NCLEX: Cardiovascular disorders

Cardiovascular disorders: Common cardiovascular disorders

Focus topic: Cardiovascular disorders

What causes it

Risk factors for arterial occlusive disease include smoking, aging, hypertension, hyperlipidemia, diabetes mellitus, and family history of vascular disorders, MI, or stroke. Causes include:

  • emboli formation
  • infection
  • thrombosis
  • trauma or fracture
  • vasculitis.

Pathophysiology

In arterial occlusive disease, obstruction or narrowing of the lumen of the aorta and its major branches causes an interruption of blood flow, usually to the legs and feet.

Prognosis? It all depends…

Focus topic: Cardiovascular disorders

Prognosis depends on the location of the occlusion, the development of collateral circulation to counteract reduced blood flow and, in acute disease, the time elapsed between occlusion and its removal.

What to look for

Signs and symptoms depend on the severity and site of the arterial occlusion. Acute arterial occlusion may produce the five classic Ps:

  • paralysis
  • pain
  • paresthesia
  • pallor
  • pulselessness.

Other signs and symptoms include:

  • unequally cool extremities when compared with each other
  • intermittent claudication
  • severe pain in the toes or feet (aggravated by elevating the extremity and sometimes relieved by keeping the extremity in a dependent position)
  • ulcers or gangrene
  • pallor on elevation, followed by redness with dependency
  • delayed capillary filling, hair loss, or trophic nail changes
  • diminished or absent extremity pulses.

What tests tell you

  • Arteriography demonstrates the type (thrombus or embolus), location, and degree of obstruction and helps evaluate the collateral circulation. It’s particularly useful for diagnosing chronic forms of the disease and evaluating candidates for reconstructive surgery.
  • Duplex Doppler ultrasonography uses ultrasound to visualize vessels and measure the speed, direction, and pattern of blood flow.
  • Plethysmography detects arterial pulsations to quantify the blood flow in an extremity.
  • Pulse volume recordings can determine the level of ischemia in an extremity.

How it’s treated

Treatment for arterial occlusive disease depends on the cause, location, and size of the obstruction.

Mild disease… moderate measures

Focus topic: Cardiovascular disorders

For patients with mild chronic disease, it usually consists of risk factor reduction, such as smoking cessation and hypertension control as well as suppportive measures such as walking exercise.
Drug therapy includes dextran and antiplatelet and hemorheologic drugs, such as aspirin, ticlopidine, pentoxifylline (Trental), and cilostazol (Pletal). Thrombolytic therapy may be used to treat an acute arterial thrombosis. Patients with hyperlipidemia may be treated with antilipemic drugs.

Severe disease… surgery

Focus topic: Cardiovascular disorders

Appropriate surgical procedures may include embolectomy, thromboendarterectomy, patch grafting, and bypass grafting. The patient may require amputation if arterial reconstructive surgery fails or complications develop.

Lower the risk

Focus topic: Cardiovascular disorders

Invasive endovascular techniques carry less risk than surgery and may include balloon angioplasty, atherectomy, and stenting. Other appropriate therapy includes heparin to prevent emboli (for embolic occlusion) and bowel resection after restoration of blood flow (for mesenteric artery occlusion).

What to do

  • For information on nursing care of patients who undergo vascular surgery.
  • Following treatment, evaluate the patient. He should be able to increase exercise tolerance without developing pain and should have normal peripheral pulses. The patient should also maintain good skin color and temperature in his extremities.

Cardiovascular disorders: Coronary artery disease

Focus topic: Cardiovascular disorders

Coronary artery disease (CAD) refers to any narrowing or obstruction of arterial lumina that interferes with cardiac perfusion. Deprived of sufficient blood, the myocardium can develop various ischemic diseases, including angina pectoris, MI, heart failure, sudden death, and cardiac arrhythmias.

Not an equal opportunity disease

Focus topic: Cardiovascular disorders

CAD affects more Whites than Blacks and more men than women. After menopause, however, the risk of CAD in women increases to equal that of men. CAD occurs more commonly in industrial countries than underdeveloped areas and affects affluent people more than poor people.

What causes it

Most commonly, atherosclerosis leads to CAD. Other possible causes include:

  • arteritis
  • coronary artery spasm
  • certain infectious diseases
  • congenital abnormalities.

Patients with certain risk factors appear to face a greater likelihood of developing CAD. These factors include:

  • family history of heart disease
  • obesity
  • smoking
  • high-fat, high-carbohydrate diet
  • sedentary lifestyle
  • menopause
  • stress
  • diabetes
  • hypertension
  • hyperlipoproteinemia.

