chronic cor pulmonale. cor pulmonale 1. acute cor pulmonale 2. chronic cor pulmonale
DESCRIPTION
Cor pulmonale Acute cor pulmonale usually refers to the development of acute pulmonary hypertension and right ventricular overload from a massive pulmonary thromboembolic event, with subsequent development of right ventricular dilationTRANSCRIPT
CHRONIC COR PULMONALE
Cor pulmonale
1. Acute cor pulmonale 2. Chronic cor pulmonale
Cor pulmonale
Acute cor pulmonale usually refers to the development of acute pulmonary hypertension and right ventricular overload from a massive pulmonary thromboembolic event, with subsequent development of right ventricular dilation
Chronic cor pulmonale: Definition
Pulmonary arterial hypertension resulting from diseases affecting the structure and/or the function of the lungs; pulmonary arterial hypertension
results in right ventricular enlargement (hypertrophy and/or dilatation) and may lead with time to right heart failure
(Weitzenblum, 2003)
Chronic cor pulmonale: key-point
- Right ventricular dilation or hypertrophy in chronic cor pulmonale is a direct compensatory effect of chronic pulmonary vasoconstriction and subsequent pulmonary artery hypertension that leads to increased right ventricular work and stress.
- When the right ventricle can no longer compensate through dilation or hypertrophy, right ventricular failure occurs.
Chronic cor pulmonale: Old Definitions
Hypertrophy of the right ventricle resulting form diseases affecting the structure and/or function of the lungs (WHO, 1963)
Hypertrophy alteration in the structure and function of the right ventricle (revision, 1970)
Pulmonary hypertension: Definition
Pulmonary hypertension complicating chronic respiratory disease is generally defined by the presence of a resting mean pulmonary artery pressure (PAP) > 20 mm Hg.
This is slightly different from the definition of primary pulmonary hypertension (PAP> 25 mmHg).
Definition
In young (< 50 years) healthy subjects PAP is most often between 10–15 mm Hg.With aging there is a slight increase in PAP, by about 1 mm Hg/10 years.
A resting PAP > 20 mm Hg is always abnormal.
In the “natural history” of COPD, pulmonary hypertension is often preceded by an abnormally large increase in PAP during exercise, defined by a pressure> 30 mm Hg for a mild level of steady state exercise.
The term “exercising” pulmonary hypertension has been used by some authors, but the term “pulmonary
hypertension” should be reserved for resting pulmonary hypertension.
Aetiology
Aetiology
Aetiology
There are three major groups of diseases which may lead to cor pulmonale:
those characterised by a limitation to airflow (COPD and other causes of chronic bronchial obstruction)
those characterised by a restriction of pulmonary volumes from extrinsic or parenchymatous origin (restrictive lung diseases)
those where the relatively well preserved mechanical properties of the lungs and chest wall contrast with pronounced gas exchange abnormalities which are partially explained by poor ventilatory drive (respiratory insufficiency of “central”origin).
Aetiology
Obstructive lung diseases:
COPD (chronic obstructive bronchitis, emphysema and their association) (80-90% of cases)
Asthma with irreversible airway obstruction
Bronchiectasis
Bronchiolitis obliterans
Aetiology
Restrictive lung diseases:
Kyphoscoliosis
Idiopathic pulmonary fibrosis
Pneumoconiosis
Aetiology
Respiratory insufficiency of “central” origin:
Central alveolar hypoventilation
Obesity-hypoventilation syndrome (formerly, “Pickwickian syndrome”)
Sleep apnea syndrome
All of the following diseases are relatively frequent causes of cor pulmonale, EXCEPT:
A. Idiopathic pulmonary fibrosisB. Bacterial pneumoniaC. PneumoconiosisD. Sleep apneaE. Kyphoscoliosis
All of the following diseases are relatively frequent causes of cor pulmonale, EXCEPT:
A. Idiopathic pulmonary fibrosisB. Bacterial pneumoniaC. PneumoconiosisD. Sleep apneaE. Kyphoscoliosis
Some COPD patients with pulmonary hypertension will never develop right heart failure:
A. TrueB. False
Some COPD patients with pulmonary hypertension will never develop right heart failure:
A. TrueB. False
Pathophysiology
Anatomic factorsDestruction or obstruction of the pulmonary vascular bed
Functional factorsAlveolar hypoxia Acute hypoxic pulmonary vasoconstriction Remodeling of the vascular bed due to chonic hypoxemia
Hypercapnia and acidosisHyperviscosityHypervolemia secondary to polycythemia
Mechanical factorsCompression of alveolar vessels
Recognized mechanisms of pulmonary hypertension in chronic obstructive pulmonary disease are all of the followings, EXCEPT:
A. Pulmonary vascular remodeling resulting from chronic alveolar hypoxia
B. Increased pulmonary vascular resistance
C. Elevated pulmonary capillary wedge pressure
Recognized mechanisms of pulmonary hypertension in chronic obstructive pulmonary disease are all of the followings, EXCEPT:
A. Pulmonary vascular remodeling resulting from chronic alveolar hypoxia
B. Increased pulmonary vascular resistance
C. Elevated pulmonary capillary wedge pressure
Clinical Assessment
The clinical signs occur late, being observed at an advanced stage of the disease far after the development of
pulmonary hypertension. Peripheral (ankle) oedema is the best sign of RHF but it is not
specific and can arise from other causes; in some patients with pulmonary hypertension, it does not occur at all.
A murmur of tricuspid regurgitation, suggesting right ventricular dilatation, is a very late sign in respiratory patients.
