John Nation RN, MSN Thanks to Nancy Jenkins Heart Failure John Nation RN, MSN Thanks to Nancy Jenkins

Overview: Incidence/ Definition A & P Review Pathophysiology Types of Heart Failure Complications Treatments Nursing Care Devices Heart Transplant

Incidence/ Definition Heart Failure- clinical condition involving impaired cardiac pumping Incidence: 5 million people in US have HF 470,000 new cases each year 1 in 100 adults has HF Most common reason for hospital admission in adults >65 years old

A & P Review:

What Causes Heart Failure? Coronary Artery Disease (CAD) Myocardial Infarction Dysrhythmias Pulmonary Emboli Hypertension Congential Heart Disease Cardiomyopathy Valve problems Endocarditits Myocarditis Idiopathic (don’t know!)

Key Terms: Cardiac Output- Stroke volume x heart rate Normal value is 4-8 Liters/min Stroke Volume- Amount of blood pumped from the heart with each heart beat Preload- the volume of blood in the ventricles at the end of diastole, before the next contraction. Afterload- the peripheral resistance that the left ventricle pumps against

Types of Heart Failure: Systolic Heart Failure: Most common type The ventricles are not providing adequate contractions (it’s not pumping well enough) Defined primarily in terms of the left ventricular ejection fraction (EF) Ejection Fraction (EF)- percentage of total ventricular filling volume that is ejected during contraction. Normal EF is 55-70%.

Ejection Fraction:

Types of Heart Failure (Cont’d): Diastolic Heart Failure: Impaired ability of the heart to relax and fill during diastole Causes decreased stroke volume (and therefore decreased cardiac output Caused largely by stiff or noncompliant ventricles Diagnosis based on heart failure symptoms with normal ejection fraction. Often caused by hypertension and myocardial fibrosis

Types of Heart Failure (Cont’d): Systolic and Diastolic Heart Failure Low ejection fraction and poor relaxing (and thus poor filling) of ventricles Often characterized by biventricular failure Often seen with dilated cardiomyopathies

Types of Heart Failure (Cont’d): Left-Sided Heart Failure: Most common form Blood backs up into left atrium and pulmonary veins Causes pulmonary congestion/ edema Right-Sided Heart Failure: Primary cause is left-sided heart failure Blood backs up into venous circulation Causes hepatomegaly, splenomegaly, peripheral edema

Cor Pulmonale:

How the Body Responds: Remember, a decrease in stroke volume leads to a decrease in cardiac output. Body attempts to increase cardiac output: Sympathetic Nervous System Neurohormonal Response Dilation of chambers of the heart Hypertrophy Natriuretic peptides

The Body’s Response: Sympathetic Nervous System: Release of catecholamines (epinephrine and norepinephrine) Causes increased heart rate & increased contractility Increases workload on heart Increases oxygen need of heart

The Body Responds (Cont’d): Neurohormonal Response: As CO decreases, blood flow to kidneys decreases: Causes activation of renin-angiotensin-aldosterone system (RAAS) RAAS causes sodium and water retention, peripheral vasoconstriction, increased BP Low CO decreases cerebral perfusion pressure: Posterior pituitary secretes more antidiuretic hormone (ADH) ADH causes more fluid retention and production of endothelin. Endothelin causes arterial vasocontriction & increased contractility of heart muscle

The Body Responds (Cont’d): Neurohormal Response (Cont’d): Due to various types of cardiac injury (ie MI), proinflammatory cytokines are released. Cause cardiac hypertrophy, pumping dysfunction, and death of cells in the heart muscle Over time, this process can lead to a systemic inflammatory response that further damages the heart

The Body Responds (Cont’d): Dilation: Chambers of the heart get larger Increase in stretch of muscle fibers due to increase in blood volume The greater the stretch, the greater the force of contraction (Frank-Starling Law) Initially, causes increase in cardiac output. After time, muscle fibers are overstretched and contraction decreases

The Body Responds (Cont’d): Hypertrophy: Increase in muscle mass of heart Increases contractility at first However, hypertrophic muscle doesn’t work as well, needs more oxygen, greater risk for rhythm problems, and has poor circulation

The Body Responds (Cont’d):

Hypertrophy vs Dilation

The Body Responds (Cont’d): Natriuretic Peptides: Atrail natriuretic peptide (ANP) & b-type natriuretic peptide (BNP) Hormones produced by the heart that promote vasodilation (decreasing preload and afterload) Increase glomerular filtration rates Block effects of RAAS

Clinical Manifestations: Acute Decompensated Heart Failure: Often presents as pulmonary edema Often associated with CAD/ MI Pale, anxious, dyspnea, possibly cyanotic, crackles, wheezing, rhonhi, blood in sputum, increased HR, S3 heart sound

Clinical Manifestations (Cont’d): Before treatment After treatment

Clinical Manifestations (Cont’d): Chronic Heart Failure: Depends on right vs left sided failure Often has signs/ symptoms of biventricular failure Fatigue Dyspnea Nocturnal Dyspnea Tachycardia Edema Nocturia Chest pain Weight changes Behavioral changes

Clinical Manifestations (Cont’d):

Complications: Hepatomegaly Dysrhythmias Pleural Effusion Thrombus Renal Failure Cardiogenic Shock

Classification: NYHA Classifications: Class I- No limitation of physical activity. Ordinary activity does not cause fatigue, dyspnea, palpitations, or anginal pain Class II- Slight limitation of physical activity. No symptoms at rest. Ordinary physical activity results in fatigue, dyspnea, palpitations, or anginal pain Class III- Marked limitation of physical ability. Usually comfortable at rest. Ordinary activity causes fatigue, dyspnea, palpitations, or anginal pain Class IV- Inability to carry on any physical activity without discomfort. Symptoms may be present at rest.

Classification (Cont’d): ACC/ AHA Stages of Heart Failure: Stage A- Patients at high risk for developing left ventricular dysfunction because of conditions that are strongly associated with development of HF Stage B- Patients who developed structural heart disease that is strongly associated with development of HF but who have no symptoms Stage C- Patients who have current or prior symptoms of HF associated with underlying structural heart disease Stage D- Patients with advanced structural heart disease and marked symptoms of HF at rest despite maximized medical therapy and who require specialized interventions

Diagnostic Tests: History and Physical CBC, BMP, cardiac enzymes, liver function tests, BNP, PT/INR Chest x-ray 12- lead ECG Echocardiogram Nuclear imaging studies Stress testing Hemodynamic monitoring Heart catheterization

Echocardiogram: Transesophageal echocardiogram TEE Echocardiogram Video

Treatment Goals: Decreasing Intravascular Volume- decreases venous return, decreases preload, more efficient contraction and increased cardiac output Decreasing Preload- vasodilator, positioning Decreasing Afterload- decreases pressure against which LV must pump Increasing Contractility- inotropes increase cardiac output

Drug Therapy: Diuretics: reduce preload Ace-Inhibitors- Furosemide (Lasix)- PO or IV, loop diuretic. Spironolactone (Aldactone)- PO, potassium sparing diuretic Metolazone (Zaroxolyn)- PO, when extra diuresis necessary Ace-Inhibitors- lisinopril first line therapy in chronic HF block conversion of angiotensin I to angiotensin II, decrease aldosterone Decrease afterload. Increase cardiac output.

Drug Therapy (Cont’d): Vasodilators: Nitrates- directly dilate vessels, decrease preload, vasodilate coronary arteries. Nitroprusside (Nipride)- reduces preload and afterload Nesiritide (Natrecor)- arterial and venous dilation B- Blockers- Carvedilol (Coreg), Metoprolol (Lopressor) Block negative effects of SNS system (such as HR) Can reduce myocardial contractility Improve patient survival

Drug Therapy (Cont’d): Positive Inotropes: Increase contractility Digoxin- increases contractility, decreases HR Watch for hypokalemia Reduces symptoms, but not shown to prolong life Dopamine Dobutamine Milrinone (Primacor) Angiotensin II Receptor Blockers (ARBs) Mostly for patients unable to tolerate Ace Inhibitors Similar effects to Ace Inhibitors Isosorbide dinitrate and hydralazine (BiDil)- for African Americans with HF.

