Heart Failure

http://www.youtube.com/watch?v=GnpLm9fzYxU

Heart Failure
An abnormal condition involving impaired cardiac pumping Heart is unable to produce an adequate cardiac output (CO) Heart failure (HF) is not a disease but a syndrome Associated with long-standing HTN and CAD Affects about 5 million people in the U.S. The most common reason for hospitalization in adults >65

Heart Failure
Characterized by
Ventricular dysfunction Reduced exercise tolerance Diminished quality of life Shortened life expectancy

Etiology & Pathophysiology

http://www.youtube.com/watch?v=3YddwXPWVSc

Primary risk factors

CAD Advancing age

Contributing risk factors

HTN Diabetes Tobacco use Obesity High serum cholesterol African American descent

Etiology and Pathophysiology

Causes of HF may be divided into two subgroups:
Primary

Precipitating

HF is classified as systolic or diastolic failure

Etiology and Pathophysiology

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)

Etiology and Pathophysiology

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

Etiology and Pathophysiology

Caused by

Left ventricular hypertrophy from chronic hypertension

Aortic stenosis
Hypertrophic cardiomyopathy
However, a majority of patients do not have
an identifiable heart disease.

Etiology and Pathophysiology

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
http://www.youtube.com/watch?v=fVzPVlsLfBM

Activated to maintain adequate CO

Sympathetic nervous system (SNS) activation: First and least effective mechanism
Increased heart rate (HR) Increased myocardial contractility Peripheral vasoconstriction

Over time, these mechanisms are detrimental as they increase the workload of the failing myocardium and the need for O2.

Compensatory Mechanisms
Neurohormonal responses: Kidneys release renin Increased sodium and water retention Increased peripheral vasoconstriction (increases BP) Response is known as the renin-angiotensinaldosterone system (RAAS).

Compensatory Mechanisms
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
Endothelin is stimulated by ADH, catecholamines, and angiotensin II, causing Arterial vasoconstriction Increase in cardiac contractility Hypertrophy

Compensatory Mechanisms
Pro-inflammatory 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
Over time, a systemic inflammatory response is mounted and results in
Cardiac wasting

Muscle myopathy
Fatigue

Consequences
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.

Consequences
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

Natriuretic peptides are endothelin and aldosterone antagonists.
Enhance diuresis

Natriuretic peptides inhibit the development of cardiac hypertrophy and may have anti-inflammatory effects.

Counter Regulatory Processes

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

TYPES OF HEART FAILURE

Left-Sided Heart Failure Left Ventricular Heart Failure (LVHF)

Most common From left ventricular dysfunction (e.g. MI, HTN, CAD, cardiomyopathy) Backup of blood into the left atrium and pulmonary veins resulting in:
Pulmonary congestion Edema

Right-Sided Heart Failure Right Ventricular Heart Failure (RVHF)

From left-sided HF, cor pulmonale, right ventricular MI Backup of blood into the right atrium and venous systemic circulation
Jugular venous distension Hepatomegaly, splenomegaly Ascites Peripheral edema

Acute Decompensated Heart Failure (ADHF)

Manifests as pulmonary edema
Lungs fill with serosanguineous fluid Often life-threatening

Early
Increased respiratory rate Decrease in PaO2

Later
Tachypnea Respiratory acidosis

Acute Decompensated Heart Failure (ADHF)

Physical findings
Orthopnea Dyspnea, tachypnea Use of accessory muscles Cyanosis Cool and clammy skin Cough with frothy, blood-tinged sputum Breath sounds: Crackles, wheezes, rhonchi Tachycardia Hypotension or Hypertension

Clinical Manifestations: Chronic HF

Fatigue
Earliest symptom

Dyspnea, orthopnea, paroxysmal nocturnal dyspnea Persistent, dry cough

unrelieved with position change or over-thecounter cough suppressants

Tachycardia

Clinical Manifestations: Chronic HF

Dependent edema
May be pitting in nature Sudden weight gain Renal failure may contribute to fluid retention

Nocturia Skin
Dusky, cool, damp to touch Lower extremities: shiny & swollen, diminished or absent hair growth, pigment changes

Clinical Manifestations: Chronic HF

Restlessness, confusion, decreased memory
Decreased CO

Chest pain (angina)

Decreased coronary artery perfusion

Weight changes
Anorexia, nausea
d/t ascites and hepatomegaly

Fluid retention

Complications: HF
Pulmonary edema Lungs fill with serosanguineous fluid

Pleural effusion
Fluid in pleural space Atrial fibrillation

Most common dysrhythmia

Loss of the atrial kick can reduce CO by 10-20% 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

Diagnostic Studies
Primary goal: Determine and treat underlying cause History and physical examination Chest x-ray
Look for heart enlargement Fluid in lungs

ECG Stress testing Cardiac catheterization

Evaluate coronary arteries

Diagnostic Studies
Hemodynamic assessment Echocardiogram Ejection fraction (EF)
Amount of blood ejected with each contraction Normal >55%

Lab Studies
Cardiac enzymes
Rule out MI

BNP http://www.youtube.com/watch?v=JJAMYHAwCMs
<100 pg/ml HF very improbable 100-500 pg/ml HF probable >500 pg/ml HF very probable

