Chapter 26 Nursing Care of Patients With Heart Failure

Chronic Heart Failure

- Signs and symptoms Fatigue and weakness are the earliest symptoms of HF . They occur from the decreased amount of oxygen reaching the tissues. fatigue worsens, especially with activity. Dyspnea is a common symptom of left-sided HF. pulmonary congestion that impairs gas exchange. between the alveoli and capillaries. • Exertional dyspnea is shortness of breath that increases with activity. • Orthopnea is dyspnea that increases when lying flat. In an upright position, gravity holds fluid in the lower extremities. In a supine position, gravitational forces are removed, allowing fluid to move from the legs to the heart, which overwhelms the already congested pulmonary system. When orthopnea is present, two or more pillows are often used for sleeping. Documentation should state the number of pillows used. For example, use of three pillows would be "three-pillow orthopnea." • Paroxysmal nocturnal dyspnea (PND) is sudden short- ness of breath that occurs after lying flat for a time. PND results from excess fluid accumulation in the lungs. A chronic, dry cough is common in HF. Pulmonary congestion causes abnormal breath sounds such as crackles and wheezes. Crackles are produced from fluid buildup. Wheezes occur from bronchiolar constriction caused by the increased fluid. The sympathetic nervous system compensates for the de- creased cardiac output in HF by releasing epinephrine and norepinephrine to increase the heart rate. Chest pain may occur from ischemia in the patient with HF. The kidneys compensate by retaining sodium and fluid, which increases the fluid volume returning to the heart. Pain also increases oxygen requirements, adding further to the cycle of HF. A breathing pattern of shallow respirations building to deep breaths followed by a period of apnea characterizes Cheyne- Stokes breathing. The apneic period occurs because the deep breathing causes carbon dioxide levels to drop to a level that does not stimulate the respiratory center. Edema occurs in HF as a result of (1) systemic blood v essel congestion and (2) sympathetic compensatory mechanisms that cause the kidneys to activate the renin-angiotensin-aldosterone system, in which antidiuretic hormone is released from the pituitary gland, causing sodium and water to be retained. distention of the jugular veins, swelling of the legs and feet, sacral edema in the individual on bed rest, and increased fluid within the abdominal cavity and organs Many patients with HF are anemic. Nocturia is an increase in urine output at night during sleep. Nocturia may occur up to six times per night, contributing to the patient's fatigue from lack of sleep. The skin, nail beds, or mucous membranes may appear blue. Cyanosis is a late sign of HF. It is associated primarily with left-sided HF. Reduced cardiac output decreases the amount of oxygen de- livered to the brain. Altered mental status, dyspnea, and fatigue inter- fere with the ability to eat. Anorexia and GI upset occur from pressure exerted by excess fluid surrounding the GI structures.

Congestive Heart Failure

An older term for HF Volume overload or "congestion" either in the lungs or periphery is not present in everyone with HF or at all times.

Cardiac Transplantation

Cardiac transplantation is reserved for patients with end-stage cardiac disease.

Overview of Heart Failure

Clinical syndrome that occurs as a result of inability of the ventricles to fill or pump enough blood to meet the body's oxygen and nutrient needs. It may cause dyspnea, fatigue, and fluid volume overload in the intravascular and interstitial spaces resulting in reduced quality and length of life. Causes of HF are varied and may include coronary artery disease(most often), myocardial infarction, cardiomyopathy, heart valve problems, and hypertension. In older adults the most common cause is cardiac ischemia.

Compensatory Mechanisms to Maintain Cardiac Output

Compensatory mechanisms help ensure that an adequate amount of blood is being pumped out of the heart. they contribute to a cycle that, instead of being helpful, leads to further HF. When the sympathetic nervous system detects low cardiac output, it speeds up the heart rate by releasing epinephrine and norepinephrine. Although this raises cardiac output the increased heart rate also increases the oxygen needs of the heart. In response to the resulting low renal blood flow, the kidneys activate the renin- angiotensin-aldosterone system, and antidiuretic hormone is released from the pituitary gland to conserve water, causing decreased urine output. This adds to the fluid retention problem already found in HF. Over time the heart responds to the increased workload by enlarging its chambers (dilation) and increasing its muscle mass (hypertrophy), referred to as remodeling. heart muscle fibers stretch to increase the force of myocardial contractions, which is known as the Frank- Starling phenomenon.

Right-sided Heart Failures

Conditions causing right-sided HF increase the work of the right ventricle. The major cause of right-sided HF is left-sided HF. When the left side fails, fluid backs up into the lungs and pulmonary pressure is increased. The right ventricle must continually pump blood against the increased fluid and pressure in the pulmonary artery and lungs. Over time this additional hypertrophies or fails because of increased pulmonary pressures, it is referred to as cor pulmonale. As blood backs up from the right ventricle, right atrial and systemic venous blood volume increases. The jugular neck veins, which are not normally visible, become distended. Edema may occur in the peripheral tissues, and the abdominal organs can become engorged. As the failure progresses, blood pools in the hepatic veins, and the liver becomes congested (hepatomegaly). Systemic venous congestion also leads to engorgement of the spleen (splenomegaly).

