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Cardiovascular > Arrhythmia management > Flashcards

Arrhythmia management Flashcards

1
Q

What are some factors that can lead to AFib?

A

-electrolyte derangements (hypokalemia hypomagnesemia)
-acidosis
-fever
-sepsis
-volume overload
-thyrotoxicosis
-withdrawal

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2
Q

What class of antiarrhythmic medication can be used for AFib rate control?

A

-class 2 (cardiac beta blocker, metoprolol)
-class 4 (L-type Ca blocker, diltiazem)

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3
Q

What class of antiarrhythmic medication can be used to convert out of AFib?

A

class 3 (K channel blocker, amiodarone)

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4
Q

What antiarrhythmic drug can be used to help distinguish between SVT and Vtach?

A

adenosine- temporarily blocks AV node so slows SVTs but doesn’t effect VTach

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5
Q

What clinical factors can lead to VT?

A

-hypokalemia
-acidosis
-catecholamine surge
-thyrotoxicosis
-ischemia

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6
Q

What is usually the cause of polymorphic VT?

A

-myocardial ischemia

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7
Q

For the rare patient with stable vitals in VT what antiarrhythmic drugs can be used?

A

-class 1 (fast Na channel blocker, procainamide)
-class 3 (K channel blocker, amiodarone)

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8
Q

Which arrhythmia is the leading cause of sudden cardiac arrest?

A

VF

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9
Q

Haloperidol is associated with which dysrhythmia?

A

VT

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10
Q

Lidocaine and other class 1b antiarrhythmics are associated with which dysrhythmia?

A

VT

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11
Q

Dobutamine is associated with which dysrhythmias?

A

arterial and ventricular tachycardias

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12
Q

Fluoroquinolones are associated with which dysrhythmia?

A

Torsades de pointes

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13
Q

Micafungin is associated with which dysrhythmias?

A

arterial and ventricular tachycardia

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14
Q

Ondansetron is associated with which dysrhythmia?

A

Torsades de pointes

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15
Q

What are some clinical factors that can lead to new first degree AV block?

A

-hypokalemia
-myocardial ischemia
-myocarditis
-medication side effects

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16
Q

Which type of AV block is at risk for progression and cardiac death?

A

Mobitz 2- nonconducted p-waves at regular intervals

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17
Q

What percent of annual ACS cases are STEMIs vs. NSTEMI?

A

30% STEMI
70% NSTEMI

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18
Q

What is the 90-day mortality of a patient who had preoperative MI?

A

30%

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19
Q

What ECG changes are concerning for STEMI?

A

-ST elevation in 2 contiguous leads
-new LBBB
-anterior ST depression suggesting a posterior MI

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20
Q

What ECG changes suggest NSTEMI?

A

new ST depression or a horizontal or downsloping ST

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21
Q

What ECG changes can be suggestive of a MI or a PE?

A

transient ST changes (< 0.5mm) and/or T wave inversion (> 2mm)

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22
Q

What biomarker is the most sensitive and specific for ACS?

A

troponins

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23
Q

What can cause a chronic troponin elevation?

A

LV hypertrophy and ventricular dilation

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24
Q

What biomarker should be used to detect new or worsening heart failure?

A

BNP

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25
Q

What is the goal time period from medical contact to cath lab balloon time for STEMI patients?

A

90 min

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26
Q

What are recommended initial treatments for STEMIs?

A

-ASA 162mg or 325mg
-unfractionated heparin or bivalirudin with ACT 200-250s

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27
Q

What is the MOA of clopidogrel or ticagrelor?

A

P2Y12 inhibitor

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28
Q

Clopidogrel or ticagrelor therapy should be held until what is determined in the cath lab?

A

coronary anatomy
-if anatomy is not amenable to PCI an emergent CABG is needed and prior P2Y12 inhibitor administration could lead to significant hemorrhage

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29
Q

Overall basic treatment for NSTEMI patients?

A

-continuous cardiac monitoring
-antianginal
-antiplatelet
-anticoagulation

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30
Q

What antiplatelet therapy should be started for NSTEMIs?

A

start ASAP
-nonenteric coated chewable 162-325mg followed by maintenance of 81-325mg
-if can’t take ASA us clopidogrel (only 300mg if unsure if pt will need CABG)
-for 12 months post NSTEMI everyone who can should get ASA and P2Y12 inhibitor

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31
Q

What anticoagulation therapy should be started for NSTEMIs?

A

-enoxaparin
-bivalirudin
-fondaparinux
-unfractionated heparin

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32
Q

What antianginal therapy should be started for NSTEMIs?

