DRUGS FOR CARDIAC DISORDERS

Congestive heart failure (CHF)

 condition when heart muscle fails to effectively pump blood through the heart & systemic
circulation  build-up of blood (congestion).

 Causes:
• damaged heart muscle
 atherosclerosis / coronary artery dse (CAD)
 cardiomyopathy

• increased demand to heart muscle to work harder

 hypertension
 valvular disease

• abnormal heart structure

 congenital cardiac defects

Left-sided Heart failure

 when LV does not contract sufficiently  excessive blood backs up into lung tissue.

 s/sxs
• pulmonary edema
o tachypnea
o dyspnea
o orthopnea
o hemoptysis
o rales /wheezes
• cardiomegaly, increase HR, S3
• anxiety
• decrease peripheral pulses

Right-sided Heart Failure

 when right side of the heart does not contract sufficiently  excessive blood backs up into
peripheral tissues.

 s/sxs:

o elevated jugular venous pressure

o hepatomegaly
o splenomegaly
o decrease renal perfusion when upright
o increase renal perfusion when supine  nocturia
o pitting edema
o weakness & fatigue
Compensatory Mechanisms in CHF

Treatment for CHF:

Nonpharmacologic measures:

1. limit salt intake to 2 gms daily.

2. limit alcohol intake
3. avoid smoking
4. low fat & low caloric diet
5. mild exercise

Pharmacologic measures:

1. cardiotonic /inotropic agents  directly stimulate heart muscle to contract

more effectively.
2. vasodilators  reduce cardiac workload
3. diuretics  reduce blood volume & heart’s workload
4. beta- blockers (in some cases)  reduce heart’s workload precipitated by
sympathetic activity.
5. beta-adrenergic agonists  increase heart contractility.

CARDIOTONIC DRUGS

I. Cardiac Glycosides
a. Digoxin ( Lanoxin, Lanoxicaps)
b. Digitoxin

II. Phosphodiesterase Inhibitors

a. Inamrinone (Inocor)
b. Milrinone (Primacor)

I. Cardiac Glycosides / Digitalis Glycosides

 increase calcium movement into heart muscle
• increase force of myocardial contraction  (+ ) inotropic effect
• increase CO & renal perfusion increase stroke volume & increase UO  decrease
blood volume
• slowed HR ( - ) chronotropic effect
• decreased conduction velocity thru AV node (-) dromotropic effect

decrease cardiac workload & relief of CHF

 primarily excreted unchanged in urine

 Indications:
1. treat CHF
2. correct atrial fibrillation
3. correct atrial flutter
4. treat paroxysmal atrial tachycardia

A. Digoxin (Lanoxin, Lanoxicaps)

 absorption rate  oral tablet  > 70%
 liquid  90%
 capsule  90-100%
 narrow margin of safety
 therapeutic serum level 0.5 to 2.0 ng/ ml
 half-life is 36 hours
 B. Digitoxin
 potent cardiac glycoside
 very long half-life

SE/Adverse effects of cardiac gycosides:

1. headache, drowsiness, fatigue, confusion
2. visual illusions, blurred vision, diplopia, photophobia
3. GI upset & anorexia
4. bradycardia

Digitalis Toxicity
 overdose or accumulation of digoxin
 s/sxs
i. confusion & delirium
ii. bradycardia
iii. anorexia, N & V, diarrhea
iv. ventricular dysrhythmias  heart block

Digoxin immune Fab (Digibind, Digifab)

 antidote to digitalis toxicity ( serum levels >10 ng / ml with serum potassium
> 5mEq/L )

Drug interactions:
1. verapamil, amiodarone, quinidine, erythromycin, tetracycline
 ncrease Tx effect & toxic effects
2. potassium- losing diuretics & cortisone  hypokalemia  increase risk of cardiac
dysrhythmias.
3. antacids  decrease digitalis absorption
4. thyroid hormones, metoclopramide or penicillamine  decrease digitalis efficacy

Nursing Responsibilities:
Before
1. Obtain a drug history.
2. Obtain baseline pulse rate.
3. Assess for S/Sxs of digitalis toxicity & report ASAP.
4. Be aware of contraindications:
a. Allergy
b. Ventricular dysrhthmias
c. Heartblock
d. Acute myocardial infarction
e. Renal insufficiency
During
1. Read labels carefully.
2. Check dosage & preparation carefully esp in children & elderly.
3. Check apical pulse rate before administering digoxin.
4. Check serum digoxin level ( 0.5 – 2.0 ng /ml)
5. Check serum potassium level (3.5 – 5.3 mEq/L)
6. Maintain emergency equipment on standby:
a. Potassium salts
b. Lidocaine
c. Phenytoin
 d. atropine
After
1. Monitor for SE/ adverse effects.
2. Monitor patients response & effectiveness.

