Drugs for Cardiac Disorders

a. Cardiac Glycosides
b. Antianginals
c. Antidysrhymthmias

CARDIAC GLYCOSIDES
 also called digitalis glycosides
 a group of drugs that inhibit the sodium-potassium pump,

increase intracellular calcium

cardiac muscle fiber contract more efficiently

 effects on the heart muscle

1. positive inotropic action (increases myocardial contraction stroke
volume)
2. negative chronotropic action (decreases heart rate)
3. negative dromotropic action (decreases conduction of the heart cells)

 effective in treating congestive heart failure (CHF) or congestive cardiac

failure (CCF)

Congestive heart failure – inability of the heart to pump blood to meet the needs
of the tissues for oxygen and nutrients
↓ Myocardial function or failure

↓ Cardiac output

↓blood flow to kidneys Baroreceptor stimulation

Activation of renin- angiotensin system

Sympathetic activation

↑ Bp, Cardiac output ↑ aldosterone synthesis and release

↑ Bp, PR,
↑ Na retention ADH release RR,Cardiac
↑ K excretion, H20 retention output, +
inotropic effect
↑ Blood volume
↑ Cardiac workload
Cardiac glycosides/antianginal drugs -1- cvb
DIGOXIN

 Pharmacodynamics:
1. Increases myocardial contraction

Increases cardiac output improves circulation and tissue perfusion

2. decrease conduction through AV node decrease heart rate

- therapeutic serum level: 0.5- 2 ng/ml

- Route of admin: PO/ IV

 Pharmacodynamics:
- Absorption rate:
tablet: > 70%
liquid: 90%
capsule: 90- 100%
- Protein binding: 25%
- Half-life: 36 hours
- Excretion: 70% urine, mostly unchanged
30% by liver metabolism

 Digitalis toxicity
- Overdose or accumulation of digoxin
- Hypokalemia increases the risk for digitalis toxicity
- Signs and symptoms
» Anorexia
» diarrhea,
» nausea and vomiting
» bradycardia (PR< 60 bppm)
» premature ventricular contractions
» cardiac dysrythmias
» headaches
» malaise
» blurred vision
» visual illusions (white, green, yellow halos around lights)
» confusion
» delirium
- Antidote: Digoxin Immune Fab (ovine, Digibind)
- binds with digoxin to form complex molecules that can be excreted
in the urine.

 Drug Interactions
- potent diuretics (furosemide, hydrochlorothiazide)

Cardiac glycosides/antianginal drugs -2- cvb

 » promotes potassium loss
- Cortisone preparations (taken systemically)
» promotes Na and retention and potassium excretion
- Antacids
» Decrease digitalis absorption if taken at the same time

***Nursing Considerations:
Clients who take potassium-wasting diuretics or a cortisone should
consume foods high in potassium or take potassium supplements as prescribed
to avoid hypokalemia and digitalis toxicity
Doses of antacids and digitalis should be staggered.

 Contraindications - Rationale
Ventricular tachycardia or fibrillation Potentially fatal and should be treated
with other drugs
Heart block Could be made worse by slowing of
conduction through AV node
AMI Increase in force of contraction could
cause more muscle damage and
infarct
Renal insufficiency Drug is excreted through the kidneys
and toxic levels could develop
Electrolyte abnormalities (↓ K, Mg, ↑ Ca) Can alter the action potential and
change the effects of the drug
Pregnant or lactating mothers Used cautiously because of the
potential adverse on the fetus or
neonate.

Nursing Process
Assessment:
 Drug and medical history
 Baseline PR. Apical pulse should be taken for a full minute and should
be >60 bpm
 If PR is less than 60bpm, withhold medication and inform the doctor.
 Assess for S/sx of digitalis toxicity

Nursing Diagnosis
 Decrease cardiac output
 Ineffective tissue perfusion
 Anxiety related to cardiac problems

Cardiac glycosides/antianginal drugs -3- cvb

Nursing Interventions:

 Do not confuse digoxin with digitoxin

- both are cardiac glycosides
Digoxin Digitoxin
Half-life 36 h 4 – 9 days
Therapeutic serum 0.5 – 2.0 ng/ml 10 – 35 ng/ml
level
Dosage: Digitalization 0.5- 1mg initially in 0.8 – 1.2 mg
2 divided doses
Maintenance 0.125 – 0.5 mg/day 0.05 – 3 mg/day

