CH 27: HF Flashcards

1
Q

is the inability of the ventricles to pump enough blood to meet
the metabolic needs of the body.

A

heart failure

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2
Q

possible disorders causing HF

A

 Coronary artery disease (CAD)
 Mitral stenosis
 Myocardial infarction (MI)
 Chronic hypertension (HTN)
 Diabetes mellitus
 Dyslipidemia
 Thyroid disorders

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3
Q

the degree to which the myocardial fibers are stretched just
prior to contraction is called

A

Preload

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4
Q

the degree of pressure in the aorta that must be overcome
for blood to be ejected from the left ventricle (the amount of peripheral resistance to the contraction of the ventricles)

A

Afterload

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5
Q

change in heart contractility

A

inotropic effect

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6
Q

drugs that increase contractility

A

positive inotropic agents

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7
Q

positive inotropic agent examples

A

Epinephrine, norepinephrine, thyroid hormone, dopamine

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8
Q

drugs that decrease contractility

A

negative inotropic agents

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9
Q

examples of negative inotropic agents

A

beta blockers -atenolol

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10
Q

most common cause of HF

A

HTN

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11
Q

increases the amount of work the heart has to do to push through the pressure

A

afterload (peripheral resistance)

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12
Q

increased after load results in:

A

left ventricular hypertrophy (LVH) – this weakens the heart –
resulting in fluid in the lungs

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13
Q

LVH results in:

A

fluid in the lungs

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14
Q

right side can weaken from increased afterload leading to:

A

peripheral edema

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15
Q

pharmacotherapy for HF is now targeted at:

A

prevention and slowing the progression

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16
Q

when HF begins the ventricles secrete:

A

B-type natriuretic peptide (BNP)

17
Q

therapeutic effects of digoxin (cardiac glycoside)

A

Positive inotropic effect. Cause the heart to beat more forcefully.
Lowers heart rate.
Makes contractions more efficient

18
Q

adverse effects of digoxin (cardiac glycoside)

A

vomiting,
fatigue,
anorexia,
visual disturbances such as seeing halos, a yellow-
green tinge, or blurring.

19
Q

monitoring for digoxin (cardiac glycoside)

A

MONITOR FOR DIGOXIN TOXICITY**
CHECK SERUM DIGOXIN LEVELS
Monitor for dysrhythmias with hypokalemia

20
Q

safety considerations for digoxin (cardiac glycoside)

A

NARROW THERAPEUTIC DOSE
DIGOXIN OVERDOSE CAN BE FATAL
Take apical pulse for 1 minute and note rate, rhythm, and quality
WITHHOLD FOR HR LESS THAN 60
Use of digoxin with diuretics can cause hypokalemia or hyperkalemia (depending on which kind) and
dysrhythmias
Use of digoxin with betablockers can cause
additive bradycardia
No potassium supplements unless approved by provider

21
Q

therapeutic effects of vasodilators

A

vessels and lower blood pressure – reduces preload

22
Q

increase the force of the myocardial contraction = increased
cardiac output

A

Cardiac Glycosides

23
Q

Increase the force of myocardial contraction = increased cardiac output

A

Phosphodiesterase inhibitors

24
Q

therapeutic effect of milrinone (Phosphodiesterase inhibitors)

A

Increase the force of contraction = increased cardiac contractility and vasodilates
Positive inotropic
Decrease left ventricle afterload

25
Q

adverse effects of milrinone (Phosphodiesterase inhibitors)

A

ventricular dysrhythmia, which may occur in 1 of every 10 patients taking the drug
Blood pressure is also continuously monitored during the infusion to prevent hypotension.
Less serious side effects include headache, nausea, and vomiting.

26
Q

safety and monitoring for milrinone (Phosphodiesterase inhibitors)

A

CONTINUOUS CARDIAC MONITORING for ventricular dysrhythmias
hypotension
Serious Toxicity can only take for 2 to 3 days – only given IV
Overdose causes hypotension

27
Q

**Signs and symptoms of Digoxin Toxicity:

A

abdominal pain,
anorexia,
nausea,
vomiting,
visual disturbance (halo), bradycardia,
ECG changes,
dysrhythmia,
headache,
seizure.