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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
CV and respiratory effects of valsalva maneuver
Decreased HR Decreased contractility Vasodilation
26
CV and respiratory effects of baroreceptor reflex
Decreased HR Decreased contractility Vasodilation
27
CV and respiratory effects of oculocardiac reflex
Bradycardia Asystole Dysrhythmias Hypotension
28
CV and respiratory effects of celiac reflex
Bradycardia Hypotension APNEA
29
CV and respiratory effects of bainbridge refles
Increased HR Decreased BP Decreased SVR Diuresis
30
CV and respiratory effects of Cushing reflex
SNS stimulation = HTN
31
CV and respiratory effects of chemoreceptor reflex
Increased respiratory drive Increased BP
32
Determinants of BP
BP = CO X SVR
33
Determinants of CO
CO = HR X SV
34
SV dependent on
Preload Contractility Afterload
35
HR determined by (3)
(+) or (-) chronotropic effects from SNS, PNS, SA node
36
Determinants of SVR
SVR = Tone X Viscocity
37
Tone dependent on
Radius Pressure gradient Vessel length
38
Viscosity dependent on
COP and Hg
39
Hemodynamic effects of Alpha 1 receptors
Vasoconstricts
40
Hemodynamic effects of Alpha 2 receptors
Blocks output (vasodilation)
41
Hemodynamic effects of Beta 1 receptors
Increased HR and contractility
42
Hemodynamic effects of Beta 2 receptors
Vasodilates Bronchodilation Increased gluconeogenesis
43
Hemodynamic effects of dopamine receptors
Vary depending on dose
44
Hemodynamic effects of muscarinic receptors
Decrease HR Activates salivary and sweat glands Decrease vascular tone (much lesser degree)
45
How is NE removed from nerve ending
Diffusion out of cleft into circulation Metabolized by COMT in cleft Reuptake into neuron, broken down by MAO
46
Receptor and hemodynamic effect of dexmedetomidine
Alpha 2 agonist Decrease BP and HR
47
Receptor and hemodynamic effect of carvedilol
Mixed alpha/beta antagonist Decrease HR and BP
48
Receptor and hemodynamic effect of NE
Alpha 1 and 2 agonist Beta 1 agonist Increase HR, contractility, PVR Vasoconstriction
49
Receptor and hemodynamic effect of epi
All Alpha and Beta agonist Increase HR, contractility Vasoconstriction Gluconeogenesis Bronchodilation
50
Receptor and hemodynamic effect of labetalol
Mixed Alpha 1, Beta1, Beta 2 antagonist Ratio 6:1 alpha:beta Vasodilation Bradycardia Bronchoconstriction
51
Receptor and hemodynamic effect of esmolol
Beta 1 antagonist Bradycardia
52
4 mechanisms of adrenergic receptor activation
Direct binding Promotion of NE release Blockade of NE reuptake Inhibition of NE inactivation
53
Catecholamines adrenergic agonists
Epi NE Isoproterenol Dopamine Dobutamine
54
Noncatecholamine adrenergic agonists
Ephedrine Phenylephrine Terbutaline
55
CV effects of beta 1 receptor activation
Increased HR, contractility, automaticity, conduction, renin release
56
cardiopulmonary and vascular effects of PDE-3 inhibitors
Inhibition of enzyme prevents cAMP breakdown and increasing intracellular concentration Increased inotropy, chronotropy, dromotropic
57
Dopamine 1-5 mcg/kg/min
Induces natriuresis
58
Dopamine 5-10 mcg/kg/min
Beta 1 activation Increased contractility and HR
59
Dopamine >10mcg/kg/min
Alpha 1
60
Increased density of receptors | Seen with chronic decrease in receptor stimulation
Up regulation
61
Decreased density of receptors | Caused by chronic increase in receptor stimulation
Down regulation
62
Mechanisms responsible for BP effects seen with propofol
Decreased SNS outflow Direct vasodilation
63
Mechanisms responsible for BP effects seen with thiopental
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
Mechanisms responsible for BP effects seen with midazolam
Profound decrease in SVR when used with opioid Less profound with diazepam
65
Mechanisms responsible for BP effects seen with etomidate
10-15% decrease in SVR will increase BP 19%
66
Mechanisms responsible for BP effects seen with ketamine
Increased PVR and SVR
67
3 benefits of using N20 in addition to other inhaled anesthetics
Hasten onset Ultrashort duration Decrease dose of other inhaled agent
68
Cardiac anesthesia dose of propofol
Hypnotic 0.2-1.5mg/kg
69
Cardiac anesthesia dose of thiopental
Hypnotic 0.5-4mg/kg
70
Cardiac anesthesia dose of etomidate
Hypnotic 0.1-0.3mg/kg
71
Cardiac anesthesia dose of fentanyl
Opioid 3-25mcg/kg
72
Cardiac anesthesia dose of Sufentanil
Opioid 0.5-2mcg/kg
73
Cardiac anesthesia dose of Remifentanil
Opioid 0.1-0.75 mcg/kg/min
74
Cardiac anesthesia dose of cisatracurium , Vecuronium, pancuronium
70-100mcg/kg
75
Cardiac anesthesia dose of succinylcholine
1-2 mg/kg
76
Primary mechanism thought to be responsible for CV effects of volatile anesthetics
Reduction in calcium influx through sarcolemma dm depression of Ca release from SR
77
Relationship between dose of volatiles on BP, SVR, HR, and CI
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