 Check the apical pulse rate before administering digoxin. Do NOT

administer if PR > 60 bpm for adult; PR> 90 bpm for infants.
 Check the serum digoxin level, to evaluate therapeutic dosing and
monitor the development of toxicity ( > 2.0ng/ml is indicative of digitalis
toxicity.)
 Check the serum potassium level. (NV: 3.5 – 5.5 mEq/L). Hypokalemia
increases the risk for digitalis toxicity.
 Administer IV doses very slowly over at least 5 minutes, to avoid cardiac
dysrythmias and adverse effects.
 Arrange for the client to be weighed at the same time each day, in the
same amount of clothes, to monitor for fluid retention and CHF.
 Avoid administering the oral drug with food or antacids, to avoid delays
in absorption.
 Maintain emergency equipment on standby: (in case severe toxicity
occurs)
- potassium salts (for treatment of hypokalemia)
- lidocaine (for treatment of arrhythmias)
- phenytoin (for treatment of seizures)
- atropine (to increase heart rate)
- Cardiac monitor
 Client teaching:
- Explain the importance of compliance to the drug therapy
- Advise client not to take OTC drugs without first consulting
the health care provider
- Instruct the client or parent of a child to check PR before
administering the drug.
- Instruct client to call the health care provider if PR < 60 bpms
or irregular
- Diet: Foods rich in potassium (fresh and dried fruits, fruit
juices, vegetables)

Cardiac glycosides/antianginal drugs -4- cvb

 - Adverse Effects:
 Dizziness, drowsiness, headache: Avoid driving or
performing hazardous tasks or delicate tasks that
require concentration if these occur.
 Nausea, GI upset, loss of appetite: Small frequent
meals may help; monitor for weight loss
 Vision changes: Yellow halos around objects: These
effects may pass with time. Take extra care in your
activities for the first few days. If these reactions do not
go away after 3 – 4 days, consult with the doctor.

PHOSPHODIESTERASE INHIBITORS
- inhibits enzyme phosphodiesterase

positive inotropic response vasodilation

- administered IV for no longer than 48 to 72 hours

- May cause severe cardiac dysrythmias, therefore ECG and cardiac status
should be monitored.
- amrinone lactate (Inocor) – incompatible with furosemide
- milrinone lactate (Primacor)

ANTIANGINAL DRUGS
 used to treat angina pectoris
 three types
a. Nitrates
b. Beta-blockers
c. Calcium channel blockers

Cardiac glycosides/antianginal drugs -5- cvb

ANGINA PECTORIS
- a condition of acute cardiac pain caused inadequate blood flow to the
myocardium resulting from either plaque occlusions within or spasms of
the coronary arteries.
↓ blood flow

↓ O2 to the myocardium

Pain
(tightness, pressure in the center of the chest,
pain radiating down the left arm)
- Types
a. Classic (stable) – occurs with stress or exertion
- caused by narrowing or partial occlusion of the coronary
arteries
b. Unstable (Preinfarction) – occurs frequently over the course of the day
with progressive severity
- caused by narrowing or partial occlusion of the coronary
arteries
- often indicates impending MI
c. Variant (prinzmetal, vasospastic) – occurs during rest
- caused by vessel spasm (vasospasm)

A. NITRATES
Short-acting: Nitroglycerin
Long-acting: isosorbide dinitrate (Isordil, Sorbitrate)
Isosorbide mononitrate (Imdur)
 Causes generalized vascular and coronary vasodilation, thus increasing
blood flow through the coronary arteries to the myocardial cells.

 Vasodilation causes blood to pool in veins and capillaries, decreasing the

volume of blood that the heart has to pump around (decrease preload)

 Relaxation of the of the vessels decreases the resistance the heart has to
pump against (decrease afterload) = decrease cardiac workload

 Combination of the these actions reduces the cardiac workload and

demand for O2 thus bringing the supply-and-demand ratio into balance.

