Nursing Care Plan: Congestive Heart Failure

Definition

Heart failure is the inability of the heart to supply blood fl~w to meet physiologic demands, without utilizing compensatory changes. There may be failure involving one or both sides of the heart, and over time, causes the development of pulmonary and systemic congestion and complica- tions. Congestive heart failure, or CHF, is a common complication after myocardial infarction and can be attributed to one-third of the deaths of patients with MIs. Usually following MI, the heart failure is left-sided since most infarctions involve damage to the left ventricle.

Heart failure can also be classified as acute or chronic. In chronic heart failure, the body experi- ences a gradual development as the heart becomes

unable to pump a sufficient amount of blood to meet the body’s demands. Chronic heart failure can become acute without any overt cause.

Often, the patient will have no early symptoms of left-sided heart failure. Symptoms of decreased cardiac output will develop once the heart fails to pump enough blood into the systemic circulation. The pressure in the left ventricle increases, which in turn causes retrograde increases of pressure in the left atrium because of the increased difficulty for blood to enter the atrium from the pulmonary veins. Blood backs up in the lung vasculature, and when the pulmonary capillary pressure is exceeded by the oncotic pressure of the proteins in the plasma fluid (usually > 30 mmHg), the fluid leaks into the interstitial spaces. When this fluid moves into the alveoli, shortness of breath, coughing, and crackles (rales) occur, and the patient progresses into overt pulmonary edema, with the classic sign of coughing up copious amounts of pink frothy sputum.

Right-sided heart failure is usually caused by left- sided heart failure, but can also be caused by pulmonary emboli, pulmonary hypertension, COPD, and the presence of right ventricular infarctions.

The lungs can accept a certain amount of fluid build-up, but eventually, if no intervention is taken, the pressure in the lungs increases to the point whereby the right ventricle cannot eject its blood into the lungs. The right ventricle fails and then the blood in the right atrium cannot drain completely, and thus cannot accept the total amount of blood from the vena cavae. Venous pooling occurs with the impairment of venous blood flow, and eventually the organs become congested with venous blood.

 Treatment of heart failure involves attempts to improve contractility of the ventricle by use of positive inotropic drugs, decrease of afterload by the use of nitrates and vasodilators, and in some instances, by use of the IABP, and decrease of pre-load by the use of diuretics, IV nitroglycerin, and fluid/sodium restrictions.

MEDICAL CARE

Oxygen: to increase available oxygen supply

Morphine: used to induce vasodilation, decrease venous return to the heart, reduce pain and anxi- ety, and decrease myocardial oxygen consumption

Cardiac glycosides: digitalis (Digoxin, Lanoxin) PO or IV to increase the force and strength of ventricular contractions and to decrease rate of contractions in order to increase cardiac output.

Diuretics: furosemide (Lasix) PO or IV, chlorothiazide (Diuril) PO, bumetanide (Bumex) PO or IV to promote excess fluid removal, to decrease edema and pulmonary venous pressure by preventing sodium and water reabsorption

Vasodilators: hydralazine (Apresoline) PO or IV, isosorbide dinitrate (Isordil) SL or PO, prazosin (Minipress) PO, minoxidil (Loniten) PO, diazox-

ide (Hyperstat) IV, sodium nitroprusside (Nipride) IV, nitroglycerine (Nitrostat, Tridil) PO, SL, IV to relax vascular smooth muscle, decrease preload and afterload, decrease oxygen demand, decrease systemic vascular resistance, and increase venous capacitance

Renin-angiotensin system inhibitors: captopril (Capoten) PO used to inhibit angiotensin converting enzyme to reduce the production of angiotensin I1 to enable the decrease in vasocon- striction and to reduce afterload

Inotropic agents: dopamine, dobutamine (Dobutrex) IV, amrinone (Inocor) IV used to increase myocardial contractility, without increas- ing the heart rate, to produce peripheral vasodilation and decrease preload and afterload

Electrolytes: mainly potassium to replace that which is lost during diuretic therapy

Laboratory: electrolyte levels to monitor for imbalances; renal profiles to monitor for kidney function problems; digoxin levels to monitor for toxicity; platelet count to monitor for thrombocytopenia from amrinone

Chest x-ray: shows any enlargement of the heart and pulmonary vein, presence of pulmonary ederna or pleural effusion

Electrocardiography: used to monitor for dysrhythmias which may occur as a result of the heart failure or as a result of digitalis toxicity

Echocardiography: used to study structural abnor- malities and blood flow through the heart

Intra-aortic balloon pump: decreases the workload on the heart, decreases myocardial oxygen demand, increases coronary perfusion, decreases afterload, decreases preload, improves cardiac output and tissue perfusion

NURSING CARE PLANS

Fluid volume excess

Related to: increased sodium and water retention, decreased organ Perfusion, compromised regulatory mechanisms, decreased cardiac output, increased ADH production.

