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heart lecture Flashcards

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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
disopyramide moa
moderate na block
26
dispyramide interactions 1. Other meds with similar effects? 1. Increased risk of QT prolongation with?
1. Other anticholinergic medications (i.e. glycopyrrolate or atropine) 1. Increased risk of QT prolongation with macrolide antibiotics (i.e. erythromycin or clarithromycin
27
disopyramide adrs
Anticholinergic-Dry mouth, constipation, urinary hesitancy Cardiac- QT prolongation
28
mexiltine moa
weak na block
29
mexilitine adrs
* GI- nausea, vomiting, heartburn * Neuro- dizziness, light-headedness, tremors, convulsion (toxic)
30
mexilitne interactions vasoconstrictor?
* Use the lowest effective dose of local vasoconstrictor
31
propafenone moa
strong na block
32
propafenone adrs
* GI: nausea, vomiting, **altered taste**, constipation * Neuro- dizziness
33
propafenone interaction * vasoconstrictors?
* Use the lowest effective dose of local vasoconstrictor
34
Class I Antiarrhythmic medications Na+ Channel blockers-Dental Implications
* 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
35
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?
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**
36
B1 selective blockers we may use at heart
* Betaxolol * Acebutelol * Esmolol * Atenolol * Metoprolol
37
metoprolol moa
B1 selective blocke fr
38
metoprolol adrs
hypotension, bradycardia, fatigue, sexual dysfunction, drowsiness
39
metoprolol interactions * fentanyl and inhaled anesthetics * Decreases the effect of? * NSAIDS?
* Increased hypotension with fentanyl and inhaled anesthetics * Decreased effect of vasoconstrictors (i.e. epinephrine) * NSAIDS may reduce the efficacy (> 3 weeks of treatment)
40
Class II Antiarrhythmic medications β-adrenoceptor blockers- Dental Implication
* 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
41
Class III Antiarrhythmic medication MOA work on what phase cardiac potential? risk?
* K+ channel blockers * Delay repolarization (prolong action potential) * QT prolongation→→→ risk of TdP
42
class 3 agents | activity of each?
* 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)
43
class 3 mnemonic
“A Big Dog Is Darn Scary” * Amiodarone, Bretylium, Dofetilide, Ibutilide, Dronedarone, Sotalol
44
amiodarone moa
K+ channel blocker, also blocks Na+ and Ca2+ channels, b receptors
45
amiodarone adrs
Effects seven organ systems: eyes, lungs, heart, thyroid, liver, GI, skin
46
amiodarone interactions * HR/BP changes with? * Increased photosensitivity with? * Many interactions secondary to?
* Bradycardia and hypotension with vasoconstrictors and inhaled anesthetics * Increased photosensitivity with tetracycline * Many interactions secondary to CYP3A4 inhibition
47
DatabaseClass III Antiarrhythmic medications K+ channel blockers- Dental Implications
* 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
Class IV Antiarrhythmic medication * Slow conduction in? * HR? * block what node? * Shorten which phase of action potential * Deceased what mechanisms of arrhythmias?
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
types of class 4 meds | selective for? names? common side effects?
50
verapmil moa
myocardial ca channel blocker
51
verapmil adrs
Constipation, dizziness, lightheadedness, hypotension, bradycardia, gingival enlargement
52
verapmil interactions *HR/BP changes with? * Many interactions secondary to?
* Bradycardia and hypotension with general and inhaled anesthetics * Many interactions secondary to CYP3A4 inhibition
53
Class IV Antiarrhythmic medications Dental Implications
* 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
class V med * Produced? * Binds to? causing? * Used to? * Half-life is? * Metabolized by? * ADRs? * dental?
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
what incrases cardiac contractility?
more Ca
56
Cardiac contractility terms * LV End Diastolic Volume (EDV) * Afterload * LV End Systolic Volume (ESV)- * Stroke Volume (SV): * Ejection Fraction (EF): * Cardiac Output (CO):
* 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
frank starling curve
too much volume reduces the ability of the actin and myosin to interact
58
Positive Inotropic medications
* Cardiac glycosides: Digoxin- inhibits Na-K ATPase * DOBUTamine- b1 adrenocepter agonist * Milrinone- phosphodiesterase inhibitor * Levosimendan- calcium sensitizer
59
digoxin mechanism
more Ca in increases contractility
60
Digoxin | moa
inhibition of Na+-K+ ATPase/ vagal tone to heart
61
digoxin adrs
(narrow therapeutic index medication): * Nausea, vomiting, diarrhea * Bradycardia/ heart block * Visual disturbances (green-yellow halo)
62
digoxin interactions * Other drugs that cause? * Increased levels with? * Increase risk of arrhythmia with?
