Exam 2: Heart Failure Text book powerpoint

*Chronic HF Ambulatory and Home Care* Explain to patient and caregiver physiologic changes that have occurred Assist patient to adapt to both the physiologic and psychologic changes Integrate patient and caregiver(s) into the overall care plan

HF is a chronic illness for most persons. When a patient is diagnosed with HF, care should focus on slowing the progression of the disease. Your important nursing responsibilities include: (1) teaching the patient about the physiologic changes that have occurred (2) assisting the patient to adapt to both the physiologic and psychologic changes (3) integrating the patient and the caregiver in the overall care plan.

Classification of Heart Failure: 1. Systolic versus diastolic 2. Left-sided versus right-sided

HF is classified as systolic or diastolic failure (or dysfunction). Patients can have isolated systolic or diastolic failure or a combination of both. Although HF is usually manifested by biventricular failure, one ventricle may precede the other in dysfunction. Normally the pumping actions of the left and right sides of the heart are synchronized, producing a continuous flow of blood. However, as a result of pathologic conditions, one side may fail while the other side continues to function normally for a period of time. Because of the prolonged strain, both sides of the heart will eventually fail, resulting in biventricular failure.

Anything that interferes with mechanisms that regulate cardiac output (CO) *Primary causes* Conditions that directly damage the heart Precipitating causes Conditions that increase the workload of ventricles

HF may be caused by any interference with the normal mechanisms regulating cardiac output (CO). CO depends on (1) preload, (2) afterload, (3) myocardial contractility, and (4) heart rate (HR). Any changes in these factors can lead to decreased ventricular function and HF. The major causes of HF may be divided into two subgroups: *primary and precipitating* *Primary causes include:* Coronary artery disease, including myocardial infarction Hypertension, including hypertensive crisis Rheumatic heart disease Congenital heart defects (e.g., ventricular septal defect) Pulmonary hypertension Cardiomyopathy (e.g., viral, postpartum, substance abuse) Hyperthyroidism Valvular disorders (e.g., mitral stenosis) Myocarditis *Precipitating causes:* often increase the workload of the ventricles, resulting in an acute condition that results in decreased cardiac function. -Anemia (decreased oxygen supply increases workload of heart to meet the demand) -Infection (increased oxygen demand) -Thyrotoxicosis (increased heart rate and workload) -Hypothyroidism (increased risk for atherosclerosis) -Dysrhythmias (decreased CO and increased workload) -Bacterial endocarditis (infection increases workload, can also cause valvular disorders) -Pulmonary embolism (increased workload to pump blood into lungs) -Paget's disease (increased workload secondary to increased vasculature bed) -Nutritional deficiencies (decreased cardiac function increases workload) -Hypervolemia (increased preload increases workload)

*Cardiac Transplantation Posttransplantation monitoring* -Acute rejection -Infection -Malignancy -Cardiac vasculopathy Immunosuppressive therapy Endomyocardial biopsy (EMB)

A variety of complications can occur after the transplant, including a risk for SCD. *Acute rejection* is an immediate posttransplant complication, and immunosuppressive therapy is the key in posttransplant management. In the first year after transplantation, the major causes of death are acute rejection and infection. Later on, malignancy (especially lymphoma) and cardiac vasculopathy (accelerated CAD) are major causes of death. Most immunosuppressive regimens include corticosteroids, calcineurin inhibitors (cyclosporine [Sandimmune, Neoral], tacrolimus [Prograf]), and antiproliferative drugs (mycophenolate mofetil [CellCept]). Because of the use of immunosuppression therapy, infection is a primary complication after transplant surgery. On a long-term basis, immunosuppressive therapy increases the risk for cancer. To detect rejection, an EMB is obtained on a weekly basis for the first month, monthly for the following 6 months, and yearly thereafter. In this procedure, a catheter is inserted into the jugular vein and moved into the right ventricle. The catheter uses a bioptome, a device with two small cups that can be closed, to remove small samples of heart muscle.

*Risk Factors* (Primary risk factors) -Hypertension -CAD

Hypertension and CAD are the primary risk factors for HF. Most patients with HF have a history of hypertension. The risk of HF increases with the severity of hypertension. Other factors, such as diabetes, advanced age, tobacco use, obesity, and high serum cholesterol, also contribute to the development of HF.

*Risk Factors* Contributing risk factors -Advanced age -Diabetes -Tobacco use -Obesity -High serum cholesterol

Hypertension and CAD are the primary risk factors for HF. Most patients with HF have a history of hypertension. The risk of HF increases with the severity of hypertension. Other factors, such as diabetes, advanced age, tobacco use, obesity, and high serum cholesterol, also contribute to the development of HF.

*Compensatory Mechanism* Sympathetic nervous system (SNS) activation 1. First and least effective mechanism 2. Release of catecholamines (epinephrine and norepinephrine) -Increased heart rate -Increased myocardial contractility -Peripheral vasoconstriction 3. Initially helpful but then harmful

Sympathetic nervous system (SNS) activation is often the first mechanism triggered in low-CO states. However, it is the least effective compensatory mechanism. In response to an inadequate stroke volume and CO, there is increased SNS activation, resulting in the increased release of catecholamines (epinephrine and norepinephrine). This results in increased HR, increased myocardial contractility, and peripheral vasoconstriction. Initially, this increase in HR and contractility improves CO. However, over time these factors are harmful as they increase the already failing heart's workload and need for oxygen. The vasoconstriction causes an immediate increase in preload, which may initially increase CO. However, an increase in venous return to the heart, which is already volume overloaded, actually worsens ventricular performance.

*ADHF Drug Therapy* 1. *Diuretics* Decrease volume overload (preload) -Furosemide (Lasix), bumetanide (Bumex) 2. *Vasodilators* Reduce circulating blood volume and improve coronary artery circulation -IV nitroglycerin -Sodium nitroprusside (Nipride) -Nesiritide (Natrecor)

*1. Diuretics* Diuretics are the mainstay of treatment in patients with volume overload. -Diuretics act to decrease sodium reabsorption at various sites within the nephrons, thereby enhancing sodium and water loss. Decreasing intravascular volume with the use of diuretics reduces venous return (preload) and subsequently the volume returning to the LV. This allows the LV to contract more efficiently. -CO is increased, pulmonary vascular pressures are decreased, and gas exchange is improved. Loop diuretics (e.g., furosemide [Lasix], bumetanide [Bumex]) can be administered by IV push and act rapidly in the kidneys. *2. Vasodilators* -*IV nitroglycerin*: is a vasodilator that reduces circulating blood volume. It also improves coronary artery circulation by dilating the coronary arteries. Therefore nitroglycerin reduces preload, slightly reduces afterload (in high doses), and increases myocardial oxygen supply. When titrating IV nitroglycerin, monitor BP frequently (every 5 to 10 minutes) to avoid symptomatic hypotension. -*Sodium nitroprusside (Nipride)* is a potent IV vasodilator that reduces both preload and afterload, thus improving myocardial contraction, increasing CO, and reducing pulmonary congestion. Complications of IV sodium nitroprusside include (1) hypotension and (2) thiocyanate toxicity, which can develop after 48 hours of use. Sodium nitroprusside is administered in an ICU, as symptomatic hypotension is the main adverse effect. -*Nesiritide (Natrecor)*, administered IV, is a recombinant form of BNP and causes both arterial and venous dilation. The main hemodynamic effects of nesiritide include (1) a reduction in PAWP and (2) a decrease in systemic BP. Although classified as a vasodilator, nesiritide is also a neurohormonal blocking agent. It can be used for short-term treatment of ADHF. Nesiritide does not require titration after the initial IV bolus. It can be given in the emergency department (ED) and a non-ICU setting. Because the main adverse effect of nesiritide is symptomatic hypotension, monitor BP closely.

Chronic Heart Failure Drug therapy *RAAS inhibitors* ACE inhibitors Angiotensin II receptor blockers Aldosterone antagonists Monitor potassium levels (hyperkalemia)

*Angiotensin-Converting Enzyme Inhibitors* ACE inhibitors are the primary drug of choice for blocking the RAAS system in HF patients with systolic failure. The conversion of angiotensin I to the potent vasoconstrictor angiotensin II needs ACE. ACE inhibitors act by blocking this enzyme, resulting in reduced levels of angiotensin II. As a result, plasma aldosterone levels are also reduced. Thus ACE inhibitors serve as neurohormonal blocking agents. Consequently, ACE inhibitors also decrease the development of ventricular remodeling by inhibiting ventricular hypertrophy. Because CO is dependent on afterload in chronic HF, the reduction in SVR seen with the use of ACE inhibitors causes a significant increase in CO. Though the use of ACE inhibitors may decrease BP, tissue perfusion is maintained or increased as a result of improved CO. In addition, diuresis is enhanced by the suppression of aldosterone. These drugs can cause hypotension, nonproductive cough, and (rarely) life-threatening angioedema *Angiotensin II Receptor Blockers* For patients who are unable to tolerate ACE inhibitors, angiotensin II receptor blockers (ARBs) are recommended. These agents prevent the vasoconstrictor and aldosterone-secreting effects of angiotensin II by binding to the angiotensin II receptor sites. *Aldosterone Antagonists* Spironolactone (Aldactone) and eplerenone (Inspra) are aldosterone antagonists. They block the harmful neurohormonal effects of aldosterone on the heart blood vessels. They are also *potassium-sparing diuretics* that promote sodium and water excretion while retaining potassium. These effects occur because these agents bind to receptors at the aldosterone-dependent sodium-potassium exchange site in the distal renal tube.

