Transcript CONGESTIVE HEART FAILURE

HEART FAILURE
by Nancy Jenkins
The most common reason for
hospitalization in adults >65
years old.
1 in 100 adults has HF
heart failure
Heart Failure- Clinical syndrome
that can result from any structural
or functional cardiac disorder that
impairs ability of ventricle to fill
with or eject blood
5 million Americans have heart
failure
•500,000 new cases every year
• 25-50 billion dollars a year to
care for people with Heart Failure
•6,500,000 hospital days / year
•300,000 deaths/year
Heart Failure
Mild
Mild
Cardiogenic shock
Cardiomyopathy
Uncompensated Heart Failure
Pulmonary Edema-ADHF
Severe End Stage
Irreversible
Control With
Drugs
Diet
Fluid
Restriction
/Same as Mild with
Morphine Sulfate
Needs new ventricle
VAD
IABP
Heart Transplant
Heart Failure Pneumonic
U
Upright Position
N
Nitrates
L
Lasix
O
Oxygen
A
Amiodorone, ACE, ARBs
D
Dig, Dobutamine
M
Morphine Sulfate
E
Extremities Up or Down
Definition Of Heart Failure
• CO=SVxHR is insufficient to meet the
metabolic needs of the body
• SV is determined by preload, afterload and
myocardial contractility
• Systolic failure- dec. contractility
• Diastolic failure- dec. filling
• EF< 40%
Heart Failure- Types
Systolic versus Diastolic
• Systolic failure is the most common cause –”poor
pump”
– **Hallmark finding: Decrease in the left ventricular
ejection fraction (EF) < 40%
• Caused by
– Impaired contractility (e.g., MI)
– Increased afterload (e.g., hypertension)
– Cardiomyopathy
– Mechanical abnormalities (e.g., valve disease)
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hypokinesis
EF- the % of total ventricular filling volume that is ejected
during systole. EF- 55-65 normal
Heart Failure
Diastolic
• Diastolic failure-”poor filling” stiff ventricles
– 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, normal ejection fraction (EF)
diastolic failure
Heart Failure
• 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)
Your patient has a normal EF but
shows signs of heart failure. Your
patient most likely has:
1. Decreased cardiac
output
2. Systolic failure
3. Diastolic failure
4. LV hypertrophy
How the Body Responds:
• Remember, a decrease in stroke volume
leads to a decrease in cardiac output.
• Body attempts to increase cardiac output:
1.
2.
3.
4.
5.
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
– What does this do to the workload on heart?
– What does this do to O2 need of the heart?
– What meds could we give to decrease this
release?
The Body Responds (Cont’d):
Neurohormonal Response:
– As CO decreases, blood flow to kidneys __________:
• Causes activation of (RAAS)
• RAAS causes _____ & _______ retention, peripheral
vasoconstriction, increased BP
– Low CO decreases cerebral perfusion pressure:
• Posterior pituitary secretes more antidiuretic hormone
(ADH)
• ADH causes more retention of _______ & 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):
Hypertrophy:
– Increase in ___________ of heart
– Increases contractility at first
– However, hypertrophic muscle doesn’t work as
well, needs more _________, greater risk for
rhythm problems, and has poor circulation
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 (_____________ Law)
– Initially, causes increase in cardiac output.
After time, muscle fibers are overstretched and
contraction decreases .CHF
The Body Responds
• Counter regulatory processes- these help protect the heart
– Natriuretic peptides: atrial natriuretic peptide (ANP)
released with cardiac muscle stretch and b-type natriuretic
peptide (BNP) released with increased pressure of LV
• Released in response to increases in atrial volume and
ventricular pressure
• Act opposite of RAAS and block effect
• Promote venous and arterial vasodilation, reducing
preload and afterload
• Increase GFR
• Prolonged HF leads to a depletion of these factorsNatrecor can be used for same effects
Which of the following are
compensatory mechanisms for HF?
1.
2.
3.
4.
Tachycardia
Hypotension
RAAS
LV hypertrophy
Pathophysiology
Structural Changes
•
•
•
•
Decreased contractility
Increased preload (volume)
Increased afterload (resistance)
Ventricular remodeling(ACE inhibitors can
prevent this)
– Ventricular hypertrophy
– Ventricular dilation
END RESULT
FLUID OVERLOAD AND EDEMA
Heart Failure
Classification Systems
• New York Heart Association Functional
Classification of HF
– Classes I to IV
• ACC/AHA Stages of HF
– Stages A to D
NYHA Classificationbased on activity
Class
Patient Symptoms
Class I (Mild)
No limitation of physical activity. Ordinary physical
activity does not cause undue fatigue, palpitation, or
dyspnea (shortness of breath).
Class II (Mild)
Slight limitation of physical activity. Comfortable at rest,
but ordinary physical activity results in fatigue,
palpitation, or dyspnea.
Class III
(Moderate)
Marked limitation of physical activity. Comfortable at
rest, but less than ordinary activity causes fatigue,
palpitation, or dyspnea.
Class IV
(Severe)
Unable to carry out any physical activity without
discomfort. Symptoms of cardiac insufficiency at rest. If
any physical activity is undertaken, discomfort is
increased.
Stage A
Stage B
Stage C
Those at high risk for
developing heart failure.
Includes people with:
•Hypertension
•Diabetes mellitus
•Coronary artery disease
(including heart attack)
•History of cardiotoxic
drug therapy
•History of alcohol abuse
•History of rheumatic
fever
•Family history of CMP
Those diagnosed with “systolic”
heart failure but have never had
symptoms of heart failure
(usually by finding an ejection
fraction of less than 40% on
echocardiogram).
Patients with known heart failure
with current or prior symptoms.
Symptoms include:
•Shortness of breath
•Fatigue
•Reduced exercise
intolerance.
•Exercise regularly
•Quit smoking
•Treat hypertension
•Treat lipid disorders
•Discourage alcohol or illicit drug use
•If previous heart attack or current
diabetes mellitus or hypertension 
angiotensin converting enzyme
inhibitor (ACE-I)
•Care measures in Stage A +
•All patients should be on ACE-I
•Beta-blockers should be added
•Surgical consultation for coronary
artery revascularization and valve
repair/replacement (as appropriate)
In this group, care measures from Stage A
apply, ACE-I and beta-blockers should be
used +
•Diuretics (water pills)
•Digoxin
•Dietary sodium (salt) restriction
•Weight monitoring
•Fluid restriction (as appropriate)
•Withdrawal of drugs that worsen the
condition
•Spironolactone when symptoms
remain severe with other therapies
AHA Newer
Heart
FailureStaging A-D
Stage D
Presence of advanced symptoms, after
assuring optimized medical care
All therapies under Stages A, B and C + evaluation
for:
•Cardiac transplantation
•Ventricular assist devices
•Surgical options
•Research therapies
•Continuous intravenous inotropic infusions
•End-of-life care
Heart Failure
Risk Factors
• Primary risk factors
– Coronary artery disease (CAD) (MI)
– Advancing age
• Contributing risk factors
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–
–
–
–
–
–
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Hypertension
Diabetes
Tobacco use
Obesity
High serum cholesterol
African American descent
Valvular heart disease
Hypervolemia
Which of the following are risk
factors for Heart Failure
1. Hypertension
2. Myocardial
Infarction
3. Diabetes
4. Valvular Disease
Classifications
• Systolic versus diastolic
– Systolic- loss of contractility get dec. CO
– Diastolic- decreased filling or preload
• Left-sided versus right –sided
– Left- lungs
– Right-peripheral
• High output- hypermetabolic state- pregnancy
• Acute versus chronic
– Acute- MI
– Chronic-cardiomyopathy
Symptoms
Left Ventricular Failure
• Signs and symptoms
–
–
–
–
–
dyspnea
orthopnea PND
fatigue
Anxiety
rales
– NOTE L FOR LEFT AND L FOR LUNGS
Which of the following is associated
with left sided failure?
1.
2.
3.
4.
crackles
hypoxemia
tachypnea
Peripheral edema
???????
• WHY DOES THIS OCCUR?
ADHF-Clinical Manifestations
• Acute decompensated heart failure (ADHF)
• When PA WEDGE pressure is approx 30mmHg
Physical findings (like ARDS) pulmonary edema
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•
•
•
•
•
•
Orthopnea, dyspnea, tachypnea
Crackles, wheezes, rhonchi
Use of accessory muscles
Cool and clammy skin
Hypoxemia, Cyanosis
4.s3 gallop The Auscultation Assistant - Rubs and Gallops
*Cough with frothy, blood-tinged sputum-why??? (later
sign)
Person literally drowning in
secretions
Immediate Action Needed
Goals of Treatment for ADHF
• MAD DOG
• Improve gas exchange (much like ARDS)
–
–
–
–
O2
intubate
elevate HOB
BIPAP
Right Heart Failure
• Signs and Symptoms
– fatigue, weakness, lethargy
– wt. gain, inc. abd. girth, anorexia,RUQ
pain
– elevated neck veins
– Hepatomegaly +HJR
– may not see signs of LVF- why??
Can Have RVF Without LVF
• What is this called and what causes it?
Cor Pulmonale
“Blue
Bloater”
This results from
pulmonary
hypertension.
How does this affect
afterload?
Heart Failure- Complications
• Pleural effusion
• Dysrhythmias-Atrial fibrillation (most
common dysrhythmia)
– **High risk of fatal dysrhythmias (e.g., sudden
cardiac death, ventricular tachycardia) with HF
and an EF <35% (Use of ICDs and CRT)
– Loss of the atrial contraction (kick) can reduce
CO by 20%
– Promotes thrombus/embolus formation
increasing risk for stroke
Heart Failure- Complications Cont.
• Hepatomegaly
– Fibrosis and cirrhosis can develop over time
– can store 10 L
• Renal insufficiency or failure
• Cardiogenic shock
• Why and what would you monitor?
Heart Failure
Diagnostic Studies
• Primary goal is to determine underlying
cause
–
–
–
–
History and physical examination( dyspnea)
Chest x-ray
12 lead ECG
Lab studies (e.g., cardiac enzymes, BNP)
electrolytes, CBC, liver function tests, PT/INR
– EF
Heart Failure
Diagnostic Studies
– Hemodynamic assessment-Hemodynamic
Monitoring-CVP- (right side) and SG(left and
right side)
– Echocardiogram-TEE best (EF) also have TTE
– Stress testing- exercise or medicine
– Cardiac catheterization- determine heart
pressures ( inc.PAW )
Nursing Assessment
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•
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•
•
•
•
Vital signs
PA readings
Urine output
---------------------------------------------------------------
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
Listen to BS frequently
Knowledge deficit
•
•
•
•
•
Low Na diet
Fluid restriction
Daily weight
When to call Dr.
Medications
3 Main Goals- in acute as well as
chronic HF
• Decrease preload
• Decrease afterload
• Increase contractility
How to Achieve Goals
• Decrease preload by :
– Dec. intravascular volume-diuretics, natrecor
– Dec venous return
• Fowlers
• MSO4 and Ntg
• Decrease afterload–
–
–
–
–
ACE (pril or ril),
ARB (sartans),
Vasodilators,
beta blockers (al or ol)
BiDil (combination drug containing isosorbide dinitrate
and hydralazine) approved only for the treatment of HF
in African Americans
Increase Contractility
• 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,
dobutamine)
– Phosphodiesterase inhibitors (e.g., milrinone)
– Question use of calcium channel blockers
– New calcium sensitizer-(levosimendan)
– CRT
Other
• Balance supply and demand of oxygen
– Inc. O2- O2, intubate, HOB up,Legs down,
mech vent with PEEP
– Dec. demand-beta blockers, rest, dec B/P
Manage symptoms
Collaborative Care:
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•
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•
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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
Heart Failure- Chronic
• Overall long term 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
PATIENT TEACHING
Joint Commission has mandated 6
areas of discharge teaching
Discharge Teaching
6 areas
•
•
•
•
•
•
Weight Monitoring
Medications
Activity
Diet
What to do if symptoms worsen
Follow-up
Weight Monitoring
• Weight reduction recommendations must be
individualized and culturally sensitive
• Same scale every day at same time
• Preferably in the morning after voiding
• Report weight gain of 3 or more pounds in
two days or 3-5 or more in 1 week.
Activity
• Instruct patient in energy-conserving and energyefficient behaviors
• Improves symptoms but often not prescribed
• Cardiac Rehab program
• Goal is 150 minutes per week
• Walking, biking, swimming or a combo is
recommended
• Nutritional therapy
Diet
– Diet and weight reduction recommendations must be
individualized and culturally sensitive
– Dietary Approaches to Stop Hypertension (DASH) diet
is recommended
• Avoid fats such as butter and margarine
• Avoid fried foods
• Read labels for hidden sodium
– Sodium is usually restricted to 2.5 g per day
• Avoid any food with more than 400mg of sodium
– Alcohol- limit women 1 drink, men 2 drinks
– Fluid restriction may or may not be required
Medications
– Medications (lifelong) diuretics, vasodilators, positive
inotropics
• Diuretics- loop, thiazides, spirinolactone (aldactone)
• Vasodilators- Ntg,
• Postive inotropics- digoxin
– Taking pulse rate
• Know when drugs (e.g., digitalis, -adrenergic
blockers) should be withheld and reported to health
care provider
• Home BP monitoring
– Signs of hypo- and hyperkalemia if taking diuretics that
deplete or spare potassium
Drug Therapy:
Diuretics:
– PO or IV, loop - _____________
– PO, potassium sparing - _____________
– When extra diuresis necessary –
Metolazone (Zaroxolyn) or Bumex
– reduce preload
• Ace-Inhibitors:
–
–
–
–
–
–
Name some: ______________
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
• Name some: _____________
• directly dilate vessels, decrease preload, vasodilate coronary arteries.
– Nitroprusside (Nipride)- reduces preload and afterload
– Nesiritide (Natrecor)- arterial and venous dilation
B- Blockers:
– Name some:__________________
• 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
– Monitor which electrolyte?
