Cardiology other Flashcards
how long should you wait to prescribe sildenafil post MI
6 months post MI
Which beta blockers have been shown to reduce mortality in HF
carvedilol and bisoprolol are the only BBs that have been shown to reduce mortality in stable heart failure
Side effects of Adenosine administration (SVT)
Flushing
chest and abdo discomfort
headache
hypotension
an ‘impending sense of doom’
what are some secondary causes of AF and why
IHD: ischemia → scarring → electrical insability.
Heart failure, HTN, valvular disease, PE:
pressure → atrial enlargement → electrical instability.
Hyperthyroidism and stimulants
increased HR → increased atrial activity.
OSA and COPD:
Oxygen deprivation → atrial remodeling.
EtoH and smoking:
Toxic effects on heart cells → electrical disruption.
Sepsis: Widespread inflammation
Electrolyte Imbalances: electrical instability
doses of NOACs to start on for AF
Dabigatrain
- 150mg BD if <80 and CrCl >50
- 110mg BD if >80 or lower CrCl 30-50
Rivaroxaban
- 20mg OD if CrCl >50
- 15mg OD if CrCl 15-49
Doses of Beta-blockers to start on for AF rate control
(and which ones do you choose?)
Bisoprolol 1.25-20mg
metoprolol 23.75-190mg
Carvedilol 3.125-50mg
avoid sotalol as it can cause arrhythmias/heart block
Doses of calcium-channel-blockers to start on for AF rate control
(and which ones do you choose?)
non-dihydropyridine CCB
1. Diltiazem
IR 60mg TDS
MR 120mg OD
- Verapamil:
IR 40mg TDS
MR 120mg OD
DO NOT USE VERAPAMIL with a BB - negative inotrope and hypotension
what would be some reasons warfarin would be preferable over DOACs for AF
Mechanical valve or mod-severe mitral stenosis
Severe renal or liver disease
Significant gastrointestinal disease: Standard-dose DOACs have a higher risk of gastrointestinal bleeding than warfarin; lower doses have comparable risk.
Antiphospholipid syndrome:
if DOACs trialled/not working/adverse affects
Managing bleeding on a DOAC
mild bleeding:
compression + supportive measures
TXA
WH DOAC for 1-2 days
moderate - severe:
discuss with haem, ABCD, refer
whats a common GI symptom of dabigatran to be aware of
dyspepsia (~30%)
Take post prandially or with PPI
Why do we worry about LBBB
because they are always pathological
myocardial infarction
HTN
aortic stenosis
cardiomyopathy
rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
how long do you see STE post STEMI, and what does it mean if they persist
ST elevation
- typically begins to resolve within hours to days after reperfusion or treatment, often normalizes within 1 to 2 weeks
- may persist longer if there is extensive myocardial damage or if the infarcted area does not fully recover.
Chronic Changes: Persistent ST elevation beyond several weeks can indicate left ventricular aneurysm formation.
how long do you see STD post NSTEMI, a
ST depression tends to normalize faster than ST elevation
often within a few days, especially if the ischemia is relieved and no further myocardial injury
Summarise HOCM, its inheritence and ECHO findings
Hypertrophic obstructive cardiomyopathy (HOCM) autosomal dominant condition of muscle tissue caused by defects in the genes encoding contractile proteins.
HOCM is important as it is the most common cause of sudden cardiac death in the young (leads to VF)
ECHOL MR SAM ASH (MR, systolic movment of mitral valve, asymmetric hypertrophy_
Features of hypokalaemia on ECG
U waves
small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT
