Drug-Induced Cardiac Disease Flashcards
(25 cards)
T or F: If a person gets QTc prolongation, they will develop torsade de pointe.
False!
Someone may have elevated QTc and never develop TdP
What is a normal QTc for men and women?
Men: <470 ms
Women: <480 ms
Why does QTc prolongation occur? (Explain the mechanism)
The plateau phase is longer (where K+/Na+&Ca+ exchange occurs). This phase is linked to the ECG’s QT interval, causing the elongation.
What is the CUTOFF for determining QTc prolongation? (2 ways)
QTc ≥ 500 ms
OR
QTc ≥ 60 ms increase from baseline
(even if QT is usually low, if increase +60 ms then diagnosed)
What are the common medications that cause QTc prolongation?
A: antiArrhythmics (Amiodarone, sotalol, dofetilide)
B: antiBiotics (-floxacins, erythromycin)
C: antipsyChotics (Class I)
D: antiDepressants (citalopram, TCAs)
E: antiEmetics (ondansetron)
F: antiFungals (-azoles)
Is drug-induced QTc prolongation dose dependent? How might disease states like AKI cause issues?
QTc prolonging drugs ARE dose dependent!
AKI may decrease renal clearance, causing increased concentration of drug
What are NON-MODIFIABLE risk factors for drug-induced Torsades? (4)
> 65 years old
Female
Genetics
Cardiac disease
What are MODIFIABLE risk factors for drug-induced Torsades? (4)
Diuretics
Electrolyte abnormalities
2+ QT prolonging drugs
Impaired organ function (think AKI/renal)
What are some approaches to managing acute drug-induced QTc prolongation?
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
What are the steps to treating drug-induced TdP? (4)
- D/C offending agents that may prolong QTc
- Mg push (no pulse) or Mg infusion (pulse)
- Transcutaneous pacing [speeds up heart to reset rhythm]
- Isoproterenol infusion
- $$ and not always available! Alt. - epinephrine or atropine
If hemodynamically unstable, use cardioversion or defibrillator
What is isoproterenol and what is it used for?
Used for last line treatment of TdP
Stimulates beta 1 & 2 receptors to increase HR and reset rhythm
AEs: angina
Monitor: HR, BP, ECG
What are the main THREE reasons for drug-induced HF?
- Sodium/volume retention
- Direct cardiotoxicity/cardiomyopathy
- Negative inotropy
What drugs can cause SODIUM/FLUID RETENTION heart failure? (3)
NSAIDs
Steroids
Thiazolidinediones [BBW avoid in NYHA 3-4 HF]
What drugs can cause CARDIOMYOPATHY heart failure? (3)
**Chemo agents (anthracyclines)
Biologics (Trastuzumab)
Alcohol
What NEGATIVE INOTROPIC drugs cause HF? (2)
Non-DHP CCBs
Beta blockers
How do anthracyclines (doxorubicin, daunorubicin) cause cardiomyopathy? What drug could prevent this? What DOSE increases risk?
- MOA = topoisomerase 2B inhibition = DNA breakdown + apoptosis
- Dexrazoxane prevents anthracycline binding
- Cumulative dose >400 mg/m2 RISK FOR TOXICITY! (Limit of 550mg)
How does trastuzumab induce cardiomyopathy?
MOA = HER2 receptor antagonism
Cardiomyopathy is usually reversible once D/C
Worse with elderly or CV comorbidities
What is the BBW on trastuzumab?
Associated with reductions in left ventricular ejection fraction (LVEF) and HF development
Trastuzumab can be combined with WHAT DRUGS (2) to improve LVEF?
ACEi/ARBs
Beta-blockers
Negative Inotropy HF:
Avoid ______ in patients with EF < 40%
Avoid ______ in patients with acute HF exacerbations
Avoid NON-DHP CCBs in patients with EF < 40%
Avoid BETA-BLOCKERS in patients with acute HF exacerbations
What two drugs can cause drug-induced myocardial ischemia and ACS?
Cocaine**
NSAIDs
How does cocaine cause myocardial ischemia/ACS?
Increases HR and contractility
Increased coronary resistance
Coronary artery thrombosis
Increased CVD risk
VASOSPASMS/VASOCONSTRICTION
Cocaine may induce an MI. What are some treatments for this?
Angina - aspirin (helps eliminate atherosclerotic MI), benzos
HTN - IV NTG, benzos
AVOID acute and beta-specific BETA BLOCKERS
What is the BBW for NSAIDs?
May increase risk of serious CV thrombotic events, MI, and stroke.