Pathophysiology

Proper cardiac functioning requires each ventricle to pump out equal amounts of blood over time. If the amount of blood returned to the heart becomes more than either ventricle can handle, the heart can no longer function effectively as a pump. Conditions that cause HF can affect one or both of the heart's pumping systems. Therefore, HF can be classified as right-sided HF, left-sided HF, or biventricular HF. The left ventricle typically weakens first because it has the greatest workload. Failure of one side eventually leads to the failure of the other side.

Pulmonary Edema (Acute Heart Failure)

Pulmonary edema, also known as acute HF, is sudden severe fluid congestion in the alveoli of the lungs and is life threatening. PE occurs with an acute event such as a MI or when the heart is severely stressed, Complications of pulmonary edema include dysrhythmias and cardiac arrest. - Signs and symptoms Pink, frothy sputum is a classic symptom of pulmonary edema caused by the increased lung congestion and pressures that allow leaking of fluid and RBCs into the alveoli. as pulmonary edema worsens, the blood pressure may fall. - Therapeutic Measures Immediate treatment is needed to prevent patients from drowning in their own secretions reduce the workload of the left ventricle in order to improve cardiac output Fowler's position allows the lungs to expand more easily. In severe cases of pulmonary edema, endotracheal intubation and mechanical ventilation may be necessary. Medications are given intravenously - Nursing Care The patient is typically critically ill and in an intensive care unit

Nutrition Notes

Taking cyclosporine with grapefruit juice may cause elevated blood levels of the drug. St. John' s wort dietary supplement can help and has interacted with cyclosporine. Temperature is monitored every 4 hours and complete blood cell count (CBC) and white blood cell (WBC) results are monitored for indications of infection.

Left sided heart failure

The left ventricle must generate a certain amount of force during contraction to eject blood into the aorta through the aortic valve. This force is referred to as after load. The pressure within the aorta and arteries acts as resistance and influences the force required to open the aortic valve to pump blood into the aorta. The pressure is called peripheral vascular resistance, or PVR. Hypertension is one of the major causes of left-sided HF because it increases the pressure within arteries. It makes the left ventricle work harder to pump blood into the aorta. Over time the strain caused by the increased workload causes the left ventricle to weaken and fail. With left-sided HF, blood backs up from the left ventricle into the left atrium and then into the four pulmonary veins and lungs. Alveolar edema is more serious because it reduces gas exchange across the alveolar capillary membrane. Shortness of breath and cyanosis may result from the decreased oxygenation of the blood leaving the lungs. If the fluid buildup is severe, acute pulmonary edema occurs, which requires immediate medical treatment.

