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NAPLEX Review > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

What is the definition of conduction?

A

The term conduction means to transmit electrical charges (or heat) through a substance

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2
Q

What is the cardiac conduction system?

A

The cardiac conduction system is the electrical signaling system that causes the atria and ventricles to contract, which pushes the blood forward

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3
Q

What is the direction of blood flow in the body?

A

Bloods flows in one direction in the body, through the heart chambers (from the atria to the ventricles), then to the lungs (to pick up oxygen) or to the body (to provide oxygen and nutrients)

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4
Q

How are the “lub-dub” sounds created in the heart?

A

The “lub-dub” sounds heard through ausculation are made by the closing of teh heart valves that occur in sequence with each heartbeat

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5
Q

Describe the S1 and S2 signals.

A

The first heart sound (S1) signals the beginning of ventricular systole and the second heart sound (S2) signals the end of ventricular systole

  • Sounds other than S1 and S2 are abnormal
  • Systole means to contract
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6
Q

What are the cause of murmurs?

A

Murmurs are caused by turbulent blood flow or regurgitation (e.g. blood flowing the wrong direction)

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7
Q

What is an arrhythmia?

A

An arrhythmia is an abnormal heart rhythm, which can cause the heart to beat too slow (bradycardia) or too fast (tachycardia)

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8
Q

What can possibly cause an arrhythmia?

A

Any change from the normals sequence of electrical impulses can cause an arrhythmia. When the electrical impulses are too fast, too slow or erratic, the heart cannot pump blood efficiently, and symptoms can develop

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9
Q

What are some symptoms of arrhythmias?

A
  • Some arrhythmias are silent and might only be detected during a medical exam while others, patients can feel that the heart is beating very fast, “fluttering” in their chest or “skipping a beat”
  • Symptoms can include dizziness, shortness of breath, fatigue, lightheadedness and chest pain
  • In severe cases, arrhythmias can lead to syncope (loss of consciousness due to decreased cardiac output), heart failure or death
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10
Q

What is an ECG and how does it work?

A

An electrocardiogram (ECG) is used to diagnose arrhythmias. An ECG machine records the electrical activity of the heart using electrodes placed on the skin

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11
Q

What is a Holter monitor?

A

A Holter monitor is an ambulatory ECG device that records the electrical activity of the heart for 24-48 hours and it is used to detect arrhythmias that are intermittent

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12
Q

What is a Zio patch?

A

Zio is a wireless adhesive patch placed directly on the chest and worn for up to 14 days

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13
Q

Where does the normal sinus rhythm originate?

A

NSR originates in the sinoatrial (SA or sinus) node

*SA node is the heart’s natural pacemaker where the electrical signal for a heartbeat begins, and the frequency of the signals determines the pace or heart rate

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14
Q

What is considered normal heart rate?

A

A normal heart rate is 60 to 100 BPM

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15
Q

What does the cardiac conduction pathway consist of and what are the main components?

A

The cardiac conduction pathway consists of a group of specialized cardiac cells (myocytes) that send electrical impulses. The main components include the SA node, AV node, bundle of His, bundle branches and Purkinje fibers

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16
Q

Describe the signaling system of the cardiac conduction system.

A

1) The electrical impulse begins in the SA node, which is a cluster of cells located at the junction of the superior vena cava and the right atrium
2) The impulse then travels from the SA node to the right and left atria, which causes the atria to contract
3) When the signal reaches the atrioventricular (AV) node, electrical conduction slows down
4) The impulses continues through the bundle of His and into the ventricles
5) The bundle of His divides into the right bundle branch for the right ventricle and the left bundle branch for the left ventricle
6) The signal continues to spread through the ventricles via the Purkinje fibers, which causes the ventricles to contract

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17
Q

Where are possible places that there could be a disruption somewhere in the conduction system?

A
  • The SA node can be firing at an abnormal rate or rhythm
  • Scar tissue from a prior heart attack can block and divert signal transmission
  • Another part of the heart may be acting as the pacemaker
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18
Q

What is the cardiac action potential?

A

Cardiac action potential refers to the movement of ions through channels in the myocytes that cause the electrical impulses in the cardiac conduction pathway. The action potentials provide the electricity needed to power the heart

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19
Q

What does it mean when it is said that the SA (pacemaker) cells have automaticity?

