CARDIOMYOPATHY AND SETM CELL THERAPY

1. Presenter : Priyanka Bhati
M.Sc. Nursing 2ND year
CON ,AIIMS
Cardiomyopathy
AND STEM CELL THERAPY

2. OBJECTIVES:
• At the end of the class, the students will be able to,
• Define cardiomyopathy
• List the different types of cardiomyopathy
• Describe dilated cardiomyopathy and its treatment.
• Explain hypertrophic cardiomyopathy and its management
• Explain restrictive cardiomyopathy.
• Formulate nursing diagnosis for patients with
cardiomyopathy.

3. INTRODUCTION
•Cardiomyopathy is an irreversible primary disease of the
heart muscle.
•Cardiomyopathy affects the myocardial layer of the heart,
but it can also affect endocardial, subendocardial and
pericardial layers.

4. Cardiomyopathy is defined as a heart muscle disease,
characterized by ventricle dilation, myocyte and wall
thickening (hypertrophy), interstitial fibrosis, decreased
contractility and conduction disturbances.
DEFINITION:

6. INCIDENCE
• Affect any age group, clinical manifestations most commonly
appear in the third or fourth decade.
• Incidence in males is twice that of females
• In blacks it is 2.4 times that of the white
• Africo- American people most affected
• The incidence of dilated cardiomyopathy DCM discovered at
autopsy is estimated to be 4.5 cases per 100,000 populations per
year, whereas the clinical incidence is 2.45 cases per 100,000
populations per year.
• DCM occurs in age group of 20-60 yrs.

7. Types of cardiomyopathy
based on etiology:
Primary cardiomyopathies are those conditions in
which the etiology of the heart disease is unknown.
Portion of the heart is involved and other cardiac
structures are unaffected.
Secondary cardiomyopathies, the cause of the
myocardial disease is known and is secondary to
another disease process.

8. WHO CLASSIFICATION OF
CARDIOMYOPATHY-FUNCTIONAL

10. CAUSES
• Unknown
• Ischemic: = 50% atherosclerosis, Kawasaki disease, anomalous origin of left
coronary artery.
• Idiopathic = 45%
• Hereditary: = 25 – 35% autosomal dominant, autosomal recessive, X-linked,
mitochondrial.
• Acute and chronic myocarditis: coxsackievirus, HIV adenovirus,
• Autoimmune diseases
• Chronic tachycardia

11. CAUSES
• Drugs: alcohol, sympathomimetics, anthracyclines, amphetamines ,cocaine and
cancer drugs doxorubicin and daunorubicin.
• End-stage hypertrophic cardiomyopathy
• Endocrine: growth hormone deficiency, hyperthyroidism, hypothyroidism,
hypocalcemia, diabetes mellitus, pheochromocytoma
• Inborn errors of metabolism
• Muscular dystrophies
• Nutritional deficiency: selenium, carnitine, thiamine
• Peripartum
• Structural heart disease
• Systemic hypertension
• Toxins: cobalt, lead

12. Heart becomes weak and the chambers get large.
Heart cannot pump enough blood out to the
body
Decreased cardiac output

13. PHYSIOLOGICAL CONSEQUNCES

14. CLINICAL MANIFESTATION -signs
• May be asymptomatic
• The onset is insidious, but sometimes symptoms of heart
failure occur suddenly
• Dyspnea ,Nocturnal dry cough
• Palpitation
• Chest pain ,pulmonary edema
• Dizziness and syncope
• CVA , Hemiplegia, Paraplegia
• Systemic embolism
• Infants and younger children have respiratory symptoms and
failure to thrive.