A

-up to 3 doses of sublingual nitroglycerin
-after that switch to IV is still having CP

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33
Q

How long after phosphodiesterase inhibitors before nitrates can be given?

A

-sildenafil and varsenafil = 24h
-tadalafil = 48h

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34
Q

Beta-blocker therapy should be started in all NSTEMI patients except for those with what?

A

-heart failure
-low CO state
-increased risk for cardiogenic shock (>70yo HR >110 SBP <120)
-PR interval > 0.24s
-2nd or 3rd degree heart block without a pacemaker
-active asthma or reactive airway disease

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35
Q

Where is atrial activity beat seen on EKG?

A

P waves in inferior leads (II, III, aVF)

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36
Q

A QRS complex that follows a p-wave in less than what amount of time means they’re not associated?

A

< 0.1s

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37
Q

Each small box on an EKG is how much time?

A

0.04s

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38
Q

What can provoke or exacerbate arrhythmias?

A

-eletrolye disturbances
-mechanical irritation of the heart
-drugs
-ischemia

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39
Q

What lab abnormalities can aggravate arrhythmic tendencies?

A

-hypo/hyperkalemia
-hypomagnesium
-alkalosis
-anemia
-hypoxemia

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40
Q

What stimuli can provoke arrhythmias that cease once the stimuli is removed?

A

-intracardiac catheters
-pacemaker malfunctions
-digitalis
-theophylline
-sympathomimetic agents (catecholamines, cocaine)

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41
Q

What drugs can be given in a HD stable patient with a new wide-complex tachycardia of unknown ventricular or atrial origin?

A

-lidocaine: if it fails to respond this supports a SVT rhythm
-procainamide or amiodarone: will help both SVT and VT but won’t help diagnosis which one
-adenosine: transiently blocks AV node so treats SVT but not VT

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42
Q

What drugs should not be given in a HD stable patient with a new wide-complex tachycardia of unknown ventricular or atrial origin?

A

Verapamil or diltiazem
-cardiodepressants and vasodilating so lower BP
-can accelerate some SVTs

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43
Q

What is the main treatment of sinus tach?

A

Treat the underlying cause

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44
Q

Why should beta-blockers be used with caution in patients with obstructive lung disease?

A

Can precipitate bronchospasm

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45
Q

Which patient populations should beta-blockers be used with caution?

A

-hypotensive
-acute infarction
-chronic CHF

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46
Q

What is the response of VT to vagal manuevers?

A

Unresponsive

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47
Q

What is the response of AFib to vagal manuevers?

A

Transient slowing of ventricular rate

48
Q

What is the response of AFlutter to vagal manuevers?

A

Unmasking of underlying flutter waves

49
Q

What disease processes is multifocal atrial tachycardia most often associated with?

A

-COPD
-metabolic derangements

50
Q

In patients with COPD what are risk factors to developing multifocal atrial tachycardia?

A

-hypoxemia
-hypercapnia
-acidosis
-alkalosis
-pulm HTN
-beta blockers

51
Q

What is the prevalence of AFib in >70yo?

A

5%

52
Q

At what rate does the atria depolarize in AFib? The AV node?

A

-up to 400/min
-rarely >180-200 per min

53
Q

What are 3 prominent risks due to AFib?

A

-hypoperfusion (rapid ventricular rate)
-embolism (clot formation in non-contractile atrium)
-cardiomyopathy (chronic tachycardia)

54
Q

In AFib what does ventricular rates >200bpm suggest? If rate is <60bpm?

A

-accelerated conduction due to vagolytic meds (type 1a antiarrhythmic) or accelerated conduction pathway
-drug effect (digitalis beta-blocker Ca-channel blocker) or conduction system disease

55
Q

An atrial diameter above what signifies conversion from AFib to NSR is unlikely?

A

4cm

56
Q

For HD stable AFib who need rate control what is the preferred choice for good ventricular function? Impaired ventricular function?

A

-Ca channel blockers or beta-blockers
-digoxin

57
Q

What is the best medication to use for rate control and rhythm conversion in AFib with a sudpected nodal bypass tract?

A

Amiodarone

58
Q

What medications can be used for AFib rhythm conversion?

A

-amiodarone: highly effective but 25% get hypotension and chemical phlebitis is common; don’t give with digoxin (can get significant bradycardia)
-procainamide: effective in 40% poor long term tolerance
-ibutilide: only parental can can as proarrhythmic

59
Q

What is the annual stroke rate in patients with AFib but without mitral valve disease or HF? With those comorbidities?

A

-1%
-6%

60
Q

Where does depolarization usually occur in Aflutter?

