MEDICAL SURGICAL NURSING

A Seminar On

 Pericarditis
 Myocarditis
 Aortic aneurysm
 Ventricular aneurysm

Submitted to : Prof. Agnet Beena Mani.

HOD. Medical surgical nursing ,

Baby Memorial College Of Nursing ,

Calicut.

Submitted by: Mrs Neeraja Madhu,

II year M.Sc Nursing ,

Baby Memorial College Of Nursing ,

Calicut .

Submitted on: 11.07. 2013

 PERICARDITIS
INTRODUCTION

The normal pericardium is a double-layered sac; the visceral pericardium is a serous

membrane that is separated by a small quantity (15–50 mL) of fluid, an ultrafiltrate of
plasma, from the fibrous parietal pericardium. The normal pericardium, by exerting a
restraining force, prevents sudden dilation of the cardiac chambers, especially of the right
atrium and ventricle, during exercise and with hypervolemia. It also restricts the anatomic
position of the heart, minimizes friction between the heart and surrounding structures,
prevents displacement of the heart and kinking of the great vessels, and probably retards the
spread of infections from the lungs and pleural cavities to the heart.

DEFINITION

Pericarditis is a condition caused by inflammation of the pericardial sac (the pericardium),

the membranous sac enveloping the heart.

CLASSIFICATION

Acute pericarditis can be classified both clinically and etiologically

Clinical Classification
I. Acute pericarditis (<6 weeks)
  A. Fibrinous
  B. Effusive (serous or sanguineous)
II. Subacute pericarditis (6 weeks to 6 months)
  A. Effusive-constrictive
  B. Constrictive
III. Chronic pericarditis (>6 months)
  A. Constrictive
  B. Effusive
  C. Adhesive (nonconstrictive)
Etiologic Classification
I. Infectious pericarditis
o Viral (coxsackievirus A and B, echovirus, mumps, adenovirus, hepatitis, HIV)
o Pyogenic (pneumococcus, streptococcus, staphylococcus, Neisseria, Legionella) 
o Tuberculous
 o Fungal (histoplasmosis, coccidioidomycosis, Candida, blastomycosis) 
o Other infections (syphilitic, protozoal, parasitic)
II. Noninfectious pericarditis
o Acute myocardial infarction
o Uremia
o Neoplasia
1. Primary tumors (benign or malignant, mesothelioma)
2. Tumors metastatic to pericardium (lung and breast cancer, lymphoma, leukemia)
o Myxedema
o Trauma
1. Penetrating chest wall
2. Nonpenetrating
o Aortic dissection (with leakage into pericardial sac)
o Postirradiation
o Familial pericarditis
o Whipple's disease
o Sarcoidosis
III. Pericarditis presumably related to hypersensitivity or autoimmunity
o Rheumatic fever
o Collagen vascular disease (SLE, rheumatoid arthritis, ankylosing spondylitis,
scleroderma, acute rheumatic fever, Wegener's granulomatosis)
o Drug-induced (e.g., procainamide, hydralazine, phenytoin, isoniazide, minoxidil,
anticoagulants, methysergide)
o Postcardiac injury
    1. Postmyocardial infarction (Dressler's syndrome)
    2. Postpericardiotomy
    3. Posttraumatic

PATHOPHYSIOLOGY
 Accumulation of fluid in the pericardial sac (pericardial effusion)

Increases pressure on the heart

Cardiac tamponade

Frequent or prolonged episodes of pericarditis

Thickening and decreased elasticity

Restrict the heart’s ability to fill properly with blood

(constrictive pericarditis).

calcification of the pericardium

Further restricting ventricular expansion during ventricular filling (diastole).

 With less filling, the ventricles pump out

less blood

Decreased cardiac output

signs and symptoms of heart failure.

Restricted diastolic filling

Increased systemic venous pressure

Peripheral edema and hepatic failure.

CLINICAL FEATURES

o The most characteristic symptom of pericarditis is chest pain, although pain also may
be located beneath the clavicle, in the neck, or in the left scapula region.
o The pain or discomfort usually remains fairly constant, but it may worsen with deep
inspiration and when lying down or turning. It may be relieved with a forward leaning
or sitting position.
o The most characteristic sign of pericarditis is a friction rub. The rub is scratching ,
grating, high pitched sound believed to arise from friction between the roughed
pericardial and epicardial surfaces. It is best heard with the stethoscope diaphragm
firmly placed at the lower sterna border of the chest.
o Timing of the pericardial rub with pulse not with the respiration helps to differentiate
it from pleural rub.
o Other signs may include mild fever, increased white blood cell count, and increased
erythrocyte sedimentation rate (ESR).
o Dyspnea and other signs and symptoms of heart failure may occur as the result of
pericardial compression due to constrictive pericarditis or cardiac tamponade.
 DIAGNOSIS
o Diagnosis is most often made on the basis of the patient’s history, signs, and
symptoms.
o An echocardiogram may detect inflammation and fluid build-up, as well as
indications of heart failure, and help to confirm the diagnosis.
o Because the pericardial sac surrounds the heart, a 12-lead ECG detects ST changes in
many, if not all, leads.
o The ECG shows ST elevation with upward concavity over the affected area, which
may be widespread. PR interval depression is a very sensitive indicator of acute
pericarditis. Later, there may be T-wave inversion, particularly if there is a degree of
myocarditis.
o BUN , Serum creatinine – uremic pericarditis
o Tuberculin skin test – tuberculous pericarditis
o Chest X ray- generally normal or non specific unless the patient has large pericardial
effusion.
o Pericardiocentesis
o Pericardial biopsy – helps o determine the cause of pericarditis
o CT Scan
o Cardiac nuclear scan

COMPLICATION

 Pericardial effusion
 Cardiac tamponade
 Heart failure
 Hemopericardium (especially patients post-MI receiving anticoagulants)

Pericardial Effusion.
o If the patient does not respond to medical management, fluid may accumulate
between the pericardial linings or in the sac. This condition is called pericardial
effusion.
o It can occur rapidly (e.g. chest trauma) or slowly (e.g. tuberculous pericarditis)
o Large effusion may compress the adjoining structures.
 o Pulmonary tissue compression may cause cough, tachypnoea, and dyspnoea.
o Phrenic nerve compression may induce hiccups and recurrent laryngeal nerve may
result in hoarseness.
o Heart sounds are generally distant and muffled, although BP is usually maintained by
compensatory mechanism.
o Fluid in the pericardial sac can constrict the myocardium and interrupt its ability to
pump. Cardiac output declines with each contraction. Failure to identify and treat this
problem can lead to the development of cardiac tamponade and the possibility of
sudden death.
Cardiac Tamponade
o Cardiac tamponade develops as the pericardial effusion increases in size.
o The signs and symptoms of cardiac tamponade begin with falling arterial pressure.
Usually, the systolic pressure falls while the diastolic pressure remains stable; hence,
the pulse pressure narrows.
o Heart sounds may progress from sounding distant to being imperceptible.
o Neck vein distention and other signs of rising central venous pressure are observed.
o These signs and symptoms occur because, as the fluid-filled pericardial sac
compresses the myocardium, blood continues to return to the heart from the
periphery but cannot flow into the heart to be pumped back into the circulation.
o Pulses paradoxus, an inspiratory drop in the systolic BP greater than 10 mm Hg,
result because the normal inspiratory decline in the systolic BP of less than 10 mm
Hg, is exaggerated in cardaiac tamponade.
o In such situations, the nurse notifies the physician immediately and prepares to assist
with pericardiocentesis. The nurse stays with the patient and continues to assess and
record signs and symptoms while intervening to decrease the patient’s anxiety.
MANAGEMENT
The objectives of treatment are targeted toward determining the etiology of the problem;
administering pharmacologic therapy for specified etiology, when known; relef of symptoms
and being alert to the possible complication of cardiac tamponade.
 Antibiotics are used to treat bacterial pericarditis
 Analgesics and bed rest are used to treat pain.
  Nonsteroidal anti-inflammatory drugs (NSAIDs) are the mainstay of treatment.
Gastrointestinal mucosa protectants guard against the side effects, but close
monitoring is essential.
 Colchicine may be added to an NSAID or given as monotherapy for both the initial
attack and to prevent recurrences.
 Corticosteroids are used only if other treatments fail, and then only in minimally
effective dosages. The use of these agents is controversial.
 The patient with pericarditis is also closely observed for development of the
complications of pericardial effusion or cardiac tamponade.

 Bacterial pericarditis - penicillin or other antimicrobial agents

 Rheumatic fever - penicillin G and other antimicrobial agents
 Tuberculosis - antituberculosis chemotherapy
 Fungal pericarditis - amphotericin B and fluconazole
 Systemic lupus erythematosus - corticosteroids
 Renal pericarditis - dialysis, biochemical control of end-stage renal disease
 Neoplastic pericarditis - intrapericardial instillation of chemotherapy; radiotherapy
 Post-MI syndrome - bed rest, aspirin, prednisone
 Postpericardiotomy syndrome (after open heart surgery) - treat symptomatically
 Emergency pericardiocentesis if cardiac tamponade develops
 Partial pericardiectomy or total pericardiectomy for recurrent constrictive pericarditis

Pericardiocentesis is usually performed when acute cardiac tamponade has reduced the
patients systolic BP 30 mm Hg or more from base line. Hemodynamic preparation for
patients being prepared for pericardiocentesis includes administration of volume expanders
and ionotropic agents.The procedure is performed in the CCU or Cath Lab under sterile
condition in conjunction with the ECG, Echocardiogram and hemodynamic measurement.

A 16- 18 G needle is inserted in the pericardial sac to remove fluid for analysis and to relieve
cardiac pressure.

