NCLEX: Cardiovascular disorders

Cardiovascular disorders: Common cardiovascular disorders

Focus topic: Cardiovascular disorders

Myocarditis

Focus topic: Cardiovascular disorders

Myocarditis, a focal or diffuse inflammation of the cardiac muscle (myocardium), may be acute or chronic and can strike at any age. In many cases, myocarditis fails to produce specific cardiovascular symptoms or ECG abnormalities. The patient will commonly experience spontaneous recovery without residual effects. Occasionally, myocarditis is complicated by heart failure and, rarely, leads to cardiomyopathy.

What causes it

Potential causes of myocarditis include:

  • viral infections (most common cause in the United States), such as coxsackievirus A and B strains and, possibly, poliomyelitis, influenza, rubeola, rubella, adenoviruses, and echoviruses
  • bacterial infections, such as diphtheria, tuberculosis, typhoid fever, tetanus, and staphylococcal, pneumococcal, and gonococcal infections
  • hypersensitivity reactions, such as acute rheumatic fever and postcardiotomy syndrome
  • radiation therapy to the chest in treating lung or breast cancer
  • chronic alcoholism
  • parasitic infections, such as toxoplasmosis and, especially, South American trypanosomiasis (Chagas’ disease) in infants and immunosuppressed adults
  • helminthic infections such as trichinosis.

Pathophysiology

Damage to the myocardium occurs when an infectious organism triggers an autoimmune, cellular, or humoral reaction; toxic inflammation can also result from a noninfectious cause. In either case, inflammation may lead to hypertrophy, fibrosis, and inflammatory changes of the myocardium and conduction system.

Feeling flabby

Focus topic: Cardiovascular disorders

The heart muscle weakens and contractility is reduced. The heart muscle becomes flabby and dilated and pinpoint hemorrhages may develop.

What to look for

Signs and symptoms of myocarditis may include:

  • fatigue
  • dyspnea
  • palpitations
  • fever
  • mild, continuous pressure or soreness in the chest
  • signs and symptoms of heart failure (with advanced disease).

What tests tell you

  • Laboratory tests may reveal elevated cardiac enzymes, such as CK and CK-MB, an increased WBC count and ESR, and elevated antibody titers (such as antistreptolysin-O titer in rheumatic fever).
  • ECG changes provide the most reliable diagnostic aid. Typically, the ECG shows diffuse ST-segment and T-wave abnormalities, such as those that occur with pericarditis, conduction defects (prolonged PR interval), and other supraventricular ectopic arrhythmias.
  • Stool and throat cultures may identify bacteria.
  • Endomyocardial biopsy provides a definitive diagnosis.

How it’s treated

Treatment includes antibiotics for bacterial infection, modified bed rest to decrease heart workload, and careful management of complications. Thromboembolism requires anticoagulant therapy. Inotropic drugs, such as dobutamine or dopamine, may be necessary. Some patients may require nitroprusside and nitroglycerin for after load reduction. Treatment with immunosuppressive drugs is controversial but may help after the acute inflammation has passed. Patients with low cardiac output may benefit from intraaortic balloon pulsation and left VADs. Patients will only receive heart transplantation as a last resort.

What to do

  • Assess cardiovascular status frequently, watching for signs of heart failure, such as dyspnea, hypotension, and tachycardia.
  • Assist the patient with bathing as necessary. Provide a bedside commode because this stresses the heart less than using a bedpan.
  • Evaluate the patient. After successful treatment, the patient should have adequate cardiac output as evidenced by normal blood pressure, warm and dry skin, normal LOC, and no dizziness. He should be able to tolerate a normal level of activity. His temperature should be normal, and he shouldn’t be dyspneic.

Pericarditis

Focus topic: Cardiovascular disorders

Pericarditis is an acute or chronic inflammation that affects the pericardium, the fibroserous sac that envelops, supports, and protects the heart. Acute pericarditis can be fibrinous or effusive, with purulent serous or hemorrhagic exudate. Chronic constrictive pericarditis characteristically leads to dense fibrous pericardial thickening. Because pericarditis commonly coexists with other conditions, diagnosis of acute pericarditis depends on typical clinical features and the elimination of other possible causes. Prognosis depends on the underlying cause. Most patients recover from acute pericarditis, unless constriction occurs.

Cardiovascular disorders

What causes it

Pericarditis may result from:

  • bacterial, fungal, or viral infection (infectious pericarditis)
  • neoplasms (primary or metastatic from lungs, breasts, or other organs)
  • high-dose radiation to the chest
  • uremia

Don’t be so sensitive!

Focus topic: Cardiovascular disorders

  • hypersensitivity or autoimmune diseases, such as rheumatic fever (the most common cause of pericarditis in children), systemic lupus erythematosus, and rheumatoid arthritis
  • postcardiac injury, such as MI (which later causes an autoimmune reaction [Dressler’s syndrome] in the pericardium), trauma, and surgery that leaves the pericardium intact but causes blood to leak into the pericardial cavity
  • neoplastic disease
  • idiopathic factors (most common in acute pericarditis)
  • less commonly, aortic aneurysm with pericardial leakage, and myxedema with cholesterol deposits in the pericardium.

Pathophysiology

As the pericardium becomes inflamed, it may become thickened and fibrotic. If it doesn’t heal completely after an acute episode, it may calcify over a long period and form a firm scar around the heart. This scarring interferes with diastolic filling of the ventricles.

What to look for
Pericarditis causes a sharp, sudden pain that usually starts over the sternum and radiates to the neck, shoulders, back, and arms. Unlike the pain of MI, pericardial pain is usually pleuritic, increasing with deep inspiration and decreasing when the patient sits up and leans forward.

One of the classics

Focus topic: Cardiovascular disorders

A classic sign, pericardial friction rub is a grating sound that occurs as the heart moves. You will usually hear the friction rub best during forced expiration while the patient leans forward or is on his hands and knees in bed. Occasionally, you’ll hear the friction rub only briefly or not at all. Pericarditis also causes signs similar to those of chronic right-sided heart failure, such as fluid retention, ascites, and hepatomegaly (with chronic constrictive pericarditis).

What tests tell you

  • Laboratory results don’t establish a diagnosis. Instead,they indicate the presence of inflammation and may help identify its cause. They may include normal or elevated WBC count (especially in infectious pericarditis), an elevated ESR, and slightly elevated cardiac enzymes (with associated myocarditis).
  • A culture of pericardial fluid obtained by open surgical drainage or cardiocentesis sometimes identifies a causative organism in bacterial or fungal pericarditis.
  • Echocardiography may establish the diagnosis of pericardial effusion by revealing an echo-free space between the ventricular wall and the pericardium.
  • Chest X-ray may show an enlarged cardiac silhouette (with large effusion).

Get the rhythm

Focus topic: Cardiovascular disorders

ECG changes in acute pericarditis may include:

  • elevated ST segments in the standard limb leads and most precordial leads without the significant changes in QRS morphology that occur with MI
  • atrial ectopic rhythms such as atrial fibrillation
  • diminished QRS voltage (in pericardial effusion).

How it’s treated

Treatment for pericarditis seeks to relieve symptoms and manage underlying systemic disease. In acute idiopathic pericarditis, post-MI pericarditis, and postthoracotomy pericarditis, treatment consists of bed rest as long as fever and pain persist and nonsteroidal anti-inflammatory drugs, such as aspirin and indomethacin (Indocin), to relieve pain and reduce inflammation. If these drugs fail to relieve symptoms, expect to administer corticosteroids.
Infectious pericarditis that results from disease of the left pleural space, mediastinal abscesses, or septicemia requires antibiotics, surgical drainage, or both. If cardiac tamponade develops, the doctor may perform emergency pericardiocentesis. Signs of cardiac tamponade include pulsus paradoxus, jugular vein distention, dyspnea, and shock.

Open a window

Focus topic: Cardiovascular disorders

Recurrent pericarditis may necessitate partial pericardiectomy, which creates a “window” that allows fluid to drain into the pleural space. In constrictive pericarditis, the surgeon may need to perform total pericardiectomy to permit adequate filling and contraction of the heart. Treatment must also include management of rheumatic fever, uremia, tuberculosis, and other underlying disorders.

What to do

  • Encourage complete bed rest.
  • Assess pain in relation to respiration and body position to distinguish pericardial pain from myocardial ischemic pain.
  •  Place the patient in an upright position to relieve dyspnea and chest pain.
  • Provide analgesics and oxygen, as ordered.
  • Reassure the patient with acute pericarditis that his condition is temporary and treatable.
  • Monitor for signs of cardiac compression or cardiac tamponade, both possible complications of pericardial effusion. Signs include decreased blood pressure, increased central venous pressure, jugular vein distention, and pulsus paradoxus. Because cardiac tamponade requires immediate treatment, keep a pericardiocentesis set at bedside whenever pericardial effusion is suspected.
  • Evaluate the patient. Evidence of successful treatment includes normal temperature, absence of pain and shortness of breath, adequate blood pressure, and warm, dry skin.

Cardiovascular disorders: Raynaud’s phenomenon

Focus topic: Cardiovascular disorders

Primary Raynaud’s phenomenon is one of several arteriospastic diseases characterized by episodic vasospasm in the small peripheral arteries and arterioles. It occurs bilaterally and usually affects the hands or, less commonly, the feet. Upon exposure to cold or stress, the patient experiences skin color changes (blanching, cyanosis, and rubor). He may develop pain, numbness, and throbbing after an attack, but his arterial pulses remain normal. Primary Raynaud’s phenomenon is usually relatively mild and rarely leads to the development of other diseases.

What causes it

The cause of primary Raynaud’s phenomenon is unknown. However, secondary Raynaud’s phenomenon is a condition commonly associated with several connective tissue disorders, such as systemic sclerosis, SLE, and polymyositis, and has a progressive course, leading to ischemia, gangrene, and amputation. Distinction between the two disorders is difficult; some patients who experience mild symptoms of secondary Raynaud’s phenomenon for several years may later develop overt connective tissue disease, such as systemic lupus erythematosus or scleroderma.

Cardiovascular disorders

Pathophysiology

Raynaud’s phenomenon is a syndrome of episodic constriction of the arterioles and arteries of the extremities, resulting in pallor and cyanosis of the fingers and toes. Several mechanisms may account for the reduced digital blood flow, including:

  • intrinsic vascular wall hyperactivity to cold
  • increased vasomotor tone due to sympathetic stimulation
  • antigen-antibody immune response (most likely because abnormal immunologic test results accompany secondary Raynaud’s phenomenon).

What to look for

After exposure to cold or stress, the patient will typically experience:

  • blanching of the skin on the fingertips, which then becomes cyanotic before changing to red and from cold to normal temperature
  • numbness and tingling of fingers
  • sclerodactyly, ulcerations, or chronic paronychia (in long-standing disease).

What tests tell you

  • Diagnosis requires that clinical symptoms last at least 2 years, after which the patient may undergo tests to rule out secondary disease processes, such as chronic arterial occlusive or connective tissue disease.
  • Antinuclear antibody (ANA) titer may identify autoimmune disease as an underlying cause of Raynaud’s phenomenon; more specific tests must be performed if ANA titer is positive.
  • Erythrocyte sedimentation rate measures inflammation. It will be elevated in secondary Raynaud’s phenomenon but not in the primary form.
  • Doppler ultrasonography may show reduced blood flow if the patient also has an associated arterial occlusive disease.

How it’s treated

Initially, the patient must avoid cold, safeguard against mechanical or chemical injury, and quit smoking. Drug therapy is usually reserved for patients with unusually severe symptoms.
Calcium channel blockers, such as nifedipine (Procardia), diltiazem (Cardizem), and nicardipine (Cardene), may be prescribed to produce vasodilation and prevent vasospasm. Adrenergic blockers, such as phenoxybenzamine or reserpine, may improve blood flow to fingers or toes.

What to do

  • For a patient with a less advanced form of illness, provide reassurance that symptoms are benign. As the disorder progresses, try to allay the patient’s fears about disfigurement.
  • Evaluate the patient. The patient who responds well to treatment will have warm hands and feet. The skin of his hands and feet will retain its normal color.

Cardiovascular disorders: Restrictive cardiomyopathy

Focus topic: Cardiovascular disorders

Characterized by restricted ventricular filling and failure to contract completely during systole, restrictive cardiomyopathy is a rare disorder of the myocardial musculature that results in low cardiac output, and eventually endocardial fibrosis and thickening. If severe, it’s irreversible.