15. Cont..
• Pulse : low amplitude and pulse alternans are common .
• BP : Low BP , Narrow pulse pressure
• Cardiomegaly( board and displaced point of max .impulse , right
ventricular heave)
• JVP : Elevated Precordium: – Apex shifted, forceful and ill sustained –
S2 may be palpable due to PH – May be parasternal lift – On
auscultation:S1 and S2 soft, S2 loud from PH , Pansystolic murmur at
mitral and tricuspid area,S3 and S4 are common

16. Diagnostic evaluation
Assessment Finding
Auscultation
Chest X-ray
ECG{RULE
OUT}
Echo { MAIN}
Point of maximal intensity away from the normal
position.
Heart sound reveal S3
Cardiomegaly with signs of pulmonary venous
hypertension.
Non-specific ST segment and T wave
abnormalities / arrhythmias
Dilated chambers with normal/decreased
wall thickness, decreased ejection fraction
(<30%)

17. Diagnostic evaluation
Assessment Finding
Left
ventriculogram
Cardiac
catheterization
Laboratory
investigations
Endomyocardial
biopsy{ NOT
DEFINITIVE}
Thin walled ventricles that are
dilated.
Coronary vasodilatation is
impaired by increased LV filling.
Cardiac troponin I is done to
detect recent MI
LFT, BUN and creatinine.
To identify the aetiology.

18. INVESTIGATIONS(HEART FAILURE EVALUATION)
• Laboratory Studies – Blood count, urinalysis, electrolytes, renal
function, glucose, LFTs (class I; level C)
• Thyroid stimulating hormone (class I; level C)
• Fe/TIBC, ferritin (class IIa, level C)
• Urinary screening for hemochromatosis (class IIa; level C)
• HIV testing (class IIb; level C)
• Electrocardiogram (class I; level C
• Chest x-ray (class I; level C)
• Echocardiogram/Doppler or radioventriculogram (class I;level C)

19. ECG changes:
• Sinus tachycardia, Bradycardia
• Low voltage ECG
• LVH or Rt or Lt Atrial hypertrophy
• Atrial or Ventricular arrythmia
• Pseudo infraction pattern(Deep but narrow ‘q’ suggestive of
antero-septal MI)
• Shallow invasion of ‘T’ wave
• LBBB, RBBB ,LAHB, LPHB, Bifascicular or Trifascicular block
• AV block( 1’or 2’ or 3’degree)

21. X-ray
• Cardiomegaly ,simulating pericardial effusion or multi valvular
disease or Ischemic cardiomyopathy.
• Pulmonary edema with Kerley’ B line.
• Pleural effusion may be present .
• Pulmonary infraction is not uncommon .
• Usually no LA enlargement so single right border. No calcified
valve and normal aorta.

22. Pulmonary edema with Kerley’ B line

23. MRI
• black blood images: enlarged cardiac chambers and thin
myocardial walls.
• Cine images: show LV hypokinesia, increased volumes, (end-
diastolic volumes that constitute a dilated CMP: > 140 mL for
the LV and > 150 mL for the RV.
• Phase-contrast sequences: impaired diastolic function.
transvalvular flow may be characterized by a restrictive
pattern .
• Late gadolinium-enhancement.

25. ENDOMYOCARDIAL BIOPSY
VENTRCULOGRAM

26. MANAGEMENT
Goal
•Enhance myocardial contractility
•Decrease afterload.

27. sw

28. Supportive medical treatment:
• Treatment of HF: – Rest – Salt and water restriction –
Diuretics (eg. Frusemide)
• Digoxin
• Vasodilators (eg.ACE inhibitor , Nitrates, Prazocin ) -
Potassium supplements -Spironolactone
• Vitamin: B1 -Levocarnitine

29. Supportive medical treatment:
• Anti arrythmic drugs: – 90% patient has complex ventricular
arrythmia –
• IF AF: Digoxin
• If VT or VF :Amiodorone.
• Long term anticoagulant therapy: – To prevent systemic and
pulmonary embolism .
• Consider adding beta blocker if symptoms persist Intravenous
Dobutamine / Dopamine.

