Cor Pulmonale Emedicine

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    eMedicine Specialties > Cardiology > Myocardial Disease and Cardiomyopathies

    Cor Pulmonale

    Al i A Sovar i, MD, Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois at ChicagoRavi H Dave, MD, Associate Professor of Medicine, University of California at Los Angeles David Geffen School of Medicine;Abraham G Kocheril , MD,FACC, FACP, FHRS, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago

    Updated: Jul 22, 2010



    Cor pulmonale is defined as an alteration in the structure and function of the right ventricle caused by a primary disorder of the

    respiratory system. Pulmonary hypertension is the common link between lung dysfunction and the heart in cor pulmonale. Right-sided

    ventricular disease caused by a primary abnormality of the left side of the heart or congenital heart disease is not considered cor

    pulmonale, but cor pulmonale can develop secondary to a wide variety of cardiopulmonary disease processes. Although cor

    pulmonale commonly has a chronic and slowly progressive course, acute onset or worsening cor pulmonale with life-threatening

    complications can occur.[1 ]


    Several different pathophysiologic mechanisms can lead to pulmonary hypertension and, subsequently, to cor pulmonale. These

    pathogenetic mechanisms include (1) pulmonary vasoconstriction due to alveolar hypoxia or blood acidemia, (2) anatomic

    compromise of the pulmonary vascular bed secondary to lung disorders (eg, emphysema, pulmonary thromboembolism, interstitial

    lung disease, adult respiratory distress syndrome, and rheumatoid disorders), (3) increased blood viscosity secondary to blood

    disorders (eg, polycythemia vera, sickle cell disease, macroglobulinemia), (4) increased blood flow in pulmonary vasculature, and (5)

    idiopathic primary pulmonary hypertension. The result is increased pulmonary arterial pressure.

    The right ventricle (RV) is a thin-walled chamber that is more a volume pump than a pressure pump. It adapts better to changing

    preloads than afterloads. With an increase in afterload, the RV increases systolic pressure to keep the gradient. At a point, a further

    increase in the degree of pulmonary arterial pressure produces significant RV dilation, an increase in RV end-diastolic pressure, and

    RV circulatory collapse. A decrease in RV output with a decrease in diastolic left ventricle (LV) volume results in decreased LV output.

    Since the right coronary artery, which supplies the RV free wall, originates from the aorta, decreased LV output diminishes blood

    pressure in the aorta and decreases right coronary blood flow. What ensues is a vicious cycle between decreases in LV and RVoutput.

    Genetic investigations have confirmed that morphogenesis of the right and left ventricle originated from different sets of progenitor

    cells and sites. This polymorphism could explain the differing rates of hypertrophy of the right and left ventricles.[2 ]

    Right ventricular overload is associated with septal displacement toward the left ventricle. Septal displacement, which is seen on

    echocardiography, can be another factor that decreases LV volume and output in the setting of cor pulmonale and right ventricular

    enlargement. Several pulmonary diseases cause cor pulmonale, which may involve interstitial and alveolar tissues with a secondary

    effect on pulmonary vasculature or may primarily involve pulmonary vasculature. Chronic obstructive pulmonary disease (COPD) is

    the most common cause of cor pulmonale in the United States.

    Cor pulmonale usually presents chronically, but 2 main conditions can cause acute cor pulmonale: massive pulmonary embolism

    (more common) and acute respiratory distress syndrome (ARDS). The underlying pathophysiology in massive pulmonary embolismcausing cor pulmonale is the sudden increase in pulmonary resistance. In ARDS, 2 factors cause RV overload: the pathologic

    features of the syndrome itself and mechanical ventilation. Mechanical ventilation, especially higher t idal volume, requires a higher

    transpulmonary pressure. In chronic cor pulmonale, right ventricular hypertrophy (RVH) generally predominates. In acute cor

    pulmonale, right ventricular dilatation mainly occurs. In the case of ARDS, cor pulmonale is associated with increased possibility of

    right to left shunt through patent foramen ovale and caries poorer prognosis.[3 ]


    United States

    z Cor pulmonale is estimated to account for 6-7% of all types of adult heart disease in the United States, with chronic obstructive

    pulmonary disease (COPD) due to chronic bronchitis or emphysema the causative factor in more than 50% of cases.

    z At present, cor pulmonale accounts for 10-30% of decompensated heart failure related admissions in the United States.[4 ]

    z Although the prevalence of COPD in the United States is about 15 million, the exact prevalence of cor pulmonale is difficult to

    determine because it does not occur in all cases of COPD, and the physical examination and routine tests are relatively

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    insensitive for the detection of pulmonary hypertension.

    z In contrast, acute cor pulmonale is usually secondary to massive pulmonary embolism.

    z Acute massive pulmonary thromboembolism is the most common cause of acute life-threatening cor pulmonale in adults.

    z In the United States, 50,000 deaths are estimated to occur per year from pulmonary emboli and about half occur within the first

    hour due to acute right heart failure.


    The incidence of cor pulmonale varies among different countries depending on the prevalence of cigarette smoking, air pollution, and

    other risk factors for various lung diseases.