*Pathophysiology Diastolic HF* -Impaired ability of the ventricles to relax and fill during diastole, resulting in decreased stroke volume and CO -Heart failure with normal EF -Result of left ventricular hypertrophy from hypertension, MI, valve disease, or cardiomyopathy

*Diastolic failure* is the inability of the ventricles to relax and fill during diastole. Decreased filling of the ventricles will result in decreased stroke volume and CO. Diastolic failure is often referred to as HF with normal EF. The diagnosis of diastolic failure is made based on the presence of HF symptoms with a normal EF. *Diastolic failure is characterized* by high filling pressures due to stiff ventricles. This results in venous engorgement in both the pulmonary and systemic vascular systems. Diastolic failure is usually the result of left ventricular hypertrophy from hypertension (most common), myocardial ischemia, valve disease (e.g., aortic, mitral), or cardiomyopathy. However, many patients will not have an identifiable heart disease.

Chronic Heart Failure (Drug therapy) Diuretics -Reduce edema, pulmonary venous pressure, and preload -Promote sodium and water excretion -Loop diuretics -Thiazide diuretics -Monitor potassium levels (hypokalemia)

*Diuretics* Diuretics are used to reduce edema, pulmonary venous pressure, and preload. If excess extracellular fluid is removed, blood volume returning to the heart can be reduced and cardiac function improved. Diuretics act on the kidney by promoting excretion of sodium and water. Many varieties of diuretics are available. Loop diuretics (e.g., furosemide [Lasix], bumetanide [Bumex]) are potent diuretics. These drugs act on the ascending loop of Henle to promote sodium, chloride, and water excretion. Problems in using loop diuretics include reduction in serum potassium levels, ototoxicity, and possible allergic reaction in patients sensitive to sulfa-type drugs. Thiazide diuretics inhibit sodium reabsorption in the distal tubule, thus promoting excretion of sodium and water. They can be added to loop diuretics to obtain results if patients become resistant to loop diuretics. Thiazide diuretics also can cause severe reductions in potassium levels. Diuretics are very effective in relieving the congestive symptoms of HF. However, their use does activate the SNS and RAAS, which can exacerbate the HF syndrome. In chronic HF, the lowest effective dose of diuretic should be used.

*Chronic HF Patient Teaching* -Signs and symptoms of HF exacerbations - what to do/report -Importance of early detection -Can have positive outlook with chronic health problem if treatment plan is followed

*Review the signs and symptoms of HF* exacerbations with the patient and caregiver, and provide them with a clear action plan should symptoms occur. Early detection of worsening HF may help to prevent an acute episode requiring hospitalization. Patients with HF are at risk for anxiety and depression. Emphasize to the patient that it is possible to live productively with this chronic health problem. Patients with HF are usually required to take drugs for the rest of their lives. This often becomes difficult because a patient may be asymptomatic when HF is under control. You must stress that the disease is chronic, and that drugs must be continued to keep the HF under control. Teach the patient the expected actions of the prescribed drugs and the signs of drug toxicity. Also teach the patient and caregiver how to take a pulse rate. The pulse rate should always be taken for 1 full minute. A pulse rate less than 50 beats/minute may be a contraindication to taking a digitalis preparation or β-adrenergic blocker unless specified otherwise by the health care provider. However, in the absence of symptoms (e.g., heart block, ventricular ectopy, syncope), a pulse rate less than 50 beats/minute may be acceptable. Include clear information about when a drug, especially digitalis and beta blockers, should be held and a health care provider called. Teach the patient the symptoms of hypokalemia and hyperkalemia if diuretics that deplete or spare potassium are ordered. Frequently the patient who takes thiazide or loop diuretics is given supplemental potassium. It may also be appropriate to instruct patients in home BP monitoring, especially for those HF patients with hypertension. The physical therapist, occupational therapist, or you can instruct the patient in energy-conserving and energy-efficient behaviors after an evaluation of daily activities has been done. For example, once you understand the patient's daily routine, suggestions can be made to simplify work or modify an activity. Exercise training (e.g., cardiac rehabilitation) improves symptoms of chronic HF but is often underprescribed. Exercise for patients with HF has been found to be safe and to improve the overall sense of well-being. It has also been correlated with mortality reduction. Frequently the patient needs a prescription for rest after an activity. Many hard-driving persons need the "permission" to not feel "lazy." Sometimes an activity that the patient enjoys may need to be stopped. In such situations, help the patient to explore alternative activities that cause less physical stress. The physical environment may require modification in situations in which there is an increased cardiac workload demand (e.g., frequent climbing of stairs). You can help the patient identify areas where outside assistance can be obtained.

*Chronic Heart Failure* (Clinical Manifestations) Fatigue Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Tachycardia

*Fatigue* Fatigue is one of the earliest symptoms of chronic HF. The patient notes fatigue after usual activities and eventually limits these activities. The fatigue is caused by decreased CO, impaired perfusion to vital organs, decreased oxygenation of the tissues, and anemia. Anemia can result from poor nutrition, renal disease, or drug therapy (e.g., angiotensin-converting enzyme [ACE] inhibitors). *Dyspnea* Dyspnea is a common manifestation of chronic HF. It is caused by increased pulmonary pressures secondary to interstitial and alveolar edema. Dyspnea can occur with mild exertion or at rest. *Orthopnea* often accompanies dyspnea. Careful questioning of patients often reveals adaptive behaviors, such as sleeping with two or more pillows or in a chair to aid breathing. *Paroxysmal nocturnal dyspnea (PND)* occurs when the patient is asleep. It is caused by the reabsorption of fluid from dependent body areas when the patient is flat. The patient awakes in a panic, has feelings of suffocation, and has a strong desire to sit or stand up. A cough is often associated with HF and may be the first clinical symptom. It begins as a dry, nonproductive cough and may be misdiagnosed as asthma or other lung disease. The cough is not relieved by position change or over-the-counter cough medicine. *Tachycardia* Tachycardia is an early clinical sign of HF. One of the body's first mechanisms to compensate for a failing ventricle is to increase the HR. Because of reduced CO, the SNS is activated, which increases HR. However, this response may be blocked or reduced in patients taking beta-blocker drugs.

*Chronic HF* *(Nutritional Therapy)* Fluid restriction not generally required If required, < 2L/day. Ice chips, gum, hard candy, ice pops to help thirst Daily weights important Same time, same clothing each day Weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3 kg) gain over a week should be reported to health care provider

*Fluid restrictions* are not commonly prescribed for the patient with mild to moderate HF. However, in moderate to severe HF and renal insufficiency, fluids are limited to less than 2 L/day. Helping patients deal with thirst as a side effect of the drugs is important. To deal with the thirst, suggest ice chips, gum, hard candy, or ice pops. Instruct patients to weigh themselves daily as this is important for monitoring fluid status. Teach patients to weigh themselves at the same time each day, preferably before breakfast and using the same scale while wearing the same type of clothing. This helps ensure valid comparisons from day to day and helps identify early signs of fluid retention. For patients with visual limitations, suggest scales with larger numbers and/or an audible response. Instruct patients to call the primary care provider if they see a weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3-kg) gain over a week.

*ADHF Drug Therapy* *Morphine* Reduces preload and afterload Relieves dyspnea and anxiety *Positive inotropes* β-adrenergic agonists (dopamine [Intropin], dobutamine [Dobutrex]) Phosphodiesterase inhibitors (inamrinone [Inocor], milrinone [Primacor]) Digitalis

*Morphine* Morphine sulfate reduces preload and afterload. It is frequently used in the treatment of ADHF and pulmonary edema. It dilates both the pulmonary and systemic blood vessels. Results include a decrease in pulmonary pressures and myocardial oxygen needs, and an improvement in gas exchange. When morphine is used, the patient often experiences relief from dyspnea and, consequently, the anxiety that often is associated with dyspnea. Use morphine cautiously in patients with ADHF. Morphine is related to more adverse events, including a greater need for mechanical ventilation, more ICU admissions, prolonged hospitalization, and higher mortality. *Positive inotropes* Inotropic therapy increases myocardial contractility. Drugs include β-adrenergic agonists, (e.g., dopamine [Intropin], dobutamine [Dobutrex], epinephrine, norepinephrine [Levophed]), phosphodiesterase inhibitors (inamrinone [Inocor], milrinone [Primacor]), and digitalis. The β-adrenergic agonists are only used for short-term treatment of ADHF. In addition to increasing myocardial contractility and SVR, dopamine dilates the renal blood vessels and enhances urine output. Unlike dopamine, dobutamine is a selective β-adrenergic agonist and works primarily on the β1-receptors in the heart. Dobutamine does not increase SVR and is preferred for short-term treatment of ADHF. Inamrinone and milrinone are two phosphodiesterase inhibitors that have been called inodilators. They increase myocardial contractility (inotropic effect) and promote peripheral vasodilation. Inhibition of phosphodiesterase increases cyclic adenosine monophosphate (cAMP). This enhances calcium entry into the cell and improves myocardial contractility. They increase CO and reduce BP (decrease afterload). Like dopamine and dobutamine, these drugs are only available for IV use. Adverse effects include dysrhythmias, thrombocytopenia, and hepatotoxicity. *Digitalis is a positive inotrope* that improves left ventricular function. Digitalis increases contractility but also increases myocardial oxygen consumption. Because digitalis requires a loading dose and time to work, it is not recommended for the initial treatment of ADHF. Currently, inotropic therapy is only recommended for use in the short-term management of patients with ADHF who have not responded to conventional pharmacotherapy (e.g., diuretics, vasodilators, morphine).

