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PHARM > heart lecture > Flashcards

heart lecture Flashcards

1
Q

heart conduction system

A
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2
Q

phases of the cardiac action potential

A
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3
Q

refactory periods of cardiac cells

A
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4
Q

EKG diagrammed

A
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5
Q

what controls the PR segement

A

AV node

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6
Q

what part of an ekg is widened in HF pts

A

QRS

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7
Q

what segment of the EKG is altered in ischmic dx

A

st segment

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8
Q

increased QT intervals are at risk for?

A

VT/ toresades de pointes

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9
Q

QT vs. QTc

A

QT is rate dependent and
must be adjusted at a HR > 60 bpm

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10
Q

Prolonged QT in men and women

A

≥ 460 msec in women
≥ 450 msec in men

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11
Q

Cardiac Arrhythmias classified by:

A

site, rate and mechanism

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12
Q

potetinal sites of Cardiac Arrhythmias

A
  • Atrial
  • Junctional
  • Ventricular
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13
Q

rates of cardiac arrhythmias

A
  • Tachycardia (HR > 100 bpm)
  • Ex. Atrial Fibrillation, SVT, Ventricular
    tachycardia, and ventricular fibrillation
  • Bradycardia (HR < 60 bpm)
  • Ex. Heart block and asystol
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14
Q

mechanisms of cardiac arrhythmias

A
  • Delayed after-depolarization
  • Re-entry
  • Ectopic pacemaker activity
  • Heart block
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15
Q

Delayed after-depolarization (DAD)

A
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16
Q

re-entry

A

will increase HR as conduction is abnormal in path

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17
Q

Vaughn-Williams Classification of Antiarrhythmic Medications

A
  • Class I – Na+ Channel blockers (Subgroups: Ia, Ib, and Ic)
  • Class II- β-adrenoceptor blockers
  • Class III- K+ Channel blockers
  • Class IV- Ca2+ Channel blockers
  • Class V- Miscellaneous
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18
Q

Class I Antiarrhythmic Medications

A

USE-DEPENDENT CHANNEL BLOCKADE
Na+ Channel blockers
* Class Ia, Ib and Ic

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19
Q

Class Ia

A
  • Moderate Na+ Channel blockade
  • Eg. quinidine, procainamide, disopyramide
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20
Q
  • Class Ib
A
  • Weak Na+ Channel blockade
  • Eg. Lidocaine, Tocainide, Mexilitine, Phenytoin
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21
Q
  • Class Ic
A
  • Strong Na+ Channel blockade
  • Eg. Moricizine, Flecainide, Propafenone
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22
Q

which class I antiarrhytmitc can incrase refactory period/QT interval?

A

Ia

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23
Q

class I antiarrhytmatics effects on cardiac potential

A
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24
Q

Mnemonic for class I

A
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25
Q

disopyramide moa

A

moderate na block

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26
Q

dispyramide interactions
1. Other meds with similar effects?
1. Increased risk of QT prolongation with?

A
  1. Other anticholinergic medications (i.e. glycopyrrolate or atropine)
  2. Increased risk of QT prolongation with macrolide antibiotics (i.e. erythromycin or clarithromycin
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27
Q

disopyramide adrs

A

Anticholinergic-Dry mouth, constipation, urinary hesitancy
Cardiac- QT prolongation

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28
Q

mexiltine moa

A

weak na block

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29
Q

mexilitine adrs

A
  • GI- nausea, vomiting, heartburn
  • Neuro- dizziness, light-headedness, tremors, convulsion (toxic)
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30
Q

mexilitne interactions
vasoconstrictor?

A
  • Use the lowest effective dose of local vasoconstrictor
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31
Q

propafenone moa

A

strong na block

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32
Q

propafenone adrs

A
  • GI: nausea, vomiting, altered taste, constipation
  • Neuro- dizziness
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33
Q

propafenone interaction
* vasoconstrictors?

