Cardiology Flashcards
Why is radial access superior to femoral access for PCI?
all cause mortalitiy
MI
Stroke
non-CABG related bleeding
NO DATA on contrast induced nephropathy
Jugular venous pressures
a = atrial contraction
c = closure of the tricuspid valve
x-decent: fall in atrial pressure during ventricular systole
v = passive filling of atrium
large v in tricuspid regurgitation
y-decent: opening of the tricuspid valve
Contraindications for balloon valvulotomy for MS
Mitral valve area >1.5cm2
Left atrial thrombus
Mod to severe MR
Severe or bicommissural calcification
Absence of commisural fusion
Severe concomitant AV disease or severe combined TS or TR
Concomitant CAD requiring bypass surgery
Murmurs and respiration
rIght is louder with inspiration
lEft is louder with Expiration
CABG vs PCI
patients with left main stem disease and low-intermediate anatomic complexity PCI with 2nd gen DES is non-inferior to CABG with respect to death, stroke or MI at 3 years
GRACE score
risk with NSTEMI
>140 is high risk and would benefit from early intervention
STEMI and early PCI
associated with reduction in death, reinfarction, recurrent ischaemia, CHF, or cardiogenic shock at 30days
features of complete heart block
syncope
heart failure
regular bradycardia
wide pulse pressure
cannon wave in neck
variable intensity of S1
Exam finding in Mitral stenosis
- reduced arterial pulse volume
- prominent ‘a’ wave in JVP, absent in AF
- prominent ‘v’ wave secondary to TR
- right ventricular heave
- palpable S2
- loud S1
- late diastolic in mild MS, becomes early in severe disease
Exam finding in Mitral stenosis
- reduced arterial pulse volume
- prominent ‘a’ wave in JVP, absent in AF
- prominent ‘v’ wave secondary to TR
- right ventricular heave
- palpable S2
- loud S1
- late diastolic in mild MS, becomes early in severe disease
SEVERE:
- mitral facies
- prominent V
- RV lift
- early opening snap following S2
- loud pulm component of S2
ECG features of pericardial tamponade
- low voltage
- electrical alternans
- PR segment depression
Posterior infarcts usually accompany which STEMI
Inferior/Lateral
Isolated posterior infarct is uncommon
Indications for PPM
PPM = permanent pacemaker
- Symptomatic sinus node dysfunction
- Acquired AV blocks in adults - Mobitz Type 2 or CHB
- Chronic bifascicular block: Mobitz Type 2 or intermittent CHB or alternating BBB
- Persistent and symptomatic 2nd or 3rd degree AV block after STEMI
- Symptomatic hypersensitive carotid sinus syndrome and neurocardiogenic syncope
- Persistent inappropriate or symptomatic bradycarida
- Sustained pause dependent VT with or without QT prolongation
Antiarrhythmic to avoid in Torsades
Class
1A: Quinidine, procainamide, disopyramide
1c: Flecainide
3: Sotalol, Amiodarone
Class I - Sodium-channel blockers.
Class II - Beta-blockers.
Class III - Potassium-channel blockers.
Class IV - Calcium-channel blockers.
Miscellaneous - adenosine. - electrolyte supplement (magnesium and potassium salts) - digitalis compounds (cardiac glycosides)
Which drugs increase digoxin level?
- Clarithromycin, erythromycin, azole
- Amiodarone, Verapamil, quinidine
- Cyclosporin
- inhibit P-glycoprotein in the kidney
What is a Hill sign and what is it associated with
Popliteal BP exceeds brachial BP by >60mmHg, associated with AR
Digoxin
Digoxin – Never first line only after B Blocker and CCB failed
Steady state is achieved after 5x T1/2 – approx. 7-10 days
Serum levels 0.5 - 0.9 ng CHF and 0.5 – 2ng in AF
Digoxin Effect
Reverse tick or sagging ST segment
Also inverted, flattened or biphasics T waves
U waves
Prolonged PR
Short QTc
Digoxin Toxicity
Clinical features include:
Gastrointestinal: Nausea, vomiting and abdominal pain (usually less prominent than with acute toxicity)
Cardiovascular: Bradycardias (1st, 2nd or 3rd degree blocks, AF with a rate <60), increased automaticity (ventricular ectopic beats, bigeminy, SVT with AV block, ventricular tachycardia) and hypotension.
CNS: Lethargy and confusion
Visual: Decreased visual acuity, yellow halos (xanthopsia) – more in chronic toxicity
Mechanism:
Direct
inhibition of Na/K ATPase on the cell surface
-> increased intracellular Na+ and increased extracellular K+
-> increased intracellular Ca2+ due to Na+/Ca2+ antiporter
-> calcium-mediated ionotropy and increased automaticity, as well as negative dromotropy due to decreased intracellular K+
Indirect
increased vagal tone (vagomimetic effect)
Toxicokinetics
Absorption – good oral absorption with oral bioavailability of 80% and peak levels at 6 hours
Distribution – 30% protein bound, Vd 10L/kg (higher in the elderly and obese)
Metabolism – minimal hepatic metabolism
Elimination – 60% renal, t ½ of 30-40 h, longer in renal failure
**Treatment: **
Digoxin immune FAB (Digibind)
Atropine for AV block and lignocaine for tachyarrthmias
Supportive therapy – treat losses, AKI and hyperkalemia
Ivabradine
Inhibits funny potassium channels in the AVN
Pt need to be in SR, EF less than 30% HR more than 70
SE: bradycardia, HTN, dizziness, AF and visual disturbances (phosphenes = flashes of light), assoc with TdP when taken with other QT prolonging drugs.
Frusemide
Ascending LoH
NKCC2
Pharmakokinetics
Onset of action – 30-60 mins
Bioavailibility – 40-70%
Elimination T1/2 – 2 hours
Excretion – renal 66% biliary 33% (check)
Metabolism – liver 10% (glucoronidation) and kidney
Perhexillene is metabolised by CYP2D6
Perhexiline is a coronary vasodilator used especially for angina of effort. It may cause neuropathy and hepatitis.
U-wave
Normal: <25% of Twave
Can appear when HR <65
Prominent U wave is seen in bradycardia and severe hypoklaemia