    Development of cor pulmonale as a result of a primary pulmonary disease usually heralds a poorer prognosis. For example, patients

    with COPD who develop cor pulmonale have a 30% chance of surviving 5 years. However, whether cor pulmonale carries an

    independent prognostic value or is simply reflecting the severity of underlying COPD or other pulmonary disease is not clear.

    Prognosis in the acute setting due to massive pulmonary embolism or ARDS has not previously been shown to be dependent on the

    presence or absence of cor pulmonale. However, a prospective, multicenter cohort study by Volschan et al indicates that in cases of

    pulmonary embolism, cor pulmonale may be a predictor of inhospital mortality.[5 ]

    The authors collected demographic, comorbidity, andclinical manifestation data on 582 patients admitted to emergency or intensive care units and diagnosed with pulmonary embolism.

    Assessing the information using logistic regression analysis, the investigators built a prediction model. Their results indicated that in

    hemodynamically stable patients with pulmonary embolism, the following factors may be independent predictors of inhospital


    z Age over 65 years

    z Bed rest for longer than 72 hours

    z Chronic cor pulmonale

    z Sinus tachycardia

    z Tachypnea



    Clinical manifestations of cor pulmonale generally are nonspecific. The symptoms may be subtle, especially in early stages of the

    disease, and mistakenly may be attributed to the underlying pulmonary pathology.

    z The patient may complain of fatigue, tachypnea, exertional dyspnea, and cough.

    z Anginal chest pain also can occur and may be due to right ventricular ischemia (it usually does not respond to nitrates) or

    pulmonary artery stretching.

    z Hemoptysis may occur because of rupture of a dilated or atherosclerotic pulmonary artery. Other conditions, such as tumors,

    bronchiectasis, and pulmonary infarction, should be excluded before attributing hemoptysis to pulmonary hypertension. Rarely,

    the patient may complain of hoarseness due to compression of the left recurrent laryngeal nerve by a dilated pulmonary artery.

    z A variety of neurologic symptoms may be seen due to decreased cardiac output and hypoxemia.

    z In advanced stages, passive hepatic congestion secondary to severe right ventricular failure may lead to anorexia, right upper

    quadrant abdominal discomfort, and jaundice.

    z Syncope with exertion, which may be seen in severe disease, reflects a relative inability to increase cardiac output during

    exercise with a subsequent drop in the systemic arterial pressure.

    z Elevated pulmonary artery pressure can lead to elevated right atrial, peripheral venous, and capillary pressure. By increasing

    the hydrostatic gradient, it leads to transudation of fluid and accumulation of peripheral edema. Although this is the simplest

    explanation for peripheral edema in cor pulmonale, other hypotheses explain this symptom, especially in a fraction of patients

    with COPD who do not show increase in right atrial pressure. A decrease in glomerular filtration rate (GFR) and filtration of

    sodium and stimulation of arginine vasopressin (which decreases free water excretion) due to hypoxemia play important

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    pathophysiologic roles in this setting and may even have a role for peripheral edema in patients with cor pulmonale who have

    elevated right atrial pressure.[6 ]


    Physical findings may reflect the underlying lung disease or pulmonary hypertension, RVH, and RV failure.

    z On inspection, an increase in chest diameter, labored respiratory efforts with retractions of the chest wall, distended neck veins

    with prominent a orv waves, and cyanosis may be seen.

    z On auscultation of the lungs, wheezes and crackles may be heard as signs of underlying lung disease. Turbulent flow through

    recanalized vessels in chronic thromboembolic pulmonary hypertension[7 ]may be heard as systolic bruits in the lungs. Splitting

    of the second heart sound with accentuation of the pulmonic component can be heard in early stages. A systolic ejection

    murmur with sharp ejection click over the region of the pulmonary artery may be heard in advanced disease, along with a

    diastolic pulmonary regurgitation murmur. Other findings upon auscultation of the cardiovascular system may be third and

    fourth sounds of the heart and systolic murmur of tricuspid regurgitation.

    z RVH is characterized by a left parasternal or subxiphoid heave. Hepatojugular reflux and pulsatile liver are signs of RV failure

    with systemic venous congestion.

    z On percussion, hyperresonance of the lungs may be a sign of underlying COPD; ascites can be seen in severe disease.

    z Examination of the lower extremities reveals evidence of pitting edema. Edema in cor pulmonale is strongly associated with

    hypercapnia.[8 ]


    Etiologies of cor pulmonale can mechanistically be categorized in 5 groups.

    1. Pulmonary vasoconstriction due to alveolar hypoxia or blood academia: This can result in pulmonary hypertension and if the

    hypertension is severe enough, it causes cor pulmonale.

    2. Various lung disorders: Parenchymal or alveolar lung disorders may anatomically compromise the vasculature beds and cause

    elevated pulmonary blood pressure. Chronic obstructive pulmonary disorder is the most common cause of cor pulmonale.

    Other lung disorders that may cause cor pulmonale are pulmonary thromboembolism, interstitial lung disease, and adult

    respiratory distress syndrome. Also, some connective tissue disorders with pulmonary involvement may result in pulmonary

    hypertension and cor pulmonale.

