how to treat primary hypertension
diuretics, ACE inhibitors, ARBs, calclium channel blockers
should you use beta blockers in CHF
only if it is compensated. it is not good to use in decompensated CHF.
drug for hypertension and diabetes
ACE inhibitors/ARBs- protective against diabetic nephropathy
amlodipine, nimodipine and nifedipine
dihyropyridine calcium channel blocker. all end in dipine
diltiazam and verapamil
non dihydropyridine calcium channel blockers
mechanism of calcium channel blockers
block L type calclium channels in cardiac and smooth muscle. no issue in skeletal muscle because not dependent on calcium inflow from the outside.
which calcium channel is best for cardiac use
Verapamil>diltiazam > dihydropyridine types
uses of non dihydropyridine calcium channel blockers
hypertension, angina, atrial fib/flutter
use of nimodipine specifically
subarachnoid hemorrage (prevents cerebral vasospasm)
hydralazine mechanism
increases cGMP which leads to smooth muscle relaxation. preferentially vasodilates the arterioles >veins so it is good for afterload reduction.
first line therapy for hypertension in pregnancy
hydralazine with methyldopa
other uses of hydralazine
severe hypertension, CHF, give with a beta blocker to prevent reflex tachycardia
strange toxicity to know of hydralazine
drug induced lupus, headache, nausea
nitroprusside
used in a hypertensive emergency. short acting, increases cGMP, via direct release of NO.
important side effect of nitroprusside
can cause cyanide toxicity by releasing the cyanide
fenoldopam mechanism
dopamine D1 receptor agonist- coronary, peripheral, renal and splanchnic vasodilation. decreases BP and increases natriuresis
nitroglycerin mechanism
vasodilates- by increasing NO in vascular smooth muscle, get increased cGMP, and smooth muscle relaxation. veins> arteries so it reduces preload mostly
uses of nitroglycerine
angina, pulmonary edema, acute coronary syndrome
Monday disease
this is in response to exposure to nitroglycerine and other veno dilating agents. this leads to tachycardia, dizziness and headaches upon return to work on Monday with renewed exposure
two partial beta agonists contra-indicated in angina
pindolol and aceutolol
best drug to decrease LDL
HMG coa reductase inhibitors
statins mechanism
inhibit conversion of HMG CoA to mevalonate, a cholesterol precursor
side effects of statins
hepatoxociticity (increased LFTs), rhabdomyalasis when used with fibrates and niacin
use of niacin
this is used to reduce LDL and it is really the only drug to effectively increase HDL.
mechanism of niacin
inhibits lipolysis in adipose tissue, reducing hepatic VLDL production
classic side effect of niacin
flushed face. this can be decreased by taking an aspirin or just with time
other side effects of niacin
hyperglycemia and hyperuricemia (makes gout worse)
which anti choelsterol agent actually increases triglycerides
bile acid resins
effect of bile acid resins
decreases LDL
mechanism of bile acid resins like choelstyramine, colestipol, colesevelam
decreases LDL by preventing intestinal re-absorption of bile acids. the liver must then use cholesterol to make more.
side effects of bile acid resins
tastes bad, GI issues, reduced absorption of fat soluble vitamins, cholesterol gallstones
ezetimibe
this is a choelsterol absorption blocker.
mechanism of ezetimibe
this prevents cholesterol absorption at small intestine brush border.
side effects of ezetimibe
can cause a rare increase in LFTs, and can cause dairrhea
patient with high triglycerides, what drug to use
fibrates.
mechanism of fibrates
increases Lipoprotein lipase to increase triglyceride clearance. also activates PPAR alpha to induce HDL synthesis.
side effects of fibrates
myositis (increased risk with use of statins too), hepatotoxicit, and cholesterol gall stones
digoxin mechanism
inhibits the Na/K pump which leads to inhibiton of the Na/Ca pump so there is more calclium in the cell- positive inoptrope. also stimulates the vagus nerve- decreases HR.
clinical use of dogoxin
used in CHF to increase contractility and in atrial fibrilation to decrease conduction at the AV node and depress the SA node
whats is an important factor leading to dig toxicity
hypokalemia. also renal failure and co-adminstration with verapamil, amiodarone and quinidine (decrease dig clearance by displacig it from tissue binding sites)
side effects of dig
nausea, vomiting, yellow blurry vision, AV block, low QT, hyperkalemia
class 1 anti arrythmics
block Na
class 1a drugs
quinidine, procainamide and disopyramide
side effect of quinidine
cinchonism (headache, tinnitus)
side effect of procainamide
drug induced lupus
side effect of disopyramide
heart failure
side effects common to all 1a
thrombocytopenia, torsades de pointes due to QT prolongation
class 1b drugs
lidocaine, mexiletine
what is special about 1b drugs
preferentially affect depolarized myocytes which are those that have been damaged by an MI. they like ischemic or depolarized perkinje cells and ventricular tissue. phenytoin can also fall into this category.
clinical use of 1b
ventricular arrythmias (post MI) and digitalis induced arrythmias
class 1c drugs
Can I have Fries Please
1C: Flecainide and Propafenone
mechanism of 1c
prolongs the refractory period but has minimal effect on action potential (unlike Class 1a and 1b)
clinical use of 1c
SVTs and atrial fibrilation
important to know about 1c
contraindicated in ischemic heart disease or post MI
class 2 antiarrythmics
beta blockers
beta blocker mechanism as an anti arrythmic
decrease SA and AV node acivitiy by decreasing cAMP and decreasing Ca current. decreases the slope of phase 4.
when are beta blockers used
to slow the rate during a fib or a flutter
beta blocker used with lipid issues
metoprolol
when should you never use a beta blocker
in a cocaine user- can get unapposed alpha adrenergic and get serious hypertension crisis
how to treat an overdose of beta blockers
glucagon
Class III anti arrythmics
potassium channel blockers. AIDS Amoiodarone Ibutilide Dofetilide Solatol
mechanism of class III
like class Ia, they increase the AP duration, increase effective refractory period but the slope of the Na first up part is NORMAL. also increase the QT interval
clinical use of Class 3
a fib and a flutter ventricular tachycardia (amiodarone, sotalol)
solatol toxicity
torsades de pointes, excessive beta blockade
side effect of Ibutilide
torsades de pointes
side effect of amiodarone
pulmonary fibrosis, hepatoxocit, hypo and hyper thryoidism, corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, bradycardia, CHF, heart block.
what labs do you need for amiodarone
PFTs, LFTs and thyroid function
what is special about amiodarone
has class I, II and III and IV effects and alters the lipid membrane
class IV anti arrythmics
these are calcium channel blockers
class IV
verapamil, diltiazem
mechanism of class IV
decrease conduction velocity, increase the effective refractory period, increase the PR interval.
clinical use of class IV
prvention of nodal arrythmias (SVT) and rate control in a fib
side effects of class IV
constipation, flushing, edema, CV effects
adenosine mechanism
increases K+ out of the cells. hyper-polarizes the cell and decreases Ica. very short acting.
use of adenosine
diagnosing and abolishing supraventricular tachycardia. very shot acting- about 15 secs. can cause flushing.
what blocks the effect of adenosine
theophylline and caffeine
clinical use of Mg2+
used to treat torsades de pointes and digoxin toxicity