Nursing

management of
patient with cardiac
disorders
 cardiac disorders
1. Coronary Artery Disease

2. Myocardial Infarction

3. Cardiogenic Shock

4. Infective Endocarditis

5. Rheumatic Endocarditis (Rheumatic Heart Disease

6. Myocarditis
7. Pericarditis

8. Cardiomyopathy

9. Acquired Valvular Disease of the Heart

10. Cardiac Dysrhythmias

11. Hypoplastic Left Heart Syndrome

 Objectives:
1. Define cardiac disorders
2. Explain anatomy and physiology.
3. Enlist types risk factor and etiological factor for cardiac disorders
4. Formulate pathophysiology
5. Discuss clinical manifestation
6. Explain medical management.
7. Explain surgical management
8. Explain nursing management.
  Anatomy and physiology.:
1. The cardiovascular system consists of the heart, the major blood vessels that
empty into or exit directly from the heart, and a vast network of smaller
peripheral blood vessels.

2. The heart itself is about the size of a person’s fist. It lies below and slightly to
the left of the midline of the sternum in the mediastinum, a portion of the
thoracic cavity that also contains the trachea and major blood vessels. The
upper portion of the heart is the base, and the tip is the apex
 Conductive system
 Cardiac cycle:
1.Coronary Artery Disease
Coronary artery disease (CAD) is the leading cause of death in the United
States. CAD is characterized by the accumulation of plaque within the layers of
the coronary arteries.

The plaques progressively enlarge, thicken, and calcify, causing a critical

narrowing (>70% occlusion) of the coronary artery lumen, resulting in a
decrease in coronary blood flow and an inadequate supply of oxygen to the
heart muscle.
Acute coronary syndrome (ACS) is an umbrella term that is used to describe
many of the complications associated with CAD.

These include unstable angina, non-ST-elevation myocardial infarction

(NSTEMI), and ST-elevation myocardial infarction (STEMI).
  Etiology:
1. Unstable or ruptured atherosclerotic plaque.

2. Coronary vasospasm.

3. Atherosclerotic obstruction without clot or vasospasm.

4. Inflammation or infection.

5. Unstable angina due to a noncardiac cause.

6. Thrombus formation with subsequent coronary artery occlusion

 RISK FACTORS
 Pathophysiology:
 Clinical manifestation:
1. Chest pain (Angina pectoris)
2. Myocardial infarction
3. Diaphoresis
4. Ecg changes
5. Dysarrithmias
6. Chest heaviness
7. Dyspnea
8. Fatigue
 Diagnostic Evaluation
1. History collection
2. Physical examination
3. Cardiac enzymes
4. Electrocardiograms
5. Echocardiograms
6. Stress Tests
7. Nuclear Imaging
8. Angiography
9. ECHOCARDIOGRAMS It is may be ordered if doctor suspects a problem
with the heart muscle or one of the valves that channel blood through the
heart.

10. STRESS TESTS They are used to show how the heart reacts to physical
exertion. Exercise stress tests are usually performed on a treadmill or
exercise bicycle.
 MEDICAL MANAGEMENT
PHARMACOLOGICAL THERAPY

Anti anginal medications :like nitrates(isd,)

Beta adrenergic blockers(atenolol)
calcium channel blockers(nefidipine)
ACE inhibitors(captopril)
statins
imipramine for analgesia
 SURGICAL INTERVENTION
1. ANGIOPLASTY

2. STENTS

3. CORONARY ARTERY BYPASS GRAFTING (CABG)

4. PTCA
 NURSING DIAGNOSIS
1. Acute pain related to imbalance to oxygen supply demand

2. Decreased cardiac output related to reduced preload afterload contractility

and heart rate secondary to hemodynamic effects of drug therapy

3. Anxiety related to chest pain, uncertain prognosis, and threatening

environment
2. ANGINA PECTORIS
  Definition:
• Angina pectoris is a clinical syndrome usually characterized by
episodes or paroxysms of pain or pressure in the anterior chest.

• The cause is insufficient coronary blood flow, resulting in a decreased

oxygen supply when there is increased myocardial demand for oxygen
in response to physical exertion or emotional stress
• In other words, A disease marked by brief sudden attacks of chest
pain or discomfort caused by deficient oxygenation of the heart
muscles usually due to impaired blood flow to the heart.

• the need for oxygen exceeds the supply.

• In general, the severity of the symptoms of angina is based on the

magnitude of the precipitating activity and its effect on activities of
daily living.
 INCIDENCE:
• An estimated 10 million people in the US suffer from angina.