    3. Blood disorders that are associated with increased blood viscosity such as polycythemia vera, sickle cell disease,


    4. Increased blood flow in the pulmonary vasculature

    5. Idiopathic primary pulmonary hypertension

    Differential Diagnoses

    Other Problems to Be Considered

    Congestive (biventricular) heart failure

    Primary pulmonic stenosis

    Primary pulmonary hypertension

    Right-sided heart failure due to congenital heart diseasesRight heart failure due to right ventricular infarction

    Ventricular septal defect

    Constrictive pericarditis

    High-output heart failure

    Infiltrative cardiomyopathies

    Atrial myxoma


    Laboratory Studies

    z Laboratory investigations are directed toward defining the potential underlying etiologies as well as evaluating complications of

    cor pulmonale. In specific instances, appropriate lab studies may include the following: hematocrit for polycythemia (which can

    be a consequence of underlying lung disease but can also increase pulmonary arterial pressure by increasing viscosity),

    serum alpha1-antitrypsin if deficiency is suspected, and antinuclear antibody level for collagen vascular disease such as

    scleroderma. Hypercoagulability states can be evaluated by serum levels of proteins S and C, antithrombin III, factor V

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    Leyden, anticardiolipin antibodies, and homocysteine.

    z Arterial blood gas tests may provide important information about the level of oxygenation and type of acid-base disorder.

    z Elevated brain natriuretic peptide (BNP) level alone is not adequate to establish presence of cor pulmonale, but it helps to

    diagnose cor pulmonale in conjunction with other noninvasive tests and in appropriate clinical settings. An elevated BNP level

    may actually be a natural mechanism to compensate for elevated pulmonary hypertension and right heart failure by promoting

    diuresis and natriuresis, vasodilating systemic and pulmonary vessels, and reducing circulating levels of endothelin and


    Imaging Studies

    A general approach to diagnose cor pulmonale and to investigate its etiology starts with routine laboratory tests, chest radiography,

    and electrocardiography. Echocardiography gives valuable information about the disease and its etiology. Pulmonary function tests

    may become necessary to confirm the underlying lung disease. Ventilation/perfusion (V/Q) scan or chest CT scan may be performed

    if history and physical examination suggest pulmonary thromboembolism as the cause or if other diagnostic tests do not suggest other

    etiologies. Right heart catheterization is the most accurate but invasive test to confirm the diagnosis of cor pulmonale and gives

    important information regarding the underlying diseases. Any abnormal result in each of these tests may need further diagnostic

    evaluation in that specific direction.

    Imaging studies may show evidence of underlying cardiopulmonary diseases, pulmonary hypertension, or its consequence, right

    ventricular enlargement.

    z Chest roentgenography: In patients with chronic cor pulmonale, the chest radiograph may show enlargement of the central

    pulmonary arteries with oligemic peripheral lung fields. Pulmonary hypertension should be suspected when the right

    descending pulmonary artery is larger than 16 mm in diameter and the left pulmonary artery is larger than 18 mm in diameter.

    Right ventricular enlargement leads to an increase of the transverse diameter of the heart shadow to the right on the

    posteroanterior view and filling of the retrosternal air space on the lateral view. These findings have reduced sensitivity in the

    presence of kyphoscoliosis or hyperinflated lungs.

    z Echocardiography: Two-dimensional echocardiography usually demonstrates signs of chronic RV pressure overload. As this

    overload progresses, increased thickness of the RV wall with paradoxical motion of the interventricular septum during systole

    occurs. At an advanced stage, RV dilatation occurs and the septum shows abnormal diastolic flattening. In extreme cases, the

    septum may actually bulge into the left ventricular cavity during diastole resulting in decreased diastolic volume of LV and

    reduction of LV output.

    z Doppler echocardiography is now used to estimate pulmonary arterial pressure, taking advantage of the functional tricuspid

    insufficiency that is usually present in pulmonary hypertension. Doppler echocardiography is considered the most reliable

    noninvasive technique to estimate pulmonary artery pressure. The efficacy of Doppler echocardiography may be limited by the

    ability to identify an adequate tricuspid regurgitant jet, which may be further enhanced by using saline contrast.

    z Ventilation/perfusion (V/Q) lung scanning, pulmonary angiography, and chest CT scanning may be indicated to diagnose

    pulmonary thromboembolism as the underlying etiology of cor pulmonale. These tests may be performed early in the

    diagnostic workup if any evidence of pulmonary embolism appears in history and physical examination. The test may also be

    considered later in the workup if other tests are not suggestive of any other etiology. Pulmonary thromboembolism has a wide

    range of clinical presentations from massive embolism with acute and severe hemodynamic instability to multiple chronic

    peripheral embolisms that may present with cor pulmonale.

    z Ultrafast, ECG-gated CT scanning has been evaluated to study RV function. In addition to estimating right ventricular ejection

    fraction (RVEF), it can estimate RV wall mass. I ts use is still experimental, but with further improvement, it may be used to

    evaluate the progression of cor pulmonale in the near future.

    z Magnetic resonance imaging (MRI) of the heart is another modality that can provide valuable information about RV mass,

    septal flattening, and ventricular function. [9 ]

    z Radionuclide ventriculography can determine RVEF noninvasively. Myocardial perfusion may also show a permanent increase

    in brightness of the right ventricle.[10 ]

    Other Tests

    Electrocardiography (ECG) abnormalities in cor pulmonale reflect the presence of RVH, RV strain, or underlying pulmonary disease.

    These electrocardiographic changes may include the following:

    z Right axis deviation

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    Medical therapy[12 ]for chronic cor pulmonale is generally focused on treatment of the underlying pulmonary disease and improving

    oxygenation and RV function by increasing RV contractility and decreasing pulmonary vasoconstriction. However, the approach might

    be different to some degree in an acute setting with priority given to stabilizing the patient.

    Cardiopulmonary support for patients experiencing acute cor pulmonale with resultant acute RV failure includes fluid loading and

    vasoconstrictor (eg, epinephrine) administration to maintain adequate blood pressure. Of course, the primary problem should be

    corrected, if possible. For example, for massive pulmonary embolism, consider administration of anticoagulation, thrombolytic agents

    or surgical embolectomy, especially if circulatory collapse is impending; consider bronchodilation and infection treatment in patients

    with COPD; and consider steroid and immunosuppressive agents in infiltrative and fibrotic lung diseases.

    Oxygen therapy, diuretics, vasodilators, digitalis, theophylline, and anticoagulation therapy are all different modalities used in the long-

    term management of chronic cor pulmonale.

    Oxygen therapy

    Oxygen therapy is of great importance in patients with underlying COPD[13 ], particularly when administered on a continuous basis.

    With cor pulmonale, the partial pressure of oxygen (PO2) is likely to be below 55 mm Hg and decreases further with exercise and

    during sleep.

    Oxygen therapy relieves hypoxemic pulmonary vasoconstriction, which then improves cardiac output, lessens sympathetic

    vasoconstriction, alleviates tissue hypoxemia, and improves renal perfusion. The Nocturnal Oxygen Therapy Trial (NOTT), a

    multicenter randomized trial, showed that continuous low-flow oxygen therapy for patients with severe COPD resulted in significantreduction in the mortality rate.[14 ]In general, in patients with COPD, long-term oxygen therapy is recommended when PaO2 is less

    than 55 mm Hg or O2 saturation is less than 88%. However, in the presence of cor pulmonale or impaired mental or cognitive

    function, long-term oxygen therapy can be considered even if PaO2 is greater than 55 mm Hg or O2 saturation is greater than 88%.

    Although whether oxygen therapy improves survival in patients with cor pulmonale due to pulmonary disorders other than COPD is

    not clear, it may provide some degree of symptomatic relief and improvement in functional status. Therefore, oxygen therapy plays an

    important role in both the immediate setting and long-term management, especially in patients who are hypoxic and have COPD.


    Diuretics are used in the management of chronic cor pulmonale, particularly when the right ventricular filling volume is markedly

    elevated and in the management of associated peripheral edema. Diuretics may result in improvement of the function of both the right

    and left ventricles; however, diuretics may produce hemodynamic adverse effects if they are not used cautiously. Excessive volumedepletion can lead to a decline in cardiac output. Another potential complication of diuresis is the production of a hypokalemic

    metabolic alkalosis, which diminishes the effectiveness of carbon dioxide stimulation on the respiratory centers and lessens

    ventilatory drive. The adverse electrolyte and acid-base effect of diuretic use can also lead to cardiac arrhythmia, which can diminish

    cardiac output. Therefore, diuresis, while recommended in the management of chronic cor pulmonale, needs to be used with great


    Vasodilator drugs

    Vasodilator drugs have been advocated in the long-term management of chronic cor pulmonale with modest results. Calcium channel

    blockers, particularly oral sustained-release nifedipine[15 ]and diltiazem, can lower pulmonary pressures, although they appear more

    effective in primary rather than secondary pulmonary hypertension.[16 ]Other classes of vasodilators, such as beta agonists, nitrates,

    and angiotensin-converting enzyme (ACE) inhibitors have been tried but, in general, vasodilators have failed to show sustained

    benefit in patients with COPD and they are not routinely used. A trial of vasodilator therapy may be considered only in patients withCOPD with disproportionately high pulmonary blood pressure.

    Beta-selective agonists

    Beta-selective agonists have an additional advantage of bronchodilator and mucociliary clearance effect. Right heart catheterization

    has been recommended during initial administration of vasodilators to objectively assess the efficacy and detect the possible adverse

    hemodynamic consequences of vasodilators.

    The Food and Drug Administration (FDA) has approved epoprostenol, treprostinil, bosentan, and iloprost for treatment of primary

    pulmonary hypertension. Epoprostenol, treprostinil, and iloprost are prostacyclin (PGI2) analogues and have potent vasodilatory

    properties.[17 ]Epoprostenol and treprostinil are administered intravenously and iloprost is an inhaler. Bosentan is a mixed endothelin-A

    and endothelin-B receptor antagonist indicated for pulmonary arterial hypertension (PAH), including primary pulmonary hypertension

    (PPH). In clinical trials, it improved exercise capacity, decreased rate of clinical deterioration, and improved hemodynamics.[17 ]

    The PDE5 inhibitor sildenafil has been intensively studied[18,19,20 ]and approved by the FDA for treatment of pulmonary hypertension.

