notes by dr Claudio Italiano
The patient with a pulmonary heart must certainly be evaluated for his
cardiology, as the pulmonary hypertension that underlies the pulmonary heart may
have caused damage to the heart or the heart can be primitively ill and
responsible for the onset and aggravation of a picture of pulmonary hypertension.
The electrocardiogram shows alterations that suggest pressure overload and volume increase of the right ventricle: vertical QRS axis, or deviated to the right, or directed posteriorly and upwards; right activation delay with more or less advanced branch block panels; prevalence of the R vector in the precordial right, flattening-inversion of the T wave in these derivations; appearance S1-Q3 S1-S2-S3; P pulmonary; of amplitude increased in II, III, aVF, expression generally of significant increase in pulmonary pressure. In addition, a pulmonary heart can generate dangerous arrhythmias, of which the most frequent are hyperkinetic and supraventricular (ectopic beats, chaotic atrial rhythm, paroxysmal or chronic atrial fibrillation in the most advanced forms), and ventricular (ectopic beats, couples, ventricular tachycardias ).
The cause of the genesis of arrhythmias may lie in the use of drugs such as digitalis, beta-stimulants, theophylline diuretics and hypoxemia with hypercapnia and disionia. Chest X-ray shows predominantly the signs of underlying bronchopneumopathy, which can often mask those of pulmonary hypertension and of the chronic pulmonary heart. The cardiac involvement is revealed by a medium-severe cardiomegaly with the prevalence of the right sections, thickening of the pulmonary ili by dilation of the trunk and of the main pulmonary branches. 2-D echocardiography allows to recognize the changes induced by the pressure overload on the main pulmonary artery and on the right ventricle; but generally also the other cardiac chambers are always dilated.
The left ventricle is instead of reduced or normal size, with displacement of the interventricular septum which in diastole appears stretched to the left and assumes paradoxical movement to the right in systole. Doppler echocardiography allows measurement of the flow velocity of the tricuspid deficiency jet, which can be used to determine the right ventricular-atrium pressure gradient. This gradient, added to the clinically measured or measured right atrial pressure, allows the estimate of systolic pressure in the right ventricle
It is certainly not simple and the writer is now treating his own joint with pulmonary hypertension that, following a chronic pleural effusion, is submitted to thoracic drainage, after thoracoscopy and thoracentesis.
The main goal of therapy is:
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Treat basic pneumopathy and respiratory failure
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Correct respiratory failure
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Prevent ventricular decompensation.
Surely it is necessary to evaluate the patient's hemogas is mainly to treat hypoxia because the reduction of hypoxia is the most important measure to reduce pulmonary hypertension (see pathophysiology of the pulmonary heart) as it is a stimulus for vasoconstriction of the arterioles of the respiratory bronchiole and this applies both to prevention and treatment of the chronic pulmonary heart and right ventricular failure.
To treat hypoxemia, it is first necessary to treat the pathology that underlies
it:
- Treating chronic obstructive bronchopneumopathy (see Bronchitis, ie using, as
appropriate, bronchodilators, both beta2 stimulants and anticholinergics,
xanthine derivatives, cortisones and ACTH, secretolytics, antibiotics, and
implement environmental measures: aerating the environment, removing dust, mold
, allergens etc.
Correct the chronic suppurative pathology, especially in bronchiectasis where
antibiotics, respiratory physiotherapy and postural drainage are to be used.
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Use the ventilators in restrictive pneumopathies, es interstitial fibrosis.
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Using respiratory analectics, correcting the deformities of the rib cage,
obesity in forms with hypoventilation
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Primary pulmonary hypertension: vasodilators (oxygen, hydralazine or derivatives,
calcium antagonists, ACE inhibitors, nitroderivatives), anticoagulants,
heart-lung transplants.
- Multiple pulmonary embolism, use of anticoagulant drugs, caval filters (tao)
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Oxygen therapy, indicated in all patients with alveolar hypoxia, as sufficient
oxygenation has been shown to prevent the occurrence of heart failure both in
the short and long term. Oxygen should be given sufficiently to return the
alveolar partial pressure to values stably above 55-60 mmHg, and should be
continued for at least 10-15 hours a day to improve the clinical picture and
prognosis at a distance.
- Particular attention in the hypercapnic patient. In case of heart failure, it is also necessary to restore the heart pump function as much as possible, with intropictive drugs such as Digital, which has recently had a revival, even if it must be used with caution for the wall stress that can determine , while being sure to point to atrial fibrillation, in right heart failure, its use is more limited because the beneficial effects of digital are not as evident as in other cardiac diseases. The drug should also be used with caution because hypoxia, acidosis, concomitant treatments facilitate the emergence of digital induced arrhythmias. A place aside of certain attention deserves diuretics and especially those of the loop (the lasix to be clear), as they find indicate in the decompensation and in the edematous subjects are very effective, and to maintain in compensation the subjects with a chronic heart lungs; however, they may aggravate pulmonary hypertension due to increased blood viscosity and bronchial secretions. On the contrary, it should be noted that the subjects with "ispissatio sanguinis" benefit from bloodletting, advisable and effective only in patients with a hematocrit higher than 55-60%.
Anticoagulants and calcium heparin is administered subcutis for prophylaxis of deep phlebothrombosis in patients with decompensation or in-bed patients. The frequent gastroduodenal pathologies of patients with chronic pulmonary heart increase the risk of full anticoagulant therapy, which should therefore be reserved only for cases of pulmonary vascular bed disease and those with previous thromboembolic complications. In COPD the onset of pulmonary hypertension affects the prognosis, contributing significantly to mortality: overall survival of COPD correlates to pulmonary arterial pressure levels more than to any other clinical or instrumental variable, with increased mortality rates of about 4 times compared to subjects with the same degree of pneumopathy but without signs of chronic pulmonary heart. Appropriate therapy usually allows a prolonged survival, even after repeated episodes of right-handed failure, which, especially in the initial phase, respond quickly enough to drugs.