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Arrhythmias Flashcards

1
Q

What is arrhytmia?

A
  • Abnormal heart rhythm, which can cause the heart to beat too slow (bradycardia) or too fast (tachycardia)
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2
Q

Sx and Diagnosis

A
  • Some might be silent and others can be shown with increased heartbeat “fluttering” in the chest or “skipping a beat”
  • Sx include; dizziness, SOB, fatigue
  • ECG is used to diagnose; Holter monitor is an ambulatory ECG device that records electrical activity of the heart within 24-48 hrs. It is used to detect intermittent arrhythmias
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3
Q

The conduction pathway

A
  1. SA node
  2. Right atrium and left atrium
  3. AV node
  4. Bundle of His
  5. Right bundle brunch for the right ventricle
  6. Left bundle brunch for the left ventricle
  7. Purkinje fibers
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4
Q

What is the heart’s natural pacemaker?

A
  • SA node
  • Arrhythmia is caused by a disruption somewhere in the conduction stystem:
    *The SA node can be firing at an abnormal rate or rhythm
    *Scar tissue from a prior heart attack can block/divert signal transmission
    *Another part of the heart may be acting as the pacemaker
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5
Q

What is cardiac action potential?

A
  • Electrical impulses in the cardiac conduction pathway
  • Action potential provide the electricity needed to power the heart
  • SA (pacemaker) cells have automacity, which means that they initiate their own action potential
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6
Q

Phase 0

A
  • A heartbeat is initiated when rapid ventricular depolirization occurs in response influx of Na; causing ventricular contraction (QRS)
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7
Q

Phase 1

A
  • Early rapid repolarization (Na channels close)
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8
Q

Phase 2

A
  • A plateau in response to an influx of Ca and efflux of K
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9
Q

Phase 3

A
  • Rapid ventricular repolarization occurs in response to an efflux of K; this causes ventricular relaxation (T wave)
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10
Q

Phase 4

A
  • Resting membrane potential is established; atrial depolarization occurs (P wave)
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11
Q

What QRS represents on the ECG?

A
  • Ventricular contraction
  • Phase 0
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12
Q

What P represents on the ECG?

A
  • Atrial contraction
  • Phase 4
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13
Q

What T represents on the ECG?

A
  • Ventricular relaxation
  • Phase 3
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14
Q

What causes arrhytmia?

A
  • Most common: MI
  • Electrolyte imbalances (K, Mg, Na, Ca)
  • Elevated sympathetic states (hyperthyroidism, infection)
  • Drugs (illicit drugs, antiarrhythmics, and drugs that prolong QT interval)
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15
Q

Supraventricular Arrhythmias

A
  • Afib is the mos common type of arrhythmia
  • Multiple waves of electrical impulses in the atria result in an irregular, rapid ventricular response
  • This makes heart unable to adequately contact which increases the risk of clot formation, leading to stroke
  • Anticoagulation is required
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16
Q

Ventricular Arrhythmias

A
  • Premature ventricular contractions (PVCs); ventricula tachycardia an ventriculat fibrillation
  • Reffered to a skipped heartbeat
  • It can be related to stress or caffeine
  • A series of pf PVCs in a row, resulting in a HR of greater than 100 BPM is known as ventricular tachycardia (VT)
  • Untreated VT can degenerate into ventricular fibrillation which is also a medical emergency
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17
Q

T/F: Prolongation of the QT interval is a risk factor for TdP and can cause sudden cardiac death

A

True

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18
Q

QT prolongation risk factors

A
  • Higher doses
  • Multiple QT-prolonging drugs taken at the same time
  • Reduced drug clearance due to renal disease, liver disease or DDIs
  • Electrolyte abnormalities, including hypokalemia and hypomagnesemia
  • Other cardiac conditions
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19
Q

Drugs that can increase or prolong the QT interval

A
  • Antiarrhythmics
    *class I and class III
  • Antibiotics
    *quinolones and macrolides
  • Azole antifungals
  • all except isavuconazonium
  • Antidepressants
    *tricyclics, SSRIs, SNRIs, mirtazapine and trazadone
  • Antiemetic drugs
    *5-HT3 receptor antagonists, droperidol and phenothiazines
  • Antipsychotics
    *chlorpromazine, clozapine, haloperidol, olanzapine, paliperidone, quetiapine, risperidone, thioridazine, ziprasidone
  • Donepezil, fingolimod, methadone, tacrolimus
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20
Q

T/F: Prior to starting non-life-threatening arrhythmia, electrolytes and toxicology screen should be checked

A

True

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21
Q

Vaughan Williams Classification

A
  • This splits drugs into categories based on their dominant electrophysiological effect
22
Q