    Sildenafil promotes selective smooth muscle relaxation in lung vasculature.[21 ]Tadalafil, another PDE5 inhibitor, was also recently

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    approved by the FDA for the treatment of PAH to improve exercise ability.[22 ]

    Not enough data are available regarding the efficacy of these drugs in patients with secondary pulmonary hypertension such as in

    patients with COPD.

    Cardiac glycosides

    The use of cardiac glycosides, such as digitalis, in patients with cor pulmonale has been controversial, and the beneficial effect of

    these drugs is not as obvious as in the setting of left heart failure. Nevertheless, studies have confirmed a modest effect of digitalis on

    the failing right ventricle in patients with chronic cor pulmonale.[23 ]It must be used cautiously, however, and should not be used during

    the acute phases of respiratory insufficiency when large fluctuations in levels of hypoxia and acidosis may occur. Patients with

    hypoxemia or acidosis are at increased risk of developing arrhythmias due to digitalis through different mechanisms including

    sympathoadrenal stimulation.


    In addition to bronchodilatory effect, theophylline has been reported to reduce pulmonary vascular resistance and pulmonary arterial

    pressures acutely in patients with chronic cor pulmonale secondary to COPD.[24 ]Theophylline has a weak inotropic effect and thus

    may improve right and left ventricular ejection. Low doses of theophylline have also been suggested to have anti-inflammatory effects

    that help to control underlying lung diseases such as COPD.[25 ]As a result, considering the use of theophylline as adjunctive therapy

    in the management of chronic or decompensated cor pulmonale is reasonable in patients with underlying COPD.


    Anticoagulation with warfarin is recommended in patients at high risk for thromboembolism. The beneficial role of anticoagulation in

    improving the symptoms and mortality in patients with primary pulmonary arterial hypertension has been demonstrated in several

    studies.[26,27,28,29 ]The evidence of benefit, however, has not been established in patients with secondary pulmonary arterial

    hypertension. Therefore, anticoagulation therapy may be used in patients with cor pulmonale secondary to thromboembolic

    phenomena and with underlying primary pulmonary arterial hypertension.

    Surgical Care

    Phlebotomy is indicated in patients with chronic cor pulmonale and chronic hypoxia causing severe polycythemia, defined as

    hematocrit of 65 or more. Phlebotomy results in a decrease in mean pulmonary artery pressure, a decrease in mean pulmonary

    vascular resistance,[30 ]and an improvement in exercise performance in such patients. However, no evidence suggests improvement

    in survival. Generally, phlebotomy should be reserved as an adjunctive therapy for patients with acute decompensation of cor

    pulmonale and patients who remain significantly polycythemic despite appropriate long-term oxygen therapy. Replacement of the

    acute volume loss with a saline infusion may be necessary to avoid important decreases in systemic blood pressure.

    No surgical treatment exists for most diseases that cause chronic cor pulmonale. Pulmonary embolectomy is efficacious for

    unresolved pulmonary emboli, which contribute to pulmonary hypertension. Uvulopalatopharyngoplasty in selected patients with sleep

    apnea and hypoventilation[31 ]may relieve cor pulmonale. Single-lung, double-lung, and heart-lung transplantation are all used to

    salvage the terminal phases of several diseases (eg, primary pulmonary hypertension, emphysema, idiopathic pulmonary fibrosis,

    cystic fibrosis) complicated by cor pulmonale. Lung transplantation may lead to a reversal of right ventricular dysfunction from the

    chronic stress of pulmonary hypertension. However, strict selection criteria for lung transplant recipients must be met because of the

    limited availability of organ donors.


    Diuretics are used to decrease the elevated right ventricular filling volume in patients with chronic cor pulmonale. Calcium channel

    blockers are pulmonary artery vasodilators that have proven efficacy in the long-term management of chronic cor pulmonale

    secondary to primary pulmonary arterial hypertension. New FDA-approved prostacyclin analogues and endothelin-receptor

    antagonists are available for treatment of PPH. The beneficial role of cardiac glycosides, namely digitalis, on the failing right ventricle

    are somewhat controversial; they can improve right ventricular function but must be used with caution and should be avoided during

    acute episodes of hypoxia.

    In the management of cor pulmonale, the main indication for oral anticoagulants is in the setting of an underlying thromboembolic

    event or primary pulmonary arterial hypertension. Methylxanthines, like theophylline, can be used as an adjunctive treatment for

    chronic cor pulmonale secondary to COPD. Besides the moderate bronchodilatory effect of methylxanthine, it improves myocardial

    contractility, causes a mild pulmonary vasodilatory effect, and enhances diaphragmatic contractility.


    Are used to decrease the elevated right ventricular filling volume in patients with chronic cor pulmonale.

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    Furosemide (Lasix)

    Example of diuretic agents used in the management of chronic cor pulmonale. Furosemide is a powerful loop diuretic that works on

    thick ascending limb of Henle loop, causing a reversible block in reabsorption of sodium, potassium, and chloride.