Complications from pericardiocentesis include arrhythmias, pneumomediastinum, pneumo

thorax, myocardial laceration, cardiac tamponade, coronary artery laceration, gastric fistula.
Medical management does not relieve constriction. Surgical pericardectomy is the definitive
treatment. It is more easily accomplished if done early in the course of the disease, when the
patient has less systemic disease and before calcification and myocardial abnormalities
develop. Preventing the development of constrictive pericarditis is the optimal method to
combat this condition, through adequate treatment of pericarditis, and draining of fluid and
pus if indicated.

CHRONIC PERICARDITIS

Chronic pericarditis is inflammation that begins gradually, is long-lasting, and results in fluid
accumulation in the pericardial space or thickening of the pericardium.

Pericarditis is considered chronic if it lasts longer than 6 months. There are two main types of
chronic pericarditis.

In chronic effusive pericarditis, fluid slowly accumulates in the pericardial space, between
the two layers of the pericardium.

CHRONIC CONSTRICTIVE PERICARDITIS

 Another complication of pericardial disease is constrictive pericarditis.
 It is important to recognize this form of pericarditis because it may be
correctable if treated early.
 The challenge with constrictive pericarditis is that it can mimic common
disorders that produce symptoms of right-sided heart failure, such as
restrictive cardiomyopathy, pulmonary embolism, pulmonary hypertension,
right ventricular infarction, mitral stenosis, and left ventricular systolic
dysfunction.
 TB that led to calcification of the pericardium was the major cause of
constrictive pericarditis in the early twentieth century. Now the most
common cause is idiopathic."
 Radiation therapy and open heart surgery are also frequent causes.
 Constrictive pericarditis causes fibrosis and calcification of the pericardium,
which inhibit normal ventricular filling while systolic contraction of the
ventricles remains normal.
 Pericardial scarring usually occurs over a period of years. Classically, the
 pericardial scarring is uniform involving all chambers of the heart.
 The restricted filling leads to equal and elevated pressures in all chambers.
 As blood flows from the right atrium to the right ventricle during diastole, the
right ventricle expands and quickly reaches the limit imposed by the rigid,
constricting pericardium.
 The ventricle is now unable to fill further, resulting in an increase in
systemic venous pressure and signs and symptoms of right heart failure.
 Decreased left ventricular filling decreases stroke volume and cardiac output,
which leads to hypotension similar to that seen with restrictive
cardiomyopathy.
 The differentiation between these two maladies can be very difficult, but is
exceedingly important in that the treatments are quite different

CLINICAL PRESENTATION
 Constrictive pericarditis can take months or years to develop.
 Early in the course of the disease, patients manifest signs and symptoms of
right heart failure often severe.
 Subsequently, they may develop signs and syrnptorns of left heart failure.
 At end stage, these patients develop cardiac cachexia with weakness, fatigue,
and tissue wasting.
 Pertinent physical findings in constrictive pericarditis include significantly
increased JVD; often kussmaul sign, a paradoxical (jugular veins normally collapse
during inspiration) increase in JVD during inspiration and a prominent y descent in
the jugular waveforms. Lung sounds may be clear despite the presence of JVD and
peripheral edema.
 In contrast to the muffled heart sound heard cardiac tamponade, an early
diastolic filling heard in constrictive pericarditis, known as dial knock.
 A pericardial knock is a high pitched sound heard early in diastole at the 4th
and 5th intercostal space along the left sternal border or at the apex of the
heart with the patient leaning forward.
 The knock occurs as a result of a constrictive pericardium abruptly empting
early rapid filling of the ventricle.
 These signs and symptoms except for the pericardial knock may be mistaken
 for restrictive cardiomyopathy.

DIAGNOSTIC TESTS
 Chest X-ray may show a calcified pericardium and often an enlargement.
 ECG findings of low voltage and sometimes atrial fibrillation are
nonspecific.
 The echocardiogram may be helpful in revealing pericardial thickening,
septal bounce during diastole, and septal shifting with inspiration.
 CT is better than MRI in providing excellent resoluion of the pericardium,
which can detect a thickened pericardium (more than 2 mm) quite
accurately. However, 20 percent of patients exhibit no signs of a thickened
pericardium.
 Cardiac catheterization may yield similar findings in both constrictive
pericarditis and retrictive cardiomyopathy. Diastolic pressures in all
chambers are usually equalized. Rapid y descent of early diastole with a rapid
upswing and plateau yields the classic "square root sign," which can be
present in both diseases.
 One distinguishing feature of constrictive pericarditis is a pulmonary artery
pressure (PAP) greater than 50 nm Hg on cardiac catheterization. This
finding can support the diagnosis of constrictive pericarditis.
 Endomyocardial biopsy is most useful and may be performed to distinguish
between constrictive pericarditis and restrictive cardiomyopathy.
 The only clinical or diagnostic findings that help to differentiate these two
maladies are the following: pericardial knock in constrictive pericarditis,
PAP greater than 60 mm Hg in restrictive cardiomyopathy, and the "septal
bounce" on echocardiogram in constrictive pericarditis.

CLINICAL MANAGEMENT
 Clinical management of constrictive pericarditis includes monitoring of
vital signs and managing symptoms of the disease process.
 Early conservative management with diuretics alleviates symptoms of
volume overload. Many of these patients will develop atrial fibrillation,
and digoxin is appropriate for rate control.
  Beta blockers and calcium channel blockers should not be used in these
patients because they slow the heart rate and may interfere with the
compensatory tachycardia.
 Surgical treatment is the only effective treatment of constrictive
pericarditis.
 A complete resection of the pericardium is performed via a median
sternotomy, often without cardiopulmonary bypass.
 The earlier in the disease process surgical intervention is accomplished, the
less ill the patient and the better the outcome. Late in the disease, removal
of the pericardium may be of little benefit to a patient who is now critically
ill and wasted.

 NURSING MANAGEMENT

Nursing Assessment

 Evaluate complaint of chest pain.

o Ask the patient if pain is aggravated by breathing, turning in bed, twisting
body, coughing, yawning, or swallowing.
o Elevate head of bed; position pillow on over-the-bed table so the patient can
lean on it.
o Assess if above intervention relieves the patient's chest pain (associated
pleuritic pain of pericarditis is usually relieved by sitting up and/or leaning
forward).
o Be alert to the patient's medical diagnoses when assessing pain. Post-MI
patients may experience a dull, crushing pain radiating to neck, arm, and
shoulders, mimicking an extension of infarction.
 Auscultate heart sounds.
o Listen for friction rub by asking patient to hold breath briefly.
o Listen to the heart with patient in different positions.
 Evaluate history for precipitating factors.

Nursing Diagnoses
  Acute Pain related to pericardial inflammation
 Decreased Cardiac Output related to impaired ventricular expansion

Nursing Interventions
Reducing Discomfort
 Give prescribed drug regimen for pain and symptomatic relief.

 Relieve anxiety of patient and family by explaining the difference between pain of
pericarditis and pain of recurrent MI. (Patients may fear extension of myocardial
tissue damage.)
 Explain to patient and family that pericarditis does not indicate further heart damage.
 Encourage patient to remain on bed rest when chest pain, fever, and friction rub
occur.
 Assist patient to position of comfort.

Maintaining Cardiac Output

 Assess heart rate, rhythm, BP, respirations at least hourly in the acute phase;
continuously if hemodynamically unstable.
 Assess for signs of cardiac tamponade increased heart rate, decreased BP, presence of
paradoxical pulse, distended neck veins, restlessness, muffled heart sounds.
 Prepare for emergency pericardiocentesis or surgery. Keep pericardiocentesis tray at
bedside.
 Assess for signs of heart failure.
 Monitor closely for the development of dysrhythmias.

Patient Education and Health Maintenance

 Teach patient the etiology of pericarditis.

 Instruct patient about signs and symptoms of pericarditis and the need for long-term
medication therapy to help relieve symptoms.
 Review all medications with the patient purpose, adverse effects, dosage, and special
precautions.
Constrictive Pericarditis. The pericardium loses its flexibility and elasticity and becomes
scarred and rigid in constrictive pericarditis. As a result, the heart is compressed and its
function is disturbed. Advances in diagnostic testing as well as in our understanding of
hemodynamics have improved early diagnosis. Traditionally, constriction has been chronic,
with sometimes surprising pericardial thickness. Recently, relatively thinner constricting
pericardia are increasingly evident, perhaps because of earlier diagnoses and a shift in
recognizable etiologies. The etiology of constrictive pericarditis is often undetermined, but it
can result from almost all the conditions that also cause acute pericarditis.

MYOCARDITIS
DEFINITION
Myocarditis is a focal or diffuse inflammation of the myocardium.
ETIOLOGY
Infections
     Viral
          Coxsackievirus
          Poliomyelitis
          Mumps
          Rubella
          Epstein-Barr
          Human immunodeficiency virus
     Bacterial
Tuberculosis
          Tetanus
          Staphylococcal
          Pneumococcal
     Fungal
     Parasitic
          Toxoplasmosis
          Cytomegalovirus
Pharmacologic agents
      Inotropes
Radiation therapy
Chemical poisons
Peripartum condition
Autoimmune
      Eosinophilia
      Asthma

PATHOPHYSIOLOGY

o The pathophysiological mechanism of myocarditis is poorly understood because there

is usually a period of several weeks after the initial infection before the development
of manifestations of myocarditis.

o Myocarditis is usually characterized by necrosis and cell injury associated with

inflammation of the heart muscle and lymphocytic inflammation in the absence of an
ischemic episode.

o As the myocardium becomes infected and necrosis occurs, an immune response is

initiated and cytokines are produced.

o The viral infection persists, and an autoimmune response is initiated, causing the body
to attack its own cells.

o These mechanisms and the viral attack of vascular endothelium, causing

microvascular spasm and reperfusion injury, are thought to produce the myocardial
damage that occurs in myocarditis.

o Cardiac tissues show multiple focal areas of myocyte loss, sheets of fibrosis, and
calcified deposits diffusely distributed across all cardiac muscle layers and chambers.