A
  • Use the lowest effective dose of local vasoconstrictor
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34
Q

Class I Antiarrhythmic medications
Na+ Channel blockers-Dental Implications

A
  • Monitor vital signs (pulse to irregularity)
  • Consider stress reduction protocol
    * Xerostomia- assess salivary flow as a factor in caries, periodontal 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 vasoconstricto
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35
Q

Class II Antiarrhythmic medications
* Block ________ stimulation to the heart: effect on heart rate and automaticity
* block what effect on Ca2+ channels?
* Slow conduction through?
* Prevent?
blocking agent of?

A

β-adrenoceptor blockers
* Block sympathetic stimulation to the heart: Decrease heart rate and automaticity
* block NE’s effects on Ca2+ channels
* Slow conduction through AV node (increase refractory period)
* Prevent ischemia

AV nodal blocking agent

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36
Q

B1 selective blockers we may use at heart

A
  • Betaxolol
  • Acebutelol
  • Esmolol
  • Atenolol
  • Metoprolol
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37
Q

metoprolol moa

A

B1 selective blocke fr

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38
Q

metoprolol adrs

A

hypotension, bradycardia, fatigue, sexual dysfunction, drowsiness

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39
Q

metoprolol interactions
* fentanyl and inhaled anesthetics
* Decreases the effect of?
* NSAIDS?

A
  • Increased hypotension with fentanyl and inhaled anesthetics
  • Decreased effect of vasoconstrictors (i.e. epinephrine)
  • NSAIDS may reduce the efficacy (> 3 weeks of treatment)
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40
Q

Class II Antiarrhythmic medications
β-adrenoceptor blockers- Dental Implication

A
  • Monitor vital signs
  • Consider stress reduction protocol
  • Shorter appointments
  • After supine positioning, have patient sit upright for at least 2 minutes before standing to avoid orthostatic hypotension
  • Use vasoconstrictors and inhaled anesthetics with caution
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41
Q

Class III Antiarrhythmic medication MOA
work on what phase cardiac potential?
risk?

A
  • K+ channel blockers
  • Delay repolarization (prolong action potential)
  • QT prolongation→→→ risk of TdP
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42
Q

class 3 agents

activity of each?

A
  • Amiodarone (exhibits all antiarrhythmic classes activity)
  • Dofetilide (pure class III activity)
  • Dronedarone (amiodarone analog- less toxic)
  • Sotalol (exhibits class III and class II activity)
  • Ibutilide (pure class III activity- only available IV)
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43
Q

class 3 mnemonic

A

“A Big Dog Is Darn Scary”
* Amiodarone, Bretylium, Dofetilide, Ibutilide,
Dronedarone, Sotalol

44
Q

amiodarone moa

A

K+ channel blocker, also blocks Na+ and Ca2+ channels, b receptors

45
Q

amiodarone adrs

A

Effects seven organ systems: eyes, lungs, heart, thyroid, liver, GI, skin

46
Q

amiodarone interactions
* HR/BP changes with?
* Increased photosensitivity with?
* Many interactions secondary to?

A
  • Bradycardia and hypotension with vasoconstrictors and inhaled anesthetics
  • Increased photosensitivity with tetracycline
  • Many interactions secondary to CYP3A4 inhibition
47
Q

DatabaseClass III Antiarrhythmic medications
K+ channel blockers- Dental Implications

A
  • Monitor vital signs
  • Consider stress reduction protocol
  • Shorter appointments
  • Delay appointment if patient in distress
  • After supine positioning, have patient sit upright
    for at least 2 minutes before standing to avoid
    orthostatic hypotension
  • Use vasoconstrictors and inhaled anesthetics with caution
    * Avoid dental light in patient’s eye/offer dark glasses (Amiodarone)
48
Q

Class IV Antiarrhythmic medication
* Slow conduction in?
* HR?
* block what node?
* Shorten which phase of action potential
* Deceased what mechanisms of arrhythmias?

