Cor pulmonale

Missov, Emil; Marco, Teresa De

doi:10.1007/s11936-000-0008-z

Cited by 6 publications

(7 citation statements)

References 59 publications

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“…Studies conducted by this method showed that RV contractility was reduced at acute exacerbations (in the case of acidosis and infection) accompanied by significant peripheral edema, whereas it was within normal range independent of PAP in clinically stable COPD patients [28,31]. In addition to the modifications above, RV dilatation may cause the interventricular septum to be pushed towards the LV, reducing the left ventricular filling and cardiac output [57]. On the other hand, increased RVSP may contribute to the preservation of LV EF by helping to release LV and pushing LV through free wall through the septum [58].…”

Section: Right Ventricular Functionsmentioning

confidence: 99%

“…These changes in intrathoracic pressure cause lowered cardiac output due to decreased systemic venous return or increase in afterload [28]. Therefore, in advanced COPD patients with mild PHT (25-30 mmHg) at rest, there is a significant increase in PAP (50)(51)(52)(53)(54)(55)(56)(57)(58)(59)(60) with an increase in cardiac output after constant moderate level exercise. When clinically assessed, an exercise at this level can coincide with daily activities, and therefore, significant PHT can develop in daily activities [31].…”

Section: Exercisementioning

confidence: 99%

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Pulmonary Hypertension in Patients with Chronic Obstructive Pulmonary Disease: A Review for Definition, Epidemiology, Pathology, and Diagnosis

Gülmez¹

2017

Gen Med

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Chronic obstructive pulmonary disease (COPD) is a type of obstructive lung disease characterized by progressive and persistent restriction of airflow with a prevalence of 19-25%. The main symptoms are shortness of breath, cough, and sputum production. Smoking is the most common cause and quitting smoking is the only action which prevents developing and progressing of COPD.Pulmonary hypertension (PHT) which is defined as a mean pulmonary artery pressure of ≥ 25 mmHg measured by right heart catheterization at rest is a common complication of COPD and it has been investigated under the title of "Class III: Pulmonary Hypertension due to Pulmonary Disease and/or Hypoxia" according to the updated clinical classification in the 5 th World Pulmonary Hypertension Symposium. Although pathogenesis is complex, it often involves HPV and pulmonary vascular remodeling. In this review, the PHT which mainly develops secondary to COPD is discussed.

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Section: Right Ventricular Functionsmentioning

confidence: 99%

Section: Exercisementioning

confidence: 99%

Pulmonary Hypertension in Patients with Chronic Obstructive Pulmonary Disease: A Review for Definition, Epidemiology, Pathology, and Diagnosis

Gülmez¹

2017

Gen Med

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“…These clinical signs reflect both a low cardiac output and the detrimental activation of neurohormones and other mediators. 2,8,9 Natriuretic peptide levels become significantly elevated in patients with right heart failure even in the absence of left ventricular dysfunction. B-type natriuret-ic peptide (BNP) levels increase in proportion to the extent of right ventricular dysfunction in PAH and are predictive of mortality in right ventricular failure.…”

Section: Clinical Manifestations and Hemodynamic Derangementsmentioning

confidence: 99%

“…The intermediate and long-term goals are to optimize the medical regimen to alleviate symptoms, prevent further disease progression, reduce morbidity and mortality, and successfully bridge the patient to lung or heart-lung transplantation in appropriate individuals. 7,8…”

Section: Goals Of Therapymentioning

confidence: 99%

Managing Right Ventricular Failure in PAH: An Algorithmic Approach

Teresa

McGlothin

2005

Advances in Pulmonary Hypertension

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Pulmonary arterial hypertension (PAH) is a disorder characterized by progressive elevation of pulmonary artery pressure (PAP) and vascular resistance in the absence of left-sided cardiac disease, pulmonary vein compression, respiratory disorders, or thromboembolic disease. It is defined by a mean PAP over 25 mmHg at rest or over 30 mmHg with exercise and a pulmonary artery occlusion pressure (PAOP) of less than 15 mmHg. PAH is associated with a poor prognosis. The estimated median survival from diagnosis is 2.8 years and the 1-year and 5-year survival rates are only 68% and 34%, respectively. 1,2 More than 70% of PAH patients will die as a result of right ventricular failure and most of the remainder from dysrhythmia. Predictors of a poor prognosis in PAH are related to the development of right ventricular failure. 1,3,4 The objectives of this review are to examine the pathophysiologic mechanisms leading to the development of right ventricular failure due to PAH, the diagnostic features of right ventricular failure, and the management of chronic right ventricular failure with emphasis on acute decompensation in this setting. Pathophysiology Clinical Manifestations and Hemodynamic DerangementsThe normal right ventricle is a thin-walled (less than 0.6 cm), trabeculated, roughly triangular structure that weighs less than 65 g in men and less than 50 g in women. 5,6 It is designed to empty its volume into a low-impedance, highcapacitance, pulmonary circulation by contracting sequentially from inflow to outflow. The pulmonary circulation can tolerate three-to fourfold increases in right-sided cardiac output without significant increases in PAP. In healthy individuals, pulmonary vascular resistance (PVR) decreases as the cardiac output rises with exercise. 7 In the setting of PAH, PVR does not sufficiently decrease with exercise, resulting in dyspnea and poor exercise capacity.Progressive PAH presents a pressure overload state to the right ventricle, increasing right ventricular workload leading to concentric hypertrophy (Figure 1). The right ventricle compensates: the walls hypertrophy while maintaining a normal or smaller chamber size, resulting in normal or reduced right ventricular wall stress. During this compensated phase of adaptive hypertrophy and normal to reduced wall stress, the ventricle is able to eject blood against the high PVR while maintaining an adequate right-sided cardiac output and normal right atrial pressure. During this phase patients exhibit few symptoms.The right ventricle can compensate only so long, initiating the symptomatic/declining phase (Figure 1). During this phase, with marked, maladaptive right ventricular hypertrophy and variable degrees of interstitial fibrosis, diastolic function may be impaired, altering the right ventricular diastolic pressure-volume relationship and leading to increases in right ventricular end-diastolic and right atrial pressures. With persistent pressure overload, the right ventricle undergoes a remodeling process eventually leading to right ventricular failu...

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“…39 In isolated patients with cor pulmonale, angiotensin-converting enzyme inhibitors have been reported to produce beneficial hemodynamic effects. 40 However, experience with angiotensin-converting enzyme inhibitor therapy is extremely limited in these patients. In elderly patients, vasodilator therapy is associated with increased incidence of symptomatic systemic hypotension.…”

Section: Treatmentmentioning

confidence: 99%