Cardiovascular

Question 1

What are 3 important side effects of clexane (enaxaparin, LMW heparin)?

Answer 1

1. Monitor the platelet function to look for heparin-induced thrombocytopenia (HIT). It is rare (less than 1% of patients with short term use).
   Platelet count should be monitored on days 0, 3, 5 and then on alternate days if treatment is continued. If the platelet count drops 30–50% below baseline, heparin or LMWH should be withheld and an alternate anticoagulant substituted. Severe HIT usually occurs between days five to ten but may occur earlier if a patient has been exposed to heparin recently (

Question 2

What is the standard dose and route of clexane?

Answer 2

40mg subcut daily

Question 3

Which agents are indicated for VTE prophylaxis in the setting of hip replacement? For how long following hip replacement should the patient be anticoagulated?

Answer 3

Patients having elective hip arthroplasty are at high risk of VTE (40-60%). Provided there are no contraindications, pharmacological thromboprophylaxis is recommended for approximately 5 weeks following hip replacement using one of the following agents:

LMWH, fondaparinux, rivaroxaban, dabigatran, or apixaban. Fondaparinux is more effective than LMWH in major orthopaedic surgery but has a higher risk of major bleeding. Rivaroxaban, dabigatran, and apixaban are relatively new orally active agents with limited post-marketing surveillance. Rivaroxaban and apixaban have been shown to be more effective than LMWH for total hip and knee replacement surgery. The effectiveness of dabigatran and LMWH is similar.

Question 4

What dose of clexane should be given to a patient with renal impairment?

Answer 4

20mg s/c per day

Question 5

What is the normal range for platelets?

Answer 5

150-400 x 109/L

Question 6

What are the AF drugs- rate and rhythm control

Answer 6

rate: digoxin, beta blockers, verapamil/diltiazem
rhythm: flecainide, sotalol, amioderone

Question 7

What is the mechanism of digoxin?

Answer 7

• increases refractory period of the AV node to improve filling time
• inhibition of the Na+/K+ ATPase–> cells extrude less sodium–> due to Na/Ca exchanged intracellular calcium is increased–>increasing the amount of calcium in the sarcoplasmic reticulum-> ionotropic= increased for of contraction per stretch
• also increases vagal tone of the heart

Question 8

what is the mechanism of amiodarone?

Answer 8

Amiodarone is categorized as a class III antiarrhythmic agent, and prolongs phase 3 of the cardiac action potential, the repolarization phase where there is normally decreased calcium permeability and increased potassium permeability. It has numerous other effects however, including actions that are similar to those of antiarrhythmic classes Ia, II, and IV.

Amiodarone shows beta blocker-like and calcium channel blocker-like actions on the SA and AV nodes, increases the refractory period via sodium- and potassium-channel effects, and slows intra-cardiac conduction of the cardiac action potential, via sodium-channel effects.