[Right ventricle insufficiency in pulmonary arterial hypertension. Physiopathologic considerations]. / Insuficiencia ventricular derecha en la hipertensión arterial pulmonar. Consideraciones fisiopatológicas.

The present review is focused on chronic RV pressure overload or Cor Pulmonale as it may occur in the setting of two distinct disorders: those associated with abnormal pulmonary gas exchange (hypoxemia and/or hypercapnia) where chronic obstructive pulmonary disease (COPD) is the leading cause, and those associated with pulmonary vascular obstruction where primary pulmonary hypertension (PDDH) is the representative example. The clinical curse, prognostic, implications, and therapeutic strategies differ considerably in these two clinical entities. Right ventricular failure (RVF) may adversely influence the natural history and prognosis of patients with diverse cardiopulmonary disorders. It has been long established that right ventricular (RV) ischemia, RV overload, and RV pressure overload, alone or in combination, are the main factors involved in the pathogenesis of RVF. From the pathophysiologic point of view, RVF of COPD is more a congestive type of failure, in which activation of renin-angiotensin system is involved. In PPH, a low cardiac output state is predominant and the precise mechanism of RVF remains unknown. Current evidence in favor of the pathogenetic role of ischemia, adrenergic overdrive, and genetic determination are all reviewed during the course.

[Development of a canine model of chronic progressive right ventricular hypertension]. / Desarrollo de un modelo canino de hipertensión ventricular derecha crónica progresiva.

INTRODUCTION: Several animal models of right ventricle hypertension (RVH) have been produced through pulmonary artery banding with linen, tygon or teflon. Nevertheless few devices attempting a progressive, step by step graduated chronic development of RVH have been reported. The present study describes the results in our animal model of chronic RVH. MATERIAL AND METHODS: We designed a software programmed to obtain hemodynamic data and installed a small occlusive hydraulic device (OHD) at the pulmonary artery trunk producing a raise in the right ventricular systolic pressure (RVSP); this pressure can be modified externally through the OHD. We studied 12 healthy mongrel dogs (18 to 28 kg of weight) in the course of 6 months. Hemodynamic measurements were performed at different RVSP at two months intervals; (Baseline, 40 mmHg and 60 mmHg). RESULTS: The software was useful to analyze several hemodynamic variables at each RVSP. At 60 mmHg, the end diastolic pressure of the right ventricle (RVEDP) increased from 4.2 +/- 0.4 mmHg to 13.2 +/- 1.1 mmHg, p < 0.000, accompanied with a fall in cardiac output adjusted to the dogs weight from 0.16 +/- 0.03 L/min/kg to 0.09 +/- 0.01 L/min/kg, p > 0.000. Also an increase of the end diastolic pressure of the left ventricle (LVEDP) from 7.4 +/- 0.8 mmHg to 16.3 +/- 2.8 mmHg, p < 0.000, was observed. RVSP was maintained in chronic condition and the intraclass correlation coefficient was 0.83, P < 0.005. CONCLUSIONS: Right ventricular chronic hypertension is created. The device is useful and reliable to maintain chronic increments of RVSP. The software permits a versatile analysis.

[Helical computerized tomography of the thorax in the diagnosis of unresolved chronic pulmonary thromboembolism]. / La tomografía computarizada helicoidal del tórax en el diagnóstico de la tromboembolia pulmonar crónica no resuelta.

We assessed the diagnostic usefulness of helical CT scan of the thorax in the setting of chronic thromboembolic pulmonary hypertension by prospectively comparing the results of helical CT scan to those of the pulmonary angiogram (gold standard). We studied 40 patients with diagnosis of pulmonary hypertension of diverse etiology (mean age: 40.7 +/- 12 y.o.; mean systolic pulmonary artery pressure: 91 +/- 33 mmHg)). Thirty of these patients fulfilled the diagnostic criteria of chronic thromboembolic pulmonary hypertension and the other ten were used as controls. Diagnosis in control patients included: primary pulmonary hypertension (4); patent ductus arteriosus (2); atrial septal defect (1); rheumatic valve disease (1); ischemic heart disease (1); and acute pulmonary embolism (1). Both helical CT scan and pulmonary angiogram were part of the routine diagnostic work up of these patients, and were, performed and interpreted almost simultaneously (within one week) by a different group of investigators in a blind manner. Only the diagnostic accuracy of the method regarding central (major arteries) vascular lesions was evaluated. Helical CT scan had an overall sensitivity of 100% (29/29), and a specificity of 91% (10/11). Positive predictive and negative predictive values were 96.6% (29/30) and 100% (10/10), respectively. Overall diagnostic accuracy was 97.5% (39/40). We conclude that helical CT scan of the thorax is an excellent alternative approach for the diagnosis of major arteries lesions in the setting of chronic thromboembolic pulmonary hypertension.

