Download Cardiac Output

Heart Failure
John Nation RN, MSN
Thanks to Nancy Jenkins
Overview:
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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?
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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
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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:
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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:
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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
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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:
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Most common form
Blood backs up into left atrium and pulmonary
veins
Causes pulmonary congestion/ edema
Right-Sided Heart Failure:
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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:
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Sympathetic Nervous System
Neurohormonal Response
Dilation of chambers of the heart
Hypertrophy
Natriuretic peptides
The Body’s Response:
Sympathetic Nervous System:
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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:
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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
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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):
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Due to various types of cardiac injury (ie MI),
proinflammatory cytokines are released.
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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:
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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:
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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:
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Atrail natriuretic peptide (ANP) & b-type
natriuretic peptide (BNP)
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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:
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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:
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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:
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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:
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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,
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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
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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:
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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)
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Block negative effects of SNS system (such as HR)
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Can reduce myocardial contractility
Improve patient survival
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Drug Therapy (Cont’d):
Positive Inotropes: Increase contractility
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Digoxin- increases contractility, decreases HR
 Watch for hypokalemia
 Reduces symptoms, but not shown to prolong life
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Dopamine
Dobutamine
Milrinone (Primacor)
Angiotensin II Receptor Blockers (ARBs)
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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
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Activity intolerance
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Decreased cardiac output
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Fluid volume excess
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Impaired gas exchange
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Anxiety
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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):
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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 (2 min 45 sec)
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:
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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:
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Persistent fluid overload despite medical therapy
Persistent unstable angina
Heart Transplantation (Cont’d):
Possible exclusion criteria (exceptions for some
patients/ differs by center):
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>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