Cardiac glycosides/antianginal drugs -6- cvb

 NITROGLYCERIN (Nitrostat, Nitro-Bid ointment, Transderm-Nitro)
 Pharmacodynamics
- acts directly on the smooth muscle of blood vessels, causing
relaxation and dilation
- decreases preload ( the amount of blood in the ventricle at the end of
diastole)
- decreases afterload (peripheral vascular resistance)
- reduces the myocardial O2 demand
Onset Peak Duration
SL 1-3 min 4min 20-30 min
Sustained 20-45 min 3-8 h
release cap
Ointment 20 – 60 min 1-2 h 2- 12 h
Patch 30 – 60 min 1-2 h 20- 24 h
IV 1-3 min 3-5 min

 Pharmacokinetics
- SL: >75 % absorbed rapidly and directly into the internal jugular vein
and the right atrium
- 40-50% absorbed in GI are inactivated by liver metabolism
- Ointment/patch: absorbed slowly through the skin
- Excretion: liver, primarily urine

 Side effects and Adverse Reactions

- headaches: most common side effects, may become less with
continued use
- hypotension
- dizziness
- weakness
- faintness
- reflex tachycardia – may occur if nitrate is given rapidly; due to
overcompensation of the cardiovascular system
- GI: Nausea, vomiting, incontinence
- Skin-related: flushing, pallor, increased perspiration
- Contact dermatitis and local hypersensitivity (with transdermal
preparation)

 Contraindications:
- marked hypotension
- Acute Myocardial infarction
- Increased intracranial pressure (relaxation of cerebral vessels may
cause intracranial bleeding)

Cardiac glycosides/antianginal drugs -7- cvb

 - Severe anemia (decrease in cardiac output may be detrimental)
- Pregnancy or lactation (because of potential adverse effects on the
neonate and ineffective blood flow to the fetus)
- Caution should be used in patients with
- hepatic and renal function – which could alter metabolism and
excretion of these drugs.
- Hypotension, hypovolemia (decreased blood volume and
conditions that limit cardiac output – because these conditions
could be exacerbated, leading in serious adverse effects.

NURSING PROCESS: Nitrates

Assessment:
- Obtain baseline vitals signs for future comparison
- Obtain health and drug history

Nursing Diagnosis
- Decreased cardiac output
- Anxiety related to cardiac problems
- Acute pain
- Activity intolerance

Nursing Interventions
 Monitor vital signs. Hypotension is associated with most antianginal
drugs
 Have the client sit or lie when taking nitrates for the first time.
 After administration, check the vital signs while the client is lying down
and then sitting up. Have client rise slowly to a standing position.
 Offer sips of water before giving SL nitrates; dryness may inhibit drug
absorption
 Apply Nitro-Bid ointment on designated mark on paper, Do NOT use
fingers because the drug can be absorbed; use a tongue blade or
gloves.
 Do not touch patch on the medicated area.
 Client teaching:
- A SL nitroglycerin tablet is used if chest pain occurs. Repeat in 5
minutes if the pain has not subsided and again in 5 minutes if it
persists. Do NOT give more than 3 tablets. If the pain persists > 15
minutes, immediate medical help is necessary.
- Instruct the client not ingest alcohol while taking nitroglycerin to avoid
hypotension, weakness and faintness.

Cardiac glycosides/antianginal drugs -8- cvb

 - Tolerance to nitroglycerin occurs. If client’s chest pain is not
completely alleviated, client should notify the health care provider.
- Demonstrate to client how to SL nitroglycerin tablets are taken.
- The tablet is placed under the tongue for quick absorption.
- Instruct the client not to swallow
- A stinging or biting sensation may indicate tablet is fresh
- The bottle is stored away from light and kept dry. The drug is
volatile.
- Keep original screw cap, amber glass bottle. The amber color of
the glass provides light protection and screw-cap closure
protects from moisture in the air, which can easily reduce the
potency of the tablets
- Instruct the client about Transderm-Nitro patch. Apply once a day,
usually in the morning. Rotation of skin sites is necessary. To
decrease the risk for skin abrasion and breakdown.
- Usually the patch is applied to the chest wall; however, the thighs and
arms are used. Avoid hairy area
- Patch must be removed nightly to allow for an 8 to 12-hour nitrate-
free interval to avoid tolerance associated with uninterrupted use or
continued dosage increases of nitrate preparation.
- Give sustained-release (SR) forms with water and caution the patient
not to chew or crush them, because these preparations needs to
reach the GIT intact.
- Side effects:
- Headaches commonly occur when first taking nitroglycerin
products and last about 30 minutes. Acetaminophen is
suggested for relief.
- If hypotension occurs, place the client in supine position with legs
elevated.
- Taper the dosage gradually (over 4 to 6 weeks) after long-term
therapy, because abrupt withdrawal could cause severe reaction,
including MI.
- Provide comfort measures to help the client tolerate drug effects:
- small frequent meals
- access to bathroom facilities if GI upset is severe
- environmental controls
- safety precautions
- orientation
- appropriate skin care