A

Unlike other myocytes, the pacemaker cells initiate their own action potential (the cells spontaneously depolarize and do not require external stimulation)

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20
Q

When is the action potential of ventricular myocyte triggered?

A

The action potential of a ventricular myocyte is triggered when a threshold voltage is reached

*This occurs in 5 phases

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21
Q

Describe the different phases of the action potential of a ventricular myocyte?

A
  • Phase 0: a heartbeat initiated when rapid ventricular depolarization occurs in response to an influx of Na (causes ventricular contraction represented by the QRS complex on the ECG)
  • Phase 1: early rapid repolarization (Na channels close)
  • Phase 2: a plateau in response to an influx of Ca and efflux of K
  • Phase 3: rapid ventricular repolarization occurs in response to an efflux of K (causes ventricular relaxation represented by the T wave on the ECG)
  • Phase 4: resting membrane potential is established (atrial depolarization occurs (represented by the P wave on the ECG)
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22
Q

What is the most common causes of arrhythmias as well as other causes?

A

Abnormalities of the heart or its conduction system can alter the cardiac action potential and lead to arrhythmias. The most common cause of arrhythmias is myocardial ischemia or infarction. Other conditions resulting in damage to cardiac tissue can cause arrhythmias, including heart valve disorders, hypertension and heart failure

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23
Q

What are some non-cardiac conditions that can trigger or predispose a patient to an arrhythmia?

A

Electrolyte imbalances (especially potassium, magnesium, sodium and calcium), elevated sympathetic states (e.g. hyperthyroidism, infection) and drugs (including illiciting drugs, antiarrhythmics and drugs that prolong the QT interval)

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24
Q

What are the two broad categories of arrhythmias?

A

Supraventricular (originating above the AV node) and ventricular (originating below the AV node)

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25
Q

What are some examples of supraventricular arrhythmias?

A

Sinus tachycardia, atrial fibrillation, atrial flutter, atrial tachycardia, and supraventricular reentrant tachycardias (formerly known as paroxysmal supraventricular tachycardias or PSVTs)

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26
Q

What is atrial fibrillation?

A

Atrial fibrillation (Afib) is the most common type of arrhythmia. It occurs when multiple waves of electrical impulses in the atria result in an irregular (and usually rapid) ventricular response

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27
Q

What are the possible consequences of atrial fibrillation?

A

The rapid ventricular rate can decrease cardiac output (because the ventricles do not have time to fill), which can lead to hypotension and worsen underlying ischemia and heart failure. Also, the atria cannot adequately contract, so B=blood becomes stagnant in the atria, which increases the risk of clot formation. A clot can embolize (break off and travel) to an artery in the brain, which can block blood flow and cause a stroke.

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28
Q

How do you reduce the risk of clotting in patients with Afib?

A

To reduce clotting risk, patients with Afib may require anticoagulation

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29
Q

Describe atrial flutter.

A

Atrial flutter is more organized and regular than Afib. It occurs most often in patients with underlying heart disease or COPD and it can progress to Afib

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30
Q

What are some examples of ventricular arrhythmias?

A

Premature ventricular contractions (PVCs), ventricular tachycardia and ventricular fibrillation

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31
Q

Describe PVCs.

A

They are referred to as a skipped heartbeat. PVCs are generated from within the ventricular tissue and it can be related to stress or too much caffeine. nicotine or exercise

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32
Q

What is ventricular tachycardia?

A

A series of PVCs in a row, resulting in a heart rate of greater than 100 BPM, is known as ventricular tachycardia (VT)

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33
Q

How is ventricular tachycardia treated?

A

VT with a pulse is treated with antiarrhythmics, whereas pulseless VT is a medical emergency and advanced cardiac life support (ACLS) should be initiated

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34
Q

What is the consequence of untreated ventricular tachycardia?

A

Untreated VT can degenerate into ventricular fibrillation (completely disorganized electrical activation of the ventricles), which is also a medical emergency

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35
Q

How is the QT interval measured and what does it indicate?