– Reduces symptoms, but not shown to prolong life
– Dopamine
Dobutamine
Milrinone (Primacor)
Angiotensin II Receptor Blockers (ARBs):
– Name some: ______________
– Mostly for patients unable to tolerate ACE Inhibitors
– Similar effects to Ace Inhibitors
Isosorbide dinitrate and hydralazine (BiDil):
– for African Americans with HF
When to call Dr.
• Symptoms worsen
–
–
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–
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Shortness of breath
Edema
Weight gain
Side effects of medications
Chest pain
4 Core Measures for Heart
Failure
• Discharge instructions- weight, activity,
medications, follow up and when to call dr.
• LV function is documented (EF)
• If EF less than 40% on ACE or ARB
• Smoking Cessation
Follow-up
• Frequent follow-up with physician
• Heart Failure Clinics
• Home health care may be needed
– Monitor symptoms
– Effects of medications and side effects
– Blood draws for potassium
• Other
– Stop smoking
– Flu and pneumonia vaccines
– Refer to local support group
Chronic HF- Devices to increase CO
• Ways to achieve goals: (inc. CO)
– CRT
– Intraaortic balloon pump (IABP) therapy
– Ventricular assist devices (VADs)
• Destination therapy—permanent, implantable VAD
Artificial Heart
Cardiomyoplasty-wrap latissimus dorsi around
heart
Ventricular reduction surgery-ventricular wall is
resected
CRT-Cardiac Resynchronization
Therapy
1.Utilizes biventricular pacing
2.Coordinates right and left
ventricle contractility
3.Normal electrical
conduction increases CO
4.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)
• Provides temporary circulatory assistance
Used
for
cardiac
shock
–
–Allows heart to rest
– ↓ Afterload
– Augments aortic diastolic
pressure
• Outcomes
– Improved coronary blood flow
– Improved perfusion of vital organs
YouTube - IABP Intraaortic Ballon Pump
Ventricular Assist Devices (VADs)
• Indications for VAD therapy
– Patients with New York Heart Association
Classification IV who have failed medical
therapy
– Bridge to transplant
– Destination therapy
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
https://www.youtube.com/watch?v=alTp5_p-dmA
• 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)
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 46 hour maximum time limit
Who receives a heart?
• Absolute indications
–
–
–
–
Cardiogenic shock
On IV inotropes (dobutamine)
Severe cardiac ischemia –not treatable
Life threatening dysrhythmias- VT
Cardiac Transplantation
Nursing Management
• Treatment of choice for patients with refractory end-stage
HF, inoperable CAD and cardiomyopathy
• 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
– The overall waiting period for a transplant is long, and
many patients die while waiting for a transplant
– Goal of the transplant evaluation process is to identify
patients who would most benefit from a new heart
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
• 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%
• 3 year survival rate is 79%
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
• Peripheral blood T lymphocyte monitoring to
assess the recipient’s immune status
• Care focuses on
–
–
–
–
Promoting patient adaptation to the transplant process
Monitoring cardiac function
Managing lifestyle changes
Providing relevant teaching
Blackboard Learning System™ (Release 6)
CHF case 4
Congestive Heart Failure:
Overview
Practice Game
http://www.quia.com/cb/107511.html
Angiotensin-converting enzyme inhibitors ,
such as captopril and enalapril, block the
conversion of angiotensin I to angiotensin II, a
vasoconstrictor that can raise BP. These drugs
alleviate heart failure symptoms by causing
vasodilation and decreasing myocardial workload.
Beta-adrenergic blockers , such as bisoprolol,
metoprolol, and carvedilol, reduce heart rate,
peripheral vasoconstriction, and myocardial
ischemia.
Diuretics prompt the kidneys to excrete sodium,
chloride, and water, reducing fluid volume. Loop
diuretics such as furosemide, bumetanide, and
torsemide are the preferred first-line diuretics
because of their efficacy in patients with and
without renal impairment. Low-dose
spironolactone may be added to a patient's
regimen if he has recent or recurrent symptoms
at rest despite therapy with ACE inhibitors, betablockers, digoxin, and diuretics.
Digoxin increases the heart's ability to contract
and improves heart failure symptoms and
exercise tolerance in patients with mild to
moderate heart failure.
Other drug options include nesiritide
(Natrecor), a preparation of human BNP that
mimics the action of endogenous BNP, causing
diuresis and vasodilation, reducing BP, and
improving cardiac output.
Intravenous (I.V.) positive inotropes such
as dobutamine, dopamine, and milrinone, as
well as vasodilators such as nitroglycerin or
nitroprusside, are used for patients who
continue to have heart failure symptoms
despite oral medications. Although these drugs
act in different ways, all are given to try to
improve cardiac function and promote diuresis
and clinical stability.