Causes of Cor pulmonale
List of causes of Cor pulmonale
Following is a list of causes or underlying conditions
(see also Misdiagnosis of underlying causes of Cor pulmonale)
that could possibly cause Cor pulmonale includes:
More causes:
see full list of causes for Cor pulmonale
Causes of Cor pulmonale (Diseases Database):
The follow list shows some of the possible medical causes of Cor pulmonale
that are listed by the Diseases Database:
Source: Diseases Database
Cor pulmonale Causes: Book Excerpts
Cor pulmonale as a complication of other conditions:
Other conditions that might have
Cor pulmonale as a complication may,
potentially, be an underlying cause of Cor pulmonale.
Our database lists the following as having
Cor pulmonale as a complication of that condition:
Cor pulmonale as a symptom:
Conditions listing Cor pulmonale
as a symptom may also be potential underlying causes of Cor pulmonale.
Our database lists the following as having
Cor pulmonale as a symptom of that condition:
Related information on causes of Cor pulmonale:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Cor pulmonale may be found in:
Causes of Cor pulmonale: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the causes of Cor pulmonale.
Pulse pressure, widened:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Aortic insufficiency
With acute aortic insufficiency, pulse pressure widens progressively as the valve deteriorates, and a bounding pulse and an atrial or a ventricular gallop develop. These signs may be accompanied by chest pain; palpitations; pallor; strong, abrupt carotid pulsations; pulsus bisferiens; and signs of heart failure, such as crackles, dyspnea, and jugular vein distention. Auscultation may reveal several murmurs, such as an early diastolic murmur (common) and an apical diastolic rumble (Austin Flint murmur).
Arteriosclerosis
With arteriosclerosis, reduced arterial compliance causes progressive widening of pulse pressure, which becomes permanent without treatment of the underlying disorder. This sign is preceded by moderate hypertension and accompanied by signs of vascular insufficiency, such as claudication, angina, and speech and vision disturbances.
Febrile disorder
A fever can cause widened pulse pressure. Accompanying symptoms vary depending on the specific disorder.
Increased ICP
Widening pulse pressure is an intermediate to late sign of increased ICP. Although a decreased LOC is the earliest and most sensitive indicator of this life-threatening condition, the onset and progression of widening pulse pressure also parallel rising ICP. (A gap of 50 mm Hg can signal a rapid deterioration in the patient’s condition.) Assessment reveals Cushing’s triad: bradycardia, hypertension, and respiratory pattern changes. Other findings include a headache, vomiting, and impaired or unequal motor movement. The patient may also exhibit vision disturbances, such as blurring or photophobia, and pupillary changes.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Cor pulmonale:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Approximately 85% of patients with cor pulmonale have COPD, and 25% of patients with COPD eventually develop cor pulmonale.
Other respiratory disorders that produce cor pulmonale include:
❑ obstructive lung diseases — for example, bronchiectasis and cystic fibrosis
❑ restrictive lung diseases — for example, pneumoconiosis, interstitial pneumonitis, scleroderma, and sarcoidosis
❑ loss of lung tissue after extensive lung surgery
❑ congenital cardiac shunts — such as a ventricular septal defect
❑ pulmonary vascular diseases — for example, recurrent thromboembolism, primary pulmonary hypertension, schistosomiasis, and pulmonary vasculitis
❑ respiratory insufficiency without pulmonary disease — for example, in chest wall disorders such as kyphoscoliosis, neuromuscular incompetence due to muscular dystrophy and amyotrophic lateral sclerosis, polymyositis, and spinal cord lesions above C6
❑ obesity hypoventilation syndrome (pickwickian syndrome) and upper airway obstruction
❑ living at high altitudes (chronic mountain sickness).
Pulmonary capillary destruction and pulmonary vasoconstriction (usually secondary to hypoxia) reduce the area of the pulmonary vascular bed. Thus, pulmonary vascular resistance is increased, causing pulmonary hypertension. To compensate for the extra work needed to force blood through the lungs, the right ventricle dilates and hypertrophies. In response to low oxygen content, the bone marrow produces more red blood cells (RBCs), causing erythrocytosis. When the hematocrit (HCT) exceeds 55%, blood viscosity increases, which further aggravates pulmonary hypertension and increases the hemodynamic load on the right ventricle. Right-sided heart failure is the result.
Cor pulmonale accounts for about 25% of all types of heart failure. It’s most common in areas of the world where the incidence of cigarette smoking and COPD is high; cor pulmonale affects middle-age to elderly men more often than women, but incidence in women is increasing. In children, cor pulmonale may be a complication of cystic fibrosis, hemosiderosis, upper airway obstruction, scleroderma, extensive bronchiectasis, neurologic diseases affecting respiratory muscles, or abnormalities of the respiratory control center.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Pulmonary hypertension:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Pulmonary hypertension begins as hypertrophy of the small pulmonary arteries. The medial and intimal muscle layers of these vessels thicken, decreasing distensibility and increasing resistance. This disorder then progresses to vascular sclerosis and obliteration of small vessels.
In most cases, pulmonary hypertension occurs secondary to an underlying disease process, including:
❑ alveolar hypoventilation from chronic obstructive pulmonary disease (most common cause in the United States), sarcoidosis, diffuse interstitial disease, pulmonary metastasis, and certain diseases such as scleroderma (In these disorders, pulmonary vascular resistance occurs secondary to hypoxemia and destruction of the alveolocapillary bed. Other disorders that cause alveolar hypoventilation without lung tissue damage include obesity, kyphoscoliosis, and obstructive sleep apnea.)
❑ vascular obstruction from pulmonary embolism, vasculitis, and disorders that cause obstruction of small or large pulmonary veins, such as left atrial myxoma, idiopathic veno-occlusive disease, fibrosing mediastinitis, and mediastinal neoplasm
❑ primary cardiac disease, which may be congenital or acquired. Congenital defects that cause left-to-right shunting of blood — such as patent ductus arteriosus or atrial or ventricular septal defect — increase blood flow into the lungs and, consequently, raise pulmonary vascular pressure. Acquired cardiac diseases, such as rheumatic valvular disease and mitral stenosis, increase pulmonary venous pressure by restricting blood flow returning to the heart.
Primary (or idiopathic) pulmonary hypertension is rare, occurring most commonly — and with no known cause — in women between ages 20 and 40. Secondary pulmonary hypertension results from existing cardiac, pulmonary, thromboembolic, or collagen vascular diseases or from the use of certain drugs.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Pulse pressure, widened:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Aortic insufficiency
With acute aortic insufficiency, pulse pressure widens progressively as the valve deteriorates, and a bounding pulse and an atrial gallop or ventricular gallop develop. These signs may be accompanied by chest pain; palpitations; pallor; strong, abrupt carotid pulsations; pulsus bisferiens; and signs of heart failure, such as crackles, dyspnea, and jugular vein distention. Auscultation may reveal several murmurs, such as an early diastolic murmur (common) and an apical diastolic rumble (Austin Flint murmur).
Arteriosclerosis
With this disorder, reduced arterial compliance causes progressive widening of pulse pressure, which becomes permanent without treatment of the underlying disorder. This sign is preceded by moderate hypertension and accompanied by signs of vascular insufficiency, such as claudication, angina, and speech and vision disturbances.
Febrile disorders
Fever can cause widened pulse pressure. Accompanying symptoms vary depending on the specific disorder.
Increased intracranial pressure
Widening pulse pressure is an intermediate to late sign of increased ICP. Although decreased LOC is the earliest and most sensitive indicator of this life-threatening condition, the onset and progression of widening pulse pressure also parallel rising ICP. (Even a gap of only 50 mm Hg can signal a rapid deterioration in the patient’s condition.) Assessment reveals Cushing’s triad: bradycardia, hypertension, and respiratory pattern changes. Other findings include headache, vomiting, and impaired or unequal motor movement. The patient may also exhibit vision disturbances, such as blurring or photophobia, and pupillary changes.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Cor pulmonale:
Causes
(Handbook of Diseases)
About 85% of patients with cor pulmonale have COPD, and 25% of patients with COPD eventually develop cor pulmonale.
Other respiratory disorders that produce cor pulmonale include:
❑ obstructive lung diseases — for example, bronchiectasis and cystic fibrosis
❑ restrictive lung diseases — for example, pneumoconiosis, interstitial pneumonitis, scleroderma, and sarcoidosis
❑ loss of lung tissue after extensive lung surgery
❑ pulmonary vascular diseases, such as recurrent thromboembolism, primary pulmonary hypertension, schistosomiasis, and pulmonary vasculitis
❑ respiratory insufficiency without pulmonary disease as seen in chest wall disorders, such as kyphoscoliosis, neuromuscular incompetence resulting from muscular dystrophy or amyotrophic lateral sclerosis, polymyositis, and spinal cord lesions above C6
❑ obesity hypoventilation syndrome (pickwickian syndrome) and upper airway obstruction
❑ living at high altitudes (chronic mountain sickness).
Pathophysiology
Pulmonary capillary destruction and pulmonary vasoconstriction (usually secondary to hypoxia) reduce the cross-sectional area of the pulmonary vascular bed. This increases pulmonary vascular resistance and causes pulmonary hypertension.
To compensate for the extra work needed to force blood through the lungs, the right ventricle dilates and hypertrophies. In response to low oxygen content, the bone marrow produces more red blood cells, causing erythrocytosis. When the hematocrit exceeds 55%, blood viscosity increases, which further aggravates pulmonary hypertension and increases the hemodynamic load on the right ventricle. Right-sided heart failure is the result.
Incidence
Cor pulmonale accounts for about 25% of all types of heart failure. It’s most common in areas of the world where the incidence of cigarette smoking and COPD is high.
Cor pulmonale affects more middle-aged to elderly men than women, but its incidence in women is increasing. In children, cor pulmonale may be a complication of cystic fibrosis, hemosiderosis, upper airway obstruction, scleroderma, extensive bronchiectasis, neurologic diseases affecting respiratory muscles, or abnormalities of the respiratory control center.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Pulmonary hypertension:
Causes
(Handbook of Diseases)
Primary pulmonary hypertension begins as hypertrophy of the small pulmonary arteries. The medial and intimal muscle layers of these vessels thicken, decreasing distensibility and increasing resistance. This disorder then progresses to vascular sclerosis and obliteration of small vessels. Because this form of pulmonary hypertension occurs in association with collagen diseases, it’s thought to result from altered immune mechanisms.
Usually, pulmonary hypertension is secondary to hypoxemia from an underlying disease process, including:
❑ alveolar hypoventilation from chronic obstructive pulmonary disease (most common cause in the United States), sarcoidosis, diffuse interstitial pneumonia, pulmonary metastasis, and certain diseases such as sclero-derma.
These diseases may cause pulmo-nary hypertension through alveolar destruction and increased pulmonary vascular resistance. Other disorders that cause alveolar hypoventilation without lung tissue damage include obesity, kyphoscoliosis, and obstructive sleep apnea.
❑ vascular obstruction from pulmonary embolism, vasculitis, and disorders that cause obstructions of small or large pulmonary veins, such as left atrial myxoma, idiopathic veno-occlusive disease, fibrosing mediastinitis, and mediastinal neoplasm.
❑ primary cardiac disease, which may be congenital or acquired. Congenital defects that cause left-to-right shunting of blood — such as patent ductus arteriosus, or atrial or ventricular septal defect — increase blood flow into the lungs and consequently raise pulmonary vascular pressure.
Acquired cardiac disease, such as rheumatic valvular disease and mitral stenosis, increases pulmonary venous pressure by restricting blood flow returning to the heart.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Pulse pressure, widened:
Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
Aortic insufficiency
With acute aortic insufficiency, pulse pressure widens progressively as the valve deteriorates, and a bounding pulse and an atrial or a ventricular gallop develop. These signs may be accompanied by chest pain, palpitations, pallor, pulsus bisferiens, and strong, abrupt carotid pulsations. Other signs of heart failure, such as crackles, dyspnea, and jugular vein distention, may also be present. Auscultation may reveal several murmurs, such as an early diastolic murmur (common) and an apical diastolic rumble (Austin Flint murmur).
Arteriosclerosis
With arteriosclerosis, reduced arterial compliance causes progressive widening pulse pressure, which becomes permanent without treatment of the underlying disorder. This sign is preceded by moderate hypertension and is accompanied by signs of vascular insufficiency, such as claudication, angina, and speech and vision disturbances.
Febrile disorders
Fever can cause widened pulse pressure. Accompanying symptoms vary depending on the specific disorder.
Increased ICP
Widening pulse pressure is an intermediate to late sign of increased ICP. Although a decreased LOC is the earliest and most sensitive indicator of this life-threatening condition, the onset and progression of widening pulse pressure also parallel rising ICP. (Even a gap of only 50 mm Hg can signal a rapid deterioration in the patient’s condition.) Assessment reveals Cushing’s triad: bradycardia, hypertension, and respiratory pattern changes. Other findings include headache, vomiting, and impaired or unequal motor movement. The patient may also exhibit vision disturbances, such as blurring or photophobia, and pupillary changes.
» READ BOOK EXCERPT ONLINE »
Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Pulse pressure, widened:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Aortic insufficiency
With acute aortic insufficiency, pulse pressure widens progressively as the valve deteriorates, and a bounding pulse and an atrial gallop or ventricular gallop develop. These signs may be accompanied by chest pain; palpitations; pallor; strong, abrupt carotid pulsations; pulsus bisferiens; and signs of heart failure, such as crackles, dyspnea, and jugular vein distention. Auscultation may reveal several murmurs, such as an early diastolic murmur (common) and an apical diastolic rumble (Austin Flint murmur).
Arteriosclerosis
With arteriosclerosis, pulse pressure progressively widens. This sign is preceded by moderate hypertension and is accompanied by signs of vascular insufficiency, such as claudication, angina, and speech and vision disturbances.
Febrile disorders
Fever can cause widened pulse pressure. Accompanying symptoms vary depending on the specific disorder but may include fatigue, chills, malaise, anorexia, tachycardia, tachypnea, and diaphoresis.
Increased intracranial pressure
Widening pulse pressure is an intermediate to late sign of increased ICP. Although decreased LOC is the earliest and most sensitive indicator of this life-threatening condition, the onset and progression of widening pulse pressure also parallel rising ICP. (Even a gap of only 50 mm Hg can signal a rapid deterioration in the patient’s condition.) Assessment reveals Cushing’s triad: bradycardia, hypertension, and respiratory pattern changes. Other findings include headache, vomiting, and impaired or unequal motor movement. The patient may also exhibit vision disturbances, such as blurring or photophobia, and pupillary changes.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Pulse pressure, widened:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Aortic insufficiency.With acute aortic insufficiency, pulse pressure widens progressively as the valve deteriorates, and a bounding pulse and an atrial or a ventricular gallop develop. These signs may be accompanied by chest pain; palpitations; pallor; strong, abrupt carotid pulsations; pulsus bisferiens; and signs of heart failure, such as crackles, dyspnea, and jugular vein distention. Auscultation may reveal several murmurs, such as an early diastolic murmur (common) and an apical diastolic rumble (Austin Flint murmur).
Arteriosclerosis.With arteriosclerosis, reduced arterial compliance causes progressive widening of pulse pressure, which becomes permanent without treatment of the underlying disorder. This sign is preceded by moderate hypertension and accompanied by signs of vascular insufficiency, such as claudication and angina.
Febrile disorder.Fever can cause widened pulse pressure. Accompanying symptoms vary depending on the specific disorder causing the fever.
Increased ICP.Widening pulse pressure is an intermediate to late sign of increased ICP. Although decreased LOC is the earliest and most sensitive indicator of this life-threatening condition, the onset and progression of widening pulse pressure also parallel rising ICP. (A gap of 50 mm Hg can signal a rapid deterioration in the patient's condition.) Assessment reveals Cushing's triad: bradycardia, hypertension, and respiratory pattern changes. Other findings include headache, vomiting, and impaired or unequal motor movement. The patient may also exhibit vision disturbances, such as blurring or photophobia, and pupillary changes.
» READ BOOK EXCERPT ONLINE »
Source: Nursing: Interpreting Signs and Symptoms, 2007
Pulmonary Hypertension:
Pulmonary Hypertension - pathophysiology
(The 5-Minute Pediatric Consult)
Structural alterations in pulmonary vessel architecture (remodeling)
- Smooth muscle hypertrophy
- Extension of blood vessel’s smooth muscle into smaller vessels
- Inflammation
Pulmonary Hypertension - etiology
- Hypoxemia-induced pulmonary hypertension
- Chronic lung disease
- Cystic fibrosis
- Bronchopulmonary dysplasia
- Interstitial lung disease
- Upper airway obstruction:
- Tonsillar and/or adenoid hypertrophy
- Obesity
- Hypoventilation:
- Neurologically mediated process
- Secondary to muscular weakness
- High pulmonary blood flow secondary to left-to-right shunting (seen in congenital heart disease):
- Patent ductus arteriosus
- Atrial septal defect
- Ventricular septal defect
- Left-sided cardiac disorders that increase pulmonary venous pressure:
- Left ventricular failure
- Mitral valve stenosis
- Obstructed anomalous pulmonary veins
- Occlusion of pulmonary vessels:
- Sickle cell disease
- Veno-occlusive disease
- Thromboembolism
- Pulmonary vasculitis:
- Systemic lupus erythematosus
- Rheumatoid arthritis
- Scleroderma
- Persistent pulmonary hypertension of the newborn
- Idiopathic cases (primary pulmonary hypertension)
» READ BOOK EXCERPT ONLINE »
Source: The 5-Minute Pediatric Consult, 2008
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