• According to the Framingham Heart Study, an estimated 500,000

new cases of stable angina occur each year.
  TYPES:
• Stable Angina

• Unstable Angina

1. Variant Angina Pectoris

2. Nocturnal Angina Pectoris

  Stable Angina
1. Character—substernal chest pain, pressure, heaviness, or discomfort. Other
sensations include a squeezing, aching, burning, choking, strangling, and/or
cramping pain.

2. Location—behind middle or upper third of sternum; the patient will generally

make a fist over the site of the pain (positive Levine’s sign, indicating diffuse
deep visceral pain) rather than point to it with his or her finger.
3. Radiation—usually radiates to neck, jaw, shoulders, arms, hands,
and posterior intrascapular area. Pain occurs more commonly on
the left side than the right.

4. Duration—usually lasts 2 to 15 minutes after stopping activity;

nitroglycerin relieves pain within 1 min
 Unstable (Preinfarction) Angina
Pectoris
1. Unstable (Preinfarction) AA change in frequency, duration, and
intensity of stable angina symptoms is indicative of progression
to unstable

2. Unstable angina pain lasts longer than 10 minutes, is unrelieved

by rest or sublingual nitroglycerin, and mimics signs and
symptoms of impending MI.ngina Pectoris
  Etiological factor:
• Development of atherosclerosis; Coronary artery disease is thought to begin with
damage or injury to the inner layer of a coronary artery, sometimes as early as
childhood. The damage may be caused by various factors, including:

1. Smoking

2. High blood pressure

3. High cholesterol

4. Diabetes or insulin resistance

5. Sedentary lifestyle
 Pathophysiology:
 Clinical manifestation:
• CARDIOVASCULAR-

Angina pectoris- it is sensation of chest pain , pressure or squeezing often due

to insufficient blood flow to the heart muscle as a result of obstruction.

Chest pain –chest pain occurs suddenly , severe immobilizing chest pain that
not relieved by rest , position change and medications.

Hypotension

tachycardia, bradcardia, or dysrhythimas,Dysarrithmias

2. RESPIRATORY-

1. Shortness of breath.

2. Pulmonary edema

3. Chest heaviness

4. Dyspnea

5. Fatigue
3. Genitourinary-

• Decreased Urinary Output May Indicate Cardiogenic Shock.

4. Gastrointestinal- Nausea And Vomiting

5. Skin- Cool, Clammy ,Diaphoretic , And Pale Appearance On Skin

 DIAGNPOSTIC EVALUATION
1.Physical Examination
2.History collection
3.Stress test
4.Chest X-ray.
5.Electrocardiogram (ECG).
6.Echocardiogram

7.Cardiac catheterization (angiogram).

 Medical Managements:
1. Variousdrugs can be used to treat coronary artery disease, including:  Vasodilators
(These drugs acts as blood vessel dilator):

2. Nitrates

3. Beta-Blockers (Decrease work load in heart): • Propranolol 20-40 mg

4. Calcium channel blocker (They improve coronary blood flow): • Nifedipine • Verapamil

5. Anticoagulant Drugs: Heparin

6. Opiate Analgesic (For reduce pain) ,Morphine sulphate

7. Thrombolytic Drugs: :Streptokinase, Urokinase

• ANTIHYPERTENSIVE MEDICINES-

1. Methyldopa - This medication is used alone or with other medications to

treat high blood pressure (hypertension). Lowering high blood pressure
helps prevent strokes, heart attacks, and kidney problems. Methyldopa
works by relaxing blood vessels so blood can flow more easily.

2. Sodium nitroprusside- It is used for lowering the blood pressure.

3. Amlodipine- Amlodipine is used with or without other medications to

treat high blood pressure. Lowering high blood pressure helps prevent
strokes, heart attacks, and kidney problems. Dose-10 mg,20 mg.
  SURGICAL MANAGEMENT
• Angioplasty
and stent
placement
(percutaneous
coronary
revascularizati
on):
 Nursing diagnosis:
1.  Impaired gas exchange related to decreased blood flow as evidenced by
breathlessness
2. Acute pain related to disease condition as evidenced by patient verbalization
3. Impaired physical mobility related to weakness as evidenced by patient is unable to
perform daily activity.
4. Imbalanced nutrition less than body requirement related to less intake of food as
evidenced by weight loss
5. Disturbed sleep pattern related to hospitalization as evidenced by patient
verbalization
6. Anxiety related to hospitalization as evidenced by patient asking too many question.
7. Knowledge deficit related to disease process and treatment as evidenced by patient is
having many doubts
3. Infective Endocarditis
  Definition:
Infective endocarditis (IE; bacterial endocarditis) is an infection of the inner
lining of the heart caused by direct invasion of bacteria or other organisms that
could potentially result in myocardial abscess or heart failure and other
complications
• Infective endocarditis, a serious infection of the endocardium of
the heart, particularly the heart valves, is associated with a high
degree of illness and death. It generally occurs in patients with
altered and abnormal heart architecture, in combination with
exposure to bacteria through trauma and other potentially high-risk
activities involving transient bacteremia.
  Types of endocarditis:
1. Acute – Affects normal heart valves – Rapidly destructive –
Metastatic foci – Commonly Staph. – If not treated, usually fatal
within 6 weeks