Accentuation of the pulmonary component of the second heart sound is only observed in patients with severe pulmonary hypertension.
Clinical Assessment: features of frank right heart failure
- Ascites and peripheral edema
- Pulsus paradoxus (a decrease of >10 mm Hg in systemic systolic BP during inspiration)
- Prominence of the jugular veins
- Sustained impulse along the lower left sternal margin (arising from RV enlargement)
NB. Cardiac findings may be obscured during auscultation by chest hyperinflation and by rotation of the heart in patients with COPD
Diagnostic techniques
Chest radiography ECG Echo
Radionuclide assessment of RV EF RV dimensions measured by MRI
Diagnostic techniques
Chest radiography
↑ Diameter of the right descending PA on posteroanterior projection
↑ Diameter of the left descending PA on left lateral projection
Loss of retrosternal airspace on lateral films (owing to RV hypertrophy)
RV silhouette often assumes lobular appearance
Diagnostic techniques: chest radiography
Diagnostic techniques
Chest radiography ECG Echo
Radionuclide assessment of RV EF RV dimensions measured by MRI
ECG (high specifity, but low sensitivity)- Right ventricular hypertrophy:R.A.D.R or R’>S in V1R<S in V6R in V1 + S in V5 or V6 = 10 mmR in V1 = 7 mm (15 mm with RBBB)RA enlargement
-S1S2S3 syndrome-Incomplete or complete RBBB-Inverted, biphasic, or flattened T waves in precordial leads- Depressed ST segments in leads II, III, aVF
Case 1
A 76-year old man admitted for dyspnea
Case 1
A 76-year old man admitted for dyspnea
Case 2
A 60-year old woman with dyspnea and pulmonary hypertension in the setting of sarcoidosis
Case 2
A 60-year old woman with dyspnea and pulmonary hypertension in the setting of sarcoidosis
Peripheral (ankle) oedema is the best clinical sign of cor pulmonale:
A. TrueB. False
Peripheral (ankle) oedema is the best clinical sign of cor pulmonale:
A. TrueB. False
A normal ECG does not exclude the presence of cor pulmonale :
A. TrueB. False
A normal ECG does not exclude the presence of cor pulmonale :
A. TrueB. False
The non-invasive diagnosis of pulmonary hypertension is presently based on Doppler echocardiography :
A. TrueB. False
The non-invasive diagnosis of pulmonary hypertension is presently based on Doppler echocardiography :
A. TrueB. False
Treatment
FEV 1
(% o
f val
ue a
t age
25)
Age (years)Adapted from Fletcher C et al. Br Med J. 1977;1:1645–1648.
COPD Risk and Smoking Cessation
0
25
50
75
100
25 50 75
Death
Disability
Never smoked or not susceptible to smoke
Smoked regularlyand susceptible toeffects of smoke
Stopped smoking at 45 (mild COPD)
Stopped smoking at 65 (severe COPD)
Treatment
Long-term oxygen therapy (LTOT)Vasodilator treatment Other (diuretics, digitalis, phlebotomy)
Indications
AbsolutePa O2 ≤55 mm Hg or Sa O2 ≤88%
In patients with cor pulmonale Pa O2 55–59 mm Hg or Sa O2 ≥89%ECG evidence of P pulmonale, hematocrit >55%, and CHD
Specific IndicationsNocturnal hypoxemia
Sleep apnea with nocturnal desaturation not corrected by constant positive airway pressure or bilevel positive airway pressureNo hypoxemia at rest, but desaturation during exercise or sleep (PaO2 <55 mm Hg)
Treatment Goals
Pa O2 ≥60 mm Hg or Sa O2 ≥90%; Appropriately adjusted O2 dose during sleep and exercise
Same as above
Appropriately adjusted O2 dose during sleep
Long-Term Oxygen Therapy: Guidelines
Appropriately adjusted O2 dose during sleep
Same as above
Treatment
Long-term oxygen therapy (LTOT)Vasodilator treatment Other (diuretics, digitalis, phlebotomy)
Treatment
Vasodilator treatment :
ACEI - ARB (captopril, enelapril, losartan): despite reductions in Ppa, no improvements in RV function and exercise tolerance were detected
CCB (nifedipine, diltiazem):only one third demostrated any reduction in Ppa
Nitrates, prostaglandins (E1 and I2 i.v.), theophylline
Treatment
Long-term oxygen therapy (LTOT)Vasodilator treatment Other (diuretics, digitalis, phlebotomy)
Treatment
Digitalis : contraindicated unless left-sided congestive heart failure present
The cardiac glycosides have been used to manage cor pulmonale for many years.
The evidence, however, does not support (!) the use of digoxin in patients with cor pulmonale unless they have concurrent LV failure or arrhythmia (rapid AF).
Treatment
Phlebotomy :
In polycythemic patients who undergo phlebotomy, the mean Ppa decreases but the cardiac output is generally unaffected.
Although rarely indicated as the sole therapy for cor pulmonale, phlebotomy might be considered for acute decompensation of cor pulmonale accompanied by severe polycythemia, or for patients who remain markedly polycythemic even after continuous oxygen therapy.
Nonetheless, it is not known whether repeated phlebotomies lead to any definite long-term benefits in pulmonary hemodynamics.
LTOT has not significantly modified the life expectancy of COPD patients with cor pulmonale :
A. TrueB. False
LTOT has not significantly modified the life expectancy of COPD patients with cor pulmonale :
A. TrueB. False
LTOT is at present the best treatment of cor pulmonale in COPD patients:
A. TrueB. False
LTOT is at present the best treatment of cor pulmonale in COPD patients:
A. TrueB. False