[Pulmonary vascular reactivity and the development of edema in the presence of prostaglandin inhibitors in the isolated canine lobe]. / Reactividad vascular pulmonar y formación de edema en presencia de inhibidores de prostaglandinas en el lóbulo canino aislado.

UNLABELLED: Alveolar hypoxia is the most powerful pulmonary vasoconstrictor. In a previous work, we did not demonstrate significant changes in vascular reactivity and edema formation in an isolated canine lobe model during alveolar hypoxia. The purpose of this study is to define vascular pulmonary reactivity and edema formation after induction of pulmonary vasoconstriction using a prostaglandin inhibitor like tiaprofenic acid and alveolar hypoxia. Six isolated canine pulmonary lobules were instrumented and studied, all of them under two conditions (normoxia FIO2 21% and hypoxia FIO2 5%) four starting in normoxia condition and 2 starting in hypoxia condition. RESULTS: No significant changes in filtration rate were found, normoxia 0.42 +/- 0.41, hypoxia 0.37 +/- 0.51 ml/min/100 g pulmonary tissue P = NS. The arterial pressure in basal conditions was 25.1 +/- 6.21, and during hypoxia increased to 37 +/- 7.19 cm H2O (Delta 12.0 +/- 1.2 cm H2O). P < 0.001. CONCLUSION: Hypoxia vascular reactivity was significantly increased in tiaprofenic acid pretreated isolated canine lobes, no changes in pulmonary permeability was found nor increased rate in edema formation.

[Continuous spectrophotometry as a method to study pulmonary edema in isolated canine pulmonary lobe]. / Espectrofotometría continua como método para el estudio del edema pulmonar en una preparación de lóbulo pulmonar canino aislado.

The aim of this paper is to introduce the spectrophotometric method to the study of pulmonary edema in isolated ex-vivo canine pulmonary lobe preparation. This spectrophotometric method is based on the on-line measure of light transmission in a column of blood, that is proportional to hematocrit. A second light is used to follow Evans blue dyed proteins. With this method we were able to measure the amount of edema in 10 isolated canine lobes. Both the filtration and reflection coefficient of the membrane as well as the characteristics of the filtrate could be calculated. The filtration coefficient was 0.6 +/- 0.4 ml/min (1.3 +/- 0.9 ml/min/100 g pulmonary, tissue) at maximum capillary pressure and the reflection coefficient was 0.53 +/- 0.07. With the spectrophotometric method we have the capability to study different aspects of lung edema formation. This method has the advantage of being exact and independent from pressure and volume induced vascular changes. It also allows the measurement of solute transport.

[Primary or of unknown etiology pulmonary hypertension: survival and its determinants]. / Hipertensión arterial pulmonar primaria o de etiología desconocida. La sobrevida y sus determinantes.

UNLABELLED: The main objective of the present study is to characterize mortality in PPH and the factors associated with survival. Our series comprises 61 patients diagnosed of PPH and prospectively followed at the Cardiopulmonary Department between the years of 1977 and 1992. Univariate and multivariate analysis were used to examine relations between survival and selected demographic, medical-history, pulmonary-function, laboratory, and hemodynamic variables. We used the date of initial diagnostic catheterization as an index for determining survival. The method of Kaplan-Meir was used to estimate overall survival distribution. RESULTS: the mean age of the group was 22.6 +/- 11 years with a female to male ratio of 3.06:1. Pulmonary hemodynamics at entry were: mean pulmonary artery pressure (PAP) = 65.5 +/- 17.5 mmHg; right atrial pressure (RAP) = 7.5 +/- 5 mmHg; cardiac index (CI) = 3.15 +/- 1.31.mi.m2; pulmonary vascular resistance (RP) = 24 +/- 11 U. The pulmonary to systemic resistance ratio (Rp/Rs) was 0.8 +/- 0.2. The median survival (MS) of the whole group 4.04 years. There was a significant difference in MS between the groups with and without vasodilator treatment (5.04 and 2.12 years respectively), however, the hemodynamic profile at entry was also different, with higher RAP, PAP, PVR, and higher Rp/Rs in the group without treatment (p < 0.05). Factors associated with poor survival (univariate) were: increased RAP, RP, and Rp/Rs and decreased forced vital capacity (FVC), decreased CI, and stroke volume index and decreased mixed venous PO2. The absence of vasodilator treatment was also associated with an increased risk of death. On the multivariate analysis, survival was associated mainly to FVC and to pulmonary hemodynamic variables. We conclude that survival in PPH is related to pulmonary hemodynamic factors at diagnosis.

