Antiarrhythmics pt 2 Flashcards

1
Q

what phase is being prolonged, what channels, and what class of drugs cauase this?

A

phase 0: fast action depoloarization in the myoctes

Na blocking drugs

class I (abc)+class III drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Left to right

A

A. class 1a: QRS increased; QT increased ; AP increased; ERP increased

B. class 1b: QRS no change; QT decreases; ERP+AP both decrease

c. class 1c: QRS increases; QT no change; ERP+AP no change

red line = after drug administration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

which class 1 drug effects sodium channels largely during their depolarized state?

A

class 1b: bind above 0mv

RAPIDLY unbinds- unbound by the time the next impulse arrives; therefore works better in fast heart rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

which drug can be used to treat re-entry and what is the MOA of this induced state?

A

Re-entry occurs when there is an accessory route refracting a depolarizing wave back to the atria: lidocaine inhibits this “two way” electrical route and permits only unidirectional electrical flow.

re-entry pathways look like this

unidirectional (normal)–> bidirectional (pathological)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

which class 1 causes CNS toxicity? what is its bother AE?

A

class1b: tremor and agitation

class 1b also causes heart block, bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MI-associated arrhythmia and Ic drugs

A

CAST trial showed almost 4x mortality in patients using class 1c antiarrhythmics following MI: DONT USE THEM

therefore ONLY USE DRUG IN NORMAL HEARTS

Monitor patient so QRS does NOT PROLONG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

bradycardia vs tachycardia: which of these conditions will class 1 drugs be beneficial?

A

tachycardia for class 1 drugs: they all have USE-dependence but especially class 1c drugs, meaning they only act when the channels are open/activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which drug class causes these changes?

A

K+ (repolarization) channel blockers: class III: amidarone, sotalol, dofetilide, ibutilide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

torsade de pontes

A

may be induced by class III and Class 1a because these drugs prolong AP, therefore QT interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

prolongs QRS, slows AV conduction, slows HR

A

Amiodarone: has class I (prolonged class I character), class II+IV (delays HR and AV conduction) characteristics.

Amiodarone is the class III drug with the lowest risk of TDP induction torsade.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

half life of amiodarone

A

58 days; lipid soluble, so accumulates in tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
A

amiodarone: photosensitivity to sun is the most common affect of amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
A

least common side effect of amidarone: blue man syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
A

pulmonary fibrosis- SE of amiodarone, “honeycombing” cxr: foamy macrophages fllled with phospholipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

tests needed for px on amiodarone

A

LVTs, TFTs, PFTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

class III drugs for cardiomyopathy

A

sotalol, dofetilide: they have reverse use dependence; this permits them to bind during the potassium resting state, when they aren’t in use. They have the greatest effect in bradycardic patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Ibutilide

A

Class III drug, Intravenous (Ibut..), 2-4 hr half life, used predominantly for cardioversion

terminates arrhythmia but can induce torsades

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
A

Class II drugs (beta blockers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
A

class II drugs (BB): blue is before red is after

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

AV block drugs

A

Class II BB and Class IV CCBs: decrease AV conduction –> type 1 AV block or type II (Mobitz 1; wenckebach)

used soley for anti-arrhythmic rates

22
Q

VTac/Vfib–>SCD. which drug would decrease rates of SCD among antiarrhythmics?

A

beta blockers: they not only slow AV conduction down but also work on ventricular myocytes as well, so they improve outcomes for patients.

23
Q
24
Q

adenosine receptors, use, and mode of delivery, SE

A

located in the AV node and blood vessels

used for AVNRT (most common SVT)

