Heart Failure and Angina Flashcards
Goals of HF Management
- decrease congestion with diuretics
- modulate neurohormonal activation w/ RAAS antagonists and B-Blockers
- improve flow, if possible with vasodilators
Digoxin MOA
inhibits Na/K pumo of cell membrane –> Na levels within cells rise, inactivating a Na/Ca symporter –> Calcium levels in cell rises –> more Ca is stored in SR –> more Ca available for contractility
Digoxin Physiologic effects
HR is slowed at the SA node and AV conduction is slowed (vagal response at low doses)
toxic levels may upset resting membrane potential and cause arrhythmias
Milrinone MOA
parenteral inotrope. inhibits phosphodiesterase, increases cAMP which increases Ca++ influx
increases Calcium = increased contractile force
Nitrate MOA
Nitrates are converted into NO in vascular smooth muscle –> NO activates guanylate cyclase which increases the conversion of GTP-cGMP –> cGMP mediates relaxation of smooth muscle
Nitrate Uses
SL –> tx of acute angina
PO/transdermal –> prophylaxis in stable angina
Nitrate physiologic effects
decreases LVEDP
decreases myocardial O2 demand
increases perfusion of tissue
Nitrate Drugs
Nitroglycerin
Isosorbide Mononitrate
Isosorbide Dinatrate
Ca++ channel blocker Drugs
verapamil
diltiazem
nifedipine (“dipines”)
CCBs MOA
blocks L-type calcium channels in cardiac smooth muscle and prevents Ca++ from entering the cell
Arterioles are more sensitive than veins
Dihydropyridines sensitivity
more effective on dilation of vasculature than supression of contractility and nodal conduction
Diltiazem and Verapamil Sensitivity
Great effect on SA/AV nodal tissue (phase 0) and muscle (phase 2). Also have vasodilatory effects
CCB uses
Angina: decreases PVR and O2 requirement of the heart. decreases arterial tone
Arrhythmia, HTN, premature labor and ICP in subarachnoid hemorrhage
CCB adverse effects
Gingival hyperplasia
AV block and bradycardia (diltiazem, verapamil)
flushing/edema/dizziness (dipines)
nausea/constipation
Ranolazine MOA
In ischemia, CVD, hypertrophy: late Na+ current fails to inactivate, which leads to increased Na+ intracellularly. THis reverses the Na/Ca exchange and increases intracellular Ca++. Calcium overload can lead to mechanical dysfunction and O2 demand/supply imbalance
Inhibits Na current