A

The QT interval is measured from the beginning of the QRS complex to the end of the T wave on an ECG. It reflects ventricular depolarization and repolarization and varies with heart rate (the QT interval is longer when the heart rate is slower

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36
Q

When can a QT interval be used?

A

A QTc interval can be used if the heart rate is < 60 BPM; when the heart rate is > 60 BPM, a QT interval corrected for heart rate (QTc) is used

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37
Q

When is a QTc interval considered prolonged?

A

A QTc interval is considered prolonged when it is > 440 milliseconds (msec), but is more worrisome when markedly prolonged (> 500 msec)

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38
Q

What is a consequence of QT prolongation?

A

Prolongation of the QT interval is a risk factor for Torsades de Pointes (TdP), a particularly lethal ventricular tachyarrhythmia that can cause sudden cardiac death

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39
Q

What increases the risk of drug-induced QT prolongation?

A
  • Higher doses (risk is concentration-dependent)
  • Multiple QT-prolonging drugs taken at the same time (additive effects)
  • Reduced drug clearance due to renal disease, liver disease, or drug interactions
  • Electrolyte abnormalities including low potassium (hypokalemia), magnesium (hypomagnesia) and calcium (hypocalcemia)
  • Other cardiac conductions; cardiac damage is a risk for arrhythmias, including TdP
  • Female gender
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40
Q

What are key drugs that can increase or prolong the QT interval?

A
  • Antiarrhythmic: class I (especially class Ia) and class III
  • Antibiotics: quinolones and macrolides
  • Azole antifungals: all except isavuconazonium
  • Antidepressants: Tricyclics, SSRIs, SNRIs, Mirtazapine and Trazodone
  • Antiemetic drugs: 5-HT3 receptor antagonists, droperidol and phenothiazines
  • Antipsychotics: chlorpromazine, clozapine, haloperidol, olanzapine, paliperidone, quetiapine, risperidone, thioridazine, ziprasidone
  • Others: donepezil, fingolimod, methadone, tacrolimus
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41
Q

How do antiarrhythmic drugs work?

A

Antiarrhythmic drugs work by affecting the electrical currents in the cells of the heart. By blocking the movement of ions in different phases of cardiac action potential, select drugs can reduce conduction velocity and/or automaticity, or prolong the refractory period, which can slow or terminate the abnormal electrical activity causing the arrhythmia

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42
Q

Where are different types of arrhythmias managed?

A

Ventricular arrhythmias are managed in a hospital or emergent setting. Supraventricular arrhythmias are managed in both inpatient and outpatient settings

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43
Q

What are labs needed prior to starting any drug for a non-life threatening arrhythmia?

A

Prior to starting any drug for a non-life threatening arrhythmia, electrolytes and a toxicology screen should be checked to identify reversible causes

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44
Q

What is the Vaughan Williams classification system?

A

The Vaughan Williams classification system is most commonly used for antiarrhythmic drugs that splits the drugs into categories based on their dominant electrophysiological effect

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45
Q

What are the Class I drugs?

A

Class Ia: Disopyramide, Quinidine, Procainamide
Class Ib: Lidocaine, Mexiletine
Class Ic: Flecainide, Propafenone

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46
Q

What are the Class II drugs?

A

Beta-blockers

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47
Q

What are the class III drugs?

A

Dronedarone, Dofetilide, Sotalol, Ibutilide, Amiodarone

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48
Q

What are class IV drugs?

A

Verapamil, Diltiazem

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49
Q

What is the MOA of class I drugs and what are the consequences of it?

A
  • MOA: Na channel blockers
  • Reduces the speed of ion conduction through sodium channels
  • Proarrhythmic (higher risk of arrhythmia) and negative ionotropic potential, which decreases the force of ventricular contraction (use caution in patients with underlying cardiac disease)
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50
Q

What is the MOA of class II drugs and its consequences?

A

MOA: beta-blockers
- Blocks the sympathetic activity that can trigger an arrhythmia; indirectly blocks calcium channels, which decrease ion conduction speed. Used primarily to slow ventricular rate in AFib

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51
Q

What is the MOA of class III drugs and its consequences?