Vaughan Williams Classification - Class 1

Hint: Double Quarter Pounder, Lettuce, Mayo, Fries Please! Because Dieting During Stress Is Always Very Difficult

A
  • Ia: Disopyramide, Quinidine, Procainamide
  • Ib: Lidocaine, Mexiletine
  • Ic: Flecainide, Propafenone
23
Q

Vaughan Williams Classification - Class II

Hint: Double Quarter Pounder, Lettuce, Mayo, Fries Please! Because Dieting During Stress Is Always Very Difficult

24
Q

Vaughan Williams Classification - Class III

Hint: Double Quarter Pounder, Lettuce, Mayo, Fries Please! Because Dieting During Stress Is Always Very Difficult

A
  • Dronedarone, Dofelitide, Sotalol, Ibulitide, Amiodarone
25
Q

Vaughan Williams Classification - Class IV

Hint: Double Quarter Pounder, Lettuce, Mayo, Fries Please! Because Dieting During Stress Is Always Very Difficult

A
  • Verapamil, Diltiazem
26
Q

Class I - Na-channel blockers

A
  • Proarrhythmic
  • Use caution with cardiac disease
27
Q

Class II - BBs

A
  • Used primarily to slow ventricular rate in Afib
28
Q

Class III - K-channel blockers

A
  • Amiodarone and dronedarone K, Ca, Na channels, and alpha- and beta- adrenergic receptors
  • Amiodarone is useful for Afib
  • Amiodarone and dofelitide are preferentially used for Afib in patients with HF
  • Sotalol blocks K channels and is a BB
29
Q

Class IV - CCBs, non-DHP

A
  • Used primarily to slow ventricular rate in Afib
  • Do not use verapamil or diltiazem in patients with HF and HFrEF
30
Q

Digoxin

A
  • Na-K-ATPase blocker
  • Supresses AV node conduction (decreases HR) by enhancing vagal tone and increases force of contraction (positive inotrope)
31
Q

Adenosine

A
  • Activates adenosine receptors to decrease AV node conduction
  • Used for paroxysmal supraventricular tachyarrhythmias (PSVTs)
32
Q

Rate Control

A
  • Goal resting HR is <80 BPM in symptomatic Afib
  • Lenient goal is <110 BPM
  • BBs and non-DHP CCBs are recommended for controlling ventricular rate in patients with Afib
  • Patients with HF wth HFrEF should not receive non-DHP CCB
33
Q

Rhythm Control

A
  • Consists of methods for conversion to NSR and maintenance of NSR
  • Anticoagulation should be started at least 3 weeks before cardioversion and continued for at least 4 weeeks after due to the risk of thromboembolism
34
Q

Rate Control vs Rhythm Control

A
  • Rate control
    *Patient remains in AFib and takes medications to control the ventricular rate (HR)
    *BBs or non-DHP CCBs are used (and sometimes digoxin)
  • Rhythm control
    *The goal is to restore and maintain NSR
    *Class Ia, Ic, or II antiarrhythmic drugs or electric cardioversion
    *If AFib is permanent, avoid thythm control strategy with antiarrhythmic drugs
35
Q

Stroke Prophylaxis

A
  • Clots can form when a patient is in AFib which can embolize (causing a stroke) when the patient returns to NSR
  • It is safer to remain in AFib with rate control than restore NSR
  • NOACs (apixaban, rivaroxaban) are preferred over warfarin for stroke prevention in non-valvular AFib
  • Warfarin is indicated for stroke prevention in patients with AFib and a mechanical heart valve
36
Q

When a rhythm control strategy is chosen, restoration and maintenance of NSR are not guaranteed. The decision for long term anticoagulation will depend on the patient’s ____ risk

37
Q

Amiodarone

A
  • Antiarrhythmic, DOC in HF
  • Nexterone, Pacerone
  • t1/2: 40-60 days
  • Decrease infusion rate or discontinue as needed for hypotension or bradycardia
  • IV: 0.22 micron filter; centeral line preferrable
  • Incompatible with heparin
  • Contains iodine
38
Q

Amiodarone - Safety/SEs/Monitoring

A
  • BW:
    *pulmonary toxicity, hepatotoxicity, proarrhythmic, must be hospitalized for IV loading (for life-threatening arryhtmias only)
  • CIs:
    *iodine hypersensitivity
  • Warnings:
    *hyper/hypothroidism - partially inhibits the conversion of T4 to T3, optic neuropathy, photosensitivity (slate-blue skin discoloration, neuropathy
  • SEs:
    *hypotension, bradycardia, corneal microdeposits, photosensitivity
  • Monitoring:
    *ECG, BP, HR, electrolytes
39
Q

Infusions >2 hours require a ___ container

Amiodarone

A

Non-PVC (e.g., polyolefin or glass)

40
Q

What container nexterone premixed IV bag comes with?