CLINICAL MANIFESTATIONS

o Myocarditis classically presents with nonspecific symptoms such as fatigue, dyspnea,

and palpitations, along with viral illness symptoms, including fever.
 o If the disease has progressed, symptoms of heart failure present, such as tachycardia,
pulmonary edema, diaphoresis, neck vein distention, and cardiomegaly.

o Symptoms of poor perfusion or cardiogenic shock can also be manifested, such as

hypotension, cool, clammy extremities, decreased urine output, and decreased level of
consciousness.

DIAGNOSTIC STUDIES

Cardiac function is evaluated through:

Echocardiography

ECG

Nuclear scans, and

Cardiac catheterization with endomyocardial biopsy.

The latter test remains the gold standard for diagnosis of myocarditis, although results remain
controversial and it is invasive and costly. In EMB several pieces of myocardial tissues are
percutaneously removed from the right ventricle with a special instrument called bioptome
and microscopically examined. A biopsy done during the initial 6 weeks of acute illness is
most diagnostic because this is a period in which lymphocytic infiltration and myocyte
damage indicative of myocardiis are present.

One study indicated that MRI may serve as a powerful, noninvasive diagnostic tool in
myocarditis.

In myocarditis, the ECG can show low-voltage QRS complexes, ST segment elevation, or
heart block. Nonsustained atrial or ventricular arrhythmias are common. An S4 and systolic
ejection murmurs may be heard on auscultation.

Laboratory values are also often inconclusive, with the presence of mild to moderate
leukocytosis and atypical lymphocytes, elevated viral titres ( usually present 8- 10 days of
illness), increased ESR and elevated myocardial enzymes such as Creatinine kinase.

MEDICAL MANAGEMENT
 o Management of myocarditis is focused on support.

o Heart failure is treated and arrhythmias are controlled.

o Inotropic support of cardiac function with amrinone, dopamine, or dobutamine may

be used. Nitroprusside and nitroglycerin may be used to reduce afterload.

o Digoxin is often used to treat ventricular failure because it improves myocardial

contractility and reduces ventricular rate. But it should be used cautiously in patients
with myocarditis, because of the increased sensitivity of the heart to the adverse
effects of this drug and potential toxicity with minimal doses.

o Bed rest is used to promote healing and minimize myocardial oxygen consumption.
Intubation, ventilation, and sedation may be necessary to decrease cardiac workload.
Extracorporeal membrane oxygenation has been used in 50 cases of pediatric and
neonatal myocarditis, with a 54% survival rate.

o Mechanical assist devices such as intra-aortic balloon pulsation and left ventricular
assist devices have been used to improve CO in myocarditis.

o Another important aspect of management is prevention of complications. If the

ejection fraction is low and there is blood stasis in the chambers, anticoagulant
therapy is necessary to prevent thrombus formation.

o The use of immunosuppression in the treatment of myocarditis is controversial. An

immunosuppressive therapy trial of myocarditis demonstrated no beneficial
effects.However, immunosuppression during the autoimmune phase of myocarditis
may be effective.

o Intravenous immunoglobulin is used on the experimental bases fot the treatment of

myocarditis.

o Antiviral agents (e.g ribavirin, alpha interferon) are undergoing clinical evaluation for
the treatment of acute viral myocarditis.

Nursing Management
o The nurse assesses the patient’s temperature to determine whether the disease is
subsiding.
o The cardiovascular assessment focuses on signs and symptoms of heart failure and
dysrhythmia.
o The patient experiencing dysrhythmias should receive continuous cardiac monitoring
with personnel and equipment readily available to treat life-threatening dysrhythmias.
o Elastic compression stockings and passive and active exercises should be used,
because embolization from venous thrombosis and mural thrombi can occur.
o Bed rest is important because it reduces myocardial oxygen demand and usually
continues until the following criteria are met:
Temperature remains normal without use of salicylates
Resting pulse rate remains less than 100 beats/min
ECG tracings show no manifestations of myocardial damage
Pericardial friction rub is not present
o Obtain a clear description of the pain or discomfort. Identify the source of greatest
discomfort as a focus for intervention.
o Administer analgesics as needed and use salicylates around the clock.
o Balance rest and activity according to the degree of pain and activity tolerance.
o Provide psychosocial support while patient is confined to hospital or home with
restrictive intravenous therapy.
o If patient received surgical treatment, provide postsurgical care and instruction.
o After surgery, monitor patient’s temperature; a fever may be present for weeks.
o A high-protein, high-carbohydrate diet helps maintain adequate nutrition in the
presence of fever and infection.
o Oral hygiene every 4 hours; small, attractive meal servings and foods that are not
overly rich, sweet or greasy stimulate the appetite.
o Instruct the client about how to reduce exposure to infection as follows:
o Take good care of the teeth and gums, obtain prompt dental care for cavities and
gingivitis
o Prophylactic medication may be needed before invasive dental procedures, and
individualized evaluation for prophylaxis medication is needed.
o Avoid people who have an upper respiratory tract infection
 o Assess for signs and symptoms of organ damage such as stroke (CVA, brain attack),
meningitis, heart failure, myocardial infarction, glomerulonephritis, and
splenomegaly.
o Instruct patient and family about activity restrictions, medications, and signs and
symptoms of infection.
o Refers to home care nurse to supervise and monitor intravenous antibiotic therapy in
the home.

AORTIC ANEURISMS
DEFINITION
An aneurysm is a distention of an artery brought about by a weakening/destruction of the
arterial wall.
o They are lined with intraluminal debris, such as plaque and thrombi.
o Because of the high pressure in the arterial system, aneurysms can enlarge, producing
complications by compressing surrounding structures; left untreated, they may
rupture, causing a fatal hemorrhage.
o A dissection occurs when the layers of the artery become separated. Blood flows
between the layers, causing further disruption of the arterial wall.
o Additionally, the intraluminal thrombus may totally occlude the artery, leading to
acute ischemia to all arteries distal to the area of thrombosis, or they may embolize
clot and/or plaque to the arteries distal to the aneurysm.
 o The aorta is the most common site for aneurysms; however, they may form in any
vessel.
o Peripheral vessel aneurysms may involve the renal artery, subclavian artery, popliteal
artery (knee), or any major artery. These produce a pulsating mass and may cause
pain or pressure on surrounding structures.

AORTIC ANEURYSM
Aortic aneurysm can be defined as the aneurysm that involves different parts of aorta
especially aortic arch, thoracic aorta and/ or abdominal aorta.
Most of the aneurysm is found in the abdominal aorta below the level of the renal arteries.
The growth rate of aneurysms is unpredictable, but arger the aneurysm there is greater risk
for rupture.
ETIOLOGY

 Aneurysms may form as the result of:

o Atherosclerosis.
o Heredity.
o Infection.
o Trauma.
o Immunologic conditions.
 False aneurysms (pseudoaneurysm) are associated with trauma to the arterial wall, as
in blunt trauma or trauma associated with arterial punctures for angiography and/or
cardiac catheterization.
 The ascending aorta and the aortic arch are the sites of greatest hemodynamic stress
and also are the most common sites of arterial dissection.
 Contributing factors include:
o Hypertension.
o Arteriosclerosis.
o Local infection, pyogenic or fungal (mycotic aneurysm).
o Congenital weakness of vessels.
o Syphilis.
o Trauma.
 PATHOPHYSIOLOGY
o Due to etiolological factors
o Dilatation of aortic wall
o Dilated aortic wall becomes lined with thrombi that can embolise
o Acute ischemic symptoms to the distal branches.

In case of atherosclerosis – the atherosclerotic plagues deposit beneath the intima – plague
formation may cause degenerative changes in the media- loss of elasticity, weakening and
eventual dilation of the aorta.

CLASSIFICATION
 Aneurysm are generally divided in to two basic classification: true and false
aneurysms. A true aneurysm is the one in which the wall of artery forms the
aneurysm, with at least one vessal layer still intact.
 The true aneurysms can be further classified in to fusiform and saccular.
 A false aneurysm or pseudoaneurysm is not an aneurysm but the disruption of all the
layers of the arterial wall resulting in bleeding that is contained by surrounding
structures.
 False aneurysm may result from trauma, infection, after peripheral artery bypass graft
surgery at the site of the graft to artery anastomosis.

 Morphologically, aneurysms may be classified as follows:

o Saccular - distention of a vessel projecting from one side
o Fusiform - distention of the whole artery (ie, entire circumference is involved)
o Dissecting - hemorrhagic or intramural hematoma, separating the medial
layers of the aortic wall
 Abdominal aortic aneurysms are described as infrarenal, when the neck of the
aneurysm is located below the level of the renal arteries, or suprarenal, when the
aneurysm is located above the level of the renal arteries or involves the renal arteries.
 Because of vascular changes that occur as a natural process of aging, all patients over
age 65 are assessed for the potential for aneurysms.

CLINICAL MANIFESTATIONS
Aneurysm of the Thoracoabdominal Aorta
From the aortic arch to the level of the diaphragm. At first, no symptoms; later, symptoms
may come from heart failure or a pulsating tumor mass in the chest.

