focus on heart failure

Focus onHeart Failure

• An abnormal condition involving impaired cardiac pumping/filling

• Heart is unable to produce an adequate cardiac output (CO) to meet metabolic needs.

Heart Failure

• Characterized by

– Ventricular dysfunction

– Reduced exercise tolerance

– Diminished quality of life

– Shortened life expectancy

Heart Failure

• Heart failure (HF) is not a disease but a “syndrome.”

• Associated with long-standing hypertension, coronary artery disease (CAD), and myocardial infarction (MI)

Heart Failure

• Affects about 5 million people in the United States

• The most common reason for hospitalization in adults >65 years old

Heart Failure

• Primary risk factors– CAD– Advancing age

• Contributing risk factors – Hypertension– Diabetes– Tobacco use– Obesity– High serum cholesterol

Etiology and Pathophysiology

• Causes of HF may be divided into two subgroups:

– Primary

– Precipitating • HF is classified as systolic or diastolic failure

(or dysfunction).


• Systolic failure– Hallmark finding: Decrease in the left ventricular

ejection fraction (EF)• Caused by

– Impaired contractile function (e.g., MI)– Increased afterload (e.g., hypertension)–Cardiomyopathy–Mechanical abnormalities (e.g., valve

disease)


• Diastolic failure– Impaired ability of the ventricles to relax and fill

during diastole, resulting in decreased stroke volume and CO

– Diagnosis based on the presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy, and normal EF


• Diastolic failure (cont’d)

– Caused by • Left ventricular hypertrophy from chronic

hypertension

• Aortic stenosis

• Hypertrophic cardiomyopathy


• 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.


• Compensatory mechanisms are activated to maintain adequate CO.– Sympathetic nervous system (SNS) activation: First

and least effective mechanism • Release of catecholamines (epinephrine and

norepinephrine)

– Increased heart rate (HR)– Increased myocardial contractility–Peripheral vasoconstriction


• Compensatory mechanisms (cont’d)– Sympathetic nervous system (SNS) activation• Over time, these mechanisms are

detrimental as they increase the workload of the failing myocardium and the need for O2.


• Compensatory mechanisms (cont’d)– Neurohormonal responses: Kidneys release renin

• Renin converts angiotensinogen to angiotensin I.

• Angiotensin I is converted to angiotensin II by a converting enzyme made in the lungs.


• Compensatory mechanisms (cont’d)– Neurohormonal responses (cont’d)

• Angiotensin II causes–Adrenal cortex to release aldosterone

(sodium and water retention)–Increased peripheral vasoconstriction

(increases BP)• Response is known as the renin-

angiotensin-aldosterone system (RAAS).



• Low CO causes a decrease in cerebral perfusion pressure.

• Antidiuretic hormone (ADH) is secreted and causes

–Increased water reabsorption in the renal tubules, leading to water retention and increased blood volume


• Compensatory mechanisms (cont’d)

– Neurohormonal responses (cont’d)• Endothelin is stimulated by ADH,

catecholamines, and angiotensin II, causing

–Arterial vasoconstriction–Increase in cardiac contractility–Hypertrophy



• Proinflammatory cytokines (e.g., tumor necrosis factor): Released by cardiac myocytes in response to cardiac injury

• Depress cardiac function by causing cardiac hypertrophy, contractile dysfunction, and death of myocytes


• Compensatory mechanisms (cont’d)

– Neurohormonal responses (cont’d)• Over time, a systemic inflammatory response

is mounted and results in

–Cardiac wasting

–Muscle myopathy

–Fatigue


• Consequences of compensatory mechanisms– Dilation

• Enlargement of the chambers of the heart that occurs when pressure in the left ventricle is elevated

• Initially an adaptive mechanism • Eventually this mechanism becomes

inadequate, and CO decreases.


Dilated & Hypertrophied Heart Chambers

Fig. 35-1. A, Dilated heart chambers. B, Hypertrophied heart chambers.

• Consequences of compensatory mechanisms– Hypertrophy

• Increase in muscle mass and cardiac wall thickness in response to chronic dilation, resulting in

–Poor contractility–Higher O2 needs–Poor coronary artery circulation–Risk for ventricular dysrhythmias


• Counter regulatory processes– Natriuretic peptides: Atrial natriuretic peptide (ANP),

b-type natriuretic peptide (BNP)• Released in response to increase in atrial

volume and ventricular pressure• Promote venous and arterial vasodilation,

reducing preload and afterload • Chronic HF leads to a depletion of these

factors.


• Counter regulatory processes (cont’d)– Natriuretic peptides are endothelin and

aldosterone antagonists. • Enhance diuresis • Block effects of the RAAS

– Natriuretic peptides inhibit the development of cardiac hypertrophy and may have antiinflammatory effects.


• Counter regulatory processes (cont’d)– Nitric oxide (NO)

• Released from the vascular endothelium in response to compensatory mechanisms

• NO relaxes arterial smooth muscle, resulting in vasodilation and decreased afterload.