*Counterregulatory Mechanisms* *(Nitric oxide (NO))* Released from the vascular endothelium in response to compensatory mechanisms NO relaxes arterial smooth muscle, resulting in vasodilation and decreased afterload

*Nitric oxide (NO)* is another counterregulatory substance released from the vascular endothelium in response to the compensatory mechanisms activated in HF. Like the natriuretic peptides, NO works to relax the arterial smooth muscle, resulting in vasodilation and decreased afterload. Cardiac compensation occurs when compensatory mechanisms succeed in maintaining an adequate CO that is needed for tissue perfusion. Cardiac decompensation occurs when these mechanisms can no longer maintain adequate CO and inadequate tissue perfusion results.

Chronic HF Nursing Dx Impaired gas exchange Decreased cardiac output Excess fluid volume Activity intolerance

*Nursing diagnoses for the patient with HF include*, but are not limited to: Impaired gas exchange related to increased preload and alveolar-capillary membrane changes Decreased cardiac output related to altered contractility, altered preload, and/or altered stroke volume Excess fluid volume related to increased venous pressure and decreased renal perfusion secondary to cardiac failure Activity intolerance related to imbalance between oxygen supply/demand secondary to cardiac insufficiency and pulmonary congestion

*Heart Failure* (Complications) -Pleural effusion -Dysrhythmias - atrial and ventricular -Left ventricular thrombus -Hepatomegaly -Renal failure

*Pleural Effusion* Pleural effusion results from increasing pressure in the pleural capillaries. A transudation of fluid occurs from these capillaries into the pleural space. (Pleural effusion is discussed in Chapter 28.) *Dysrhythmias* Chronic HF causes enlargement of the chambers of the heart. This enlargement (stretching of the atrial and ventricular walls) can cause changes in the normal electrical pathways. When numerous sites in the atria fire spontaneously and rapidly (atrial fibrillation), the organized atrial depolarization (contraction) no longer occurs. Atrial fibrillation also promotes thrombus formation within the atria. Thrombi may break loose and form emboli. This places patients with atrial fibrillation at risk for stroke. They require treatment with cardioversion, antidysrhythmics, and/or anticoagulants. Patients with HF are also at risk for ventricular dysrhythmias (e.g., ventricular tachycardia [VT], ventricular fibrillation [VF]). VT and VF can lead to sudden cardiac death (SCD). *Left Ventricular Thrombus* With ADHF or chronic HF, the enlarged LV and decreased CO combine to increase the chance of thrombus formation in the LV. Once a thrombus has formed, it may also decrease left ventricular contractility, decrease CO, and further worsen the patient's perfusion. The development of emboli from the thrombus also places the patient at risk for stroke. *Hepatomegaly* HF can lead to severe hepatomegaly, especially with RV failure. The liver becomes congested with venous blood. The hepatic congestion leads to impaired liver function. Eventually liver cells die, fibrosis occurs, and cirrhosis can develop (see Chapter 44). *Renal Failure* The decreased CO that accompanies chronic HF results in decreased perfusion to the kidneys and can lead to renal insufficiency or failure.

*Chronic Heart Failure* (Clinical Manifestations) Skin changes Behavioral changes Chest pain Weight changes

*Skin Changes* Because tissue capillary oxygen extraction is increased in a person with chronic HF, the skin may appear dusky. Often the lower extremities are shiny and swollen, with diminished or absent hair growth. Chronic swelling may result in pigment changes. This causes the skin to appear brown or brawny in areas covering the ankles and lower legs. *Behavioral Changes* Cerebral circulation may be reduced with chronic HF secondary to decreased CO. The patient or caregiver may report unusual behavior, including restlessness, confusion, and decreased attention span or memory. This may also be secondary to poor gas exchange and worsening HF. It is often seen in the late stages of HF. *Chest Pain* HF can precipitate chest pain (angina) due to decreased coronary artery perfusion from decreased CO and increased myocardial work. Chest pain may accompany either ADHF or chronic HF. *Weight Changes* Many factors contribute to weight changes. First there may be a progressive weight gain from fluid retention. Renal failure may also contribute to fluid retention. Abdominal fullness from ascites and hepatomegaly frequently causes anorexia and nausea. As HF advances, the patient may have cardiac cachexia with muscle wasting and fat loss. This can be masked by the patient's edematous condition and may not be seen until after the edema subsides.

*ADHF* (Collaborative Management) -Ultrafiltration (aquapheresis) for patients with volume overload and resistance to diuretics -Circulatory assist devices for patients with deteriorating HF Intraaortic balloon pump (IABP) Ventricular assist devices (VADs) -Treat any anxiety and/or depression

*Ultrafiltration (UF)* or *aquapheresis* is an option for the patient with volume overload. It is a process to remove excess salt and water from the patient's blood. UF can rapidly remove intravascular fluid volume while maintaining hemodynamic stability. The ideal patients for UF are those with major pulmonary or systemic volume overload who have shown resistance to diuretics and are hemodynamically stable. UF also may be an appropriate adjunctive therapy for patients with HF and coexisting renal failure. *Circulatory assist devices* are used to manage patients with worsening HF. -The *intraaortic balloon pump (IABP)* is a device that increases coronary blood flow to the heart muscle and decreases the heart's workload through a process called counterpulsation. The IABP is placed in the aorta. It is useful in hemodynamically unstable patients because it decreases SVR, PAWP, and PAP leading to improved CO. *Ventricular assist devices (VADs)* can be used to maintain the pumping action of a heart that cannot effectively contract by itself. A VAD is a battery-operated, mechanical pump that is surgically implanted. Assess patients with HF for *depression and anxiety* and, if appropriate, initiate treatment plans. Coexisting psychologic disorders, especially depression and negative thinking, contribute to an increased risk of mortality and higher readmission rates and health care costs in patients with HF. In addition, patients with psychologic disorders have poorer treatment compliance and self-care

*Chronic HF Drug Therapy* β-adrenergic blockers Vasodilators -Nitrates -BiDil Positive inotropic agents -Digitalis

*β-Adrenergic Blockers* β-adrenergic blockers directly block the negative effects of the SNS (e.g., increased heart rate) on the failing heart. They can also help in reducing the effect of renin. Because beta blockers can reduce myocardial contractility, care must be taken to start slowly. Dosage is increased every 2 weeks as tolerated by the patient. Major adverse effects include edema, worsening of HF, hypotension, fatigue, and bradycardia. Three beta blockers are approved for use in HF patients: carvedilol (Coreg), bisoprolol (Zebeta), and metoprolol CR/XL (Toprol XL). Vasodilators *Nitrates* Nitrates cause vasodilation by acting directly on the smooth muscle of the vessel wall. Nitrates are of particular benefit in the management of myocardial ischemia related to HF because they promote vasodilation of the coronary arteries. One specific problem with the use of nitrates in HF is nitrate tolerance. In addition, men with HF may experience erectile dysfunction and as a result take an erectile agent (e.g., sildenafil [Viagra]). Erectile agents are contraindicated in patients taking nitrates as together they could produce symptomatic hypotension. *BiDil* A combination drug containing isosorbide dinitrate and hydralazine (BiDil) is used for the treatment of HF in African Americans who are already being treated with standard therapy. The drug is only approved for use with this ethnic group. How these two drugs work together is not fully known. As an antihypertensive agent, hydralazine relaxes the arteries and decreases the work of the heart. The antianginal agent, isosorbide dinitrate, relaxes the veins as well as the arteries. Isosorbide seems to work by releasing nitric oxide at the blood vessel wall, but its effect usually wears off after half a day. Hydralazine may prevent this loss of effect. Common side effects of isosorbide/hydralazine are headache and dizziness. *Positive Inotropes* *Digitalis* preparations (e.g., digoxin [Lanoxin]) increase the force of cardiac contraction (inotropic action). They also decrease the HR (chronotropic action). These actions allow for more complete emptying of the ventricles. This reduces the volume remaining in the ventricles during diastole. CO increases due to the increased stroke volume from improved contractility. Patients taking a digitalis preparation are at risk for digitalis toxicity. Hypokalemia, secondary to the use of potassium-depleting diuretics (e.g., thiazides, loop diuretics), is one of the most common causes of digitalis toxicity. Low serum potassium enhances the action of digitalis, causing a therapeutic dose to reach toxic levels. Similarly, hyperkalemia inhibits the action of digitalis, resulting in a subtherapeutic dose. Both hypokalemia and hyperkalemia also cause dysrhythmias. Monitor serum potassium levels of all patients taking digitalis preparations and potassium-depleting and potassium-sparing diuretics. Other electrolyte imbalances, such as hypercalcemia and hypomagnesemia, can also precipitate digitalis toxicity.