A
  • Non-PVC, non-DEHP GALAXY plastic container

Premixed IV bags has longer stability

41
Q

Amiodarone DDIs

A
  • It is an inhibitor of CYP450 2D6, 3A4, and P-gp
  • When starting amiodarone:
    *Lower digoxin by 50%
    *Lower warfarin by 30-50%
    *Do not exceed 20 mg/day of simvastatin or 40 mg/day of lovastatin
  • Additive effects may occur if used with drugs that lower HR, including;
    *Non-DHP CCB, digoxin, BBs, clonidine
  • Sofosbuvir can enhance bradycardic effect; do not use with amiodarone
42
Q

Non-DHP CCBs

A
  • Diltiazem (Cardizem, Tiazac)
  • Verapamil (Calan SR)
  • Warnings: HF (may worsen symptoms)
  • SEs: edema, arrhythmias, constipation (more with verapamil) gingival hyperplasia
43
Q

Non-DHP CCBs - DDIs

A
  • Additive effects can occur if used with other drugs that decrease HR; amiodarone, digoxin, BBs, clonidine
  • Non-DHP CCBs are CYP3A4 substrates so do not use with grapefruit
  • They are also P-gp substrates and CYP34 inhibitors; lower doses of simvastatin and lovastatin
44
Q

Digoxin

A
  • Digitek, Digox, Lanoxin
  • Dose: 0.125 - 0.25 mg PO daily
  • Theraoeutic range: 0.8 - 2 ng/mL for AFib
  • CrCl <50 ml/min: lower the dose or frequency
  • Lower dose bt 20-25% when converting from PO to IV
  • Initial s/sx of toxicity: N/V, loss of appetite and bradycardia
  • Severe s/sx of toxicity: blurred/double vision, greenish-yellow halos
  • Used in combination with BBs and non-DHP CCB
  • Antidote: DigiFab
  • Hypokalemia, hypomagnesemia, and hypercalcemia increase the risk of digoxin toxicity
45
Q

Digoxin - DDIs

A
  • Substrate of P-gp. Levels increase with inhibitors, including amiodarone, diltiazem, verapamil
  • Decrease digoxin dose by 50% with amiodarone
  • Additive effects occur with drugs that decrease HR, including amiodarone, non-DHP CCB, BBs and clonidine
46
Q

Class Ia Drugs

Disopyramide, Quinidine, Procainamide

A
  • Disopyramide
    *Warnings: proarrhythmic
    *SEs: anticholinergic effects
  • Quinidine
    *Take with food
    *Warnings: proarrhythmic, hemolysis risk (avoid in G6D deficiency), can cause positive coombs test
    *SEs: DILE, diarrhea (35%), stomach cramping (22%), cinchonism (tinnitus, hearing loss, blurred vision, headache, delirium)
  • Procainamide - injection
    *Active metabolite, N-acetyl procainamide (NAPA), is renally cleared
    *Therapeutic level: 4-10 mcg/mL
    *BW: agranulocytosis, antinuclear antibody (ANA), DILE
    *Warnings: proarrhythmic
    *Metabolism of procainamide to NAPA occurs by acetylation; slow acetylators are risk at toxicity
47
Q

Class Ib Drugs

Lidocaine

A
  • Useful for ventricular arrhythmias only
  • Lidocaine - injection
    *Used for refractory VT/cardiac arrest
48
Q

Class Ic Drugs

Flecainide, Propafenone

A
  • Flecainide
    *BW: proarrhythmic
    *CIs: HF, MI
  • Propafenone
    *CIs: HF, MI
    *Warnings: proarrhythmic
    *SEs: taste disturbance (metallic)
49
Q

Class III Drugs

Dronedarone

A
  • Dronedarone
    *BW: increased risk of death, stroke and HF in patients with decompensated HF or permanent AFib
    *CIs: hepatic failure, pulmonary disease (including pulmonary fibrosis)
    *SEs: QT prolongation
  • Not contain, iodine and has little effect on thyroid function
  • Avoid use with strong CYP34 inhibitors and inducers and drugs that prolong QT interval
50
Q

Class III Drugs

Sotalol

A
  • Non-selective BB
  • CrCl <60 mL/min
  • BW: adjust dosing interval based on CrCl to derease proarrhythmia, QT prolongation is related to the concentration
51
Q

Class III Drugs

Ibutilide, Dofetilide

A
  • Ibutilide
    *Injection
    *Correct hypokalemia and hypomagnesemia
  • Dofetilide
    *BW: initiated with continuous ECG monitoring and assess CrCl for a minimum of 3 days; proarrhythmic
    *DOC in HF
52
Q

Adenosine

A
  • Injection
  • t1/2: less than 10 sec
  • Used in PSVTs

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