30. • Implantable cardiac defibrillators.
• Biventricular pacemakers.(CRT)
OTHER MANAGEMEMT

31. HEART TRANSPLANT
•Heterotopic Procedure Orthotopic procedure

32. EMERGING THERAPIES
• Agents to eradicate persistent
viral infections and
immunomodulatory agents.
• Stem cells for cardiac
regeneration and gene therapy
approaches are in clinical trials.

33. Prevention
• Modification of contributory factor:
• Avoid alcohol
• Avoid pregnancy
– Genetic counselling
– Limit exercise
– Weight reduction
– Control of blood pressure
– Prompt control of Infection
– Correction of anemia and malnutrition

34. Complication of DCM
• Heart failure
• Arrythmias : AF ,SVT,PVCs ,VT VF
• AV blocks:1’ 2’ and CHB
• BBB : RBBB ,LBBB, LAHB ,LPHB
• Systolic or pulmonary embolism
• Syncope
• Sudden cardiac death

35. PROGNOSTIC FEATURES
• VENTRICULOGRAPHIC FINDINGS
• Degree of impairment in LVEF – Extent of left ventricular enlargement –
Coexistent right ventricular dysfunction – Ventricular mass/volume ratio –
Global wall motion abnormalities – Left ventricular sphericity .
• CLINICAL FINDINGS
• Favorable prognosis: NYHA < IV, younger age, female sex
• Poor prognosis: Syncope, persistent S3 gallop, rightsided heart failure, AV or
bundle branch block, hyponatremia, troponin elevation, increased BNP,
maximum oxygen uptake < 12 ml/kg/min.

36. HYPERTROPHIC CARDIOMYOPATHY

37. DEFINITION
• HCM is a disorder of cardiac muscle characterized by myocardial
hypertrophy.
• It most commonly affects the intraventricular septum and
disorganization of the cardiac
myocytes and myofibrils.
• It is the most common cause of
sudden cardiac death in
young competitive athletes.

38. Common causes
•Genetic(autosomal dominant) or familial.
•Hypertension.
•Ischemia( coronary artery disease).
•Aortic stenosis.
•Idiopathic.

39. PATHOPHYSIOLOGY
• Involves 4 interrelated process
• LVOT
• Diastolic dysfunction
• Myocardial ischemia
• Mitral regurgitation
Pathophysiology
 Left ventricular hypertrophy (thick ventricular wall)  
ventricular chamber size  hold less blood   CO
  pressure in the ventricles and lungs
 changes in the cardiac muscles  interfere with the heart's electrical
signals, leading to arrhythmias  sudden cardiac arrest

40. PATHOPHYSIOLOGY
Hypertrophy and
asymmetric septal wall
Changes in left
ventricular cavity shape
Misaligned papillary
muscles.
systolic anterior motion of
the mitral valve during
systole

41. Inward movement of the mitral valve leaflet
due to increased pressure in the LVOT(
Venturi phenomenon)
Mitral regurgitation, Cresendo- decresendo
murmur ,
Blockage of blood flow, during increased HR ,
The blood flow to heart is compromised
This condition is also known as idiopathic
hypertrophic subaortic stenosis(IHSS

42. LV Outflow Obstruction in HCM
• Long-standing LV outflow obstruction is a major determinant for
heart failure symptoms and death in HCM patients Subaortic
outflow obstruction is caused by systolic anterior motion (SAM) of
the mitral valve – leaflets move toward the septum.

43. LV Outflow Obstruction in HCM
• Explanations for the SAM of the mitral valve
• 1. Mitral valve is pulled against the septum by contraction of the
papillary muscles, which occurs because of the valve's abnormal
location and septal hypertrophy altering the orientation of the
papillary muscles.
• 2. Mitral valve is pushed against the septum because of its
abnormal position in the outflow tract.
• 3. Mitral valve is drawn toward the septum because of the lower
pressure that occurs as blood is ejected at high velocity through a
narrowed outflow tract (Venturi effect).

44. THE VENTURI EFFECT

45. Physiological Consequences of Obstruction
• Elevated intraventricular pressures.
• Prolongation of ventricular relaxation .
• Increased myocardial wall stress .
• Increased oxygen demand.
• Decrease in forward cardiac output .

46. CLINICAL
MANIFESTATIONS

47. CLINICAL MANIFESTATIONS
• SUDDEN DEATH
• Rapid, pounding heartbeat.
• Chest tightness or pressure.
• Fatigue.
• Fluid retention resulting in swollen feet or ankles or unexplained
weight gain.
• In children and adolescents, pre-syncope and syncope identify patients
at increased risk of sudden death.
Often diagnosis is made during screening. Sometimes, the first sign is
sudden death.

48. Diagnostic studies
•History and physical examination
•Palpation and auscultation of the chest.( Split S2, harsh
systolic ejection murmur worsening with Valsalva (
crescendo decrescendo murmur)
•S4 heard
•ECG findings- (ST segment changes, not specific, SVT ,VT)
may be normal .
•Echocardiogram( MAINSTAY OF DIAGNOSIS)
•Chest X ray.
•Biopsy –myofibril disarray

49. Physical Examination
• Holosystolic murmur at the apex and axilla of mitral
regurgitation is heard in patients with systolic anterior
motion of the mitral valve and significant LV outflow
gradients
• Diastolic decrescendo murmur of aortic regurgitation is
heard in 10% of patients, although mild aortic regurgitation
can be detected by Doppler echocardiography in 33% of
patients

50. Electrocardiogram in HCM
• LVH with nonspecific ST/T wave abnormalities .
• Left or right axis deviation, Conduction abnormalities .
• Abnormal and prominent Q wave in the anterior precordial and
lateral limb leads A fib with preexcitation implies poor
prognosis.
• Findings on Holter monitoring include APC’s VPC’s, sinus pauses,
wandering atrial pacemaker, atrial tachycardia, AF/flutter and
nonsustained ventricular tachycardia.

51. Electrocardiogram in HCM

52. ECHO
2-D echocardiography is diagnostic for HCM.
 Abnormal systolic anterior leaflet motion of
the mitral valve .
 LV hypertrophy.
 Left atrial enlargement .
 Diastolic dysfunction.
 Small ventricular chamber size .
 Septal hypertrophy with septal to free wall
ratio greater than 1.4:1 (absolute septal wall
thickness >15mm) .
 SAM of anterior and rarely posterior mitral
valve leaflet and mitral regurgitation .
 Decreased mid aortic flow .
 Partial systolic closure of the aortic valve in
mid systole.

53. Cardiac MRI in HCM
• Useful when echocardiography is questionable, particularly
with apical hypertrophy .
• Cines loops typically show obstruction and velocity mapping is
useful in the assessment of peak velocities .
• SAM of the mitral valve is clearly seen on cardiac MRI.
• Improvement in obstruction after septal ablation or
myomectomy can be demonstrated, as can the location and
size of the associated infarction, which are useful for planning
repeat procedures.
• Cardiac MRI tagging identifies abnormal patterns of strain,
shear, and torsion in cases of HCM, demonstrating significant
dysfunction in hypertrophic areas of the ventricle.

54. Cardiac MRI in HCM
• Gadolinium contrast cardiac MRI - differentiating HCM from
other causes of cardiac hypertrophy and other types of
cardiomyopathy such as, amyloidosis, athletic heart, and
Fabry’s disease
• Late gadolinium enhancement occurring in HCM represents
myocardial fibrosis
• The greater the degree of late gadolinium enhancement, the
more likely that the particular HCM patient has 2 or more risk
factors for sudden death.
• More likely the patient has or will develop progression of
ventricular dilation toward heart failure, thereby indicating a
poorer prognosis

55. Cardiac Catheterization
• Diagnostic cardiac catheterization is useful to determine the degree of
LVOT obstruction, cardiac hemodynamics, the diastolic characteristics of
the left ventricle, LV anatomy and coronary anatomy
• Reserved for situations when invasive modalities of therapy, such as a
pacemaker or surgery, are being considered
• Therapeutic cardiac catheterization interventions, include transcatheter
septal alcohol ablation
• The arterial pressure tracing found on cardiac catheterization may
demonstrate a "spike and dome" configuration

