March 29, 2018 | Author: cristianamihaila | Category: Heart Failure, Echocardiography, Heart, Atrium (Heart), Chronic Obstructive Pulmonary Disease



Cor pulmonalePage 1 of 13 Official reprint from UpToDate® www.uptodate.com Print | Back Cor pulmonale Author Herbert P Wiedemann, MD Section Editor James K Stoller, MS, MD Deputy Editor Kevin C Wilson, MD Last literature review for version 16.1: January 31, 2008 | This topic last updated: September 2, 2004 INTRODUCTION — Cor pulmonale is the alteration of right ventricular structure or function that is due to pulmonary hypertension caused by diseases affecting the lung or its vasculature. Rightsided heart disease resulting from primary disease of the left side of the heart or from congenital heart disease is not considered within this constellation of disorders [1,2] . Although most of the conditions that cause cor pulmonale are chronic and slowly progressive, patients may also present with acute and life-threatening symptoms. Such abrupt decompensation occurs when the right ventricle is unable to compensate for the imposition of sudden additional demands, resulting either from progression of the underlying disease or a superimposed acute process. The etiology, clinical characteristics, and treatment of cor pulmonale will be reviewed here. Detailed discussions of the clinical characteristics and treatment of both primary and secondary causes of pulmonary hypertension are presented separately. (See "Overview of pulmonary hypertension", see "Diagnostic evaluation of pulmonary hypertension", see "Pathogenesis of pulmonary hypertension", and see "Treatment of pulmonary hypertension"). ETIOLOGY — Cor pulmonale is a state of cardiopulmonary dysfunction that may result from several different etiologies and pathophysiologic mechanisms (show table 1). (See "Overview of pulmonary hypertension"). Possible mechanisms include [3] : Pulmonary vasoconstriction (secondary to alveolar hypoxia or blood acidosis) Anatomic reduction of the pulmonary vascular bed (emphysema, pulmonary emboli, etc) Increased blood viscosity (polycythemia, sickle-cell disease, etc) Increased pulmonary blood flow. The most frequent cause of cor pulmonale is chronic obstructive pulmonary disease (COPD) due to chronic bronchitis or emphysema [1,4,5] . In patients with COPD, an increased incidence of right ventricular involvement may correlate with increasing severity of lung dysfunction. As an example, right ventricular hypertrophy is present in 40 percent of patients with an FEV1 <1.0 L and in 70 percent of those with an FEV1 <0.6 L [1] . However, the presence of hypoxemia, hypercapnia, and polycythemia also independently predict the development of right ventricular hypertrophy in COPD, although not as strongly as abnormal pulmonary mechanics. http://www.uptodate.com/online/content/topic.do?topicKey=copd/7135&view=print 7/23/2008 Hoarseness can result from compression of the left recurrent laryngeal nerve by a dilated main pulmonary artery. lethargy. and exertional syncope reflect an inability to increase cardiac output during stress because of vascular obstruction in the pulmonary arterioles. The mechanism by which angina occurs is variable. Typical exertional angina can occur in patients with primary or secondary pulmonary hypertension. which may even become palpable. the development of pulmonary hypertension and peripheral edema heralds a poor prognosis. and this risk is greatest for patients with a pulmonary artery trunk diameter ≥40 mm [7. The second heart sound may also be narrowly split. Fatigue.8] . for example. lethargy. symptoms directly attributable to pulmonary hypertension. angina can also be caused by dynamic compression of the left main coronary by an enlarged pulmonary artery.do?topicKey=copd/7135&view=print 7/23/2008 . However. In COPD. and those whose pulmonary vascular resistance exceeds 550 dynes-sec/cm(5) rarely survive for more than 3 years [1.com/online/content/topic. CLINICAL CHARACTERISTICS — The clinical detection and assessment of cor pulmonale are difficult due to the subtle and often nonspecific signs and symptoms. rather than having a substantial direct effect on mortality. Auscultation of the heart also may reveal a systolic ejection murmur and. sometimes