CARDIOMYOPATHY

PRESENTER:
DAINY THOMAS MSc NURSING IST YEAR STUDENT, AIIMS.

MODERATOR:
MADAM RACHEL ANDREWS LECTURER, AIIMS.

INTRODUCTION

OBJECTIVES
      

Define cardiomyopathy. Explain the types of cardiomyopathy. List down the etiological factors. Describe the pathophysiology of cardiomyopathy. Enlist the clinical features. Explain the medical and surgical management. Discuss the nursing management.

LAYERS OF HEART
  

Epicardium Myocardium Endocardium Pericardium

Definition


Diseases that involve the myocardium primarily and are not the result of hypertension, or congenital, valvular, coronary or arterial or pericardial abnormalities.

Cardiomyopathy

-"heart

muscle

disease"

deterioration of the function of the myocardium (i.e., the actual heart muscle) for any reason.

Definition
 Disease of the heart muscle in which the heart loses its ability to pump blood effectively.  Heart muscle- enlarged or abnormally thick or rigid.  Rare cases- heart muscle tissue- replaced with scar tissue.  Disease progresses heart becomes weaker and less able to pump blood to heart failure, arrhythmias, systemic and pulmonary edema and, more rarely, endocarditis.

Incidence
3rd most common form of heart disease in U.S. 2nd most common cause of adolescent sudden death. Directly affects cardiac structure and

impairs myocardial function.

Classification
 

Extrinsic or Intrinsic cardiomyopathy . Extrinsic - primary pathology - outside the myocardium itself.

 

Most common cause - ischemia. WHO- specific cardiomyopathies.

Classification


Intrinsic - Weakness in the heart muscle that is not due to an identifiable external cause (idiopathic cardiomyopathies).

Consist of a variety of disease states, each with their own causes.

According to the structural and functional abnormalities

   

Dilated cardiomyopathy (DCM) Hypertrophic cardiomyopathy (HCM) Restrictive or constrictive cardiomyopathy Arrhythmogenic right ventricular cardiomyopathy (ARVC)

 

Unclassified cardiomyopathy Ischemic cardiomyopathy

Types
Primary/intrinsic cardiomyopathies
Genetic
Hypertrophic cardiomyopathy (HCM) Arrhythmogenic right ventricular

cardiomyopathy (ARVC) Isolated ventricular non-compaction Mitochondrial myopathy

Types
Mixed
Dilated cardiomyopathy (DCM) Restrictive cardiomyopathy (RCM)

Acquired
Takotsubo cardiomyopathy Loeffler endocarditis

Secondary/extrinsic cardiomyopathies


Metabolic/storage
Amyloidosis  Hemochromatosis


Endocrine
Diabetic cardiomyopathy  Hyperthyroidism  Acromegaly


Inflammatory


Chagas disease

Toxicity
Chemotherapy  Alcoholic cardiomyopathy


 

Nutritional diseases Other



"Ischemic cardiomyopathy

Neuromuscular


Muscular dystrophy

Types and Causes:

Ischemic cardiomyopathy - caused by CAD & MI , which leave scars in the heart muscle Idiopathic cardiomyopathy - the cause is unknown. Hypertensive cardiomyopathy - seen in people who have high BP for a long time, particuarly when it has gone untreated for years. Infectious cardiomyopathy - HIV, viral myocarditis Diabetes and thyroid disease

Types and Causes:

Alcoholic cardiomyopathy - usually begins about 10 years after sustained, heavy alcohol consumption. Toxic cardiomyopathy due to cocaine, amphetamines, and some chemotherapy drugs (doxorubicin, daunorubicin) Peripartum cardiomyopathy: This type appears in women during the last trimester of pregnancy or after childbirth. Radiotherapy (cobalt)

DILATED CARDIOMYOPATHY

Most common cause of clinical syndrome of heart failure

Dilated Cardiomyopathy
Defined - a ventricular chamber exhibiting increased diastolic and systolic volumes and a low < 45% ejection fraction.  Generally occurs - 20 to 60 years  More common in men Heart muscle begins to dilate or stretch and become thinner Ventricular chamber size Over time, the heart becomes weaker Heart failure


Anatomical specimen

DILATED CMP
    

LV and or RV dilatation Systolic dysfunction CCF Arrhythmias Emboli

Hypertrophic Cardiomyopathy
 Occurs when the heart muscle thickens abnormally (left ventricle)  Obstructive type - septum thickens and bulges into the LV blocks the flow of blood into the aorta the ventricle must work much harder to pump blood past the blockage and out to the body. Symptoms - chest pain, dizziness, SOB, or fainting  Can also affect the MV, causing blood to leak backward through the valve.