*Pathophysiology Mixed Heart Failure* Mixed systolic and diastolic failure Seen in disease states such as dilated cardiomyopathy (DCM) Poor EFs (<35%) High pulmonary pressures Biventricular failure Both ventricles may be dilated and have poor filling and emptying capacity

-Mixed systolic and diastolic failure is seen in disease states such as dilated cardiomyopathy (DCM). -DCM is a condition in which poor systolic function is further compromised by dilated left ventricular walls that are unable to relax. These patients often have extremely low EFs (less than 35%), high pulmonary pressures, and biventricular failure (both ventricles are dilated and have poor filling and emptying capacity).

Acute Decompensated Heart Failure (ADHF) Clinical Manifestations -Can manifest as pulmonary edema -Life-threatening situation - alveoli fill with fluid -Most commonly associated with left-sided HF

ADHF can manifest as pulmonary edema. This is an acute, life-threatening situation in which the lung alveoli become filled with serosanguineous fluid. The most common cause of pulmonary edema is left-sided HF secondary to CAD. As pulmonary edema progresses, it inhibits oxygen and carbon dioxide exchange at the alveolar-capillary interface. A. Normal relationship. B. Increased pulmonary capillary hydrostatic pressure causes fluid to move from the vascular space into the pulmonary interstitial space. C. Lymphatic flow increases in an attempt to pull fluid back into the vascular or lymphatic space. D. Failure of lymphatic flow and worsening of left heart failure result in further movement of fluid into the interstitial space and into the alveoli.

*Compensatory Mechanism* *(Ventricular remodeling)* Results from SNS activation and neurohormonal responses Hypertrophy of ventricular myocytes Ventricles larger but less effective in pumping Can cause life-threatening dysrhythmias and sudden cardiac death

Activation of the SNS and the neurohormonal response lead to elevated levels of norepinephrine, angiotensin II, aldosterone, ADH, endothelin, and proinflammatory cytokines. Together, these factors result in an increase in cardiac workload, myocardial dysfunction, and ventricular remodeling. Remodeling involves hypertrophy of the ventricular myocytes, resulting in large, abnormally shaped contractile cells. This altered geometric shape of the ventricles eventually leads to increased ventricular mass, increased wall tension, increased oxygen consumption, and impaired contractility. Although the ventricles become larger, they become less effective pumps. Ventricular remodeling is a risk factor for life-threatening dysrhythmias and sudden cardiac death (SCD).

*Chronic HF Pt. teaching Activity/rest* Energy-conserving and energy-efficient behaviors Exercise training (cardiac rehab) Increase gradually Avoid heat and cold extremes Rest after exertion Avoid emotional upsets

Activity Program 1. Increase walking and other activities gradually, provided they do not cause fatigue or dyspnea. Consider a cardiac rehabilitation program. 2. Avoid extremes of heat and cold. Rest The physical therapist, occupational therapist, or you can instruct the patient in energy-conserving and energy-efficient behaviors after an evaluation of daily activities has been done. For example, once you understand the patient's daily routine, suggestions can be made to simplify work or modify an activity. Exercise training (e.g., cardiac rehabilitation) improves symptoms of chronic HF but is often underprescribed. Exercise for patients with HF has been found to be safe and to improve the overall sense of well-being. It has also been correlated with mortality reduction. Increase walking and other activities gradually, provided they do not cause fatigue or dyspnea. Avoid extremes of heat and cold. Frequently the patient needs a prescription for rest after an activity. Many hard-driving persons need the "permission" to not feel "lazy." Avoid emotional upsets. Verbalize any concerns, fears, feelings of depression, etc., to health care provider.

Chronic HF Nursing Assessment *Objective data* Skin color and temperature Edema Respiratory rate and sounds Frothy, blood-tinged sputum Heart rate and sounds Abdominal distention Changes in LOC

Additional focused assessment findings include: Integumentary Cool, diaphoretic skin; cyanosis or pallor, peripheral edema (right-sided heart failure) Respiratory Tachypnea, crackles, rhonchi, wheezes; frothy, blood-tinged sputum Cardiovascular Tachycardia, S3, S4, murmurs; pulsus alternans, PMI displaced inferiorly and posteriorly, lifts/heaves, jugular vein distention Gastrointestinal Abdominal distention, hepatosplenomegaly, ascites Neurologic Restlessness, confusion, decreased attention or memory

M.W. is a 78-year-old woman admitted to the hospital with shortness of breath. She has a history of hypertension and CAD. What factors in M.W.'s history increase her risk for heart failure? What other factors might you question M.W. about?

Advanced age, hypertension, MI, not taking cardiac drugs Diabetes, high cholesterol, obesity, smoking, thyroid disorders, history of rheumatic heart disease, infections, valvular disorders, anemia See next two slides

Heart Failure

An abnormal clinical syndrome involving inadequate cardiac pumping/filling -Insufficient blood supply/oxygen to tissues -Used to be called congestive heart failure (CHF) *Teacher Comment* Heart failure (HF) is an abnormal clinical syndrome that involves inadequate pumping and/or filling of the heart. This results in the inability of the heart to provide sufficient blood to meet the oxygen needs of the tissues. In clinical practice, the terms acute and chronic HF have replaced the term "congestive HF" (CHF), because not all HF involves pulmonary congestion. However, the term CHF is still commonly used.

The home care nurse visits a patient with chronic heart failure who is taking digoxin (Lanoxin) and furosemide (Lasix). The patient complains of nausea and vomiting. Which action is most appropriate for the nurse to take? a. Perform a dipstick urine test for protein. b. Notify the health care provider immediately. c. Have the patient eat foods high in potassium. d. Ask the patient to record a weight every morning.

Answer: b Rationale: Administration of furosemide increases excretion of potassium and may cause hypokalemia. The risk for digitalis toxicity increases if potassium levels are below normal and digoxin is administered. Signs and symptoms of digitalis toxicity include anorexia, nausea and vomiting, visual disturbances (such as "yellow" vision), and dysrhythmias.

A patient with left-sided heart failure is prescribed oxygen at 4 L/min per nasal cannula, furosemide (Lasix), spironolactone (Aldactone), and enalapril (Vasotec). Which assessment should the nurse complete to best evaluate the patient's response to these drugs? a. Observe skin turgor b. Auscultate lung sounds c. Measure blood pressure d. Review intake and output

Answer: b Rationale: Left-sided heart failure will prevent normal blood flow and will cause blood to back up into the left atrium and into the pulmonary veins. The increased pulmonary pressure causes fluid extravasation from the pulmonary capillary bed into the interstitium and then the alveoli, which manifests as pulmonary congestion and edema. The most important assessment to determine if the drugs are improving the patient's condition is to auscultate lung sounds. The other assessments are important, but the best indicator of improvement of left ventricular function is a reduction in adventitious lung sounds (crackles).

A patient with a history of chronic heart failure is hospitalized with severe dyspnea and a dry, hacking cough. Assessment findings include pitting edema in both ankles, blood pressure 170/100 mm Hg, pulse 92 beats/minute, and respirations 28 breaths/minute. Which explanation, if made by the nurse, is most accurate? a. "The assessment indicates that venous return to the heart is impaired, causing a decrease in cardiac output." b. "The manifestations indicate impaired emptying of both the right and left ventricles, with decreased forward blood flow." c. "The myocardium is not receiving enough blood supply through the coronary arteries to meet its oxygen demand." d. "The patient's right side of the heart is failing to pump enough blood to the lungs to provide systemic oxygenation."

Answer: b Rationale: The patient is experiencing acute decompensated heart failure with symptoms of both right- and left-sided heart failure. Left-sided heart failure prevents normal, forward blood flow and causes pulmonary congestion. Right-sided heart failure causes a backup of blood and results in venous congestion.

