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CARDIOTONICS AND CORONARY VASODILATORS. NURS 1950: Pharmacology I. Objective 1: describe the relationship of calcium to electrical activity of the heart Resting: Preload: Afterload :. repolarization. Heart dependent upon influx of calcium

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slide2

Objective 1: describe the relationship of calcium to electrical activity of the heart

  • Resting:
  • Preload:
  • Afterload:
repolarization
repolarization
  • Heart dependent upon influx of calcium
  • Ca+ enters channels in the cardiac cell membrane and go into the cell along with Na
  • K+ comes out
  • Cardiac cells contract
slide5

The ANS is the primary controller of heart rate

  • Cholinergic (parasympathetic) vagal fibers are close to the SA node
  • Stimulation with acetylcholine slows the heart rate
slide6

Sympathetic (adrenergic) nerves also innervate the heart

  • Stimulation causes norepinephrine to be released.
  • Increases heart rate, slows refractory period
how cardiac drugs work
How cardiac drugs work
  • 1. Increase or decrease the force of myocardial action
  • Positive inotropics
  • Negative inotropics
slide10

2. Increase or decrease heart rate by altering SA node impulse conduction

  • Positive chronotropics
  • Negative chronotropics
slide11

3. Increase or decrease conduction of AV impulses

  • Positive dromotropics
  • Negative dromotropics
cardiac glycosides
Cardiac glycosides
  • Digoxin & relatives
  • Come from Natural sources
  • Helpful in CHF
  • Have a positive inotropic effect
slide16

Increases mechanical efficiency of heart

  • This pumps more blood
  • With increased blood to kidneys, diuresis occurs, edema reduced
  • Cardiac glycosides also have negative chronotropic effect,
  • Negative dromotropic effect
slide17

Action

    • Thought that they cause release of free calcium within the cardiac muscle cell
    • Also change the electrical activity of myocardium
slide18

Decrease velocity of electrical conduction, prolong refractory period in AV conduction system

  • Increase vagal tone
slide19

Objective 5: relate how the effects of digitalis are beneficial to the client with CHF

  • Recall the signs/symptoms of CHF
  • How do you think cardiac glycosides improve this condition?
slide21

What is atrial fibrillation?

  • What activity of the cardiac glycosides improve this condition?
slide22

Chronotropic/dromotropic effects

    • Suppress impulse conduction through the AV node
    • This prevents excessive atrial activity from reaching ventricles
slide23

Objective 7: list the generic and brand names of the digitalis preparations

  • Digitalis preparations similar in pharmacological properties, toxic effects
prototype
Prototype
  • Digoxin (Lanoxin, Lanoxicaps): oral or IV
  • Onset 30-120 minutes oral
  • Peaks 2-6 hrs
  • Duration 2-4 days
  • Eliminated by kidney
    • Used most often as rapid onset, short duration
slide25

Must take apical pulse 1 minute before administration

  • Hold if under 60, contact MD
  • Blood levels needed
slide27

Digitalization is the administration of digitalis that is more than the maintenance dose

  • This raises the blood level quickly to therapeutic range
    • May also be called a loading dose
slide28

Example

    • Oral dose of digoxin 0.5-0.75 mg
    • 0.25-0.5 mg then given every 6-8 hours until desired blood level reached
    • Then maintenance dose: 0.125-0.5 mg daily
slide30

Digitalis toxicity:

    • GI distress: N/V, anorexia, and/or diarrhea (flu like symptoms)
    • May have excessive salivation and abdominal pain
    • Neurological: restless, irritable, lethargy, drowsiness, and/or confusion
slide31

May have vision changes, changes in color

    • May have halos, amblyopia and diplopia
    • Cardiac effects: development of arrhythmias (bradycardia, primary AV block)
contraindications
Contraindications
  • Toxicity predisposition: hypokalemia as cardiac muscles more sensitive to the glycosides
  • Renal impairment as 60-90% excreted by kidney
  • IV administration: rapid accumulation can occur
slide34