Volatile most associated with increased HR
Desflurane Sevo can at > 1 MAC
79
Effects of modern volatile agents on conduction, contractility, dysrhythmia potential, baroreflexes, and ischemic heart
Depress contractility and BP Prolong AV conduction and QT interval Predispose to catecholamine induced dysrhythmia Attenuate baroreflexes in dose dependent fashion
80
Effect of volatile on coronary blood flow
Decreased coronary vascular resistance but coronary blood flow also decreased due to effects on DBP
81
Volatile considered to be agent of choice for pt with cerebrovascular disease undergoing cardiac surgery
Isoflurane
82
Non anesthetic drugs considered to have a synergistic relationship with volatiles on hemodynamics
Synergistic with ACE Less with beta blockers Limitations interaction with CBD
83
How does N20 interact with volatiles to impact hemodynamics
Decreased CO and SV Also decreased MAC requirements
84
How does fentanyl interact with volatiles to impact hemodynamics
Decreases MAC, SVR, HR
85
How does propofol interact with volatiles to impact hemodynamics
Dose related circulatory depression Decreased CO and BP
86
How does dexmedetomidine interact with volatiles to impact hemodynamics
Modestly affects circulatory effects Decreased HR and SVR
87
Circulatory effects of N20 and how affected by other anesthetic agents
Activates SNS = increased SVR Increased CVP and arterial pressure SNS response intact w/ other volatiles When given with opioids augments cardiac depression
88
Effect of moderate to high dose opioids on hemodynamics
More disinfectant bradycardia and vasodilation
89
Possible mechanisms for hemodynamic effect of opioids
Influence of SNS outflow from SNS Bradycardia due to direct stimulant effect on central vagal nuclei
90
Opioid considered to have most favorable effect on HR and BP for intubation and intraop BP control
Sufentanil
91
Effects of fentanyl sufentanil on epi and NE levels
NE level lower with sufentanil Lower epi intraop with Demerol
92
Effect of CPB on drug absorption
Reduced oral or IM absorption
93
Effect of CPB on drug distribution
Decreased volume of distribution Decreased pulmonary drug distribution- increased systemic drug levels
94
Effects of CPB on drug elimination
Decreased drug clearance Decreased renal function
95
3 drug classes commonly used as anti-ischemic therapy in pt with CAD
Nitrates Beta blockers Calcium channel blockers
96
MOA of NTG causing vasodilation
Converted to nitric oxide in smooth muscle Vasodilation Enhances myocardial oxygen delivery and reduces demand
97
Start to see decrease in SVR with NTG at what dose
> 50 mcg/min
98
4 beneficial effects of NTG in pt with CAD
Decreased PCWP/LVEDP Decreased wall tension Decreased myocardial O2 demand Decreased ischemia
99
Dose dependent effects of NTG on venous and arterial blood vessels
Larger doses = arterial vasodilation
100
How NTG better suited for pulmonary HTN than other more potent arterial vasodilators
Vasodilation of pulmonary arteries and veins more than systemic Decreased RAP Decreased PCWP Decreased PAP
101
Unique effects of NTG on coronary artery flow
Potent coronary vasodilators Smaller coronaries dilate more Reverses or prevents vasospasm
102
How use of NTG improves CPP
CBP improves as PCWP decreases Reduces subendocardial pressure Improves collateral flow
103
In pt with CHF NTG effect on cardiac performance
Decreased mitral regurg and afterload Increased CO
104
Effect of NTG on cardiac performance in pt with normal LV
Inadequate preload = decreased CO
105
Effect of NTG on cardiac performance in pt with ischemic heart disease
Decreased wall tension, O2 demand, ischemia Improved cardiac function
106
Benefits of beta blockade in pt with ischemic heart disease
- 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
Dose of esmolol
5-20 mg Half life 9.5 minutes
108
Dose of metoprolol
Bolus 1-5 mg Half-life 3-6 minutes
109
Dose of labetalol
Bolus 2.5-5mg Half-life 2-6 hours
110
3 mechanisms by which calcium blocking drugs reduce myocardial oxygen demand
Depress contractility Decreased HR Decreased afterload (SBP)
111
2 drugs with primary action on heart CBD
Diltiazem Verapamil
112
Primary action on arterioles (2) CBD
Nicardipine Nifedipine
113
First line anti-hypertensive drug for heart failure pt with HTN
ACE inhibitor | Angiotensin converting enzyme inhibitors
114
4 advantages of ACEI over conventional anti-hypertensives
Free of CNS effects Free of myocardial depressant effects Metabolic changes not seen Rebound HTN not seen
115
2 hemodynamic concerns associated with ACEI and ARBs during general anesthesia
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
Dose of hydralazine
2.5-10 mg IV or IM Slow onset - 10 minutes Offset 4 hours
117
Why thiosulfate used with nitroprusside
Reacts with sulfur do now Effectively detoxifies cyanide

Cardiothoracic Pharmacology (3 decks)

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