B. BETA-BLOCKERS (Beta-Adrenergic Blocking Agents)

 blocks the beta1 and beta2 receptor sites
 decrease the effects of the sympathetic nervous system by blocking the
action of cathecolamines (epinephrine and norepinephrine)

Cardiac glycosides/antianginal drugs -9- cvb

  Beta1-receptors are primarily located in the heart
- stimulation increases myocardial contractility and heart rate

Beta1-receptors

heart kidney

↑ heart contraction ↑ renin secretion

↑ heart rate ↑ angiotensin

↑ blood pressure
 Beta2-receptors are found mostly in the smooth muscles of the lung,
arterioles of the skeletal muscles and uterine muscles
- stimulation causes:
1. relaxation of the smooth muscles of the lungs, resulting to
bronchodilation
2. an increase in the blood flow in skeletal muscles
3. relaxation of the uterine muscle, resulting in a decrease in
uterine contraction.
Beta2 - receptor

Smooth muscle of GIT lungs uterus liver

↓ Gastrointestinal tone Activation of

bronchodilation relaxation of the
and motility glycogenolysis
uterine smooth
muscle
Increased blood
sugar

Cardiac glycosides/antianginal drugs - 10 - cvb

  Types of Beta-blockers
 Non-selective beta-blockers- blocks beta1 and beta2
- examples: propanolol (Inderal)
nadolol (Corgard)
pindolol (Visken)
 Selective beta-blockers- act more strongly on the beta1 receptor
- decreases the pulse rate and avoiding bronchonconstriction because of
the relative lack of activity at the beta2 receptor.
- examples: atenolol (tenormin)
Metoprolol (Lopressor, Toprol-XL)

 Pharmacodynamics:
 Blockage of the beta-receptors in the heart and the juxtoglumerular
apparatus of the nephron account for most of the therapeutic benefit of these
drugs
 Decreases the force of myocardial contraction

Reduces the O2 demand by the myocardium

 Juxtaglumerular cells are not stimulated to release renin

Decreases Bp

Onset of action Peak Duration

Propanolol 30 min 1 – 1.5 h 4 to 12 hours
Atenolol 60 min 2–4h 24 h

 Pharmacokinetics:
Absorption Halflife excretion
Propanolol Well orally 3 – 6h Liver
Atenolol Well orally 6–7h Kidneys, feces
Metoprolol Well orally 3–7h liver

 Side effects and Adverse Reactions

- bradycardia
- hypotension
- CNS effects: fatigue, dizziness, depression, paresthesia, sleep disturbances,
memory loss and disorientation
- GIT: GI upset, N/V, diarrhea, gastric pain, even colitis
- Genitourinary tract: decreased libido, impotence, dysuria
- nonselective beta blockers: bronchospasm
- behavioral or psychotic response
- impotence (with use of Inderal)

Cardiac glycosides/antianginal drugs - 11 - cvb

  Contraindications and Cautions
Contraindications Rationale
Bradycardia, heart blocks, These conditions may be
shock CHF exacerbated by cardiac-
suppressing effects these drugs
Brochospasm, COPD, acute These conditions could be made
asthma worse by the blocking of
sympathetic bronchodilation
Pregnancy Because neonatal apnea,
bradycardia, and hypoglycemia
may occur
Lactation Because of potential effects on
the neonate: slowed heart rate,
hypotension, hypoglycemia