2. Subacute – Often affects damaged heart valves – Indolent nature

– If not treated, usually fatal by one year
  Etiological factor:
Bacterial Endocarditis
1. Dental manipulation
2. Dental disease (caries, abscess)
3. Extra cardiac infection (lung, urinary tract,
4. skin, bone, abscess)
5. Instrumentation (urinary tract, GI tract, IV infusions)
6. Cardiac surgery
7. Injection drug use
8. w`xzzcvfghjk6as
  Causative organism:
1. Infecting Organisms Common bacteria –

2. Alpha haem streptococci (viridans – S. mitis, S. sanguis)

3. SUBACUTE – Enterococci (E. faecalis)

4. SUBACUTE – Coagulase Negative Staphylococci –

5. PROSTHETIC VALVES, SUBACUTE

6. Less common bacteria – S. aureus

7. ACUTE – B-Haemolytic streptococci ,Streptococcus pneumonia Not so common –

Fungi – Pseudomonas / Coliforms
 Pathophysiology:
  Clinical manifestation:
• General Manifestations

1. Fever, chills, sweats (fever may be absent in older patients or

those with uremia).

2. Anorexia, weight loss, weakness.

3. Cough, back and joint pain (especially in patients over age 60). 4.
Splenomegaly
• Skin and Nail Manifestations

1. Petechiae—conjunctiva, mucous membranes.

2. Splinter hemorrhages in nailbeds.

3. Osler’s nodes—painful red nodes on pads of fingers and toes; usually late sign of infection
and found with a subacute infection.

4. Janeway’s lesions—light pink macules on palms or soles, nontender, may change to light
tan within several days or fade in 1 to 2 weeks; usually an early sign of endocardial
infection.

5. Clubbing of fingers and toes—primarily occurs in patients who have an extended course of
untreated infective endocarditis
• Heart Manifestations

1. New pathologic or changing murmur—no murmur with other signs and

symptoms may indicate right-sided heart infection.

2. Tachycardia—related to decreased CO.

3. Symptoms consistent with heart failure.

• Central Nervous System Manifestations

1. Localized headaches.

2. Transient cerebral ischemia or other neurological symptoms.

3. Altered mental status, aphasia.

4. Hemiplegia.

5. Cortical sensory loss.

6. Roth’s spots on fundi (retinal haemorrhages)

• Pulmonary Manifestations

1. Usually occur with right-sided heart involvement.

2. Pneumonitis, pleuritis, pulmonary edema, infiltrates. Embolic Phenomena

3. Lung—haemoptysis, chest pain, shortness of breath.

• Kidney—haematuria, abnormal urine colour.

• Spleen—pain in left upper quadrant of abdomen radiating to left shoulder.

• Heart—MI, aortic insufficiency, heart failure.

• Brain—sudden blindness, paralysis, brain abscess, meningitis, CVA.

• Blood vessels—mycotic aneurysms.

• Abdomen—melena, acute pain.

 Diagnostic Evaluation
• Physical examination:

Major Criteria

1. Blood cultures—at least two positive serial blood cultures (90% of IE patients have
positive blood cultures).

2. Endocardial involvement (diagnosed with echocardiography)—identification of

vegetations and assessment of location and size of lesions.

3. New valvular insufficiency/regurgitation.

4. Development of partial dehiscence of prosthetic valve.

• Minor Criteria

1. Predisposing cardiac condition or IV drug use.

2. Fever higher than 100.4° F (38° C).
3. Vascular factors—pulmonary complication, emboli, Janeway’s lesions.
4. Immunologic factors—Osler’s nodes, Roth’s spots, rheumatoid factor.
5. Microbiology—positive cultures, but not meeting major criteria.
6. Echocardiogram—consistent with disease, but not meeting major
criteria
• History collection

1.Electrocardiogram (ECG).