A

MOA: Block calcium from entering cell through voltage sensitive “slow” L-type channels
* Slow conduction in SA and AV node (non dihydropyridine)
* decrease heart rate
* AV block
* Shorten plateau (phase 2) of action potential
* Deceased delayed after-depolarization (DAD)
* decrease ectopic beats

49
Q

types of class 4 meds

selective for? names? common side effects?

A
50
Q

verapmil moa

A

myocardial ca channel blocker

51
Q

verapmil adrs

A

Constipation, dizziness, lightheadedness, hypotension, bradycardia, gingival enlargement

52
Q

verapmil interactions
*HR/BP changes with?
* Many interactions secondary to?

A
  • Bradycardia and hypotension with general and inhaled anesthetics
  • Many interactions secondary to CYP3A4 inhibition
53
Q

Class IV Antiarrhythmic medications
Dental Implications

A
  • Monitor vital signs
  • Consider stress reduction protocol
  • Shorter appointments
  • After supine positioning, have patient sit upright
    for at least 2 minutes before standing to avoid
    orthostatic hypotension
  • Use vasoconstrictors and inhaled anesthetics with caution
    * Place on frequent recall to monitor for gingival hyperplasia
54
Q

class V med
* Produced?
* Binds to? causing?
* Used to?
* Half-life is?
* Metabolized by?
* ADRs?
* dental?

A

adenosine
* 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 red blood cells and vascular endothelium
* ADRs= flushing, chest pain, shortness of breath
* No dental implication

55
Q

what incrases cardiac contractility?

A

more Ca

56
Q

Cardiac contractility terms
* LV End Diastolic Volume (EDV)
* Afterload
* LV End Systolic Volume (ESV)-
* Stroke Volume (SV):
* Ejection Fraction (EF):
* Cardiac Output (CO):

A
  • LV End Diastolic Volume (EDV)- amount of blood in left ventricle at the end of diastole= LV EDV = Preload
  • Afterload- pressure heart has to overcome to eject blood, Afterload =Systemic blood pressure
  • LV End Systolic Volume (ESV)- amount of blood in left ventricle at the endof systole
  • Stroke Volume (SV): SV= EDV – ESV (mL)
  • Ejection Fraction (EF): EF= SV/EDV X 100% (%)
  • Cardiac Output (CO): CO= HR X SV (mL/min
57
Q

frank starling curve

A

too much volume reduces the ability of the actin and myosin to interact

58
Q

Positive Inotropic medications

A
  • Cardiac glycosides: Digoxin- inhibits Na-K ATPase
  • DOBUTamine- b1 adrenocepter agonist
  • Milrinone- phosphodiesterase inhibitor
  • Levosimendan- calcium sensitizer
59
Q

digoxin mechanism

A

more Ca in increases contractility

60
Q

Digoxin

moa

A

inhibition of Na+-K+ ATPase/ vagal tone to heart

61
Q

digoxin adrs

A

(narrow therapeutic index medication):
* Nausea, vomiting, diarrhea
* Bradycardia/ heart block
* Visual disturbances (green-yellow halo)

62
Q

digoxin interactions
* Other drugs that cause?
* Increased levels with?
* Increase risk of arrhythmia with?

A
  • Other drugs that cause bradycardia or hypokalemia
  • Increased levels with macrolide antibiotic
  • Increase risk of arrhythmia with adrenergic agonists or succinylcholine
63
Q

Digoxin- Dental Implications

A
  • Monitor vital signs
    * Increased gag reflex may make dental procedures,
    such as taking radiographs or impressions difficult
  • After supine positioning, have patient sit upright
    for at least 2 minutes before standing to avoid
    orthostatic hypotension (bradycardia)
  • Use vasoconstrictors with caution (adrenergic stimulation)
    * Avoid dental light in patient’s eye/offer dark glasses
  • Stress reduction protoco
64
Q

dobutamine mechanism

A

increases cAMP leading to increased Ca

65
Q

dobutamine moa

A

B1 agonist

66
Q

dobutamine adrs
* heart rate and blood pressure?
* EKG?
* Chest?

