Heart Failure

• Characterized by •Not a disease but a

Heart Failure “syndrome.”
– Ventricular dysfunction
•Associated with long-
The most common reason for
– Reduced exercise
hospitalization in adults >65 standing hypertension,
years old! tolerance coronary artery disease
– Diminished quality of life (CAD), and myocardial
•An abnormal condition involving impaired cardiac pumping/filling infarction (MI)
– Shortened life expectancy
•Heart is unable to produce an adequate cardiac output (CO) to meet
metabolic needs

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Etiology and Pathophysiology Heart Failure

Etiology and Pathophysiology
• Causes of HF may be divided into two
subgroups: • Systolic failure- most common cause
– Hallmark finding: Dec. in *left ventricular ejection
– Primary fraction (EF)
• Due to
– Precipitating – Impaired contractile function (e.g., MI)
– Increased afterload (e.g., hypertension)
• HF is classified as systolic or diastolic – Cardiomyopathy
failure (or dysfunction). – Mechanical abnormalities (e.g., valve disease)

Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.

Heart Failure Heart Failure

Etiology and Pathophysiology Etiology and Pathophysiology
• Diastolic failure
– Impaired ability of ventricles to relax and fill • Mixed systolic and diastolic failure
during diastole > dec. stroke volume and CO – Seen in disease states such as dilated
cardiomyopathy (DCM)
– Diagnosis based on presence of pulmonary – Poor EFs (<35%)
congestion, pulmonary hypertension, – High pulmonary pressures
ventricular hypertrophy • Biventricular failure (both ventricles may
– *normal ejection fraction (EF)- Know why! be dilated and have poor filling and
emptying capacity)
 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
90/140= 64% EF- 55-65 (75)
– Diastolic failure- dec. filling normalClick for animated EF

– Mixed Quick-what is EF?

Heart Failure- Heart Failure

(progression) Cardiogenic shock
Cardiomyopathy
Click here for Online Lecture
Mild
Mild CDHF(Pulmonary Edema) Severe End Stage (Interactive)
Irreversible or
Control
With Needs new ventricle Click here for Online Lecture (Read)
Drugs Emergency-Upright, O2, morphine, etc
Diet
VAD
Fluid IABP
Restriction Heart Transplant

Heart Failure
•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
Click here for Online Lecture (Interactive)
•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 *Use these links to supplement learning
and legs causes fluid to "seep" out of blood vessels ; inc. weight
Click here for Online Lecture (Read)
 Factors effecting
heart pump
Heart Failure -congestive heart failure)
effectiveness Preload
• Pathophysiology-Compensatory mechanisms
• Volume of blood in ventricles at end • Sympathetic nervous system (SNS)
diastole – 1.Inc heart rate-tachycardia
• Depends on venous return – 2.Inc myocardial contractility>ventricular dilation
• Depends on compliance – 3. Peripheral vasoconstriction
Afterload – 3.Myocardial hypertrophy
• Hypoxia >dec. contractility
•Force needed to eject blood into circulation
•Arterial B/P, pulmonary artery pressure
•Valvular disease increases afterload American Heart Assn-Media files Animations

Heart Failure- Etiology and Pathophysiology

Heart Failure
Etiology and Pathophysiology
• Compensatory mechanisms- activated to
maintain adequate CO
– Neurohormonal responses:
• Renin converts angiotensinogen to angiotensin 1
• Angiogensin I converted to angiotensinI I - converting
enzyme made in lungs > adrenal cortex to release
aldosterone (Na and H2O retention) > Inc peripheral
vasoconstriction > Inc BP (RAAS)
• Low CO > dec. cerebral perfusion > ADH secreted > inc
H2O in renal tubules > H2) retention & blood volume
– contractile dysfunction, and myocyte cell death
• Compensatory mechanisms- activated to maintain
adequate CO
– Neurohormonal responses:
• Endothelin stimulated by ADH, catecholamines, and angiotensin II,
causing
– Arterial vasoconstriction
– Increase cardiac contractility
– Hypertrophy
– Proinflammatory cytokines (e.g., tumor necrosis factor)
• Released by cardiac myocytes in response to cardiac
injury
• Depress cardiac function > cardiac hypertrophy,

Heart Failure Etiology and Pathophysiology Dilated & Hypertrophied Heart

Chambers
• Consequences of compensatory mechanisms
– Dilation-enlargement of chambers of heart that occurs when
pressure in left ventricle is elevated; Initially adaptive
mechanism
• Eventually mechanism inadequate> CO dec.
– Hypertrophy -inc in muscle mass & cardiac wall thickness in
response to chronic dilation, resulting
• poor contractility>inc O2 needs>poor coronary artery
circulation>risk for ventricular dysrhythmias

Fig. 35-1. A, Dilated heart chambers. B, Hypertrophied heart chambers.

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Elsevier Inc.
 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

Pathophysiology-
Heart Failure- Etiology and Pathophysiology
Structural Changes with HF
• Counter regulatory processes • Dec. contractility
– Natriuretic peptides- endothelin and aldosterone
antagonists • Inc. preload (volume)
• Enhance diuresis ;Block effects of RAAS • Inc. afterload (resistance)
– Natriuretic peptides- inhibit development of cardiac
hypertrophy; may have antiinflammatory effects • **Ventricular remodeling (ACE inhibitors
– Nitric oxide (NO) can prevent this)
• Released from vascular endothelium in response to – Ventricular hypertrophy
compensatory mechanisms
– Ventricular dilation
• Relaxes arterial smooth muscle >resulting in
vasodilation and decreased afterload.

Pathophysiology-Questions??
• Homeostatic Compensatory mechanisms
Result of
Compensator • Sympathetic Nervous System-(beta blockers effect?)
y – 1. Vascular system- norepinephrine- vasoconstriction
Mechanisms (What effect on afterload?)
> – 2. Kidneys
• A. Dec. CO and B/P > renin angiotensin release. (ACE)
Heart Failure • B. Aldosterone release > Na and H2O retention
Heart Failure – 3. Liver- stores venous volume (ascites, +HJR,
Explained 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?
 Match these medication to their primary effect on preload or
afterload or both or neither
• 1. furosemide
• 2. morphine
• 3 nitroprusside (Nipride)
• 4 digitalis
• 5. nestiritide
• 6. captopril
• 7. metoprolol
1. furosemide (Lasix- loop diuretic – preload)
2. morphine reduces preload and afterload; dilates
pulmonary and systemic blood vessels; used for
ADHF
3. nitroprusside- (Nipride) (ADHF) IV use, potent
, reduces preload and afterload, improves
myocardial contraction, inc CO, dec. pulmonary
congestion,,,only use 48 hrs in IC
4. digitalis-positive inotrope, improves myocardial
contractility, inc myocardial oxygen consumption *
Neither
5. nestiritide- (Natrecor) synthetic BNP- causes
both arterial and venous dilitation; reduces PAWP;
inc CO; neurohormonal blocking agent; dec.
preload and afterload- use only for ADHF
6. captopril- (Capoten)- ACE inhibitor-
neurohormonal blocking agent; dec ventricular
remodeling, inc CO, dec. SVR; promote diuresis;
dec preload & afterload
7. metroprolol-directly block negative effects of
SNS on failing heart as inc HR; No effect on 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
preload, afterload causes that inc. pressure or volume overload as in Heart failure

Left-Sided Heart Failure

Types of Heart Failure
• Left-sided HF (most common) from left
ventricular dysfunction (e.g., MI
hypertension, CAD, cardiomyopathy)
– Backup of blood into left atrium and
pulmonary veins
• Pulmonary congestion
• Edema
Fig. 35-2. Pathophysiology of heart failure. Elevated systemic vascular resistance results in left-sided
heart failure that leads to right-sided heart failure. Systemic vascular resistance and preload are
exacerbated by the renin-angiotensin-aldosterone system. ADH, Antidiuretic hormone; LA, left atrium;
LV, left ventricle; LVEDP, left ventricular end-diastolic pressure; RV, right ventricle.
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Types of Heart Failure Signs/Symptoms HF

• Right-sided HF from left-sided HF, cor
pulmonale, right ventricular MI
– Backup of blood into right atrium and
venous systemic circulation
• Jugular venous distention
• Hepatomegaly, splenomegaly
• Vascular congestion of GI tract
• Peripheral edema
• Fatigue. Weakness, lethargy
• Wt gain, inc abd girth, anorexia,
RUQ pain
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Elsevier Inc.
Can You Have RVF Without LVF? END RESULT
• What is this called? FLUID OVERLOAD > Acute Decompensated Heart
COR PULMONALE Failure (ADHF)/Pulmonary Edema

>Medical
Emergency!

Left Ventricular Failure (ADHF) Heart Failure

• Signs and symptoms *whn PA wedge aprox Clinical Manifestations
30 mm Hg • Acute decompensated heart failure
– Dyspnea- wheezing (ADHF)
– orthopnea PND – > Pulmonary edema, often life-threatening
– Cheyne Stokes • Early
– Fatigue, pallor, cyanosis –Inc in respiratory rate
– Anxiety, inc HR, BP –Dec in PaO2
– S3 gallopThe Auscultation Assistant - Rubs and • Later
Gallops –Tachypnea
– NOTE L FOR LEFT AND L FOR LUNGS –Respiratory acidemia
– Rales,copious pink, frothy sputum

Heart Failure
Clinical Manifestations Pulmonary Edema
• Acute decompensated heart
failure (ADHF)
•Physical findings
• Physical findings •*Cough with frothy,
blood-tinged sputum-
• Orthopnea
why??? > (see next
• Dyspnea, tachypnea slide)
• Use of accessory •Breath sounds:
muscles Crackles, wheezes,
Fig. 35-3. As pulmonary edema progresses, it inhibits oxygen and carbon dioxide exchange at the
• Cyanosis rhonchi alveolar-capillary interface. A, Normal relationship. B, Increased pulmonary capillary hydrostatic pressure

• Cool and clammy skin •Tachycardia causes fluid to move from the vascular space into the pulmonary interstitial space. C, Lymphatic flow
increases in an attempt to pull fluid back into the vascular or lymphatic space. D, Failure of lymphatic flow
•Hypotension or and worsening of left heart failure result in further movement of fluid into the interstitial space and into
the alveoli.
hypertension
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Elsevier Inc.
 Acute Decompensated Heart
Failure (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 Copyright © 2011, 2007 by Mosby, Inc., an affiliate of Elsevier Inc.
filtration through the loose junctions of the
pulmonary capillaries. 38

Clinical Manifestations: Chronic HF Clinical Manifestations: Chronic HF

• Fatigue
• Nocturia
• Dyspnea, orthopnea, paroxysmal nocturnal
dyspnea • Skin
• Persistent, dry cough, unrelieved with position – Dusky, cool, damp to touch
change or over-the-counter cough suppressants • Lower extremities: Shiny and swollen, diminished or
• Tachycardia absent hair growth, pigment changes
• Restlessness, confusion, decreased memory
• Dependent edema • Chest pain (angina)
– Edema may be pitting in nature • Weight changes
– Sudden weight gain of >3 lb (1.4 kg) in 2 days – Anorexia, nausea
Copyright may indicate
© 2011, 2007 by an exacerbation of HF. Copyright © 2011, 2007 by
Mosby, Inc., an affiliate of
Elsevier Inc.
– Fluid retention
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Elsevier Inc.

What Signs and symptoms are present in these slides common to chronic heart
failure?
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 Heart Failure
Complications Diagnostic Studies
• **High risk of fatal dysrhythmias (e.g., sudden • Primary goal- determine underlying
cardiac death, ventricular tachycardia) with
cause
HF and an EF <35%
– History and physical examination( dyspnea)
– Chest x-ray
– ECG
– HF lead to severe hepatomegaly, especially
with RV failure – Lab studies (e.g., cardiac enzymes, BNP-
• Fibrosis and cirrhosis - develop over time
(beta natriuretic peptide- normal value less
than 100) electrolytes
– Renal insufficiency or failure
– EF

Heart Failure
Diagnostic Studies
Transesophage
• Primary goal- determine underlying al
cause echocardiogram
– Hemodynamic assessment-Hemodynamic
Monitoring-CVP- (right side) and Swan Ganz (left TEE
and right side)
– Echocardiogram-TEE best
– Stress testing- exercise or medicine
– Cardiac catheterization- determine heart
pressures ( inc.PAW )
– Ejection fraction (EF)

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

But
 Therapies

Stage A At high risk for developing heart failure. Exercise regularly

Includes people with: Quit smoking
Hypertension Treat hypertension
Diabetes mellitus Treat lipid disorders
CAD (including heart attack) Discourage alcohol or illicit drug
History of cardiotoxic drug therapy use
History of alcohol abuse If previous heart attack/ current
History of rheumatic fever diabetes mellitus or HTN, use ACE-
Family history of CMP I

Stage B Those diagnosed with “systolic” heart Care measures in Stage A +

failure- have never had symptoms of heart
failure (usually by finding an ejection
fraction of less than 40% on
echocardiogram
Stage C Patients with known heart failure with
current or prior symptoms.
Symptoms include: SOB, fatigue
Reduced exercise intolerance
Stage D Presence of advanced symptoms, after
assuring optimized medical care
Should be on ACE-I
Add beta -blockers
Surgical consultation for coronary
artery revascularization and valve
repair/replacement (as appropriate
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
All therapies -Stages A, B and C +
evaluation for:Cardiac transplantation,
VADs, surgical options, research
therapies, Continuous intravenous
inotropic infusions/ End-of-life care

Nursing and Collaborative Nursing and Collaborative Management

Management ADHF
• Overall goals of therapy for ADHF and • High Fowler’s position
chronic HF • Supplemental oxygen
– Decrease patient symptoms. • Continuous ECG monitoring
– Improve LV function. • Ultrafiltration: Option for patients with volume
overload
– Reverse ventricular remodeling.
– Improve quality of life. • Circulatory assist devices used to treat patients
with deteriorating HF.
– Decrease mortality and morbidity.
• Address coexisting psychologic disorders

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Elsevier Inc. Elsevier Inc.

Nursing and Collaborative Management

Nursing and Collaborative Management ADHF
ADHF
• Dec intravascular volume • Dec afterload

– Reduces venous return and preload – Improves CO and decreases pulmonary congestion
• IV sodium nitroprusside (Nipride)
• Loop diuretics (e.g., furosemide [Lasix])
• Morphine sulfate
• Ultrafiltration or aquapheresis
• Nesiritide (Natrecor)
• Dec venous return (preload)
• Improve gas exchange and oxygenation
– Reduces amount of volume returned to LV during
diastole – Supplemental oxygen
• High-Fowler’s position – Morphine sulfate
• IV nitroglycerin – Noninvasive ventilatory support (BiPAP)
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Elsevier Inc. Elsevier Inc.
 Nursing and Collaborative Management
ADHF
Summary Treatment Goals-ADHF/Pulmonary Edema)
• Improve cardiac function

– If do not respond to conventional pharmacotherapy (e.g., • MAD DOG

diuretics, vasodilators, morphine sulfate)
• Inotropic therapy
– Digitalis
– -Adrenergic agonists (e.g., dopamine)
– Phosphodiesterase inhibitors (e.g., milrinone)
• 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

• Hemodynamic monitoring – D- Diuretics

– O- oxygen /measure sats;
• Reduce anxiety • Hemodynamics, careful observation
– G- blood gases
– Distraction, imagery
– Think physiology
– Sedative medications (e.g., morphine sulfate,
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benzodiazepines)
Mosby, Inc., an affiliate of
Elsevier Inc.

Heart Failure (ADHF)Pneumonic Collaborative Management

U Upright Position
(emergency mgt >recall for later!) Chronic HF
N Nitrates • Main treatment goals
– Treat the underlying cause and contributing
factors.
L Lasix
– Maximize CO.
O Oxygen
– Provide treatment to alleviate symptoms.
A ACE, ARBs, Amiodorone
– Improve ventricular function.
D Dig, Dobutamine
– Improve quality of life.
– Preserve target organ function.
M Morphine Sulfate – Improve mortality and morbidity.
E Extremities Down Copyright © 2011, 2007 by
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Elsevier Inc.