NonNon-obstructive type
-

The

entire

ventricle

may

become

thicker

(symmetric ventricular hypertrophy) or it may happen only at the bottom of the heart (apical hypertrophy).
-

The right ventricle also may be affected.

Pathophysiology: 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

Causes:
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Inherited because of a gene mutation Develop over time because of high blood pressure or aging

Often, the cause is unknown.

Restrictive Cardiomyopathy


Tends to mostly affect older adults

Ventricles - stiff and rigid due to replacement of the

normal heart muscle with abnormal tissue, such as scar tissue ventricles cannot relax normally and expand to fill with blood atria to become enlarged blood flow in the heart is reduced complications - heart failure or arrhythmias occur.

Causes:
Radiation treatments, Infections, or Scarring after surgery Hemochromatosis Amyloidosis Sarcoidosis

Major Risk Factors

Family history of cardiomyopathy, heart failure, or sudden cardiac death Disease or condition that can lead to cardiomyopathy: CAD A previous heart attack Myocarditis Long-term alcoholism Long-term high blood pressure Diabetes and other metabolic diseases

Clinical Manifestations
 

Remain stable without symptoms. Signs and symptoms of heart failure (eg, dyspnea on exertion, fatigue). PND, cough (especially with exertion), and orthopnea. Fluid retention, peripheral edema, and nausea, (poor perfusion of GI system). Chest pain, palpitations, dizziness, nausea, and syncope with exertion. HCM- cardiac arrest -initial manifestation in young people, including athletes.

CLINICAL MANIFESTATIONS
Symptoms of heart failure Pulmonary congestion (left HF) Dyspnea (rest, exertional, nocturnal), Orthpnea Systemic congestion (right HF) Edema, Nausea, Abdominal pain, Nocturia Low cardiac output Fatigue and Weakness Hypotension, Tachycardia, Tachypnea, JVD If EF<20% high risk for embolism and SV arrhythmias

Assessment and Diagnostic Findings

Physical examination : Tachycardia, extra heart sounds, Signs and symptoms of heart failure Patient history -Myocardial Infarction. Echocardiogram Radionuclide imaging

Assessment and Diagnostic Findings

ECG - Dysrhythmias and changes of LVH. Chest X-ray - Heart enlargement, pulmonary congestion. Cardiac catheterization CAD Endomyocardial biopsy- Analyze myocardial tissue cells.

DIAGNOSIS


Cardiac catheterization  Age >40, ischemic history, abnormal ECG  LVEDV,LA, PCWP, RVEDV, RA, CVP

Chest X-Ray PA view X-

NORMAL

2D Echo finding M Mode

Parasternal longitudinal view

Massive cardiomegaly water bottle shaped heart

TREATMENT


Manage any conditions that cause or contribute to the cardiomyopathy

Control symptoms so that the person can live as normally as possible

 

Stop the disease from getting worse Reduce complications and the chance of sudden cardiac death

Medications:


Diuretics -remove excess fluid and sodium from the body.

Angiotensin-converting enzyme (ACE) inhibitors - lower blood pressure and reduce stress on the heart.

Beta-blockers- slow the heart rate by reducing the speed of the heart's contractions and also lower BP.

Calcium channel blockers- slow a rapid heartbeat by reducing the force and rate of heart contractions, decrease BP

Medications


Digoxin - increases the force of heart contractions and slows

the heartbeat.


Anticoagulants- prevent blood clots from forming, used in

the treatment of dilated cardiomyopathy.



Antiarrhythmics - keep the heart beating in a normal rhythm. Antibiotics- used before dental or surgical procedures, help to

prevent endocarditis.


Corticosteroids, which reduce inflammation.

Contd
Treatment of CCF Avoid dehydration Cardiac pacing Mx of arrhythmias ICD implantation Cardiac transplantation Stem cell transplantation

Lifestyle Changes


Quit smoking Lose excess weight Eat a low-salt diet Get moderate exercise, such as walking Avoid strenous exercise Fluid restriction, <2l/ day.

Lifestyle Changes
   

Avoid the use of alcohol and illegal drugs Get enough sleep and rest Reduce stress Treat underlying conditions, such as DM and high BP.