A

Low in the right atrium

61
Q

What are frequent causes of Aflutter?

A

-PNA
-exacerbation of COPD
-post thoracic surgery

62
Q

What are common atrial rates in Aflutter? Ventricular rate?

A

-260-340bpm
-½ to ¼ of the atrial rate

63
Q

What is the most effective way to get rhythm conversion in Aflutter?

A

Electric cardioversion

64
Q

What does sinus bradycardia in a patient with recent posterior or inferior MI signify?

A

Ischemia of nodal tissue

65
Q

When treating sinus bradycardia what medications can be used and their doses?

A

-atropine 0.5 - 1mg q3 - 5min
-dopamine 5 - 20mcg/kg/min
-epinephrine 2 - 10mcg/min
-isoproterenol 2 - 10mcg/min

66
Q

What can a new 1st degree AV block signify?

A

Drug toxicity or progressive conduction system disease

67
Q

When is pacing indicated for 1st degree AVB?

A

When accompanied by RBBB and L anterior fasicular block in the setting of myocardial ischemia or infection

68
Q

What is characteristic of a mobitz 1 AVB?

A

Weneckebach
-progressive prolongation of PR interval with eventual failure to transmit an atrial impulse
-RR intervals progressively shorten
-often accompanies inferior MI

69
Q

What is frequently the cause of mobitz 1?

A

-digitalis toxicity
-intrinsic heart disease

70
Q

What is the significance of mobitz 1 after an anterior infarct?

A

Suggests extensive myocardial damage and a guarded prognosis

71
Q

What is characteristic of a mobitz 2 AVB?

A

-constant PR intervals but inconsistent conduction of atrial depolarization
-originates below the level of the AV node in the His-Purkinje system
-often progresses to symptomatic type 3 AVB
-generally requires transvenous pacing

72
Q

What are potential causes of 3rd degree AVB?

A

-degenerative myocardial disease
-myocarditis
-MI
-infiltration of conducting system
-toxic concentration of digitalis

73
Q

What are the treatments for symptomatic AFib or AFlutter?

A

-cardioversion
-amiodarone
-digoxin
-esmolol
-diltiazem
-procainamide
-prevent recurrence with Ca channel blockers or beta blockers

74
Q

What are the treatments for symptomatic bradycardia?

A

-correct underlying cause
-atropine/oxygen
-isoproterenol/pacing
-catecholamine infusion

75
Q

What are the treatments for symptomatic PVCs?

A

-lidocaine
-procainamide

76
Q

What are the treatments for monomorphic VT?

A

-cardioversion
-lidocaine
-procainamide
-sotalol
-amiodarone

77
Q

What are the treatments for polymorphic VT?

A

-cardioversion
-isoproterenol
-Mg
-pacing

78
Q

What are the treatments for VF?

A

-cardioversion
-lidocaine

79
Q

What is the MOA and examples of class 1a antiarrhythmic drugs?

A

Depresses conduction and accelerates repolarization
-procainamide
-quinidine
-disopyramide

80
Q

What is the MOA and examples of class 1b antiarrhythmic drugs?

A

Depresses conduction and accelerates repolarization
-lidocaine
-phenytoin
-tocainide

81
Q

What is the MOA and examples of class 1c antiarrhythmic drugs?

A

Markedly reduces conduction
-encainide
-flecainide

82
Q

What is the MOA and examples of class 2 antiarrhythmic drugs?

A

Beta blockers
-metoprolol
-propranolol
-esmolol

83
Q

What is the MOA and examples of class 3 antiarrhythmic drugs?

A

Prolongs repolarization
-amiodarone
-sotalol
-bretylium

84
Q

What is the MOA and examples of class 4 antiarrhythmic drugs?

A

Slow Ca channel blockers, decreases automaticity, blocks nodal conduction
-verapamil
-diltiazem
-nicardipine

85
Q

What is the cardiac arrest, critical ventricular arrhythmia, and less critical ventricular arrhythmia dosing of amiodarone?

A

-300mg IV push
-150mg IV over 15min
-1mg/min loading dose over 6hrs then 0.5mg/min for another 540mg

86
Q

What are the most common side effects of amiodarone? The less common more concerning SE?

A

-GI and neurological
-pulmonary toxicity (esp. with preexisting lung fibrosis), liver injury, thyroid dysfunction

87
Q

Amiodarone can raise plasma levels of which drugs?

A

-digoxin
-quinidine
-procainamide
-flecainide
-potentiates anticoagulant effect of warfarin

88
Q

What is the MOA of propranolol?