A

MOA: K-channel blockers

  • Amiodarone and dronedarone block K channels (primarily), Ca channels, Na channels and alpha- and beta- adrenergic receptors
  • Amiodarone is useful for different types of arrhythmias, including Afib
  • Amiodarone and dofetilide are preferentially used for Afib in patients with HF
  • Sotalol blocks K channels and is a beta-blocker
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52
Q

What is the MOA of Class IV drugs and its consequences?

A

MOA: Ca-channel blockers, non-dihydropyridine

  • Used primarily to slow ventricular rate in AFib
  • Negative inotropic effect (decreased contraction force), which can cause cardiac decompensation
  • Do not use verapamil or diltiazem in patients wth heart failure and reduced ejection fraction (HFrEF)
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53
Q

What is the MOA of Digoxin and its consequences?

A

MOA: Na-K-ATPase blocker
- Suppresses AV node conduction (decreased heart rate) by enhancing vagal tone and increasing the force of contraction (positive inotrope)

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54
Q

What is the MOA of Adenosine and its consequences?

A

MOA: activates adenosine receptors to decrease AV node conduction
- Used for paroxysmal supraventricular tachyarrhythmias

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55
Q

What are the two main strategies for guideline-recommended treatment for most types of AFib?

A

Rate control and rhythm control

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56
Q

What is paroxysmal Afib?

A

Afib that terminates spontaneously or with intervention within 7 days of onset; episodes may recur with variable frequency

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57
Q

What is persistent Afib?

A

Continuous Afib that is sustained > 7 days

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58
Q

What is long-standing persistent Afib?

A

Continuous AFib that is sustained > 12 months

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59
Q

What is permanent Afib?

A

Term used when a joint decision has been made by the clinician and patient to cease further attempts to restore and/or maintain NSR; this is a treatment choice rather than a characteristic of the arrhythmia iself

60
Q

What is valvular Afib?

A

AFib with moderate to severe mitral stenosis or with a mechanical heart valve; long-term anticoagulation with warfarin is indicated

61
Q

What is non-valvular AFib?

A

AFib without moderate to severe mitral stenosis or a mechanical heart valve

62
Q

What is the goal resting HR in patients with symptomatic AFib?

A

The goal resting HR is < 80 BPM in patients with symptomatic AFIb

*A more lenient goal of < 110 BPM may be reasonable in patients who are asymptomatic and have preserved left ventricular function

63
Q

What is rate control?

A

Patient remains in AFib and takes medications to control the ventricular rate (HR)

64
Q

What medications are used for rate control?

A

Beta-blockers (preferred) or non-DHP calcium channel blockers are recommended for controlling ventricular rate in patients with AFib

*Patients with HFrEF should not receive a non-DHP CCB

65
Q

What can be added to first line agents for rate control?

A

Digoxin is not first-line for ventricular rate control, but can be added for refractory patients or used in those who cannot tolerate beta-blockers or non-DHP CCBs

66
Q

What does rhythm control consist of?

A

Rhythm control consists of methods for conversion to NSR and maintenance of NSR

67
Q

What is the most effective method of conversion to NSR?

A

Conversion to NSR is most effective with direct current (electrical) cardioversion, a medical procedure that delivers a high-energy shock through the chest wall. The shock breaks the incorrect cycle, stops the arrhythmia and allows the sinus node to begin firing again with a NSR

68
Q

What are medications that can be used for pharmacologic cardioversion?

A

Amiodarone (oral and IV), dofetilide, flecainide, ibutilide and propafenone

69
Q

What is needed prior to cardioversion?

A

Cardioversion has a high risk of thromboembolism so patient should be started on therapeutic anticoagulation at least three weeks before cardioversion and continued for at least four weeks after successful cardioversion to NSR

70
Q

What is the goal INR of patients taking warfarin for anticoagulation?

A

2-3

71
Q

What are recommended options for maintenance of NSR?

A

Dofetilide, dronedarone, flecainide, propafenone or sotalol

72
Q

When is Amiodarone generally recommended?

A

Due to toxicities, amiodarone is recommended only when other drugs have failed or are contraindicated (e.g. heart failure)

73
Q

What is something important to note with rhythm control?

A

If AFib is permanent, avoid a rhythm-control strategy with antiarrhythmic drugs (risk outweighs benefit)

74
Q

What are the boxed warnings associated with Amiodarone?

