Unit 5 - Rx of Cardio Flashcards
Cardiotonic drugs
Drugs increase the STRENGTH of heart.
Drugs for a FAILING heart (CHF)
– Heart becomes weaker as a pump.
– Over many years or rapidly in response to injury
Cardiotonic drugs
Goals for treatment
increase CO and pumping efficiency while reducing cardiac work (increase preload and decrease afterload)
*cardiac glycosides (digoxin)
MOA
MOA: increases contractility in the heart muscle
- increases intracellular calcium ion concentration and increases the force of contraction
- increases CO and relieves edema if present
*cardiac glycosides (digoxin)
S/E
- narrow therapeutic window, long half life
- development of arrhythmia - many kinds esp. ventricular
- can induce AV block
- GI
- Visual: single color vision (yellow/green), halos around obj
*cardiac glycosides (digoxin)
also used to treat ATRIAL FLUTTER (has muscarinic effect on atria)
arrhythmia(s)
- abnormal pacemaker activity: cell takes over the pacing of the heart at a rate that is diff from what it ought to be
- ectopic pacemakers: cells generating impulse outside of the SA node
- 1st cell to reach threshold will begin to pace the heart
4 classes of drugs for arrhythmias
- Na+ channel blockers
- calcium channel blockers
- blocking beta receptors
- K+ channel blockers
sodium channel blockers
delay upward spike –> will take longer to trigger the action potential.
delay phase 4 to spike of AP
calcium channel blockers
same MOA as above
increases intracellular calcium ion concentration and increases the force of contraction
blocking beta receptors
slows automaticity
potassium channel blockers
will cause the cell to take longer to get back to resting membrane potential and slows the HR.
Makes the whole AP process take longer
Class 1: Na+ channel blockers
Bind to channels in the inactive and active state, they prolong the period in which these channels don’t work
drugs will lengthen the time it takes for the channel to go back to the resting state
especially effective in sites of ischemia
Quinidine
- Na+ channel blocker
- not widely used, antimuscarinic effect
- blocks open and active Na+ channels
- stop an arrhythmia
- chiefly a cardiac depressant
- effective ORALLY
- PROBLEM: potentil for generating arrhythmias due to lengthening of AP
- S/E: cinchonism…similar to aspirin toxicity
Lidocaine
Na+ channel blocker
- used for VENTRICULAR ARRHYTHMIAS (esp. v-fib)
- effective w/ less tendency for cardiotoxicity
- used IV, first pass metabolism
An antiarrythmic agent that is used for ventricular arrhythmias in emergency situations because it has a rapid onset and a short duration of action and does not have an anticholinerigc effect is:
lidocaine
In a patient with complete heart block, ventricular rate:
is decreased over its former rate
Which antilipemic agent inhibits the enzyme necessary for cholesterol synthesis?
statins
What class of drug is indicated for the control of blood pressure because it acts by inhibiting vasoconstriction and decreases fluid retention?
ACE inhibitor
Coumarin derivatives are:
anticoagulants
A cardiac glycoside is often indicated for a patient with congestive heart failure because it has the effect of increasing the force of contraction and decreasing the rate of contraction. This class of drug is said to have a(n) ______________ effect.
positive inotropic and negative chronomtropic
When there is a mismatch in oxygen supply and demand a patient may present with chest pain. To address the chest pain, a drug that relaxes smooth muscle, decreasing blood pressure and ultimately decreases the work of the heart would be prescribed. What class of drug can accomplish this goal?
nitroglycerine
A major side effect of cardiac glycosides is:
ventricular tachycarida
Atrial flutter is:
treated with a cardiac glycoside or an antiarrythmic agent since both are effective
The antihypertensive agent(s) that shows an increased efficacy for African American patients is (are):
calcium channel blockers and diuretics
*Amiodarone
K+ channel blocker
Na+ channel blocker
- also blocks Ca+2 and beta-adrenergic receptors
- effective in ORALLY suppressing arrhythmias
- less likely to produce arrhythmias
- very long half life, tendency to go crystalize in the tissue (pulmonary fibrosis is limiting side effect)
- crystal formation in cornea
Class 2: Beta adrenergic antagonists
- SLOW the heart down and suppresses arrhythmias
- decrease catecholamine induced automaticity (epi or nor-epi)
Class 3: Potassium channel blocker (sodalol) (adenosine)
- prolongs AP and refractory period
- if you lengthen the AP it takes longer to get back to resting potential and longer until cells can fire again
- produces same arrhythmias as Quinidine.