used via IV

because of vascular receptors–> vasodilation, flushing

25
Magnesium
only used in Trsades: blocks calcium influx during phase 2
26
atropine: can be used as an anti-arrhythmic. ## Footnote Hot as a hare: increased body temperature Blind as a bat: mydriasis (dilated pupils) Dry as a bone: dry mouth, dry eyes, decreased sweat Red as a beet: flushed face Mad as a hatter: delirium
27
adenosine block
theophylline and caffeine
28
patient has reduced EF: this drug is available. what is it?
digoxin
29
what is the outcome and drug used in this scene?
digoxin; increases contractility by decreasing Ca2+ loss by inhibiting K/Na ATPase in other words, more Calicum inside myocyte
30
second MOA of Digoxin (not the same as the Na/K pump inhibitor
31
hypokalemia and renal clearance
digoxin: patients will need K sparring diuretics
32
GI: N/V Neuro: confusion/delerious Visual changes: scotomas, blindness
digoxin
33
digoxin
34
digoxin toxicity
35
Fab binding, produced by sheep, bound to albumin as haptan --\> leading to antibody against \_\_\_\_
Digibind: synthetic anitbody that binds digoxin and corrects HYPERkalemia. Digoxin can cause both hyperkalemia and hypokalemia
36
``` A rapid form of polymorphic VT associated with the evidence of prolonged ventricular repolarization (long QT syndrome). ```
torsades de pontes: class 1a and class III drugs may induce, amiodarone has the lowest risk
37
a triggered activity resulting from early afterdepolarizations
torsades: a triggered activity resulting from early afterdepolarizations that prolongs the QT interval 1. _Triggered activity_: **depolarizing oscillations in the membrane potential induced by the preceding action potentials** 2. _Early afterdepolarizations_: * **Often associated with the *_impaired function of potassium channels_* leading to a *_prolonged period of repolarization_*** * **Abnormal depolarizations occur during phase 2 or phase 3 of AP** * **due to the opening of Ca2+ (2) or Na+ (3) channels, respectively**
38
A type of a triggered activity resulting from delayed afterdepolarization
1. Digoxin: 1. Occur during phase 4 1. results from increased cytosolic Ca2+ due to Ca2+ overload 2. Spontaneous Ca release from SR 1. activates 3Na+/Ca2+ exchange leading to a net depolarizing current
39
Atrial fibrillation RATE control: mnenomic
* Atrial fibrillation: * Ventricular rate control * Calcium channel blockers * Beta-blockers * Digoxin * Amiodarone * "D CABs are slower"
40
Paroxysmal/Persistant AF: Step 1 --\> two PWs + the "goal" of this tx
1. assess liver function ---\> 2. No HF and LVEF is = or \> 40% 1. --\> CCB or BB 1. Worked? No--\> CCB AND Digoxin or BB and Digoxin 1. Worked? No--\> Amiodarone 3. HF + LVEF less than 40% 1. bb 1. worked? no--\> bb + digoxin 1. worked? no --\> amiodarone 4. **_Goal less than 100 bpm or 20% reduction rate reduction with symptom relief._** **_HINT: Heartfailure + is treated the same way as heartfailure - but without the CCB. End of._**
41
Rhythm control (conversion to sinus rhythm)
1. Rhythm control (conversion to sinus rhythm) 1. Cardioversion using direct current cardioversion 2. Pharmacologic (chemical) cardioversion 1. Amiodarone 2. Flecainide 3. Dofetilide 4. Ibutilide 5. Propafenone 3. "I FAPD"
42
Maintenance of sinus rhythm after the conversion to sinus rhythm
1. Maintenance of sinus rhythm after the conversion to sinus rhythm: FAPD + drone + soda + catheter ablation 1. Dronedarone 2. Flecainide 3. Propafenone 4. Sotalol 5. Amiodarone 6. Dofetilide 7. Catheter ablation 2. All the drugs used for cardioversion EXCEPT ibutilide 3. New additions include dronedarone, sotalol, and catheter ablation
43
Decision algorithm for conversion of hemodynamically stable AF to sinus rhythm
1. 2. 1. AF \< or equal to 40 hrs 1. direct current cardioversion 1. feasible/desirable? 1. no 1. No HF and LVEF \> or = 40%? 1. yes 1. IFAPD 2. No​​​​ 1. IDA
44
AFIB: which two things do you need to control
Ventricular rate (D-CAB), SA rhythm (I FAPD)
45
SVT
1. Paroxysmal supraventricular tachycardia 1. _termination_ 1. – **Adenosine** 2. – Verapamil or diltiazem 3. – Beta-blockers 4. – Digoxin 5. – Amiodarone 2. _Prevention_ 1. – Verapamil 2. – Digoxin 3. – Catheter ablation
46
PSVT termination
1. PSVT 1. Vagal maneuvers. Worked? 1. No--\> adenosine 1. Worked? No--\> 1. **_No HF and LVEF above/equal to 40%?_** 1. _Yes_--\> *Verapimil + Diltiziem* 1. worked? no--\> *BBlocker* 1. worked? no --\> *digoxin* 2. _No_--\> *Digoxin* 1. worked? no --\> *amiodarone* 1. worked? no--\> *diltiazam* 2.
47
Tx for AV block
1. mostly asymptomatic, just monitor 2. Acute high grade AV block that is symptomatic 1. atropine--\> epinephrine if needed 3. Long-standing AV second or third degree block--\> if patient is on drugs, discontinue them --\> pacemaker if that doesnt work
48
Polymorphic Ventricular Tachycardia
Torsades 1. if drug induced, discontinue 2. if hemodynamically unstable, DCC 3. if hemodynamically stable: a. correct electrolyte imbalance b. MgSulfate (regardless of Mg status) c. Transvenous temporary pacemaker for overdrive pacing or isoproterenol i.v.
49
Polymorphic Ventricular Tachycardia: prevent
1. prevent QT prolongation 2. Do not give TdP-inducing drugs if QTc is \>450 ms 3. If a completely reversible cause cannot be identified, consider implantation of ICD (implantable cardioverter defibrillator)
50
1. Tx Digoxin overdose Digoxin-induced arrhythmias 1.  Cancel digoxin 2.  Anti-digoxin antibodies (Digibind, Digifab) 3.  Potassium supplementation to upper normal levels