Left Ventricular Outflow Tract Surgery.

u

Myectomy (myotomymectomy)- some of the heart tissue is excised.

Removing the MV , chordae, and papillary muscles. MV then is replaced with a low-profile disk valve. Open-heart surgery for hypertrophic obstructive cardiomyopathy

Heart Transplantation
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Orthotopic transplantation - most common Recipients heart- removed, donor heart is implanted at the vena cava and pulmonary veins.

Some remove the recipients heart leaving a portion of the recipients atria (with the vena cava and pulmonary veins) in place.

Heart Transplant (cont.)

Orthotopic transplantation
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Donor heart - implanted by suturing the donor atria to the residual atrial tissue of the recipients heart.

Both techniques then connect the recipients pulmonary artery and aorta to those of the donor heart.

Heterotopic transplantation
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Less common. Donor heart - placed to the right and slightly anterior to the recipients heart.

Recipients heart -not removed. Transplanted heart - denervated Sympathetic and vagus nerves do not affect the transplanted heart.

Heterotopic transplantation
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Resting rate of transplanted heart approx 70 - 90 bpm, increases gradually if catecholamines are in the circulation.

Patients gradually

and

their exercise (extended

warm-up and cool-down periods.

u

Atropine does not increase the heart rate of these patients.

Heart Transplant :Contra indications

u

Advanced age Poor blood circulation throughout the body Diseases of the kidney, lungs, or liver that can't be reversed. History of cancer or malignant tumors. Inability or unwillingness to follow lifelong medical

instructions
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Pulmonary arterial hypertension that can't be reversed. Active infection throughout the body.

Heart Transplant (cont.)

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Organs are matched for blood type and size of donor and recipient.

Guidelines on how a donor heart is selected :  The donor meet the legal requirement for brain death  Consent forms are signed  Younger than 65 years of age  Have little or no history of heart disease or trauma to the chest  Not exposed to hepatitis or HIV  Donor heart must be transplanted within 4 hrs. After removal from the donor

Heart Transplant (cont.)

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A bypass machine is hooked up to the arteries and veins of

the heart. The machine pumps blood through the patient's lungs and body while the diseased heart is removed and the donor heart is sewn into place.
u

Watching for Signs of Rejection

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Shortness of breath , Fever Fatigue , Weight gain Reduced amounts of urine Preventing Infection

Postoperative Course


Balance the risk of rejection with the risk of infection.

Complex regimen of diet, medications, activity, follow-up laboratory studies, biopsies (to diagnose rejection), and clinic visits.

Patients

receive or

cyclosporine mycophenolate

or

tacrolimus, and

azathioprine

mofetil,

corticosteroids (prednisone) to minimize rejection.

Complications
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Rejection and infection Accelerated atherosclerosis of the coronary arteries (cardiac allograft vasculopathy [CAV]or accelerated graft atherosclerosis [AGA])

Hypertension Osteoporosis

Complications
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Post transplantation lymphoproliferative disease Cancer - skin and lips Weight gain, obesity, diabetes, dyslipidemias (eg, hypercholesterolemia), hypotension, renal failure,

CNS,

respiratory,

and

GI

disturbances

corticosteroids or other immunosuppressants.

Complications
u

Immunosuppressant medication toxicities Psychosocial stresses Guilt Anxiety about the new heart Depression or fear when rejection is identified Difficulty with family role changes

Mechanical Assist Devices and Total Artificial Hearts.



Patients who cannot be weaned from cardiopulmonary bypass

Patients in cardiogenic shock may benefit from a period of mechanical heart assistance.

 

Intra-aortic balloon pump- most common This pump decreases the work of the heart during contraction but does not perform the actual work of the heart.

Ventricular Assist Devices.

Can circulate as much blood per minute as the patients heart. Used to support one ventricle. Some combined with an oxygenator-

extracorporeal membrane oxygenation (ECMO). Used for the patient whose heart cannot pump adequate blood through the lungs or the body.

Left Ventricular Assist Device (LVAD)

VADs
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3 basic types of devices: centrifugal, pneumatic, and electric or electromagnetic.

Centrifugal VADs - external, nonpulsatile, coneshaped devices with internal mechanisms that spin rapidly, creating a vortex (tornado-like action) that pulls blood from a large vein into the pump and then pushes it back into a large artery.

Pneumatic VADsVADs

External or implanted pulsatile devices with a flexible reservoir housed in a rigid exterior.

Usually fills with blood drained from the patients atrium or ventricle.