A

-nonspecific beta-blocker
-negative inotrope and chronotrope
-decreases rate of SA node and conduction velocity

89
Q

Which are the cardioselective beta-blockers?

A

-metoprolol
-carvedilol

90
Q

Which beta-blocker ultrashort acting making it good for SVT management without depressing myocardial function?

A

Esmolol

91
Q

What are Ca channel blockers good for?

A

-converting AVNRT and AVRT to NSR
-slows ventricular response of AFib and flutter

92
Q

What are two of the more serious complications of verapamil?

A

-can cause high degree AVB or asystole
-decreases contractility and vasodilation to point of hypotension (esp in elderly and volume deplete)

93
Q

What can be given prior to verapamil for to avoid extreme hypertension?

A

IV Ca gluconate

94
Q

What is the major use of digitalis?

A

Slow AV conduction in AFib and flutter

95
Q

What is the typical Afib/flutter dosing of digitalis?

A

0.125 - 0.25mg IV q4-6hr

96
Q

What does lidocaine do as type 1b antiarrhythmic?

A

Suppresses ventricular irritability but little effect on SVT

97
Q

In what scenario is lidocaine good for?

A

Myocardial ischemia with VT

98
Q

What attribute of lidocaine causes it to require several loading doses to achieve and maintain effect?

A

It distributes into multiple compartments
-also means it does not need a taper to stop

99
Q

What drug class can be exacerbated by lidocaine?

A

Neuromuscular effects of paralytics

100
Q

What can procainamide be used for?

A

SVT and ventricular arrhythmias
-type 1a antiarrhythmic

101
Q

What consideration must be made when procainamide is to be used in patient with AFib/flutter?

A

Controlling conduction rate with beta-blockers Ca channel blockers or digitalis
-alone it can accelerate ventricular rate

102
Q

What is the dosing of procainamide?

A

-loading 100mg q5min for total of 1gm
-infusion 2 - 6mg/min

103
Q

What arrhythmia can procainamide precipitate?

A

Torsades de pointes

104
Q

What syndrome can be induced in prolonged periods of procainamide use?

A

Lupus-like syndrome
-in as many as 20%
-50% develop positive ANA

105
Q

Which analgesic drug class is contraindicated in pts w/ a STEMI due to increased mortality?

A

NSAIDS

106
Q

How long after onset of symptoms does it take for the majority of infarct to occur in a MI? For the infarct to be complete?

A

-4hrs
-6hrs

107
Q

What is the medication recommendation for pts within 1yr of coronary stent placement who need urgent noncardiac surgery on ASA and plavix?

A

stop plavix for 5 days but continue ASA

108
Q

At what CHA2DS2-VASc does a pt need perioperative anticoagulation bridging?

A

4 or greater

109
Q

What are the components of CHA2DS2-VASc?

A

-CHF
-HTN
-age >75 (2 points)
-DM
-stroke (CVA/TIA/TE)
-vascular disease
-age 65-74 (1 point)
-sex category (female gets 1 point)

110
Q

What is the most common location of a spontaneous ectopic foci in paroxysmal AFib?

A

in nearly 90% of pts the point of origin is in the pulmonary veins

111
Q

What type of MI would ST elevations in leads 2, 3, aVF be concerning for?

A

inferior STEMI

112
Q

What are the components of the TIMI (thrombolysis in myocardial infarction) score for periop risk stratification?

A

-age >/= 65
->/= 3 risk factor for CAD
-aspirin use in last 7 days
-recent severe symptoms of angina (>/= 2 in last 24hrs)
-elevated cardiac markers
-ST deviation >/= 5mm
-prior coronary artery stenosis 50%

-measures the risk of death, new/recurrent MI, or need for urgent revascularization w/in 14 days
-each component is worth 1 point, >/= 5 is high risk

113
Q

For pts w/ drug eluding coronary stents what is the ideal time frame for them to use dual antiplatelet therapy?

A

1 year
-studies show that for at least 6 months they have an increased risk of stent thrombosis
-stop clopidogrel (or other P2Y12 inhibitor) and continue ASA

114
Q

How long should surgery be delayed after the placement of coronary stents?

A

-30 days after bare metal stent
-6 months after drug eluding stent

115
Q

What medication should be used to treat Wolfe-Parkinson-White? Which should be avoided?

A

-procainamide (increases refractory period and decreases accessory pathway conduction)

-agents that slow AV node (adenosine, amiodarone, digoxin, verapamil) cause an increased ventricular rate d/t more atrial activity passing through the accessory pathway –> VT

Cardiovascular (6 decks)

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