Cardiovascular disorders

Pathophysiology

Fatty, fibrous plaques progressively occlude the coronary arteries, reducing the volume of blood that can flow through them, leading to myocardial ischemia.

A precarious balance

Focus topic: Cardiovascular disorders

As atherosclerosis progresses, luminal narrowing and vascular changes impair the diseased vessel’s ability to dilate. This causes a precarious balance between myocardial oxygen supply and demand, threatening the myocardium beyond the lesion.

When the balance tips…

Focus topic: Cardiovascular disorders

When oxygen demand exceeds what the diseased vessels can supply, localized myocardial ischemia results. Transient ischemia causes reversible changes at the cellular and tissue levels, depressing myocardial function. Untreated, it can lead to tissue injury or necrosis. Oxygen deprivation forces the myocardium to shift from aerobic to anaerobic metabolism. As a result, lactic acid (the end product of anaerobic metabolism) accumulates and cellular pH decreases.

…things fall apart

Focus topic: Cardiovascular disorders

The combination of hypoxia, reduced energy availability, and acidosis rapidly impairs left ventricular function. The strength of contractions drops in the affected myocardial region as the fibers shorten inadequately, with less force and velocity. Plus, the ischemic section’s wall moves abnormally. This typically results in the heart ejecting less blood with each contraction. If blood flow through the coronary arteries isn’t restored, an MI will result. If blood flow is restored, aerobic metabolism and contractility return.

What to look for

Angina, the classic symptom of CAD, occurs as a burning, squeezing, or crushing tightness in the substernal or precordial chest. It may radiate to the left arm, neck, jaw, or shoulder blade. Women, however, may experience atypical chest pain. Angina has four major forms:

  • stable — pain that’s predictable in frequency and duration and relieved with nitrates and rest
  • unstable — increased pain that’s easily induced
  • Prinzmetal’s or variant — pain that results from unpredictable coronary artery spasm

Cardiovascular disorders

  • microvascular — angina-like chest pain in a patient with normal coronary arteries that results from impaired vasodilator reserve.
    Other signs and symptoms of CAD include:
  • nausea
  • vomiting
  • weakness
  • diaphoresis
  • cool extremities.

What tests tell you

  • ECG shows ischemia and, possibly, arrhythmias such as premature ventricular contractions. A pain-free patient may have a normal ECG. Arrhythmias may occur without infarction, secondary to ischemia.
  • Exercise ECG may provoke chest pain and signs of myocardial ischemia in response to physical exertion.
  • Coronary angiography reveals coronary artery stenosis or obstruction and collateral circulation and shows the condition of the arteries beyond the narrowed area.

Keep on running

Focus topic: Cardiovascular disorders

  • During treadmill exercise, myocardial perfusion imaging with thallium-201 detects ischemic areas of the myocardium, visualized as “cold spots.”
  • Laboratory evaluation of cardiac markers may be performed to confirm or rule out a diagnosis of MI. The patient may also undergo serum lipid studies to detect and classify hyperlipidemia.
  • An elevated Hb A1C level indicates an increased risk for atherosclerosis and adverse cardiac events; an elevated C-reactive protein level points to a higher cadiac risk. Although these two tests alone can’t determine if a patient with angina has CAD, they do help detect a higher risk for CAD.

How it’s treated

For patients with angina, CAD treatment seeks to reduce myocardial oxygen demand or increase oxygen supply. Nitrates reduce myocardial oxygen consumption. Beta-adrenergic blockers can reduce the workload and oxygen demands of the heart by reducing heart rate and peripheral resistance to blood flow. If angina results from coronary artery spasm, the patient may receive calcium channel blockers. Antiplatelet drugs minimize platelet aggregation and the danger of coronary occlusion. Antilipemic drugs can reduce elevated serum cholesterol or triglyceride levels.
Obstructive lesions may call for coronary artery bypass surgery or PTCA. Other alternatives include laser angioplasty, minimally invasive surgery, rotational atherectomy, and stent placement.

What to do

  • Monitor blood pressure and heart rate during an anginal episode.
  • Take an ECG before administering nitroglycerin or other nitrates for angina.
  • Record the duration of pain, the amount of medication required to relieve it, and accompanying symptoms. Keep nitroglycerin available for immediate use.
  • Evaluate the patient. Note if the patient experiences pain or shortness of breath at rest or with usual activity. Assess whether he can tolerate activity.

Cardiovascular disorders: Dilated cardiomyopathy

Focus topic: Cardiovascular disorders

Dilated cardiomyopathy occurs when myocardial muscle fibers become extensively damaged. This disorder interferes with myocardial metabolism and grossly dilates every heart chamber, giving the heart a globular shape. Dilated cardiomyopathy leads to intractable heart failure, arrhythmias, and emboli. Usually not diagnosed until its advanced stages, this disorder carries a poor prognosis.