Classifications of Heart Failure

New York Heart Association
Functional classification of HF
Class I not limited with normal physical activity by symptoms Class II ordinary physical activity results in fatigue, dyspnea, or other symptoms Class III marked limitation in normal physical activity Class IV symptoms at rest or with any physical activity

Acute Heart Failure Nursing and Collaborative Management

Overall goals of therapy:
Decrease patient symptoms Improve LV function Reverse ventricular remodeling Improve quality of life Decrease mortality and morbidity

Acute Heart Failure Nursing and Collaborative Management

Core measures in the acute management
Joint Commission
Discharge instructions (meds, diet, weight control) Assessment of LV function Treatment with ACE inhibitors or ARBs Smoking cessation

Acute Heart Failure Nursing and Collaborative Management

Decrease intravascular volume
Reduces venous return and preload
Loop diuretics (e.g. furosemide)
May increase risk of dysrhythmias

Decrease venous return (preload)

Reduces the amount of volume returned to the LV during diastole
High fowlers position IV NTG

Acute Heart Failure Nursing and Collaborative Management

Decrease afterload
Improves CO and decreases pulmonary congestion
IV sodium nitroprusside (Nipride)
Also reduces preload NEED TO MONITOR BP FREQUENTLY

Morphine
Reduces preload and afterload Also used to reduce anxiety Causes vasodilation need to monitor for hypotension

Acute Heart Failure Nursing and Collaborative Management

Improve gas exchange and oxygenation
Supplemental oxygen Morphine
Dilates pulmonary and systemic blood vessels and decreases pulmonary pressures

Non-invasive ventilatory support

BiPAP, CPAP

Intubation and ventilation

Acute Heart Failure Nursing and Collaborative Management

Improve cardiac function enhance contractility
For patients who do not respond to conventional pharmacotherapy Inotropic therapy
Digitalis
Increases left ventricular function Slows heart rate MONITOR HR PRIOR TO ADMIN

B-andrenergic agonists (e.g dopamine)

Enhances UO

Phosphodiesterase inhibitors (e.g. milrinone

More effective than dopamine and dobutamine

Acute Heart Failure Nursing and Collaborative Management

Prevent ventricular remodeling
ACE inhibitors
i.e. captopril, enalapril, lisinopril Side effects : cough, hyperkalemia, hypotension Use in caution with decreased renal function

ARBs
i.e. irbesartan, losartan, valsartan Used in those who cannot tolerate ACE inhibitors

Acute Heart Failure Nursing and Collaborative Management

Reduce anxiety
Distraction, imagery Sedative medications
Morphine Lorazepam Alprazolam

Chronic Heart Failure Nursing and 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

Chronic Heart Failure Nursing and Collaborative Management

Oxygen administration Physical and emotional rest Nonpharmacologic therapies
Cardiac resynchonization therapy (CRT) Biventricular pacing Cardiac transplantation Intra-aortic balloon pump (IABP) therapy Ventricular assist devices (VADs) Destination therapy permanent, implantable VAD

Chronic Heart Failure Nursing and Collaborative Management

Therapeutic objectives for drug therapy
Identification of the type of HF and underlying causes Correction of sodium and water retention and volume overload Reduction of cardiac workload Improvement of myocardial contractility Control of precipitating and complicating factors

Chronic Heart Failure Nursing and Collaborative Management

Nutritional Therapy
Diet and weight reduction recommendations must be individualized and culturally sensitive Dietary Approaches to Stop Hypertension (DASH) diet is recommended Sodium is usually restricted to 2.5 gm. per day

Chronic Heart Failure Nursing and Collaborative Management

Fluid restriction not generally required Daily weights are important Weight gain should be reported to health care provider
3lbs (1.4kg) over 2 days 3-5lb (2.3kg) over a week

NURSING DIAGNOSES

Activity Intolerance
Encourage rest periods Monitor patients response
Respiratory rate Heart rate Blood pressure

Teach patient activities to minimize oxygen consumption

Self-monitoring Pacing techniques

Fluid Volume Excess

Daily weight I/O Monitor electrolytes Monitor for S/Sx of hypervolemia
Lung sounds Blood pressure Respiratory rate Edema

Impaired Gas Exchange

Monitor respiratory status
Rate Depth Effort

Auscultate lungs Monitor for dyspnea Administer oxygen as ordered

Anxiety
Provide reassurance and create trust Explain all procedures Instruct in relaxation techniques Medication as needed

Knowledge Deficiency
Common S/Sx of disease Measures to decrease episodes Medication regimen Decrease side effects Smoking cessation

HOME MANAGEMENT

Planning Overall Goals

Decrease in symptoms Decrease or absence of edema Increase in exercise tolerance Compliance with the medical regimen No complications r/t HF

Health Promotion
Treatment or control of underlying heart disease Anti-dysrhythmic agents or pacemaker for patients with serious dysrhythmias or conduction disturbances Flu and pneumonia vaccinations Patient teaching Home nursing care for f/u and to monitor patients response to treatment may be required

Ambulatory & Home Care

Explain physiologic changes that have occurred to patient Assist patient to adapt to both the physiologic and psychological changes
Anxiety and depression are common

Integrate patient and support system in the overall care plan

Patient Education
http://www.youtube.com/watch?v=3IZfGGWEtf4 Lifelong medications Taking pulse rate
Know when drugs should be withheld and reported to heath care provider

Home BP monitoring Signs of hypo and hyperkalemia Weight diary