What causes it

The cause of primary restrictive cardiomyopathy remains unknown. In amyloidosis, infiltration of amyloid into the intracellular spaces in the myocardium, endocardium, and subendocardium may lead to restrictive cardiomyopathy syndrome.

Pathophysiology

In restrictive cardiomyopathy, left ventricular hypertrophy and endocardial fibrosis limit myocardial contraction and emptying during systole as well as ventricular relaxation and filling during diastole. As a result, cardiac output falls.

What to look for

Restrictive cardiomyopathy produces:

  • fatigue
  • dyspnea
  • orthopnea
  • chest pain
  • generalized edema
  • liver engorgement
  • peripheral cyanosis
  • pallor
  • S3 or S4 gallop rhythms.
Cardiovascular disorders

What tests tell you

  • ECG may show low-voltage complexes, hypertrophy, or AV conduction defects. Arterial pulsation reveals blunt carotid upstroke with small volume.
  • Chest X-ray shows massive cardiomegaly, affecting all four chambers of the heart (in advanced stages).
  • Echocardiography rules out constrictive pericarditis as the cause of restricted filling by detecting increased left ventricular muscle mass and differences in end-diastolic pressures between the ventricles.
  • Cardiac catheterization demonstrates increased left ventricular end-diastolic pressure and also rules out constrictive pericarditis as the cause of restricted filling.
  • Endomyocardial biopsy may reveal amyloidosis.

How it’s treated

Although no therapy currently exists for restricted ventricular filling, digoxin, diuretics, and a sodium-restricted diet can ease symptoms. Anticoagulant therapy may prevent thrombophlebitis in the patient on prolonged bed rest.

What to do

  • In the acute phase, monitor heart rate and rhythm, blood pressure, and urine output.
  • Be supportive and understanding, and encourage the patient to express his fears.
  • Provide appropriate diversionary activities for the patient restricted to prolonged bed rest.
  • If the patient needs additional help in coping with his restricted lifestyle, refer him for psychosocial counseling.
  • Evaluate the patient. When assessing his response to therapy, look for adequate tissue perfusion, demonstrated by good color; warm, dry skin; and clear lungs. The patient should maintain his weight and level of activity. He should have adequate blood pressure and no dizziness or edema.

Cardiovascular disorders: Thrombophlebitis

Focus topic: Cardiovascular disorders

An acute condition characterized by inflammation and thrombus formation, thrombophlebitis may occur in deep (intermuscular or intramuscular) or superficial (subcutaneous) veins.

Cardiovascular disorders

That’s deep

Focus topic: Cardiovascular disorders

Deep vein thrombophlebitis commonly begins in the small veins, such as the soleal venous sinuses or calf veins. Clots can also form or extend into the large veins, such as the vena cava and the femoral, iliac, and subclavian veins. Usually progressive, this disorder may lead to pulmonary embolism, a potentially fatal condition.

So superficial

Focus topic: Cardiovascular disorders

Superficial thrombophlebitis is usually self-limiting and rarely leads to pulmonary embolism.

What causes it

Although deep vein thrombophlebitis may be idiopathic, it usually results from endothelial damage, accelerated blood clotting, or reduced blood flow. Superficial thrombophlebitis may follow:

  • trauma
  • infection
  • I.V. drug abuse
  • chemical irritation caused by prolonged I.V. use
  •  coagulation problems.

Risk on the rise

Focus topic: Cardiovascular disorders

Certain risk factors appear to increase the risk of developing deep vein or superficial thrombophlebitis. These include:

  • immobility
  • trauma
  • childbirth
  • use of hormonal contraceptives
  • major abdominal surgery
  • joint replacement.

Pathophysiology

Alteration in the epithelial lining causes platelet aggregation and fibrin entrapment of RBCs, WBCs, and additional platelets. The thrombus initiates a chemical inflammatory process in the vessel epithelium that leads to fibrosis, which may either occlude the vessel lumen or embolize.

