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Pharmacology I > The Heart > Flashcards

The Heart Flashcards

1
Q

what is the order of the conduction system

A
  • SA node -> AV node -> bundle of his -> Purkinje fibers
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2
Q

what happens in phase 0 of cardiac AP

A
  • rapid depolarization
  • Na+ channels open
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3
Q

what happens in phase 1 of cardiac AP

A
  • partial repolarization
  • Na+ channels close
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4
Q

what happens in phase 2 of cardiac AP

A
  • plateau
  • Ca2+ channels open
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5
Q

what happens during phasse 3 of cardiac AP

A
  • repolarization
  • Ca2+ channels close
  • K+ channels open
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6
Q

what happens in phase 4 of cardiac AP

A
  • pacemaker/resting
  • degradation of membrane potential slowly- Ca2+ channels
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7
Q

whatis the absoluate refractory period

A

cannot be stimulated

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8
Q

what is the relative refractory period

A
  • below the threshold
  • respond to greater than normal stimulus
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9
Q

what are the 3 types of refractory period

A
  • absolute refractory period
  • relative refractory period
  • supernormal excitatory period
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10
Q

what happens during the P wave

A

atrial depolarization

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11
Q

what happens during the PR interval

A

time to start of atrial depolarization to start of ventricular depolarization

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12
Q

what happens during th QRS complex

A

ventricular depolarization also includes atrial repolarizationwh

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13
Q

what happens during the T wave

A

ventricular repolarization

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14
Q

what happens during the QT interval

A

time between start of ventricular depolarization and end of repolarization

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15
Q

QT is ______ and must be adjusted at a HR of ______ bpm

A

rate dependent; greater than 60 bpm

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16
Q

what is prolonged QT in men and women

A
  • women: greater than 460msec
  • men: greater than 450 msec
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17
Q

what are the sites of arrhythmias

A
  • atrial
  • junctional
  • ventricular
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18
Q

what are examples of tachycardia

A
  • a fib
  • SVT
  • ventricular tachycardia
  • ventricular fibrillation
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19
Q

what are examples of bradycardia

A

heart block and asystole

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20
Q

what are the mechanissm of cardiac arryhthmias

A
  • delayed after depolarization
  • re-entry
  • ectopic pacemaker activity
  • heart block
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21
Q

what are class I antiarrhythmic medications

A
  • Na+ channel blockers
  • subgroups: Ia, Ib, and Ic
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22
Q

what are class II antiarrhythmic medications

A

beta adrenoreceptor blockers

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23
Q

what are class III antiarrhythmic medications

A

K+ channel blockers

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24
Q

what are class IV antiarrhythmic medications

A

Ca2+ channel blockers

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25
Q

what are class V antiarrhythmic medications

A

miscellaneous

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26
Q

what phase do B agonists work on

A

stimulate phase 4

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27
Q

where do class I antiarrhythmic medications work

A

inhibit phase 0

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28
Q

where do class II antiarrhythmic medications work

A

stimulate phase 2

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29
Q

where do class IV antiarrhythmic medications work

A

inhibit phase 2

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30
Q

where do class III antiarrhythmic medications work

A

inhibit phase 3

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31
Q

what do class Ia antiarrhythmic meds do and give examples

A
  • moderate Na+ channel blockade
  • quinidine, procainamide, disopyramide
  • increase ERP
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32
Q

what do class Ib antiarrhythmic meds do

A
  • weak Na+ channel blockade
  • Lidocaine, tocainide, mexilitine, phenytoin
  • decrease ERP
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33
Q

what do class Ic antiarrhythmic meds do and what are exmaples

A
  • strong Na+ channel blockade
  • moricizine, flecainide, porpafenone
  • increased ERP = increased QT duration
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34
Q

what is the brand name, MOA, use, ADRs, and drud-drug interactions of disopyramide