[High altitude pulmonary edema. Physiopathologic considerations apropos of a case]. / Edema pulmonar de las alturas. Consideraciones fisiopatólogicas a propósito de un caso.

High Altitude Pulmonary Edema (HAPE) generally appears in persons who climb over 2,500 meters (8,300 feet) above sea level, or in residents at altitudes beyond 3,000 meters (10,000 feet) who go down to sea level for a short period of time and return to their place of residence. Although dozens of cases have been reported, their etiopathogenesis is unknown, although both hydrostatic and permeability factors have been implied in its genesis. In this paper we describe the first HAPE case reported in the national literature and the factors implied in its physiopathology are reviewed.

[10 years' experience in the use of vasodilator agents in the treatment of primary pulmonary arterial hypertension (P-PAH) (1977-1987)]. / Diez años de experiencia con el uso de vasodilatadores en el tratamiento de la hipertensión arterial pulmonar primaria (HAP-P) (1977-1987).

We analyze the experience derived from the use of vasodilating therapy in Primary Pulmonary Hypertension (PPH) at our institution in the last ten years. Important aspects such as complications, long-term hemodynamic effects and survival are particularly emphasized. We have consecutively studied forty patients (29 females, 11 males) with a mean age of 21 +/- 1.6 years. The follow-up period is 50 +/- 8 months and the drugs used were: Hydralazine (HDL) and Nifedipine (NFD). On the basis of their hemodynamic response the patients were divided into two groups: twenty responders (R) and twenty non-responders (NR). Both groups seem to have a different clinical and hemodynamic basal profile; most of the patients in the R group had a better functional class (NYHA: I-II) than those NR (III-IV). Also, the R group had a lower basal Pp (49 vs 77 mmHg, p less than 0.05), lower Rp (17 vs 29 U/m2, p less than 0.05) and lower Rp/Rs ratio (0.59 vs 1.05, p less than 0.05). The R group has continued on long-term vasodilator therapy with NFD (n-13) and HDL (n-7) and most of them showed a significant improvement in their quality of life and still maintain a good hemodynamic response. Only minor side effects were associated with the medication. The NR group, on the other hand, has shown progressive clinical deterioration. Eight patients in the NR group and three in the R group have died. The five-year probability of survival in the R group is 86% whereas it is only 45% in the NR group. We conclude that vasodilator therapy significantly improves quality of life, with minimum untoward effects, in selected patients with PPH. The R group probably reflects a different patient population or a different stage of the disease and therefore its better long-term prognosis cannot be attributable solely to the use of these drugs.

[The respiratory center in normal subjects at 2,240 meters above sea level. The ventilatory and occlusion pressure (P 0.1) responses upon CO2 stimulation]. / Estudio del centro respiratorio en sujetos normales a 2,240 metros sobre el nivel del mar. La respuesta ventilatoria y de la presión de oclusión (P 0.1) al estímulo del CO2.

Altitude hypoxia imposes acute changes and long term adjustments in the ventilation of human beings. Most of the present knowledge of the respiratory center behavior at high altitude derives from the studies of ventilatory response to both hypoxia and hypercapnea. Other indexes of respiratory center output such as the occlusion pressure (P 0.1) response to a variety of stimuli are at present being evaluated. We could not find, however, studies on the P 0.1 responses to CO2 at high altitude. In this study we analyze the ventilatory and P 0.1 responses to CO2 in a group of 32 normal subjects, all of them natives and residents of Mexico city (altitude of 2,240 meters) and we compared them with those reported at sea level. The slope of both, the ventilatory and P 0.1 responses to CO2 was found to be similar to that reported at sea level; 4.52 +/- 1.29 L. min. mmHg and 0.07 +/- 0.01 cm H2O/mmHg respectively. The crossing over of such responses, however, is shifted to the left of the reported at sea level. This means higher levels of both ventilation and P 0.1, for the same level of end-tidal PCO2, at high altitude. This finding might be explained in the basis of the so-called "acclimatization to hypocapnea".

[Effects of body posture on mechanical lung function in the obese patient]. / Los effectos de la posición corporal sobre la función mecánica del pulmón en el obeso.

The pulmonary mechanics of twelve obese patients were studied: the static and dynamic compliance, the maximum pressure of elastic recoil, and the expiratory flow curves breathing room air and a mixture of He-O2. Also analyzed were the closing capacity, the closing volume and the slope of the alveolar plateau (phase III), in the erect and supine positions. Our data confirm that the tests that explore the small airways are abnormal in the obese patients. The results obtained, allow us to assure that the pulmonary mechanics in the obese patients are affected by the change of position, as is shown by the closing volume and closing capacity when assuming the supine position when compared to orthostatism, as well as the decrease in vital capacity. These alterations were not found in non-obese patients which were used as controls.

[Microscopic pulmonary arteriovenous fistulas]. / Fístulas arteriovenosas pulmonares microscópicas.

A case of pulmonary arterio-venous microfistula in a fifteen year old male is reported. He referred dyspnea and cyanosis for 3 and 2 years respectively. Physical examination was normal except for finger clubbing. Chest radiograph and EKG were also normal. Lung function tests showed hypoxemia due to an increase in veno-arterial shunt (Qs/Qt). Its localization was not apparent by routine studies such as phonocardiogram, echocardiogram, right heart catheterization and pulmonary angiogram. However, a contrast echocardiogram and selective occlusion of the right and left pulmonary arteries performed with a Dotter-Lucas catheter were suggestive of an intrapulmonary localization of the shunt. A lung biopsy confirmed the diagnosis.

[Arteriovenous shunting in obesity, its relation to lung volume]. / El corto-circuito venoarterial en al obesidad, su dependencia del volumen pulmonar.

Thirty-five patients with an average overweight of 67.1% were studied. Pulmonary restriction of a variable degree was found in 68.6/; in 60% due to reduction of respiratory reserve volume. Bronchial obstruction was detected in 57% as measured by forced midexpiratory flow (25-75%). In addition, 14% showed a decrease of 75-85% in forced expiratory flow, which suggested that the pathology was located in the small respiratory airways. The PaO2 while breathing room air and in a resting state was of 52.6 +/- 9.42 mmHg, and after breathing it increased to 69.07 +/- 11.01 mmHg. The PaO2 breathing inspiratory fractions of 99.6% O2 in a resting condition was 309.34 +/- 70.07 mmHg, and after deep breathing it rose to 354.0 +/- 64.27 mmHg. The mechanisms which produce hypoxemia in the obese were analysed and it was concluded that they were due fundamentally to alterations of the ventilation perfusion ratio and to an increase of the venous-arterial shunt. In some cases, alveolar hypoventilation contributed (Pickwick syndrome). By increasing the pulmonary volume with deep breathing, the ventilation perfusion ratio improves or becomes normal, likewise, the venous-arterial shunt can improve or persist as the only cause of hypoxemia.

El corto-circuito venoarterial en la obesidad, su dependencia del volumen pulmonar. / Arteriovenous shunt in obesity, its dependence to pulmonary volume

Se estudiaron 35 pacientes con sobrepeso corporal del 67.1% en promedio. El 68.6% tenian restriccion pulmonar de grado variable, en el 60% a expensas de reduccion del VER. Existio broncobstruccion en el 57% a juzgar por el FEF de 25-75%; ademas 14% tuvieron disminucion del FEF entre 75-85% lo que sugiere patologia de la via aerea menor. La PaO2 respirando aire ambiente en reposo fue de 52.6 mmHg +/- 9.42 y despues de realizar respiraciones profundas se elevo a 69.07 mmHg +/- 11.01. La PaO2 respirando O2 FI 99.6% en condiciones basales fue de 309.34 mmHg +/- 70.07 y despues de respiraciones profundas ascendio a 354.0 +/- 64.27. Se analizaron los mecanismos productores de hipoxemia en el obeso y se concluyo que eran debidos fundamentalmente a alteraciones de la relacion V/Q y al aumento del corto circuito v-a. En algunos casos contribuye la hipoventilacion alveolar (Sindrome de Pickwick). Al aumentar el volumen pulmonar con respiraciones profundas la relacion V/Q mejora o se normaliza; asimismo, el corto circuito v-a puede mejorar o persistir como unica causa de hipoxemia