What causes it

The primary cause of dilated cardiomyopathy is unknown. Although the relationship remains unclear, it occasionally occurs secondary to:

  • viral or bacterial infections
  • hypertension
  • peripartum syndrome (related to toxemia)
  • ischemic heart disease or valvular disease
  • drug hypersensitivity or chemotherapy
  • cardiotoxic effects of drugs or alcohol.

Pathophysiology

Dilated cardiomyopathy is characterized by a grossly dilated, hypodynamic ventricle that contracts poorly and, to a lesser degree, by myocardial hypertrophy.

Cardiovascular disorders

Pump up the volume

Focus topic: Cardiovascular disorders

All four chambers enlarge as a result of increased volumes and pressures. Thrombi commonly develop within these chambers from blood pooling and stasis, which may lead to embolization. If hypertrophy coexists, the heart ejects blood less efficiently. A large volume remains in the left ventricle after systole, causing heart failure from backward blood flow.

What to look for

The patient may develop:

  • shortness of breath (orthopnea, exertional dyspnea, or paroxysmal nocturnal dyspnea)
  • fatigue
  • irritating dry cough at night
  • edema
  • liver engorgement
  • jugular vein distention
  • peripheral cyanosis
  • sinus tachycardia
  • atrial fibrillation
  • diffuse apical impulses
  • pansystolic murmur (mitral and tricuspid insufficiency secondary to cardiomegaly and weak papillary muscles)
  • S3 and S4 gallop rhythms.

What tests tell you

  • ECG and angiography rule out ischemic heart disease. ECG may also show biventricular hypertrophy, sinus tachycardia, atrial enlargement and, in 20% of patients, atrial fibrillation.
  • Chest X-rays may show cardiomegaly (usually affecting all heart chambers), pulmonary congestion, or pleural effusion.
  • MUGA scanning and echocardiography show decreased left ventricular function and decreased wall motion.

How it’s treated
Treatment seeks to correct the underlying causes and to improve the heart’s pumping ability. Angiotensin- converting enzyme (ACE) inhibitors reduce after load through vasodilation, thereby reducing heart failure. Diuretics are commonly given with an ACE inhibitor to reduce fluid retention.

When the ACE doesn’t fly right

Focus topic: Cardiovascular disorders

For those without improvement of symptoms on an ACE inhibitor and diuretic, digoxin (Lanoxin) may improve myocardial contractility. Hydralazine and isosorbide dinitrate in combination produce vasodilation. Antiarrhythmics, cardioversion, and pacemakers may control arrhythmias. Anticoagulants may be prescribed to reduce the risk of emboli. Treatment may also include oxygen, a sodium-restricted diet, and bed rest.

Selective surgery

Focus topic: Cardiovascular disorders

Surgical interventions in carefully selected patients may include revascularization, such as CABG, if dilated cardiomyopathy results from ischemia. Valvular repair or replacement may help if dilated cardiomyopathy results from valve dysfunction. Cardiomyoplasty — in which the latissimus dorsi muscle is wrapped around the ventricles to help the ventricles pump more efficiently — may work when other medical treatment fails. A cardiomyo stimulator delivering bursts of electrical impulses during systole can help the myocardium contract. If the patient doesn’t respond to other treatments, he may require a ventricular assist device and eventual heart transplantation.

Living the good life

Focus topic: Cardiovascular disorders

For all patients with dilated cardiomyopathy, lifestyle changes can help. As applicable, patients should stop smoking and drinking alcohol; adopt a low-fat, low-sodium diet; and maintain appropriate physical activity.

What to do

  • Monitor for signs of progressive heart failure (decreased arterial pulses and increased jugular vein distention) and compromised renal perfusion (oliguria, increased blood urea nitrogen [BUN] and serum creatinine levels, and electrolyte imbalances).
  • Weigh the patient daily.
  • Check blood pressure and heart rate frequently.
  • Monitor the patient receiving diuretics for signs of resolving congestion (decreased crackles and dyspnea) or too vigorous diuresis. Check serum potassium level for hypokalemia, especially if therapy includes digoxin.
  • Offer support, and encourage the patient to express his feelings.
  • Evaluate the patient. Look for adequate tissue perfusion, as evidenced by good color; warm, dry skin; and clear lungs. The patient should maintain his weight and level of activity. He should also have adequate blood pressure and no dizziness or edema.