Class 4: Calcium channel blockers (verapamil)
- works same way as Na+ channel blockers, they have a preference for open/active channels
(BUT they work at SA and AV nodes, places where calcium currents are driving the current) - effective for atrial arrhythmias and circus movements
- can weaken cardiac muscle for time
HTN
- CVD #1 killer in US
- essential HTN: no identifiable cause that you can treat. Treatment aimed at symptoms
- Sx are unnoticeable
risk factors: wt, sex, FHx, genetics
Targets for treatment
- CO: sympatholytics
- Vascular resistance: sympatholytics, direct acting vasodilators, drugs that interfere w/ RAA system
- fluid volume: diuretics (first line Rx)
damage to cardiovascular system
- hypertrophy to the heart
1. heart is stretched and leads to remodeling cardiomyopathies
2. bigger the heart, the more wall tension the heart has to generate to push blood against the pressure - vascular damage
1. elevate pressure can damage the blood vessels
Centrally acting sympatholytic (clonidine)
- MOA: alpha-2 adrenergic agonist in the brain. Receptors are turned on it decreases sympathetic outflow (will see decrease in vascular resistance and decrease in CO)
- Uses: HTN, when no other Rx work
- S/E: sedation and depression (rebound HTN)
2nd or 3rd line Rx
Centrally acting
guanefidine, reserpine
MOA: prevents release of nor-epi from nerve terminals
– Decrease vascular resistance and a decrease of CO
– 2nd line Rx
S/E: severe hypotension
– Reserpine can cross the BBB and can cause depletion of catecholamines, commonly causes depression
Alpha (1) Blockers (prazosin)
MOA: block alpha receptors in peripheral arterioles. The arterioles dilate and BP falls.
– Drugs are very useful in lowering BP
S/E: 1st dose hypotension –> dizziness (postural hypotension)
– Drowsiness
– Fluid retention – tachycardia
Beta Blocker (propranolol)
MOA: blocks beta adrenergic receptors, decreasing cardiac output and HR –> decreasing BP
– Decrease in vascular resistance and dilation arterioles
Indications: HTN, arrhythmias
S/E: decrease in contractility of heart, rebound HTN
Contraindications: asthma (b-2 receptors)
Calcium channel blockers (verapamil)
MOA: blocks calcium channels in smooth muscle and cardiac muscle.
– Not all Ca++ channel blockers are the same; some work better for arrythmias (verapamil), some are better for the blood vessels (nifedipine)
S/E: decrease contractility in the heart
ACE inhibitors
MOA: inhitbits angiotensin converting enzyme
– Decreases BP in practically everyone
Indications: HTN, also CHF
Adverse effects: common dry cough
C/I: pregnancy due to tendency toward renal stress, potential renal failure
Angiotensin 2 receptor blocker
Same action as ACE inhibitor
- No cough
calcium channel blockers
MOA: cause vasodilation
Therapeutic uses: HTN, suptraventricular tachycardia, angina
Note: better antihypertensive agent for African Americans (in combo w/ diuretics)
C/I: not for patients w/ CHF
Diuretics
Often first line therapy
If one drug only is being used, it is usually a diuretic
MOA: reduces hypervolemia
– Also appears to relax blood vessels
Antihypotensive Agents (aka pressor)
These drugs increase BP
How?
– Increase peripheral resistance (alpha agonist)
– Increase CO (beta agonist)
– Increase (replace) fluid volume (whole blood)
Therapeutic uses: chronic symptomatic hypotension, acute hypotension, replace blood volume
*Antianemic / Hemopoietic Drugs
Rx that replace missing factors for blood formation
– Iron, vitamin B12, folic acid (antinomic agents)
Therapeutic uses: treat anemias
Drugs affecting Coagulation
- Hemostatics
- Anticoagulants
- Thrombolytics
*Hemostatics
speed UP blood clotting
– Used to treat hemorrhage
*Anticoagulants
slow DOWN blood clotting, decrease risk of clotting
- Work by blocking formation of thrombin and fibrin, decreases platelet aggregation
- Therapeutic uses: venous thrombosis, prevent coronary thrombosis, any condition that results in blood remaining in heart after systole
*Thrombolytics
drugs that dissolve clots
– MOA: cause plasminogen to convert to plasmin
– Therapeutic use: any clot
Antilipemic Agents
- Fibroic Acid Derivatives
- Niacin
- Bile sequestrant
- Statins
*Statins
MOA: inhibit enzyme for cholesterol synthesis
– Can greatly reduce LDL cholesterol (30- 40%)
Adverse effect:
– May negatively affect the liver
– Muscle pain, weakness
- deplete CoEnzyme Q10, recommend supplement so minimize S/E
*First line of therapy for CHF
- ACE inhibitor - inhibit enzyme that converts angiotensin 1 to angiotensin 2
- beta blockers also used for CHF
- direct vasodilators
arrhythmias
abnormal rate or rhythm
Action Potential (AP)
- depolarization - cell stimulated, Na+ channels open, Na+ rush in (inside + , outside -)
- threshold - reached, then…
- AP
- re-polarization - K+ channels
