Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pulm/Tox > Drug-Induced Cardiac Disease > Flashcards

Drug-Induced Cardiac Disease Flashcards

1
Q

T or F: If a person gets QTc prolongation, they will develop torsade de pointe.

A

False!
Someone may have elevated QTc and never develop TdP

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

What is a normal QTc for men and women?

A

Men: <470 ms
Women: <480 ms

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

Why does QTc prolongation occur? (Explain the mechanism)

A

The plateau phase is longer (where K+/Na+&Ca+ exchange occurs). This phase is linked to the ECG’s QT interval, causing the elongation.

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

What is the CUTOFF for determining QTc prolongation? (2 ways)

A

QTc ≥ 500 ms
OR
QTc ≥ 60 ms increase from baseline
(even if QT is usually low, if increase +60 ms then diagnosed)

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

What are the common medications that cause QTc prolongation?

A

A: antiArrhythmics (Amiodarone, sotalol, dofetilide)
B: antiBiotics (-floxacins, erythromycin)
C: antipsyChotics (Class I)
D: antiDepressants (citalopram, TCAs)
E: antiEmetics (ondansetron)
F: antiFungals (-azoles)

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

Is drug-induced QTc prolongation dose dependent? How might disease states like AKI cause issues?

A

QTc prolonging drugs ARE dose dependent!

AKI may decrease renal clearance, causing increased concentration of drug

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

What are NON-MODIFIABLE risk factors for drug-induced Torsades? (4)

A

> 65 years old
Female
Genetics
Cardiac disease

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

What are MODIFIABLE risk factors for drug-induced Torsades? (4)

A

Diuretics
Electrolyte abnormalities
2+ QT prolonging drugs
Impaired organ function (think AKI/renal)

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

What are some approaches to managing acute drug-induced QTc prolongation?

A

Avoid QTc prolonging drugs in patients with QTc > 450 ms
Reduce dose/DC if drug increases QTc by >60 ms
DC if drug increases QTc > 500
*Maintain K > 4 and Mg > 2 mEq/L
Avoid 2+ QTc prolonging drugs
Avoid QTc prolonging drugs in patients with hx of TdP

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

What are the steps to treating drug-induced TdP? (4)

A
  1. D/C offending agents that may prolong QTc
  2. Mg push (no pulse) or Mg infusion (pulse)
  3. Transcutaneous pacing [speeds up heart to reset rhythm]
  4. Isoproterenol infusion
    • $$ and not always available! Alt. - epinephrine or atropine

If hemodynamically unstable, use cardioversion or defibrillator

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

What is isoproterenol and what is it used for?

A

Used for last line treatment of TdP

Stimulates beta 1 & 2 receptors to increase HR and reset rhythm
AEs: angina
Monitor: HR, BP, ECG

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

What are the main THREE reasons for drug-induced HF?

A
  1. Sodium/volume retention
  2. Direct cardiotoxicity/cardiomyopathy
  3. Negative inotropy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What drugs can cause SODIUM/FLUID RETENTION heart failure? (3)

A

NSAIDs
Steroids
Thiazolidinediones [BBW avoid in NYHA 3-4 HF]

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

What drugs can cause CARDIOMYOPATHY heart failure? (3)

A

**Chemo agents (anthracyclines)
Biologics (Trastuzumab)
Alcohol

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

What NEGATIVE INOTROPIC drugs cause HF? (2)

A

Non-DHP CCBs
Beta blockers

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

How do anthracyclines (doxorubicin, daunorubicin) cause cardiomyopathy? What drug could prevent this? What DOSE increases risk?

A
  • MOA = topoisomerase 2B inhibition = DNA breakdown + apoptosis
  • Dexrazoxane prevents anthracycline binding
  • Cumulative dose >400 mg/m2 RISK FOR TOXICITY! (Limit of 550mg)
17
Q

How does trastuzumab induce cardiomyopathy?

A

MOA = HER2 receptor antagonism
Cardiomyopathy is usually reversible once D/C
Worse with elderly or CV comorbidities

18
Q

What is the BBW on trastuzumab?

A

Associated with reductions in left ventricular ejection fraction (LVEF) and HF development

19
Q

Trastuzumab can be combined with WHAT DRUGS (2) to improve LVEF?

A

ACEi/ARBs
Beta-blockers

20
Q

Negative Inotropy HF:
Avoid ______ in patients with EF < 40%
Avoid ______ in patients with acute HF exacerbations

A

Avoid NON-DHP CCBs in patients with EF < 40%
Avoid BETA-BLOCKERS in patients with acute HF exacerbations

21
Q

What two drugs can cause drug-induced myocardial ischemia and ACS?

A

Cocaine**
NSAIDs

22
Q

How does cocaine cause myocardial ischemia/ACS?

A

Increases HR and contractility
Increased coronary resistance
Coronary artery thrombosis
Increased CVD risk
VASOSPASMS/VASOCONSTRICTION

23
Q

Cocaine may induce an MI. What are some treatments for this?

A

Angina - aspirin (helps eliminate atherosclerotic MI), benzos
HTN - IV NTG, benzos

AVOID acute and beta-specific BETA BLOCKERS

24
Q

What is the BBW for NSAIDs?

A

May increase risk of serious CV thrombotic events, MI, and stroke.

25
Q

When is the risk highest for developing NSAID-induced MI? Does higher dose mean higher risk?

A

Highest risk early in therapy! -> WITHIN 7 DAYS

higher dose = higher risk
>1.2 grams/day ibuprofen
>750 mg/day naproxen

Pulm/Tox (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions