eMedicine Specialties > Pulmonology > Pulmonary Hypertension

Pulmonary Hypertension, Secondary

Author: Nader Kamangar, MD, FACP, FCCP, FAASM, Associate Professor of Clinical Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Multi-campus Pulmonary and Critical Care Fellowship Program, University of California, Los Angeles, David Geffen School of Medicine; Medical Director, Hospitalist/Intensivist Program, Olive View-UCLA Medical Center; Associate Program Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA Medical Center/West Los Angeles Veterans Affairs Medical Center
Coauthor(s): Shahriar Pirouz, MD, Resident Physician, Department of Internal Medicine, Olive View University of California Los Angeles Medical Center; Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Contributor Information and Disclosures

Updated: Feb 10, 2010

Introduction

Background

Pulmonary hypertension (PH) defined as a mean pulmonary arterial (PA) pressure of greater than 25 mm Hg at rest or greater than 30 mm Hg during exercise, is characterized by a progressive and sustained increase in pulmonary vascular resistance that eventually leads to right ventricular (RV) failure. Pulmonary hypertension is a life-threatening condition if untreated; treatment success rates vary based on etiology.
 
Cardiac disorders, pulmonary disorders, or both in combination are the most common causes of secondary pulmonary hypertension. Cardiac diseases produce pulmonary hypertension via volume or pressure overload, although subsequent intimal proliferation of pulmonary resistance vessels adds an obstructive element. Perivascular parenchymal changes along with pulmonary vasoconstriction are the mechanism of pulmonary hypertension in respiratory diseases.
 
Therapy for pulmonary hypertension is targeted at the underlying cause and its effects on the cardiovascular system. Novel therapeutic agents such as prostacyclin and others undergoing clinical trials have led to the possibility of specific therapies for these once untreatable disorders.

Gross pathology on a patient who died from severe...

Gross pathology on a patient who died from severe pulmonary hypertension secondary to persistent patent ductus arteriosus.

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Gross pathology on a patient who died from severe...

Gross pathology on a patient who died from severe pulmonary hypertension secondary to persistent patent ductus arteriosus.



Another view (of picture in Media File 1) of gros...

Another view (of picture in Media File 1) of gross pathology on a patient who died from severe pulmonary hypertension secondary to persistent patent ductus arteriosus.

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Another view (of picture in Media File 1) of gros...

Another view (of picture in Media File 1) of gross pathology on a patient who died from severe pulmonary hypertension secondary to persistent patent ductus arteriosus.



During a pulmonary arterial thromboendarterectomy...

During a pulmonary arterial thromboendarterectomy, a bilateral proximal thrombus was carefully dissected and extracted, leading to the resolution of secondary pulmonary artery hypertension.

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During a pulmonary arterial thromboendarterectomy...

During a pulmonary arterial thromboendarterectomy, a bilateral proximal thrombus was carefully dissected and extracted, leading to the resolution of secondary pulmonary artery hypertension.

The following clinical guideline summaries are available:

Frequency

United States

The overall prevalence of pulmonary hypertension in the general population is unknown, owing to the heterogeneity of the disease. In specific subgroups of pulmonary hypertension patients, studies have estimated the prevalence as follows:  

  • In an observational study of 277 patients with HIV infection, .46% of patients had pulmonary hypertension.5 In comparison with prior studies, no change in prevalence rate was seen with modern highly active antiretroviral treatment (HAART).6   
  • A systematic review of several studies of patients with obstructive sleep apnea (OSA) estimated the prevalence of pulmonary hypertension at 15-20%.7  
  • A systematic review of several studies among patients with chronic obstructive pulmonary disease (COPD) estimated the prevalence of pulmonary hypertension at 10-30%.8  
  • In scleroderma patients, the incidence has been estimated to be 6-60% of all patients, with the variance based on the extent of disease.9

Mortality/Morbidity

Based on the US Centers for Disease Control and Prevention (CDC) Pulmonary Hypertension Surveillance from 1980-2002, the following was reported10 :  

  • The age-standardized death rates for the total US population increased from 5.2 deaths to 5.4 deaths per 100,000 population.
  • The main increase in death rates was seen among women, with 3.3 deaths to 5.5 deaths per 100,000 population, and blacks, with 4.6 deaths to 7.3 deaths per 100,000 population.
  • The death rate in males decreased over this time, from 8.2 deaths to 5.4 deaths per 100,000 population.

Clinical

History

The clinical manifestations of secondary pulmonary arterial hypertension (SPAH) are frequently masked by the underlying etiology. Obtaining a careful history may help exclude some of the numerous causes of secondary pulmonary hypertension.
 
Important clues to a specific secondary cause include past history of heart murmur, deep venous thrombosis or pulmonary embolism, Raynaud phenomenon, arthritis or arthralgias, rash, heavy alcohol consumption, hepatitis, heavy snoring, daytime hypersomnolence, morning headaches, morbid obesity, and a family history of hypertension.

Patients with SPAH often have nonspecific symptoms that reflect the underlying etiology. Other symptoms include the following: 

  • Dyspnea upon exertion
  • Fatigue
  • Lethargy
  • Syncope with exertion
  • Chest pain

Less common symptoms include the following:

  • Cough
  • Hemoptysis
  • Hoarseness (due to compression of the recurrent laryngeal nerve by the distended pulmonary artery)

Typical exertional angina has been reported in as many as 8.5% of patients with SPAH secondary to mitral stenosis. This most likely occurs because of the pulmonary artery distension, right ventricular ischemia, or both in combination.

Physical

Physical examination findings may include the following:

  • The intensity of the pulmonic component of the second heart sound (P2) may be increased, and a systolic ejection murmur may be heard over the left sternal border. The P2 may demonstrate fixed or paradoxic splitting. A right ventricular heave may be palpated.
  • A prominent a wave may be observed in the jugular venous pulse, and a right-sided fourth heart sound (S4) with a left parasternal heave may be heard.
  • Right ventricular failure leads to systemic venous hypertension and cor pulmonale. Signs are the high-pitched systolic murmur of tricuspid regurgitation, hepatomegaly, a pulsatile liver, ascites, and peripheral edema. In this scenario, a right ventricular third heart (S3) sound is also heard.
  • Signs of underlying cardiac, pulmonary, liver, or collagen-vascular disease are often present.

Causes

Pulmonary hypertension was previously divided into 2 categories: primary pulmonary hypertension and secondary pulmonary hypertension, based on identifiable etiology. In 1998, the World Health Organization (WHO) proposed a clinical classification of pulmonary hypertension based on similarities in pathophysiology, clinical presentation, and therapeutic options.

  • Group 1, pulmonary arterial hypertension (PAH), with 2 subgroups
    • Subgroup 1 - Patients with sporadic and familial idiopathic pulmonary arterial hypertension (IPAH)
    • Subgroup 2 - Conditions with known localization of lesions the small pulmonary arterioles, including collagen-vascular disease (scleroderma/CREST syndrome), congenital left-to-right shunts, portopulmonary hypertension, HIV-associated pulmonary hypertension, newborn pulmonary hypertension, and drug-induced (eg. anorexigens) pulmonary hypertension
  • Group 2, pulmonary venous hypertension: This group consists of left-sided myocardial and valvular diseases and extrinsic compression of the pulmonary veins (eg tumors) and pulmonary veno-occlusive disease.
  • Group 3, pulmonary hypertension associated with lung diseases and/or hypoxemia: This group consists of diseases causing inadequate arterial oxygenation. The 3 main groups are those due to lung disease (eg, COPD, interstitial lung disease), impaired respiration (eg, OSA,11 alveolar hypoventilation disorders), and long-term exposure to high altitude.
  • Group 4, pulmonary hypertension due to chronic thrombotic and/or embolic disease, with 2 subgroups
    • Subgroup 1 - Chronic thromboembolic pulmonary hypertension (CTEPH) of proximal arteries
    • Subgroup 2 - Pulmonary embolisms within distal pulmonary arteries, which may be due to thrombosis, tumor, parasites, in situ thrombosis, or sickle cell disease
  • Group 5, pulmonary hypertension due to direct effect of pulmonary vasculature: This group consists of inflammatory diseases effecting pulmonary vasculature including, schistosomiasis, sarcoidosis, histocytosis X, and fibrosing mediastinitis.

Functional classifications of PAH

The classes listed below are based on information adapted from the executive summary of the world symposium on Primary Pulmonary Hypertension in Evian, France in 1998.

  • Class I: These are patients with pulmonary hypertension but without resulting limitation of physical activity. Ordinary physical activity does not cause undue dyspnea or fatigue, chest pain, or near syncope.
  • Class II: These are patients with pulmonary hypertension resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity causes undue dyspnea or fatigue, chest pain, or near syncope.
  • Class III: These are patients with pulmonary hypertension resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary activity causes undue dyspnea or fatigue, chest pain, or near syncope.
  • Class IV: These are patients with pulmonary hypertension with an inability to perform any physical activity without symptoms. These patients manifest signs of right-sided heart failure. Dyspnea and/or fatigue may even be present at rest. Discomfort is increased by any physical activity.

More on Pulmonary Hypertension, Secondary

Overview: Pulmonary Hypertension, Secondary
Differential Diagnoses & Workup: Pulmonary Hypertension, Secondary
Treatment & Medication: Pulmonary Hypertension, Secondary
Follow-up: Pulmonary Hypertension, Secondary
Multimedia: Pulmonary Hypertension, Secondary
References
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Further Reading

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Contributor Information and Disclosures

Author

Nader Kamangar, MD, FACP, FCCP, FAASM, Associate Professor of Clinical Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Multi-campus Pulmonary and Critical Care Fellowship Program, University of California, Los Angeles, David Geffen School of Medicine; Medical Director, Hospitalist/Intensivist Program, Olive View-UCLA Medical Center; Associate Program Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA Medical Center/West Los Angeles Veterans Affairs Medical Center
Nader Kamangar, MD, FACP, FCCP, FAASM is a member of the following medical societies: American Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Shahriar Pirouz, MD, Resident Physician, Department of Internal Medicine, Olive View University of California Los Angeles Medical Center
Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Oleh Wasyl Hnatiuk, MD, Program Director, National Capital Consortium, Pulmonary and Critical Care, Walter Reed Army Medical Center; Associate Professor, Department of Medicine, Uniformed Services University of Health Sciences
Oleh Wasyl Hnatiuk, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

 
 
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