A
  • Increased heart rate and blood pressure
  • Arrhythmias
  • Chest pain
67
Q

dobutamine interactions

A

none

68
Q

milrinone mechanism

A

prevents cAMP breakdown

69
Q

milrinone moa

A

PDE3 inhibitor= more cAMP

70
Q

Milrinone adrs
* cardiac rhythm?
* bp?
* Chest?

A
  • Arrhythmias (ectopic beats, NSVT, VT)
  • Hypotension
  • Chest pain
71
Q

milrinone interactions

A

none

72
Q

levosimendan mech

A
73
Q

levosimendan moa

A

Sensitize troponin to Ca2+ (inotropy) and KATP channel activation in smooth muscle (vasodilation)

74
Q

levosimendan adrs
* rhythm? less than what other drug?
* bp?
* Head?

A
  • Arrhythmias (ectopic beats, NSVT, VT)- supposedly less than DOBUTamine
  • Hypotension
  • Headache
75
Q

Myocardial Oxygen Supply is a function of:

A
  1. Arterial O2 content
    * decreased with anemia and hypoxia
  2. Coronary blood flow
    * decreased with atherosclerosis and vasospasm
  3. Myocardial Oxygen Supply is a function of Heart Rate
    Cardiac myocytes supplied with blood during diastole
    decreased Heart rate = decreased time in diastole
76
Q

Myocardial Oxygen Demand (MVO2) determinants

A
  1. Heart rate
  2. Myocardial contractility
  3. Myocardial wall stress
    * Preload
    * Afterload
77
Q

good surrgate marker for mvo2

A

Double Product= HR X SBP

78
Q

autonomics at the heart and their actions

A
79
Q

CAD forms

A
80
Q

spectrum of ACS

A
81
Q

pathphys of IHD/ACS

A
82
Q

Antianginal medications and their mech
* Organic nitrates-
* Calcium channel blockers-
* b-adrenocepter antagonists-
* Ranolazine-
* Ivabradine-

A
  • Organic nitrates- increase myocardial O2 supply
  • Calcium channel blockers- increase myocardial O2 supply and decrease O2 demand
  • b-adrenocepter antagonists- decrease myocardial O2 demand
  • Ranolazine- improves angina w/o changing BP or HR
  • Ivabradine- not approved for angina in U.S
83
Q

med effects on mvo2:
nitrates, b-blockers, nifedipine, vemapril, diltiazem

A
84
Q

nitrates MOA for angina

A
85
Q

forms of nitrate meds

A
  • Organic nitrates: Nitroglycerin and Isosorbide dinitrate/mononitrate
  • Sodium Nitroprusside (not metab by s-nitroso-thiol)
86
Q

major side effects of nitrates

A
  • Headache
  • Syncope/hypotension
  • Tachycardia
  • Tolerance (saturation of enzyme)- “nitrate holiday”
  • Methemoglobinemia
87
Q

when are nitrates contra

A

Contraindicated with PDE-5 Inhibitors

88
Q

available forms of nitrates

A
89
Q

Isosorbide Mononitrate moa

A

stim cGMP production (NO to GC)

90
Q

isosorbide mononitrate adrs

A
  • Headache (common), flushing, dizziness, postural hypotension
91
Q

isosorbide mono interactions
increased effects with?

A

Increased effects with other vasodilator type medications

92
Q

Organic nitrates- Dental Implications

A
  • Monitor vital signs
  • Stress reduction protocol
  • After supine positioning, have patient sit upright
    for at least 2 minutes before standing to avoid
    orthostatic hypotension
  • Use vasoconstrictors with caution
    * Sublingual nitroglycerin available for acute angina attack
93
Q

Calcium Channel Blockers for angina moa

A

Block calcium from entering cell through voltage
sensitive “slow” L-type channels

94
Q

ca channel block used for angina results
* conduction? which class?
* heart rate?
* block where
* state of arterioles?
* arterial pressure and wall tension
* myocardial contractility
* Increase flow where?