A
  • brand name: norpace, norpace CR
  • MOA: Na+ channel blockade (moderate)
  • use: tx of PVC and VT
  • ADRs: anticholinergic- dry mouth, constipation, urinary hesitancy, cardiac QT prolongation
  • drug: drug interactions: other anticholinergic meds, increased risk of QT prolongation with macrolide antibiotics
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35
Q

what is the brand name, MOA, use, ADRs, and drud-drug interactions of mexiletine

A

brand name: mexitil
- MOA: Na+ channel blockade- weark
- use: treatment of documented life threatening ventricular dysrhythmias
- ADRs: nausea, vomiting, heartburn, dizziness, light headedness, tremors, convulsion
- Drug: drgu interactions: use the lowest effective dose of vasoconstrictor

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36
Q

what is the brand name, MOA, use, ADRs, and drud-drug interactions of propafenone

A

brand name: rythmol/rythmol SR
- MOA: Na+ channel blockade- strong
- use: treatment of documented life threatening ventricular dysrhythmias
- ADRs: nausea, vomiting, altered taste, constipation, dizziness
- Drug: drgu interactions: use the lowest effective dose of vasoconstrictor

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37
Q

what are the dental implications with Na+ channel blockers

A
  • monitor vital signs - pulse to irregularity
  • considers tress reduction protocol
  • xerostomia- assss salivary flow as a factor of caries, perioodntal disease and candidiasis- most significant with Ia medications
  • after supine positioning have patient sit upright for at least 2 minutes before standing to avoid orthostatic hypotension
  • avoid or limit dose of vasoconstrictor
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38
Q

what do beta adrenoreceptor blockers/class II meds do

A
  • block sympathetic stimulation to the heart
  • decrease HR
  • decrease automaticity
  • block NEs effects on Ca2+ channels
  • slow conduction through AV nodes ( increase refractory period)
  • prevent iscemia
  • AV nodal blocking agent
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39
Q

what is the receptor affinity for metoprolol, betaxolol, acebutol, esmolol, atenolol, nebivolol

A

B1&raquo_space;» B2

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40
Q

what is the receptor affinity for propranolol, careolol, penbutolol, pindolol, timolol

A

B1= B2

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41
Q

what is the receptor affinity for butoxamine

A

B2&raquo_space;> B1w

42
Q

what is the receptor affinity for labetalol and carvedilol

A

B1 = B2 > A1 > a2

43
Q

what is the mnemonic for B1 selective antagonist

A
  • “Beta blockers Acting Exclusively At Myocardium”
  • Betaxolol
  • Acebutol
  • Esmolol
  • Atenolol
  • Metoprolol
44
Q

what is the brand name, MOA, use, ADRs, and drud-drug interactions of metoprolol

A
  • brand name: lopressor (tartrate), Toprol XL (succinate)
  • MOA: selective B1 adrenoreceptor blocker
  • use: hypertension, CAD, angina, HF, supraventricular arrhythmias
  • ADRs: hypotension, bradycardia, fatigue, sexual dysfunction, drowsiness
  • drug: drug interactison: icnreased hypotension with fentanyl and inhaled anesthetics. decreased effect of vasoconstrictors
  • NSAIDS may reduce the efficacy greater than 3 weeks of tx
45
Q

what are the dental implications for B adrenoreceptor blockers

A
  • monitor vital signs
  • consider stress reduction protocol
    -shorter apppointments
  • after supine positioning ahve patient sit upright for at least 2 monutes before standing to avoid orthostatic hypotension
  • use vasoconstrictors and inhaled anesthetics with caution
46
Q

what do class III antiarrhythmic medication

A
  • K+ channel blockers
  • delay repolarization ( prolong AP)
  • QT prolongation -» risk of Tdp
  • agents: amiodarone (all classes activity)
  • dofetilide ( pure class III)
  • dronedarone (amiodarone analog- less toxic)
  • sotalol ( exhibits class III and II activity)
  • ibutilide ( pure class III activity)
47
Q