Chronic HF
Chronic HF
Collaborative Management Collaborative Management
• Therapeutic objectives for drug
• O2 (non-rebreather if emergency); morphine, diuretics,
etc-dec preload, afterload
therapy
• Physical/ emotional rest – Identification of type of HF & underlying
• Nonpharmacologic therapies *See at end of slides causes
– Cardiac resynchronization therapy (CRT) or – Correction of Na & H2O retention and
biventricular pacing volume overload
– Cardiac transplantation – Reduction of cardiac workload
– Intraaortic balloon pump (IABP) therapy – Improvement of myocardial contractility
– Ventricular assist devices (VADs) – Control of precipitating and complicating
factors
– Destination therapy—Permanent, implantable VAD
 Chronic HF-Collaborative Management
Chronic HF Drug therapy
Collaborative Management
– Vasodilators
– Diuretics
• Drug therapy • ACE inhibitors- pril or
• Thiazide
ril *first line heart
– Positive inotropic agents • Loop failure
• Digitalis • Spironolactone • Angiotensin II
• Calcium sensitizers- (Levosimendan) new receptor blockers
under research; cardioprotective, inc. cardiac
contractility
• Nitrates
– BiDil (combination drug containing • -Adrenergic
isosorbide dinitrate and hydralazine) blockers- al or ol
approved only for the treatment of HF in • Nesiritide- Natrecor
African Americans (BNP)

Chronic HF- Collaborative Management Chronic HF

• Nutritional therapy
Nursing Management
– Fluid restriction may or may not be required
• Nursing diagnoses
– Daily weights important
• Same time, same clothing each day – Activity intolerance
– *Weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb – Decreased cardiac output
(2.3 kg) gain over a week-report to health care provider – Fluid volume excess
– Diet/weight reduction recommendations-individualized
and culturally sensitive
– Impaired gas exchange
– DASH diet recommended – Anxiety
– Sodium- usually restricted to 2.5 g per day – Deficient knowledge
– Potassium encouraged unless on K sparing diuretics
(Aldactone)

Chronic HF Chronic HF
Nursing Management Nursing Management
• Health Promotion • Health Promotion
– Treatment or control of underlying heart – Patient teaching: medications, diet, and
disease key to preventing HF and episodes exercise regimens
of ADHF (e.g., valve replacement, control of • Exercise training (e.g., cardiac rehabilitation)
hypertension) improves symptoms but often underprescribed

– Antidysrhythmic agents or pacemakers for – Home nursing care for follow-up and to
monitor patient’s response to treatment
patients with serious dysrhythmias or
may be required
conduction disturbances
– Flu and pneumonia vaccinations
 Chronic HF Chronic HF
Nursing Management Nursing Management
• Acute Intervention • Planning: Overall Goals
– HF -progressive disease—treatment plans – Dec in symptoms (e.g., shortness of breath,
established with quality-of-life goals fatigue)
– Symptom management controlled with self- – Dec in peripheral edema
management tools (e.g., daily weights)
– Inc in exercise tolerance
– Salt -restricted
– Compliance with the medical regimen
– Energy- conserved
– No complications related to HF
– Support systems - essential to success of
entire treatment plan

Chronic HF- Nursing Management

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
• Ambulatory and Home Care
– Explain physiologic changes that have occurred
– Assist patient to adapt to physiologic and
psychologic changes
– Integrate patient and patient’s family or support
system in overall care plan
• Implementation: Patient Education
– Home BP monitoring
– Drug knowledge
– Signs of hypo- and hyperkalemia if taking diuretics
that deplete or spare potassium
– Instruct in energy-conserving and energy-efficient
behaviors

Decreased cardiac output

• Activity Intolerance • Fluid Volume
– 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
Excess • Plan frequent rest periods
– Give diuretics and
• Monitor VS and O2 sat at rest and during activity
provide BSC
– Teach side effects of • Take apical pulse
meds • Review lab results and hemodynamic monitoring
– Teach fluid restriction results
– Teach low sodium • Fluid restriction- keep accurate I and O
diet
• Elevate legs when sitting
– Monitor I and O and
daily weights • Teach relaxation and ROM exercises
– Position in semi or
high fowlers
– Listen to BS
 Knowledge deficit
• Low Na diet
• Fluid restriction
PATIENT TEACHING • Daily weight
• When to call Dr.
• Medications