• Left-sided HF (most common) from left ventricular dysfunction (e.g., MI hypertension, CAD, cardiomyopathy)– Backup of blood into the left atrium and

pulmonary veins • Pulmonary congestion • Edema

Types of Heart Failure

Left-Sided Heart Failure

Fig. 35-2. Pathophysiology of heart failure. Elevated systemic vascular resistance results in left-sided heart failure that leads to right-sided heart failure. Systemic vascular resistance and preload are exacerbated by the renin-angiotensin-aldosterone system. ADH, Antidiuretic hormone; LA, left atrium; LV, left ventricle; LVEDP, left ventricular end-diastolic pressure; RV, right ventricle.

• Right-sided HF from left-sided HF, cor pulmonale, right ventricular MI– Backup of blood into the right atrium and venous

systemic circulation• Jugular venous distention• Hepatomegaly, splenomegaly• Vascular congestion of GI tract• Peripheral edema

Types of Heart Failure

• Pulmonary edema, often life-threatening – Early

• Increase in the respiratory rate • Decrease in PaO2

– Later • Tachypnea • Respiratory acidemia

Clinical Manifestations: Acute Decompensated Heart Failure (ADHF)

Pulmonary Edema

Fig. 35-3. 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 flowand worsening of left heart failure result in further movement of fluid into the interstitial space and into the alveoli.

• Physical findings–Orthopnea–Dyspnea, tachypnea–Use of accessory muscles–Cyanosis–Cool and clammy skin

Clinical Manifestations: ADHF

• Physical findings– Cough with frothy, blood-tinged sputum– Breath sounds: Crackles, wheezes, rhonchi – Tachycardia– Hypotension or hypertension

Clinical Manifestations: ADHF

• Fatigue• Dyspnea, orthopnea, paroxysmal nocturnal

dyspnea • Persistent, dry cough, unrelieved with position

change or over-the-counter cough suppressants

• Tachycardia

Clinical Manifestations: Chronic HF

• Dependent edema

– Edema may be pitting in nature – Sudden weight gain of >3 lb (1.4 kg) in 2 days may

indicate an exacerbation of HF.


• Nocturia

• Skin

– Dusky, cool, damp to touch – Lower extremities: Shiny and swollen, diminished

or absent hair growth, pigment changes


• Restlessness, confusion, decreased memory

• Chest pain (angina)

• Weight changes

– Anorexia, nausea

– Fluid retention


• Pleural effusion• Atrial fibrillation (most common dysrhythmia)

– Promotes thrombus/embolus formation, increasing risk for stroke

– Treatment can include rate control, cardioversion, antidysrhythmics, and/or systemic anticoagulation.

Complications: HF

• High risk of fatal dysrhythmias (e.g., sudden cardiac death, ventricular tachycardia) with HF and an EF <35%

• HF can lead to severe hepatomegaly, especially with RV failure. – Fibrosis and cirrhosis can develop over time.

• Renal insufficiency or failure

Complications: HF

• Primary goal: Determine and treat underlying cause

– History and physical examination

– Chest x-ray

– ECG

– Lab studies (e.g., cardiac enzymes, BNP)

Diagnostic Studies

• Primary goal: Determine and treat underlying cause (cont’d)– Hemodynamic assessment– Echocardiogram– Stress testing– Cardiac catheterization– Ejection fraction

Diagnostic Studies

• New York Heart Association Functional Classification of HF

– Classes I to IV

• ACC/AHA Stages of HF

– Stages A to D

Classification Systems

• Overall goals of therapy for ADHF and chronic HF – Decrease patient symptoms.– Improve LV function.– Reverse ventricular remodeling.– Improve quality of life.– Decrease mortality and morbidity.

Nursing and Collaborative Management

• High Fowler’s position• Supplemental oxygen• Continuous ECG monitoring• Ultrafiltration: Option for patients with

volume overload

Nursing and Collaborative Management ADHF

• Circulatory assist devices are used to treat patients with deteriorating HF.

• Coexisting psychologic disorders should be addressed.


• Decrease intravascular volume

– Reduces venous return and preload

• Loop diuretics (e.g., furosemide [Lasix])

• Ultrafiltration or aquapheresis


• Decrease venous return (preload) – Reduces the amount of volume returned to the LV

during diastole

• High-Fowler’s position

• IV nitroglycerin


• Decrease afterload– Improves CO and decreases pulmonary congestion

• IV sodium nitroprusside (Nipride)

• Morphine sulfate

• Nesiritide (Natrecor)


• Improve gas exchange and oxygenation

– Supplemental oxygen

– Morphine sulfate

– Noninvasive ventilatory support (BiPAP)


• Improve cardiac function – For patients who do not respond to conventional

pharmacotherapy (e.g., diuretics, vasodilators, morphine sulfate)

• Inotropic therapy

–Digitalis–-Adrenergic agonists (e.g., dopamine)–Phosphodiesterase inhibitors (e.g.,

milrinone)• Hemodynamic monitoring


• Reduce anxiety

– Distraction, imagery– Sedative medications (e.g., morphine sulfate,

benzodiazepines)


• 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.

