CPTP4.24 Flashcards
Difference between paroxysmal and persistent AF?
Paryoxsmal self terminates!
When is rhythm control preferred?
Reversible cause, HF mainly due to AF, new onset, clinical judgement
Options for rate control?
First line is cardioselective B-blocker or rate-limiting CCB. Digoxin monotherapy can be used if sedentary. If B-blocker and CCB alone not enough, consider dual therapy with any two of: B-blocker, diltiazem, digoxin. If have LVF, give B-blocker and digoxin.
Choice of B-blockers for AF?
Sotalol contraindicated (torsade); can use carvedilol, bisprolol, atenolol, metoprolol. All can be negative inotropes and chronotropes. Chronically get fatigue and cold extremities.
CCBs in AF?
Non-DHP. L-type CCB. -ve inotropes and chronotropes. AEs include headache, constipation, ankle oedema, hypotension. Bad in HF.
Digoxin in AF?
Less effective than other two. Consider in sedentary. Risk of toxicity in renal impairment. Acts by increasing vagal tone (reduces rate) but positively inotropic. Mostly renally eliminated and narrow Tw. Stops K+/Na+ antiporter. Means less Na+ outside of cell so less of a gradient to then remove calcium.
Pill in the pocket for AF?
Use for paroxysmal. Must have no history of LVF/IHD/valve disease, infrequent symptomatic AF episodes, able to understand treatment.
Cardioverting?
If unstable, do DC cardioversion regardless of anticoagulated. If <48 hours and stable, can do either. If choose pharma, then flecainide best in first 12 hours, then equal, but bad for structural heart disease. Amiodarone not good for thyroid disease. Both can cause hypotension and HF but amiodarone less so. If >48 hours, need three weeks anticoagulation then DC, then four weeks after. Can give rate control in the meantime. Also need echo for elective.
Amiodarone?
Class III antiarrhythmic. Indicated for rhythm control. If going to do elective DC cardioverson, give before and after. Extensive tissue binding and has chronic adverse effects of photosensitivity, hepatotoxicity, pulmonary fibrosis, thyroid disease, hypotension, blue skin. Acutely (IV) can get thrombophlebitis.
Warfarin?
Vit K reductase inhibitor. Affected by illness, NSAIDs and many drug interactions. Induced by alcohol (chronic), St Johns Wort, rifampicin, carbamazepine, phenytoin. Inhibited by macrolies, azoles, non-DHP CCBs, amiodarone, valproate. Takes 2-3 days to work because only acts on synthesis of new factors. Requires monitoring, hepatically excreted, need steady state and >50% in therapeutic range. 3% risk of bleeding per year. OD.
NOACs?
Can be factor Xa inhibitors (rivaroxaban, epixaban) or direct thrombin inhibitors (dabigatran). Do not need INR monitoring but are expensive and antidotes are not widespread. GI side effects and GI bleeds, less ICH. Metabolism inhibited by amiodarone and verapamil.
Managing paroxysmal AF?
Standard B-blocker, or pill-in-the-pocket.
Reversing warfarin?
- No bleeding, INR <8 = omit/reduce, consider PO vit K. If INR >8, give 1mg Vit K PO.
- Bleeding. Minor = PO vit K. Significant, stable = IV vit K, consider FFP. Life/limb/site threatening, IV vit K AND beriplex.
Epidemiology of poisoning?
Mostly affects children 1-5, or AYA (M=F).
Poisons most likely to cause death?
Paracetamol, TCAs, opiates (!!!), carbon monoxide.