Heart Failure Flashcards
Define heart failure
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)
signs and symptoms
Left-sided heart failure:
Pulmonary edema
Coughing
Dyspnea
Right-sided heart failure:
Jugular vein distention
Ascites
Pedal edema
Identify diagnostic studies performed for heart failure
Diagnostic studies:BNP,Echocardiography to determine ejection fraction (EF),Echocardiogram
decompensated heart failure
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.
compensated heart failure
In compensated heart failure, symptoms are stable, and many overt features of fluid retention and pulmonary oedema are absent.
inotropic
Positive inotropic drugs – increase the force of myocardial contraction
Negative inotropic drugs – reduce the force of contraction
chronotropic
Positive chronotropic drugs – increase rate at which heart beats/ increase heart rate
Negative chronotropic drugs – reduce rate at which heart beats/ reduce heart rate
dromotropic
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
Diuretics (furosemide, Lasix) MOA
Decreases Na, Cl, and K reabsorption in thick ascending limb of the loop of Henle in the nephron which results in profound diuresis
Drug effects diuretics
Reduced blood volume decreases venous pressure (preload) and arterial pressure (afterload). Reduced pulmonary and peripheral edema.
Indications diuretics
Acute and chronic HF
Dosages and Routes diuretics
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.
Adverse effects diuretics
Hypokalemia (↑ risk of digoxin toxicity)
Severe hypotension
Nursing implications diuretics
Assess patient’s fluid volume status
Assess vital signs
Assess labs
Patient education diuretics
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
labs to monitor when taking diuretics
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.
Drugs that inhibit the RAAS e.g. ACE inhibitors MOA (pril meds)
Inhibits ACE which prevents the conversion of angiotensin I to angiotensin II (a powerful vasoconstrictor). Also reduces aldosterone secretion. Suppress degradation of kinins (vasodilator).
drug effects ace inhibitors
Arteriolar and venous dilation results in reduced preload, afterload, ↓ pulmonary & pedal edema, and increased cardiac output. ↑ kinins reduces cardiac remodeling.
indications ace
Cornerstone of HF therapy
Adverse effects ace
Hypotension (0.9-6.7%)
Cough (9%)
Hyperkalemia
Angioedema
Drugs that inhibit the SNS e.g. beta-blockers(lol meds) MOA
Protect heart from excessive sympathetic stimulation
Drug effects beta- blockers
Improve LV ejection fraction (1-3 months), slow the progression of HF, reduce need for hospitalization, and prolong survivial.
Dosages and routes beta blockers
Start low and go slow. Excessive beta blockade can reduce ventricular contractility
Contraindications beta blockers
Heart block
Adverse effects beta blockers
Fluid retention/ worsening HF
Bradycardia/ heart block
Hypotension
Cardiac Glycosides Mechanism of action
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.
Drug effects glycosides
Positive inotropic effect increases the force of ventricular contraction which increases cardiac output. Increased CO, can reverse all the overt manifestations of HF.
Indications: glycosides
Second-line heart failure; atrial fibrillation
Precautions: glycosides
Lasix (secondary to risk of hypokalemia)
Adverse effects: glycosides
Digoxin toxicity
Cardiac dysrhythmia
digoxin (Lanoxin)
Very narrow therapeutic window.
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
Nursing implications: glycosides
Monitor vital signs
Monitor for EKG changes
Monitor labs – K+, digoxin level (CRITICAL)
Patient education: glycosides
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)
Mechanism of action/drug effects:Vasodilator
ex.Bidil (37.5 mg of hydralizine/ 20 mg isosorbide dinitrate)
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)
B-type Natriuretic Peptide Mechanism of action/ Drug effects:
Examples:
nesiritide (Natrecor)
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).
Indication/ Route: B-type
Acutely decompensated CHF via continuous intravenous infusion only.