Cardiovascular disorders

Cardiovascular disorders: Endocarditis

Focus topic: Cardiovascular disorders

Endocarditis — infection of the endocardium, heart valves, or cardiac prosthesis — results from bacterial or fungal invasion. Untreated endocarditis usually proves fatal, but with proper treatment, 70% of patients recover. Prognosis becomes much worse when endocarditis causes severe valvular damage, leading to insufficiency and heart failure, or when it involves a prosthetic valve.

What causes it

Most cases of endocarditis occur in patients who abuse I.V. drugs or those with prosthetic heart valves, mitral valve prolapse, or rheumatic heart disease.
Other predisposing conditions include congenital abnormalities (coarctation of the aorta and tetralogy of Fallot), subaortic and valvular aortic stenosis, ventricular septal defects, pulmonary stenosis, Marfan syndrome, degenerative heart disease, and syphilis.

When bugs attack

Focus topic: Cardiovascular disorders

Causative organisms may include group A nonhemolytic streptococci, Pneumococcus, Staphylococcus, Enterococcus and, rarely, Gonococcus.

Pathophysiology

Infection causes fibrin and platelets to aggregate on the valve tissue and engulf circulating bacteria or fungi. They form friable verrucous (wartlike) vegetative growths on the heart valves, endocardial lining of a heart chamber, or endothelium of a blood vessel. Such vegetations may cover the valve surfaces, causing ulceration and necrosis; they may also extend to the cordae tendineae. Ultimately, they may embolize to the spleen, kidneys, central nervous system, and lungs.

What to look for

Early clinical features are usually nonspecific and include:

  • weakness
  • fatigue
  • weight loss
  • norexia
  • arthralgia
  • night sweats
  • intermittent fever (may recur for weeks)

Cardiovascular disorders

  • loud, regurgitant murmur that is typical of the underlying rheumatic or congenital heart disease
  • murmur that changes or appears suddenly, accompanied by fever.

Lots of spots

Focus topic: Cardiovascular disorders

Other indications of endocarditis include:

  • petechiae on the skin (especially common on the upper anterior trunk); the buccal, pharyngeal, or conjunctival mucosa; and the nails (splinter hemorrhages)
  • Osler’s nodes (small nodules on the fingers or toes)
  • Roth’s spots (white spots surrounded by hemorrhage on the retina)
  • Janeway lesions (irregular, red lesions on the hands; rare).

When veggies are bad for you

Focus topic: Cardiovascular disorders

In subacute endocarditis, embolization from vegetating lesions or diseased valve tissue can cause several kinds of problems:

  • Splenic infarction causes pain in the left upper quadrant that radiates to the left shoulder as well as abdominal rigidity.
  • Renal infarction results in hematuria, pyuria, flank pain, and decreased urine output.
  • Cerebral infarction causes hemiparesis, aphasia, and other neurologic deficits.
  • Pulmonary infarction — which occurs most commonly in right-sided endocarditis and is common among I.V. drug abusers and after cardiac surgery— can cause cough, pleuritic pain, pleural friction rub, dyspnea, and hemoptysis.
  • Peripheral vascular occlusion results in numbness and tingling in an arm, leg, finger, or toe or impending peripheral gangrene.

What tests tell you

  • Three or more blood cultures, with samples drawn at least 1 hour apart during a 24-hour period, identify the causative organism in up to 90% of patients. The remaining 10% may have negative blood cultures, possibly suggesting fungal infection.
  • Echocardiography, including transesophageal echocardiography, may identify vegetations and valvular damage.
  • ECG readings may show atrial fibrillation and other arrhythmias that accompany valvular disease.
  • Laboratory abnormalities include elevated white blood cell (WBC) count; abnormal histocytes (macrophages); elevated erythrocyte sedimentation rate (ESR); normocytic, normochromic anemia (in subacute bacterial endocarditis); and rheumatoid factor (occurs in about half of all patients).

How it’s treated

Treatment seeks to eradicate the infecting organism. It should start promptly and continue over several weeks.

Germ warfare

Focus topic: Cardiovascular disorders

The practitioner bases antibiotic selection on sensitivity studies of the infecting organism — or the probable organism, if blood cultures are negative. I.V. antibiotic therapy usually lasts 4 to 6 weeks and may be followed by oral antibiotics.
Supportive treatment includes bed rest, antipyretics for fever and aches, and sufficient fluid intake. Severe valvular damage, especially aortic insufficiency, or infection of a cardiac prosthesis may require corrective surgery if refractory heart failure develops.