*Compensatory Mechanism* Neurohormonal responses -Kidneys release renin and initiate the RAAS system -Posterior pituitary gland secretes antidiuretic hormone (ADH) -Endothelin released by vascular endothelial cells -Proinflammatory cytokines

As the CO falls, blood flow to the kidneys decreases. This is sensed by kidneys as decreased volume. In response, the kidneys release renin, which converts angiotensinogen to angiotensin I. Angiotensin I is subsequently converted to angiotensin II by a converting enzyme made in the lungs. *Angiotensin II causes* (1) the adrenal cortex to release aldosterone, which results in sodium and water retention, and (2) increased peripheral vasoconstriction, which increases BP. This response is known as the renin-angiotensin-aldosterone system (RAAS). *Low CO causes* a decrease in cerebral perfusion pressure. In response, the posterior pituitary gland secretes antidiuretic hormone (ADH), also called vasopressin. ADH increases water reabsorption in the kidneys, causing water retention. As a result, blood volume is increased in a person who is already volume overloaded. *Other factors* also contribute to the development of HF. The production of endothelin, a potent vasoconstrictor produced by the vascular endothelial cells, is stimulated by ADH, catecholamines, and angiotensin II. Endothelin results in further arterial vasoconstriction and an increase in cardiac contractility and hypertrophy. Locally, proinflammatory cytokines are released by cardiac cells in response to various forms of cardiac injury (e.g., MI). Two cytokines, tumor necrosis factor (TNF) and interleukin-1 (IL-1), further depress cardiac function by causing cardiac hypertrophy, contractile dysfunction, and cardiac cell death. Over time, a systemic inflammatory response also occurs. This accounts for the cardiac and skeletal muscle myopathy and fatigue that accompany advanced HF.

Heart Failure

Associated with cardiovascular diseases ↑ in incidence and prevalence ↑ with age Common cause for hospital admission and readmissions *Teacher Comment* HF is associated with numerous types of cardiovascular diseases, particularly long-standing hypertension, coronary artery disease (CAD), and myocardial infarction (MI). It is a major health problem in the United States. In contrast to other cardiovascular diseases, HF is increasing in incidence and prevalence. This is due to improved survival after cardiac events and the increased aging population. Currently, about 5.7 million people in the United States have HF. The American Heart Association (AHA) estimates that 670,000 new cases are diagnosed each year. HF is primarily a disease of older adults and approximately 10 in every 1000 persons over the age of 65 have HF. The incidence of HF is similar in men and women. HF is the most common reason for hospital admission in older adults. This places a significant economic burden on the health care system. The complex, progressive nature of HF often results in poor outcomes, the most costly being hospital readmissions.

*Cardiac Transplantation* 1. Treatment of choice for patients with refractory end-stage HF, inoperable CAD, and cardiomyopathy 2. Selection process to identify patients who would most benefit from a new heart 3. Candidates must undergo physical, diagnostic, and psychologic evaluation

Cardiac transplantation is the transfer of a healthy donor heart to a patient with a diseased heart. This surgery is used to treat a variety of terminal or end-stage heart conditions, including end-stage heart failure refractory to medical care. In the United States, over 2000 cardiac transplants are done each year. However, thousands more adults would benefit from a heart transplant if more donated hearts were available. The 1-year transplant survival rate is 88% for males and 86% for females. The 5-year survival rate is 73% for males and 69% for females. A careful selection process ensures that hearts are distributed fairly and to those who will benefit most from the donor heart. The United Network for Organ Sharing (UNOS) is in charge of a system that gives organs fairly to people. Once an individual meets the criteria for cardiac transplantation, a complete physical examination and diagnostic workup are done. In addition, the patient and caregiver undergo a comprehensive psychologic evaluation. This includes assessing coping skills, support systems, and commitment to follow the rigorous regimen that is essential to a successful transplantation. The complexity of the transplant process may be overwhelming to a patient with inadequate support systems and a poor understanding of the lifestyle changes needed after transplant.

*Chronic Heart Failure* (Clinical Manifestations) Dependent on age, underlying type and extent of heart disease, and which ventricle is affected *(FACES)* *F*atigue Limitation of *A*ctivities *C*hest congestion/cough *E*dema *S*hortness of breath

Chronic HF is characterized as progressive worsening of ventricular function and chronic neurohormonal activation that result in ventricular remodeling. This process involves changes in the size, shape, and mechanical performance of the ventricle. The clinical manifestations of chronic HF depend on the patient's age, the underlying type and extent of heart disease, and which ventricle is failing to pump effectively. The Heart Failure Society of America (HFSA) developed the acronym, FACES (fatigue, limitation of activities, chest congestion/cough, edema, and shortness of breath) to help educate patients on identifying HF symptoms.

*Pulmonary Edema* (Clinical Manifestation) Anxious, pale, cyanotic Cool and clammy skin Dyspnea Orthopnea Tachypnea Use of accessory muscles Cough with frothy, blood-tinged sputum Crackles, wheezes, rhonchi Tachycardia Hypotension or hypertension

Clinical manifestations of pulmonary edema are distinct. The patient is usually anxious, pale, and possibly cyanotic. The skin is clammy and cold from vasoconstriction caused by stimulation of the SNS. The patient will have dyspnea (shortness of breath) and orthopnea (shortness of breath that occurs when lying down). Respiratory rate is often greater than 30 breaths per minute and use of accessory muscles to breathe may be noted. There may be coughing with the production of frothy, blood-tinged sputum. Auscultation of the lungs may reveal crackles, wheezes, and rhonchi throughout the lungs. The patient's HR is rapid, and BP may be elevated or decreased depending on the severity of the HF.

Dilated and Hypertrophied Heart

Compare and contrast dilation and hypertrophy; dilation refers to size of filling space; hypertrophy refers to thickness of muscle.

*Chronic HF Nursing Implementation* Health promotion Identify and treat risk factors for HF to prevent or slow progression Flu and pneumonia vaccinations for patients with HF

Currently, there is a campaign to aggressively identify and treat risk factors for HF to prevent or slow the progression of the disease. For example, teach a patient with hypertension or hyperlipidemia measures to manage BP or cholesterol with drugs, diet, and exercise. Patients with valvular disease should have valve replacement planned before lung congestion develops. Coronary revascularization procedures should be done in patients with CAD. The use of antidysrhythmic agents or pacing therapy is indicated for patients with serious dysrhythmias or conduction disturbances. In addition, encourage patients with HF to obtain vaccinations against the flu and pneumonia.

*Diagnostic Testing* Determine and treat underlying cause Endomyocardial biopsy (EMB) Echocardiography and/or nuclear imaging Chest x-ray ECG, stress test Cardiac catheterization BNP (NT-proBNP), ABGs

Diagnosing HF is often difficult since neither patient signs nor symptoms are highly specific, and both may mimic many other medical conditions (e.g., anemia, lung disease). A primary goal in diagnosis is to find the underlying cause of HF. *Endomyocardial biopsy (EMB)* may be done in patients who develop unexplained, new-onset HF that is unresponsive to usual care. EF is used to differentiate systolic and diastolic HF. This distinction is important to make in the early treatment of HF. EF is measured using echocardiography and/or nuclear imaging studies. Other useful diagnostic tests include chest x-ray, electrocardiogram (ECG), stress testing, and heart catheterization. *Laboratory studies* also aid in the diagnosis of HF. In general, BNP levels correlate positively with the degree of left ventricular failure. Many labs routinely measure the N-terminal prohormone of BNP (NT-proBNP). This is a more precise assay to aid in the diagnosis of HF. Levels will be temporarily higher in patients receiving nesiritide (Natrecor) and may be high in patients with chronic, stable HF. Conditions other than HF can cause increases in BNP or NT-proBNP levels (e.g., pulmonary embolism, renal failure, acute coronary syndrome). ABGs will be used to determine adequate oxygenation.

*Chronic HF Pt. teaching Dietary therapy* Written plan Reading labels for sodium No added salt Daily weights Smaller, more frequent meals

Dietary Therapy 1. Consult the written diet plan and list of permitted and restricted foods. 2. Examine labels to determine sodium content. Also examine the labels of over-the-counter drugs, such as laxatives, cough medicines, and antacids for sodium content. 3. Avoid using salt when preparing foods or adding salt to foods. 4. Weigh yourself at the same time each day, preferably in the morning, using the same scale and wearing the same or similar clothes. 5. Eat smaller, more frequent meals.

*Compensatory Mechanism* *(Dilation)* Enlargement of chambers of the heart that occurs when pressure in the left ventricle is elevated Initially effective Eventually this mechanism becomes inadequate and CO decreases

Dilation is an enlargement of the chambers of the heart. It occurs when pressure in the heart chambers (usually the LV) is elevated over time. The muscle fibers of the heart stretch in response to the volume of blood in the heart at the end of diastole. The degree of stretch is directly related to the force of the contraction (systole) (this is the Frank-Starling law). This increased contraction initially leads to increased CO and maintenance of BP and perfusion. Dilation starts as an adaptive mechanism to cope with increasing blood volume. Eventually this mechanism becomes inadequate because the elastic elements of the muscle fibers are overstretched and can no longer contract effectively, thereby decreasing the CO.

Chronic HF Nutrition Therapy

Discuss how to read food labels; note the amount of sodium per serving; 1/5 of daily recommended intake per a serving that is only 1/8 of total caloric intake (2000 calorie diet)!