What to look for

Clinical features vary with the site and length of the affected vein. Deep vein thrombophlebitis may produce:

  • severe pain
  • fever
  • chills
  • malaise
  • nonpitting edema greater than 1″ (2.5 cm) of the affected arm or leg
  • possible warmth to the touch in the affected area
  • positive Homans’ sign (pain on dorsiflexion of the foot); falsepositives are common.
    Signs and symptoms of superficial thrombophlebitis occur along the length of the affected vein. They include:
  • heat
  • pain
  • swelling
  • redness
  • tenderness
  • induration
  • lymphadenitis (with extensive vein involvement)
  • palpable cord.

What tests tell you

  • Doppler ultrasonography identifies reduced blood flow to a specific area and any obstruction to venous flow, particularly in ilio femoral deep vein thrombophlebitis.
  • CT angiography can help visualize the thrombus.
  • Phlebography (also called venography), which is performed infrequently, shows filling defects and diverted blood flow.

How it’s treated

Treatment aims to control thrombus development, prevent complications, relieve pain, and prevent recurrence of the disorder. Symptomatic measures include bed rest, with elevation of the affected arm or leg; warm, moist soaks to the affected area; and analgesics, as ordered. After an acute episode of deep vein thrombophlebitis subsides, the patient may begin to walk while wearing antiembolism stockings (applied before getting out of bed).

You can never be too thin…

Focus topic: Cardiovascular disorders

Treatment for thrombophlebitis may also include anticoagulants (initially, unfractionated or low-molecular-weight heparin [Lovenox]; later, warfarin) to prolong clotting time. Before any surgical procedure, discontinue the full anticoagulant dose as ordered to reduce the risk of hemorrhage. After some types of surgery, especially major abdominal or pelvic operations and joint replacements, prophylactic doses of anticoagulants may reduce the risk of deep vein thrombophlebitis and pulmonary embolism.

Acute, but not so cute

Focus topic: Cardiovascular disorders

For lysis of acute, extensive deep vein thrombosis, treatment may include thrombolytics such as alteplase. In rare cases, deep vein thrombophlebitis may cause complete venous occlusion, and embolectomy may need to be performed.

Superficial treatment

Focus topic: Cardiovascular disorders

Therapy for severe superficial thrombophlebitis may include an anti-inflammatory drug, such as indomethacin, along with antiembolism stockings, warm soaks, and elevation of the patient’s leg. A patient with a high risk for deep vein thrombophlebitis and pulmonary embolus combined with contraindications to anticoagulant therapy or with a high risk for bleeding complications might undergo insertion of a vena caval umbrella or filter.

What to do

  • To prevent thrombophlebitis in high-risk patients, perform ROM exercises while the patient is on bed rest. Use an intermittent external venous compression device during lengthy surgical or diagnostic procedures. Apply antiembolism stockings postoperatively, and encourage early ambulation.
  • Remain alert for signs of pulmonary emboli, such as sudden sharp chest pain that’s worse on inspiration, crackles, dyspnea, hemoptysis, sudden changes in mental status, restlessness, and hypotension.
  • Closely monitor anticoagulant therapy to prevent serious complications such as internal hemorrhage. Watch for signs of bleeding, such as dark, tarry stools; coffee-ground vomitus; and ecchymoses. Encourage the patient to use an electric razor and to avoid medications that contain aspirin.

Keep it flowing

Focus topic: Cardiovascular disorders

To prevent venostasis in patients with thrombophlebitis, take the following steps:

  • Enforce bed rest, as ordered, and elevate the patient’s affected arm or leg. If you plan to use pillows for elevating the leg, place them to support the entire length of the affected extremity and to avoid compressing the popliteal space.
  • Apply warm soaks to improve circulation to the affected area and to relieve pain and inflammation. Give analgesics to relieve pain as ordered.
  • Measure and record the circumference of the affected arm or leg daily. Compare this with the circumference of the other arm or leg. To ensure accuracy and consistency of serial measurements, mark the skin over the area and measure at the same spot daily.
  • Administer heparin I.V. or S.C. as ordered. Use an infusion monitor or pump to control the flow rate of I.V. infusions.
  • Evaluate the patient. After successful therapy, the patient shouldn’t feel pain in the affected area or have a fever. He should  also have normal skin temperature and pulses in the affected armor leg.
Cardiovascular disorders

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