Defining characteristics: edema, weight gain, intake greater than output, increased blood pressure, increased heart rate, shortness of breath, dyspnea, orthopnea, crackles (rales), S3 gallop, oliguria, jugular vein distention, pleural effusion, specific gravity changes, altered electrolyte levels

Outcome Criteria

Blood pressure will be maintained within normal limits and edema will be absent or minimal in all body parts.

Fluid volume will be stabilized with balanced intake and output.

INTERVENTIONS	RATIONALES
Monitor vital signs and hemodynamic readings if available.	Fluid volume excess will cause increases in blood pressure, and CVP and pulmonary artery pressures, and these changes will be reflected from the development of pulmonary congestion and heart failure.
Auscultate lungs for presence of crackles (rales), or other adventitious breath sounds. Observe for presence of cough, increased dyspnea, tachypnea, orthopnea or paroxysmal nocturnal dyspnea.	May indicate pulmonary edema from cardiac decornpensation and pulmonary congestion. Pulmonary edema symptoms reflect leftsided heart failure. Right sided heart failure may have slower onset, but symptoms of dyspnea, orthopnea, and cough are more difficult to reverse.
Observe for jugular vein distention and dependent edema. Note presence of generalized body edema (anasarca).	May indicate impending congestive failure and fluid excess. Peripheral edema begins in feet and ankles, or other dependent areas and ascends as failure progresses. Pitting will usually occur only after 10 or more pounds of excess fluid is retained. Anasarca will be seen only with right heart failure or bi-ventricular failure.
Investigate abrupt complaints of dyspnea, air hunger, feeling of impending doom or suffocation.	Excessive fluid build-up can promote other complications such as pulmonary edema or pulmonary embolus and inter- vention must be immediate.
Determine fluid balance by measuring intake and output, and observing for decreases in output and concentrated urine.	Renal perfusion is impaired with excessive fluid volume, which causes decreased cardiac output leading to sodium and water retention and oliguria.
Weigh daily and notify MD of greater than 2 lblday increase.	Abrupt changes in weight usually indicate excess fluid
Provide patient with fluid intake of 2 L/day, unless fluid restriction is warranted.	Fluids may need to be restricted due to cardiac decompensation. Fluids maintain hydration of tissues.
Administer diuretics as ordered (furosemide, hydralazine, spirolactone with hydrochlorothiazide).	Drugs may be necessary to cor- rect fluid overload depending on emergent nature of problem. Diuretics increase urine flow rate and may inhibit reabsorp- tion of sodium and chloride in the renal tubules.
Monitor electrolyte for imbalances. Note increasing lethargy, hypotension, or musde cramping.	Hypokalemia can occur with the administration of diuretics. Signs of potassium and sodium deficits may occur due to fluid shifts with diuretic therapy.
Place and maintain patient in semi Fowler's position.	Diuresis may be enhanced by recumbent position due to increased glomerular filtration and decreased production of ADH.
Auscultate bowel sounds and observe for abdominal distention, anorexia, nausea, or constipation. Provide small, easily digestible meals.	CHF progression can impair gastric motility and intestinal function. Small, frequent meals may enhance digestion and pre- vent abdominal discomfort.
Measure abdominal girth if warranted.	Progressive right sided heart failure can cause fluid to shift into the peritoneal space and cause ascites.
Palpate abdomen for liver enlargement; note any right upper quadrant tenderness or pain.	Progressive heart failure can lead to venous congestion, abdominal distention, liver engorgement, and pain. Liver function may be impaired and can impede drug metabolism.
Assist with dialysis or hemofiltration as warranted.	Mechanically removing excess fluid may be performed to rapidly reduce circulating volume in cases refractory to other medical therapeutics.