Fistulas arteriovenosas pulmonares microscopicas. / Microscopic pulmonary arteriovenous fistula

Se comunica el caso de un varon de 15 anos de edad en quien se establecio el diagnostico de fistulas arteriovenosas pulmonares microscopicas. Su sintomatologia basica era disnea y cianosis progresivas de 3 y 2 anos respectivamente. El examen fisico, con excepcion del hipocratismo digital, era normal. La radiografia de torax y el electrocardiograma eran tambien normales. En las pruebas de funcion respiratoria se encontraba hipoxemia severa (PaO2 = 41 mmHg), cuyo mecanismo fisiopatologico fundamental era el de aumento importante del cortocircuito veno-arterial (Qs/Qt). La localizacion de este Qs/Qt, fue intensamente investigada a traves de fono y ecocardiografia y por cateterismo derecho, los que resultaron normales. La angiografia pulmonar no mostro alteraciones significativas. A pesar de ello, un estudio de ecocardiografia con contraste realizado en cavidades ventriculares sugirio la existencia del cortocircuito a nivel intrapulmonar, dato que fue ratificado por el estudio hemodinamico con oclusiones selectivas de las ramas de la arteria pulmonar realizado con cateter de Dotter-Lucas, el que demostro aumento del cortocircuito en ambos pulmones. El estudio histopatologico de la biopsia pulmonar confirmo el diagnostico de fistulas arteriovenosas microscopicas intrapulmonares

Los efectos de la posicion corporal sobre la funcion mecanica del pulmon en el obeso / Effects of body position on the mechanical pulmonary function of the obese

Se estudio la mecanica pulmonar de doce pacientes obesos: su distensibilidad estatica y dinamica, la presion maxima de retraccion elastica y las curvas espiratorias de flujo-volumen, respirando aire ambiente y mezcla de HeO2. Se analizo, igualmente, la capacidad de cierre, el volumen de cierre y la pendiente de la fase III en ortostatismo y en decubito dorsal. Se confirma que todos los parametros que exploran la via aerea menor son anormales en el paciente obeso. Nuestros datos permiten asegurar que el cambio de posicion influye sobre la mecanica pulmonar del obeso, como lo demuestra el aumento del volumen de cierre y la capacidad de cierre al adoptar la posicion de decubito supino en relacion con el ortostatismo (p menor ou igual 0.001), asi como la documentada disminucion de la capacidad vital. Estos cambios no se prestaron en los sujetos normales que se usaron como testigos

[Use of final positive expiratory pressure (FPEEP) in the management of acute respiratory insufficiency]. / El uso de la presión positiva espiratoria final (PPEF) en el manejo de la insuficiencia respiratoria aguda.

A group of 19 patients with acute respiratory failure (ARF) of diverse etiology received as a part of their treatment positive and expiratory pressure (PEEP). All of them were evaluated clinically and with several respiratory parameters. The response to treatment, complications and mortality rates are analyzed. The addition of PEEP in the management of this patients was accompanied by a significant increase of the PAO2 (p < 0.001) and a simultaneous decrease in the following parameters: FiO2/PaO2 index, Alveolo-arterial oxygen gradient (A-aDO2) and the pulmonary shunt (Qs/Qt). No hemodynamic deterioration was observed. None of the clinical parameters such as: blood pressure, heart rate and diuresis was significantly modified; neither a significant change in the arterious-venous oxygen gradient (a-vDO2) was detected. Pneumothorax as a complication of the use of PEEP was present in the 10.4% of the patients. The course of the ARF was toward the improvement in most of them at the end of the evolution. The high mortality rate in this study was considered to be secondary to uncontrollable sepsis and also to the presence of multiple organ failure. In none of the cases the poor outcome was secondary to refractory acute hypoxemia. PEEP which is one of the varieties of continuous positive pressure ventilation (CPPV) represents one of the most importants therapeutic advances in the last decade in the management of patients with acute respiratory failure.