Angina and congestive heart failure Flashcards
What are 4 drug classes used to treat angina?
Organic nitrates
Ca2+ blockers
K+ activators
If current inhibitors
What is isosorbide mononitrate?
Increases levels of cGMP which sequests Ca2+ out, causing weaker contraction of the heart muscle. It also causes vasodilation in the peripheries which reduce pre and after load.
Name two types of organic nitrates and two side effects
Glycerol trinitrate, and isosorbide mononitrate
Given sublingually
Headache, postural hypotension, reflex tachycardia, methaemoglobinamia
What are Ca2+ blockers and how do they work?
Verapimil, amlodipine, diltiazem, nifedipine
Reduced force of contraction
What is a contraindication of Ca2+ blocker during angina?
Using B-blockers
What is diltiazem and what side effects does it have?
It is a Ca2+ blocker, and it can cause constipation, bradycardia, high degree AV block
What is ivabradine?
If inhibitor of funny current to slow heart rate, reduce pacemaker activity.
What is the gold standard treatment for congestive heart failure?
- Carvidelol Beta blocker
- Spironolactone
- Captopril
How would you treat overdose of cardiac glycoside?
KCl if hypokalaemic Withdraw the drug immediately Antibodies to free glycosides Anti-dysrhythmic drugs e.g. lignocaine, phentoiyn Electrical defibrillation
When would you use vasodilators and how do they work to treat congestive heart failure?
When the ACE inhibitors don’t work
Hydralazine, nitrates reduce preload and afterload.
What is a long term side effect of hydralazine?
SLE like syndrome, methylanemoglobinanaemia
What do you use during acute heart failure and how does it work? How would you administer it?
B agonists IV dobutamine injection. This increases the force of contraction by increases cAMP
What are side effects of cardiac glycosides?
Dysrhythmia, nausea, vomiting, excessive bradycardia, vagal effects, gastric irritation, retinal effects, renal dysfunction
Reduced function when using K+ sparing diuretics
What is the mechanism of cardiac glycosides?
Inhibits the Na/K+ ATPase channels by competing with K+. This then reduces Na+ gradient, causing less Ca2+ to be transported out the cell. Instead Ca2+ moves into the sarcoplasmic reticulum. It enhances the force of contraction when an action potential arrives. This reduces central venous pressure and reduces oedema. It also reduces tachycardia with vagal effects. It increases refractory period of AV node to promote better filling.
What is milrenone, how would you administer it?
Phosphodiesterase inhibitor type III PDE3 administered by IV infusion or injection. It increases levels of cAMP to promote contractility by prolonging Ca2+ influx.
