Mechanism: blocks inactivated channels: prefers the tissues to be partially depolarized (slow conduction in hypoxic & ischemic tissues), increases threshold for excitation & less excitation of hypoxic tissue (accelerated phase 3)
decreases APD: due to block of slow Na "window" currents but increases diastole & extends their time to recover
Clinical use: acute ventricular dysrhythmias (post MI) and digitalis-induced dysrhythmias
IB is Best for MI
Antiarrhythmic Drug: Class Ib- Lidocaine
Uses: tx for: post MI, open heart surgery, digoxin therapy
Side Effects: CNS toxicity (seizures), less cardiotoxic than conventional anti-arrhythmias
Administration: IV (to prevent 1st pass effects)
'li don't know what to do, so I'll work on good and bad tissue' :)
Antiarrhythmic Drug: Class Ib- Mexiletine
Clinical use: same as lidocaine
Antiarrhythmic Drug: Class Ic- General
Drugs: Flecainimide, Encainide, Propafenone
Mechanism: blocks fast Na channels (espeically Purkinje tissue), no effect on APD, no ANS effects
Toxicity: contraindicated post-MI, prodysrhythmic if used in prophylactic VT tx,significantly prolongs the refractory period in AV node
IC is Contraindicated in MI, flee from using it after an MI
Antiarrhythmic Drug: Class II - Beta Blockers (general)
Toxicity: reflex tachy, hypotension, flushing, "Monday Disease" in industrial exposure - dev't of tolerance for VD action during work week and loss of tolerance over weekend = tachy, dizziness & headache on reexposure
Antihypertensive Drug: Vasodilators: Direct acting thru K channels: Minoxidil
Mechanism: K channel opener = hyperpolarizes and relaxes vascular SM
Clinical use: severe htn
Toxicity: hypertrichosis (hirsuitism), pericardial effusion, reflex tachy, angina, Na retension, T wave changes on EKG
What is the drug of choice for methemoglobinemia?
Mechanism: causes the met-Hbg to form free Hbg again)
Pulmonary Hypertension: Bosentan
Note: Endothelin (ET1) is a powerful VC thru ET-A and ET-B receptor
Mechanism: Bosentan is an ETA receptor
Side effects: anything associated with VD (headache, flushing, hypotension, etc.)
CONTRAINDICATED IN PREGNANCY
Pulmonary Hypertension: Epoprostenol
Mechanism: is a prostacylcine that causes VD
Administration: infusion pumps
Pulmonary Hypertension: Sildenafil *
Mechanism: inhibits type V phosphodiesterase (PDE5 = increases cGMP = relaxes arteries) to reduce the hypertension
What are the suitable antihypertensive drugs for a pt with angina?
What are the suitable antihypertensive drugs for diabetic patients?
ACEI (protective against diabetic nephropathy)
diuretics (thiazides first line)
What are the suitable antihypertensive drugs for pts w/ heart failure?
Beta blockers (for compensated CHF but contraindicated in decompensated CHF)
diuretics (K sparing)
What are the suitable antihypertensive drugs post-MI?
What are the most suitable antihypertensive drugs for pts w/ BPH?
What are the most suitable antihypertensive drugs for pts with dyslipidemia?
What is the most suitable antihypertensive drug for pts with essential hypertension?
Diuretics (thiazide unless contraindicated)
Malignant hypertension treatment includes:
1. Nitroprusside: short acting, increases cGMP = direct release of NO, CN toxicity
2. Fenoldopam: D1 receptor agonist - relaxes vascular SM
3. Diazoxide: K channel opener: hyperpolarizes and relaxes vascular SM, can cause hyperglycemia by reducing insulin release
Inotropic Drug: Cardiac Glycoside: Digoxin
Characteristics: 75% bioavailability, 20-40% protein bound, t1/2=40 hours (thus need loading dose), urinary excretion
Mechanism: direct inhibition of Na/K ATPase = inhibition of Na/Ca exchanger/antiport = increases Ca = + inotropy, also stimulates the vagus nerve
Clinical use: CHF (increases contractility), atrial fib (decreases conduction at AV node & depression of SA node), SVT (except Wolff-Parkinson-White sydnrome)
Cholinergic - n/v/d, blurry yellow vision (think Van Gogh)ECG - increase PR, decreased QT, scooping (hockey stick) depression of ST segment, T wave inversion, dysrhythmia, hyperK