what is the mnemonic for class III drugs

A
  • A Big Dog Is Darn Scary
  • amiodarone
  • bretylium
  • dofetilide
  • Ibutilide
  • Dronedarone
  • Sotalol
48
Q

what is the brand name, MOA, use, ADRs, and drud-drug interactions of amiodarone

A
  • brand name: cordarone or pacerone
  • MOA: K+ channel blocker, also blocks Na+ and Ca2+ channels, beta receptors
  • use: supraventricular and ventricular arrhythmias
  • ADRs: seven organ systems: eyes, lungs, heart, thyroid, liver, GI, skin
  • drug to drug itneractions: bradycardia and hypotension with vasoconstrictors and inhaled anesthetics. increased photosensitivity with tetracycline. many interactions secondary to CYP3A4 inhibition
49
Q

what are the most effective and most toxic class III drugs

A

amiodarone

50
Q

what are the dental implications with class III drugs

A
  • monitor vital signs
  • consider stress reduction protocol- short appointments, delay appointment if pt is in distress
  • after supine positioning, have pt sit upright for at least 2 minutes before standing to avoid orthostatic hypotension
  • use vasoconstrictors and inhaled anesthetics with caution
  • avoid dental light in patients eyes/offer dark glasses with amiodarone
51
Q

what is the MOA with class IV drugs

A
  • calcium channel blockers
  • block calcium from entering the cell through voltage sensitive slow L type channels
  • slow conduction in SA and AV node (non-dihydropyridine)
  • decreased HR
  • AV block
  • shorten plateau ( phase 2) of AP
  • deceased delayed after depolarizaation (DAD)
  • decreased ectopic beats
52
Q

describe dihydropyridine class IV drugs

A
  • selective for smooth muscle
  • end in “dipine”
  • common side effects: reflex tachycardia, hypotension, peripheral edema, gingival hyperplasia
53
Q

describe non- dihydropyridine class IV drugs

A
  • selective for myocardium
  • diltiazem and verapamil
  • common SE: bradycardia/AV block, hypotension, edema, gingival hyperplasia
54
Q

what is the brand name, MOA, use, ADRs, and drud-drug interactions of verapamil

A
  • brand name: calan, isoptin, or verlan
  • MOA: non dihydropyridine calcium channel blocker
  • use: angina, a fib, hypertension
  • ADRs: constipation, dizziness, lightheadedness, hypotension, bradycardia, gingival enlargement
  • drug: drug interactions: bradycardia and hypotension with general and inhaled anesthetics. many interactions secondary to CYP3A4 inhibition
55
Q

what are the dental implications with Class IV drugs

A
  • monitro vital signs
  • consider stress reduction protocol
  • shorter appointments
  • after supine positioning have pt sit upright for at least 2 minutes before standing to avoid orthostatic hypotension
  • use vasoconstrictros and inhaled anesthetics with caution
  • place on frequent recall to monitor for gingival hyperplasia
56
Q

describe adenosine

A
  • class V antiarrhythmic meds
  • produced endogenously
  • binds to the A1 receptor in the AV node causing AV node block
  • used to terminate SVT
  • half life is 20-30 seconds
  • metabolized by RBCs and vascular endothelium
  • ADRs = flushing, chest pain, SOB
  • no dental implications
57
Q

what is EDV

A

amount of blood in LV after diastole

58
Q

LV EDV =

A

preload

59
Q

what is afterload

A

pressure heart must overcome to eject blood

60
Q

afterload =

A

systemic BP

61
Q

what is ESV

A

amount of blood in LV at the end of systole

62
Q

what is the formula for SV

A

SV = EDV - ESV

63
Q

what is the formula for ejection fraction

A

EF = SV/EDV x100%

64
Q

what is the formula for CO

A

CO= HR x SV

65
Q

what is inotropy

A

ability of the heart to contract

66
Q

what are the positive inotropic medications

A
  • cardiac glycosides
  • digoxin- inhibits Na-K ATPase
  • DOBUTamine -B1 adrenoreceptor agonist
  • milrinone- phosphodiesterase inhibitor
    -levosimendan- calcium sensitizer
67
Q

what is the brand name, MOA, use, ADRs, and drud-drug interactions of digoxin

A
  • brand name: Digitek, lanoxicaps, Lanoxin
  • MOA: inhibition of Na-K+ ATPase/ increases vagal tone to heart
  • use: HF, A fib (rate-control)
  • ADRs: narrow therapeutic index. nausea, vomiting, diarrhea. bradycardia/heart block, visual disturbances (green-yellow halo)
  • drug: drug interactions: other drugs that cause bradycardia or hypokalemia. increased levels with macrolide antibiotic. increase risk of arrhythmia with adrenergic agonists or succinylcholine
68
Q

what are the dental implications with positive inotropic medications

A
  • monitor vital signs
  • increased gag reflex may make dental procedures such as taking radiographs or impressions difficult
  • after supine positioning have pt sit upright for at least 2 minutes before standing to avoid orthostatic hypotension
  • use vasoconstrictors with caution - adrenergic stimulation
  • avoid dental light in pt eyes
  • stress reduction protocol
69
Q

what is the brand name, MOA, use, ADRs, and drud-drug interactions of DOBUTamine

A
  • brand name: Dobutrex
  • MOA: beta1 adrenergic receptor agonist
  • use: acute depressed HF, cardiogenic shock
  • ADRs: increased HR and BP, arrythmias, chest pain
  • drug: drug interactions: none of significance
70
Q

what are the dental implications with DOBUTamine

A

none

71
Q

what is the brand name, MOA, use, ADRs, and drud-drug interactions, and dental implications of milrinone

A

brand name: primacor
- MOA: phosphodiesterase 3 enzyme inhibitor
- use: acute decompensated HF, cardiogenic shock
- ADRs: arrhythmias, hypotension, chest pain
- drug: drug interations: none
- dental implications: none

72
Q

what is the brand name, MOA, use, ADRs, and drud-drug interactions, and dental implications of levosimendan

A
  • brand name: simdax ( not available in US)
  • MOA: sensitize to troponin to Ca2+ and KAtp channel activation in smooth muscle
  • use: acute decompensated HF
  • ADRs: Arrhythmias, hypotension, headache
  • drug: drug interactions: none
  • dental implications: none
73
Q

what is the function of myocardial O2 supply

A
  • arterial O2 content: decreased anemia and hypoxia
  • coronary blood flow: decreased atherosclerosis and vasospasm
74
Q

myocardial oxygen supply is a function of:

A

HR

75
Q

cardiac myocytes supplied with blood during:

A

diastole

76
Q

increased HR = _____ time in diastole

A

decreased

77
Q

what are the MVO2 determinants

A
  • HR
  • myocardial contractility
  • myocardial wall stress: preload and afterload
78
Q

what do B1 adrenoreceptors do

A
  • sympathetic NS
  • increased force of contraction (positive inotropic effect_
  • increased HR (positive chronotropic effect)
  • increased automaticity
  • repolarization
  • reduced cardiac efficiency
79
Q

what do muscarinic receptors do

A
  • parasympathetic NS
  • cardiac slowing
  • decreased automaticity
  • inhibition of AV node conduction
80
Q

coronary artery disease can lead to:

A
  • stable ischemic disease
  • acute coronary syndromes: UA, NSTEMI, STEMI
81
Q

what ACS syndroms have No ST elevation to the most ST elevation

A
  • UA -> NSTEMI -> STEMI
82
Q

what is the pathophysiology of IHD and ACS

A

mismatch of myocardial O2 supply and demand

83
Q

what are the antianginal meds and what do they do

A
  • organic nitrates: increased myocardial O2 supply
  • calcium channel blockers - increased myocardial O2 supply and decreased O2 demand
  • Beta- adrenoreceptor antagonists: decreased myocardial O2 demand
  • ranolazine: improves angina without changing BP or HR
  • Ivabradine- not approved for use in US
84
Q

double product =

A

HR x SBP

85
Q

what are the forms of antianginal meds

A
  • organic nitrates: nitroglycerin and isosorbide dinitrate/mononitrate
  • sodium nitroprusside
86
Q

what are the major SE of antianginal meds

A
  • headache
  • tachycardia
  • methemoglobinemia
  • syncope/hypotension
  • tolerance
87
Q

antianginal meds are contraindcated with:

A

PDE-5 inhibitors

88
Q

what are the available products for organic nitrates

A
  • SL tablets
  • spray
  • intravenous
  • ointment
  • patch
  • capsules
  • LA tablets (ISMN and ISDN)
89
Q

which organic nitrate forms are immediate relief

A

SL tablets, spray, IV, ointment

90
Q

what is the brand name, MOA, use, ADRs, and drug to drug interactions for isosorbide mononitrate

A
  • brand name: Imdur, Ismo
  • MOA: stimulate production of intracellular cGMP
  • use: angina and HF
  • ADRs: headache, flushing, dizziness, postural hypotension
  • drug: drug interactions: increased effects with other vasodilator type meds
91
Q

what are the dental implications with organic nitrates

A
  • monitor vital signs
  • stress reduction protocol
  • after supine positioning, have pt sit upright for at least 2 mins before standing to avoid orthostatic hypotension
  • use vasoconstrictors with caution
  • sublingual nitroglycerin available for acute angina attack
92
Q

what is the MOA for calcium channel blockers for anitanginal meds

A
  • block calcium from entering cell through voltage sensitive slow L-type channels
  • slow conduction in SA and AV node: decreased HR, AV block
  • vasodilation of arterioles
  • decrease arterial pressure and wall tension
  • decrease myocardial contractility
  • increase flow through areas of fixed coronary obstruction
93
Q

what are the two types of antianginal medications that are calcium channel blockers

A
  • dihydropyridine
  • non- dihydropyridine
94
Q

what is the brand name, MOA, use, ADRs, and drud-drug interactions of amlodipine

A
  • brand name: norvasc
  • MOA: dihydropyridine calcium channel blocker
  • use: angina, HTN, vasospastic angina
  • ADRs: edema, dizziness, lightheadedness, hypotension, flushing, gingival enlargement
  • drug: drug interactions: hypotension with sedative, opioids, general and inhaled anesthetics. NSAIDs reduce bloos pressure lowering effect
95
Q

what do beta adrenoreceptor blockers do as antianginal meds

A
  • block sympathetic stimulation to the heart
  • decrease HR
  • decrease Automaticity
  • block NEs affects on Ca2+ channels
  • slow conduction through AV node (increase refractory period)
  • prevent ischemia
  • decrease myocardial oxygen demand
  • decrease HR, contractility and SBP
96
Q

prefer _________ B1 selective agents for angina

A

non-selective

97
Q

what are the most common meds used to treat angina

A

beta blockers

98
Q

what is the MOA of ranolazine

A
  • inhibits late inward sodium curren in ischemic myocardium - reduced myocardial wall tension and O2 consumption
  • at higher concentrations inhibits rapid delayed rectifier potassium current - prolonged action potenial and QT interval
99
Q

what is the brand name, MOA, use, ADRs, and drud-drug interactions, and dental implications of Ranolazine-

A
  • brand name: ranexa
  • MOA: inhibition of late inward sodium current
  • use: angina
  • ADRs: bradycardia, hypotension, dizziness, QT prolongation, TdP, xerostomia
  • drug:drug interactions: many due to CYP 450 3A4 metabolism
  • dental implications: assess salivary flow as a factor in caries, periodontal disease and candidiasis. use of vasoconstrictors and inhaled anesthetics with caution
100
Q
A

Pharmacology I (12 decks)

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