Complications of Heart Failure

The liver and spleen enlarge from the fluid congestion, which causes impaired function, cellular death, and scarring. leakage of fluid Thrombosis and emboli can occur. leads to stasis of blood. Cardiogenic shock is a life-threatening condition. - Diagnostic tests Serum laboratory tests can elevate contributing factors for HF, such as an elevated serum blood urea nitrogen (BUN) and serum creatinine from renal failure, elevated liver enzymes from liver damage, elevated ferritin with he- mochromatosis (iron overload), and thyroid function tests. • A serum B-type natriuretic peptide (BNP) or N-terminal proBNP (NT-proBNP) level may be obtained. Elevated levels indicate HF and severity; higher levels of this cardiac biomarker correlate with a worse prognosis. BNP is made by the heart to regulate blood volume to reduce cardiac workload. When the heart has to work harder over time, it releases more BNP. • Elevated serum cystatin C (a protein produced by all nu- cleated cells) is a risk factor for HF. • A chest x-ray examination shows the size, shape, and any enlargement of the heart as well as congestion in the pulmonary vessels. • Cardiac dysrhythmias that precipitate and contribute to HF are diagnosed with an electrocardiogram (ECG; see Chapters 21 and 25). • Echocardiography may measure ventricular size, wall thickness, motion, and ejection fraction and assess valvular function. • Exercise stress testing and nuclear imaging studies show activity tolerance, which is usually limited in HF. • Cardiac magnetic resonance imaging (MRI) shows both moving and still pictures of the heart and major blood vessels. Cardiac structure and function are analyzed to determine treatment for cardiac disease. • Cardiac catheterization and angiography are used to detect underlying heart disease that may be the cause of HF. • Sleep studies may be done because sleep apnea or breath- ing disorders can contribute to HF. • Measurement of the pressure in the heart and lungs is done with hemodynamic monitoring to guide medical therapy. - Therapeutic measures Treatment of HF focuses on (1) identify- ing and correcting the underlying cause, (2) increasing the strength of the heart's contraction, (3) maintaining optimum water and sodium balance, and (4) decreasing the heart' s workload. One of the major problems caused by HF is a reduction in oxygen delivered to the tissues. fatigue, dyspnea, altered mental status, and cyanosis. Severe symptoms may require bed rest. For stable HF, a regular exercise program, such as one set up with referral to a cardiac rehabilitation program, has shown to improve cardiac function and reduce HF effects. Dietary sodium is restricted to decrease fluid retention. A healthy weight range should be maintained. low-sodium diet. There is no cure for HF. Medications, however, can improve symptoms and quality of life. • Stage A refers to people at high risk of HF. • Stage B is those who have no HF symptoms but do have structural heart disease. • Stage C applies to people with current or past symptoms of HF with structural heart disease. This includes most patients with HF. • Stage D includes those with refractory HF. ARBs - Angiotensin receptor blockers. They are used for their vasodilation effect, which lowers blood pressure and reduces workload on the heart. lowering blood pressure and workload on the heart. Beta- blockers block the adverse effects of the SNS. Diuretics reduce fluid volume and decrease pulmonary venous pressure, which in turn decreases cardiac workload. Potassium supplements are often given with potassium-wasting diuretics. Spironolactone (Aldactone) blocks the effects of aldosterone, which causes the retention of sodium and fluid. Potassium must be monitored carefully. Inotropic drugs strengthen ventricular contraction to increase cardiac output. usually used short term. In addition to improving contraction strength, digitalis preparations decrease conduction time within the heart. Obtaining an apical pulse rate before ad- ministration of digitalis is required. Monitoring of serum drug levels is necessary to detect toxic levels of the drug. Cardiac resynchronization therapy (CRT) restores normal contraction timing of the ventricles. A right and left ventricular lead stimulates the ventricles to synchronize their contractions in response to the atrial event. Mechanical assistive devices can provide temporary support to patients in cardiogenic shock and act as a bridge to trans- plantation. increase the cardiac output. For acute care, an intra- aortic balloon pump (IABP) increases circulation to the coronary arteries and reduces the work of the heart. Ventricular assist devices (VADs) are implanted mechanical devices that assist cardiac pumping. These devices maintain cardiac output and allow the failing ventricle to rest. HF causes may be treated surgically with coronary artery by- pass for coronary artery disease or valve replacement for valvular disease. Once these conditions are treated, HF symptoms should resolve.

Nursing Process for the Patient with Chronic Heart Failure

The major focus of nursing care for chronic HF patients is to improve oxygenation and decrease the body's need for oxygen with rest, positioning, medications, fluid balance, and oxygen consumption control. For chronic HF, oxygen is administered at 2 to 6 L/min via nasal cannula. A balance of rest and activity that does not produce signs or symptoms of oxygen deprivation is essential. Semi-Fowler's or high-F owler's position makes breathing easier. Monitoring daily weights for weight gain is important in detecting fluid retention. until 5 to 10 pounds of e xtra fluid are present. Tell patients to report weight gains of 2 to 3 pounds over 1 to 2 days. Increased oxygen consumption by the heart should be avoided. Sustained tachycardia increases the oxygen needs of the heart and should be reported promptly to the HCP for treatment. Constipation should be prevented because straining during defecation, known as the Valsalva maneuver, increases the heart's workload by increasing venous return to the heart. Fatigue should be avoided by alternating activity with periods of rest. HF is a progressive, chronic condition, and patients may require lifetime medication. Diuretics require monitoring of the patient's potassium levels and blood pressure. If too much fluid is removed, the patient may become hypotensive, and orthostatic hypotension can develop. Can be dizzy and at risk of falling. Before administration of a digitalis drug, which slows the heart rate, the patient' s apical pulse should be counted for 1 minute. If the pulse is below 60 beats/min, no- tify the HCP to determine if the drug should be given. Some patients are given digitalis even if their heart rates are be- tween 50 and 60 beats/min, as long as their heart's conduction system is normal or if the rate is due to other medications such as a beta blocker. hypokalemia increases the heart's sensitivity to digitalis. Patient can become toxic when hypokalemia is present. Medications with vasodilating effects reduce the heart's workload by decreasing vascular pressure. Blood pressure is monitored when administering vasodilators. • Take drug during the day before 1600 to decrease being awakened at night to void (if desired). • Have a readily available and obstacle-free bathroom or commode to prevent incontinence and falls. • Eat high-potassium foods if taking a potassium-wasting diuretic. •Weigh ones self daily, and report weight gains of 2 to 3 pounds over 1 to 2 days.