 Pulse and BP difference in upper extremities if aneurysm interferes with circulation in

left subclavian artery
 Pain and pressure symptoms
 Constant, boring pain because of pressure
 Intermittent and neuralgic pain because of impingement on nerves
 Dyspnea, causing pressure against trachea
 Cough, often paroxysmal and brassy in sound
 Hoarseness, voice weakness, or complete aphonia, resulting from pressure against
recurrent laryngeal nerve
 Dysphagia due to impingement on esophagus
 Edema of chest wall is infrequent
 Dilated superficial veins on chest
 Cyanosis because of vein compression of chest vessels
 Ipsilateral dilatation of pupils due to pressure against cervical sympathetic chain
 Abnormal pulsation apparent on chest wall, due to erosion of aneurysm through rib
cage in syphilis

Abdominal Aneurysm

 Many of these patients are asymptomatic

 Abdominal pain is most common, either persistent or intermittent , often localized in
middle or lower abdomen to the left of midline
 Lower back pain
 Feeling of an abdominal pulsating mass, palpated as a thrill, auscultated as a bruit
 Hypertension
 Distal variability of BP, pressure in arm greater than thigh
 If rupture, will present with hypotension and/or hypovolemic shock

Most abdominal aneurysms occur between ages 60 and 90. Rupture of the aneurysm is likely
if there is coexistent hypertension or if the aneurysm is larger than 6 cm.
 DIAGNOSTIC EVALUATION

 Abdominal or chest X-ray may show calcification that outlines aneurysm.

 CT scanning and ultrasonography are used to detect and monitor size of aneurysm.
 MRI/MRA.
 Spiral CT gives three-dimensional view of the aneurysm and any attendant
atherosclerosis
 Arteriography allows visualization of aneurysm and vessel.

COMPLICATIONS

 Rupture of aneurysm – if the rupture occurs posteriorly in the retroperitoneal space,

bleeding may be tamponaded by surrounding structures, preventing exsanguination
and death. In this case patient may have severe back pain and may or may not have
back or flank ecchymosis ( grey turne’s sign).If the rupture occurs anteriorly in the
abdominal cavity most of the patient may die of massive hemmorhage.It the patient
does not reach the hospital he may develop hypovolemic shock.
 Fatal hemorrhage
 Myocardial ischemia
 Stroke
 Paraplegia due to interruption of anterior spinal artery
 Abdominal ischemia
 Ileus
 Graft occlusion
 Graft infections
 Acute renal failure
 Impotence
 Lower extremity ischemia
 Trash toes results from distal emobolization of plaque and blood clots

AORTIC RUPTURE
Rupture of aorta is the most common blunt injury of the great vessels. A ruptured aneurysm
carries a mortality risk of above 90%. And the emergency surgical repair is the only chance
for the survival.

Etiology

 Decelerating injury suffered in automobile accidents

 Hypertension

Most common sites of rupture of aorta

 Descending aorta just distal to the origin of left subclavian vein.

 Ascending aorta just above the aortic valve

Clinical manifestations

 Chest and/ or mid scapular pain

 Hypertension of the upper extremities
 Murmers
 Increased pulse amplitude

Patients with aortic rupture may have injury to the CNS, Abdominal viscera, skeleton which
may mask the signs of aortic rupture.

Diagnosis

1. Chest x ray

Injury to the aortic isthmus

 widening of the superior mediastinal shadow

 Depression of the left main bronchus
 Displacement of the trachea and esophagus to the right
 Obliteration of the aortic knob shadow

Injury to the aortic arch and ascending aorta

  Widening of the mediastinum
2. Aortography
3. Constrast CT

MANAGEMENT OF AORTIC ANEURYSM

 Management of aortic aneurysm is individualised .Sugery is conducted as soon as

possible.

Indication for surgery

o Leaking or ruptured aneurysm

o Symptomatic aneurysm(aneurysm causing pain, ureteric obstruction or embolism)
o Expanding aneurysm – expanding at a rate of > 0.5 cm in 1 year.
o Size : aneurysm of > 5.5 cm dm or any saccular aneurysm.

 Those patients with trauma to the CNS, Contaminated wound, and respiratory
insufficiency from lung contusion, cardiac blunt trauma, retroperitoneal hematoma or
other medical co morbidities are treated with either percutaneous endovascular
stenting of the tear or medical therapy to be followed by delayed surgical repair.
 The medical management consists of maintain the mean systemic blood pressure
below 70 mm Hg to control the aortic wall tension and are continued until other
injuries or complication cease.
 Surgery on aorta presents high risks associated with compromising circulation to the
major organs and tissues.
 Unlike traditional cardiac surgery, the use of cardiopulmonary bypass (CPB) may be
limited in some cases because clamping of the aorta is hindered by the location of the
injury.

 A number of techniques have been used to minimise the risks and to improve the
outcome associated with high risk procedure including hypothermic circulatory arrest
 (HCA), left heart bypass and separate cerebral perfusion catheters which may vary
according to the type of aortic surgery being performed.

 The incisional approach, the use of CPB, and specialized techniques used to provide
neurologic protection vary depending on the type of aortic surgery being performed.

 When surgery is performed on the ascending aorta for repair of either a Type A
dissection or an aneurysm, the goals are similar. These include maintaining
myocardial blood flow via the coronary ostia, restoring functions of the aortic
valve, and preventing rupture into the pericardium, which could lead to
tamponade and death.

 The ascending aorta is accessed via a median sternotomy. The patient is placed
on CPB, usually via cannulation of the right atrium and either the aorta distal to
the surgical site or one femoral artery.

 The degree of damage to the aorta and the aortic valve is then assessed. If the
dissection or aneurysm involves the aortic valve or the aortic tissue has
deteriorated (common in Marfan syndrome), a composite graft is used for repair
(Bentall procedure).

 This consists of a Dacron tube with an aortic valve sewn into one end. The graft
is attached to the aortic annulus and the coronary arteries are then reimplanted in
the graft.

 If the aortic tissue is structurally viable and the valve leaflets are intact, a valve
sparing procedure may be performed. Although technically more demanding,
this approach is preferred by some because it avoids the long-term
anticoagulation therapy required with prosthetic valves.

 Surgical repair of dissections or aneurysm involving the aortic arch is more

complicated, because the vessels branching from this area -the innominate,
carotid, and subclavian arteries supply blood flow to the upper body, including
the brain.
 During repairs to the arch, the brachiocephalic vessels must first be removed
from the diseased section of the aorta, and then reimplanted in the graft. This is
typically performed with a period of circulatory arrest to allow the operation on
a bloodless field.

 Circulatory arrest is performed under deep hypothermia, with the patient cooled
systemically to 15- 18° C-the point at which EEG silence occurs. Systemic
cooling is performed through the bypass circuit until the desired temperature is
reached and EEG silence is confirmed.

 In emergent situations where EEG monitoring is not available this cooling is

performed over a period of 45minutes or less as research has shown this allows
for EEG silence in most patients.

 CPB is then halted and the surgical repair is completed as quickly as possible.
The goal is to perform the procedure in 40 minutes or less periods of HCA
beyond this time are associated with increased neurologic dysfunction.

 During HCA, a variety of cerebral protection techniques are employed to

minimize neurologic damage that can occur secondary to emboli or from global
ischemia.

 These include packing the head in ice, providing antegrade or retrograde

cerebral circulation with strategically positioned catheters, and administering
protective medications like barbiturates, steroids, lidocaine, magnesium.

 Of these methods, the use of antegrade cerebral perfusion is currently believed to

convey the most neurologic benefit, with some suggesting that this provides the
ability to safely extend the period of HCA to 90 minutes for complicated repairs.

 Repairs to the descending aorta are typically done via a left thoracotomy and may
be performed with full, partial or no CPB in an attempt to minimize ischemia to
the spinalcord and the kidneys. When full bypass is used, the femoral cannulation
is generally performed.
 Distal perfusion may be augmented with left heart bypass, in which a centrifugal
pump is used to circulate oxygenated blood between the left atrium and a point in
the aorta Distal to the surgical repair. HCA is an alternative approach, with a
recent study indicating improved mortality and fewer complications (renal failure
and paraplegia) when this technique was used for aneurysm repair of the- the
distal aorta.

 For traumatic injuries or rupture, a "clamp and go" technique may be used in
which clamps are applied on both sides of the damaged area and the graft is
quickly interpositioned. This method may also be used for uncomplicated aneu-
rysm repairs in which the anticipated period for clamping the aorta is 30 minutes
or less.

 The most devastating complication of surgery on the distal aorta is paraplegia,

which occurs secondary to interruption of blood flow to the spinal cord.

 Patients with extensive thoracoabdominal aneurysms (Crawford I and II ) and

those with active dissection are at greatest risk. The process for injury to the
spinal cord is complex and involves several factors perfusion, metabolic demand,
and reperfusion injury.

 Several intervention have been used in an attempt to mitigate the risk of spinal
cord injury, including regional hypothermic cooling of the spinal cord,
perioperative drainage of cerebral spinal fluid, maintenance of distal aortic
perfusion with left heart bypass, and reimplantation of critical intercostal arteries
into the graft.

 Pulmonary complications are also common after surgery on the descending or

thoracoabdominal aorta. This is partially attributable to the high prevalence of
smoking and COPD in this patient population. In addition, the surgery typically
requires a period of one-lung ventilation as well as a thoracotomy incision and
the need to cut through the diaphragm to access the aorta.

 Newer surgical approaches that protect the phrenic nerve and preserve as much
diaphragm as possible have helped to improve outcomes somewhat, but the
 number of patients requiring mechanical ventilation longer than 48 hours is still
as high as 11% to 34% in some series. The incidence of tracheostomy in patients
with pulmonary complications has been reported to be between 7% and 11 %.

 Risk of compromised flow to the kidneys occurs as a consequence of the

dissection/aneurysm itself, from the absence of perfusion during cross-clamping,
and because of hypotension during the perioperative period. In addition,
preoperative renal insufficiency and ruptured aneurysms are known predictors of
acute postoperative renal failure. Outcomes can be improved with adequate
hydration, judicious use of contrast dye, distal perfusion techniques, and renal
artery reconstruction when needed.

 During repair of an AAA, access is obtained via a midline incision or through a

retroperitoneal approach. The latter approach is associated with a decrease in
pulmonary complications. In elective cases, heparinization is used to minimize
the risk of embolic complications, but this is not feasible for repair of a ruptured
aneurysm.

 Open repair consists of clamping the aorta first distally and then proximally, to
isolate the aneurysm. The aneurysm is then incised and a Dacron tube graft is
anastomosed to the proximal and distal aorta. If the iliac arteries are involved, a
bifurcated graft may be used.

 Cross-clamping the proximal aorta is associated with an increase in cardiac

workload, while cross-clamping the distal aorta results in temporary ischemia to
the lower body, including the kidneys. Complications for this procedure include
myocardial infarction, colon ischemia, renal failure, and lower extremity
emboliythrombosis

Interventional Therapies

Within the past decade, a number of interventional options have become available for
the treatment of aortic conditions. Options to restore flow through the aorta now include
endovascular placement of stents and catheter-guided fenestration. Recent studies have
shown that these techniques may offer improved outcomes, even in high-risk
patients.

 Percutaneous balloon fenestration is used to create a tear in the dissection flap

between the true and the false lumen, to restore flow into the aorta. A needle
attached to a guidewire is positioned within the false lumen at the desired
location, and a balloon catheter is used to create a tear.
 Although this may restore flow to compromised arterial branches, it carries
the risk of embolism from thrombosis within the false lumen as well as an
increased risk for future arterial rupture.
 An alternative is to use a fenestrated stent graft designed with openings that
can be positioned to allow flow into branch arteries while maintaining patency
of the aortic lumen.
 Endovascular stent grafts were first used in the abdominal aorta in 1990.
Initially used only in the elective repair of abdominal aneurysms, stent use has
now evolved to include treatment of thoracic aneurysm and Type B
dissections as well.
 Aortic stent grafts are available in a variety of configurations-straight tube,
bifurcated, branch graft-depending on the area of the aorta that requires repair.
All of the grafts are deployed via the femoral artery, and positioned with the the
use of fluoroscopy.
 Data on thorasic stents are more limited because of the newness of the
technology, but a recent report indicated accepted rate of mortality and
morbidity with stents placed for both elective and emergent repair of the
thoracic aorta.

Medical management

Drug Dose Action

Elanapril 0.625 mg IV over 5 min, then every Decreases blood pressure by
6 hr inhibiting conversion of
(vasotec) angiotensin I to angiotensin II
(potent vasoconstrictor).

Esmolol 0.25-0.5 mcg/kg bolus, followed Cardioselective agents block

by infusion of 50-200 meg/kg/min OR beta] receptors to decrease
2.5-5 mg IV over 2 min; repeat up contractility and heart rate,
to total dose of 15mg thus decreasing BP.
Metoprolol
Labetalol Intermittent boluses of 20-40 mg Is a combined alpha and
administered over 2 min, or as infusion at
beta blocker. Blocks alpha
1-4 mg/min receptors to decrease SVR
and BP; blocks beta 1
receptors to prevent reflex
tachycardia.
Dilzem Bolous dose of 0.25 mg/kg iv over 5 Calcium channel blockers
minutes followed by infusion of 5-15
verapamil
mg/hr
Nicardipine 2.5 mg over 5 minutes may be Blocks transport of
repeated 4 times. Followed by calcium in to the smooth
infusion at 2-4 mg/hr muscle cells lining the
vasculature, causing
vasodilation and decrease
in SVR.
Fentanyl 25-100 mcg IV bolous Opiod analgesic and
sedatives
Morphine 2- 10 mg IV EVERY 2-4 HRS.
sulphate
Sodium 1.1- 8 mcg/kg/min infusion Relaxes arterial and
nitroprusside venous smooth muscles
to decrease both preload
and after load
phenylephrine 10- 100 mcg/ min Stimulate alpha 1
receptors to cause vaso
constriction.

NURSING MANAGEMENT
NURSING ASSESSMENT

 In patient with thoraco abdominal aortic aneurysm, be alert for sudden onset of sharp,
ripping, or tearing pain located in anterior chest, epigastric area, shoulders, or back,
indicating acute dissection or rupture.
 In patients with abdominal aortic aneurysm, assess for abdominal (particularly left
lower quadrant) pain and intense lower back pain caused by rapid expansion. Be alert
 for syncope, tachycardia, and hypotension, which may be followed by fatal
hemorrhage due to rupture.

NURSING DIAGNOSES

 Ineffective Tissue Perfusion (vital organs) related to aneurysm or aneurysm rupture or

dissection
 Risk for Infection related to surgery
 Acute Pain related to pressure of aneurysm on nerves and postoperatively
 Potential for complication related to the use of hypothermic circulatory arrest,
including hypothermia, bleeding and neurological injuries.
 Potential for ischemic complication related to location of aortic injury,
surgical approach and pre exiting disease.

Nursing Interventions
Maintaining Perfusion of Vital Organs
Preoperatively:

 Assess for chest pain and abdominal pain.

 Prepare patient for diagnostic studies or surgery as indicated.
 Monitor for signs and symptoms of hypovolemic shock.
 Perform neurovascular checks to distal extremities.

Postoperatively:

 Monitor vital signs frequently.

 Assess for signs and symptoms of bleeding:
o Hypotension
o Tachycardia
o Tachypnea
o Diaphoresis
 Monitor laboratory values as ordered.
 Monitor urine output hourly.
  Assess abdomen for bowel sounds and distention. Observe for diarrhea, which occurs
sooner than one would expect bowel function.
 Perform neurovascular checks to distal extremities.
 Assess feet for signs and symptoms of embolization:
o Cold feet
o Cyanotic toes or patchy blue areas on plantar surface of feet
o Pain in feet
 Maintain I.V. infusion to administer medications to control BP and provide fluids
postoperatively.
 Position patient to avoid hip flexion, keeping knees below the level of the hips when
sitting in chair.
 If thoracoabdominal aneurysm repair has been performed, monitor for signs and
symptoms of spinal cord ischemia:
o Pain
o Numbness
o Paresthesia
o Weakness

Preventing Infection

 Monitor temperature.
 Monitor changes in WBC count.
 Monitor incision for signs of infection.
 Administer antibiotics, if ordered.

Relieving Pain

 Administer pain medication as ordered or monitor patient-controlled analgesia.

 Keep head of bed elevated no more than 45 degrees for the first 3 days
postoperatively to prevent pressure on incision site.
 Rarely administer nasogastric decompression for ileus following surgery, until bowel
sounds return.
 Assess abdomen for bowel sounds and distention.
Hypothermia

 Continuously monitor the temperature

 Apply warm air blankets as needed
 Administer meperidine as needed to treat shivering

Bleeding

 Maintain patency of chest tubes.

 Monitor postoperative lab results for Hct/Hgb, aPTI, and platelets;
 Obtain additional coagulation studies for continued bleeding.
 Administer blood products and medication for bleeding.
 Maintain MAP 70-80 mm Hg in patients who are actively bleeding.

Neurological dysfunction

 Allow patient to awaken as soon as possible, to evaluate neurologic status

 Complete assessment of cognitive function, as well as gross motor movement and
sensation

Myocardial ischemia

 Continuously monitor the ECG for ST changes

 Administer perioperative beta blockers as ordered.

Spinal cord ischemia/ para plegia

 Optimize perfusion to spinal cord by maintaining adequate blood pressure.

 If a lumbar drain is placed, maintain system at prescribed level and drain CSF as
needed to maintain CSF pressure
<10 mm Hg.
 Perform hourly assessments for neurologic impairment, including numbness, tingling,
or weakness in lower extremities.

Renal dysfunction

 Monitor urine output hourly.

 Monitor filling pressures and maintain preload with fluids as needed.
 Maintain adequate blood pressure for renal perfusion
GI DYSFUNCTION

 Maintain an NG tube to low continous suction until bowel sounds are heard
 Monitor for signs of ischemic bowel, including abdominal pain, distention,
persistant acidosis, diarrhea

Distal embolisation

 Perform neurovascular check to the distal extremities for motor function,

capillary refill, sensation and pulses.

Patient Education and Health Maintenance

 Instruct patient about medications to control BP and the importance of taking them.
 Discuss disease process and signs and symptoms of expanding aneurysm or
impending rupture, or rupture, to be reported.
 For postsurgical patients, discuss warning signs of postoperative complications (fever,
inflammation of operative site, bleeding, and swelling).
 Encourage adequate balanced intake for wound healing.
 Encourage patient to maintain an exercise schedule postoperatively.
 Instruct patient that due to use of a prosthetic graft to repair the aneurysm, he will
require prophylactic antibiotic use for invasive procedures, including routine dental
examinations and dental cleaning.

Evaluation: Expected Outcomes

 Tissue color, sensation, and temperature normal; nontender, nonswollen, and intact
 Afebrile, no signs of infection
 Reports control of pain with medication

VENTRICULAR ANEURYSM

DEFINITION
  Ventricular aneurysm usually refers to a thin and stretched area of the ventricle where
mature scar tissue has replaced most of the myocardium.
 Left ventricular aneurysm is defined as a localized protrusion of the left ventricular
(LV) cavity during systole and diastole with akinetic or dyskinetic walls.
 Ventricular aneurysm results when the infracted myocardial wall become thinned and
bulges out during contraction.