56. Cardiac Catheterization
• Approximately one fourth of patients demonstrate pulmonary
hypertension - usually mild
• Results in characteristic change recorded on arterial pressure tracing -
exhibits a pulse pressure that fails to increase as expected or actually
decreases (the so-called Brocken broughBraunwald phenomenon)
• One of the more reliable signs of dynamic obstruction of the LVOT,
intensity of murmur also increased

57. GOAL
• The main goals of management are alleviate
symptoms, prevent complications and decrease risk
of sudden death
• Improve ventricular filling.
• Reduce ventricular contractility
• Relieve left ventricular outflow obstruction.
TO DECREASE
CONTRACTILITY
TO IMPROVE FILLING

58. MANAGEMENT OF HCM
• Medical therapy
• Device therapy
• Surgical septal myomectomy
• Alcohol septal ablation

59. MANAGEMENT OF
HCM
Beta-blockers( Mainstay)
Increase ventricular diastolic filling/relaxation (decreases HR)
Decrease myocardial oxygen consumption
Have not been shown to reduce the incidence of SCD
Verapamil - Augments ventricular diastolic filling/relaxation
Amiodarone
Disopyramide - Used in combination with beta-blocker
Negative inotrope – Diuretics
DIGOXIN IS CONTRAINDICATED IN HYPERTROPHIC
CARDIOMYOPATHY.

60. Dual-Chamber Pacing
• Proposed benefit:
• Pacing the RV apex will decrease the outflow tract gradient by decreasing
projection of basal septum into LVOT
• Several RCTs have found that the improvement in subjective measures
provided by dual-chamber pacing is likely a placebo effect
• Objective measures such as exercise capacity and oxygen consumption
are not improved

61. SURGICAL MANAGEMENT OF
HCM:
Mitral valve replacement: Septal myectomy:

62. SYMPTOMATIC
MANAGEMENT
Percutaneous Transluminal Septal Myocardial
Ablation(PTSMA)

63. Alcohol Septal Ablation
• Successful short-term outcomes
• LVOT gradient reduced from a mean of 60-70 mmHg to <20 mmHg
• Symptomatic improvements, increased exercise tolerance
• Long term data not available yet
• Complications
• Large MI
• Complete heart block
• No randomized efficacy trials yet for alcohol septal ablation vs.
surgical myectomy

64. Sudden Cardiac Death in HCM
Most frequent in young
adults<30-35 yrs old
Primary VF/VT
Tend to die during or just
following vigorous physical
activity
Often is 1st clinical
manifestation of disease
HCM is most common cause
of SCD among atheletes.

65. RESTRICTIVE CARDIOMYOPATHY

66. RESTRICTIVE CARDIOMYOPATHY
• It is a disease of the heart muscle that impairs
diastolic filling and stretch.
• Systolic function remains unaffected.
• Least common of the cardiomyopathic
conditions.
• The heart chambers are unable to fill with
blood because the heart muscle is stiff.

67. RESTRICTIVE CARDIOMYOPATHY
• The average age at diagnosis is 5 to 6 years.
• RCM appears to affect girls somewhat more often than boys.
• There is a family history of cardiomyopathy in approximately 30% of
cases.
• In most cases the cause of the disease is unknown (idiopathic),
although a genetic cause is suspected in most cases of pediatric RCM

68. CAUSES
•Endomyocardial fibrosis
•Sarcoidosis
•amyloidosis
•Lofflers syndrome
•Neoplastic tumor
•Ventricular thrombus
•Fibrosis of different etiology
•Radiation to the thorax

69. PATHOPHYSIOLOGY
Increase in stiffness of the ventricular walls
Impaired diastolic filling of the ventricle(pulmonary
congestion, decreased CO)
Reducing preload and end-diastolic volume
Heart failure
As the disease progresses Systolic dysfunction

70. Disease course
• The most common symptoms at first may appear to be lung related. Children
with RCM frequently have a history of “repeated lung infections” or “asthma.”
• In these cases, referral to a cardiologist eventually occurs when a large heart
is seen on chest x-ray. The second most common reason for referral is an
abnormal physical finding during a doctor’s examination.
• Children who have ascites hepatomegaly and edema are often sent to see a
gastroenterologist first.