*Cardiac Transplantation* Transplant candidates are placed on a list Stable patients wait at home and receive ongoing medical care Unstable patients may require hospitalization for more intensive therapy Overall waiting period for a heart is long; many patients die during this time

Donor and recipient matching is based on body and heart size, and an immunologic evaluation. The immunologic assessment includes ABO blood type, antibody screen, panel-reactive antibody (PRA) level, and human leukocyte antigen typing (explained in Chapter 14). Once a person is accepted as a transplant candidate (this may happen quickly during an acute illness or after a longer period), he or she is placed on a transplant list. Patients may wait at home and receive ongoing medical care if their condition is stable. If their condition is not stable, they may require hospitalization for more intensive therapy. Therapy may include implantation of bridge devices (VADs) to assist the heart while awaiting transplant. Unfortunately, the overall waiting period for a new heart is long. Many patients die while waiting for a transplant.

*Chronic HF Nursing Interventions* Alternate rest with activity Provide diversionary activities Monitor response to activity Collaborate with OT/PT Reduce anxiety Evaluate support system Patient teaching

Encourage alternate rest and activity periods to reduce cardiac workload and conserve energy. Provide calming diversionary activities to promote relaxation to reduce O2 consumption and to relieve dyspnea and fatigue. Monitor patient's O2 response (e.g., pulse rate, cardiac rhythm, and respiratory rate) to self-care or nursing activities to determine the level of activity that can be performed. Collaborate with occupational and/or physical therapists to plan and monitor activity/exercise program. Instruct patient and caregivers on activity restriction and progression to allay fears and anxiety. Establish a supportive relationship with the patient and caregiver(s) to promote adherence with the treatment plan. Evaluate and encourage use of support systems. Teach patient and caregiver techniques of self-care that will minimize O2 consumption (e.g., self-monitoring and pacing techniques for performance of ADLs). Inform the patient of the purpose for and benefits of the prescribed activity/exercise.

*Compensatory Mechanisms* *(Hypertrophy)* Increase in muscle mass and cardiac wall thickness Initially effective Over time leads to poor contractility, increased O2 needs, poor coronary artery circulation, and risk for ventricular dysrhythmias

Hypertrophy is an increase in the muscle mass and cardiac wall thickness in response to overwork and strain. *It occurs* slowly because it takes time for this increased muscle tissue to develop. Initially, the increased contractile power of the muscle fibers leads to an increase in CO and maintenance of tissue perfusion. *Over time*, hypertrophic heart muscle has poor contractility, requires more oxygen to perform work, has poor coronary artery circulation (tissue becomes more easily ischemic), and is prone to dysrhythmias.

Acute Decompensated Heart Failure (ADHF) (Clinical Manifestations *Early* → increased pulmonary venous pressure Increase in the respiratory rate Decrease in Pao2 *Later* → interstitial edema Tachypnea *Further progression* → alveolar edema Respiratory acidemia

In *acute decompensated HF (ADHF)*, there is an increase in the pulmonary venous pressure caused by failure of the LV. This results in engorgement of the pulmonary vascular system. As a result, the lungs become less compliant, and there is increased resistance in the small airways. In addition, the lymphatic system increases its flow to help maintain a constant volume of the pulmonary extravascular fluid. *This early stage* is clinically associated with a mild increase in the respiratory rate and a decrease in partial pressure of oxygen in arterial blood (Pao2). If pulmonary venous pressure continues to increase, the increase in intravascular pressure causes more fluid to move into the interstitial space than the lymphatics can remove. Interstitial edema occurs at this point. *Tachypnea develops* and the patient becomes symptomatic (e.g., short of breath). If the pulmonary venous pressure increases further, the alveoli lining cells are disrupted and a fluid containing red blood cells (RBCs) moves into the alveoli (alveolar edema). As the disruption becomes worse from further increases in the pulmonary venous pressure, the alveoli and airways are flooded with fluid. *This is accompanied* by a worsening of the arterial blood gas values (i.e., lower Pao2 and possible increased partial pressure of carbon dioxide in arterial blood [Paco2] and progressive respiratory acidemia).

*Chronic HF* *(Collaborative Management)* Oxygen therapy -Relieves dyspnea and fatigue Physical and emotional rest -Conserve energy and decrease oxygen needs -Dependent on severity of HF Structured exercise program

In a person with HF, oxygen saturation of the blood can be reduced because the blood is not adequately oxygenated in the lungs. Administration of oxygen improves saturation and assists in meeting tissue oxygen needs. This helps to relieve dyspnea and fatigue. Optimally, either pulse oximetry or arterial blood gases (ABGs) are used to monitor the need for and effectiveness of oxygen therapy. Physical and emotional rest allows the patient to conserve energy and decreases the need for additional oxygen. The degree of rest recommended depends on the severity of HF. A patient with severe HF may be on bed rest with limited activity. A patient with mild to moderate HF can be ambulatory with restriction of strenuous activity. The patient should be instructed to participate in prescribed activities with adequate recovery periods. A structured exercise program, such as cardiac rehabilitation, should be offered to all patients with chronic HF.

Cardiac Transplant Endomyocardial biopsies are obtained from the right ventricle weekly for the first month, monthly for the following 6 months, and yearly thereafter to detect rejection

In an EMB, a catheter is put into the jugular vein and is advanced into the right ventricle. The catheter has a bioptome at its end—a set of two small cups that can be closed to pinch off and remove small samples of heart muscle.

*Chronic HF Evaluation* Monitoring to assess outcomes and prevent/ limit future hospitalizations Vital signs Weight Pulse oximetry Dyspnea Home health nurses can be essential Can use electronic monitoring

Managing HF patients out of the hospital is a priority. Effective home health care can prevent or limit future hospitalizations by providing ongoing assessments (e.g., monitoring vital signs and weight, evaluating response to therapies). Many agencies offer specialized programs dedicated to managing HF patients at home. For example, these programs may include the use of telehealth monitoring technology (e.g., electronic scale, BP cuff, pulse oximeter) to collect physiologic data. The technology may also be able to audibly ask the patient questions such as, "Are you short of breath today?" Results are transmitted telephonically or by computer to the home care agency. Once received, the data are reviewed. Based on the findings, the patient may be called to further assess the situation or a visit may be scheduled. *Home health nurses* frequently work with protocols set up with the patient's health care team. The protocols enable you and the patient to identify problems, such as an increase in weight or dyspnea as evidence of worsening HF. Interventions can be started to prevent hospitalization. These may include changing drugs and restricting fluids. Home health nursing care of HF patients is vital in reducing the number of hospitalizations, increasing functional capacity, and increasing the quality of life.

*Chronic HF Nursing Interventions* Basic principles of care HF is a progressive disease: establish treatment plans and quality-of-life goals Use of self-management tools for symptom management Restrict salt (and water at times) Conserve energy Maintain support systems

Many persons with HF will experience one or more episodes of ADHF. When they do, they are usually admitted through the ED, initially stabilized, and then managed in an ICU, an intermediate care unit, or a specialized HF unit with continuous ECG monitoring capability. Successful HF management depends on several important principles: (1) HF is a progressive disease, and treatment plans are established along with quality of life goals (2) symptom management is controlled by the patient with self-management tools (e.g., daily weights, drug regimens, diet and exercise plans) (3) salt and, at times, water must be restricted (4) energy must be conserved (5) support systems are essential to the success of the entire treatment plan. The nursing care plan for the patient with HF applies to the patient with stabilized ADHF or chronic HF (see NCP 35-1). Reduction of anxiety is an important nursing function, since anxiety may increase the SNS response and further increase myocardial workload. Reducing anxiety may be facilitated by a variety of nursing interventions and the use of sedatives (e.g., benzodiazepines, morphine sulfate). The Joint Commission has selected three core measures in the management of patients with HF to reflect standards of evidence-based care (Table 35-10). The AHA has developed a program, Get With The Guidelines-Heart Failure, to improve adherence to standards of evidence-based care of patients hospitalized with HF. Together, these approaches work to ensure high-quality care for patients with HF.

*Chronic HF* *(Collaborative Management)* Biventricular pacing/cardiac resynchronization therapy (CRT) -With implantable cardioverter-defibrillator (ICD) IABP and VADs as bridge or destination therapy for stage IV HF

Nonpharmacologic therapies are an integral part of the care of HF patients. One therapy is biventricular pacing or cardiac resynchronization therapy (CRT). Traditional pacemakers pace one or two chambers (e.g., right atrium and/or right ventricle). In HF, neurohormonal effects and cardiac remodeling can result in dyssynchrony of the ventricular contractions. This contributes to poor CO. In CRT, an extra pacing lead is placed in the coronary vein of the left ventricle. This lead coordinates right and left ventricular contractions through biventricular pacing. The ability to have normal electrical conduction (synchrony) between the right and left ventricles increases left ventricular function and CO. Life-threatening ventricular dysrhythmias (e.g., ventricular tachycardia) can cause SCD. The addition of an implantable cardioverter-defibrillator (ICD) with CRT is often warranted. Several mechanical options are available to sustain HF patients with deteriorating conditions, especially those awaiting cardiac transplantation. These include the intraaortic balloon pump (IABP) and ventricular assist devices (VADs). The limitations of bed rest, infection, and vascular complications preclude long-term use of IABP. VADs provide highly effective long-term support and have become standard care in many heart transplant centers. VADs are used as a bridge to transplantation. They effectively increase cardiac function until a donor heart becomes available for the patient. The use of a permanent, implantable VAD, known as destination therapy, is an option for some HF patients with advanced NYHA Functional Class IV who are not candidates for heart transplantation.

