not all drugs are good drugs: Cardio Flashcards
Difference between QTc prolongation and Torsades
QTc prolongation puts you at high risk for Torsades, Torsades is a life threatening arrhythm
* QT prolongation creates additional time in the plateau phase where another action potential can come in, if that does happens, that’s torsades
What is considered QT prolongation
> 500 or >60 from baseline
QT prolonging drugs
- anti-Arrhythmics: amiodarone, sotalol, dofetilide
- anti-Biotics: fluoquinolones (-floxacin), macrolide (erythrmoycin)
- anti-psyChotics: first gen more so than second
- anti-Depressants: citalopram, TCAs
- anti-Emetics: ondasetron and reglan (to some extent)
- anti-Fungals: -azole antifungals
Risk factors for drug induced QT prolongation
- Non-modifable
- > 65
- Female
- Genetics
- Cardiac disease
- Modifable
- Diuretic treatment
- Electrolyte abnormality
- Use of multiple agents
- Organ function
- Diuretic treatment
Approach to QT prolongation
- Avoid drugs QT prolonging drugs in pts with pre-treatment interval >450
- Reduce dose or dc proloning agents if QT increases >60 from bbaseline
- DC if QT increases to >500
- Maitain K >4 and Mg >2
- Avoid admin of multiple QT prolonging drugs
- Avoid use of QT prolonging drugs in pts with a hx of Torsades
Risk for QT prolongation is ____ dependent
Risk is drug [ ] dependent
- DDIs and organ dysfunction that increases [ ] increase risk
- Just because a patient has been on the drug, doesn’t mean it is safe for the patient right now
Torsades treatment
- DC offending agents
- Mg is treatment of choice
- Give bolus if pt has no pulse
- Give IV if pt HAS pulse
- Assess other electrolytes
- K should be > 4
- Ca may need to be repleted as well
- IF THE ABOVE DON’T WORK: transcutaneous pacing - increase HR pace to faster than the arryhtmia
- Can also do this with drugs: isoproterenol infusion (expensive) → alternatives are epinephrone or atropine
- if at any point it is hemodynamically unstable -> cardiovert or defibrillate
- Can also do this with drugs: isoproterenol infusion (expensive) → alternatives are epinephrone or atropine
Isoproterenol
- MOA: beta 1 and 2 agonsit → increase HR , contracitliy, and vasodilation
- AE: angina
- Monitor: HR, BP, ECG
- Continuous infusion, immediate onset
Drugs taht can cause HF d/t myopathy
- Chemo agents: antrhacyclines (doxorubicin, daunorubicin), alkylating agents
- mAbs: trastuzumab
- EtOH
Anthracyclines: MOA in causing HF
Topoisomerase 2B is blocked → cause DNA breadkown and cell death
Anthracyclines: risk factors for developing HF
- Life time dose dependent: lifetime limit is 550mg/m^2
- Radiation therapy
- Co admin with potentially cardiotoxic agents
- Age
- Preexisting CV disease or rissk factors
- Obestiy
- Smokign
Trastuzumab: MOA in causing HF
Inhibits HER2 receptor → increased ROS and angiotensin II and reduces NO → makes heart work harder → reversible HF
Approaches to trastuzumab induced HF
- Consider dose reduction or dc
- Can dose adust based on the EF
- If pt must stay on it, consider HF meds during treatment if EF declines
- ACE/ARB > beta blocker
EtOH: MOA in causing HF
directly toxic to myocardium
Drugs that can cause HF d/t Na and fluid retention
-
NSAIDs: avoid the drugs if possible and if necessary, minimize dose adn duration
- Makes it harder for heart to work
- Steroids: avoid the drugs if possible and if necessary, minimize dose adn duration
-
Thiazolidineoids: BBW to avoid in pts with NYHA III-IV HF
- Can icnrease progression towards HF