* Other drugs that cause bradycardia or hypokalemia * Increased levels with macrolide antibiotic * Increase risk of arrhythmia with adrenergic agonists or succinylcholine
63
Digoxin- Dental Implications
* 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
dobutamine mechanism
increases cAMP leading to increased Ca
65
dobutamine moa
B1 agonist
66
dobutamine adrs * heart rate and blood pressure? * EKG? * Chest?
* Increased heart rate and blood pressure * Arrhythmias * Chest pain
67
dobutamine interactions
none
68
milrinone mechanism
prevents cAMP breakdown
69
milrinone moa
PDE3 inhibitor= more cAMP
70
Milrinone adrs * cardiac rhythm? * bp? * Chest?
* Arrhythmias (ectopic beats, NSVT, VT) * Hypotension * Chest pain
71
milrinone interactions
none
72
levosimendan mech
73
levosimendan moa
Sensitize troponin to Ca2+ (inotropy) and KATP channel activation in smooth muscle (vasodilation)
74
levosimendan adrs * rhythm? less than what other drug? * bp? * Head?
* Arrhythmias (ectopic beats, NSVT, VT)- supposedly less than DOBUTamine * Hypotension * Headache
75
Myocardial Oxygen Supply is a function of:
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
Myocardial Oxygen Demand (MVO2) determinants
1. Heart rate 2. Myocardial contractility 3. Myocardial wall stress * Preload * Afterload
77
good surrgate marker for mvo2
Double Product= HR X SBP
78
autonomics at the heart and their actions
79
CAD forms
80
spectrum of ACS
81
pathphys of IHD/ACS
82
Antianginal medications and their mech * Organic nitrates- * Calcium channel blockers- * b-adrenocepter antagonists- * Ranolazine- * Ivabradine-
* 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
med effects on mvo2: nitrates, b-blockers, nifedipine, vemapril, diltiazem
84
nitrates MOA for angina
85
forms of nitrate meds
* Organic nitrates: Nitroglycerin and Isosorbide dinitrate/mononitrate * Sodium Nitroprusside (not metab by s-nitroso-thiol)
86
major side effects of nitrates
* Headache * Syncope/hypotension * Tachycardia * Tolerance (saturation of enzyme)- "nitrate holiday" * Methemoglobinemia
87
when are nitrates contra
Contraindicated with PDE-5 Inhibitors
88
available forms of nitrates
89
Isosorbide Mononitrate moa
stim cGMP production (NO to GC)
90
isosorbide mononitrate adrs
* Headache (common), flushing, dizziness, postural hypotension
91
isosorbide mono interactions increased effects with?
Increased effects with other vasodilator type medications
92
Organic nitrates- Dental Implications
* 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
Calcium Channel Blockers for angina moa
Block calcium from entering cell through voltage sensitive “slow” L-type channels
94
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?
* 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
amlodipine moa
Dihydropyridine calcium channel blocker
96
amlodipine adrs
* Edema (common), dizziness, lightheadedness, hypotension, flushing, gingival enlargement (rare- but more common than non-DHP
97
amlodipine interactions * Hypotension with? * NSAIDS?
* Hypotension with sedatives, opioids, general and inhaled anesthetics * NSAIDS reduce blood pressure lowering effect
98
Antianginal Medications Calcium channel blockers- Dental Implication
* 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
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?
* 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
preferred b blockers for angina
Prefer long-acting b1 selective agents for angina
101
b blockers dental implications
* 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
Ranolazine mechanism
* 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
ranolazine adrs
* Bradycardia, hypotension, dizziness, QT prolongation, TdP, **xerostomia**
104
ranolazine interactions: Many due to?
Many due to CYP 450 3A4 metabolism
105
ranolazine dental implications
* Assess salivary flow as a factor in caries, periodontal disease, and candidiasis * Use vasoconstrictors and inhaled anesthetics with caution
106
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?
* 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
amlodipine interactions * Hypotension with? * NSAIDS?
* Hypotension with sedatives, opioids, general and inhaled anesthetics * NSAIDS reduce blood pressure lowering effect

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