Use cautiously Rationale

Diabetes and hypoglycemia Because of the blocking of the
normal signs and symptoms of
hypoglycemia and hyperglycemia
Thyrotoxicosis Because of the adrenergic
blocking effects on the thyroid
gland
Hepatic dysfunction Condition may interfere with the
metabolism of these drugs

 Nursing Interventions:
- Do not stop these drugs abruptly after chronic therapy but taper gradually over
2 weeks because long term use of these drugs can sensitize the myocardium
to cathecolamines and severe reactions could occur. Withdrawal symptoms,
such as reflex tachycardia and pain may be severe.
- Continuously monitor patient receiving IV form of these drugs to avert serious
complications caused by rapid symphathetic blockade.
- Arrange for supportive care and comfort measures (rest, environmental
control) to relieve CNS effects
- Institute safety measures if CNS effects occur to prevent patient injury
- Provide small, frequent meals and mouth care to help relieve the discomfort of
GI effects
- Instruct the client how to take pulse rate. Advise the client to call physician if
dizziness or faintness occurs, this may indicate hypotension.

Cardiac glycosides/antianginal drugs - 12 - cvb

 C. CALCIUM-CHANNEL BLOCKERS or Calcium blockers
- amlodipine (Norvasc)
- diltiazem (Cardizem, Cardizem SR)
- nicardipine (Cardene)
- nifedipine (Adalat, Procardia)
- verapamil (Calan, Isoptin)

 prevent the movement of calcium into the cardiac and smooth muscle cells
when the cells are stimulated

interferes with its ability to contract

 leads to loss of smooth muscle tone, vasodilation and decreased peripheral

resistance

decrease venous return (preload)

resistance the heart has to pump against (afterload)

decrease in cardiac workload and oxygen consumption

 Phamacodymanics:
 calcium-channel blockers inhibit the movement of calcium ions across
the membranes of the myocardial cells and arterial muscle cells

alters action potential and blocking muscle cell contraction

depress myocardial contractility

slow cardiac impulse formation in the conductive tissue
relax and dilates arteries

fall in the Bp
decrease in the venous return

decrease in cardiac workload

decrease O2 consumption of myocardium

 Nifedipine, most potent of the calcium blockers promotes vasodilation of

coronary and peripheral vessels
Onset of action Duration
Verapamil 10 min PO:3 – 7 h
IV: 2 h
Nifedipine 30 min 6–8h
Diltiazem 30 min 6–8h

Cardiac glycosides/antianginal drugs - 13 - cvb

  Pharmacokinetics:
- generally well absorbed
- metabolized in the liver
- excreted in urine
- can cross placenta and enter breast milk

 Contraindications
Contraindications Rationale
Heart block Condition could be exacerbated by the
conduction-slowing effects of these drugs
Renal and hepatic These could alter metabolism and
dysfunction excretion of these drugs
Pregnancy, lactation Because of the potential adverse effects
on the fetus or neonate

 Adverse Effects
- CNS effects: dizziness, light-headedness, headache and fatigue
- GI effects: nausea, hepatic injury
- Cardiovascular effects: hypotension, bradycardia, peripheral edema
heart block
- Skin effects: flushing, rash

***Nursing Consideration: Serum liver enzymes should be checked

periodically

 Drug-drug interaction
- increased serum level and toxicity of cyclosporine if taken with
diltiazem
- increased risk of heart block and digoxin toxicity if combined with
verapamil (Verapamil increases digoxin serum levels)
- Verapamil is also associated with serious respiratory depression when
given with general anesthetics or as an adjunct to anesthesia

 Nursing Interventions:
- Instruct the client how to take pulse rate. Advise the client to call
physician if dizziness or faintness occurs, this may indicate
hypotension.
- Monitor the patient carefully (Bp, cardiac rhythm, cardiac output) while
the drug is being titrated or dosage is being changed, to ensure early
detection of potentially serious adverse effects
- Provide comfort measures to help client tolerate drug effects

Cardiac glycosides/antianginal drugs - 14 - cvb

 - Inform the client not discontinue these drugs without the health care
provider’s approval. Withdrawal symptoms, such as reflex tachycardia
and pain may be severe.

Cardiac glycosides/antianginal drugs - 15 - cvb