What to do

  • Obtain a patient history of allergies.
  • Administer antibiotics on time to maintain consistent blood levels. Check dilutions for compatibility with other patient medications, and use a compatible solution (for example, add methicillin to a buffered solution).
  • Evaluate the patient. The patient has recovered from endocarditis if he maintains a normal temperature, clear lungs, stable vital signs, and adequate tissue perfusion and is able to tolerate activity for a reasonable period and maintain normal weight.Heart failure

When the myocardium can’t pump effectively enough to meet the body’s metabolic needs, heart failure occurs. Pump failure usually occurs in a damaged left ventricle but may also happen in the right ventricle. Usually, left-sided heart failure develops first. Heart failure is classified as:

  • acute or chronic
  • left-sided or right-sided (see Understanding left- and right sided heart failure.
  • systolic or diastolic.

Quality time

Focus topic: Cardiovascular disorders

Symptoms of heart failure may restrict a person’s ability to perform ADLs and severely affect quality of life. Advances in diagnostic and therapeutic techniques have greatly improved outcomes for these patients.  However, prognosis still depends on the underlying cause and its response to treatment.

Cardiovascular disorders

Cardiovascular disorders

Cardiovascular disorders

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What causes it

Cardiovascular disorders that lead to heart failure include:

  • atherosclerotic heart disease
  • MI
  • hypertension
  • rheumatic heart disease
  • congenital heart disease
  • ischemic heart disease
  • cardiomyopathy
  • valvular diseases
  • arrhythmias.

Noncardiovascular causes of heart failure include:

  • pregnancy and childbirth
  • increased environmental temperature or humidity
  • severe physical or mental stress
  • thyrotoxicosis
  • acute blood loss
  • pulmonary embolism
  • severe infection
  • chronic obstructive pulmonary disease.

Pathophysiology

The patient’s underlying condition determines whether heart failure is acute or chronic. Heart failure is commonly associated with systolic or diastolic overloading and myocardial weakness. As stress on the heart muscle reaches a critical level, the muscle’s contractility is reduced and cardiac output declines. Venous input to the ventricle remains the same, however.

The body’s responses to decreased cardiac output include:

  • reflex increase in sympathetic activity
  • release of renin from the juxtaglomerular cells of the kidney
  • anaerobic metabolism by affected cells
  • increased extraction of oxygen by the peripheral cells.

Adept at adaptation

Focus topic: Cardiovascular disorders

When blood in the ventricles increases, the heart compensates, or adapts. Compensation may occur for long periods before signs and symptoms develop. Adaptations may be short- or long term. In short-term adaptations, the end-diastolic fiber length increases, causing the ventricular muscle to respond by dilating and increasing the force of contractions. (This is called the Frank- Starling curve.) In long-term adaptations, ventricular hypertrophy increases the heart muscle’s ability to contract and push its volume of blood into the circulation.

What to look for

Clinical signs of left-sided heart failure include:

  • dyspnea, initially upon exertion
  • paroxysmal nocturnal dyspnea
  • Cheyne-Stokes respirations
  • cough
  • orthopnea
  • tachycardia
  • fatigue
  • muscle weakness
  • edema and weight gain
  • irritability
  • restlessness

Cardiovascular disorders

  • shortened attention span
  • ventricular gallop (heard over the apex)
  • bibasilar crackles
  • frothy, blood-tinged sputum.

The patient with right-sided heart failure may develop:

  • edema, initially dependent
  • jugular vein distention
  • hepatomegaly.

What tests tell you

  • Blood tests may show elevated BUN and creatinine levels, elevated serum norepinephrine levels, and elevated transaminase and bilirubin levels if hepatic function is impaired.
  • Elevated blood levels of B-type natriuretic peptide (BNP) may correctly identify heart failure in as many as 83% of patients.
  • ECG reflects heart strain or ventricular enlargement (ischemia). It may also reveal atrial enlargement, tachycardia, and extrasystoles, suggesting heart failure.
  • Chest X-ray shows increased pulmonary vascular markings, interstitial edema, or pleural effusion and cardiomegaly.
  • MUGA scan shows a decreased ejection fraction in left-sided heart failure.
  • Cardiac catheterization may show ventricular dilation, coronary artery occlusion, and valvular disorders (such as aortic stenosis) in both left- and right-sided heart failure.
  • Echocardiography may show ventricular hypertrophy, decreased contractility, and valvular disorders in both left- and right-sided heart failure. Serial echocardiograms may help assess the patient’s response to therapy.
  • Cardiopulmonary exercise testing to evaluate the patient’s ventricular performance during exercise may show decreased oxygen uptake.

How it’s treated

Treatment for heart failure can be planned by using the New York Heart Association classification system and the patient’s BNP level to determine his degree of heart failure.

Cardiovascular disorders

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