Collaborative Management Chronic HF

• Oxygen administration• Physical and emotional rest• Nonpharmacologic therapies

– Cardiac resynchronization therapy (CRT) or biventricular pacing

– Cardiac transplantation


• Nonpharmacologic therapies (cont’d)

– Intraaortic balloon pump (IABP) therapy

– Ventricular assist devices (VADs)

– Destination therapy—Permanent, implantable

VAD


• Therapeutic goals for drug therapy– Identification of type of HF and causes– Correction of sodium and water retention and

volume overload– Reduction of cardiac workload– Improvement of myocardial contractility– Control of precipitating and complicating factors


• Drug therapy

– Diuretics

• Thiazide

• Loop

• Spironolactone


• Drug therapy (cont’d)

– ACE inhibitors

– Angiotensin II receptor blockers

– Aldosterone antagonists

– Nitrates

– -Adrenergic blockers


• Drug therapy (cont’d)

– Positive inotropic agents

• Digitalis

• Calcium sensitizers– BiDil (combination drug containing isosorbide

dinitrate and hydralazine)


• Nutritional therapy– Diet and weight reduction: Individualize

recommendations and consider cultural background

– Recommend Dietary Approaches to Stop Hypertension (DASH) diet.

– Sodium is usually restricted to 2.5 g per day.


• Nutritional therapy– Fluid restriction not generally required– Daily weights are 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.


• Assessment– Subjective data

• Past health history• Functional health patterns• Medications

– Objective data

• Physical examination

Nursing Management Chronic HF

• Nursing diagnoses

– Activity intolerance

– Fluid volume excess

– Impaired gas exchange

– Anxiety

– Deficient knowledge


• Planning: Overall goals– Decrease in symptoms (e.g., shortness of breath,

fatigue)– Decrease in peripheral edema– Increase in exercise tolerance– Compliance with the medical regimen– No complications related to HF


• Health promotion– Treatment or control of underlying heart disease

key to preventing HF and episodes of ADHF (e.g., valve replacement, control of hypertension, coronary revasculariztion)

– Early detection of worsening HF may prevent future hospitalizations.


• Health promotion– Patient/caregiver teaching: Medications, diet, and

exercise regimens • Exercise training (e.g., cardiac

rehabilitation) improves symptoms but is often underprescribed.

– Home nursing care may be required for follow-up and to monitor patient’s response to treatment.


• Acute intervention– HF is a progressive disease—Treatment plans are

established with quality-of-life goals.– Symptom management is controlled with the use

of self-management tools (e.g., daily weights).


• Acute intervention

– Salt must be restricted.

– Energy must be conserved.– Support systems are essential to the success of

the entire treatment plan.


• 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) or support

system into the overall care plan.


• Implementation: Patient education– Medications (lifelong)– Taking pulse rate

• Know when drugs (e.g., digitalis, -adrenergic blockers) should be withheld and reported to health care provider.


• Implementation: Patient and caregiver education– Home BP monitoring– Signs of hypokalemia and hyperkalemia if taking

diuretics that deplete or spare potassium– Instruct patient in energy-conserving and energy-

efficient behaviors.


• Evaluation

– Respiratory status

– Fluid balance

– Activity tolerance

– Anxiety control

– Knowledge of disease process


• Treatment of choice for patients with refractory end-stage HF, inoperable CAD, and cardiomyopathy– Goal of the transplant evaluation process is to

identify patients who would most benefit from a new heart.

Nursing Management 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.


• Bridge to transplantation devices• Surgery involves removing the recipient’s

heart, except for the posterior right and left atrial walls and their venous connections.

• Recipient’s heart is replaced with the donor heart.


• Donor sinoatrial (SA) node is preserved so that a sinus rhythm may be achieved postoperatively.

• Immunosuppressive therapy usually begins in the operating room.


• Infection is the primary complication, followed by acute rejection, in the first year after transplantation.

• Malignancy (especially lymphoma) and coronary artery vasculopathy are major causes of death after the first year.


• 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.


• Nursing care focuses on – Promoting patient adaptation to the transplant

process

– Monitoring cardiac function

– Managing lifestyle changes

– Providing relevant teaching


Case Study

78

Case Study• 68-year-old woman is admitted to the

hospital for shortness of breath.

• She was diagnosed 4 years ago with HF after failing to follow the recommended medical regimen for an MI she suffered 6 years ago.

Case Study

• States she was taking a diuretic but ran out 4 days ago; has not been able to refill her prescription

• States she noticed some swelling in her feet that seemed worse than usual

Case Study

• Physical examination–Alert and oriented to person, place,

and time–Fine crackles bilateral lower lobes–Shortness of breath on minimal

exertion

Case Study

• Physical examination (cont’d)

–O2 saturation 89%, room air

–S1 and S2 without murmur or extra heart sounds

–Capillary refill sluggish in lower extremities, normal in upper extremities

–2+ edema bilateral lower extremities

Discussion Questions

1. What is the priority of care for her?

2. How would you evaluate whether your nursing actions were successful?

3. What teaching measures would you use to prevent a reoccurrence of ADHF?

focus on heart failure

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