Collaborative Care: Treat underlying cause (if possible) Oxygen therapy PRN Cardiac rehab Daily weights Drug therapy education Sodium restriction Strict Input/ output Symptom education Home health Specialty clinics

Discharge Teaching- JCAHO- Weight Monitoring Medications Activity Diet What to do if symptoms worsen Follow-up

Nursing Diagnosis Activity intolerance Decreased cardiac output Fluid volume excess Impaired gas exchange Anxiety Deficient knowledge

Decreased cardiac output Plan frequent rest periods Monitor VS and O2 sat at rest and during activity Take apical pulse Review lab results and hemodynamic monitoring results Fluid restriction- keep accurate I and O Elevate legs when sitting Teach relaxation and ROM exercises

Activity Intolerance Provide O2 as needed practice deep breathing exercises teach energy saving techniques prevent interruptions at night monitor progression of activity offer 4-6 meals a day

Fluid Volume Excess Give diuretics and provide BSC Teach side effects of meds Teach fluid restriction Teach low sodium diet Monitor I and O and daily weights Position in semi or high fowlers

Knowledge deficit Low Na diet Fluid restriction Daily weight When to call Dr. Medications

Treatment: Devices: Cardiac Resynchronization Therapy (CRT): Utilizes biventricular pacing Coordinates right and left ventricle contractility Normal electrical conduction increases CO For patients with Class III and IV HF Patients with HF caused by ischemia and EF <35% may need implantable cardiac defibrillator (ICD) as well due to risk of dysrhythmias

Intraaortic Balloon Pump (IABP): Temporary circulatory assistance Reduces afterload Improves coronary blood flow Helps aortic diastolic pressure IABP Video

Ventricular Assist Devices (VAD): Circulatory device that provides cardiac output in addition to that of native heart Usually takes blood from left ventricle then pumps to the aorta Many different types, primarily Heartmate II and PVAD Heartmate II much easier to transport, continous flow to put blood out to body VAD Patient Video Heartmate II Thoratec Video

PVAD/ IVAD

Heartmate II:

VADs (Cont’d) Either bridge to transplant or as destination therapy Must meet criteria for implantation Be able to manage pump at home (in many cases) Require anticoagulation therapy

Heart Transplantation: First performed in 1967 Over 2000 each year in US Long wait time, not enough hearts From harvest to transplantation there is a 4-6 hr maximum time

Heart Transplantation (Cont’d): Absolute Indications: Cardiogenic shock Dependence on IV inotropes (ie dobutamine) Severe cardiac ischemia not able to be fixed by PCI or CABG Symptomatic, refractory life threatening dysrhythmias (ie V-tach) Relative Indications: Persistent fluid overload despite medical therapy Persistent unstable angina

Heart Transplantation (Cont’d): Possible exclusion criteria (exceptions for some patients/ differs by center): >65 yrs old Severe pulmonary HTN (irreversible) Irreversible kidney or liver disease not explained by HF Severe chronic lung disease Active infection Cancer in last 5 yrs Other conditions as well, this is guiding list.

Heart Transplant List: Each patient has a Status ranking Status 1a: critically ill, hospitalized Status 1b:require IV medications (inotrops) or heart assist device Status 2: not hospitalized, do not require IV medications Status 7: Temporarily inactive

Cardiac Transplantation 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

Cardiac Transplantation Infection is the primary complication followed by acute rejection in the first year after transplantation Beyond the first year, malignancy (especially lymphoma) and coronary artery vasculopathy are major causes of death One year survival rate is 85-90% Three year survival rate is 79% Local Transplant Story

Cardiac Transplantation 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 Endomyocardial Biopsy Video

Decreased cardiac output Systolic failure Diastolic failure Your patient has a normal EF but shows signs of heart failure. Your patient most likely has: Decreased cardiac output Systolic failure Diastolic failure LV hyypertrophy

True or False: Lasix increases preload.

Which of the following is associated with left sided failure? crackles hypoxemia tachypnea Peripheral edema

Which of the following are compensatory mechanisms for HF? Tachycardia Hypotension RAAS LV hypertrophy

One of the first signs of Heart failure often is: Decreased cardiac output Edema Fatigue Atrial fibrillation

B. Blood urea nitrogen (BUN) C. Potassium The nurse is caring for a hospitalized client with heart failure who is receiving captopril (Capoten) and spironolactone (aldactone). Which lab value will be most important to monitor? A. Sodium B. Blood urea nitrogen (BUN) C. Potassium D. Alkaline phosphatase (ALP)