2.Echocardiogram

3.Cardiac catheterization (angiogram).

4.Transoesophageal Echo (TOE)

  Medical management:
1. IV antimicrobial therapy, based on sensitivity of causative agent (6 weeks of
therapy is recommended for most patients except uncomplicated right-sided IE
in whom 2 weeks of therapy is recommended).

2. Bactericidal serum levels of selected antibiotics are monitored by serial titers;

if serum lacks adequate bactericidal activity, more antibiotic or a different
antibiotic is needed.

3. Note that missed doses of antibiotics due to the patient’s unavailability while
off the unit for diagnostic tests are given after return to the unit.
4. Notify health care provider if doses will be missed to ensure that appropriate alternative
measures are taken.

5. Missed antibiotic doses may have irreversible deleterious consequences.

6. Audiogram obtained before antibiotic regimen initiated.

7. Urine cultures obtained after 48 hours to assess efficacy of drug therapy.

8. Repeat blood cultures obtained after 48 hours to assess efficacy of drug therapy.

9. Close follow-up by cardiologist.

10. Supplemental nutrition

  Antibiotic Regimens for Prophylaxis
Antibiotic Regimens for Prophylaxis of Endocarditis in Adults with High-Risk
Cardiac Lesions A. Standard oral regimen

Amoxicillin: 2 g PO 1 h before procedure B. Inability to take oral medication

Ampicillin: 2 g IV or IM within 1 h before procedure C. Penicillin allergy

Clarithromycin or azithromycin: 500 mg PO 1 h before procedure

Cephalexinc: 2 g PO 1 h before procedure

Clindamycin: 600 mg PO 1 h before procedure

Penicillin allergy, inability to take oral medication

Cefazolinc or ceftriaxonec: 1 g IV or IM 30 min before procedure

Clindamycin: 600 mg IV or IM 1 h before procedure

  Surgical management:
Indications: –
1. Congestive cardiac failure
2. perivalvular invasive disease
3. uncontrolled infection despite maximal antimicrobial therapy
4. Presence of prosthetic valve endocarditis unless late infection
5. Large vegetation
6. Major embolus
7. Heart block
• Valvotomy
• Valvuloplasty
 Nursing diagnosis:
1. Decreased Cardiac Output related to structural factors (incompetent
valves).

2. Ineffective Tissue Perfusion (renal, cerebral, cardiopulmonary, GI, and

peripheral) related to interruption of blood flow.

3. Imbalanced Nutrition: Less Than Body Requirements related to

anorexia

4. Anxiety related to acute illness and hospitalization.

4. Myocarditis
  Definition:
1. Myocarditis is a focal or diffuse inflammation of the myocardium.

2. Myocarditis can cause heart dilation, thrombi on the heart wall (mural
thrombi), infiltration of circulating blood cells around the coronary vessels
and between the muscle fibers, and degeneration of the muscle fibers
themselves.

3. Myocarditis causes the heart muscle to become thick and swollen.

  ETIOLOGY:
1. 50% etiologies are Idiopathic.

There are 2 main types of etiologies are related to myocarditis.

2. Infectious causes

3. Non infectious causes

1. Infectious causes
1. Virus- Coxsackie A and B , HIV, Influenza

2. Bacterial infection-

Diphtheria, Lyme’s disease (also known as Lyme borreliosis, is an infectious

disease caused by bacteria of the Borrelia type which is spread by deer
ticks).

Rickettsial infection.
3. Fungal infection. :

• Protozoal Infection (e.g. Chagas disease caused by Trypanosoma

leads to necrosis of heart muscle)

• Metazoal infection.

• Parasitic infection.

• Spirochetal infection.
 2.NON INFECTIOUS CAUSE:
1. Granulomatous inflammatory disease (eg. sarcoidosis, giant cell myocarditis). • Rheumatic
fever. • Transplant rejection.

2. Patients receiving immunosuppressive therapy .

3. It can develop in patients with infective endocarditis , Crohn disease, and systemic lupus
erythematous.

4. Results from an inflammatory reaction to toxin such as alcohol, radiation (especially to the
left chest or upper back) , chemicals, and drugs (Anthracyclines for cancer therapy)
 Pathophysiology
 CLINICAL MANIFESTATION:
• Symptoms depend on type of infection, degree of myocardial damage,
capacity of myocardium to recover, and host
• resistance. Can be acute or chronic and can occur at any age.
• Symptoms may be minor and go unnoticed.
• Fatigue and dyspnea.
• Palpitations.
• Occasional precordial discomfort/vague chest pain.
• Cardiac enlargement

• Abnormal heart sounds: murmur, S3 or S4 , or friction rubs.