accompanied by right ventricular failure. Severe right ventricular failure leading to passive hepatic congestion may lead to complaints such as anorexia and right upper quadrant discomfort. for example. http://www. Subendocardial right ventricular ischemia induced by hypoxemia and increased transmural wall tension may play a role [6] . a change that will not be present if right ventricular depolarization is delayed because of concurrent right bundle branch block. a diastolic pulmonary regurgitation murmur. Patients who develop peripheral edema have a five year survival of only approximately 30 percent. Symptoms — There are. Even in severe COPD. the development of cor pulmonale in COPD may just reflect the severity of the underlying obstructive disease and its effect on mortality. and syncope with exertion. the development of peripheral edema in patients with COPD is not necessarily a reliable marker of pulmonary hypertension. As an example. including dyspnea on exertion. however.5] . (See "Natural history and prognosis of COPD"). in more severe disease. fatigue. Less common symptoms include cough and hemoptysis. However. The initial physical finding of pulmonary artery hypertension is increased intensity of the pulmonic component of the second heart sound. even in the absence of epicardial coronary disease. chest pain. Physical findings — The physical examination should detect findings characteristic of pulmonary hypertension and right ventricular hypertrophy. such levels are far below those found in many patients with pulmonary arterial hypertension or chronic unresolved pulmonary emboli.uptodate. it is uncommon to observe mean pulmonary artery pressures above 40 mmHg.Cor pulmonale Page 2 of 13 PROGNOSIS — The development of cor pulmonale associated with pulmonary hypertension often has important prognostic implications. such as elevated jugular venous pressure with a prominent V wave. depending upon the etiology of the hypertension. for example.11] . including the following techniques [15] : Chest radiography Electrocardiography Two dimensional and Doppler echocardiography (which can provide an indirect measurement of pulmonary artery pressure when tricuspid regurgitation is present) Pulmonary function tests Radionuclide ventriculography Magnetic resonance imaging http://www. Edema — Although some patients with severe COPD develop edema in association with clear evidence of right heart failure. Hypoxemia can cause renal vasoconstriction. (See "Pathophysiology and etiology of edema in adults"). Hypercapnia is associated with an appropriate increase in proximal bicarbonate reabsorption. Right ventricular failure leads to systemic venous hypertension. but these findings may be obscured. Although ascites is uncommon. which serves to minimize the fall in arterial pH. associated with a right-sided fourth heart sound and either a left parasternal heave or a downward subxiphoid thrust. In severe emphysema. EVALUATION — Because of the nonspecificity of symptoms and signs. which may develop or be exacerbated during a course of steroid therapy [1. suggesting that the high PCO2 rather than cardiac dysfunction may be responsible for the sodium retention in cor pulmonale [12] . leading to a reduction in urinary sodium excretion [14] .5] . (See "Chapter 3A: Cell model for proximal transport"). ancillary evaluation may be useful. even in severe cor pulmonale. and pulmonary artery pressure and arterial blood gases are stable [9] . Another contributing factor to sodium retention may be hypoxemia. the increased anteroposterior diameter of the chest makes auscultation difficult and changes the position of the right ventricular impulse.com/online/content/topic. a right ventricular third heart sound. extracardiac changes that may be seen include hepatomegaly. since it also promotes the passive reabsorption of NaCl and H2O [13] . and peripheral edema. and a high-pitched tricuspid regurgitant murmur.do?topicKey=copd/7135&view=print 7/23/2008 . Edema seems to occur primarily in patients with hypercapnia. This can produce a variety of findings. both in the resting state and with exercise [10. a pulsatile liver (if tricuspid regurgitation is prominent). but also can contribute to edema formation. other patients with edema have no hemodynamic signs of right ventricular failure. The pathogenesis of edema in such patients is not well understood: the cardiac output and glomerular filtration rate are usually normal or near normal.uptodate.Cor pulmonale Page 3 of 13 Right ventricular hypertrophy is characterized by a prominent A wave in the jugular venous pulse. The right-sided murmurs and gallops are augmented with inspiration. At a later stage. Findings that may be seen in chronic right ventricular overload include: Right axis deviation and R/S ratio greater than 1 in lead V1. The latter is not due to an intrinsic abnormality of the tricuspid valve. but the presence of electrocardiographic changes of cor pulmonale in these settings connotes a poor prognosis [16. Electrocardiogram — The electrocardiogram may demonstrate signs of right ventricular hypertrophy or strain (show ECG 1). it is a secondary manifestation of dilatation of the tricuspid annulus and right ventricle [19] . Right ventricular enlargement can also lead to a decrease in the retrosternal space.uptodate. However. Incomplete or complete right bundle branch block. leading to oligemic lung fields. The elevation in pressure leads to increased thickness of the right ventricle with paradoxical bulging of the septum into the left ventricle during systole (show figure 2). http://www. the diameter of the descending branch of the right pulmonary artery is greater than 20 mm in width. the peripheral vessels are attenuated. However.17] . In 95 percent of patients with COPD and pulmonary hypertension. and the septum shows abnormal diastolic flattening. associated with right atrial dilatation and tricuspid regurgitation. these findings may be obscured in the presence of kyphoscoliosis. the findings are absent in patients without the disease) but a low sensitivity (ie. hyperinflated lungs. Increased P wave amplitude in lead II (P pulmonale) due to right atrial enlargement (show figure 1 and show ECG 2). (See "ECG tutorial: Chamber enlargement and hypertrophy"). a classic pattern of an S wave in lead I with a Q and inverted T wave in lead III may be seen. Right ventricular failure may result in right ventricular and right atrial dilatation on chest radiography.do?topicKey=copd/7135&view=print 7/23/2008 . Two-dimensional echocardiography — Most patients with pulmonary arterial hypertension have two-dimensional echocardiographic signs of chronic right ventricular pressure overload show echocardiogram 1 show echocardiogram 2 show echocardiogram 3 show echocardiogram 4 [18] .Cor pulmonale Page 4 of 13 Right heart catheterization Lung biopsy Chest radiograph — The characteristic chest radiograph in pulmonary arterial hypertension shows enlargement of the central pulmonary arteries (show radiograph 1). this is eventually followed by right ventricular hypokinesis. Most electrocardiographic criteria show a high specificity (ie. The sensitivity of the electrocardiogram is even worse in patients with biventricular hypertrophy or COPD. or interstitial lung disease. left ventricular enlargement. such as occurs with acute pulmonary embolism. In addition. right ventricular dilatation occurs. the findings are present in patients with the disease) for the detection of RVH.com/online/content/topic. In acute cor pulmonale. Stress on the right heart initially produces hyperkinesis. This technique takes advantage of the functional tricuspid insufficiency usually present in PAH.uptodate. Right-sided cardiac catheterization — Catheterization of the right heart is the gold standard http://www. Pulmonary function tests — Pulmonary function tests should be performed in patients with a suggestive history of underlying lung disease and in those with normal cardiac function.do?topicKey=copd/7135&view=print 7/23/2008 . jugular venous distension. and the pulmonary artery pressure (PAP) is then calculated by the modified Bernoulli equation: PAP systolic = (4 x tricuspid jet velocity squared) + RAP where RAP is the right atrial pressure estimated from the size and respiratory variation of flow in the inferior vena cava. and the RV/LV ratio was increased. and hepatomegaly.21] . The use of saline contrast significantly enhanced the sensitivity of Doppler ultrasound in detecting tricuspid regurgitation. Tricuspid