Heart Failure
Heart Failure(progression)
CDHF(Pulmonary Edema) Severe End Stage
Mild
Mild
Control
With
Drugs
Cardiogenic shock
Cardiomyopathy
Irreversible
Needs new ventricle
Emergency-Upright, O2, morphine, etc
Diet
Fluid
Restriction
VAD
IABP
Heart Transplant
Heart Failure- Clinical syndrome
can result from any structural or
functional cardiac disorder that
impairs ability of ventricle to fill with
or eject blood
Impact!
Heart Failure
open !
Click to
5 million Americans- have heart
failure
500,000 new cases every year
25-50 billion dollars a year to
care for people with HF
6,500,000 hospital days / year and
300,000 deaths/year
Definition-Heart Failure (HF)
Key Concepts
CO = SV x HR-becomes insufficient to
meet metabolic needs of body
SV- determined by preload, afterload
and myocardial contractility
EF< 40% (need to understand)
*Classifications HF
Systolic failure- dec. contractility
Diastolic failure- dec. filling
Mixed
90/140= 64% EF- 55-65 (75)
normal
Keys to understanding HF
All organs (liver, lungs, legs, etc.) return blood to heart
When heart begins to fail/ weaken> unable to pump blood forward-fluid backs up >
Inc. pressure within all organs.
Organ response
LUNGS: congested > stiffer , inc effort to breathe; fluid starts to escape into alveoli; fluid
interferes with O2 exchange, aggravates shortness of breath.
Shortness of breath during exertion, may be early symptoms > progresses > later require
extra pillows at night to breathe > experience "P.N.D." or paroxysmal nocturnal dyspnea .
Pulmonary edema
Legs, ankles, feet- blood from feet and legs > back-up of fluid and pressure in these areas,
heart unable to pump blood as promptly as received > inc. fluid within feet and legs
causes fluid to "seep" out of blood vessels ; inc. weight
Heart Failure
Heart Failure (ADHF)Pneumonic
(emergency mgt >recall for later!)
U Upright Position
N Nitrates
L Lasix
O Oxygen
A ACE, ARBs, Amiodorone
D Dig, Dobutamine
M Morphine Sulfate
E Extremities Down
Heart Failure
Click here for Online Lecture
(Interactive)
or
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Heart Failure
Etiology and Pathophysiology
Systolic failure- most common cause
Hallmark finding: Dec. in *left ventricular
ejection fraction (EF)
Due to
Impaired contractile function (e.g., MI)
Increased afterload (e.g., hypertension)
Cardiomyopathy
Mechanical abnormalities (e.g., valve
disease)
Heart Failure
Etiology and Pathophysiology
Diastolic failure
Impaired ability of ventricles to relax
and fill during diastole > dec. stroke
volume and CO
Diagnosis based on presence of
pulmonary congestion,
pulmonary hypertension, ventricular
hypertrophy
*normal ejection fraction (EF)Know why!
Heart Failure
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)
Factors effecting heart
pump effectiveness
Preload
Volume of blood in ventricles at end
diastole
Depends on venous return
Depends on compliance
Afterload
Force needed to eject blood into circulation
Arterial B/P, pulmonary artery pressure
Valvular disease increases afterload
Cardiomegaly/ventricular remodeling occurs as heart overworked> changes in size, shape, and function
of heart after injury to left ventricle. Injury due to acute myocardial infarction or due to causes that inc.
pressure or volume overload as in Heart failure
American Heart Assn-Media
files Animations
Heart Failure
(AKA-congestive heart failure)
Pathophysiology
A. Cardiac compensatory mechanisms
1.tachycardia
2.ventricular dilation-Starlings law
3.myocardial hypertrophy
Hypoxia leads to dec. contractility
Pathophysiology-Summary
B. Homeostatic Compensatory mechanisms
Sympathetic Nervous System-(beta blockers block this)
1. Vascular system- norepinephrine- vasoconstriction
(What effect on afterload?)
2. Kidneys
A. Dec. CO and B/P > renin angiotensin release. (ACE)
B. Aldosterone release > Na and H2O retention
3. Liver- stores venous volume (ascites, +HJR,
Hepatomegaly- can store 10 L. check enzymes
Counter-regulatory Inc. Na > release of ADH (diuretics)
*Release of atrial natriuretic factor > Na and H20
excretion, prevents severe cardiac decompensation
What is BNP? What drug is synthetic form BNP?
Heart Failure
Etiology and Pathophysiology
Compensatory mechanismsactivated to maintain adequate CO
Neurohormonal responses: Endothelin
-stimulated by ADH, catecholamines, and
angiotensin II >
Arterial vasoconstriction
Inc. in cardiac contractility
Hypertrophy
Heart Failure
Etiology and Pathophysiology
Compensatory mechanisms- activated to
maintain adequate CO
Neurohormonal responses:
Proinflammatory cytokines (e.g., tumor necrosis
factor)
Released by cardiac myocytes in response to
cardiac injury
Depress cardiac function >
cardiac hypertrophy, contractile
dysfunction, and myocyte cell death
Heart Failure
Etiology and Pathophysiology
Compensatory mechanismsactivated to maintain adequate CO
Neurohormonal responses: Over time >
systemic inflammatory response >
results
Cardiac wasting
Muscle myopathy
Fatigue
Heart Failure
Etiology and Pathophysiology
**Counter regulatory processes
Natriuretic peptides: atrial natriuretic
peptide (ANP) and b-type natriuretic peptide
(BNP)- *also dx test for HF
Released in response to inc. in atrial volume
and ventricular pressure
Promote venous and arterial vasodilation,
reduce preload and afterload
Prolonged HF > depletion of these factors
Heart Failure
Etiology and Pathophysiology
Counter regulatory processes
Natriuretic peptides- endothelin and
aldosterone antagonists
Enhance diuresis
Block effects of the RAAS
Natriuretic peptides- inhibit
development of cardiac
hypertrophy; may have
antiinflammatory effects
Result of
Compensato
ry
Mechanisms
>
Heart Failure
Heart Failure E
xplained
PathophysiologyStructural Changes with HF
Dec. contractility
Inc. preload (volume)
Inc. afterload (resistance)
**Ventricular remodeling (ACE inhibitors
can prevent this)
Ventricular hypertrophy
Ventricular dilation
Ventricular remodeling
END RESULT
FLUID OVERLOAD > Acute Decompensated
Heart Failure (ADHF)/Pulmonary Edema
>Medical
Emergency!
Heart Failure
Classification Systems
New York Heart Association
Functional Classification of HF
Classes I to IV
ACC/AHA Stages of HF (newer)
Stages A to D
ACC/AHA Stages
NY ASSN Funct Class
Therapies
Stage A
At high risk for developing heart failure.
Includes people with:
Hypertension
Diabetes mellitus
CAD (including heart attack)
History of cardiotoxic drug therapy
History of alcohol abuse
History of rheumatic fever
Family history of CMP
Exercise regularly
Quit smoking
Treat hypertension
Treat lipid disorders
Discourage alcohol or illicit drug
use
If previous heart attack/ current
diabetes mellitus or HTN, use ACEI
Stage B
Those diagnosed with systolic heart
failure- have never had symptoms of
heart failure (usually by finding an ejection
fraction of less than 40% on
echocardiogram
Care measures in Stage A +
Should be on ACE-I
Add beta -blockers
Surgical consultation for coronary
artery revascularization and valve
repair/replacement (as appropriate
Stage C
Patients with known heart failure with
current or prior symptoms.
Symptoms include: SOB, fatigue
Reduced exercise intolerance
All care measures from Stage A apply,
ACE-I and beta-blockers should be used
+ Diuretics, Digoxin,
Dietary sodium restriction
Weight monitoring, Fluid restriction
Withdrawal drugs that worsen
condition
Maybe Spironolactone therapy
Stage D
Presence of advanced symptoms, after
assuring optimized medical care
All therapies -Stages A, B and C +
evaluation for:Cardiac transplantation,
VADs, surgical options, research
therapies, Continuous intravenous
inotropic infusions/ End-of-life care
Heart Failure
Etiology and Pathophysiology
Primary risk factors
Coronary artery disease (CAD)
Advancing age
Contributing risk factors
Hypertension
Diabetes
Tobacco use
Obesity
High serum cholesterol
African American descent
Valvular heart disease
Hypervolemia
CHF-due to
1. Impaired cardiac function
Coronary heart disease
Cardiomyopathies
Rheumatic fever
Endocarditis
2. Increased cardiac workload
Hypertension
Valvular disorders
Anemias
Congenital heart defects
3.Acute non-cardiac conditions
Volume overload
Hyperthyroid, Fever,infection
Classifications- (how to describe)
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
Acute versus chronic
Acute- MI
Chronic-cardiomyopathy
Symptoms
Left Ventricular Failure
Signs and symptoms
dyspnea
orthopnea PND
Cheyne Stokes
fatigue
Anxiety
rales
NOTE L FOR LEFT AND L FOR LUNGS
Why does this occur??
Heart Failure
Clinical Manifestations
Acute decompensated heart failure
(ADHF)
> Pulmonary edema, often lifethreatening
Early
Increase in the respiratory rate
Decrease in PaO2
Later
Tachypnea
Respiratory acidemia
Heart Failure
Clinical Manifestations
Acute decompensated
heart failure (ADHF)
Physical findings
*Cough with frothy,
Physical findings
blood-tinged sputum Orthopnea
why??? > (see next
Dyspnea, tachypnea
slide)
Use of accessory
Breath sounds:
muscles
Crackles, wheezes,
rhonchi
Cyanosis
Cool and clammy skin Tachycardia
Hypotension or
hypertension
Complete Case study of Heart Failure in Lewis online resour
Acute Decompensated Heart Failur
e (ADHF) Pulmonary Edema
As the intracapillary pressure increases, normally
impermeable (tight) junctions between the alveolar cells
open, permitting alveolar flooding to occur.
Pulmonary edema begins with an
increased filtration through the loose
junctions of the pulmonary capillaries .
ADHF/Pulmonary Edema
(advanced L side HF)
When PA WEDGE pressure is approx
30mmHg
Signs and symptoms
1.wheezing
2.pallor, cyanosis
3.Inc. HR and BP
4.s3 gallop
The Auscultation Assistant - Rubs and
Gallops
5.rales,copious pink, frothy
sputum
Person literally drowning in
secretions
Immediate Action Needed
Goals of Treatment-ADHF/Pulmonary Edema)
MAD DOG
Improve gas exchange
Start O2/elevate HOB/intubate
Morphine dec anxiety/afterload
A- (airway/head up/legs down)
D- (Drugs) Dig not first now- but drugs as
IV nitroglycerin; IV Nipride, Natrecor
D- Diuretics
O- oxygen /measure sats;
Hemodynamics, careful observation
G- blood gases
Think physiology
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
What does this
show?
What is present in this extremity, common to right sided HF?
Can You Have RVF Without LVF?
What is this called?
COR PULMONALE
Heart Failure
Complications
Pleural effusion
Atrial fibrillation (most common
dysrhythmia)
Loss of atrial contraction (kick)
-reduce CO by 10% to 20%
Promotes thrombus/embolus
formation inc. risk for stroke
Treatment may include cardioversion,
antidysrhythmics, and/or
anticoagulants
Heart Failure
Complications
**High risk of fatal dysrhythmias (e.g.,
sudden cardiac death, ventricular
tachycardia) with HF and an EF <35%
HF lead to severe hepatomegaly,
especially with RV failure
Fibrosis and cirrhosis - develop over time
Renal insufficiency or failure
Heart Failure
Diagnostic Studies
Primary goal- determine underlying
cause
History and physical
examination( dyspnea)
Chest x-ray
ECG
Lab studies (e.g., cardiac enzymes,
BNP- (beta natriuretic peptide- normal
value less than 100) electrolytes
EF
Heart Failure
Diagnostic Studies
Primary goal- determine underlying
cause
Hemodynamic assessment-Hemodynamic
Monitoring-CVP- (right side) and Swan Ganz
(left and right side)
Echocardiogram-TEE best
Stress testing- exercise or medicine
Cardiac catheterization- determine
heart pressures ( inc.PAW )
Ejection fraction (EF)
Transesophage
al
echocardiogra
m
TEE
But
Nursing Assessment
Vital signs
PA readings
Urine output
-What else!!
Chronic HF
Nursing Management
Nursing diagnoses
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
Chronic HF
Nursing Management
Planning: Overall Goals
Decrease in symptoms (e.g.,
shortness of breath, fatigue)
Decrease in peripheral edema
Increase in exercise tolerance
Compliance with the medical regimen
No complications related to HF
How to Achieve Goals
Decrease preload
Dec. intravascular volume
Dec venous return i.e.
Fowlers
MSO4 and Ntg
Decrease afterload
Inc. cardiac performance(contractility)
CRT (cardiac resynchronization therapy)
Balance supply and demand of oxygen
Inc. O2- O2, intubate, HOB up, legs down, mech
vent with PEEP (if ADHF/PE)
Dec. demand- use beta blockers, rest, dec B/P
Manage symptoms
Chronic HF
Nursing Management
Health Promotion
Treatment or control of underlying
heart disease key to preventing HF
and episodes of ADHF (e.g., valve
replacement, control of hypertension)
Antidysrhythmic agents or
pacemakers for patients with serious
dysrhythmias or conduction
disturbances
Flu and pneumonia vaccinations
Chronic HF
Nursing Management
Health Promotion
Treatment or control of underlying
heart disease key to preventing HF
and episodes of ADHF (e.g., valve
replacement, control of hypertension)
Antidysrhythmic agents or
pacemakers for patients with serious
dysrhythmias or conduction
disturbances
Flu and pneumonia vaccinations
Chronic HF
Nursing Management
Health Promotion
Patient teaching: medications, diet,
and exercise regimens
Exercise training (e.g., cardiac
rehabilitation) improves symptoms but
often underprescribed
Home nursing care for follow-up and
to monitor patients response to
treatment may be required
Heart Failure
Nursing and Collaborative Management
Overall goals- to therapy for ADHF &
chronic HF
Dec. patient symptoms
Improve LV function
Reverse ventricular remodeling
Improve quality of life
Dec. mortality and morbidity
ADHF
Nursing and Collaborative Management
Improve cardiac function
For patients who do not respond to conventional
pharmacotherapy - (e.g.- O2, even intubate,
high Fowlers, diuretics, vasodilators, morphine
sulfate)
Inotropic therapy
Digitalis
-Adrenergic agonists (e.g., dopamine)
Phosphodiesterase inhibitors (e.g.,
milrinone)
Caution re- calcium channel blockersdec. contractility- only amilodopine
(Norvasc) approved even in mild heart
failure)
Chronic HF
Collaborative Management
Main treatment goals
Treat underlying cause & 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 HF
Collaborative Management
O2 (non-rebreather if emergency);
morphine, diuretics, etc-dec
preload, afterload
Physical and emotional rest
Nonpharmacologic therapies
Cardiac resynchronization therapy
(CRT) or biventricular pacing
Cardiac transplantation
CRT-Cardiac Resynchronization
Therapy
HOW IT WORKS:
Standard implanted pacemakers equipped with two wires (or
"leads") conduct pacing signals to
specific regions of heart (usually
at positions A and C). Biventricular
pacing devices have added a third
lead (to position B) that is
designed to conduct signals
directly into the left ventricle.
Combination of all three lead >
synchronized pumping of
ventricles, inc. efficiency of each
beat and pumping more blood on
the whole.
Chronic HF
Collaborative Management
Therapeutic objectives for drug
therapy
Identification of type of HF &
underlying causes
Correction of Na & H2O retention and
volume overload
Reduction of cardiac workload
Improvement of myocardial
contractility
Control of precipitating and
complicating factors
Chronic HF-Collaborative Management
Drug therapy
Diuretics
Thiazide
Loop
Spironolacton
e
Vasodilators
ACE inhibitors- pril
or ril *first line
heart failure
Angiotensin II
receptor blockers
Nitrates
-Adrenergic
blockers- al or ol
NesiritideNatrecor (BNP)
Chronic HF
Collaborative Management
Drug therapy (contd)
Positive inotropic agents
Digitalis
Calcium sensitizers- (Levosimendan)
new under research; cardioprotective, inc.
cardiac contractility
BiDil (combination drug containing
isosorbide dinitrate and hydralazine)
approved only for the treatment of HF
in African Americans
Chronic HF
Collaborative Management
Nutritional therapy
Diet/weight reduction
recommendations-individualized and
culturally sensitive
Dietary Approaches to Stop
Hypertension (DASH) diet
recommended
Sodium- usually restricted to 2.5 g
per day
Potassium encouraged unless on K
sparing diuretics (Aldactone)
Chronic HF
Collaborative Management
Nutritional therapy
Fluid restriction may or may not be
required
Daily weights important
Same time, same clothing each day
*Weight gain of 3 lb (1.4 kg) over 2
days or a 3- to 5-lb (2.3 kg) gain over
a week-report to health care provider
Chronic HF-End Stage >ADHF
Collaborative Management
Nonpharmacologic therapies (contd)
Intraaortic balloon pump (IABP) therapy
Used for cardiogenic shock
Allows heart to rest
Ventricular assist devices (VADs)
Takes over pumping for the ventricles
Used as a bridge to transplant
Destination therapy-permanent, implantable
VAD
Cardiomyoplasty- wrap latissimus dorsi around heart
Ventricular reduction -ventricular wall resected
Transplant/Artificial Heart
Intraaortic Balloon Pump (IABP)
Provides temporary circulatory assistance
Afterload
Augments aortic diastolic pressure
Outcomes
Improved coronary blood flow
Improved perfusion of vital organs
Intraaortic balloon pump
IABP Machine
Enhanced External
Counterpulsation-EECP
The Cardiology Group, P.A.