    20-80 mg/d PO/IV/IM; may titrate to maximum dose of 600 mg/d


    1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; do not administer more frequent than q6h

    1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg


    Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and

    antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides

    and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken

    concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently with this



    Documented hypersensitivity; hepatic coma; anuria; concurrent severe electrolyte depletion



    C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus


    Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few

    months of therapy and periodically thereafter

    Calcium channel blockers

    These agents inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and

    conduction velocity.

    Nifedipine (Procardia)

    Especially in the sustained-release form, nifedipine is a calcium channel blocker that has proven to be fairly effective in the

    management of chronic cor pulmonale caused by primary pulmonary hypertension. Modifies the entry of calcium into the cells by

    blocking the slow or voltage-dependent calcium channels, resulting in vasodilation, which improves myocardial oxygen delivery.

    Sublingual administration generally is safe, despite theoretical concerns.



    10-30 mg SR cap PO tid; not to exceed 120-180 mg/d

    30-60 mg SR tab PO qd; not to exceed 90-120 mg/d


    Not recommended


    Monitor oral anticoagulants when used concomitantly; coadministration with any agent that can lower BP, including beta-blockers and

    opioids, can result in severe hypotension; H2 blockers (cimetidine) may increase toxicity


    Documented hypersensitivity


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    C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus


    Aortic stenosis; angina; congestive heart failure; pregnancy; nursing mothers; may cause lower extremity edema; allergic hepatitis

    has occurred but is rare

    Cardiac glycosidesThese agents decrease AV nodal conduction primarily by increasing vagal tone.

    Digoxin (Lanoxin)

    Has a positive inotropic effect on failing myocardium. Effect is achieved via inhibition of the Na+/K+-ATPase pump, leading to

    increase in intracellular sodium concentration along with concomitant increase in intracellular calcium concentration by means of

    calcium-sodium exchange mechanism. Net result is augmentation of myocardial contractility.



    0.125-0.375 mg PO qd; may be administered qod; available in PO/IV/IM preparations


    8-10 mcg/kg/d PO/IV/IM; maximum dose 100-150 mcg/kg/d


    Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone,

    propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine,

    flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline,

    tolbutamide, and verapamil; medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines,

    cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment

    combinations (eg, carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine),

    aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid


    Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus




    C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus


    Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients;

    hypercalcemia predisposes patient to digitalis toxicity; hypocalcemia can make digoxin ineffective until serum calcium levels are

    normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients

    diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism,

    hypoxia, and acute myocarditis


    These agents may reduce incidence of embolisms when used fast, effectively, and early.

    Warfarin (Coumadin)

    Most commonly used oral anticoagulant. Interferes with hepatic synthesis of vitamin K-dependent coagulation factors. Used for

    prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders.



    2-10 mg/d PO qd; adjust dose to an INR of 1.5:2 or higher depending on the condition requiring anticoagulation

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    Administer weight-based dose of 0.05-0.34 mg/kg/d PO/IV; adjust dose according to desired INR


    Griseofulvin, carbamazepine, glutethimide, estrogens, nafcillin, phenytoin, rifampin, barbiturates, cholestyramine, colestipol, vitamin

    K, spironolactone, oral contraceptives, and sucralfate may decrease anticoagulant effects; oral antibiotics, phenylbutazone,

    salicylates, sulfonamides, chloral hydrate, clofibrate, diazoxide, anabolic steroids, ketoconazole, ethacrynic acid, miconazole, nalidixic

    acid, sulfonylureas, allopurinol, chloramphenicol, cimetidine, disulfiram, metronidazole, phenylbutazone, phenytoin, propoxyphene,sulfonamides, gemfibrozil, acetaminophen, and sulindac may increase anticoagulant effects


    Documented hypersensitivity; severe liver or kidney disease; open wounds; GI ulcers



    D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus


    Dose needs to be adjusted to INR; caution in bleeding tendency and hazardous active hemorrhagic conditions, malignant

    hypertension, patients at high risk of recurrent trauma, (eg, people with alcoholism or psychosis, unsupervised patients who are

    senile); warfarin anaphylaxis, hepatic, renal, thyroid, allergic, and hematologic hypocoagulable conditions and disorders; do not switch

    brands after achieving therapeutic response; caution in active tuberculosis or diabetes; patients with protein C or S deficiency are at

    risk of developing skin necrosis


    Potentiate exogenous catecholamines and stimulate endogenous catecholamine release and diaphragmatic muscular relaxation,

    which, in turn, stimulates bronchodilation.

    Theophylline (Aminophyllin, Theo-24, Theolair, Theo-Dur)

    Mechanism of action is not well defined yet. Was formerly thought that this drug increases intracellular cyclic AMP by causing

    inhibition of phosphodiesterase; however, current data do not support that.



