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:1. Sympathetic Nervous System

2. Neurohormonal Response

3. Dilation of chambers of the heart

4. Hypertrophy

5. 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 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

True or False: Lasix increases preload.

1) True

2) False