It then forces pressurized air into the rigid housing, compressing the reservoir and returning the blood to the patients circulation, usually into the aorta.

Electric or electromagnetic VADs

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Similar to the pneumatic VADs, But instead of pressurized air, one or more flat metal plates are pushed against the reservoir to return the blood to the patients circulation.

Total Artificial Hearts.

 

Designed to replace both ventricles. Some require the removal of the patients heart to implant the total artificial heart; others do not.

Temporary treatments while the patients own heart recovers or until a donor heart becomes available for transplantation (ie, bridge to transplant).

NURSING DIAGNOSES
u

u u u u

Decreased cardiac output related to structural disorders caused by cardiomyopathy or to dysrhythmia from the disease process and medical treatments. Diagnostic Assessment Review ECG Echocardiography Cardiac catheterization

Patient Monitoring
u

Obtain BP hourly or more frequently if the patients condition is unstable.

Monitor hourly urine output to evaluate effects of decreased intervention. cardiac output or pharmacologic

Analyze ECG rhythm strip at least every 4 hours and note rate.

Continuously monitor oxygen status with pulse oximetry.

Monitor

patient that

activities may

and adversely

nursing affect

interventions oxygenation.

Patient Assessment
u

Obtain vital signs every 15 minutes during acute phase.

Assess the patient for changes in neurological function hourly and as clinically indicated.

Assess for skin warmth, color, and capillary refill time.

Assess

for

chest

discomfort

because

myocardial ischemia may result from poor perfusion.

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Assess heart and lung sounds to evaluate the degree in heart failure.

Patient Management
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Provide oxygen at 2 to 4 L/min to maintain or improve oxygenation.

Minimize oxygen demand by maintaining the patient at bed rest.

Provide liquid diet on acute phase, Administer diuretic as prescribed to reduce preload and afterload.

Monitor

serum

potassium

before

and

after

administration of loop diuretics.

u

Prophylactic heparin may be ordered to prevent thromboembolus formation secondary to venous poisoning.

Institute

pressure

ulcer

prevention

strategies

secondary to hypoperfusion or vasoconstriction agents.

Obstructive Hypertrophic Cardiomyopathy: Cardiomyopathy: Nursing Implications

u

Electrolyte monitoring Maintain an adequate hydration status Vigilant monitoring for tachycardias or dysrhythmias.

Emotional support, frequent teaching Counseling to assist in patient and family coping should be strongly encouraged.

Lifelong dental prophylaxis with antibiotics is necessary.

Medic-alert bracelets are recommended Nitroglycerin and positive inotropic agents are not standard therapy in the patient with HCM.

Diuretics may be used, however, when initiated, close supervision of electrolyte and hydration status must be maintained.

Monitor for dysrhythmias - primary focus. Dehydrationand obstruction. preload and HR LVOTgradient

Restrict from playing competitive sports, the rationale should be explained thoroughly (i.e., complications secondary to dehydration and

increased heart rate).

Severe problems may also present after exercise when decreasing heart rate and vasodilatation occurs.

Make aware of the potential complications so they may take the necessary precautions.

Ineffective cardiopulmonary, cerebral, peripheral, and renal tissue perfusion related to decreased peripheral blood flow (resulting from decreased cardiac output)

Impaired gas exchange related to pulmonary congestion caused by myocardial failure (decreased cardiac output)

NURSING DIAGNOSES
Activity intolerance related to decreased cardiac output or excessive fluid volume, or both Anxiety related to the change in health status and in role functioning. Powerlessness related to disease process Noncompliance with medication and diet therapies

SUMMARY
u

Nursing care of the patient is composed of advocacy, emotional support, complication prevention, monitoring, and education. Consideration must be given to the presenting symptoms, lifestyle expectations, impact of treatment selection, risks, benefits, psychological implications, and insurance concerns. Therefore, the nurse must have understanding of the complexities of this disease and its varied treatment options to be able to provide the appropriate individualized care that all patients

CONCLUSION

BIBLIOGRAPHY
u u u

http://www.medscape.com/viewarticle/495035_5 http://nursingcrib.com/category/nursing-care-plan/ inomemoirofaschizo.blogspot.com/2009/08/reviewyour-medical-surgical-nursing.html o.in/#sclient=psyab&hl=en&site=&source=hp&q=n ursing+management+of+cardiomyopathy&pbx=1& oq=nursing+management+of+cardiomyopathy&aq= f&aqi=&aql=&gs_sm=e&gs_u