Discharge or Maintenance Evaluation

·         Patient will have no edema or fluid excess.

·         Fluid balance will be maintained and blood pressure will be within normal limits of baseline.

·         Lung fields will be clear, without adventitious breath sounds, and weight will be stable.

·         Patient will be able to accurately verbalize understanding of dietary restrictions and medications.

Decreased cardiac output

Related to: damaged myocardium, decreased con- tractility, dysrhythmias, conduction defects, alteration in preload, alteration in afterload, vasoconstriction, myocardial ischemia, ventricular hypertrophy, accumulation of blood in lungs or in systemic venous system

Defining characteristics: dependent edema, elevated blood pressure, elevated mean arterial pressure greater than 120 mmHg, elevated systemic vascular resistance greater than 1400 dyne-secondslcm5, cardiac output less than 4 L/min or cardiac index less than 2.5 L/min/m2, tachycardia, cold, pale extremities, absent or decreased peripheral pulses, EKG changes, hypotension, S3 or S4, gallops, decreased urinary output, diaphoresis, orthopnea, dyspnea, crackles (rales), frothy blood-tinged sputum, junggular vein distention, edema, chest pain, confusion, restlessness

Outcome Criteria

Vital signs and hemodynamic parameters will be within normal limits for patient, with no dysrhythmias noted.

Patient will be eupneic with no adventitious breath sounds or abnormal heart tones.

INTERVENTIONS	RATIONALES
Determine level of cardiac function and existing cardiac and  other conditions.	Additional disease states and complications may place an additional workload on an already compromised heart.
Auscultate apical pulses and monitor heart rate and rhythm. Monitor BP in both arms.	Decreased contractility will be compensated by tachycardia, especially concurrently with heart failure. Blood volume will be lowered if blood pressure is increased resulting in increased afterload. Pulse decreases may be noted in association with toxic levels of digoxin, and peripheral pulses may be hard to accurately determine if per- fusion is decreased. Hypotension may occur as a result of ventricular dysfunction and poor perfusion of rhe myocardium.
Measure cardiac output and cardiac index, and calculate hernodynamic pressures every 4 hours and prn.	Provides measurement of cardiac function and calculated measurements of preload and afterload to facilitate titration of vasoactive drugs and manipulation of hemodynamic pressures.
Monitor EKG for dysrhythmias and treat as indicated.	Conduction abnormalities may occur due to ischemic myocardium affecting the pumping efficiency of the heart.
Observe for development of new S3 or S4 gallops.	S3 gallops are usually associated with congestive heart failure but can be found with rnitral regurgitation and left ventricular overload after MI. S4 gallops can be associated with myocardial ischemia, ventricular rigidity, pulmonary hypertension, or systemic hy- pertension, which can decrease cardiac output.
Auscultate for presence of murmurs and lor rubs.	Indicates disturbances of normal blood flow within the heart related to  incompetent valves, septal defects, or papillary muscle/chordae tendonae complications post MI. Presence of a rub with an MI is associated with pericarditis and/ or pericardial effusion.
Observe lower extremities for edema, distended neck veins, cold hands and feet, mottling, oliguria.	Reduced venous return to the heart can result in low cardiac output; oliguria results from decreased venous return due to fluid retention.
Position in semi-Fowler’s position.	Promotes easier breathing and prevents pooling of blood in the pulmonary vasculature.
Administer cardiac glycosides, nitrates, vasodilators, diuretics, and antihypertensives as ordered.	Used in the treatment of vasoconstriction and to reduce heart rate and contractility, reduces blood pressure by relaxation of venous and arterial smooth muscle which then in turn increases cardiac output and decreases the workload on the heart.
Titrate vasoactive drugs as ordered per MD parameters.	Maintains blood pressure and heart rate at levels to optimize cardiac output function.
Weigh every day.	Weight gain may indicate fluid retention and possible impending congestive failure.
Arrange activities so as to not overtax patient.	Avoids over-fatiguing patient and decreasing cardiac output further. Balancing rest with activity minimizes energy expenditure and myocardial oxygen demands by maintaining cardiac output.

Discharge or Maintenance Evaluation

·        Patient will have no chest pain or shortness of breath.