    Loading dose: 5.6 mg/kg IV over 20 min (based on aminophylline)

    Maintenance dose: IV infusion at 0.5-0.7 mg/kg/h; also available in oral preparation


    1 year: Administer as in adults


    Effects may decrease with aminoglutethimide, barbiturates, carbamazepine, ketoconazole, loop diuretics, charcoal, hydantoins,

    phenobarbital, phenytoin, rifampin, isoniazid, and sympathomimetics; effects may increase with allopurinol, beta-blockers,

    ciprofloxacin, corticosteroids, disulfiram, quinolones, thyroid hormones, ephedrine, carbamazepine, cimetidine, erythromycin,

    macrolides, propranolol, and interferon


    Documented hypersensitivity; uncontrolled arrhythmias; peptic ulcers; hyperthyroidism; uncontrolled seizure disorders



    C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

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    Has low serum therapeutic-to-toxicity ratio, and, therefore, serum level monitoring is important; peptic ulcer; hypertension;

    tachyarrhythmias; hyperthyroidism; compromised cardiac function; do not inject IV solution faster than 25 mg/min; patients diagnosed

    with pulmonary edema or liver dysfunction are at greater risk of toxicity because of reduced drug clearance

    Endothelin receptor antagonists

    Competitively bind to endothelin-1 (ET-1) receptors ETA and ETB causing reduction in pulmonary artery pressure (PAP), pulmonary

    vascular resistance (PVR), and mean right atrial pressure (RAP).

    Bosentan (Tracleer)

    Endothelin receptor antagonist indicated for the treatment of pulmonary arterial hypertension in patients with WHO Class II-IV

    symptoms, to improve exercise ability and decrease rate of clinical worsening. Inhibits vessel constriction and elevation of blood

    pressure by competitively binding to endothelin-1 (ET-1) receptors ETA and ETB in endothelium and vascular smooth muscle. This

    leads to significant increase in cardiac index (CI) associated with significant reduction in pulmonary artery pressure (PAP), mean right

    atrial pressure (RAP), pulmonary vascular resistance (PVR), and, to a lesser extent, systemic vascular resistance (SVR). Due to

    teratogenic potential, can only be prescribed through the Tracleer Access Program (1-866-228-3546).



    40 kg: 62.5 mg PO bid for 4 wk initially, then increase to 125 mg PO bid


    Not established; 62.5 mg PO bid recommended if 12 years; not to exceed 125 mg/d


    Toxicity may increase when administered concomitantly with inhibitors of isoenzymes CYP450 2C9 and CYP450 3A4 (eg,

    ketoconazole, erythromycin, fluoxetine, sertraline, amiodarone, and cyclosporine A); induces isoenzymes CYP450 2C9 and CYP450

    3A4 causing decrease in plasma concentrations of drugs metabolized by these enzymes including glyburide as well as other

    hypoglycemics, cyclosporine A, hormonal contraceptives, simvastatin, and possibly other statins; hepatotoxicity increases with

    concomitant administration of glyburide


    Documented hypersensitivity; coadministration with cyclosporine A or glyburide



    X - Contraindicated; benefit does not outweigh risk


    Causes at least 3-fold elevation of liver aminotransferases (ie, ALT, AST) in about 11% of patients; may elevate bilirubin (serum

    aminotransferase levels must be measured prior to initiation of treatment and then monthly); caution in patients with mildly impaired

    liver function (avoid in patients with moderate or severe liver impairment); not recommended while breastfeeding; monitor hemoglobin

    levels after 1 and 3 mo of treatment and every 3 mo thereafter; exclude pregnancy before initiating treatment and prevent thereafter

    by use of reliable contraception; headache and nasopharyngitis may occur

    Ambrisentan (Letairis)

    Endothelin receptor antagonist indicated for pulmonary arterial hypertension in patients with WHO class II or III symptoms. Improves

    exercise ability and decreases progression of clinical symptoms. Inhibits vessel constriction and elevation of blood pressure by

    competitively binding to endothelin-1 receptors ETA and ETB in endothelium and vascular smooth muscle. This leads to significant

    increase in cardiac index associated with significant reduction in pulmonary artery pressure, mean right atrial pressure, pulmonary

    vascular resistance, and, to a lesser extent, systemic vascular resistance (SVR). Because of the risks of hepatic injury and

    teratogenic potential, only available through the Letairis Education and Access Program (LEAP). Prescribers and pharmacies must

    register with LEAP in order to prescribe and dispense. For more information, see or call (866) 664-LEAP(5327).


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    5 mg PO qd initially; may increase to 10 mg PO qd if 5 mg/d tolerated; do not chew, crush, or split tab


    Not established


    Glycoprotein-P, OATP, UGTs (ie, 1A9S, 2B7S, 1A3S), CYP2C19, and CYP3A substrate; coadministration with CYP3A (eg,cyclosporine, atazanavir, clarithromycin, indinavir, itraconazole, ketoconazole, nefazodone, nelfinavir, ritonavir, saquinavir,

    telithromycin) or 2C19 inhibitors (eg, omeprazole) may decrease elimination and therefore increase serum levels; CYP3A and 2C19

    inducers (eg, rifampin) may increase metabolism and therefore decrease serum levels





    X - Contraindicated; benefit does not outweigh risk


    Common adverse effects include peripheral edema, nasal congestion, sinusitis, and facial flushing; caution with mild hepatic

    impairment or history of moderate-to-severe hepatic impairment; hepatic injury may occur (monitor bilirubin, ALT, and AST values at

    baseline and then monthly); may use in women of childbearing potential only after negative pregnancy test result and must use 2

    reliable methods of contraception (unless tubal sterilization or Copper T 380A or LNg 20 IUD inserted); may decrease hemoglobin

    and hematocrit values (monitor at baseline, 1 mo, and then periodically)


    Further Inpatient Care

    Appropriate treatment is directed both at the underlying etiology and at correction of hypoxia when present.