71. Disease course
• Referral to a cardiologist is made when additional cardiac signs or
symptoms occur, a chest x-ray is found to be abnormal or no specific
gastrointestinal cause is found for the edema or enlarged liver.
• In approximately 10% of cases, fainting is the first symptom causing
concern.
• Unfortunately, sudden death has been the initial presentation in some
patients.

73. ASSESSMENT FINDINGS
•Most common symptoms are dyspnea and
edema.
- Ascites may be evident.
•Auscultation:
- AV valve regurgitation.
•Echo:
- Biatrial enlargement due to rigid ventricular
walls is seen.(balloning of the RA and LA)
- PA pressure is greater than 50mm of Hg in
patients with RCM.
- Ejection fraction is 25-50%

74. COMPLICATIONS OF
CARDIOMYOPATHY
• Congestive cardiac failure.
• Arrhythmias.
• Thrombus and emboli.
• Stroke.
• Valvular disorders.
• Cardiac arrest.
• Infective endocarditis for patients HOCM.

75. STEM CELL THERAPY
• Stem cell therapy has emerged as a promising strategy for the
treatment of dead myocardium, directly or indirectly, and seems to
offer functional benefits to patients.
• The ideal candidate donor cell for myocardial reconstitution is a
stem-like cell that can be easily obtained, has a robust proliferation
capacity and a low risk of tumor formation and immune rejection,
differentiates into functionally normal cardiomyocytes, and is
suitable for minimally invasive clinical transplantation.

77. Types of Stem Cells for Cardiac Cell Therapy
• Skeletal Myoblasts Autologous transplantation of SKMs
• Bone Marrow-Derived Stem Cells
• Bone Marrow-Derived Mesenchymal Stem Cells
• Adipose-Derived Mesenchymal Stem Cells
• Cardiac Stem Cells
• Cardiosphere-Derived Cells
• Embryonic Stem Cells and Induced Pluripotent Stem Cells

78. • The variable and moderate benefits associated with stem cell
treatments were initially ascribed to inefficient cell delivery, with only
10% (or less) of the cells retained in the heart after 24 hours
regardless of the cell type or delivery route.
• The cells are usually washed out through the coronary venous system
or mechanically ejected from the injection site .
• Repeated administrations of BMCs, MSCs, and CDCs were
demonstrated to boost therapeutic benefits.

79. Route
• The following are three routes for delivering stem cells for cardiac
therapy:
• systemic intravenous infusion, Uptake only 0.04%
• intracoronary infusion, balloon catheters to infuse stem cells , uptake
1.3% to 2.6%
• and intramyocardial injection(open-chest surgery) Uptake of 6.2%

80. STEM CELL THERAPY
• Effects of stem cell therapy on dilated cardiomyopathy
• Rong Jiao, MD, Yuan Liu, MD, Wen-Jian Yang, MD, Xiao-Yan Zhu, MD, Jin
Li, MD, and Qi-Zhu Tang, 2014
Abstract
Objectives:
• To perform a meta-analysis of clinical trials and investigate the effect of
stem cell therapy on dilated cardiomyopathy.
Methods:
• A systematic literature search was carried out between May 2012 and July
2013 in PubMed, Medline, Cochrane Library, and Excerpta Medica
Database (EMBASE). The study took place in the Department of
Cardiology, Renmin Hospital of Wuhan University, Wuhan, China. The
weighted mean difference (WMD) was calculated for left ventricular
ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD),
mortality and heart transplantation, and the 6-minute walk test (6-MWT)
distance using the RevMan 5.0 software.