Treatment

    • Hold the drug
    • Use digoxin immune fab (Digibind)
      • Antigen-binding fragments combine with digoxin to neutralize its action
lisinopril animation
Lisinopril Animation

Click here to view an animation on the topic of lisinopril.

diuretics
Diuretics

Prototype drug: furosemide (Lasix)

Mechanism of action: to increase urine flow, reducing blood volume and cardiac workload

Primary use: to reduce edema and pulmonary congestion

Adverse effects: dehydration, electrolyte imbalance, hypotension, ototoxicity

furosemide animation
Furosemide Animation

Click here to view an animation on the topic of furosemide.

cardiac glycosides1
Cardiac Glycosides

Prototype drug: digoxin (Lanoxin)

Mechanism of action: to cause more forceful heartbeat, slower heart rate

Primary use: to increase contractility or strength of myocardial contraction

Adverse effects: neutropenia, dysrhythmias, digitalis toxicity

beta adrenergic blockers
Beta-Adrenergic Blockers

Prototype drug: Metoprolol (Lopressor, Troprol XL)

Mechanism of action: block cardiac action of sympathetic nervous system to slow heart rate and B/P, reducing workload of heart

Primary use: to reduce symptoms of heart failure and slow progression of disease

Adverse effects: fluid retention, worsening of heart failure, fatigue, hypotension, bradycardia, heart block

vasodilators
Vasodilators

Drugs: hydralazine (Apresoline); (isosorbide dinitrate (Isordil)

Mechanism of action: to relax blood vessels

Primary use: to lower blood pressure

Used for clients who cannot take ACE inhibitors

Adverse reactions: reflex tachycardia, orthostatic hypotension

phosphodiesterase inhibitors
Phosphodiesterase Inhibitors

Prototype drug: milrinone (Primacor)

Mechanism of action: to block enzyme phosphodiesterase in cardiac and smooth muscle

Primary use: as short-term therapy for heart failure

Adverse effects: hypokalemia, hypotension, ventricular dysrhythmias

slide46

Objective 11: describe the nursing responsibilities associated with administering cardiac glycosides preparations

slide47

Take apical pulse 1 full minute

  • Hold if under 60, over 100 in adults
  • Report any evidence of irregular rhythm
  • Observe for toxicity S/S
  • Monitor K+ if on diuretics
  • Encourage K+ rich foods
slide48

Teach client to take pulse

  • Teach S/S of toxicity
  • If hypothyroid, sensitive to digitalis
  • Draw blood levels periodically
angina
Angina
  • Atherosclerosis narrows heart’s vessels
  • Blood flow impeded
  • Demand exceeds supply = anginal pain
goals
Goals
  • Drugs are used to dilate coronary arteries
  • This brings in oxygen and nutrients
  • Supply = demand so no pain
slide53

Nitroglycerin

  • Calcium channel blockers
  • Beta blockers
  • ACE inhibitors
slide54

Nitroglycerin drugs

  • Works by relaxing arterial and venous smooth muscle
  • Dilate coronary arteries
slide55

Liquid nitroglycerin unstable, highly volatile

  • Oral tablets stable, non-explosive
  • Can be given sublingual for rapid, predictable action
  • Can be transmucosal, aerosol translingual spray, IV, transdermal
slide57

Ointment: placed on paper with inches marked off

  • Amount prescribed placed on the paper, taped into place
  • 4-8 hours of action
  • (Nitro-bid, Nitrol)
slide58

Nitroglycerin patches: worn 12-14 hours

  • “Patch-off” period of 6-12 hours
  • Prevents tolerance
  • (Transderm-Nitro, Nitro-Dur)
slide60

Long acting forms for prophylaxis

    • Erythrityl tetranitrate (Cardilate)
    • Pentaerythritol tetranitrate (PETN)
slide62

Tolerance

  • Headache
  • Postural hypotension
  • Dizziness
  • Weakness
  • Syncope
    • Don’t use alcohol with nitros
slide64

