1

B2. HEART FAILURE: a clinical syndrome resulting from structural or functional cardiac disorders that impair the
ability of the ventricles to fill or eject blood.
 ACUTE HEART FAILURE is the abrupt onset of a myocardial injury (such as a massive MI) resulting in
suddenly decreased cardiac function and signs of decreased cardiac output.

 CHRONIC HEART FAILURE:

 Refers to the development of symptoms over months to years.
 Chronic symptoms represents the baseline condition, the limitations the patient lives with on a daily basis.

ETIOLOGY:
1. Increase cardiac workload
2. Structural or functional alterations in the myocardium
3. Obstruction with pumping capacity of the heart

*MOST COMMON CAUSE:

a. Coronary artery disease- Ischemia & MI - primary cause is atherosclerosis
b. Cardiomyopathy
 3 TYPES:
1. Dilated cardiomyopathy - most common cause
2. Hypertrophic cardiomyopathy
3. Restrictive cardiomyopathy
c. Hypertension
d. Valvular heart disease
e. Renal dysfunction with volume overload

SYSTEMIC CONDITIONS THAT MAY CONTRIBUTE TO THE DEVELOPMENT OF HF:

1. Increased metabolic rate e.g fever and thyrotoxicosis
2. Iron overload e.g from hemochromatosis
3. Hypoxia
4. Severe anemia when S.Hct is <25%

OTHER FACTORS:
a. Acidosis (respiratory and metabolic)
b. Electrolyte abnormalities
c. Antiarryhthmic medication

COMPENSATORY MECHANISM: this is activated when cardiac output is insufficient to meet the demands 
tissue hypoxia.
 It may initially increase cardiac output but eventually will have a damaging effect on pumping
action of the heart.
A. SYMPATHETIC NERVOUS SYSTEM STIMULATION – immediate response→ increases catecholamine 
1. Increase heart rate and BP
2. Improved stroke volume
 STARLING’s LAW (Frank Starling Mechanism)
 Overstretching the muscle fiber beyond its limit ineffective contraction
 LIMITATION: after a critical point is reached this reduces the force of contraction and
cardiac output.

B. RENIN-ANGIOTENSIN SYSTEM ACTIVATION – due to decrease perfusion to the kidneys 

1. Increase vasoconstriction
2. Increase preload and afterload
3. Angiotensin II contributes to ventricular remodelling

C. OTHER CHEMICAL RESPONSES: most of this actions contribute to the worsening of the condition
a. Release of pro-inflammatory cytokines
b. Natriuretic peptide
 B-type Natriuretic Peptide (BNP) produced and released by the ventricles related to fluid overload as a
result of HF.
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c.Endothelin secreted by endothelial cells when stretched

D. MYOCARDIAL HYPERTROPHY – with or without chamber dilation (enlargement of the myocardium)

ALL COMPENSATORY MECHANISM MAY INCREASE MYOCARDIAL OXYGEN CONSUMPTION AND
CARDIAC RESERVE IS EXHAUSTED → CLINICAL MANIFESTATION OF HF

PATHOPHYSIOLOGY:

MYOCARDIAL DYSFUNCTION

CO

SYSTEMIC BP * ACTIVATION OF BARORECEPTORS

PERFUSION TO KIDNEYS

*ACTIVATION OF RENIN- VASOMOTOR CENTER STIMULATED

ANGIOTENSIN-ALDOSTERONE SYSTEM

ACTIVATION OF SNS

ALDOSTERONE/ADH

CATECHOLAMINES

. Na & H2O RETENTION

.ARGININE VASOPRESSIN VASOCONSTRICTION

. ENDOTHELIN AFTERLOAD

. CYTOKINES BP

VENTRICULAR REMODELLING HR

INCREASE ALDOSTERONE/ RELEASE OF CYTOKINES VENTRICULAR REMODELLING ( ADAPTATION OF

CHAMBERS AND MYOCARDIUM TO INCREASED PRESSURE AND FLUID VOLUME)

HYPERTROPHY AND DILATION OF VENTRICLES FORCE OF CONTRACTION → CO

ENLARGED CELLS IMPAIRED CONTRACTILITY FAILURE IN COMPENSATORY MECHANISM HF S/SX
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TYPES OF HF:
1. LEFT SIDED HEART FAILURE:
 refers to the failure of the left ventricle to fill or empty properly leading to increased pressures inside the
ventricle and congestion in the pulmonary vascular system.
 TYPICAL CAUSE: Hypertension, cad, valvular heart disease
 RESULT TO: Decreased cardiac output and pulmonary congestion  decreased tissue perfusion
 It is classified further into:
a. SYTOLIC HEART FAILURE: (SYSTOLIC DYSFUNCTION)
o Often referred to as: Forward failure
o It is defined as an ejection fraction of less than 40% and is caused by decreased contractility.
Low EF (EJECTION FRACTION) – hallmark of Systolic heart failure
o Ejection fraction drops to 40% with ventricular dilation → symptoms of inadeqaute tissue
perfusion and pulmonary and systemic congestion
b. DIASTOLIC HEART FAILURE: (DIASTOLIC DYSFUNCTION)
 often referred to as heart failure with preserved left ventricular function.
 It is caused by impaired relaxation and filing.

2. RIGHT SIDED HEART FAILURE: refers to failure of the right ventricle to pump adequately.
 The most common cause is left-sided heart failure but it can exist in the presence of a perfectly normal left
ventricle and does not lead to left-sided heart failure..
 Due to: Inability of the right ventricle to empty completely  increased volume and pressure in the venous
system  peripheral edema/fluid accumulation in the abdomen

CLINICAL MANIFESTATION:
1. LEFT-SIDED HEART FAILURE:
 DYSPNEA * PND (Paroxysmal Nocturnal Dyspnea)
 SOB – DYSPNEA ON EXERTION
 CRACKLES – at the base of the lungs
 ORTHOPNEA – sleep with the head propped-up in 2-3 pillows
 DRY-HACKING COUGH – (nocturnal) – early sign
 TACHYCARDIA
 S3 GALLOP
 PALPITATIONS
 PALLOR
 DECREASED URINE OUTPUT
 *ACTIVITY INTOLERANCE @ REST – indicate a critical level of heart decompensation
 FATIGUE
 WEAKNESS
 SEVERE HF – expectorate frothy, pink-sputum

2.RIGHT-SIDED HEART FAILURE:

 JUGULAR VEIN DISTENTION
 PERIPHERAL EDEMA (feet, legs and sacrum) + swelling of fingers
 LIVER ENLARGEMENT/TENDERNESS (+ RUQ pain)
 Hepatosplenomegaly
 ASCITES
 NAUSEA as GIT becomes congested
 ANOREXIA

 ABDOMINAL DISTENTION
 NOCTURIA
 FATIGUE
 Weight gain

3. BIVENTRICULAR FAILURE:
 MANIFESTATION OF BOTH RIGHT AND LEFT FAILURE
 PAROXYSMAL NOCTURNAL DYSPNEA – fluid that accumulates in the dependent extremities during
the day may be reabsorbed into the circulating volume when patient lies down  shifting fluid into
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the alveoli  fluid filled alveoli cannot exchange oxygen and carbon dioxide DOB with difficulty in
sleeping
 DYSPNEA (AT REST AND ACTIVITY)
 S3 & S4 GALLOP

LABORATORY/DIAGNOSTIC TEST:
1. S. ELECTROLYTES
2. Liver Function Test
3. ABG
4. BNP
5. CXR
6. Echocardiography
7. ECG

PHARMACOLOGIC THERAPY:
1. ACE INHIBITOR – Angiotensin-Converting Enzyme Inhibitors
2. ANGIOTENSIN II RECEPTOR BLOCKERS – ex. Valsartan (Diovan)
3. HYDRALAZINE/ISOSORBIDE DINITRATE
 Nitrates ex. Isosorbide Dinitrate
 Hydralazine
4. BETA-BLOCKERS –routinely given with ACE inhibitors
 Example – Carvedilol, Metoprolol
5. DIURETICS
 Loop ( Lasix)
 Thiazide diuretic
 Spironolactone
6. DIGITALIS (Digoxin) – an essential agent for the treatment of HF
 It improves contractility, increasing left ventricular output
 Note for signs and symptoms of Digitalis Toxicity
 For Digoxin toxicity – Digoxin Immune Fab (Digibind)
7. Ca CHANNEL BLOCKERS – such as Verapamil (Isoptin), Nifedipine (Adalat), Diltiazim ( Cardizem)
8. INOTROPICS such as Milrinone(Primacor), Dobutamine ( Dobutrex)
9. IV VASODILATORS such as Nitroprusside (Nipride), Nitroglycerin or Nesiritide ( Natrecor)

OTHER INTERVENTION:
1. CORONARY ARTERY REVASCULARIZATION:
 CORONARY ARTERY BYPASS
 IMPLANTABLE CARDIOVERTER DEFIB.
 CARDIAC RESYNCHRONIZATION THERAPY

CABG: Artery or vein from another part of the body is connected to the blocked coronary artery allow a new
route of oxygen-rich blood around the blockage to the heart muscles.

IMPLANTABLE CARDIOVERTER DEFIBRILLATOR (ICD): This uses electrical pulses to help control life-threatening
arrythmias

CARDIAC RESYNCHRONIZATION THERAPY (CRT): Use of biventricular pacemaker to treat electrical conduction
defects. It synchronizes the contraction of the right and left ventricles.

2.Surgery
A. Cardiac Transplant:
Two types:
a. ORTHOTOPIC transplant
b. HETEROTOPIC transplant – also known as piggy back heart
 Major post-operative concern – infection, rejection
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b.VAD (Ventricular Assist Device)

C. Other Surgical Therapies: Ventricular Reconstructive Procedures:
C.1. Partial L ventriculectomy (PLV)
C.2 Endoventricular Circular Patch Cardioplasty
C.3. Acrn Cardiac Support Device
C.4. Myosplint

3.CARDIAC REHABILITATION: a medically supervised program that helps improve the health and well-
being of people with cardiac problem
 DONE WHEN CLIENT IS FREE OF SYMPTOMS
 Begins upon admission for emergency care, continues for months and even years after
discharged from health care facility
 Goal: To help patient live a life that is full, vital and productive but within the heart’s ability to respond to
an increase stress or activity.

 Objectives:
A. Limit the effects and progression of atherosclerosis
B. Return patient to work and pre-illness lifestyle
C. Enhance the psychosocial and vocational status of the patient
D. Prevent another cardiac event

 ACTIVITIES:
a. EXERCISE – gradually implemented from the hospital onwards and terminated if any one of the
following occurs: Cyanosis, Cold sweats, faintness, extreme fatigue, severe dyspnea, pallor, chest pain,
PR >100/min, Dysrhythmias, BP >160/95
b. TEACHING/ counselling:
 Control HPN
 Diet
 Weight reduction program
 Progressive exercise
 Stress management technique
 Resumption of sexual activity after 4-6 weeks from discharge

4.NUTRITIONAL THERAPY
 Follow a Low Na ( no more than 2 g/day)
 Limit fluid intake

5. OXYGEN THERAPY

 Cardiogenic Pulmonary Edema - a life-threatening event that can result from severe HF (with fluid
overload), acute MI, mitral valve disease, and possibly dysrhythmias
 Manifestation:
•Crackles
• Dyspnea at rest
• Disorientation or acute confusion
•Tachycardia
• Hypertension or hypotension
• Reduced urinary output
• Cough with frothy, pink-tinged sputum
• Premature ventricular contractions and other dysrhythmias
• Anxiety
• Restlessness
• Lethargy
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MEDICAL MANAGEMENT: ACUTE PHASE

1. OXYGEN THERAPY VIA:
 FACE MASK – use of nonrebreather mask to provide increase concentration of the low-flow system
and can deliver an FiO2 >90%
o IF RESPIRATORY FAILURE IS SEVERE OR PERSISTS
 ET and MECHANICAL VENTILATION WITH PEEP – reduce venous return, decrease fluid movement
from the pulmonary capillaries to the alveoli and improve oxygenation

2. PHARMACOLOGY:
a. DIURETICS
o Furosemide (Lasix) – IV
o In lieu of furosemide – Bumetanide ( Bumex)and Metolazone ( Zaroxolyn)

b.Infusion with Vasodilators such as Nitroglycerin or Nitroprusside – enhance relief of symptoms of

pulmonary edema; contraindicated in clients who are hypotensive
b.1.INFUSION WITH NESERITIDE, DOBUTAMINE AND MILRINONE
 Neseritide ( Natrecor) – a BNP (Beta-type Natriuretic Peptide)indicated for acutely
decompensated HF
o It binds to vascular smooth muscles and endothelial cells  causing dilation of arteries and veins
o It suppresses neurohormone responsible for fluid retention  Promotes diuresis

 Milrinone ( Primacor) – delays the release of Ca from the intracellular reservoir and prevents
the uptake of extracellular calcium by cells
o Major side effect: hypotension, GI dysfunction, Ventricular dysrhythmia

 Dobutamine (Dobutrex) – inotropic agent

o A catecholamine – stimulates Beta 1
o Major action: increase contractility of the heart

c. Other medicines:
c.1. Anticoagulant – indicated for clients with HX of embolic events or atrial fibrillation or mural
thrombus
c.2. Anti-anginal – to treat underlying cause of HF
C.3. Anti-inflammatory drugs – such as NSAID’s

 NURSING DIAGNOSIS: ACUTE HF

 INEFFECTIVE AIRWAY CLEARANCE
 INEFFECTIVE BREATHING PATTERN
 IMPAIRED GAS EXCHANGE
 FLUID VOLUME EXCESS

 NURSING INTERVENTION: “ EMERGENT” CARE – care is directed towards ABC

1. ENSURE AIRWAY PATENCY
 Assess the effectiveness of the respiratory efforts and airway clearance
 Encourage to cough out secretions
 Provide nasotracheal suctioning
2. BREATHING:
 BE PREPARED TO ASSIST WITH INTUBATION AND MECHANICAL VENTILATION
 Assess the respiratory status – including RR, effort. Use of accessory muscle, sputum
characteristics, skin color
 Auscultate chest crackles and adventitious sound
 POSITION IN high fowlers or UPRIGHT with legs dangling
 Administer oxygen by mask or ventilator
3. ASSESS CIRCULATION
o Maintain and monitor hemodynamic status
o Maintain in cardiac monitor to detect dysrhythmias
o Assess heart sounds for possible S3, S4
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a. INITIATE IV LINE
b. Administer drugs as ordered
c. INSERT FOLEY CATHETER; RECORD I & O, WEIGH OD
d. RESTRICT FLUID INTAKE AS ORDERED
e. MONITOR O2 SATURATION AND OTHER LABORATORY RESULTS; REFER
f. BE PREPARED TO INITIATE ROTATING TOURNIQUETS ( dry phlebotomy)
 To pool blood in the extremities to relieve congestion in the lungs
 BP cuff on 3 extremities, one extremity should be free at all times, inflate on each of the 3
extremities to the level of the diastolic pressure
 Release BP cuff every 15 minutes – one cuff and placed it on the uncuffed extremity using a
systematic clockwise rotation
 No extremity must be compressed for periods longer than 15 minutes and no less than 5
minutes
 DO NOT deflate all the cuffs at the same time
 It removes about 1 liter of circulating blood
g. PROVIDE EMOTIONAL SUPPORT – explain all procedure, and the rationale, maintain close contact.

 NURSING INTERVENTION: HEART FAILURE

1. DECREASED CARDIAC OUTPUT:
o Monitor and record vs
o Auscultate heart and breath sounds regularly
o Note and report manifestations of cardiac output
o Administer oxygen as needed administer prescribed meds as ordered
o Encourage client to rest
o Promote psychologic rest and decrease anxiety

2. FLUID VOLUME EXCESS

o Assess respiratory status
o Refer if client manifests s/sx of pulmonary edema
o MIO
o Measure abdominal girth q shift
o Maintain bedrest with head of the bed elevated to 45°
o Assess for other manifestations of fluid volume excess
o Monitor and record hemodynamic parameters
o Adm. Diuretics and other medicines as ordered
o Restrict fluids as ordered

OTHER NURSING DIAGNOSIS:

2. ACTIVITY INTOLERANCE
3. KNOWLEDGE DEFICIT ON LOW Na DIET and IF NECESSARY Low Kcal diet
o TEACH CLIENT TO READ FOOD LABEL “HIDDEN Na”
o Provide a list of High Na, High fat, high cholesterol
4. POWERLESSNESS
5. ANXIETY

 HEART TRANSPLANT:
Two types:
1. ORTHOTOPIC transplant – the client’s heart is replaced by a donors heart
2. HETEROTOPIC transplant – also known as piggy back heart

 Indications and Selection

 Indicated for individual who: can no longer be managed with conventional medical therapy , no surgical
options offers favorable long-term outcomes, individual’s short-term prognosis is poor without
transplantation
 Heart transplant recipients: neonates to patients in their 60s
 Advance age >70 - contraindicated
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 Medical Contraindication
 ABSOLUTE
• Elevated pulmonary artery pressures
• Irreversible severe renal, hepatic, or pulmonary disease
• Kidney dysfunction
• Chronic liver dysfunction
• Recent or unresolved pulmonary infarction
• Active uncontrolled infection
• Active malignancy or recent malignancy with high risk of recurrence

 RELATIVE :
• Advanced age (>70 years of age)
• Diabetes mellitus with end-organ damage and/or poor glycemic control
• Obesity
• Severe cachexia or malnutrition
• Systemic disease with a high probability of recurrence in the transplanted heart
• Severe peripheral vascular disease or cerebrovascular disease
• History of multiple prior sternotomies
• High level of allosensitization

 Heart Transplantation Surgical Procedure

1. Biatrial Technique
Orthotopic Heart transplantation:
 All of the recipient’s heart is removed except the posterior walls of the atria that contain the orifices of the
pulmonary veins and vena cava.
 Four major anastomoses performed: the right and left atria, the aorta, and the pulmonary artery.
 The donor heart is denervated, resulting in a faster resting heart rate of 90 to 100 beats/min.
 The rate of the transplanted heart is the normal intrinsic rate generated by the donor sinoatrial (SA) node
located in the right atrium.
 Disadvantage: The loss of normal atrial anatomy increased the risk of mitral and tricuspid valve
regurgitation, atrial septal aneurysm, atrial thrombus formation, and tachydysrhythmias.

