Pulmonary insufficiency. Incompetence of the pulmonary valve is relatively frequent, especially the physiological one, which has become more evident since the incorporation of echo-doppler techniques as a conventional diagnostic instrument in cardiology.
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- 1 Etiology
- 2 Pathophysiology
- 3 Clinic
- 4 Physical examination
- 5 Electrocardiogram
- 6 Chest x-ray
- 7 Echocardiography
- 8 Cardiac catheterization
- 9 Natural history
- 10 Treatment
- 11 Sources
The differentiation between primary or secondary valve dysfunction is very important in the evaluation of tricuspid or pulmonary valve disease. In the adult, valve disease of the right chambers, especially regurgitant, is commonly the result of pulmonary hypertension secondary to heart disease of the left chambers , primary lung disease, or pulmonary vascular disease; the toxic oil syndrome has been the origin of pulmonary hypertension and pulmonary insufficiency (PI).
The most frequent cause of IP is valve ring dilation, secondary to pulmonary hypertension of any etiology. Unlike pulmonary stenosis , IP is rarely of congenital origin and can be manifested by idiopathic dilation of the pulmonary artery. It can also be caused by a connective disease, such as Marfan syndrome. Infectious endocarditis can cause acute PI, especially in people addicted to intravenous drugs and is the second most prevalent cause after pulmonary hypertension. Yatrogenesis due to surgical repair of PD or pulmonary balloon valvuloplasty is another possible etiology, appearing slightly in 90% of this percutaneous technique. It is also a common finding after correction of tetralogy of Fallot. Often, light IP is a casual finding on Doppler echocardiography. Other less frequent causes correspond to rheumatic involvement, tuberculosis , chest trauma and carcinoid syndrome .
Difficulty in normal closing of the pulmonary sigmoids causes, during ventricular diastole, the reflux of part of the blood volume ejected into the pulmonary artery, with the subsequent volume overload of the right ventricle. It has good tolerance for a long time, unless it is complicated by pulmonary hypertension.
Idiopathic dilation of the pulmonary artery constitutes a clinical entity that causes pulmonary regurgitation, with the following characteristics: marked dilation of the trunk of the pulmonary artery and the pulmonary annulus, with a normal right ventricle and pulmonary valve and a non-significant gradient of obstruction. This dilation may be a consequence of a connective tissue abnormality. Hemodynamically, a slight degree pulmonary valve pressure gradient and a discrete elevated cardiac index are produced.
Most cases with mild grades experience a benign clinical course. When pulmonary hypertension appears, it is accompanied by symptoms of right ventricular systolic dysfunction, and syncope, fatigue or dyspnea may appear . Patients with PI secondary to infective endocarditis may present with septic pulmonary embolism, pulmonary hypertension, and severe right ventricular dysfunction. However, the predominant symptomatology is that corresponding to the pathology that triggers pulmonary hypertension (most common etiology). When PI accompanies a carcinoid syndrome, episodes of facial redness, diarrhea and bronchospasm are observed, among other symptoms.
Upon palpation, a hyperdynamic right ventricle can be seen in the left parasternal area, the prominent pulmonary artery can cause systolic pulsations in the 2nd left intercostal space, and it is also possible to palpate both systolic and diastolic fremites. Upon cardiac auscultation and in the presence of pulmonary hypertension, the second noise, its pulmonary component, is accentuated. There may be wide splitting of the second noise due to prolonged right ventricular ejection imposed by increased stroke volume. A systolic, nonvalvular ejection click, due to sudden expansion of the pulmonary artery due to increased right ventricular systolic volume, precedes an expulsive mesosystolic murmur in the 2nd left intercostal space.
A third and fourth noise that increases with inspiration, of right origin, are frequently heard at the level of the 4th left intercostal space. In the absence of pulmonary hypertension, the regurgitating diastolic murmur is severe, with the epicenter in the third and fourth left intercostal space. It has a short rhomboidal morphology, increases with inspiration and inhalation of amyl nitrite.