• Signs of heart failure (eg, pulsus alternans, dyspnea, crackles, lower-

extremity edema, low urine output).

• Fever with tachycardia or other sign of viral infection, such as headache,

joint pain, and sore throat. 6. Joint pain or swelling; leg swelling
 Diagnostic Evaluation
1. History collection.

2. Physical examination :-A physical examination may show no abnormalities, or may

reveal the following: - I. Abnormal heartbeat II. Fever III. Tachycardia IV. Edema in
the legs.

3. An Electrocardiogram : T wave inversions; saddle- shaped ST segment elevations may

be present.

4. Chest X-Ray .

5. Lab test- elevated WBC count, increase ESR, elevated C-reactive protein (CRP) ,
elevated cardiac biomarkers.
6. Echocardiogram- dysrhythmias .

7. Magnetic resonance imaging (MRI)

scan

8. Heart biopsy

9. Nuclear imaging using gallium or

indium (antimyosin antibodies)—helps
detect myocardial inflam
  MEDICAL MANAGEMENT:
1. Diuretic and digoxin therapy for heart failure and atrial fibrillation.

2. Antidysrhythmic therapy (usually amiodarone).

3. Strict bed rest to promote healing of damaged myocardium.

4. Antimicrobial therapy if causative bacteria are isolated.

5. Anticoagulation therapy

6. ACE inhibitor or beta-adrenergic blocker (should be used with caution; may cause
hypotension)—to strengthen the heart’s pumping ability and to reduce its workload, thus
improve left ventricular systolic dysfunction
7. In severe cases, aggressive therapy may be necessary:

8. inotropes, such as dobutamine and dopamine; IABP (counter pulsation

therapy); temporary artificial heart (assist device);

9. consideration of urgent heart transplantation.

10. IV immunoglobulin has antiviral effects; immunosuppressive regimen of

steroids and cyclosporine or azathioprine

11. improves systolic function.

  NURSING MANAGEMENT :
1. Hyperthermia related to inflammatory/infectious process.

2. Decreased Cardiac Output related to decreased cardiac

contractility and dysrhythmias

3. Activity Intolerance related to impaired cardiac performance and

febrile illness.
5. Pericarditis
 Definition:
• Pericarditis is an inflammation of the pericardium, the membranous sac
enveloping the heart. It is usually a manifestation of a more generalized
disease
• The pericardium is a fibroelastic sac made up of visceral and parietal layers
separated by a (potential) space, the pericardial cavity.
• In healthy individuals, the pericardial cavity contains 15 to 50 mL of an
ultrafiltrate of plasma.
  Acute and recurrent pericarditis.
1. Cardiac tamponade is an acute type of pericardial effusion in which the heart is compressed,
either by blood or by a penetrating injury, so that its normal function is impeded.

2. Pericardial effusion is an outpouring of fluid into the pericardial cavity seen in pericarditis.

3. Constrictive pericarditis is a condition in which a chronic inflammatory thickening of the

pericardium compresses the heart so it is unable to fill normally during diastole.
 Pathophysiology
 Clinical Manifestations
1. Pain in anterior chest, aggravated by thoracic motion—may vary from mild to
sharp and severe; located in precordial area (may be felt beneath clavicle, neck,
scapular region); may be relieved by leaning forward.

2. Pericardial friction rub—scratchy, grating, or creaking sound occurring in the

presence of pericardial inflammation, Edema, ascites, and dyspnea—from
pericardial effusion and

3.cardiac tamponade
4. Fever, sweating, chills—due to inflammation of pericardium.

5. Dysrhythmias.

6. Light-headedness or feeling like you might faint

7. Flu-like symptoms such as headache, body aches, joint pain, fever or sore throat

8. Swelling of the legs, ankles and feet

9. Rapid or irregular heartbeat (arrhythmias)

10. Shortness of breath, at rest or during activity

  Diagnostic Evaluation
1. Echocardiogram—most sensitive method for detecting pericardial effusion.

2. Chest x-ray—may show enlarged cardiac silhouette with clear lung fields.

3. ECG—to evaluate for MI (acute stage of pericarditis, ST elevation is found

in several or all leads).

4. WBC count and differential indicating infection.

5. Antinuclear antibody serologic tests elevated in lupus erythematosus.

6. Purified protein derivative test positive in tuberculosis.

7. ASO titers—elevated if rheumatic fever is present.

8. BUN—to evaluate for uraemia.

9. Elevated erythrocyte sedimentation rate and serum C-reactive

10. protein levels.