A
  • Slow conduction in SA and AV node (non dihydropyridine)
  • decreased heart rate
  • AV block
  • Vasodilatation of arterioles
  • Decrease arterial pressure and wall tension
  • Decrease myocardial contractility
  • Increase flow through areas of fixed coronary obstruction
95
Q

amlodipine moa

A

Dihydropyridine calcium channel blocker

96
Q

amlodipine adrs

A
  • Edema (common), dizziness, lightheadedness, hypotension, flushing, gingival enlargement (rare- but more common than non-DHP
97
Q

amlodipine interactions
* Hypotension with?
* NSAIDS?

A
  • Hypotension with sedatives, opioids, general and inhaled anesthetics
  • NSAIDS reduce blood pressure lowering effect
98
Q

Antianginal Medications
Calcium channel blockers- Dental Implication

A
  • Monitor vital signs
  • Consider stress reduction protocol
  • Shorter appointments
  • After supine positioning, have patient sit upright
    for at least 2 minutes before standing to avoid
    orthostatic hypotension
  • Use vasoconstrictors and inhaled anesthetics with caution
    * Place on frequent recall to monitor for gingival hyperplasia
99
Q

β-adrenoceptor blockers
* sympathetic stimulation to the heart?
* heart rate and automaticity?
* NE’s effects on Ca2+ channels?
* conduction through AV node? result?
* ischemia?
* myocardial oxygen demand?
* HR,contractility, SBP?

A
  • Block sympathetic stimulation to the heart
  • Decrease heart rate and Decrease automaticity
  • block NE’s effects on Ca2+ channels
  • Slow conduction through AV node (increase
    refractory period)
  • Prevent ischemia
  • Decrease myocardial oxygen demand
  • decrease HR,contractility, SBP
100
Q

preferred b blockers for angina

A

Prefer long-acting b1 selective agents for angina

101
Q

b blockers dental implications

A
  • Monitor vital signs (heart rate should be low)
  • Stress reduction protocol
  • Shorter appointments
  • After supine positioning, have patient sit upright for at least 2 minutes before standing to avoid orthostatic hypotension
  • Use vasoconstrictors and inhaled anesthetics with caution
  • Use lowest effective dose of local anesthetics
102
Q

Ranolazine mechanism

A
  • inhibits late inward sodium current (Ina) in ischemic myocardium = reduced myocardial wall tension and O2 consumption
  • At higher concentrations inhibits rapid delayed rectifier potassium current (Ikr) = prolonged action potential and QT interval
103
Q

ranolazine adrs

A
  • Bradycardia, hypotension, dizziness, QT prolongation, TdP, xerostomia
104
Q

ranolazine interactions:
Many due to?

A

Many due to CYP 450 3A4 metabolism

105
Q

ranolazine dental implications

A
  • Assess salivary flow as a factor in caries, periodontal disease, and candidiasis
  • Use vasoconstrictors and inhaled anesthetics with caution
106
Q

ca channel block used for angina results
* conduction? which class?
* heart rate?
* block where
* state of arterioles?
* arterial pressure and wall tension
* myocardial contractility
* Increase flow where?

A
  • Slow conduction in SA and AV node (non dihydropyridine)
  • decreased heart rate
  • AV block
  • Vasodilatation of arterioles
  • Decrease arterial pressure and wall tension
  • Decrease myocardial contractility
  • Increase flow through areas of fixed coronary obstruction
107
Q

amlodipine interactions
* Hypotension with?
* NSAIDS?

A
  • Hypotension with sedatives, opioids, general and inhaled anesthetics
  • NSAIDS reduce blood pressure lowering effect

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