    Further Outpatient Care

    z Patients with cor pulmonale generally require close attention in the outpatient setting.

    z Regular assessment of oxygen needs and pulmonary function are appropriate.

    z Many patients benefit from a formal program of pulmonary rehabilitation.


    Complications of cor pulmonale include syncope, hypoxia, pedal edema, passive hepatic congestion, and death.


    z The prognosis of cor pulmonale is variable depending upon underlying pathology.

    z Patients with cor pulmonale due to COPD have a high 2-year mortality.

    Patient Education

    Patient education regarding the importance of adherence to medical therapy is vital because appropriate treatment of both hypoxia

    and underlying medical illness can improve mortality and morbidity.


    Medicolegal Pitfalls

    z Making a diagnosis of cor pulmonale should be followed by further investigation to determine the underlying lung pathology.

    Sometimes a common lung disease such as COPD is not the only lung pathology as the cause of cor pulmonale; other lung

    diseases may coexist.

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    z When diagnosing cor pulmonale, considering the possibility of thromboembolic disease and primary pulmonary hypertension

    as possible etiologies is important.

    z Note the importance of continuous supplemental oxygen therapy in appropriate patients, as well as the dangers of cigarette

    smoking while using supplemental oxygen. Elevation of carboxyhemoglobin in the blood due to smoking can significantly

    decrease the effect of O2 on arterial O2 content.


    Media file 1: This ECG shows some typical abnormalities that may be seen in cor pulmonale and other chronic

    pulmonary diseases: (1) R/S ratio >1 in V1 and

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    cor pulmonale, pulmonary hypertension, cardiopulmonary disease, COPD, chronic obstructive pulmonary disease, ARDS, acute

    respiratory distress syndrome, right heart failure, right ventricular failure, right ventricular hypertrophy, RVH, pulmonary

    thromboembolism, interstitial lung disease, polycythemia vera, macroglobulinemia, pulmonary embolism, pulmonary emboli, diastolic

    pulmonary regurgitation murmur

    Contributor Information and Disclosures


    Al i A Sovari , MD, Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois at ChicagoAli A Sovari, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians,

    American Heart Association, American Medical Association, and Heart Rhythm Society

    Disclosure: Nothing to disclose.


    Ravi H Dave, MD, Associate Professor of Medicine, University of California at Los Angeles David Geffen School of Medicine

    Disclosure: Nothing to disclose.

    Abr aham G Kocheril , MD, FACC, FACP, FHRS, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at


    Abraham G Kocheril, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Cardiology,

    American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society,

    Central Society for Clinical Research, Heart Failure Society of America, and Illinois State Medical Society

    Disclosure: Nothing to disclose.

    Medical Editor

    Gregory J Dehmer, MD, Director, Division of Cardiology, Scott & White Healthcare; Professor of Medicine, Texas A&M Health

    Science Center College of Medicine

    Gregory J Dehmer, MD is a member of the following medical societies: American College of Cardiology, American Heart Association,

    Society for Cardiac Angiography and Interventions, and Society of Cardiac Angiography and Interventions

    Disclosure: Nothing to disclose.

    Pharmacy Editor

    Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

    Disclosure: eMedicine Salary Employment

    Managing Editor

    Seite 15 von 16Cor Pulmonale: [Print] - eMedicine Cardiology


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    Steven J Compton, MD, FACC, FACP, Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska

    Regional Hospitals

    Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American

    College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart

    Rhythm Society

    Disclosure: Nothing to disclose.

    CME Editor

    Amer Sul eman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of

    Cardiology, Medical City Dallas Hospital

    Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association,

    American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal

    Society of Medicine, and Society of Cardiac Angiography and Interventions

    Disclosure: Nothing to disclose.

    Chief Editor

    Henry H Ooi, MBBCh, BAO, MRCPI, Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs

    Medical Center; Cardiologist, Heart Failure and Cardiac Transplant Program, Vanderbilt University Medical Center

    Henry H Ooi, MBBCh, BAO, MRCPI is a member of the following medical societies: American College of Cardiology, American Heart

    Association, Heart Failure Society of America, and International Society for Heart and Lung Transplantation

    Disclosure: Nothing to disclose.

    Ack now ledgments

    The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Robert S Crausman, MD, MMS and Nidal A Yunis, MD tothe development and writing of this article.

    Further Reading

    Clinical trials

    Educational and Supportive Interventions to Prevent Cardiopulmonary Rehospitalization

    Identification of Genetic Markers for Cardiopulmonary Diseases (Genotype)

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