II. Phosphodiesterase Inhibitors:

 block breakdown of cAMP  ow more calcium to enter heart muscle

more intense contraction & increase sympathetic stimulation

increase SV & CO vasodilation, increase HR, BP & workload

 reserve for use if no response with other agents.

A. Amrinone ( Inocor)
B. Milrinone ( Primacor)

Adverse effects:
1. ventricular arrhythmias
2. hypotension
3. chest pain
4. GI upset
5. thrombocytopenia

Nursing responsibilities:
• protect drug from light.
• Monitor PR & BP.
• Monitor platelet counts.
 ANTIANGINAL DRUGS

Coronary Artery Disease (CAD):

 develops when changes in the intima of coronary artery occur.
• atheromas (fatty tumors) in intima
attract platelets & immune factors

cause swelling & larger deposit

narrowing of coronary artery

lose elasticity & unable to meet needs of tissues

Angina Pectoris (“suffocation of the chest)

 acute cardiac pain caused by inadequate blood flow to myocardium
• plaque occlusions in coronary arteries or
• spasms

decrease in O2 to myocardium

anginal pain
 tightness
 pressure in center of chest
 pain radiating to left arm or neck

Types of Angina:
1. Classic (Stable)
• occurs with stress or exertion.

2. Unstable (Preinfarction )
• occurs frequently over the course of the day with progressive severity.
• occurs even at rest.

3. Prinzmetal’s (Variant, Vasospastic )

• caused by spasm of coronary vessel
• occurs often at same time each day.
• occurs during rest.

Myocaridal infarction:
 complete occlusion of coronary vessel  cells become ischemic  necrotic 
die.
  S/sxs:
 excruciating chest pain
 nausea
 severe sympathethic stress reaction

 MC cause of death  fatal arrhythmias.

Treatment to control angina:

Nonpharmacologic measures:

1. avoid heavy meals.

2. avoid smoking
3. avoid extreme weather changes
4. avoid strenuous exercise & emotional upset
5. proper nutrition
6. moderate exercise
7. adequate rest & relaxation.

Pharmacologic measures:
1. Nitrates
2. Calcium channel blockers effective for variant (vasospastic ) angina pectoris
3. Beta- blockers  effective for stable angina

Antianginal Drugs:

I. Nitrates
1. Nitroglycerin (Nitro-Bid, Nitrostat, Transderm- Nitro)
2. Amyl nitrate
3. Isosorbide dinitrate (Isordil)
4. Isosorbide mononitrate (Imdur, Monoket)

II. Beta-blockers
A. Non-selective
1. Propanolol ( Inderal)
2. Nadolol (Corgard)
3. Pindolol (Visken)

B. Selective
1. Metoprolol (Toprol, Lopressor)
2. Atenolol (Tenormin)

III. Calcium-channel blockers

1. Verapamil (Calan)
2. Nifedipine (Procardia)
3. Diltiazem (Cardizem)

I. Nitrates
 cause generalized vascular & coronary vasodilation.

decrease venous return increase blood flow to myocardial cells

 reduces myocardial ischemia
lowers systemic blood pressure
• decrease preload
• decrease afterload

decrease cardiac workload & demand for oxygen

1. Nitroglycerin
 Nitrate of choice in acute anginal attack
 Sublingual (SL) tablet
• MC used
• absorbed rapidly & directly into:
 internal jugular vein &
 right atrium
• ave. dose 0.4mg or gr 1/150 following cardiac pain
• onset of action: 1-3 min. & effects lasts for 10 minutes
• decompose when exposed to light

 also available in:

o ointment,
o transdermal patch
o aerosol spray
o IV forms

2. Amyl nitrate
 Inhaled
 onset of action: 30 secs.

3. Isosorbide dinitrate (Isordil)

4. Isosorbide mononitrate (Imdur, Monoket)
 oral drugs
 slower onset of action
 last upto 4 hrs

SE/ Adverse reactions:

1. headaches
2. hypotension , dizziness & weakness
3. flushing
4. N & V, anorexia
5. reflex tachycardia

Drug- interactions:
1. beta-blockers
2. calcium channel blockers enhance hypotensive effect of nitrates
3. vasodilators
4. alcohol
5. IV nitroglycerin  antagonize effects of heparin.
 6. ergot derivatives  risk of hypertension & decrease nitrate efficacy.