Chronic HF-End Stage >ADHF

Collaborative Management Cardiac Transplantation
Nursing Management
• Nonpharmacologic therapies (cont’d)
– Intraaortic balloon pump (IABP) therapy • Treatment of choice for patients with
• Used for cardiogenic shock; allows heart to rest refractory end-stage HF, inoperable CAD and
– Ventricular assist devices (VADs) cardiomyopathy
• Takes over pumping for the ventricles – Goal of transplant evaluation process -
• Used as a bridge to transplant
identify patients who would most benefit
– Destination therapy-permanent, implantable VAD
from a new heart
– Cardiomyoplasty- wrap latissimus dorsi around heart
– Ventricular reduction -ventricular wall resected
– Transplant/Artificial Heart

CRT-Cardiac Resynchronization Intraaortic Balloon Pump (IABP)

Therapy • Provides temporary
circulatory assistance
– ↓ Afterload
HOW IT WORKS:
– Augments aortic
Standard implanted pacemakers -
diastolic pressure
equipped with two wires (or "leads")
conduct pacing signals to specific • Outcomes
regions of heart (usually at – Improved coronary
positions A and C). Biventricular
pacing devices have added a third
blood flow
lead (to position B) that is designed – Improved
to conduct signals directly into the perfusion of vital
left ventricle. Combination of all organs
three lead > synchronized pumping
of ventricles, inc. efficiency of each
beat and pumping more blood on
the whole.
 Enhanced External
Counterpulsation-EECP
The Cardiology Group, P.A.

Pumps during diastole-

increasing O2 supply to
coronary arteries. Like
IABP but not invasive.

Ventricular
Ventricular Assist
Assist Devices
Devices (VADs)
(VADs) Patient Teaching-Cleveland Clinic for Heart
Failure LVAD devices

• 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

Schematic Diagram of Left VAD

Left ventricular assist

device
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”.
 Left Ventricular reduction
Surgery-Bautista
procedure…indicated in
some cases…

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

Click here for UTube Cardiac Transplantation

Artificial Heart animination!
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 recipient’s heart, Click here to Perform a
Heart Transplant…(your
except for posterior right and left atrial walls patient with end stage heart
and their venous connections failure may require this!)

• Recipient’s 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

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
What’s New in Heart Failure?
Go here for updates on Heart Failure!
Go here for UTube videos- great visuals
HeartNet/Ventricular Support System
End Stage Heart Failure- newest Therapies
Muscle cell transplant (stem cell); Angiogensis
Myoblasts for the Heart - Watch WebMD Video
The 10 Commandments of Heart Failure Treatment
6. Consider adding 25 mg spironolactone in most class III or IV
patients. Do not start if the serum creatinine level is > 2.5 mg
per dL (220 µmol per L).
7. Use metoprolol (Lopressor), carvedilol (Coreg) or bisoprolol
(Zebeta) (beta blockers) in all class II and III heart failure
patients unless there is a contraindication. Start with low
doses and work up. Do not start if the patient is
decompensated.
8. Use digoxin in most symptomatic heart failure patients.
9. Encourage a graded exercise program.
10. Consider a cardiology consultation in patients who fail to
improve.
ACE = angiotensin-converting enzyme.
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 recipient’s immune status
• Care focuses:
– Promoting patient adaptation to transplant process
– Monitoring cardiac function & lifestyle changes
– Providing relevant teaching
10 Commandments of Heart Failure Treatment
1. Maintain patient on 2- to 3-g sodium diet. Follow daily weight. Monitor
standing blood pressures in the office, as these patients are prone to
orthostasis. Determine target/ideal weight, which is not the dry weight.
In order to prevent worsening azotemia, some patients will need to have
some edema. Achieving target weight should mean no orthopnea or
paroxysmal nocturnal dyspnea. Consider home health teaching.
2. Avoid all nonsteroidal anti-inflammatory drugs because they block the
effect of ACE inhibitors and diuretics. The only proven safe calcium
channel blocker in heart failure is amlodipine (Lotrel /Norvasc).
3. Use ACE inhibitors in all heart failure patients unless they have an
absolute contraindication or intolerance. Use doses proven to improve
survival and back off if they are orthostatic. In those patients who
cannot take an ACE inhibitor, use an angiotensin receptor blocker like
irbesartan (Avapro).
4. Use loop diuretics (like furosemide [Lasix]) in most NYHA class II
through IV patients in dosages adequate to relieve pulmonary
congestive symptoms. Double the dosage (instead of giving twice daily)
if there is no response or if the serum creatinine level is > 2.0 mg per dL
(180 µmol per L).
5. For patients who respond poorly to large dosages of loop diuretics,
consider adding 5 to 10 mg of metolazone (Zaroxolyn) one hour before
the dose of furosemide once or twice a week as tolerated.
WebMD- Patient Medications for Heart Failure!