regurgitation was detected in 95 percent of these patients. Despite these potential problems. and there was a 97 percent correlation with the pressure measured by catheterization. Thus. Echocardiographic cor pulmonale was said to be present when the right ventricular free wall thickness was >0. Doppler ultrasound examination was able to identify tricuspid regurgitation in 80 percent of 69 patients with catheterization-documented pulmonary arterial hypertension (PA systolic pressure above 35 mmHg) [22] . For example. Doppler estimation using tricuspid regurgitation is far more sensitive than the clinical examination and can make an accurate diagnosis in the majority of patients. enlarged pulmonary arteries on the chest radiograph.Cor pulmonale Page 5 of 13 Doppler echocardiography — Doppler echocardiography is the most reliable noninvasive estimation of the pulmonary artery pressure. It is important to appreciate that only severe interstitial lung disease (with lung volume below 50 percent of normal) produces secondary pulmonary hypertension. Another study of 33 patients with severe COPD compared clinical and echocardiographic criteria in establishing the diagnosis of PAH [23] . parasternal heave. the latter finding is not indicative of interstitial lung disease as a cause of secondary pulmonary arterial hypertension.6 cm in the subxiphoid view. The maximum tricuspid regurgitant jet velocity is recorded. PA systolic pressure was greater than 40 mmHg by tricuspid jet Doppler with saline contrast. The efficacy of Doppler echocardiography may be limited by the ability to identify an adequate tricuspid regurgitant jet. The accuracy was even higher in patients with more severe disease (PA systolic pressure above 50 mmHg). acoustic windows in patients with COPD may be limited by the increased anteroposterior diameter of the chest. while a mild restrictive defect can be produced by pulmonary arterial hypertension itself. Other findings associated with pulmonary hypertension are pulmonic insufficiency and midsystolic closure of the pulmonic valve [20. Cor pulmonale was identified by clinical criteria in only 39 percent of patients versus 75 percent with echocardiography. It may also be less sensitive because of alterations induced by the underlying disease. edema. Clinical criteria included right ventricular hypertrophy on the electrocardiogram. This is illustrated by the following observations: In one report.com/online/content/topic. and physical findings such as a loud pulmonic heart sound. however. in the patient over 40 years of age or with risk factors for coronary disease. which does not exclude significant pulmonary artery hypertension [21] . quantification. Current indications include: When echocardiography does not permit measurement of a tricuspid regurgitant jet. Oxygen therapy improves arterial oxygen content. the right ventricle increases stroke volume and cardiac output.Cor pulmonale Page 6 of 13 for the diagnosis. At present. (See "Long-term supplemental oxygen therapy"). TREATMENT — The medical management of patients with cor pulmonale has centered upon attempts to improve oxygenation (with hypoxemic patients) or right ventricular contractility.com/online/content/topic. diuretic therapy might improve the function of both right and left ventricles (the latter effect being achieved as left http://www. as well as attempts to decrease pulmonary vascular resistance and vasoconstriction (primarily via vasodilators). providing enhanced delivery to the heart.uptodate. This section will discuss the management of patients with cor pulmonale. (See "Management of stable chronic obstructive pulmonary disease" and see "Treatment of pulmonary hypertension"). the mechanisms have not been fully elucidated. When therapy will be determined by precise measurement of pulmonary vascular resistance and the response to vasodilators. thereby decreasing pulmonary vascular resistance. When symptoms are exertional. Diuretics — If right ventricular filling volume is markedly elevated. for example. Right heart catheterization can also be used to determine the potential reversibility of pulmonary arterial hypertension with vasodilators. Issues related to the treatment of COPD in general are discussed in detail