Dilated Heart Chambers

Note the enlarged heart chambers with cardiac dilation.

Hypertrophied Heart Chambers

Note the thickened ventricular walls with hypertrophy

Cardiac Transplant *Nursing care focuses on* Promoting patient adaptation to the transplant process Monitoring cardiac function Managing lifestyle changes Providing ongoing teaching

Nursing management throughout the posttransplant period focuses on promoting patient adaptation to the transplant process, monitoring cardiac function, managing lifestyle changes, and providing ongoing teaching to the patient and caregiver.

Chronic HF Nursing Assessment Subjective data Past health history -Any cardiac history or diseases that increase risk for cardiac dysfunction Drugs -Any cardiac drugs, estrogens, steroids, NSAIDs, OTC drugs, herbs

Obtain the following important health information from the patient: *Past health history*: CAD (including recent MI), hypertension, cardiomyopathy, valvular or congenital heart disease, diabetes mellitus, hyperlipidemia, renal disease, thyroid or lung disease, rapid or irregular heart rate. *Drugs:* Use of and compliance with any cardiac drugs; use of diuretics, estrogens, corticosteroids, nonsteroidal antiinflammatory drugs, over-the-counter drugs, herbal supplements. Carefully review the patient's current prescription and over-the-counter drugs. Assess for use of any nonsteroidal antiinflammatory drugs (NSAIDs) as they can contribute to sodium retention.

Chronic HF Nursing Assessment *Subjective data*

Obtain the following important health information related to pertinent functional health patterns: Elimination: Nocturia, decreased daytime urinary output, constipation Activity-exercise: Dyspnea, orthopnea, cough (e.g., dry, productive); palpitations; dizziness, fainting Number of pillows used for sleeping Paroxysmal nocturnal dyspnea Insomnia Chest pain or heaviness RUQ pain, abdominal discomfort Behavioral changes Visual changes

Chronic HF Nursing Assessment *Subjective data* Fatigue, depression, anxiety Usual sodium intake Nausea/vomiting/anorexia Stomach bloating Weight gain Ankle swelling

Obtain the following important health information related to pertinent functional health patterns: Health perception-health management: Fatigue, depression, anxiety Nutritional-metabolic: Usual sodium intake; nausea, vomiting, anorexia, stomach bloating; weight gain, ankle swelling

Chronic HF pt. teaching Ongoing monitoring -Know FACES -Reappearance of symptoms -What to report -Regular follow-up -Support group Health promotion -Vaccinations -Reduce risk factors

Ongoing Monitoring 1. Know the signs and symptoms of worsening heart failure. FACES: fatigue, limitation of activities, chest congestion/cough, edema, shortness of breath. 2. Recall the symptoms experienced when illness began. Reappearance of previous symptoms may indicate a recurrence. 3. Report immediately to health care provider any of the following: Weight gain of 3 lb (1.4 kg) in 2 days, or 3 to 5 lb (1.4 to 2.3 kg) in a week Difficulty breathing, especially with exertion or when lying flat Waking up breathless at night Frequent dry, hacking cough, especially when lying down Fatigue, weakness Swelling of ankles, feet, or abdomen; swelling of face or difficulty breathing (if taking ACE inhibitors) Nausea with abdominal swelling, pain, and tenderness Dizziness or fainting 4. Follow up with health care provider on regular basis. 5. Consider joining a local support group with your family members and/or caregiver(s). Health Promotion 1. Obtain annual flu vaccination. 2. Obtain pneumococcal vaccine (e.g., Pneumovax) and revaccination after 5 years (for people at high risk of infection or serious disease). 3. Develop plan to reduce risk factors (e.g., BP control, smoking cessation, weight reduction).

*Pathophysiology Heart Failure in General* Ventricular failure leads to: -Low blood pressure (BP) -Low CO -Poor renal perfusion Abrupt or subtle onset Compensatory mechanisms mobilized to maintain adequate CO

The patient with ventricular failure of any type may have low blood pressure (BP), low CO, and poor renal perfusion. -HF can have an abrupt onset as with acute MI or it can be a subtle process resulting from slow, progressive changes. The overloaded heart uses compensatory mechanisms to try to maintain adequate CO. *The main compensatory mechanisms* include (1) sympathetic nervous system activation, (2) neurohormonal responses, (3) ventricular dilation, and (4) ventricular hypertrophy.

*ADHF* (Collaborative Management) Continuous monitoring and assessment: VS, O2 saturation, urinary output Hemodynamic monitoring if unstable Supplemental oxygen Mechanical ventilation if unstable High Fowler's position

Patients with ADHF need continuous monitoring and assessment. This may be done in an intensive care unit (ICU) if the patient is unstable. In the ICU, you will monitor ECG and oxygen saturation continuously. Vital signs and urinary output are assessed at least every hour. Some patients with ADHF require hospitalization but are more stable. They are often admitted to a telemetry or step-down unit for treatment. You should assess these patients every 4 hours (e.g., vital signs, pulse oximetry) for adequate oxygenation. Record intake and output and daily weights to evaluate fluid status. The patient may have *hemodynamic* monitoring including intraarterial BP and pulmonary artery pressures (PAPs). If a pulmonary artery catheter is placed, you will evaluate CO and pulmonary artery wedge pressure (PAWP). Therapy is titrated to maximize CO and reduce PAWP. A normal PAWP is generally between 8-12 mm Hg. Patients with ADHF may have a PAWP as high as 30 mm Hg. Supplemental oxygen helps increase the percentage of oxygen in inspired air. In severe pulmonary edema, the patient may need noninvasive ventilatory support (e.g., bilevel positive airway pressure [BiPAP]) or intubation and mechanical ventilation). BiPAP is also effective in decreasing preload. If the patient is *dyspneic*, place in a high Fowler's position with the feet horizontal in the bed or dangling at the bedside. This position helps decrease venous return because of the pooling of blood in the extremities. This position also increases the thoracic capacity, allowing for improved breathing.

*Chronic HF Nutritional Therapy* (Low sodium diet) Individualize recommendations and consider cultural background (www.nhlbi.nih.gov/health/index.htm#recipes) Recommend Dietary Approaches to Stop Hypertension (DASH) diet Sodium is usually restricted to 2 g/day

Poor adherence to a low-sodium diet and failure to take prescribed drugs as directed are the two most common reasons for readmissions of HF patients to the hospital. Therefore, it is critical that you accurately assess a patient's diet. Obtain a detailed diet history. Determine not only what foods the patient eats but also when, where, and how often the patient dines out. In addition, assess the sociocultural value of food. Use this information to assist the patient in making appropriate dietary choices when developing a diet plan. The National Heart, Lung, Blood Institute (NHLBI) provides helpful dietary guidelines for heart-healthy food preparation for people of various cultures (e.g., Hispanics, Native Americans, Asian Americans, African Americans). These are available online at www.nhlbi.nih.gov/health/index.htm#recipes. Diet and weight management recommendations must be individualized and culturally sensitive if the necessary changes are to be made. The edema associated with chronic HF is often treated by dietary restriction of sodium. Teach the patient what foods are low and high in sodium and ways to enhance food flavors without the use of salt (e.g., substituting lemon juice, various spices). The degree of sodium restriction depends on the severity of the HF and the effectiveness of diuretic therapy. The Dietary Approaches to Stop Hypertension (DASH) diet is effective as a first-line therapy for many individuals with hypertension This diet is now also widely used for the patient with HF, with or without hypertension. The average American adult's daily intake of sodium ranges from 7 to 15 g. A commonly prescribed diet for a patient with HF is a 2-g sodium diet All foods high in sodium (over 400 mg per serving) should be avoided. On this diet, processed meats, cheese, bread, cereals, canned soups, and canned vegetables must be limited. Teach the patient and caregiver how to read labels to look for sodium content. The patient and caregiver should also be aware of the high sodium content of most restaurant foods

Chronic HF Nursing Assessment *Objective data* Serum electrolytes BUN, creatinine Liver function tests NT-proBNP or BNP Chest x-ray Echocardiogram ECG O2 saturation

Possible Diagnostic findings Altered serum electrolytes (especially Na+ and K+) ↑ BUN, creatinine, or liver function tests ↑ NT-proBNP or BNP Chest x-ray demonstrating cardiomegaly, pulmonary congestion, and interstitial pulmonary edema Echocardiogram showing increased chamber size, decreased wall motion, decreased EF or normal EF with evidence of diastolic failure Atrial and ventricular enlargement on ECG ↓ O2 saturation