Medical Treatment-Drug Therapy (typical)
• Cardiac Glycoside-Digoxin
• Positive inotropes-dobutamine, Primacor. Natrecor
• Antihypertensives- WHY
• ACE inhibitors- stops remodeling (pril or ril)
– Catopril,enalapril,cozar,lisinopril
• Preload reduction *MSO4- important,
– Vasodilators-nitrates
– Diuretics-lasix, HCTZ, (Aldactone and Inspra)
– Beta blockers- dec. effects of SNS (Coreg)
– *Caution with CALCIUM CHANNEL BLOCKERS-
dec cardiac contractility
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.
Heart Failure Case Study! (#1)
Complete and check your answers!
Patient with Shortness of Breath (#2)
Congestive Heart Failure (#3)
Heart failure case study (#4)
Heart Failure Challenge Game
Meds!
Angiotensin-converting enzyme inhibitors , such as captopril and enalapril,
block 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 kidneys to excrete sodium, chloride, and water, reducing fluid
volume. Loop diuretics such as furosemide, bumetanide, and torsemide are
preferred first-line diuretics because of 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, beta-blockers, 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
ER Decision-Making
Go here for physician
discussion/decision-making re- The
patient with heart failure in ER
Prioritization and Delegation
• Two weeks ago, a 63 year old client with heart failure
received a new prescription for carvedilol (Coreg) 3.125
mg orally. Upon evaluation in the outpatient clinic these
symptoms are found. Which is of most concern?
• A. Complaints of increased fatigue and dyspnea.
• B. Weight increase of 0.5kg in 2 weeks.
• C. Bibasilar crackles audible in the posterior chest.
• D. Sinus bradycardia, rate 50 as evidenced by the EKG.
• 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)
•C. Potassium
#26
• A cardiac surgery client is being ambulated when
another staff member tells them that the client has
developed a supraventricular tachycardia with a rate
of 146 beats per minute. In what order will the nurse
take these actions?
• A. Call the client’s physician.
• B. Have the client sit down.
• C. Check the client’s blood pressure.
• D. Administer oxygen by nasal cannula
•B, D, C. A
• As charge nurse in a long-term facility that has RN,
LPN and nursing assistant staff members, a plan for
ongoing assessment of all residents with a diagnosis
of heart failure has been developed. Which activity is
most appropriate to delegate to an LVN team leader?
• A. Weigh all residents with heart failure each morning
• B. Listen to lung sounds and check for edema
weekly.
• C. Review all heart failure medications with residents
every month.
• D. Update activity plans for residents with heart
failure every quarter.
B. Listen to lung sounds and check for edema weekly
#27
• The echocardiagram indicates a large thrombus in
the left atrium of a client admitted with heart failure.
During the night, the client complains of severe,
sudden onset left foot pain. It is noted that no pulse is
palpable in the left foot and that it is cold and pale.
Which action should be taken next?
• A. Lower his left foot below heart level.
• B. Administer oxygen at 4L per nasal cannula.
• C. Notify the physician about the assessment data.
• D. Check the vital signs and pulse oximeter.
Notify the physician about the assessment data