates beta 2

75
Q

Preganglionic release which NTS sympathetic pathway

A

Acetylcholine.

76
Q

Postganglionic sympathetic fibers release

77
Q

Termination of NE due to

A

Reuptake, dilution by diffusion or metabolism by MAO

78
Q

Dexmedetomidine receptor and hemodynamic effects

A

Alpha 2 agonist

79
Q

Receptor for carvedilol and hemodynamic effects

A

Mixed alpha beta antagonist

80
Q

Receptor and hemodynamic effects of NE

A

Nonselective alpha beta

81
Q

Receptor and hemodynamic effects epi

A

Non selective alpha beta

More beta 1

82
Q

Receptor and hemodynamics for labetalol

A

Mixed alpha beta antagonist

83
Q

Esmolol receptor and hemodynamic effects

A

Beta 1 antagonist

84
Q

Four mechanisms of adrenergic receptor activation

A

Binding

Promote NE release

Block NE reuptake

Inhibition of NE inactivation

85
Q

Ex of catecholamines

A

Epi

NE

Isoproterenol

Dopamine

Dobutamine

86
Q

Examples of non- catecholamines adrenergic agonists

A

Ephedrine-alpha and beta

Phenylephrine- alpha 1

Terbutaline- beta 2

87
Q

Clinical uses of alpha 1 activation

A

Nasal decongestant

Hemostasis

Adjunct to LA

Mydriasis

Elevation of BP (neo, NE)

88
Q

Adverse effects of alpha 1 activation

A

Hypertension

Necrosis (extravasation of IV)

Bradycardia

89
Q

CV effects of beta 1 activation

A

Increased HR, contractility, automaticity, conduction through AV node

Renin release from JG cells

90
Q

4 therapeutic applications of beta 1 activation

A

Initiate contraction in arrest

Increase contractility in failing heart

Increase CO in shock

Improve AV conduction when AVB present

91
Q

Adverse effects of beta 1 activation

A

Tachycardia

Dysrhythmias

Increased MVO2 = angina

92
Q

Beta 2 receptor activation

A

Bronchodilation

Tocolysis on uterus

93
Q

Overall CV effects of PDE-3 inhibitors

A

Vasodilation
Increased organ perfusion
Decreased SVR
Decreased BP

Increased contractility, HR, SV, EF

Decreased preload and PCWP

94
Q

Dopamine 1-5mcg/kg/min

A

Induces natures is

Binds with D1 receptor dilating renal and mesenteric blood vessels

95
Q

Dopamine at 5-10 mcg/kg/min

A

Primarily beta1 with increase in contractility and HR

96
Q

Dopamine at >10mcg/kg/min

A

Primarily alpha1

97
Q

Uses of vasopressin

A

Potent vasoconstriction

Volume loss in DM

Bleeding esophageal varicose

Vasoplegia with CPB

98
Q

Most anesthetics and surgical stimulation

A

Alter ANS, autonomic reflexes, vasomotor control by pons/medulla

99
Q

Increased density or receptors

A

Up regulation

Chronic decrease in receptor stimulation

100
Q

Decreased density of regulation

A

Down regulation

Result of chronic increase in receptor stimulation

101
Q

Factors influencing hemodynamic response to induction agents

A 
Premedication
Dose
Speed of administration
CV disease and compensation
EF
Emotional state
Baseline autonomic tone
Home meds
Influence of adjuvant drugs
Age
DM
HTN
102
Q

Variables affecting anesthesia induction drug dose selection

A 
Weight
Adjuvant anesthetics
Elderly
Trauma
Poor heart function
Timing
103
Q

Hemodynamic effects of propofol

A

Decrease in BP ***

Decrease preload, contractility, afterload (CO, SV)

104
Q

Vasodilator effect of propofol due to

A

Decrease in sympathetic outflow

Direct vasodilation

105
Q

Hemodynamic effects of thiopental

A

Increase HR
Decrease CI, BP, LVEDP
Histamine release

Decrease sympathetic outflow
Decrease contractility

106
Q

Hemodynamic effects of methohexital

A

Increase in HR

Decrease in BP, profound hypotension

Decreased sympathetic outflow

107
Q

Hemodynamic effects of diazepam

A

Decreased BP but slow onset and easier to control

Decree in MVO2 and LVEDP

HR decrease w/ sleep

Combine with opiate = profound decrease in SVR

108
Q

hemodynamic effects of midazolam

A

Decrease in BP (more than Valium)

Mild increase in HR (5-15%)

109
Q

Hemodynamic effects of Etomidate

A

DRUG THAT CHANGES HEMODYNAMIC VARIABLES THE LEAST

Very useful with hypovolemic

110
Q

Hemodynamic effects of Ketamine

A

Increase MVO2

Increase PVR and SVR

111
Q

Benefits of using N2O

A

Hasten onset
Short duration
Decrease dosage of other volatiles

112
Q

Indications for inhaled induction

A

Compromised airway

Children

Indwelling ETT, trach

Needle phobia

113
Q

Dosage for cardiac anesthesia

Propofol

A

0.2-1.5mg/GI

114
Q

Dosage for cardiac anesthesia

Thiopental

A

0.5-4mg/kg

115
Q

Dosage for cardiac anesthesia

Etomidate

A

0.1-0.3mg/kg

116
Q

Dosage for cardiac anesthesia

Fentanyl

A

3-25mcg/kg

117
Q

Dosage for cardiac anesthesia

Sufentanil

A

0.5-2mcg/kg

118
Q

Dosage for cardiac anesthesia

Remifentanil

A

0.1-0.75mcg/kg/min

119
Q

Dosage for cardiac anesthesia

Cisatricurium

A

70-100mcg/kg

120
Q

Dosage for cardiac anesthesia

Vecuronium

A

70-100 mcg/kg

121
Q

Dosage for cardiac anesthesia

Pancuronium

A

70-100 mcg/kg

122
Q

Dosage for cardiac anesthesia

Succinylcholine

123
Q

Effects associated with intubation after induction with etomidate

A

Increase HR 15%
CI 19%
SVR 4%

124
Q

Effects associated with intubation after induction with propofol

A

Increase HR 15%
SV 9%
CI 18%

125
Q

Effects associated with intubation after induction with midazolam

A

Increase HR 4%
SVR 5%
CI 9%

126
Q

Primary mechanism responsible for the CV effects of volatile anesthetics

A

Reduce intracellular calcium concentration

Reduce influx through sarcolemma and release from SR

127
Q

Relationship between dose of volatiles and BP

A

decrease in dose related fashion

Due to decreased SVR

128
Q

Relationship between dose of volatiles and SVR

A

Decrease in dose dependent fashion

Iso most

129
Q

Relationship between dose of volatiles and CI

A

Decreases due to vasodilation and preload reduction

HR increases and compensatory so CI sustained

130
Q

Relationship between dose of volatiles and HR

A

Increased due to modulation of SA automaticity, modulation of baroreceptors reflex, SNS activation

Des most

131
Q

Effect of N20 on MACBAR of sevo

132
Q

Effect of N20 on MACBAR of des

133
Q

Addiction of 1.5-3mcg/kg fentanyl decreases MACBAR to

Cardiothoracic Pharmacology (3 decks)

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