11. Elevated cardiac biomarkers –troponin and MB fraction of

12. creatinine kinase.

13. Pericardiocentesis—for examination of pericardial fluid for etiologic diagnosis

and relief from cardiac tamponade.

14. Cardiac MRI or CT.

  Medial Management
1. Bacterial pericarditis—penicillin or other antimicrobials.

2. Rheumatic fever—penicillin G and other antimicrobials

3. Tuberculosis—antituberculosis chemotherapy

4. Fungal pericarditis—amphotericin B and fluconazole.

5. Systemic lupus erythematosus—corticosteroids.

6. Renal pericarditis—dialysis, biochemical control of end-stage renal

disease.
7. Neoplastic pericarditis—intrapericardial instillation of chemotherapy; radiotherapy.

8. Post-MI syndrome—bed rest, aspirin, prednisone.

9. Post pericardiotomy syndrome (after open heart surgery)— treat symptomatically.

10. Emergency pericardiocentesis if cardiac tamponade develops.

11. Partial pericardiectomy (pericardial “window”) or total pericardiectomy for recurrent

constrictive pericarditis.

12. NSAIDs are recommended for symptom relief of acute pericarditis; colchicine and
steroid regimen are used as adjunct to NSAID therapy.
 Nursing Diagnoses
1. Acute Pain related to pericardial inflammation.

2. Decreased Cardiac Output related to impaired ventricular expansion.

3. Activity Intolerance related to impaired cardiac performance and

febrile illness.

4. Anxiety related to fear of death and hospitalization.

5. Fatigue related to disease process.

6. Cardiomyopathy
  Definition:
• Cardiomyopathy refers to disease of the heart muscle or electrical dysfunction.
Causes of cardiomyopathy are classified as primary or secondary.

• Primary cardiomyopathies have genetic, mixed, or acquired etiologies,

whereas secondary cardiomyopathies have infiltrative, toxic, or inflammatory
causes.

• The four main types are dilated, hypertrophic, restrictive (less common), and
arrhythmogenic right ventricular cardiomyopathy
  Types of cardiomyopathy:
1. DILATED CARDIOMYOPATHY DCM

• is the most common form of cardiomyopathy, with an incidence of 5 to 8 cases per 100,000
people per year and increasing (Braunwald et al., 2001).

• CM occurs more often in men and African Americans, who also experience higher mortality
rates (Braunwald et al., 2001).

• DCM is distinguished by significant dilation of the ventricles without significant concomitant

hypertrophy (ie, increased muscle wall thickness) and systolic dysfunction. DCM was
formerly named congestive cardiomyopathy, but DCM may exist without signs and symptoms
of congestion.
 2. HYPERTROPHIC CARDIOMYOPATHY
1. In HCM, the heart muscle increases in size and mass, especially along the septum

2. The increased thickness of the heart muscle reduces the size of the ventricular cavities
and causes the ventricles to take a longer time to relax, making it more difficult for the
ventricles to fill with blood during the first part of diastole and making them more
dependent on atrial contra filling.

3. The increased septal size may misalign the papillary muscles so that the septum and
mitral valve obstruct the flow of blood from the left ventricle into the aorta during
ventricular contraction. Hence, HCM may be obstructive or nonobstructive.
4. Hence, HCM may be obstructive or nonobstructive.

5. Because of the structural changes, HCM had also been called idiopathic hypertrophic
subaortic stenosis (IHSS) or asymmetric septal hypertrophy (ASH).

6. Structural changes may also result in a smaller than normal ventricular cavity and a higher
velocity flow of blood out of the left ventricle into the aorta, which may be detected by
echocardiography (Braunwald et al., 2001).

7. HCM may cause significant diastolic dysfunction, but systolic function can be normal or
high, resulting in a higher than normal ejection fraction.
 3.RESTRICTIVE CARDIOMYOPATHY
1. Restrictive cardiomyopathy (RCM) is characterized by diastolic dysfunction caused by rigid
ventricular walls that impair ventricular stretch and diastolic filling

2. Systolic function is usually normal. Because RCM is the least common cardiomyopathy,
representing approximately 5% of pediatric cardiomyopathies, its pathogenesis is the least
understood (Shaddy, 2001).

3. Restrictive cardiomyopathy can be associated with amyloidosis (in which amyloid, a protein
substance, is deposited within the
 4.ARRHYTHMOGENIC RIGHT VENTRICULAR
CARDIOMYOPATHY
• ARVC occurs when the myocardium of the right ventricle is progressively infiltrated and
replaced by fibrous scar and adipose tissue.

