Arrhythmias Flashcards
(52 cards)
1
Q
What is arrhytmia?
A
- Abnormal heart rhythm, which can cause the heart to beat too slow (bradycardia) or too fast (tachycardia)
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
3
Q
The conduction pathway
A
- SA node
- Right atrium and left atrium
- AV node
- Bundle of His
- Right bundle brunch for the right ventricle
- Left bundle brunch for the left ventricle
- Purkinje fibers
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
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
6
Q
Phase 0
A
- A heartbeat is initiated when rapid ventricular depolirization occurs in response influx of Na; causing ventricular contraction (QRS)
7
Q
Phase 1
A
- Early rapid repolarization (Na channels close)
8
Q
Phase 2
A
- A plateau in response to an influx of Ca and efflux of K
9
Q
Phase 3
A
- Rapid ventricular repolarization occurs in response to an efflux of K; this causes ventricular relaxation (T wave)
10
Q
Phase 4
A
- Resting membrane potential is established; atrial depolarization occurs (P wave)
11
Q
What QRS represents on the ECG?
A
- Ventricular contraction
- Phase 0
12
Q
What P represents on the ECG?
A
- Atrial contraction
- Phase 4
13
Q
What T represents on the ECG?
A
- Ventricular relaxation
- Phase 3
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)
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
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
17
Q
T/F: Prolongation of the QT interval is a risk factor for TdP and can cause sudden cardiac death
A
True
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
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
20
Q
T/F: Prior to starting non-life-threatening arrhythmia, electrolytes and toxicology screen should be checked
A
True
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
A
- BBs
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
Vaughan Williams Classification - Class IV
## Footnote
Hint: Double Quarter Pounder, Lettuce, Mayo, Fries Please! Because Dieting During Stress Is Always **V**ery **D**ifficult
* **V**erapamil, **D**iltiazem
26
Class I - Na-channel blockers
* Proarrhythmic
* Use caution with cardiac disease
27
Class II - BBs
* Used primarily to slow ventricular rate in Afib
28
Class III - K-channel blockers
* 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
Class IV - CCBs, non-DHP
* Used primarily to slow ventricular rate in Afib
* Do not use verapamil or diltiazem in patients with HF and HFrEF
30
Digoxin
* Na-K-ATPase blocker
* Supresses AV node conduction (decreases HR) by enhancing vagal tone and increases force of contraction (positive inotrope)
31
Adenosine
* Activates adenosine receptors to decrease AV node conduction
* Used for paroxysmal supraventricular tachyarrhythmias (PSVTs)
32
Rate Control
* 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
Rhythm Control
* 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
Rate Control vs Rhythm Control
* 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
Stroke Prophylaxis
* 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
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
Clot
37
Amiodarone
* 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
Amiodarone - Safety/SEs/Monitoring
* **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
Infusions >2 hours require a **___** container
## Footnote
Amiodarone
Non-PVC (e.g., polyolefin or glass)
40
What container nexterone premixed IV bag comes with?
* Non-PVC, non-DEHP GALAXY plastic container
## Footnote
Premixed IV bags has longer stability
41
Amiodarone DDIs
* 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
Non-DHP CCBs
* Diltiazem (Cardizem, Tiazac)
* Verapamil (Calan SR)
* Warnings: HF (may worsen symptoms)
* SEs: edema, arrhythmias, constipation (more with verapamil) gingival hyperplasia
43
Non-DHP CCBs - DDIs
* 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
Digoxin
* 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
Digoxin - DDIs
* 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
Class Ia Drugs
## Footnote
Disopyramide, Quinidine, Procainamide
* **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
Class Ib Drugs
## Footnote
Lidocaine
* Useful for ventricular arrhythmias only
* Lidocaine - injection
*Used for refractory VT/cardiac arrest
48
Class Ic Drugs
## Footnote
Flecainide, Propafenone
* **Flecainide**
*BW: proarrhythmic
*CIs: HF, MI
* **Propafenone**
*CIs: HF, MI
*Warnings: proarrhythmic
*SEs: taste disturbance (metallic)
49
Class III Drugs
## Footnote
Dronedarone
* **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
Class III Drugs
## Footnote
Sotalol
* 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
Class III Drugs
## Footnote
Ibutilide, Dofetilide
* **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
Adenosine
* Injection
* t1/2: less than 10 sec
* Used in PSVTs