81. CONT…
Results:
• Seven trials with 599 participants evaluated the association between
the stem cell therapy and control groups. Compared with the control
group, stem cell therapy group improved the LVEF (WMD: 3.98%, 95%
confidence interval [CI]: 0.55 - 7.41%, p=0.02) and the 6-MWT
distance (WMD: 132.12 m, 95% CI: 88.15-176.09 m, p<0.00001), and
reduced mortality and heart transplantation (odds ratio [OR]: 0.48,
95% CI: 0.29-0.80, p=0.005). However, the LVEDD showed no
significant difference between the 2 groups (WMD: -1.53 mm, 95% CI:
-1.15-0.10 mm, p=0.10).
Conclusion:
• This meta-analysis demonstrated that stem cell therapy improves
cardiac function and reduces mortality in dilated cardiomyopathy
patients, which suggested that stem cell therapy may represent a new
therapy option for dilated cardiomyopathy.

83. NURSING MANAGEMENT

84. NURSING ASSESSMENT
• Take proper History
• Assess sign and symptoms
• Assess the psychosocial factors and stressors among pt
Physical assessment
oVitals
oPulse pressure
oWeight –gain/loss
oPoint of maximum impulse
oCheck for s3 and s4
oPulmonary assessment for crackles
oJugular venous distention
oEdema and severity

85. •Assess BP, heart rate & respiratory rate.
•Assess for change in mental status.
•Monitor intake and output regularly.
•Assess peripheral pulse for strength and quality.
•Encourage physical and psychological rest.
•Administer prescribed medications and evaluate
responses
Decreased cardiac output related to
structural disorders caused by
cardiomyopathy

86. •Monitor intake and output every 4 hourly.
•Weigh patients daily.
•Assess for the presence of peripheral edema
•Assess for jugular vein distension, hepatomegaly and
abdominal pain
•Follow low sodium diet and fluid restriction
•Auscultate breath sounds 2 hourly for the presence of
crackles and monitor for sputum production
•Administer diuretics as ordered and evaluate
effectiveness
Excess fluid volume related to decreased
contractility of heart

87. •Assess respiratory rate, rhythm and saturation
•Auscultate breath sounds every 2 hourly
•Encourage client to turn, cough and deep breath.
Use incentive spirometer 2 hourly.
•Provide fowler’s position to facilitate breathing and
observe for PND.
•Administer oxygen as ordered.
•Obtain ABG if ordered
•Administer diuretics as ordered
Impaired gas exchange related to
pulmonary congestion caused by
myocardial failure

88. .
•Assess for the manifestations of angina
•Assess respirations, BP, & HR with each episode of chest pain
•Obtain a 12 lead ECG each time chest pain recurs
•Administer nitrates, monitor response, notify if pain does not
abate in 15 – 20 min
•Provide care in a calm environment that minimizes anxiety
•Instruct patient to avoid physical exertion if pain occurs
•Stay with patient until discomfort is relieved.
Angina related to decreased coronary
perfusion

89. Summary
•Definition
•Types
•Causes
•Clinical classification
•Dilated cardiomyopathy
•Hypertrophic cardiomyopathy
•Restrictive cardiomyopathy
•Nursing management.

90. Conclusion
Although cardiomyopathy affects the
myocardium of the heart, the management
of each cardiomyopathy is different.
Hence, early diagnosis should be done to
prevent complications.

91. References
•Lewis, “medical surgical nursing, assessment
and management of clinical problems, 6th
edition, mosby publications, page no:852-
857.
•Susan woods, “cardiac nursing” 5th edition,
lippincott publications, page no:782-786.
•https://www.hindawi.com/journals/acp/2017/94
04057/
•https://www.ncbi.nlm.nih.gov/pmc/articles/PMC
4362159/#targetText=Conclusion%3A,therapy%2
0option%20for%20dilated%20cardiomyopathy.

92. THANK YOU