HF Nursing Interventions Monitor respiratory status Administer oxygen therapy Semi-Fowler's position Monitor hemodynamic status Daily weights I&O Administer prescribed drugs Monitor edema

Respiratory Monitoring Monitor pulse oxymetry, respiratory rate, rhythm, depth, and effort of respirations to evaluate changes in respiratory status. Auscultate breath sounds, noting areas of decreased/absent ventilation and presence of adventitious sounds to detect presence of pulmonary edema. Monitor for increased restlessness, anxiety, and work of breathing to detect increasing hypoxemia. Oxygen Therapy Administer supplemental O2 or other noninvasive ventilator support (e.g., bilevel positive airway pressure [BiPAP]) as needed to maintain adequate O2 levels. Monitor the O2 liter flow rate and position of O2 delivery device to ensure O2 is adequately delivered. Change O2 delivery device from mask to nasal prongs during meals as tolerated to sustain O2 levels while eating. Monitor the effectiveness of O2 therapy to identify hypoxemia and establish range of O2 saturation. Positioning Position to alleviate dyspnea (e.g., semi-Fowler's position), as appropriate, to improve ventilation by decreasing venous return to the heart and increasing thoracic capacity. Hemodynamic Monitoring Perform a comprehensive assessment of peripheral circulation (e.g., check peripheral pulses, edema, capillary refill, color, and temperature of extremity) to determine circulatory status. Note signs and symptoms of decreased cardiac output (e.g., chest pain, S3, S4, jugular vein distention) to detect changes in status. Monitor fluid balance (e.g., I/O and daily weight) to evaluate renal perfusion. Continuously monitor cardiac rhythm to detect dysrhythmias. Administer prescribed diuretics, as appropriate, to treat hypervolemia. Monitor for therapeutic effect of diuretic (e.g., increased urine output, decreased CVP/PCWP, and decreased adventitious breath sounds) to assess response to treatment. Monitor potassium levels after diuresis to detect excessive electrolyte loss. Monitor changes in peripheral edema to assess response to treatment.

*Right-Sided Heart Failure* Right ventricular dysfunction Blood backs up into the right atrium and venous circulation Jugular venous distention Hepatomegaly, splenomegaly Vascular congestion of GI tract Peripheral edema Most commonly caused by left-sided HF

Right-sided HF occurs* when the right ventricle (RV) fails to contract effectively. Right-sided HF causes a backup of blood into the right atrium and venous circulation. *Venous congestion* in the systemic circulation results in jugular venous distention, hepatomegaly, splenomegaly, vascular congestion of the gastrointestinal (GI) tract, and peripheral edema. The *primary cause of right-sided HF* is left-sided HF. In this situation, left-sided HF results in pulmonary congestion and increased pressure in the blood vessels of the lung (pulmonary hypertension). -Eventually, chronic pulmonary hypertension (increased right ventricular afterload) results in right-sided hypertrophy and HF. Right-sided HF may result from an acute condition such as RV infarction or pulmonary embolism. Cor pulmonale (right ventricular dilation and hypertrophy caused by pulmonary disease) can also cause right-sided HF.

*Pathophysiology of Systolic Heart Failure* Inability to pump blood forward *Caused by*: -Impaired contractile function -Increased afterload -Cardiomyopathy -Mechanical abnormalities Decreased left ventricular ejection fraction (EF)

Systolic failure results from an inability of the heart to pump blood effectively. The left ventricle (LV) in systolic failure loses its ability to generate enough pressure to eject blood forward through the aorta. Over time, the LV becomes dilated and hypertrophied. *caused by* impaired contractile function (e.g., MI), increased afterload (e.g., hypertension), cardiomyopathy, and mechanical abnormalities (e.g., valvular heart disease). The hallmark of systolic failure is a decrease in the left ventricular ejection fraction (EF). The EF is defined as the amount of blood ejected from the LV with each contraction. Normal EF is 55% to 60%. Patients with systolic HF generally have an EF less than 45%. It can be as low as 10%.

*Chronic HF pt. teaching Drug therapy* Expected actions Signs of drug toxicity How to take pulse and what to report Signs and symptoms of hypokalemia and hyperkalemia BP monitoring as needed

Teach the patient the expected actions of the prescribed drugs and the signs of drug toxicity. Also teach the patient and caregiver how to take a blood pressure and pulse rate. The pulse rate should always be taken for 1 full minute. A pulse rate less than 50 beats/minute may be a contraindication to taking a digitalis preparation or β-adrenergic blocker unless specified otherwise by the health care provider. However, in the absence of symptoms (e.g., heart block, ventricular ectopy, syncope), a pulse rate less than 50 beats/minute may be acceptable. Include clear information about when a drug, especially digitalis and β-blockers, should be held and a health care provider called. Teach the patient the *symptoms of hypokalemia* and *hyperkalemia if diuretics* that deplete or spare potassium are ordered. Frequently the patient who takes thiazide or loop diuretics is given supplemental potassium. It may also be appropriate to instruct patients in home *BP monitoring*, especially for those HF patients with hypertension.

Classification System

The New York Heart Association (NYHA) developed functional guidelines for classifying people with heart disease based on the person's tolerance to physical activity. Because the NYHA system only reflects exercise capacity, the American College of Cardiology/American Heart Association (ACC/AHA) developed a staging system that identifies disease progression and treatment strategies. This system allows for identification of people at risk for developing HF but who do not currently have heart disease. The ACC/AHA encourages clinicians to actively address the patient's risk factors and treat any existing conditions to prevent further disease progression. This may help to reduce the growing number of HF patients.

*Counterregulatory Mechanisms* Natriuretic peptides -Atrial natriuretic peptide (ANP), b-type natriuretic peptide (BNP) Released in response to increased blood volume in heart *Causes* diuresis, vasodilation, and lowered BP Counteracts effects of SNS and RAAS

The body's ability to try to maintain balance is demonstrated by several counterregulatory processes. Natriuretic peptides (atrial natriuretic peptide [ANP] and brain, or b-type, natriuretic peptide [BNP]) are hormones produced by the heart muscle. ANP is released from the atria and BNP is released from the ventricles in response to increased blood volume in the heart. The natriuretic peptides have renal, cardiovascular, and hormonal effects. *Renal effects include* (1) increased glomerular filtration rate and diuresis (2) excretion of sodium (natriuresis). *Cardiovascular effects include* (1) vasodilation (2) decreased BP. *Hormonal effects include* (1) inhibition of aldosterone and renin secretion (2) interference of ADH release. The combined effects of ANP and BNP help to counter the adverse effects of the SNS and RAAS in patients with HF.

*Chronic HF Collaborative Management* *(Main treatment goals)* Treat the underlying cause and contributing factors Maximize CO Provide treatment to alleviate symptoms Improve ventricular function Improve quality of life Preserve target organ function Improve mortality and morbidity

The main goals in the treatment of chronic HF are to treat the underlying cause and contributing factors, maximize CO, provide treatment to reduce symptoms, improve ventricular function, improve quality of life, preserve target organ function, and improve mortality and morbidity risks.

*Left-Sided Heart Failure* Most common form Results from left ventricular dysfunction Blood backs up into left atrium and pulmonary veins Increased pulmonary pressure causes fluid leakage →→ pulmonary congestion and edema

The most common form of HF is left-sided HF. Left-sided HF results from left ventricular dysfunction. This prevents normal, forward blood flow and causes blood to back up into the left atrium and pulmonary veins. The increased pulmonary pressure causes fluid leakage from the pulmonary capillary bed into the interstitium and then the alveoli. This manifests as pulmonary congestion and edema.

Chronic HF Planning Overall goals

The overall goals for the patient with HF include (1) a decrease in symptoms (e.g., shortness of breath, fatigue) (2) a decrease in peripheral edema (3) an increase in exercise tolerance (4) compliance with the medical regimen (5) no complications related to HF.

*Cardiac Transplantation* Heart retrieval first step Second step is removal of recipient's heart except for portions of atria (two different approaches) and venous connections Final step is implantation of donor heart

The surgical procedure actually involves multiple surgeries. First, the donor heart is retrieved. The donor is usually someone who has suffered irreversible brain injury (brain death). Most donor hearts are obtained at sites distant from the institution performing the transplant. A team of physicians, nurses, and technicians goes to the hospital of the donor to remove donated organs once brain death of the donor has been determined. The retrieved organs are transported on ice until they can be implanted. For the heart, this is optimally less than 4 hours. Often the donor heart is flown to the recipient's hospital. Second, the donated heart is implanted into the recipient. Two different approaches are used in this surgery. In the biatrial approach, the recipient's damaged heart is removed at the midatrial level and the donor heart connected at the left atrium, pulmonary artery, aorta, and right atrium. In the bicaval approach, the right atrium of the recipient's heart (with the SA node and maintenance of atrial conduction) is preserved and then the donor heart is connected. Cardiopulmonary bypass is needed during the surgical procedure to maintain oxygenation and perfusion to vital organs.