separately. right heart catheterization assessments of pulmonary vascular resistance and the vasodilator response are usually adequate to guide therapeutic decisions. Renal vasoconstriction also may be relieved. such as sustained release calcium channel blockers [5] . Lung biopsy — Pathologic assessment of pulmonary artery hypertension requires lung biopsy. resulting in an increase in urinary sodium excretion [14] . When left heart catheterization is also required. as a result. and simultaneous measurement of left-sided pressures during exercise is also indicated.do?topicKey=copd/7135&view=print 7/23/2008 . Two major (and not mutually exclusive) hypotheses may explain the survival benefit of oxygen therapy [4] : Oxygen therapy relieves pulmonary vasoconstriction. and other vital organs. focusing primarily on the treatment of those with cor pulmonale and COPD. This procedure is indicated only when the necessary information cannot be obtained with Doppler echocardiography. pathologic examination has been used intraoperatively to look for evidence of irreversible pulmonary artery pathology. brain. and characterization of pulmonary arterial hypertension. Oxygen therapy — Long-term oxygen therapy improves the survival of hypoxemic patients with COPD. Historically. sustained release) or diltiazem (120 to 720 mg/d orally. verapamil. However. eg. nitrates. clinical studies do not support the use of digitalis in patients with cor pulmonale. On the other hand. The use of vasodilators in patients with COPD can be associated with worsening of arterial oxygenation and/or systemic hypotension. In some studies. probably resulting from the fact that these patients are limited more by lung mechanics than by the degree of pulmonary hypertension [4.do?topicKey=copd/7135&view=print 7/23/2008 . it can be assumed that renal perfusion and therefore flow to other organs are being maintained. since a drop in cardiac output may result if right ventricular filling volume and pressure are reduced too dramatically in pulmonary hypertension. Vasodilators — Several vasodilator agents (including hydralazine. nor does it increase maximal exercise performance. which can have important implications in patients with severe lung disease. excessive volume depletion must be avoided. (See "Causes of metabolic alkalosis").com/online/content/topic. As long as these parameters remain stable. As a result.25] . diuretic therapy may improve cardiovascular performance in some patients with significant volume overload of the right ventricle. and ACE inhibitors) have been utilized in an attempt to ameliorate pulmonary hypertension. However. Evidence of sustained efficacy (beyond three to six months) is relatively uncommon [26-28] . therefore. the use of digoxin in COPD patients with normal left ventricular function does not improve right ventricular ejection fraction at rest or during exercise. Digoxin — Except in cases of coexistent left ventricular failure. (See "Use of digoxin in heart failure due to systolic dysfunction"). A reduction in pulmonary vascular resistance of http://www.uptodate. short-term but modest reductions in pulmonary artery pressure have been documented. In this setting. the use of vasodilator medications for patients with COPD has generally dropped from routine clinical practice. leading to difficulty weaning from a ventilator. Nevertheless.Cor pulmonale Page 7 of 13 ventricular diastolic filling is enhanced through reduction in dilation of the right ventricle). sustained release) is recommended in order to objectively assess efficacy and detect possible adverse hemodynamic consequences. patients with severe and persistent pulmonary hypertension despite oxygen and bronchodilator therapy may be candidates for a trial of vasodilator therapy. right heart catheterization is recommended during the initial administration of the vasodilator. although these effects usually are not severe. either sustained release nifedipine (30 to 240 mg/d orally. further fluid removal should cease if there is an otherwise unexplained elevation in these tests. A simple method to assess volume status is to monitor the BUN and plasma creatinine concentration. nifedipine. vasodilators generally do not result in sustained or significant improvement and may be associated with adverse side effects: Short-term studies usually fail to document an improvement in exercise capacity or functional status. Alkalosis suppresses ventilation.24. Overall. Specifically. Another potentially important complication of diuretic therapy in the patient with cor pulmonale is the development of metabolic alkalosis. Overall. the use of phlebotomy should generally be reserved as adjunctive therapy in acute management of the markedly polycythemic patient who has an acute decompensation of cor pulmonale. phlebotomy (to achieve a hematocrit of about 50 percent) is associated with a decrease in mean pulmonary artery pressure and pulmonary vascular resistance.Cor pulmonale Page 8 of 13 more than 20 percent (provided that cardiac output does not decrease and pulmonary artery pressure does not increase) is a reasonable criterion that has been suggested as evidence of efficacy [5] . State of the art: Pathophysiology of cor pulmonale in chronic obstructive pulmonary disease (Parts 1 & 2). as well as an improvement in exercise performance [4] . As a result. (See "Treatment of pulmonary hypertension"). BC Decker. HM (Eds). ML. (See "Role of methylxanthines in the treatment of COPD"). Philadelphia. experience a reduction in dyspnea (as documented in at least one double-blind trial) even without a reduction in airflow obstruction [29] . Am J Respir Crit Care Med 1994. W.uptodate.120. it is reasonable to consider the use of theophylline as adjunctive therapy in the management of chronic or decompensated cor pulmonale in patients with COPD. However. thereby worsening pulmonary hypertension. CW. Use of UpToDate is subject to the Subscription and License Agreement. especially during exercise [4. HP. the application of continuous oxygen therapy in appropriately selected patients should reduce the number of COPD patients who become severely polycythemic. This may account for the dyspnea experienced by some patients receiving this agent.do?topicKey=copd/7135&view=print 7/23/2008 . 150:833. Matthay. Cor pulmonale. Inc 1990. RA.com/online/content/topic. at least until further evidence either supporting or refuting this approach is available. Wiedemann. the use of almitrine in the management of COPD is not currently recommended. Specifically. Barton. In: Decision Making in Emergency Medicine. therefore. for example. Schumaker. or for the rare patient who remains significantly polycythemic despite appropriate long-term oxygen therapy. Theophylline and the sympathomimetic amines — Theophylline and the sympathomimetic amines (terbutaline. p. Phlebotomy — In patients with severe polycythemia (hematocrit above 55 percent). these agents may [4] : Improve myocardial contractility Provide some degree of pulmonary vasodilation Enhance diaphragm endurance Such effects may explain why some patients treated with theophylline.31] . 2. almitrine appears to improve gas exchange largely by enhancing hypoxic pulmonary vasoconstriction. Almitrine — The well documented ability of almitrine to improve arterial PO2 in patients with COPD led to initial enthusiasm regarding the potential clinical utility of this agent [30] . etc) may have salutary effects not related to bronchodilation. MacNee. However. despite enhanced arterial oxygenation. http://www. As a result. REFERENCES 1. Callaham. CR. Wiedemann. Matthay. Fuso. N. In: Pearlman. Cassidy. 5th ed. SM. 14. New York. T. Klinger. WB Saunders. Mechanisms for development of functional tricuspid regurgitation determined by pulsed Doppler and two dimensional echocardiography. Bourdarias. et al. Klein. 40:910. Clin Sci 1982. SS (Eds). 23. O. DS. 9. Echocardiographic pattern of acute cor pulmonale. Oswald. p. 62:255. J Am Coll Cardiol 1985. HP. Am J Cardiol 1984. 1989. Singh. Am J Cardiol 1999. Inc. Mesquita. Textbook of clinical echocardiography. 19. RL. Am J Med 1985. Thorax 1985. HP. 84:891. JP. Am Rev Respir Dis 1993. Himelman. 148:1414. et al. 1:1184. HP. Oedema in cor pulmonale. Arch Intern Med 1982. M.com/online/content/topic. Wiedemann. In: Heart Disease: Textbook of Cardiovascular Medicine. MH. 12. NM. 13. Investigation and management of pulmonary hypertension in chronic obstructive pulmonary disease.Cor pulmonale Page 9 of 13 3. 