Pharmacology quiz 4 Flashcards
(42 cards)
Early after depolarization
- cause
- mechanism for which arrhythmogenesis in which abnormality?
- treatment
- drugs to avoid
Cause
- slow HR and AP prolongation -> recovery of inactivated Na/Ca channels -> trigger of spontaneous AP
- happens DURING AP
LONG QT SYNDROME
Treatment
- Na channel blockers (C1) -> quinidine, lidocaine
- beta-blockers -> suppress L-type Ca channel + stimulate K channels -> net inc in outward current
AVOID
-k channel blockers -> prolong APD
Delayed afterdepolarization
- mech
- treatment.
Fast HR -> overload of Ca in SR -> dumping of Ca -> buildup of Na inside cell through NCX -> trigger spontaneous AP
- happens AFTER complete repolarization of an AP
- more likely in presence of catecholamines
TREATMENT
- beta blockers -> lower HR -> reduce Ca influx and uptake
- Na channel blockers -> block generation of spontaneous AP
3 channel problems than can prolong the APD
Drug induced LQTs due block of which channel?
- decrease outward K
- increase inward Na or Ca
Ikr channel
Drug of choice for rapid termination of AVNRT
Adenosine
What anti-arrhythmic is contraindicated in adults w/ WPW syndrome due to inc mortality?
DIGOXIN - accelerates conduction in accessory pathway -> inc risk of VF
Class Ia drugs
- mech
- indications
- example drug
- side effects
- effect on mortality (CAST).
1a -> QUINIDINE
- prolong APD, ERP, QT interval
- rhythm control in atrial flutter or afib
- risk for TdP
- has class III actions -> blocks K channels
- diarrhea, cinchonism, thrombocytopenia
SLE like syndrome -> procainamide
Effect of class I drugs on mortality (CAST)
Mortality is DOUBLED in patients with MI and LV dysfx
-slow conduction in border zone tissue -> make VT worse
- inc rate of atrial to vent transmission in atrial flutter
- > need to give an AVN blocking drug (Ca channel blocker)
-inc threshold for pacing and defib
Beta blockers - Class II
- most effective drug in txing?
- which one is used?
- is it selective?
arrhythmias and preventing SCD in patients with:
- Ischemic heart disease -> reduce HR
- HF -> stop remodeling process
- Congenital LQTs
- post MI -> reduce mortality
METOPROLOL
-beta-1 selective
Side effect of beta blockers?
CIs?
Cardiodepressant
Contraindicated in
- severe HF,
- severe bradycardia,
- AV block > 1st degree;
- use with caution with Ca channel blockers
- Bronchospasm – contraindicated in asthma
- Other: insomnia, depression, dizziness, etc
Effect of beta blockers on the following channels -ICa-L -IK-r HCN (If) -NCX
Suppress all EXCEPT for IK-r (shortens APD)
What’s the most effective drug for rhythm control in AF?
AMIODARONE - Class III
Class III - amiodarone
- indications
- effect on mortality
- Effective in acute management of sustained VT/VF
- Given IV
- in the out of hospital and emergency setting and in ICU
- improves survival to hospital admission in patients w/ shock-resistant VF - Most effective drug for maintaining sinus rhythm in AF
- Used with ICD in VT/VF to reduce number of shocks
No effect on mortality
Cardioversion of AF
- which drugs are best
- which is best in context of WPW syndrome
Flecainide (class 1C), ibutilide (III), and dofetilide (III) are the most efficacious agents for medical conversion of AF
Procainamide (1A) - AF + WPW
Adverse effects of amiodarone
- pulmonary fibrosis
- lots of drug drug ix
- deposition of pigment when exposed to sun
- gray/blue skin
What are the issues with Class III drugs ASIDE from amiodarone
promotes the development of EAD, or can convert borderline DAD into EAD, lead to TdP and SCD.
Class IV drug
- name
- mech
- indication
- adverse effect
DILTIAZEM
Reduces inward Ca current in nodal cells. Decrease conduction velocity. Effect on AVN > sinus node.
Rate control in AF;
Termination and suppression of SVT
Cardiac: sinus bradycardia, AV block. Negative inotropic effects will worsen heart failure.
Hypotension due to vasodilation
How can you tx tosades de pointes and digoxin toxicity?
Mg++
MoA of digoxin
indications
-blocks Na/K-ATPase -> inc intracellular Na -> reversal of NCX -> inc intracellular Ca -> inc contractility
INDICATIONS
- inc CO -> good for HF
- release ACh from cholinergic nerve terminals -> inhibits depolarization of AV nodal cells -> slows conduction at AVN -> good for rate control atrial flutter or afib
What’s better in AF management - controlling rate or controlling rhythm
AFFIRM trial - BOTH have equal outcomes with regards to mortality
Decreasing MLA in the presence of (fill in) correlates with (increase/decreased) plaque burden.
TCFA - thin-cap fibroatheroma
INCREASED
Statins lead to a decrease in which 3 end points?
Is this independent or dependent on baseline LDL levels?
- overall mortality = 12%
- coronary mortality = 19%
- strokes = 17%
Independent
What did the REVERSAL trial establish?
Aggressive tx is better (atorvastatin 80 mg > pravastatin 40mg) -> greater dec in atheroma volume
What did the TNT trial show?
Lower primary endpoints in intensively txed group (80mg ator - 77mg/dl LDL-C > 10mg ator - 101mg/dl)
for 2ndary prevention
What did the JUPITER trial show?
Satin use beneficial for PRIMARY prevention among patients w/out significant elevations of LDL-C at baseline
-but statins can inc risk of diabetes