ETIOLOGY
1. Coronary artery disease
2. Acute myocardial infarction
 greater than 80% of left ventricular aneurysms involve the anterior wall
and/or apex and are associated with high-grade stenosis or complete occlusion
of the proximal or mid-left anterior descending coronary artery(lad)
 Approximately 50% of left ventricular aneurysms occuring after acute mi
appear within 48 h from the onset of chest pain. The remainder appear within
two weeks. Once formed, LVA rarely resolves.
3. Chest trauma causing myocardial contusion
4. Coronary artery laceration resulting in mi.
5. Traumatic rupture of the left ventricle may also result in pseudoaneurysm formation.
6. Spontaneous closure of a ventricular septa1 defect - aneurysm of the membranous
ventricular septum is an uncommon anomaly that develops as a result of the
spontaneous closure of a ventricular septa1 defect.
7. Aortic insufficiency, endocarditis, and arrhythmias
8. Chagas’ disease
9. Cardiac sarcoidosis
10. Presence of lewitic gummas in the myocardium.
11. Midventricular hypertrophy and obstruction

PATHOHYSIOLOGY
LVA formation results from expansion of infarcted tissue within the first 2 to 14 days of MI.
 In the early stages after MI, specimens of necrotic tissue are compliant and expansile,
accepting a significant fraction of the stroke volume.
  The ventricle may dilate using the Frank-Starling mechanism as an acute
compensatory measure.
 If the LVA is large enough (20% of LV perimeter)
 congestive heart failure may develop.
 In addition, increased oxygen requirements (increased heart rate, contractility, wall
stress) may result in infarct extension and rupture of the myocardial wall.
 In the chronic stages of LVA, scar tissue is noncompliant.
 Left ventricular dilation may persist to maintain a normal stroke volume.
 Left ventricular dysfunction is primarilydiastolic secondary to reduced compliance.
The presence of systemic arterial hypertension has been implicated in the development of
postinfarction LVA.
The pathophysiology can be summarised as:

Etiological factors

Acute necrosis of the portion of the left ventricle,

with resulting healing by fibrosis and scar

Disorders in the contraction of left ventricle varying fron hypokinesia to akinesia

Left ventricular aneurysm

Distension of ventricular aneurysm

Increased work load of left ventricle

Persistant cardiac failure or ventricular arrhythmias

CLINICAL MANIFESTATIONS
Angina
Systemic arterial hypertension
Sinus tachycardia
Rales
Ventricular gallop

DIAGNOSIS
 History collection
 Physical examination
 Cardiac enzymes- elevated
 ECG- The electrocardiogram usually shows large Q waves in the precordial leads.
Persistent ST-segment elevation after healing of acute MI
 Chest x – ray - Chest x-ray is usually nondiagnostic. A definite localized bulge or
calcification may suggest the diagnosis of LVA
 Contrast ventriculography is the “gold standard” for making the clinical diagnosis of
LVA. Thrombus formation in the LVA may also be seen.
 Concomitant coronary arteriography will define the coronary anatomy.
 Echocardiography – Twodimensional (2-D) echocardiography provides excellent
sensitivity and specificity in the diagnosis of LVA. Two-dimensional
echocardiography is more sensitive than contrast ventriculography in detecting mural
thrombi in the LVA cavity. Two-dimensional echocardiography is also helpful in the
setting of chest trauma and suspected cardiac involvement.
 Equilibrium radionuclide ventriculography (technetium- 99m gated blood pool
scanning) is also a noninvasive method that provides high accuracy in the diagnosis of
LVA
 Thallium-201 scintigraphy is highly accurate for the detection of LVA.

COMPLICATIONS
 Arrhythmias- Refractory Ventricular Arrhythmias
 Angina pectoris- The occurrence of angina pectoris indicates the presence of ischemic
but viable myocardium either in the same vascular territory of LVA or, more
commonly, in a different vascular territory.
 Thromboembolism
 LV dysfunction
 Congestive heart failure- Congestive heart failure results from poor LV systolic
function (LVA usually > 20% of LV) and from diastolic dysfunction (impaired LV
filling due to stiff noncompliant scar tissue). Mitral regurgitation secondary to LV
dilation or ischemic involvement of papillary muscle may be present. Congestive
heart failure occurs in 29 % of patients with LVA and is a major cause of death.
  Rupture of LVA - Rupture of LVA is extremely rare unless reinfarction occurs at the
border of the LVA.
MANAGEMENT
 Treatment of LV aneurysm has classically included medical therapy, surgical repair,
and cardiac transplantation.
 Small aneurysms with no clot and no elevation of the LV end-diastolic pressure
should be followed up medically with noninvasive techniques if the patient is
asymptomatic.
 Patients with asymptomatic moderate-sized LV aneurysms with a global ejection
fraction of 0.55 or greater and a normal contractile ejection fraction may be treated
medically if the patient has no serious coronary disease.
 However, when the contractile ejection fraction is less than 0.50, the risk of
deterioration is great and the patient should be considered for operation unless the
aneurysm is small.
 Even with more extensive LV damage, many seemingly “hopeless” cases may be
successfully treated with aneurysm repair when the contractile ejection fraction is
0.25 to 0.30 if the mean pulmonary artery pressure is less than 40 mm Hg and the
cardiac index is greater than or equal to 2.1 L . min-1 .m-2
 If there is an associated cardiomyopathy due to a cause other than ischemia, a poor
outcome may be expected. Clearly, transplantation should be performed as a
treatment of choice when the contractile ejection fraction is less than 0.25 and when
there is right ventricular dysfunction, permanent mitral insufficiency, and poor target
coronary arteries for bypass.

LV aneurysmectomy
 Aneurysmectomy is the most effective form of therapy for patients with symptomatic
aneurysms of the left ventricle following myocardial infarction.
 Operation should not be undertaken less than 2 months following myocardial
infarction unless there is severe hemodynamic derangement.
 Circulatory assist devices, such as the intra-aortic balloon pump, have been of
particular help in this group of severely ill patients.
 Results of elective aneurysmectomy performed 2 months or more following
myocardial infarction are quite good, with the long-term outlook for the patient
 generally depending on the function of the uninvolved myocardium and the status of
the remaining coronary circulation.
 When ventricular irritability results in life-threatening arrhythmia, aneurysmectomy
must often be performed.

INDICATION
o Refractory Ventricular Arrhythmias
Left ventricular aneurysmectomy was first reported to control severe ventricular tachycardia
Subsequent reports were associated with significant operative mortality (up to 42%) and poor
control of VT since LV aneurysmectomy did not reliably remove the anhythmogenic focus
(> 75% had recurrent VT).
o Congestive Heart Failure
o Angina Pectoris
The myocardial ischemia in the patient with an LV aneurysm is aggravated by increased wall
tension. Angina may be the major symptom in a patient with an isolated ventricular aneurysm
when the oxygen demand exceeds its supply.
o Thromboembolism
Another clear indication for repair of LV aneurysms is systemic arterial emboli, many of
which may be "silent." One half of patients with LV aneurysms who undergo operation or
autopsy have mural thrombi . It is our contention that when transmural infarction has resulted
in stasis and endocardia1 injury with the formation of irregular mural thrombi, there is rarely,
if ever, a true healing with fibrosis or neoendocardium over such thrombi.
o Left Ventricular Pseudoaneurysm (LVPA)

Vasodilators, diuretics, and digoxin are used to treat heart failure. Anticoagulant drugs are
used to prevent the formation of blood clots. Antiarrhythmic drugs are used to treat cardiac
arrhythmias.

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infarction. World Journal of Surgery
http://link.springer.com/article/10.1007%2FBF01556520
14. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1422601/

15. http://www.nursing-nurse.com/medical-and-nursing-management-of-myocarditis-559/

16. http://www.merckmanuals.com/home/heart_and_blood_vessel_disorders/pericardial_diseas
e/chronic_pericarditis.html

CHRONIC PERICARDITIS

Chronic pericarditis is inflammation that begins gradually, is long-lasting, and results in fluid
accumulation in the pericardial space or thickening of the pericardium.

Pericarditis is considered chronic if it lasts longer than 6 months. There are two main types of
chronic pericarditis.
In chronic effusive pericarditis, fluid slowly accumulates in the pericardial space, between
the two layers of the pericardium.

CHRONIC CONSTRICTIVE PERICARDITIS

 Another complication of pericardial disease is constrictive pericarditis.
 It is important to recognize this form of pericarditis because it may be
correctable if treated early.
 The challenge with constrictive pericarditis is that it can mimic common
disorders that produce symptoms of right-sided heart failure, such as
restrictive cardiomyopathy, pulmonary embolism, pulmonary hypertension,
right ventricular infarction, mitral stenosis, and left ventricular systolic
dysfunction.
 TB that led to calcification of the pericardium was the major cause of
constrictive pericarditis in the early twentieth century. Now the most
common cause is idiopathic."
 Radiation therapy and open heart surgery are also frequent causes.
 Constrictive pericarditis causes fibrosis and calcification of the pericardium,
which inhibit normal ventricular filling while systolic contraction of the
ventricles remains normal.
 Pericardial scarring usually occurs over a period of years. Classically, the
pericardial scarring is uniform involving all chambers of the heart.
 The restricted filling leads to equal and elevated pressures in all chambers.
 As blood flows from the right atrium to the right ventricle during diastole, the
right ventricle expands and quickly reaches the limit imposed by the rigid,
constricting pericardium.
 The ventricle is now unable to fill further, resulting in an increase in
systemic venous pressure and signs and symptoms of right heart failure.
 Decreased left ventricular filling decreases stroke volume and cardiac output,
which leads to hypotension similar to that seen with restrictive
cardiomyopathy.
 The differentiation between these two maladies can be very difficult, but is
exceedingly important in that the treatments are quite different
 CLINICAL PRESENTATION
 Constrictive pericarditis can take months or years to develop.
 Early in the course of the disease, patients manifest signs and symptoms of
right heart failure often severe.
 Subsequently, they may develop signs and syrnptorns of left heart failure.
 At end stage, these patients develop cardiac cachexia with weakness, fatigue,
and tissue wasting.
 Pertinent physical findings in constrictive pericarditis include significantly
increased JVD; often kussmaul sign, a paradoxical (jugular veins normally collapse
during inspiration) increase in JVD during inspiration and a prominent y descent in
the jugular waveforms. Lung sounds may be clear despite the presence of JVD and
peripheral edema.
 In contrast to the muffled heart sound heard cardiac tamponade, an early
diastolic filling heard in constrictive pericarditis, known as dial knock.
 A pericardial knock is a high pitched sound heard early in diastole at the 4th
and 5th intercostal space along the left sternal border or at the apex of the
heart with the patient leaning forward.
 The knock occurs as a result of a constrictive pericardium abruptly empting
early rapid filling of the ventricle.
 These signs and symptoms except for the pericardial knock may be mistaken
for restrictive cardiomyopathy.

