Other cardiovascular drugs Flashcards
Digoxin
1) How does digoxin work?
2) Name 2 side effects of digoxin
3) Name a contraindication of digoxin
4) Name 2 consequences of digoxin toxicity
5) Name a factor that increase the chance of getting digoxin toxicity
6) What ECG change is associated with taking digoxin?
7) What is the 1st line treatment for severe digoxin toxicity?
1) Blocks the Na+/K+ pump. It reduces HR by decreasing conduction through the AV node and also has a weak positive inotropic effect
2) Decreased appetite, headache, dizziness, vomiting and visual disturbances
3) WPW syndrome, hypertrophic cardiomyopathy
4) Arrhythmias, lethargy, nausea and vomiting, yellow-green visual disturbances, diarrhoea
5) Hypokalaemia, renal failure, MI and increasing age, hypo: thermia, albuminaemia, phosphatemia, and hyper: calcaemia, natraemia. Acidosis, drugs i..e CCBs, amiodarone, spironolactone and drugs that cause hypokalemia i.e. diuretics
6) Downsloping ST segment
7) Digibind
Ivabradine
1) How does this drug work?
2) Name a contraindication of this drug
1) Blocks the pacemaker funny sodium channels, which slows HR without significantly dropping BP
2) Acute MI, bradycardia, long QT syndrome, shock
Ranolazine
1) How does it work?
2) Name 2 scenarios that this drug needs to used in caution
1) Inhibits late sodium current
2) HF, elderly, weight is <60Kg, prolonged QT interval
Nicorandil
1) How does it work?
2) Name a contraindication
1) K+ channel activator
2) Acute pulmonary oedema, LV failure, severe hypertension, hypovolaemia
Adenosine
1) The effects of adenosine are enhanced by what drug, and blocked by what drug?
2) Patients should avoid adenosine with what condition and why?
3) What is it’s MoA?
4) How does it need to be given and why?
5) Name 2 side effects
1) Enhanced by dipyridamole and blocked by theophyllines
2) Asthmatics due to bronchospasm risk
3) Causes transient heart block in the AV node
4) Large calibre cannula due to having a short half life (10s)
5) Chest pain, bronchospasm, transient flushing, enhance conduction down accessory pathways resulting in increased ventricular rates (i.e. WPW syndrome)