2. Bicaval Technique
 an alternative to the standard surgical approach
 The anastomotic sites include the left atrial cuff, which contains the orifices of pulmonary veins, the
superior and inferior vena cava, as well as the aorta and the main pulmonary artery
 Benefits include preserved SA node function with decreased incidence of atrial dysrhythmias, and mitral
and tricuspid regurgitation

 POSTOPERATIVE MEDICAL AND NURSING MANAGEMENT

 NURSING DIAGNOSES
• Decreased Cardiac Output related to alterations in preload
• Decreased Cardiac Output related to alterations in afterload
• Decreased Cardiac Output related to alterations in heart rate or rhythm
• Risk for Infection: Immunosuppressive medications required to prevent rejection of transplanted organ
• Disturbed Body Image related to actual change in body structure, function, or appearance
• Anxiety related to threat to biologic, psychologic, and social integrity,

 Priority Nursing diagnoses is Decreased Cardiac Output

 Possible causes for a decrease in cardiac output include rightheart dysfunction, dysrhythmias, hypothermia,
myocardial depression, tamponade, and rejection

1. Monitor VS, Hemodynamic status, attached to cardiac monitor, administer beta-adrenergic anatagonist e.g.
Isoproterenol , inotropic and vasodilator post-op period
2. Temporary pacing is required occasionally, and fewer than 10% of transplant recipients require a permanent
pacemaker implant.
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 Signs and Symptoms of Rejection

 fatal unless emergency hemodynamic support can be performed
 Acute cellular rejection in heart transplant recipients can occur at any time, although it is most likely to
occur during the first 3 to 6 months after transplantation.

 SIGNS AND SYMPTOMS OF HEART TRANSPLANT REJECTION

Rub (pericardial friction) Enlarged cardiac silhouette
ECG voltage decreased Pulmonary crackles, wheezes
JVD Increased weight
Edema (peripheral, sudden onset) SOB
Cardiac dysrhythmias (atrial, brady) Onset of hypotension
Tiredness Disturbance in mood
Intolerance of exercise Echo findings (systolic function, LV mass/thickness)
Onset of low-grade fever
New S3 or S4

 Rejection Surveillance
 Diagnosis of rejection is determined by fluoroscopic or echocardiography-guided endomyocardial biopsy.
 Endomyocardial biopsy - gold standard of rejection surveillance
 Treatment of acute rejection episodes:require IV corticosteroids.
 Strategies include augmenting current maintenance immunosuppression or switching to alternatives such
as Tacrolimus,Mycophenolate Mofetil, or Rapamycin.
 Other agents used for recurrent rejection include Polyclonal antibodies, such as antilymphocyte globulin or
antithymocyte globulin.

 Infection Surveillance
 high priority for the immunocompromised person in the early postoperative period
 Use aseptic technique for all intravenous line and dressing changes.
 Use reverse isolation
 Development of fever : An elevated temperature generally is considered significant when it reaches 38° C
(100.4° F).
 Nurses must be suspicious of any new productive cough, dry cough, change in type of secretions, or change
in chest xray findings.
 Cytomegalovirus (CMV) - transmitted through organ and blood product donation.
 Antiviral agent (ganciclovir) - used as prophylaxis and treatment of CMV infections.

 Patient Education
 Patients and caregivers are taught about transplant medications, self-monitoring for signs of infection and
rejection, safety precautions, and are provided with guidelines for maintaining a heart-healthy diet and
increasing physical activity.
 Teach and require patients to check their blood glucose, blood pressure, temperature, and daily weight at
home.

References:

Hinkle, J.L. & Cheever, K.H. (2018). Brunner & Suddarth's Textbook of Medical-Surgical Nursing (14th
ed.). Philadelphia: Wolters Kluwer.

Urden, L.D., Stacey, K.M., Lough, M.E. (2014) Critical Care Nursing Diagnosis and Management (7th
Ed.) St. Louis: Elsevier

LeMone, P., Burke, K.M., Bauldoff, G., & Gubrud, P. (2015). Medical-Surgical Nursing: Critical
Reasoning in Patient Care (6th ed.). Upper Saddle River, NJ: Pearson/Prentice Hall.

Prepared by: Mrs. Robeanna M. Diesto, MN