A
  • Pulmonary toxicity; check baseline chest X-ray, PFTs
  • Hepatotoxicity; check baseline LFTs
  • For life threatening arrhythmias only; proarrhythmic must be hospitalized for IV loading dose
75
Q

What are contraindications of Amiodarone?

A

Iodine hypersensitivity, severe sinus-node dysfunction causing marked decreased HR, 2nd/3rd degree heart block (unless using artificial pacemaker), bradycardia causing syncope, cardiogenic shock

76
Q

What are some warnings associated with Amiodarone?

A

Hyper- and hypo-thyroidism (hypo is more common) - amiodarone partially inhibits peripheral conversion of T4 to T3, optic neuropathy (visual impairment), photosensitivity (slate-blue skin discoloration), neurotoxicity (peripheral neuropathy), severe skin reactions (SJS/TEN). Correct hypokalemia, hypomagnesemia, hypocalcemia prior to use

77
Q

What are some monitoring parameters of Amiodarone?

A

ECG, BP, HR, electrolytes, LFTs every 6 months, thyroid function (TSH and free T4) every 3-6 months, chest x-ray at least annually, regular eye exams

78
Q

What are some notes associated with Amiodarone?

A
  • Infusions > 2 hours require a non-PVC container (e.g. polyolefin or glass); PVC tubing is okay
  • Premixed IV bags: longer stability, non-PVC, available concentrations
  • Antiarrhythmic DOC in heart failure
  • Decrease infusion rate or discontinue as needed for hypotension or bradycardia
  • Oral/IV can provide rate control (due to beta-blocking properties) when other measures are unsuccessful or contraindicated
  • IV: use 0.22 micron filter; central line preferable
  • Incompatible with heparin (flush line with saline); many Y-site, additive incompatibilities
  • Amiodarone (chemical structure) contains iodine
  • Teratogenic, excreted in breast milk; avoid in pregnancy/breastfeeding when possible
79
Q

What are some Amiodarone drug interactions?

A
  • Amiodarone can increase then level of many other drugs: it is an inhibitor of CYP2C9 (moderate), 2D6 (moderate), 3A4 (weak) and P-gp
  • When starting amiodarone, decrease digoxin by 50%, decreased warfarin by 30-50% and do not exceed 20 mg/day of simvastatin or 40 mg/day of lovastatin
  • Additive effects can occur when used with other drugs that decrease HR, including non-DHP CCB, digoxin, beta-blockers, clonidine and dexmedetomidine (Precedex)
  • Sofosbuvir can enhance the bradycardic effect of amiodarone; do not use together
80
Q

What are examples of non-DHP calcium channel blockers?

A

Diltiazem and Verapamil

81
Q

What are contraindications of non-DHP calcium channel blockers?

A

Severe hypotension (SBP < 90 mmHg), 2nd/3rd degree heart block/sick sinus syndrome (unless the patient ha a pacemaker), cardiogenic shock, HFrEF, Wolff-Parkinson-White syndrome

82
Q

What are some warnings associated with non-DHP calcium channel blockers?

A

Hypotension, heart failure (may worsen symptoms), 1st degree AV block with sinus bradycardia, increased LFTs

83
Q

What are some side effects of non-DHP calcium channel blockers?

A

Edema, arrhythmias, constipation (more with verapamil), gingival hyperplasia, HA, dizziness

84
Q

What are monitoring parameters of non-DHP calcium channel blockers?

A

ECG, BP, HR, electrolytes, LFTs

85
Q

What are some notes about non-DHP calcium channel blockers?

A

Only non-DHP CCBs are used as antiarrhythmics

86
Q

What are drug interactions of Verapamil and Diltiazem?

A
  • Additive effects can occur when used with other drugs that decrease HR, including amiodarone, digoxin, beta-blockers, clonidine and dexmedetomodine (Precedex)
  • Non-DHP CCBs are CYP3A4 substrates. Use strong CYP3A4 inducers/inhibitors with caution, and in some cases, avoid. Do not take with grapefruit
  • Diltiazem and verapamil are substrates of P-gp and inhibitors of CYP3A4. They can increase the concentration of other drugs (e.g. statins)
87
Q

What is a contraindication of Digoxin?