·        Vital signs and hemodynamic parameters will be within normal limits for age and disease condition.

·        Minimal activity will be tolerated without fatigue or dyspnea.

·        Urinary output will be adequate. Cardiac output will be adequate to ensure adequate perfusion of all body systems.

Impaired gas exchange

Related to: ventilationlperfusion imbalance caused from excess fluid in alveoli and reduction of air exchange area in lung fields, fluid collection shifts into the interstitial space

Defining characteristics: confusion, restlessness, irritability, hypoxia, hypercapnea, dyspnea, orthopnea, abnormal ABGs, abnormal oxygen saturation

Outcome Criteria

Patient will have adequate oxygenation with respiratory status within limits of normal based on age and other conditions, and ABGs will be within normal limits.

INTERVENTIONS	RATIONALES
Monitor respiratory status for rate, Regularity, depth, ease of effort at rest or with exertion, inspiratory/expiratory ratio.	Changes in respiratory pattern or patency of airway may result in gas exchange Imbalances.
Observe for presence of cyanosis and mottling; monitor oximetry for oxygen saturation; monitor ABGs for ventilation/perfusion problems.	Cyanosis results from decreases in Oxygenated hemoglobin in the blood and this reduction leads to hypoxia. Reading of 90% on pulse oximeter correlates with pO2 of GO.
Monitor for mental status changes, deterioration in level of consciousness, restlessness, irritability, easy fatigueability.	Hypoxia affects all body systems and mental status changes can result from decreased oxygen to brain tissues.
Position in semi or high Fowler's position.	Promotes breathing and lung expansion to enhance gas distribution.
Administer oxygen via nasal cannula at 2-3 L/min, or other delivery systems.	Maintains adequate oxygenation without depression of respiratory drive. CO2 may be retained with higher flow rates when used in patients with COPD.
Assist with placement of ETT and placement on mechanical ventilation.	Mechanical ventilation may be required if respiratory failure is progressive and Adequate oxygen levels cannot be Maintained by other delivery systems.

Discharge or Maintenance Evaluation

·        Patient will exhibit no ventilation/perfusion imbalances.

·        Patient will be eupneic with no adventitious breath sounds.

·        ABGs will be within acceptible ranges for patient with adequate oxygenation of all tissues.

·        Patient will be able to verbalize/demonstrate the correct use of oxygen.

Risk for impaired skin integrity

Related to: bed rest, decreased tissue perfusion, edema, immobility, decreased peripheral perfusion, shearing forces or pressure, secretions, excretions, altered sensation, skeletal prominence, poor skin turgor, altered metabolic rate

Defining characteristics: disruption of skin surface, pressure areas, reddened areas, blanched areas, mottling, warmth, firmness to area of skin, irritated tissues, excoriation of skin, maceration of skin, lacerations of skin, pruritis, dermatitis

Outcome Criteria

Patient will have and maintain skin integrity.

INTERVENTIONS	RATIONALES
Monitor mobility status and patient's ability to move self.	Immobility is the primary cause of skin breakdown.
Inspect all skin surfaces, espe- cially bony prominences, for skin breakdown, altered circulation to areas, or presence of edema.	Skin is at risk because of decreased tissue perfusion, immobility, decreased peripheral perfusion, and possible nutritional alterations.
Provide skin care to blanched or reddened areas.	Stimulates blood flow and decreases tissue hypoxia. Excess dryness or moistness of skin can promote breakdown.
Provide eggcrate mattress, alternating pressure mattress, sheepskin, elbow protectors, heel protectors, etc.	These items can reduce pressure on skin and may improve circulation.
Reposition frequently, at least every 2 hours. Assist with ROM exercises. Maintain body alignment. Raise head of bed no higher than 30 degrees.	Improves circulation by reduction of time pressure is on any one area. Proper body alignment prevents contractures. Elevations higher than this may promote pressure and friction from sliding down, and shearing force may result in breakdown of skin.
Avoid subcutaneous or IM injections when possible.	Edema and tissue hypoxia impede circulation which can cause decreased absorption of medication and can predispose patient to tissue breakdown and development of abscess/ infection.

Discharge or Maintenance Evaluation

·        Patient will have intact skin, free of redness, irritation, rashes, or bruising. Patient will be able to verbally relate measures to reduce chance of tissue injury.