99:1600. C. 111:209. et al. Silvestry. Campbell. MJ. 16. Welsh. Kudo. The management of acute and chronic cor pulmonale. Morrison. et al. Pulmonary hemodynamics in patients with chronic obstructive pulmonary disease before and during an episode of peripheral edema. 11:523. 78:87. Reihman. Relief of right ventricular angina and increased exercise capacity with long term oxygen therapy. 70:657. 5. SM. NS. LJ. Effect of hypoxemia on sodium and water excretion in chronic obstructive lung disease. 15. http://www. JR. Improved recognition of cor pulmonale in patients with severe chronic obstructive pulmonary disease. Matthay. F. Am J Med 1988. 142:1326. Richens. Kawut. Brown. Haimowitz. RB. Van Tosh. C. p. LR. DA. Abnormalities of sodium and H2O handling in chronic obstructive lung disease. 18. E (Ed). 1995. Salvaterra. MO. 83:984. 10. 6:359. JM. 7. Extrinsic compression of the left main coronary artery by the pulmonary artery in patients with long-standing pulmonary hypertension. 105:1377. 53:160. 17. Cor pulmonale. et al. Apprill. Dubourg. Chest 1994. Ebejer. Weinberger. 100:534. Ikari. Philadelphia. Struve. The cause of oedema in cor pulmonale. Farber. Weinberger. A. M. 25:708. Likelihood of left main coronary artery compression based on pulmonary trunk diameter in patients with pulmonary hypertension. Weitzenblum. et al. Higgens. 915. SN. Hill. MH. Jardin. Marcel Dekker. et al. H. PG. Rubin. 24. et al. Am J Med 2004. EJM. Chest 1991. et al. Castro. Cor pulmonale in chronic obstructive pulmonary disease: circulatory pathophysiology and management. Matthay. Schafer. Ferrari. A. De Rosa. 99:715. Noninvasive estimation of right ventricular systolic pressure by doppler ultrasound in patients with tricuspid regurgitation. Braunwald. P. RA. 21. Electrocardiographic signs of chronic cor pulmonale: A negative prognostic finding in chronic obstructive pulmonary disease. T. 8. Farber. MO. FE. DH. Circulation 1984. L. Berger. Short. E. 1997. Clin Chest Med 1990. S (Ed). VA. 22. Lancet 1960. Chest 1997. Popp. Quantitative assessment of pulmonary hypertension in patients with tricuspid regurgitation using continuous wave doppler ultrasound. JK. Yock. Wiedemann. JA. Otto.do?topicKey=copd/7135&view=print 7/23/2008 . DA. Chest 1991. M.uptodate. Saunders. Roberts. et al. Scharf. RA. 6. 1604. Mechanism coupling the absorption of solutes and water in the proximal nephron. Kidney Int 1984. 20. Right ventricular dysfunction in chronic obstructive pulmonary disease. Acute hemodynamic effects of nifedipine at rest and during maximal exercise in patients with chronic cor pulmonale. SM. Incalzi. C. 11. RA. 116:369. RA. Mikami. CG. Howard. Sakurai. M. In: Heart-Lung Interactions in Health and Disease. Philadelphia. Circulation 1999. 4. 31. Hedenstierna. et al. RA. in chronic obstructive lung disease. DA. 68:351. Sustained-release theophylline reduces dyspnea in non-reversible obstructive airway disease. Am Rev Respir Dis 1989. RC. 27. 133:385. P. Long-term treatment with a new calcium antagonist. Doria. Am Rev Respir Dis 1986. T. et al. Mullins RC III. Nyquist. Ripe.but not long-term treatment of pulmonary hypertension in patients with chronic obstructive pulmonary disease. et al. 30. 28. C. MacNee. Rubin. The effects of hydralazine on exercise capacity in pulmonary hypertension secondary to chronic obstructive pulmonary disease. Bell. West LG. W. PE. 105:342.uptodate.com/online/content/topic. Am Rev Respir Dis 1989. Matthay. A comparison of the effects of almitrine or oxygen breathing on pulmonary arterial pressure and right ventricular ejection fraction in hypoxic chronic bronchitis and emphysema. K. 134:559. GB. Eur J Respir Dis 1986. LJ. Rhind. JJ. Bratel. Dal Nogare. AR. Snyder. Connaughton. felodipine.Cor pulmonale Page 10 of 13 25. Biernacki. Mahler. Galli. Whyte. O. E. 139:120.do?topicKey=copd/7135&view=print 7/23/2008 . Am Rev Respir Dis 1986. The effect of almitrine bismesylate on hypoxemia in chronic obstructive pulmonary disease. 26. Ann Intern Med 1986. 