Objective 15: identify the nursing responsibilities associated with administering the nitroglycerin preparations

slide65

Teach: when angina occurs, take 3 tabs in 15 min; if no pain relief, call 911

  • Keep nitro in original container, cap tightly closed
  • Store in cool, dry place
  • Rotate sites of topical applications
  • Monitor BP during therapy
slide66

Shelf-life is 6 months. If burning/stinging sensation under tongue, drug still potent

  • Replace 3 months after opening bottle
slide69

Examples: propranolol, Atenolol

  • Decrease heart rate, contractility
    • Results in reduction of myocardial oxygen consumption
    • Better if used with nitrates
      • Can not use in COPD, CHF, heart block, bradycardia, DM
slide70

When used with nitrates, hypotensive episodes more likely to occur

  • Drugs used
    • Atenolol (Tenormin)--prototype
    • Metoprolol (Lopressor)
    • Nadolol (Corgard)
    • Propranolol (Inderal)
examples calcium channel blockers
Examples: calcium channel blockers
  • Nifedipine (Adalat, Procardia)
  • DiltiazemHCl (Cardizem, Dilacor SR)--prototype
  • Verapamil (Calan, Isoptin)
  • Bepridil (Vascor)
  • NicardipineHCl (Cardene)
slide74

These drugs create coronary vasodilation, increased coronary blood flow, lowered blood pressure, increased cardiac output, and relax coronary artery spasms

nitrates
Nitrates

Prototype drug: nitroglycerin (Nitrostat)

Mechanism of action: relax both arterial and venous smooth muscle; dilate coronary arteries

Short acting-terminate acute angina episode

Long-acting-decrease severity and frequency of episodes

nitrates continued
Nitrates (continued)

Primary use: for lowering myocardial oxygen demand

Adverse effects: hypotension, dizziness, headache, flushing of face, rash

beta adrenergic blockers1
Beta-Adrenergic Blockers

Prototype drug: atenolol (Tenormin)

Mechanism of action: to reduce the cardiac workload by slowing heart rate and reducing contractility

Primary use: for prophylaxis of stable angina

Adverse effects: fatigue, insomnia, drowsiness, impotence, bradycardia, confusion

calcium channel blockers
Calcium Channel Blockers

Prototype drug: diltiazem (Cardizem)

Mechanism of action: to reduce cardiac workload by relaxing arteriolar smooth muscle; dilate coronary arteries

Primary use: for lowering blood pressure; bring more oxygen into myocardium

Adverse effects: hypotension, bradycardia, heart failure, constipation, headaches, dizziness, edema

examples ace inhibitors
Examples: ACE inhibitors
  • Captopril (Capoten)
  • Lisinopril (Prinivil)--prototype
  • Ramipril (Altace)
ace inhibitors
ACE Inhibitors

Prototype drug: lisinopril (Prinivil, Zestril)

Mechanism of action: to enhance excretion of sodium and water

Primary use: to decrease blood pressure and reduce blood volume; dilate veins

Adverse effects: first-dose hypotension, cough, hyperkalemia, renal failure

assessment
Assessment
  • Frequency, nature, precipitants of angina attack
  • Lifestyle changes made
  • Effectiveness of coronary vasodilators in relief of pain
  • Monitor VS, esp. BP
nursing diagnoses
Nursing diagnoses
  • Ineffective tissue perfusion, cardiac function RT angina
  • Risk for injury RT side effects of coronary vasodilators
  • Deficient knowledge RT health alteration and medication regimen
goals1
Goals
  • Client will
    • Verbalize decrease in attacks
    • Not experience injury due to coronary vasodilitation
    • Verbalize s/s of drug toxicity and report to MD
implementation
Implementation
  • What teaching is done for clients taking nitroglycerin?
  • What teaching is done for clients taking calcium channel blockers, ACE inhibitors, beta blockers?
  • What will the nurse monitor when clients are on these medications?