Nursing responsibilities:

1. Be aware of contraindications!
a. marked hypotension
b. acute myocardial infarction
c. severe anemia
d. head trauma / cerebral hemorrhage
e. pregnancy & lactation
2. Monitor VS.
3. Have client sit or lie down when taking nitrate for the 1st time.
4. Offer sips of water before giving SL nitrates.
5. Give SL preparations under tongue or in buccal pouch.
6. Rotate sites of topical forms.
7. Nitro-Bid ointment  use tongue blade or gloves.
8. translingual spray  used under tongue, not inhaled.
9. Break amyl nitrate & wave under nose.
10. Nitrol patch – removed nightly to allow for an 8-12 hr night-free interval.
11. taper dosage gradually over 4-6 wks.
12. Proper storage.

II. Beta-blockers
 block release of catecholamines (Epi & Norepi)

block stimulatory effects of SNS

decrease HR & BP
decrease myocardial contractility

reduce need for O2 consumption & cardiac workload

reduce anginal pain

 Indications:
1. antianginal  long term mgt of stable angina pectoris
2. anti-dysrhythmic
3. antihypertensive

 well-absorbed orally
 teratogenic effects in animal studies
 SE/ adverse reactions:
o decrease in PR & BP
 o dizziness, fatigue, emotional depression
o GI upset
o CHF & arrhythmias
o Bronchospasm & cough

A. Nonselective
 decrease PR & cause bronchoconstriction
 SE
• bronchospasm
• behavioral/ psychotic response
• impotence

1. Propanolol (Inderal)
 onset of action:30 min , half-life 3-6hrs
 long-term mgmt of angina
 used to prevent reinfarction in stable pxs 1-4 wks after MI.

2. Nadolol (Corgard)
3. Pindolol (Visken)
B. Selective
 act more strongly with beta 1 receptor.
 decrease PR & avoid bronchoconstriction

1. Metoprolol (Lopressor, Toprol)

• onset of action: 15 min , half-life:3-7 hrs, doa:6-12 hrs
• Tx of angina & prevent reinfarction within 3-10days after MI

2. Atenolol (Tenormin)
• onset of action: 60 min, half-life : 6-7hrs, doa: 24 hrs

Drug- interactions:
1. beta-blockers + clonidine  paradoxical hypertension
2. beta-blockers + NSAIDS  decrease antihypertensive effect
3. beta- blockers + ergot alkaloids  peripheral ischemia
4. beta-blockers + insulin / antidiabetic agents  change in blood glucose

Nursing Responsibilities:
1. Beware of CI!
a. bradycardia
b. heartblock & cardiogenic shock
c. asthma & COPD
d. preg & lactation
2. Donot discontinue drug abruptly.
III. Calcium Channel blockers
 prevent movement of calcium into cardiac & smooth muscle cells

loss of muscle tone

vasodilation
decreased peripheral resistance

decrease preload & afterload

decrease cardiac workload & O2 consumption

 indications:
1. control of variant (vasopastic) angina
2. control of classic (stable) angina
3. atherosclerosis

 well-absorbed, metabolized in liver, excreted in urine.

 fetal toxicity in animal studies

 SE/adverse effects:
1. dizziness, headache
2. nausea & hepatic injury
3. hypotension & bradycardia
4. flushing

1. Verapamil (Calan)
 also used to treat rapid cardiac dysrhythmias
 bradycardia
 onset of action: 10 min, doa: 3 -7hrs – oral, 2hrs - IV

2. Nifedipine (Adalat,Procardia)
 most potent
 hypotension onset of action: 30 min., doa: 6- 8 hrs
3. Diltiazem (Cardizem)

Others:
4. Nicardipine (Cardene)
5. Amlodipine (Norvasc)
6. Bepridil (Vascor)
7. Felodipine (Plendil)

Drug Interactions:
1. Diltiazem + Cyclosporine  increase toxicity
2. Verapamil + Digoxin  increase risk of digoxin toxicity & heartblock
3. Verapamil + general anesthetics  respiratory depression

Nursing responsibilities:
1. Beware of contraindications:
a. Allergy
b. Heartblock
 c. Renal/hepatic dysfunction
d. Preg & lactation
2. Monitor BP & heart rhythm carefully.