139:492. Am Rev Respir Dis 1985. W. Nifedipine reduces pulmonary pressure and vascular tone during short. K. 29. Prince. The effect of six months of daily treatment with the beta-2 agonist oral pirbuterol on pulmonary hemodynamics in patients with chronic hypoxic cor pulmonale receiving long-term oxygen therapy. G. et al. et al. 131:22. Agostoni. GRAPHICS Major causes of cor pulmonale Lung disease Chronic obstructive pulmonary disease Cystic fibrosis Interstitial lung diseases Disorders of the pulmonary circulation Pulmonary thromboembolism Primary pulmonary hypertension Tumor emboli Sickle cell anemia Schistosomiasis Pulmonary veno-occlusive disease Neuromuscular diseases Amyotrophic lateral sclerosis Myasthenia gravis Poliomyelitis Guillain-Barré syndrome Spinal cord lesions Bilateral diaphragmatic paralysis Thoracic cage deformities Kyphoscoliosis Disorders of ventilatory control Primary central hypoventilation Sleep apnea syndromes http://www. E. tall R wave in V1 (as part of a qR complex). and peaked P waves in lead II consistent with concomitant right atrial enlargement. delayed precordial transition zone with prominent S waves in leads V5 and V6. The characteristic features include marked right axis deviation (+210º which is equal to -150º).do?topicKey=copd/7135&view=print 7/23/2008 .com/online/content/topic. http://www. MD.Cor pulmonale Page 11 of 13 Pulmonary artery hypertension Chest radiograph in PA view showing enlarged pulmonary arteries (arrows) due to pulmonary hypertension induced by anomalous pulmonary venous drainage. inverted T waves and ST depression in V1 to V3 consistent with right ventricular "strain". to primary pulmonary hypertension. MD. Courtesy of Ary Goldberger. Right ventricular hypertrophy Right ventricular hypertrophy due. Courtesy of Sven Paulin.uptodate. in this case. it also becomes peaked due to the increase in amount of depolarized tissue. scarring.28 mV) in lead II. II. MD.com/online/content/topic. followed by left atrial (LA) activation. due to dilatation. the P wave amplitude is increased (0.Cor pulmonale Page 12 of 13 Right atrial enlargement The left panel shows the normal pattern of atrial activation as it would appear on lead II of the electrocardiogram: activation of the right atrium (RA) occurs first. The synchronous electrical activity has an additive effect upon the surface ECG. and V1. results in simultaneous activation of the right and left atria. In right atrial enlargement (middle panel).uptodate. hypertrophy. The amplitude of the P wave may become significantly increased in the presence of right atrial hypertrophy.12 sec) are increased in lead II and there is deep terminal negativity in V1.12 sec) and notched in leads I and II and the terminal segment has a negative deflection that is deep and delayed in V1. Biatrial enlargement (right panel) has characteristics of both atrial abnormalities: the P wave amplitude (0. or a conduction abnormality.do?topicKey=copd/7135&view=print 7/23/2008 . Representation of echocardiographic findings in secondary pulmonary hypertension http://www. Courtesy of Morton Arnsdorf. resulting in a relatively narrow P wave which is of increased amplitude (P pulmonale). The right panel shows the pattern in a patient with right atrial enlargement: delayed activation of the right atrium. Atrial enlargement P wave morphology with atrial enlargement in leads I.22 mV) and duration (0. The P waves in left atrial enlargement (left panel) are wide (>0. 76. Pearlman. C. Click here to renew your subscription.uptodate. | Subscription and License Agreement | Support Tag: [ecapp1103p.utd. Otto. Cardiomyopathies. The main findings are right ventricular enlargement (RVE). Philadelphia. right ventricular hypertrophy (RVH). right atrial enlargement (RAE). Saunders. Inc. There is also paradoxic bulging of the septum into the left ventricle during systole. AS (Eds). functional tricuspid regurgitation (TR) with a detectable regurgitant jet. 1995. All rights reserved. Adapted from Otto. http://www.152-B37FCB4B4F-2579] Licensed to: UpToDate Guest Pass | Your UpToDate subscription will expire in 9 day(s).com/online/content/topic. In: Textbook of Clinical Echocardiography. and a mid-systolic notch on the pulmonary artery flow tracing.do?topicKey=copd/7135&view=print 7/23/2008 .6.Cor pulmonale Page 13 of 13 Schematic representation of two-dimensional echocardiographic changes in secondary pulmonary hypertension. hypertensive and pulmonary heart disease. © 2008 UpToDate.com-82. C.
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