DIAGNOSTIC TESTS
 Chest X-ray may show a calcified pericardium and often an enlargement.
 ECG findings of low voltage and sometimes atrial fibrillation are
nonspecific.
 The echocardiogram may be helpful in revealing pericardial thickening,
septal bounce during diastole, and septal shifting with inspiration.
 CT is better than MRI in providing excellent resoluion of the pericardium,
which can detect a thickened pericardium (more than 2 mm) quite
accurately. However, 20 percent of patients exhibit no signs of a thickened
pericardium.
 Cardiac catheterization may yield similar findings in both constrictive
 pericarditis and retrictive cardiomyopathy. Diastolic pressures in all
chambers are usually equalized. Rapid y descent of early diastole with a rapid
upswing and plateau yields the classic "square root sign," which can be
present in both diseases.
 One distinguishing feature of constrictive pericarditis is a pulmonary artery
pressure (PAP) greater than 50 nm Hg on cardiac catheterization. This
finding can support the diagnosis of constrictive pericarditis.
 Endomyocardial biopsy is most useful and may be performed to distinguish
between constrictive pericarditis and restrictive cardiomyopathy.
 The only clinical or diagnostic findings that help to differentiate these two
maladies are the following: pericardial knock in constrictive pericarditis,
PAP greater than 60 mm Hg in restrictive cardiomyopathy, and the "septal
bounce" on echocardiogram in constrictive pericarditis.

CLINICAL MANAGEMENT
 Clinical management of constrictive pericarditis includes monitoring of
vital signs and managing symptoms of the disease process.
 Early conservative management with diuretics alleviates symptoms of
volume overload. Many of these patients will develop atrial fibrillation,
and digoxin is appropriate for rate control.
 Beta blockers and calcium channel blockers should not be used in these
patients because they slow the heart rate and may interfere with the
compensatory tachycardia.
 Surgical treatment is the only effective treatment of constrictive
pericarditis.
 A complete resection of the pericardium is performed via a median
sternotomy, often without cardiopulmonary bypass.
 The earlier in the disease process surgical intervention is accomplished, the
less ill the patient and the better the outcome. Late in the disease, removal
of the pericardium may be of little benefit to a patient who is now critically
ill and wasted.
AORTIC RUPTURE

Rupture of aorta is the most common blunt injury of the great vessels. A ruptured aneurysm
carries a mortality risk of above 90%. And the emergency surgical repair is the only chance
for the survival.

Etiology

 Decelerating injury suffered in automobile accidents

  Hypertension

Most common sites of rupture of aorta

 Descending aorta just distal to the origin of left subclavian vein.

 Ascending aorta just above the aortic valve

Clinical manifestations

 Chest and/ or mid scapular pain

 Hypertension of the upper extremities
 Murmers
 Increased pulse amplitude

Patients with aortic rupture may have injury to the CNS, Abdominal viscera, skeleton which
may mask the signs of aortic rupture.

Diagnosis

1. Chest x ray

Injury to the aortic isthmus

 widening of the superior mediastinal shadow

 Depression of the left main bronchus
 Displacement of the trachea and esophagus to the right
 Obliteration of the aortic knob shadow

Injury to the aortic arch and ascending aorta

 Widening of the mediastinum

2. Aortography
3. Constrast CT

MANAGEMENT OF AORTIC ANEURYSM

  Management of aortic aneurysm is individualised .Sugery is conducted as soon as
possible.

Indication for surgery

o Leaking or ruptured aneurysm

o Symptomatic aneurysm(aneurysm causing pain, ureteric obstruction or embolism)
o Expanding aneurysm – expanding at a rate of > 0.5 cm in 1 year.
o Size : aneurysm of > 5.5 cm dm or any saccular aneurysm.

 Those patients with trauma to the CNS, Contaminated wound, and respiratory
insufficiency from lung contusion, cardiac blunt trauma, retroperitoneal hematoma or
other medical co morbidities are treated with either percutaneous endovascular
stenting of the tear or medical therapy to be followed by delayed surgical repair.
 The medical management consists of maintain the mean systemic blood pressure
below 70 mm Hg to control the aortic wall tension and are continued until other
injuries or complication cease.
 Surgery on aorta presents high risks associated with compromising circulation to the
major organs and tissues.
 Unlike traditional cardiac surgery, the use of cardiopulmonary bypass (CPB) may be
limited in some cases because clamping of the aorta is hindered by the location of the
injury.

 A number of techniques have been used to minimise the risks and to improve the
outcome associated with high risk procedure including hypothermic circulatory arrest
(HCA), left heart bypass and separate cerebral perfusion catheters which may vary
according to the type of aortic surgery being performed.

 The incisional approach, the use of CPB, and specialized techniques used to provide
neurologic protection vary depending on the type of aortic surgery being performed.

 When surgery is performed on the ascending aorta for repair of either a Type A
dissection or an aneurysm, the goals are similar. These include maintaining
 myocardial blood flow via the coronary ostia, restoring functions of the aortic
valve, and preventing rupture into the pericardium, which could lead to
tamponade and death.

 The ascending aorta is accessed via a median sternotomy. The patient is placed
on CPB, usually via cannulation of the right atrium and either the aorta distal to
the surgical site or one femoral artery.

 The degree of damage to the aorta and the aortic valve is then assessed. If the
dissection or aneurysm involves the aortic valve or the aortic tissue has
deteriorated (common in Marfan syndrome), a composite graft is used for repair
(Bentall procedure).

 This consists of a Dacron tube with an aortic valve sewn into one end. The graft
is attached to the aortic annulus and the coronary arteries are then reimplanted in
the graft.

 If the aortic tissue is structurally viable and the valve leaflets are intact, a valve
sparing procedure may be performed. Although technically more demanding,
this approach is preferred by some because it avoids the long-term
anticoagulation therapy required with prosthetic valves.

 Surgical repair of dissections or aneurysm involving the aortic arch is more

complicated, because the vessels branching from this area -the innominate,
carotid, and subclavian arteries supply blood flow to the upper body, including
the brain.

 During repairs to the arch, the brachiocephalic vessels must first be removed
from the diseased section of the aorta, and then reimplanted in the graft. This is
typically performed with a period of circulatory arrest to allow the operation on
a bloodless field.

 Circulatory arrest is performed under deep hypothermia, with the patient cooled
systemically to 15- 18° C-the point at which EEG silence occurs. Systemic
 cooling is performed through the bypass circuit until the desired temperature is
reached and EEG silence is confirmed.

 In emergent situations where EEG monitoring is not available this cooling is

performed over a period of 45minutes or less as research has shown this allows
for EEG silence in most patients.

 CPB is then halted and the surgical repair is completed as quickly as possible.
The goal is to perform the procedure in 40 minutes or less periods of HCA
beyond this time are associated with increased neurologic dysfunction.

 During HCA, a variety of cerebral protection techniques are employed to

minimize neurologic damage that can occur secondary to emboli or from global
ischemia.

 These include packing the head in ice, providing antegrade or retrograde

cerebral circulation with strategically positioned catheters, and administering
protective medications like barbiturates, steroids, lidocaine, magnesium.

 Of these methods, the use of antegrade cerebral perfusion is currently believed to

convey the most neurologic benefit, with some suggesting that this provides the
ability to safely extend the period of HCA to 90 minutes for complicated repairs.

 Repairs to the descending aorta are typically done via a left thoracotomy and may
be performed with full, partial or no CPB in an attempt to minimize ischemia to
the spinalcord and the kidneys. When full bypass is used, the femoral cannulation
is generally performed.

 Distal perfusion may be augmented with left heart bypass, in which a centrifugal
pump is used to circulate oxygenated blood between the left atrium and a point in
the aorta Distal to the surgical repair. HCA is an alternative approach, with a
recent study indicating improved mortality and fewer complications (renal failure
and paraplegia) when this technique was used for aneurysm repair of the- the
distal aorta.
 For traumatic injuries or rupture, a "clamp and go" technique may be used in
which clamps are applied on both sides of the damaged area and the graft is
quickly interpositioned. This method may also be used for uncomplicated aneu-
rysm repairs in which the anticipated period for clamping the aorta is 30 minutes
or less.

 The most devastating complication of surgery on the distal aorta is paraplegia,

which occurs secondary to interruption of blood flow to the spinal cord.

 Patients with extensive thoracoabdominal aneurysms (Crawford I and II ) and

those with active dissection are at greatest risk. The process for injury to the
spinal cord is complex and involves several factors perfusion, metabolic demand,
and reperfusion injury.

 Several intervention have been used in an attempt to mitigate the risk of spinal
cord injury, including regional hypothermic cooling of the spinal cord,
perioperative drainage of cerebral spinal fluid, maintenance of distal aortic
perfusion with left heart bypass, and reimplantation of critical intercostal arteries
into the graft.

 Pulmonary complications are also common after surgery on the descending or

thoracoabdominal aorta. This is partially attributable to the high prevalence of
smoking and COPD in this patient population. In addition, the surgery typically
requires a period of one-lung ventilation as well as a thoracotomy incision and
the need to cut through the diaphragm to access the aorta.

 Newer surgical approaches that protect the phrenic nerve and preserve as much
diaphragm as possible have helped to improve outcomes somewhat, but the
number of patients requiring mechanical ventilation longer than 48 hours is still
as high as 11% to 34% in some series. The incidence of tracheostomy in patients
with pulmonary complications has been reported to be between 7% and 11 %.