• Initially, only localized areas of the right ventricle are affected, but as the disease progresses,
the entire heart is affected. Eventually, the right ventricle dilates and develops poor
contractility, right ventricular wall abnormalities, and dysrhythmias.

• The prevalence of ARVC is unknown because many cases are not recognized. ARVC should be
suspected in patients with ventricular tachycardia originating in the right ventricle (ie, a left
bundle branch block configuration on ECG) or sudden death, especially among previously
symptom-free athletes
 5.UNCLASSIFIED CARDIOMYOPATHIES

• Unclassified cardiomyopathies are different from or have characteristics

of more than one of the previously described cardiomyopathies.

• Examples of unclassified cardiomyopathies include fibroelastosis,

noncompacted myocardium, systolic dysfunction with minimal dilation,

and mitocho
  Etiological factor:
1. Nutritional deficiency (carnitine or selenium).

2. Viral infection (myocarditis), human immunodeficiency virus.

3. Collagen vascular disease (systemic lupus erythematosus).

4. Cardiotoxic drugs (doxorubicin).

5. Cocaine abuse.

6. Infants of diabetic mothers

7. Sustained tachycardia (ectopic atrial tachycardia).

8. Catecholamine surge; hyperthyroidism

Pathophysiology:
  Clinical manifestation:
1. Signs of CHF—tachycardia, tachypnoea, dyspnoea, crackles, hepatosplenomegaly.

2. Decreased exercise tolerance, fatigue, sweating.

3. Poor weight gain, nausea, abdominal tenderness.

4. Ventricular arrhythmia.

5. Chest pain.

6. Syncope

7. paroxysmal nocturnal dyspnea, cough (especially with exertion), and orthopnea

  Diagnostic Evaluation:
1. Auscultation: systolic regurgitant murmur (if mitral or tricuspid insufficiency
is present), S2 is normal or narrowly split, prominent S3 gallop.

2. ECG: tachycardia, abnormal ST segments, arrhythmia, ectopic atrial

tachycardia, deep Q waves, LVH.

3. Chest x-ray: cardiomegaly, pulmonary congestion.

4. Two-dimensional echocardiogram: increased wall thickness, poor ventricular

systolic function, dilated heart chambers; AV valve insufficiency.
5. Cardiac MRI will provide useful information on cardiac function and may
demonstrate ventricular hypertrophy or fibrosis.

6. Cardiac catheterization: not needed for initial diagnosis; endomyocardial biopsy (to
rule out myocarditis); assess

7. PVR.
Medical management:
General Measures

• Identify and treat the underlying cause.

• Maximize caloric intake: fortify formula; supplemental nasogastric feedings.

• Supplemental oxygen, as needed.

• Activity restriction (usually self-imposed by the younger child and infant).

Restrict participation in strenuous and competitive sports.
 Treatment of Systolic Dysfunction with Dilated
Cardiomyopathy
1. Diuretics: furosemide, spironolactone.

2. Inotropics: digoxin.

3. Afterload reduction: captopril, enalapril, lisinopril.

4. Anticoagulation: warfarin, low-molecular-weight

heparin (enoxaparin).
5. Anti-arrhythmics.

6. Placement of an automatic implantable cardioverter-defibrillator.

7. Biventricular pacing.

8. Cardiac transplant
 Treatment of Diastolic Dysfunction with
Hypertrophic Cardiomyopathy
1. Beta-adrenergic blockers: propranolol.

2. Calcium channel blockers: verapamil.

3. AV sequential pacing.

4. Myomectomy or myotomy
 Treatment of Diastolic Dysfunction with Restrictive
Cardiomyopathy
1. Diuretics.

2. Anticoagulation.

3. Permanent pacemaker for advanced heart block

 Nursing Diagnoses
1. Decreased Cardiac Output related to impaired systolic or diastolic ventricular
function.

2. Imbalanced Nutrition: Less Than Body Requirements related to increased metabolic

demands and poor feeding from dyspnea, fatigue, and poor appetite

3. Ineffective Family Coping related to chronic illness

7.Hypoplastic Left Heart Syndrome
 Definition:
• Hypoplasic left heart syndrome (HLHS) is a constellation of leftsided heart abnormalities that include:

1. Critical mitral stenosis or atresia.

2. Hypoplastic LV.

3. Critical aortic stenosis or atresia.

4. Hypoplastic ascending aorta with severe coarctation of the aorta.

5. Associated anomalies include CoA (75%), ASD (15%), and VSD (10%).

• HLHS accounts for 1% of all CHDs. It is the most common cause of death from cardiac defects in the
first month of life.
  Etiological factor:
• the cause of genetic. Babies with mutations (changes) in specific
genes may have a higher risk of HLHS. These genes are known as
GJA1 or NKX2-5.
Pathophysiology:
 Clinical Manifestations
• Neonate may appear completely well initially, but becomes critically ill when the PDA
closes.

