Cardiac Glycosides and Heart Failure Flashcards

1
Q

What are the normal compensatory mechanisms the body has for someone in heart failure?

A

RAA system - increase in volume and vasoconstriction helps perfusion

Sympathetic stimulation - increases contractility and HR

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2
Q

What is the bad thing about the compensatory mechanisms our body has for heart failure?

A

In the long run our body wont be able to keep up these mechanisms and they will just end up making the heart failure worse.

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3
Q

What are some drug classifications that we use to treat heart failure? And if these fail to treat the heart failure what do we turn to? Why?

A

ACE inhibitors
ARBS
Diuretics
Beta-Blockers

If these dont work then we turn to cardiac glycosides, they are a last resort because of the risk for adverse effects

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4
Q

Where is digoxin originally derived from?

A

the foxglove/digitalis plant

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5
Q

What is the therapeutic action of cardiac glycosides?

A

increases the force of contraction, decreases the rate and conduction of the SA node

Decrase HR = Increased filling time = increased pre-load = increased contractility

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6
Q

How can digoxin be administered?

A

PO or IV

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7
Q

If digoxin is given IV, how long should it be pushed?

A

Infuse over 5 minutes

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8
Q

Other than treatment of heart failure, what other thing do cardiac glycosides have a therapeutic outcome for?

A

Atrial dysrhythmias

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9
Q

Does digoxin have a high risk for toxicity?

A

YES YES YES

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10
Q

What are some adverse effects of cardiac glycosides?

A

Dysrhythmias

Bradycardia (can be a sign of toxicity)

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11
Q

What are some things that cause the dysrhythmias in people taking cardiac glycosides?

A

hypokalemia (this medication doesnt cause it)

High serum drug levels (major decrease in HR = other pacemakers kick in)

Heart disease (damaged tissue = dysrhythmias)

MONITOR HEART RATE!!!!!!

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12
Q

Patients with this specific disorder are contraindicated for the use of cardiac glycosides.

A

ventricular dysrhythmias

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13
Q

What can bradycardia associated with taking cardiac glycosides be a sign of?

A

toxicity

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14
Q

Because of the risk for bradycardia what should the nurse do before administering a cardiac glycoside?

A

assess the apical HR of the patient before administration and if it is less that 60 HOLD the medication and call the physician

RATE AND RHYTHM

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15
Q

How would you describe the therapeutic range for cardiac glycosides? Give a range in numbers as well.

A

Very narrow (0.5-2.0)

Toxicity has occurred from 1.5-1.7

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16
Q

What does hypokalemia have to do with cardiac glycosides?

A

If the patient is hypokalemic the risk for toxicity increases, so it is crucial to monitor the patients potassium especially if taking a medication that lowers potassium

17
Q

What are some general signs of toxicity from cardiac glycosides?

A

fatigue

weakness

vision changes (yellow/green/white halos around lights

18
Q

What are some things that the patient might exhibit in early toxicity with cardiac glycosides?

A

Really tired, weak, no appetite

19
Q

What are some GI effects that might occur with cardiac glycoside toxicity?

A

anorexia

nausea

vomiting

abdominal pain

20
Q

What are some CNS effects that might occur from cardiac glycoside toxicity?

A

fatigue

weakness

visual changes (diplopia, blurred vision, yellow/green/white halos around lights)

21
Q

what are some drug-drug interactions that cardiac glycosides have?

A

Thiazide and loop diuretics (cause hypokalemia)

ACE inhibitors and ARBS can cause hyperkalemia which decreases therapeutic effects

Quinidine and verapimil increase risk for toxicity

22
Q

What are some main patient teaching points for cardiac glycosides?

A

eat high potassium foods (spinach, green leafy veggies, potatoes)

Check HR before administering (hold if below 60)

signs of hypokalemia (nausea, vomiting, weakness) and signs of toxicity

dont stop suddenly

dont double dose if a dose is missed (take it as soon as remembered then take scheduled dose

Keep lab appointments

Antidote - digibind

23
Q

What is the mechanism of action for epinephrine?

A

Alpha 1, Beta 1 & 2 stimulation increase HR, contractility, vasoconstrict, and bronchdilate

alpha 1 - vasoconstrict

Beta 1 - Increase HR and contractility

Beta 2 - bronchodilate

24
Q

When is epinephrine commonly used?

A

Shock

Asthma

Cardiac arrest

Anaphylaxis

USED IN ACUTE SITUATIONS

25
Q

What are some nursing considerations for epinephrine?

A

continuous cardiac monitoring

monitor for dysrhythmias, angina, hypertension

watch out for extravasation - tissue necrosis around the site of administration

26
Q

What is the mechanism of action for dobutamine?

A

beta 1 stimulation increases HR and contractility, also has a bit of vasodilation effect so the BP effects are less profound

27
Q

when is dobutamine used?

A

Heart failure (for more chronic issues)

28
Q

What is a primary nursing consideration for dobutamine?

A

continuous cardiac monitoring

29
Q

What is the effect of low dose dopamine?

A

dilates renal arteries 1-3mcg/kg/minute

30
Q

What is the effect of a moderate dose of dopamine?

A

(beta 1) - dilates renal arteries, increases HR, increases contractility, increases rate of conduction 3-10mcg/kg/minute

31
Q

What is the effect of high dose dopamine?

A

Beta 1 and alpha 1 - vasoconstriction and renal artery constriction, increase in HR and contractility

USUALLY USED FOR CARDIOGENIC SHOCK

32
Q

What are some nursing considerations for dopamine?

A

Closely monitor IV site for extravasation tissue necrosis

Many drug-drug interactions

Usually for emergent situations

Administer using IV pump and increase/decrease dose slowly (every 5 minutes) based on BP