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25 Cards in this Set

  • Front
  • Back
Positive Inotropic Agents:
1. what they do.
2. treatment for:
3. 2 main categories
1.increase force of myocardial contraction: increase cardiac output
2.treatment for failing heart
3.
a. cardiac glycosides
b. phosphodiesterase inhibitors
Conduction System of Heart
1. SA Node: pacemaker of heart. Determines pulse rate
2. AV Node: between R Atrium & R ventricle.
3. Bundle of HIS: in ventricle septum.
How does blood travel through the heart?
into R atrium...to R ventricle...to lungs...to L atrium...to L ventricle.
L Ventricle is strongest part of heart - must pump blood out to body.
How do electricle impulses travel through heart?
Pumping of heart is dependent on electrical impulses from SA Node, to AV node, to bundle of HIS, to purkinji fibers.
Congestive Heart failure
Is a pathologic state, the heart is unable to pump enough blood.
May effect one or both ventricles
Ejection Fraction Decreased
What is Ejection Fraction
Amount of blood ejected with each contraction compared with the total amount of blood in the ventricle before contraction. (should be 65%)
What will eventually happen when Ejection Fraction is decreased.
Blood will back up to the lungs (fluid in lungs) adn can back up to the liver.
Symptoms of Congestive Heart failure
-dyspnia (trouble breathing)
-cough
-jugular vein destended due to blood backed up
-ascites (fluid accumulating in abdominal and chest cavity)
Who is commonly effected by congestive heart failure
Elderly
and in Peds with congenital heart defects
When blood supply to organs is decreased, leads to reduced kidney functions.
Causes of congestive heart failure
*Cardiac defect:
-MI
-Valve insufficiency: leaking valves
* Defect outside of the heart
-coronary artery disease
-diabetes
-increased workload: ex: high B.P., anemia - heart has to beat faster, thyroid disease (hypo or hyperthroidism), hypervolemia- too much blood, error in hospitals
Cardiac Arrhythmias are what:
abnormal H.R.
normally conduction systme causes chambers to contract rhythmically.
Supraventricular arrhythmias(atrial fibrillation, atrial flutter)
-1. av node is circumvented.
-2.Impulses arrive in ventricle before ventricle is ready to contract.
-
what is the refractory period
the time when the cardiac cells are readjusting their sodium and potassium levels and the cardiac cells are not able to depolarize again. After depolarization, the electrical stimulation has been generated.
Cardiac Glycosides:
Drug that does what?
Restores heart rythem.

Digoxin - example of a cardiac glycoside

Helps heart prefor it's duty
Restores heart to normal sinus rhythm
Mechanism of action and drug effects for DIGOXIN
*Change electrical conduction in the heart*
-EFFECTS_
1. positive inotropic effect: increase force adn velocity of myocardial contraction - helps eject more blood.
2. negative chonotropic effect: Decreased heart rate - promotes pos. inotropic effect - decr. # times heart beats to make heart more effecient. Allows heart to stay in a contracted state and better able to push out more blood.
3. Neg dromotropic effect: Decreases conduction at the SA Node to slow H.R.
Therapeutic Uses for Cardiac glycosides (DIGOXIN)
CHF - to treat congestive heart failure.
SUPRAVENTRICULAR ARRHYTHMIAS:
(treatment of)
Side and Adverse Effects of DIGOXIN
Due to a Narrow Therapeutic Window:
1. Low potassium levels increase it's toxicity
- Careful monitoring in necessary

TOXIC SYMPTOMS:
1. Bradycardia, dysrhythmia, anorexia
2. N&V, headache, fatigue, confusion
3. Visual disturbances
What to do for Toxicity/Overdose
1.Before each dose, check pulse/HR. If HR > 60, give next dose, if HR<60 call Dr.
2.Potassium increase will decrease toxicity of Digoxin (determine potassium levels)
3.Check for dysrhythmias - heart monitoring
4.Check for Digibind: an antibody that works against digoxin and binds to it to take it away.
Drug Profile for:
Lanoxin, LanoxiCaps (Digoxin)
- improves myocardial contractility
- Normal levels are .05-2.0
Patient Teaching /Nursing Considerations:
DIGOXIN
- Apical pulse: always check HR before next dose.
-Teaching:
1. take same time of day
2. never double up/skip doses
3. Don't chg. Brands
4. Watch for side effects
5. Eat hi potassium foods
PHOSPHODIESTERASE INHIBITORS
1.Who uses them
2.what are mechanism of actions
1. For patients with congestive heart failure that are worse off - not going to make it.
2.-inhibit teh enzyme phosphodiesterase
-inodilators
The effects of Phosphodiesterase Inhibitors
1. positive inotropic: improving force of contraction of heart.
2. vasodilation: heart does not have to work so hard.
3. May have increased H.R.
Therapeutic Uses for Phosphodiesterase Inhibitors.
For:
CHF: congestive heart failure
End stage Heart failure
ex. need heart transplant
patient is being kept
comfortable but heart
will not improve.
Drug Profile: Phospho. inhib.

PRIMACOR, INOCOR
1. how administered
2. side effects
3. nursing considerations
1.IV adm. only
2.-Ventricular dysrhythmias
-hypotension - low B.P.
3.-check electrolytes before
adm.
-monitor cardiac function
during adm.
-monitor b.p.
A MISCELLANEOUS HEART FAILURE
AGENT: Newest Class

NATRECOR
1. Used where.
2. Used how.
1. In ICU's
2. To improve quality of
for end stage people.
Has vasodilating
properties on both
arteries and veins.
-Classified as a recombinant version of human B-type natriuretic peptide (hBNP).
Patient Teaching Tips for:
Misc. Heart Failure Agent
1. Take at the same time every day.
2. Never double up or skip doses.
3. Don't change brands.
4. Watch OTC's adn Herbal remedies.
5. Pt. checks own pulse.
6. report wgt gain
7. don't take with dairy products or antacids.
8. comsume high potassium foods.
9. Don't D/C abruptly