Pumps during diastoleincreasing O2 supply to
coronary arteries. Like
IABP but not invasive.
Ventricular
Assist
Devices
Ventricular Assist Devices
(VADs)
(VADs)
Indications for VAD therapy
Extension of cardiopulmonary bypass
Failure to wean
Postcardiotomy cardiogenic shock
Bridge to recovery or cardiac
transplantation
Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Patients with New York Heart Association
Classification IV who have failed medical therapy
Patient Teaching-Cleveland Clinic for Heart Fai
lure LVAD devices
Schematic Diagram of Left VAD
Left ventricular assist d
evice
HeartMate II
The HeartMate II -one of several new LVAD devices- designed to last longer with simplicity
of only one moving part; also much lighter and quieter than its predecessors; major
differences is rotary action which creates a constant flow of blood, not pumping action.
Cardiomyoplasty technique: left latissimus dorsi muscle
(LDM) transposed into chest through a window created by
resecting the anterior segment of 2nd rib (5 cm). LDM is
then wrapped around both ventricles. Sensing and pacing
electrodes are connected to an implantable cardiomyostimulator
Left Ventricular reduction Surg
ery-Bautista
procedureindicated in some
cases
Click here for UTube
Artificial Heart animination!
Cardiac Transplantation
Nursing Management
Treatment of choice for patients with
refractory end-stage HF, inoperable CAD
and cardiomyopathy
Goal of transplant evaluation process identify patients who would most
benefit from a new heart
Cardiac Transplantation
Nursing Management
Transplant candidates- placed on a list
Stable patients wait at home and
receive ongoing medical care
Unstable patients -may require
hospitalization for more intensive
therapy
Overall waiting period for a transplant
is long; many patients die while
waiting for a transplant
Cardiac Transplantation
Nursing Management
Surgery involves removing recipients
heart, except for posterior right and left
atrial walls and their venous connections
Recipients heart replaced with donor
heart
Donor sinoatrial (SA) node is preserved
so that a sinus rhythm may be
achieved postoperatively
**Immunosuppressive therapy
usually begins in operating room
Click here to Perform a Heart
Transplant(
your patient with end stage
heart failure may require this!)
Cardiac Transplantation
Nursing Management
Infection- primary complication
followed by acute rejection in first year
post transplantation
After first year, malignancy (especially
lymphoma) and coronary artery
vasculopathy = major causes of death
Cardiac Transplantation
Nursing Management
Endomyocardial biopsies -obtained from
right ventricle weekly for first month,
monthly for following 6 months, and then
yearly to detect rejection
Heartsbreath test is used along with
endomyocardial biopsy to assess organ rejection
Peripheral blood T lymphocyte
monitoring- assess recipients immune status
Care focuses:
Promoting patient adaptation to transplant
process
Monitoring cardiac function & lifestyle changes
Providing relevant teaching
PATIENT TEACHING
Chronic HF
Nursing Management
Implementation: Patient education
Medications (lifelong)
Taking pulse rate
Know when drugs (e.g., digitalis, adrenergic blockers) should be
withheld and reported to health
care provider
Chronic HF
Nursing Management
Acute Intervention
HF -progressive diseasetreatment
plans
established with quality-oflife goals
Symptom management controlled
with self-management tools (e.g.,
daily weights)
Salt -restricted
Energy- conserved
Support systems - essential to success
of entire treatment plan
Chronic HF- Nursing
Management
Ambulatory and Home Care
Explain physiologic changes that have
occurred
Assist patient to adapt to physiologic and
psychologic changes
Integrate patient and patients family or
support system in overall care plan
Implementation: Patient Education
Home BP monitoring
Signs of hypo- and hyperkalemia if taking
diuretics that deplete or spare potassium
Instruct in energy-conserving and energyefficient behaviors
