Cardiovascular Drugs Flashcards
what is arrhythmia?
alteration in normal impulse pathway
alteration in transmission pathway
what is an ectopic focus?
source of rhythm start
are ventricular alterations life threatening?
yes
what are a major cause of sudden cardiac death?
ventricular arrhythemias
T/F drug treatment can cause arrhythmias
True
T/F non drug treatment is preferable?
True
what are some non drug treatments?
pacemaker
cadioversion- global depolarization of heart
automatic defibultaor implanted
surgeries to remove ectopic forcus- ablation
class 1 drugs fro arrhythmias are what
sodium channel blockers
class 2 drugs for arrhythmias are what
beta blockers
class 3 drugs for arrhythmias are what?
K channel blockers
how do class 1 work?
local anesthetics, decrease rate of depolarization
what are the 1a drugs?
qpd
quinidine
procainamide
disopyramide
quinidine
for ALL arrhythmias, depresses all muscle function
- anticholinergic effects (antivagel)
quinidine SE
GI- nausea, vomitting, anorexea
CNS- tinnitus, alteration in color/vision
procainamide
like quinidine. analog of cocain. does NOT enter CNS
procainamide
in slow acetylators, lupus like syndromes
disopyramide
strong antivegal effect
- antimuscarinic effects- dry mouth, constipation
1b drugs for arrhythmias
lidocaine
mexiletine
lidocaine
give IV, 1st pass metal.
- less likely to cause arrhythmias but can enter CNS, tremors, seizures
what is a good use of lidocaine?
use for treating ventricular tachcardia (fast heart beat)
mexiletine
like lidocaine but given orally. `
class 2 works how?
blocks beta 1 receptors on heart. slows HR
class 2 drugs
propranolol
metoprolol
esmolol
class 2 SE
bradycardia
hypotension
propranolol
decrease firing rate
metoprolol
more selective, less B2 effects
esmolol
more rapid onset of action
class 3 drugs
sotalol
amiodarone
dronedarone
sotalol
Beta blocker that also blocks K channels
amiodarone
ultimate drug!
acts like all 4 classes of antiarrhythmias
most effective in cardiac arrest
SE of amiodarone
Potentially fatal pulmonary fibrosis- alters lung tissue
liver damage
deposits in cornea and skin (cuz of iodine, blue/gray skin)
GI upset
dronedarone
fewer SE, less efficacy, analog of amiodarone
class 4 drugs are what
calcium channel blockers
class 4 drugs
verapamil
nifedipine
diltiazem
all Ca channel blockers work how?
blocks Ca transport in cardiac cells
increases refractory period
class 4’s are not useful for what?
ventricular arrhythmias, they are also vasodilator
“other” drugs for arrhythmias
adenosine
adenosine
IV, binds to adenosine receptor, decrease firing rate of AV node. very short half-life.
Angina
not enough blood flow to heart muscle, chest pain, usually after exercise, at rest its called “unstable angina”
treatment of angina?
increase bloodflow to heart, decrease O2 demand.
basic treatment of angina?
behavioral, diet, exercise, stop smoking.
Drugs to treat angina?
nitrates
nitroglycerin
isosorbide dinitrate
nitroglycerin
sublingually. rapidly dilates all blood vessels, including coronary arteries
mechanism of nitro.
activates NO which activates guanylate cyclase which activates cGMP which causes vasodilation
SE of nitro
hypotension, skin flossing, headache.
one big problem of taking a lot of nitroglycerin?
rapid tolerance.
what is another nitrate used for angina?
isosorbide dinitrate
isosorbide dinitrate
slow release nitrate formulation. can be given orally.
other angents used for angina
- agents that decrease heart work
- beta blockers
- calcium channel blockers
what is congestive heart failure?
heart doesn’t contract enough, rest of body doesn’t get enough blood flow.
- tissue not oxygenated blood.
- heart begins to enlarge which causes…
- pulmonary congestion…which causes
- decrease ability to breath and kidney not well perfused
- kidney causes retention of sodium ions + H20- edema
why is it called CONGESTIVE heart failure?
lots of fluid retention- pitting edema if not treated.
how does the heart adapt to failure?
- apparent loss of blood- increase in E and NE and All.
leads to increase BP, HR, and vasoconstriction - increase blood volume- All, increase sodium retention, increase aldosterone secretion, increase sodium potassium exchanger.
- enlargement of heart- Incrase force of contraction due to stretching of cardiac muscle
why are these compensations so dangerous?
are what actually is damaging the heart. its a cycle, heart can’t repair itself
two basics treatments of cardiac insufficiency
- incrase force of muscle contraction
2. inotropic agents
how do inotropic agents work?
all increase amount of calcium in heart muscle
cardiac glycosides are naturally occurring? T/F
True, found in plants
main cardiac glycosides
digoxin, given orally
mechanism of action of digoxin?
all about Calcium
Digoxin inhibits the sodium potassium ATPase….Na remains high in the cell…meaning that Ca will not be exchanged as much…Ca will be high in the cell leading to greater contractility and also increase duration of contraction.
in order for muscle to relax what must be removed
calcium
toxic effects of digoxin
- cardiac arrhythmias- cuz you prolong contractility
2. CNS- yellow/green vision, hallucinations, severe nausea cuz chemoreceptors activated
digoxin poisiing cured by what?
anti digtoxin antibodies
digoxin has greater effects in someone who is
hypokalemia
other inotropic agents?
dobutamine- beta 1 agonist- incrase force of contraction
current best treatment of CHF
- ACE inhibitors. decrease BP, fluid retention
- Beta blockers. decrease fluid retention
- vasodilators. decrease BP
what do all these drugs have in common?
agents that inhibit bodies compensatory changes in heart failure. (don’t want heart to work as hard)
agents that increase blood flow to certain organs
vardenafil
avanafil
tadalafil
sildenafil
the -nafils do what?
inhibit type V cGMP phosphodiesterase, leads to more smooth muscle relaxation instead of cGMP getting broken down
SE of these drugs
- slight decrease in BP
- do not use with alpha blockers or nitrates- major BP drop
- stroke, heart attack
- impaired blue green color
- NAION- damage to retina
what are these drugs also useful for?
pulmonary hypertension- pulmonary artery also has cGMP PDE that can be inhibited.
alprostadil
injectable prostaglindin E1 PGE1, causes vasodilation when injected dirtily into penis
