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Running Head: CONGESTIVE HEART FAILURE

Congestive Heart Failure

Adrianne Bazo

Montana Tech Nursing Department

NURS 1566 Core Concepts of Adult Nursing

March 14, 2008

Noel Mathis RN, BSN, MSN

Congestive Heart Failure

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Congestive heart failure occurs when there is a malfunction in the pumping action of

either the left ventricle, right ventricle, or both which causes blood to pool in the

pulmonary arteries and/or veins. This pooling causes pulmonary congestion (fluid build

up in the lungs), reduced cardiac output, increased strain on the heart, decreased

efficiency of the heart muscle contraction, reduced stroke volume, increased heart rate,

and hypertrophy; leading to increased risk of cardiac arrest and a decreased blood supply

to the rest of the body. Since blood is the oxygen/nutrient supply to the cells, the effects

of CHF are systemic.

Risk factors for developing CHF are disorders that increase cardiac workload and

disorders that disrupt the pumping ability of the heart. Examples of such diseases are,

CAD, cardiomyopathy, acute myocardial infarction, disease of the heart valves, fluid

volume overload, hypertension, COPD, pulmonary hypertension, and anemia.

My patient had triple bypass surgery six years ago, so the cause of her CHF is most likely

from acute myocardial infarction.

The diagnosis of CHF is primarily made from a composite of patient history, physical

exam, laboratory studies, and radiographs. Lab studies that indicate CHF are, low serum

sodium and Hct from hemodilution and inadequate oxygen levels in the arteries from

poor pulmonary perfusion. The effects of CHF cause reduced renal funciton producing

elevated blood urea nitrogen and creatinine levels.

The treatment of CHF is directed on decreasing the effects of the underlying causes.

Pharmaceuticals are used to decrease excess fluid (diuretics), and improve cardiac output

(ACE inhibitors, Beta-adrenergic blockers, inotropics, and nitrates). Nonpharmaceutical

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interventions to decrease cardiac workload and increase myocardial oxygenation include

intra-aortic balloon pump, ventricular assist devices, and biventricular pacing. Also a diet

low in sodium is recommended.

My patient presents with peripheral edema, low SaO2 oxygenation, rales heard in the

lower 2/3 of the posterior lungs, shortness of breath, low Hct (30.5), high total carbon

dioxide, high Lactate dehydrogenase (778), and high natriuretic peptide (823). Lactate

dehydrogenase and natriuretic peptide are indicators of tissue damage and degree of heart

failure. My patient’s clinical presentation of heart failure, both pulmonary and systemic

effects, indicates that her CHF is from both right and left ventricle malfunction. She is

being treated with aspirin 81 mg to reduce platelet aggregation. Lisinopril 10 mg (a ACE

inhibitor), Spironlactone 50mg (a potassium sparing diuretic), and Potassium CL 10 mEq

(a mineral and electrolyte replacements/supplements).