1. Once the PDA begins to close:

2. Tachypnea due to CHF.

3. Decreased urine output.

4. Poor feeding and feeding intolerance.

6. Pallor; Gray.

7. Weak peripheral pulses.

8. Cyanosis.

9. Metabolic acidosis.

10. Lethargic; change in level of alertness.

  Diagnostic Evaluation
1. Auscultation: single S2; usually no heart murmur is present, but
occasionally a soft systolic ejection murmur may be heard. As CHF
develops, gallop rhythm may be heard.

2. Chest x-ray: cardiac silhouette varies (normal to increased size);

increased pulmonary markings and pulmonary edema.

3. ECG: RV hypertrophy; decreased electrical forces in V5 and V6.

4. Two-dimensional echocardiogram with Doppler study and color flow
mapping identifies the structural abnormalities and the altered blood
flow patterns.

5. A cardiac catheterization is usually not needed for initial diagnosis. It

may be performed if a balloon atrial septostomy is needed to improve
oxygenation.
  Medical Management
1. Resuscitation and stabilization with PGE1 infusion.

2. Inotropic support, as needed (dopamine, dobutamine).

3. Intubate and ventilate, as needed.

4. Correct metabolic acidosis.

5. Assess hepatic, renal, and neurologic function.

6. Infective endocarditis prophylaxis (lifelong).

7. Refer for surgical intervention.

• Cardiac Catheterization

• May need balloon atrial septostomy to allow unrestrictive LA to

RA blood flow
  Surgical Management
 Palliative, staged repair:

• Stage I Norwood (neonate): reconstruction of the hypoplastic aorta using the PA and an
aortic or pulmonary allograft, an atrial septectomy, repair of the coarctation and placement
of a BT shunt.

• Stage II bidirectional Glenn shunt (ages 6 to 9 months): transect the SVC off the right
atrium and directly suture end to side to right PA; ligate BT shunt.

• Stage III Fontan (ages 12 to 18 months): IVC to PA connection (extracardiac conduit or

intracardiac baffle).
• Cardiac transplantation.
  Nursing Diagnosis:
1. Impaired Gas Exchange related to altered pulmonary blood flow or pulmonary
congestion.

2. Decreased Cardiac Output related to decreased myocardial function.

3. Activity Intolerance related to hypoxia or decreased myocardial function.

4. Imbalanced Nutrition: Less Than Body Requirements related to excessive energy

demands required by increased cardiac workload

5. Risk for Infection related to chronic illness.

6. Fear and Anxiety related to life-threatening illness

  Bibliography
1. Allen, K. B. (2011). Patient characteristics and operative risk with stand-alone trans myocardial
revascularization. Journal of the American College of Cardiology, 57(14, Suppl. S), E1140.

2. Anderson, J. L., Adams, C. D., Antman, E. M., et al. (2011). 2011 ACCF/AHA focused update incorporated into
ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST elevation myocardial
infarction: A report of the American College of Cardiology Foundation/American Heart Association Task Force
on Practice Guidelines. Journal of American College of Cardiology, 57(19), 1920−1959.

3. Berndt, N. C., Bolman, C., de Vries, H., et al. (2013). Smoking cessation treatment practices: recommendations
for improved adoption on cardiology wards. Journal of Cardiovascular Nursing, 28(1), 35−47.

4. Brown, J. L., Bogaev, R. C., & O’Connell, J. (2011). Short-term mechanical management of cardiogenic shock.
Current Treatment Options in Cardiovascular
6. Medicine, 13(4), 343–353.

7. Byrne, J. G., Rezai, K., Sanchez, J. A., et al. (2011). Surgical management of
endocarditis: The Society of Thoracic Surgeons clinical practice guideline. Annals of
Thoracic Surgery, 91(6), 2012

8. Lippincoote manual of nursing practice 10 th edition, wolter klumer part two medical
surgical nursing part II cardiovascular heath, page number 735 to 780.

9. lewis Dirkenson hetikemper bucher medical surgical nursing, 10 th edition.section 6

priblem of oxygenation: transport page number 821 to 830.

10. Dymistifield medical surgical nursing,chapter 1 cardiovascular system page number 60 to

68.