Heart Failure Flashcards

1
Q

Define heart failure

A

Heart failure (HF) is a pathologic state in which the heart is unable to pump blood in sufficient amounts to meet the body’s metabolic needs (decreased CO)

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2
Q

signs and symptoms

A

Left-sided heart failure:
Pulmonary edema
Coughing
Dyspnea

Right-sided heart failure:
Jugular vein distention
Ascites
Pedal edema

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3
Q

Identify diagnostic studies performed for heart failure

A

Diagnostic studies:BNP,Echocardiography to determine ejection fraction (EF),Echocardiogram

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4
Q

decompensated heart failure

A

Decompensated heart failure refers to a deterioration, which may present either as an acute episode of pulmonary oedema or as lethargy and malaise, a reduction in exercise tolerance, and increasing breathlessness on exertion.

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5
Q

compensated heart failure

A

In compensated heart failure, symptoms are stable, and many overt features of fluid retention and pulmonary oedema are absent.

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6
Q

inotropic

A

Positive inotropic drugs – increase the force of myocardial contraction
Negative inotropic drugs – reduce the force of contraction

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7
Q

chronotropic

A

Positive chronotropic drugs – increase rate at which heart beats/ increase heart rate
Negative chronotropic drugs – reduce rate at which heart beats/ reduce heart rate

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8
Q

dromotropic

A

Positive dromotropic drugs – drugs that accelerate conduction through the conduction system of the heart/ accelerate how quickly electrical impulses travel through the conduction system of the heart  sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, and Purkinje fibers.
Negative dromotropic drugs – drugs that reduce conduction through the heart

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9
Q

Diuretics (furosemide, Lasix) MOA

A

Decreases Na, Cl, and K reabsorption in thick ascending limb of the loop of Henle in the nephron which results in profound diuresis

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10
Q

Drug effects diuretics

A

Reduced blood volume decreases venous pressure (preload) and arterial pressure (afterload). Reduced pulmonary and peripheral edema.

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11
Q

Indications diuretics

A

Acute and chronic HF

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12
Q

Dosages and Routes diuretics

A

Oral: 20-80 mg/daily or BID; max dose 600 mg/day
IV: 20-40 mg/dose IV x 1, may increase by 20mg q 2 hours.

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13
Q

Adverse effects diuretics

A

Hypokalemia (↑ risk of digoxin toxicity)

Severe hypotension

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14
Q

Nursing implications diuretics

A

Assess patient’s fluid volume status
Assess vital signs
Assess labs

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15
Q

Patient education diuretics

A

Avoid taking late in the afternoon due to nocturia.
Eat foods rich in potassium (bananas, oranges, potatoes, tomatoes, meats, fish, wheat bread, legumes). K+ supplement may be necessary
Report signs of hypokalemia (e.g. lethargy, weakness, leg cramps) to provider immediately

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16
Q

labs to monitor when taking diuretics

A

Monitor electrolytes, renal and hepatic function, serum glucose, and uric acid levels before and periodically throughout therapy. Commonly ↓ serum potassium. May cause ↓ serum sodium, calcium, and magnesium concentrations. May also cause ↑ BUN, serum glucose, creatinine, and uric acid levels.

17
Q

Drugs that inhibit the RAAS e.g. ACE inhibitors MOA (pril meds)

A

Inhibits ACE which prevents the conversion of angiotensin I to angiotensin II (a powerful vasoconstrictor). Also reduces aldosterone secretion. Suppress degradation of kinins (vasodilator).

18
Q

drug effects ace inhibitors

A

Arteriolar and venous dilation results in reduced preload, afterload, ↓ pulmonary & pedal edema, and increased cardiac output. ↑ kinins reduces cardiac remodeling.

19
Q

indications ace

A

Cornerstone of HF therapy

20
Q

Adverse effects ace

A

Hypotension (0.9-6.7%)
Cough (9%)
Hyperkalemia
Angioedema

21
Q

Drugs that inhibit the SNS e.g. beta-blockers(lol meds) MOA

A

Protect heart from excessive sympathetic stimulation

22
Q

Drug effects beta- blockers

A

Improve LV ejection fraction (1-3 months), slow the progression of HF, reduce need for hospitalization, and prolong survivial.

23
Q

Dosages and routes beta blockers

A

Start low and go slow. Excessive beta blockade can reduce ventricular contractility

24
Q

Contraindications beta blockers

A

Heart block

25
Q

Adverse effects beta blockers

A

Fluid retention/ worsening HF
Bradycardia/ heart block
Hypotension

26
Q

Cardiac Glycosides Mechanism of action

A

Inhibits the sodium-potassium adenosine triphosphatase pump. This cause an accumulation of calcium within the cardiac myocytes. The calcium then augments contractile force by facilitating the interaction of myocardial actin and myosin.

27
Q

Drug effects glycosides

A

Positive inotropic effect increases the force of ventricular contraction which increases cardiac output. Increased CO, can reverse all the overt manifestations of HF.

28
Q

Indications: glycosides

A

Second-line heart failure; atrial fibrillation

29
Q

Precautions: glycosides

A

Lasix (secondary to risk of hypokalemia)

30
Q

Adverse effects: glycosides

A

Digoxin toxicity

Cardiac dysrhythmia

31
Q

digoxin (Lanoxin)

Very narrow therapeutic window.

A

Drug levels must be monitored
0.5 to 0.8 ng/mL (old upper limit 2 ng/mL)
Low potassium levels increase its toxicity. Electrolyte (serum K+) levels must be monitored.
Normal range 3.5 – 5 mEq / L

32
Q

Nursing implications: glycosides

A

Monitor vital signs
Monitor for EKG changes
Monitor labs – K+, digoxin level (CRITICAL)

33
Q

Patient education: glycosides

A

Teach to monitor pulse rate and regularity
Signs and symptoms of dig toxicity (anorexia, nausea, vomiting, yellow tinge to vision, halos)
Monitor for signs and symptoms of hypokalemia (lethargy, muscle weakness, leg cramps)

34
Q

Mechanism of action/drug effects:Vasodilator

ex.Bidil (37.5 mg of hydralizine/ 20 mg isosorbide dinitrate)

A
Isosorbide dinitrate (Isordil) belongs to same family as nitroglycerin. Causes selective dilation of veins which ↓preload and reduces congestive symptoms.
Hydralize (Apresoline) causes selective dilation of arterioles which can improve cardiac output (decreased afterload) and renal blood flow (increase urine output/decrease volume)
35
Q

B-type Natriuretic Peptide Mechanism of action/ Drug effects:
Examples:
nesiritide (Natrecor)

A

A synthetic form of BNP produced by recombinant DNA technology. Causes suppression of RAAS, suppression of SNS, direct dilation of arterioles and veins (↓ preload and ↓ afterload).

36
Q

Indication/ Route: B-type

A

Acutely decompensated CHF via continuous intravenous infusion only.