A

Ventricular fibrillation

88
Q

What are some warnings associated with Digoxin?

A

2nd/3rd degree heart block without a pacemaker, Wolff-Parkinison-White syndrome with AFib, vesicant (avoid extravasation)

89
Q

What are some side effects associated with Digoxin?

A

Dizziness, mental disturbances, N/V/D

90
Q

What are some monitoring parameters of Digoxin?

A

ECG, HR, BP, electrolytes, renal function and digoxin level (drawn 12-24 hours after dose)

91
Q

What are the toxicities associated with Digoxin?

A
  • Initial s/sx of toxicity: N/V, loss of appetite and bradycardia
  • Severe s/sx of toxicity: blurred/double vision, greenish-yellow halos around lights or objects, altered color perception, abdominal pain, confusion, delirium, prolonged PR interval, arrhythmias
92
Q

What are some notes associated with Digoxin?

A
  • Not usually given alone for rate control (used in combination with a beta-blocker or non-DHP CCB)
  • Antidote: DigiFab
  • Hypokalemia, hypomagnesemia and hypercalcemia increases the risk of digoxin toxicity
  • Hypothyroidism can increase digoxin levels
93
Q

What are some drug interactions with Digoxin?

A
  • Digoxin is substrate of P-gp. Levels increased with inhibitors, including amiodarone, dronedarone, diltiazem, verapamil, clarithromycin, itraconazole adn many other drugs. With amiodarone or dronedarone, decrease digoxin dose by 50%
  • Additive effects can occur when used with other drugs that decrease HR, including amiodarone, non-DHP CCB, beta-blockers, clonidine and dexmedetomidine (Precedex)
94
Q

What are some examples of Class Ia drugs?

A

Disopyramide, Quinidine, Procainamide

95
Q

What is a boxed warning of Disopyramide?

A

Reserve use for patients with life-threatening ventricular arrhythmias

96
Q

What are contraindications of Disopyramide?

A

2nd/3rd degree heart block (unless patient has a functional artificial pacemaker), cardiogenic shock, congenital QT syndrome, sick sinus syndrome

97
Q

What are some warnings associated with Disopyramide?

A

Proarrhythmic, hypotension, HF, BPH/urinary retention/narrow angle glaucoma, myasthenia gravis (due to anticholinergic effects)

98
Q

What are some side effects of Disopyramide?

A

Anticholinergic effects (e.g. dry mouth, constipation, urinary retention), hypotension

99
Q

What is a boxed warning of quinidine?

A

May increase mortality in treatment of AFib or atrial flutter; control AV conduction before initiating

100
Q

What are contraindications of Quinidine?

A

Concurrent use of quinolones that prolong QT interval or ritonavir; 2nd/3rd degree heart block or idoventricular conduction delays (unless patient has a functional artificial pacemaker), thrombocytopenia, thrombotic thrombocytopenic purpura (TTP), myasthenia gravis

101
Q

What are some warnings associated with Quinidine?

A

Proarrhythmic, hepatotoxicity, hemolysis risk (avoid in G6PD deficiency), can cause positive Coombs test

102
Q

What are some side effects associated with Quinidine?

A
  • Drug-induced lupus erythematosus (DILE), diarrhea (35%), stomach cramping (22%), rash, lightheadedness
  • Cinchonism (e.g. overdose): symptoms include tinnitus, hearing loss, blurred vision, headache, delirium
103
Q

What are some notes associated with Quinidine?

A
  • Avoid changes in Na intake: decrease Na intake can increase quinidine levels
  • Alkaline foods/alkaline urine in increases quinidine levels and can lead to toxicity
104
Q

What are some boxed warnings of Procainamide?

A
  • Potentially fatal blood dyscrasias (e.g. agranulocytosis); monitor patient closely in the first 3 months and periodically thereafter
  • Long-term use leads to positive antinuclear antibody (ANA) in 50% of patients, which can result in drug-induced lupus erythematosus (DILE) in 20-30% of patients
  • Reserve use for patients with life-threatening ventricular arrhythmias
105
Q

What are contraindications of Procainamide?