When the systolic pressure of the pulmonary artery exceeds 60 mmHg, the dilation of the pulmonary ring causes a high-speed regurgitant jet that is manifested by the auscultation, on the left parasternal border, of a diastolic murmur of acute tone, in decrescendo, which begins after the pulmonary component of the second noise and which constitutes the so-called Graham Stell murmur of IP, which increases with inspiration and decreases during the pressure phase of the Valsalva maneuver. This murmur resembles that of aortic regurgitation, but is accompanied by semiology of hypertension.severe lung. Unlike aortic valve disease, stenotic and regurgitating lesion rarely coexists in pulmonary valve disease due to the unusual rheumatic etiology and the low pressure of the pulmonary artery relative to the aortic valve. Carcinoid syndrome is an exception to this, since it is very common that both types of injuries occur in lung involvement .
In idiopathic dilation of the pulmonary artery, we can find the following auscultatory findings: pulmonary ejection click, ejection systolic murmur in the area of the pulmonary focus, as well as a wide splitting of the second noise.
In PI in the absence of pulmonary hypertension, a pattern of right ventricular diastolic overload can be seen on the electrocardiogram (ECG), with rSr ‘or rsR’ morphology in right precordial leads. Regurgitation secondary to pulmonary hypertension manifests with a classic pattern of right ventricular hypertrophy. Similarly, alterations of the atriogram corresponding to the underlying pathology can be observed.
Both the pulmonary artery and the right ventricle appear enlarged in significant pulmonary insufficiency, but are entirely nonspecific findings.
IP constitutes the most frequent physiological regurgitation, that is, without structural heart disease. In different series its presence has been described, by pulsed, continuous or color Doppler, in 60% to 100% of healthy subjects.
It is common to find in the evolved IP a dilation of the right ventricle, as well as hypertrophy of this cavity if it is accompanied by pulmonary hypertension. An abnormal or paradoxical movement of the ventricular septum is characteristic of situations of volume overload of the right ventricle. In M mode, movement of the pulmonary valve suggests the cause of the regurgitation; thus, the absence of the “a” wave and the systolic notch in the posterior leaflet should suggest pulmonary hypertension. It is also possible to appreciate the imageflutter or flutter valve over the tricuspid valve. Both with M-mode or two-dimensional echocardiography, the presence of vegetations can be observed in cases of endocarditis and the etiology of lung failure. Pulsed Doppler is a very precise technique for diagnosing pulmonary insufficiency of any etiology, it shows inverted flow in the pulmonary artery. Color Doppler shows abnormal, regurgitant flow that recedes into the right ventricular outflow tract.
The diagnosis of pulmonary regurgitation is often made by echocardiography, so it is recommended to periodically repeat this technique in patients at risk of manifesting it, such as corrected pulmonary stenosis (either by surgery or by percutaneous valvulotomy) or in corrected Fallot.
The echocardiogram is the primary means of diagnosis of idiopathic pulmonary artery dilation. Some authors propose these two parameters for diagnostic confirmation:
- Ratio of the pulmonary artery at its bifurcation / aorta diameter 2 cm behind the aortic valveequal to or greater than 1.4.
- Pulmonary artery / aorta diameter ratio equal to or greater than 1.5.
It is of little use in diagnosing IP. The echocardiogram is much more sensitive in its diagnosis, since this regurgitation is not easily demonstrable with angiography. However, it can be useful for the calculation of pulmonary vascular resistance in patients with associated pulmonary hypertension.
Most patients with mild pulmonary insufficiency have a benign clinical course. In contrast, the moderate to severe grade shows an evolution towards chronic right ventricular volume overload, with ventricular dilation and systolic dysfunction. The evolution of cardiac lesions in the patient with carcinoid syndrome is very rapid, leading to right heart failure, although death occurs from systemic disease, rarely from pulmonary valve disease .
Usually no specific therapy is required in the treatment of lung failure. It is essential to identify and treat the specific etiology of regurgitation and selectively treat this disorder, be it endocarditis, pulmonary hypertension, or carcinoid syndrome. Conventional digital and diuretic medical treatment will be used in the case of right heart failure.
Surgical treatment is reserved for severe regurgitation, with evidence of progressive dilatation of the ventricular cavity or at the onset of right ventricular systolic dysfunction. A small number of patients operated on for tetralogy of Fallot and with significant residual IP, is the most common indication for surgery in pulmonary regurgitation. In these cases, the use of bioprosthesis is preferable, due to the lower risk of thrombosis . However, the result of the valve replacement has not yet been validated in a sufficient evolutionary control. Some cases with endocarditis over the pulmonary valve may require valvulectomy .