 Risk of compromised flow to the kidneys occurs as a consequence of the

dissection/aneurysm itself, from the absence of perfusion during cross-clamping,
and because of hypotension during the perioperative period. In addition,
 preoperative renal insufficiency and ruptured aneurysms are known predictors of
acute postoperative renal failure. Outcomes can be improved with adequate
hydration, judicious use of contrast dye, distal perfusion techniques, and renal
artery reconstruction when needed.

 During repair of an AAA, access is obtained via a midline incision or through a

retroperitoneal approach. The latter approach is associated with a decrease in
pulmonary complications. In elective cases, heparinization is used to minimize
the risk of embolic complications, but this is not feasible for repair of a ruptured
aneurysm.

 Open repair consists of clamping the aorta first distally and then proximally, to
isolate the aneurysm. The aneurysm is then incised and a Dacron tube graft is
anastomosed to the proximal and distal aorta. If the iliac arteries are involved, a
bifurcated graft may be used.

 Cross-clamping the proximal aorta is associated with an increase in cardiac

workload, while cross-clamping the distal aorta results in temporary ischemia to
the lower body, including the kidneys. Complications for this procedure include
myocardial infarction, colon ischemia, renal failure, and lower extremity
emboliythrombosis

Interventional Therapies

Within the past decade, a number of interventional options have become available for
the treatment of aortic conditions. Options to restore flow through the aorta now include
endovascular placement of stents and catheter-guided fenestration. Recent studies have
shown that these techniques may offer improved outcomes, even in high-risk
patients.

 Percutaneous balloon fenestration is used to create a tear in the dissection flap

between the true and the false lumen, to restore flow into the aorta. A needle
attached to a guidewire is positioned within the false lumen at the desired
location, and a balloon catheter is used to create a tear.
  Although this may restore flow to compromised arterial branches, it carries
the risk of embolism from thrombosis within the false lumen as well as an
increased risk for future arterial rupture.
 An alternative is to use a fenestrated stent graft designed with openings that
can be positioned to allow flow into branch arteries while maintaining patency
of the aortic lumen.
 Endovascular stent grafts were first used in the abdominal aorta in 1990.
Initially used only in the elective repair of abdominal aneurysms, stent use has
now evolved to include treatment of thoracic aneurysm and Type B
dissections as well.
 Aortic stent grafts are available in a variety of configurations-straight tube,
bifurcated, branch graft-depending on the area of the aorta that requires repair.
All of the grafts are deployed via the femoral artery, and positioned with the the
use of fluoroscopy.
 Data on thorasic stents are more limited because of the newness of the
technology, but a recent report indicated accepted rate of mortality and
morbidity with stents placed for both elective and emergent repair of the
thoracic aorta.

Medical management

Drug Dose Action

Elanapril 0.625 mg IV over 5 min, then every Decreases blood pressure by
6 hr inhibiting conversion of
(vasotec) angiotensin I to angiotensin II
(potent vasoconstrictor).

Esmolol 0.25-0.5 mcg/kg bolus, followed Cardioselective agents block

by infusion of 50-200 meg/kg/min OR beta] receptors to decrease
2.5-5 mg IV over 2 min; repeat up contractility and heart rate,
to total dose of 15mg thus decreasing BP.
Metoprolol
Labetalol Intermittent boluses of 20-40 mg Is a combined alpha and
administered over 2 min, or as infusion at
beta blocker. Blocks alpha
1-4 mg/min receptors to decrease SVR
and BP; blocks beta 1
receptors to prevent reflex
tachycardia.
Dilzem Bolous dose of 0.25 mg/kg iv over 5 Calcium channel blockers
minutes followed by infusion of 5-15
verapamil
mg/hr
Nicardipine 2.5 mg over 5 minutes may be Blocks transport of
 repeated 4 times. Followed by calcium in to the smooth
infusion at 2-4 mg/hr muscle cells lining the
vasculature, causing
vasodilation and decrease
in SVR.
Fentanyl 25-100 mcg IV bolous Opiod analgesic and
sedatives
Morphine 2- 10 mg IV EVERY 2-4 HRS.
sulphate
Sodium 1.2- 8 mcg/kg/min infusion Relaxes arterial and
nitroprusside venous smooth muscles
to decrease both preload
and after load
phenylephrine 10- 100 mcg/ min Stimulate alpha 1
receptors to cause vaso
constriction.

Nursing management in the post operative period

Potential for complication related to the use of hypothermic circulatory arrest,

including hypothermia, bleeding and neurological injuries.

Intervention

Hypothermia

 Continuously monitor the temperature

 Apply warm air blankets as needed
 Administer meperidine as needed to treat shivering

Bleeding

 Maintain patency of chest tubes.

 Monitor postoperative lab results for Hct/Hgb, aPTI, and platelets;
 Obtain additional coagulation studies for continued bleeding.
 Administer blood products and medication for bleeding.
 Maintain MAP 70-80 mm Hg in patients who are actively bleeding.
Neurological dysfunction

 Allow patient to awaken as soon as possible, to evaluate neurologic status

 Complete assessment of cognitive function, as well as gross motor movement and
sensation

Potential for ischemic complication related to location of aortic injury, surgical

approach and pre exiting disease.

Myocardial ischemia

 Continuously monitor the ECG for ST changes

 Administer perioperative beta blockers as ordered.

Spinal cord ischemia/ para plegia

 Optimize perfusion to spinal cord by maintaining adequate blood pressure.

 If a lumbar drain is placed, maintain system at prescribed level and drain CSF as
needed to maintain CSF pressure
<10 mm Hg.
 Perform hourly assessments for neurologic impairment, including numbness, tingling,
or weakness in lower extremities.

Renal dysfunction

 Monitor urine output hourly.

 Monitor filling pressures and maintain preload with fluids as needed.
 Maintain adequate blood pressure for renal perfusion

GI DYSFUNCTION

 Maintain an NG tube to low continous suction until bowel sounds are heard
 Monitor for signs of ischemic bowel, including abdominal pain, distention,
persistant acidosis, diarrhea

Distal embolisation

 Perform neurovascular check to the distal extremities for motor function,

capillary refill, sensation and pulses.
Nursing management for myocarditis

The nurse can help in identifying the cause of cardiomyopathy or myocarditis through a careful and detailed nursing history.
Advances in understanding of causes of cardiomyopathies make genetic counseling and screening strategies even more critical.
Advanced practice nurses are in a unique position to detect, educate, and treat familial diseases. As expert clinicians, they assess disorders
from a holistic perspective using comprehensive physical examination and detailed history, , including assessment of family history,
psychosocial influences, and functional abilities.
The nurse must be attentive to family history so identification of a familial disease can be made and other family members might be
screened.
Young family members should be screened prior to participation in sports.
Genetic testing may identify those likely to develop the disease, although this testing is not a readily available option in most
laboratories. Guidelines have been published recently for genetic testing in families where sudden cardiac death has occurred.
The nurse must probe to find out the concerns of the patient and the family, and try to address each of them. It is crucial that the patient
with a disease such as cardiomyopathy at high risk for sudden death wear a medical alert bracelet in case of emergency and that family
members be trained in basic life support rechniques The nurse is also in the best position to monitor the patient f\ worsening of symptoms
and for response to medical treatment Evaluation of heart sounds, lung sounds, vital signs, and peripr eral perfusion, as well as
interpretation of laboratory results a. key nursing responsibilities.
Signs of congestion and decreased CO must be detected and reported early to ensure the most effective treatment.
This assessment involves accurate hemodynarn measurements and assessments, which guide therapy.
The ni titrates medications and fluids to improve cardiac function, monitor ring the effects and side effects. Patients with poor perfusion.
is seen in cardiac disease, are at increased risk for skin breakdov The nurse is responsible for assessment and prevention of t, complication.
The nurse optimizes the patient's oxygenan through position changes, pulmonary toilet, monitoring and terpretation of arterial blood gases,
and oxygen administration ventilator management. Infection control is also critical. Because lethal arrhythmias can occur, emergency
equipment should readily available.
If a ventricular assist device is used in the course of treatrne for cardiomyopathy or myocarditis, the nurse monitors the effective of this
therapy. When the patient is to have surgery, preoperative education can allay many fears if the patient and family have opportunity to ask
questions and are prepared for the postopertive course. Teaching needs to be individualized, with deterrn, tion of the best method for the
patient and family. After surg the nurse is responsible for postoperative hemodynamic mon ing, pain control, and respiratory care.
Recognition of symptoms of excess use of drugs or alcohol or withdrawal from these stances is necessary.r" Complications need to be
prevented or rected immediately. Patients with HCM who have undergone tal ablation must be monitored closely for conduction def The
temporary pacemaker is employed as needed. Patients are monitored for enzymes and ECG changes.
Emotional support and education are key componen nursing care of patients with cardiomyopathy and myocar In a familial disease,
a patient may be grieving for a family member while coping with his or her own new diagnosis. : may need assistance coping with this
stressful crisis. Emo needs are particularly important in cardiomyopathy beca its wide-ranging impact on the lives of both the patient
family. Individual counseling, support groups, or both c~ effective.
The patient and his or her family must be educated aboi, diornyopathy and myocarditis, its treatments and possible plications. To
make the diagnosis, the patient undergoe tests, such as echocardiography and cardiac catheterization. test that is done should be
explained to the patient. The p care needs to be discussed and agreed on. If anticoagulan used, side effects and their symptoms, as well
as dietary in tions, need to be explained. Other dietary considerations II' addressed, such as fluid and salt restriction, and the nut leader of
the multidisciplinary team can ensure that the p multiple needs are met.
Research has shown the addition of a I-hour, nurse ea delivered teaching session at the time of hospital disch _ suited in improved
clinical outcomes, increased self-care adherence, and reduced cost of care in patients with sYSt failure. 9 I As a leader of the health care
team, the nurse social workers, chaplains, mental health professionals, d and others to the needs of the patient and coordinate rh
disciplinary care.