A

Heart block, systemic lupus erythematosus (TdP)

106
Q

What is a warning associated with Procainamide?

A

Proarrhyhtmic

107
Q

What are side effects of Procainamide?

A

Hypotension, rash

108
Q

What are some notes associated with Procainamide?

A

Metabolism of procainamide to NAPA occurs by acetylation: slow acetylators are at risk for drug accumulation and toxicity; fast acetylators can have subtherapeutic drug concentrations and reduced efficacy

109
Q

What are the Class Ib drugs?

A

Lidocaine and Mexilitine

110
Q

What is a boxed warning of Mexiletine?

A

Reserve use for patients with life-threatening ventricular arrhythmias, abnormal liver function seen in patients with CHF or ischemia

111
Q

What are contraindications of Class Ib drugs?

A

2nd/3rd degree heart block (unless patient has a function artificial pacemaker)

112
Q

What are contraindications of Lidocaine?

A

Wolff-Parkinson-White syndrome, Adam-Stokes syndrome, allergy to corn or corn-related products or amide-type anesthetics

113
Q

What is a contraindication of Mexiletine?

A

Cardiogenic shock

114
Q

What are some warnings associated with class Ib drugs?

A

Caution in the elderly, hepatic impairment and HF

115
Q

What are some warnings associated with Mexiletine?

A

Blood dyscrasias, severe skin reactions (DRESS)

116
Q

What are some notes associated with Lidocaine?

A

Lidocaine is primarily used topically or locally for numbing

117
Q

What are some examples of Class Ic drugs?

A

Flecainide and Propafenone

118
Q

What are some boxed warnings of Flecainide?

A
  • When treating atrial flutter, 1:1 atrioventricular conduction may occur; pre-emptive negative chronotropic therpay can increase the risk
  • Proarrhythmic effects, especially in AFib (do not use in chronic AFib)
  • Reserve use for patients with life-threatening ventricular arrhythmias
119
Q

What are contraindications of Flecainide?

A

2nd/3rd degree heart block (unless patient has a functional artificial pacemaker), cardiogenic shock, structural heart disease (e.g. myocardial infarction, heart failure), concurrent use of ritonavir

120
Q

What are some warnings associated with Flecainide?

A

Avoid use in severe hepatic impairment

121
Q

What are some side effects of Flecainide?

A

Dizziness, visual disturbances, dyspnea

122
Q

What is a boxed warning of Propafenone?

A

Reserve use for patients with life-threatening ventricular arrhythmias

123
Q

What are contraindications of Propafenone?

A

Sinoatrial and atrioventricular disorders (unless patient has a functional artificial pacemaker), sinus bradycardia, cardiogenic shock, hypotension, structural heart disease (e.g. heart failure, myocardial infarction), bronchospastic disorders

124
Q

What is a warning of Propafenone?

A

Proarrythmic

125
Q

What are side effects of Propafenone?

A

Taste disturbance (metallic), dizziness, visual disturbances, N/V

126
Q

What are some notes of Propafenone?

A

Propafenone has a significant beta-blocking effects, negative inotropic and proarrhythmic properties (contraindicated in HF)

127
Q

What are examples of Class III drugs?

A

Dronedarone, Sotalol, Ibutilide, Dofetilide

128
Q

What is a boxed warning of Dronedarone?

A

Increased risk of death, stroke and HF in patients with decompensated HF (NYHA Class IV or any NYHA class with a recent hospitalization due to HF) or permanent AFib

129
Q

What are contraindications of Dronedarone?

A

Concurrent use of strong CYP3A4 inhibitors and QT-prolonging drugs, pregnancy, 2nd/3rd degree hear block (unless patient has functional pacemaker), symptomatic HF, HR < 50 BPM, QTc > 500 msec, PR interval > 280 msec, lung or liver toxicity from previous amiodarone use, hepatic impairment, nursing mothers

130
Q

What are some warnings associated with Dronedarone?

A

Hepatic failure (especially in the first 6 months), pulmonary disease (including pulmonary fibrosis and pneumonitis), marked increased SCr, prerenal azotemia and ARF (usually in the setting of heart failure or hypovolemia), decreased Mg, and decreased K with administration of K-depleting diuretics

131
Q

What are side effects of Dronedarone?

A

QT prolongation, increased SCr, diarrhea, bradycardia, asthenia

132
Q

What are some notes associated with Dronedarone?

A
  • Unlike amiodarone, dronedarone does not contain iodine and has little effect on thyroid function
  • Dronderarone is a moderate inhibitor of CYP2D6, 3A4, and P-gp nad a major substrate of CYP3A4; avoid use with strong inhibitors and inducers of CYP3A4 and with drugs that prolong the QT interval; decreased digoxin dose by 50% and use lower doses of statins metabolized by CYP3A4, or use alternate statin; monitor INR if on warfarin
133
Q

What are boxed warnings of Sotalol?

A
  • Initiation (or reinitiation) and dosage increases should be done in a hospital with continuous ECG monitoring and experienced staff
  • Adjust dosing interval based on CrCl to decrease risk of proarrhythmia; QT prolongation is directly related to sotalol concentration
134
Q

What are contraindications of Sotalol?

A
  • 2nd/3rd degree heart block (unless patient has a functional artificial pacemaker), congenital or acquired long QT syndrome, sinus bradycardia, uncontrolled HF, cardiogenic shock, asthma
  • For Betapace AF, Sotylize, sotalol injection: QTc > 450 msec, bronchospatic conditions, CrCl < 40 mL/min, K < 4 mEq/L, sick sinus syndrome
135
Q

What are side effects of sotalol?

A

Bradycardia, palpitations, chest pain, dizziness, fatigue, dyspnea, N/V, tdP, HF, bronchoconstriction

136
Q

What are notes associated with Sotalol?

A

Betapace should not be substituted with Betapace AF since it is distributed with educational information specifically for patients with AFib/atrial flutter

137
Q

What is a boxed warning of Ibutilide?

A

Proarrhyhtmic; confirm that benefits of maintaining NSR outweigh the risks

138
Q

What are side effects of Ibutilide?

A

Ventricular tachycardias (e.g. TdP), hypotension, QT prolongation

139
Q

What are notes associated with Ibutilide?

A

Correct hypokalemia and hypomagnesemia prior to use and throughout treatment

140
Q

What are some of the boxed warnings of Dofetilide?

A

Must be initiated (or reinitiated) in a setting with continuous ECG monitoring, experienced staff and ability to assess CrCl for a minimum of 3 days; proarrhythmic (QT prolongation)

141
Q

What are contraindications of Dofetilide?

A

Prolonged QTc > 440 msec at baseline; do not use with cimetidine, dolutegravir, hydrochlorothiazide, itraconazole, ketoconazole, megestrol, prochlorperazine, trimethoprim, verapamil (these drugs can inhibit renal tubular secretion of dofetilide)

142
Q

What are side effects of Dofetilide?

A

Ventricular tachycardias (e.g. TdP), increase QT interval

143
Q

What are notes of Dofetilide?

A

Antiarrhyhtmic DOC in heart failure

144
Q

What is a contraindication of Adenosine?

A

2nd/3rd degree heart block, sick sinus syndrome or symptomatic bradycardia (except in patients with a functional pacemaker), bronchospastic lung disease

145
Q

What are side effects of Adenosine?

A

Transient new arrhythmia, facial flushing, chest pain/pressure, GI distress, transient decrease in blood pressure, dyspnea

146
Q

What are some counseling points regarding Amiodarone?

A
  • Can cause lung damage, liver damage, eye damage (nerve damage and corneal deposits), hypothyroidism or hyperthyroidism, photosensitivity, skin discoloration to a blue-gray color
  • Avoid grapefruit
  • Many drug interactions (enzyme inhibitor)
147
Q

What are counseling points of Digoxin?

A
  • Early symptoms of overdose include loss of appetite and nausea. If this occurs, check heart rate. If bradycardic, a digoxin level should be checked
  • Symptoms of severe overdose include vision changes (e.g. blurred or yellow/green vision), confusion, hallucinations and feeling like you might pass out
  • Avoid dehydration; an overdose can occur more easily if you are dehydrated
  • Many drug interactions

NAPLEX Review (45 decks)

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