Heart rate dynamics during a treadmill cardiopulmonary exercise test in optimized beta-blocked heart failure patients

BACKGROUND: Calculating the maximum heart rate for age is one method to characterize the maximum effort of an individual. Although this method is commonly used, little is known about heart rate dynamics in optimized beta-blocked heart failure patients. AIM: The aim of this study was to evaluate heart rate dynamics (basal, peak and percent heart rate increase) in optimized beta-blocked heart failure patients compared to sedentary, normal individuals (controls) during a treadmill cardiopulmonary exercise test. METHODS: Twenty-five heart failure patients (49±11 years, 76 percent male), with an average LVEF of 30±7 percent, and fourteen controls were included in the study. Patients with atrial fibrillation, a pacemaker or noncardiovascular functional limitations or whose drug therapy was not optimized were excluded. Optimization was considered to be 50 mg/day or more of carvedilol, with a basal heart rate between 50 to 60 bpm that was maintained for 3 months. RESULTS: Basal heart rate was lower in heart failure patients (57±3 bpm) compared to controls (89±14 bpm; p<0.0001). Similarly, the peak heart rate ( percent maximum predicted for age) was lower in HF patients (65.4±11.1 percent) compared to controls (98.6±2.2; p<0.0001). Maximum respiratory exchange ratio did not differ between the groups (1.2±0.5 for controls and 1.15±1 for heart failure patients; p=0.42). All controls reached the maximum heart rate for their age, while no patients in the heart failure group reached the maximum. Moreover, the percent increase of heart rate from rest to peak exercise between heart failure (48±9 percent) and control (53±8 percent) was not different (p=0.157). CONCLUSION: No patient in the heart failure group reached the maximum heart rate for their age during a treadmill cardiopulmonary exercise test, despite the fact that the percentage increase of heart rate was similar to sedentary normal subjects. A heart rate increase in optimized beta-blocked...

Effect of saline infusion for the maintenance of blood volume on pulmonary gas exchange during temporary abdominal aortic occlusion

We analyzed the effects of saline infusion for the maintenance of blood volume on pulmonary gas exchange in ischemia-reperfusion syndrome during temporary abdominal aortic occlusion in dogs. We studied 20 adult mongrel dogs weighing 12 to 23 kg divided into two groups: ischemia-reperfusion group (IRG, N = 10) and IRG submitted to saline infusion for the maintenance of mean pulmonary arterial wedge pressure between 10 and 20 mmHg (IRG-SS, N = 10). All animals were anesthetized and maintained on spontaneous ventilation. After obtaining baseline measurements, occlusion of the supraceliac aorta was performed by the inflation of a Fogarty catheter. After 60 min of ischemia, the balloon was deflated and the animals were observed for another 60 min of reperfusion. The measurements were made at 10 and 45 min of ischemia, and 5, 30, and 60 min of reperfusion. Pulmonary gas exchange was impaired in the IRG-SS group as demonstrated by the increase of the alveolar-arterial oxygen difference (21 ± 14 in IRG-SS vs 11 ± 8 in IRG after 60 min of reperfusion, P = 0.004 in IRG-SS in relation to baseline values) and the decrease of oxygen partial pressure in arterial blood (58 ± 15 in IRG-SS vs 76 ± 15 in IRG after 60 min of reperfusion, P = 0.001 in IRG-SS in relation to baseline values), which was correlated with the highest degree of pulmonary edema in morphometric analysis (0.16 ± 0.06 in IRG-SS vs 0.09 ± 0.04 in IRG, P = 0.03 between groups). There was also a smaller ventilatory compensation of metabolic acidosis after the reperfusion. We conclude that infusion of normal saline worsened the gas exchange induced by pulmonary reperfusion injury in this experimental model.

Effect of pentoxifylline on lung inflammation and gas exchange in a sepsis-induced acute lung injury model

Experimental models of sepsis-induced pulmonary alterations are important for the study of pathogenesis and for potential intervention therapies. The objective of the present study was to characterize lung dysfunction (low PaO2 and high PaCO2, and increased cellular infiltration, protein extravasation, and malondialdehyde (MDA) production assessed in bronchoalveolar lavage) in a sepsis model consisting of intraperitoneal (ip) injection of Escherichia coli and the protective effects of pentoxifylline (PTX). Male Wistar rats (weighing between 270 and 350 g) were injected ip with 10(7) or 10(9) CFU/100 g body weight or saline and samples were collected 2, 6, 12, and 24 h later (N = 5 each group). PaO2, PaCO2 and pH were measured in blood, and cellular influx, protein extravasation and MDA concentration were measured in bronchoalveolar lavage. In a second set of experiments either PTX or saline was administered 1 h prior to E. coli ip injection (N = 5 each group) and the animals were observed for 6 h. Injection of 10(7) or 10(9) CFU/100 g body weight of E. coli induced acidosis, hypoxemia, and hypercapnia. An increased (P < 0.05) cell influx was observed in bronchoalveolar lavage, with a predominance of neutrophils. Total protein and MDA concentrations were also higher (P < 0.05) in the septic groups compared to control. A higher tumor necrosis factor-alpha (P < 0.05) concentration was also found in these animals. Changes in all parameters were more pronounced with the higher bacterial inoculum. PTX administered prior to sepsis reduced (P < 0.05) most functional alterations. These data show that an E. coli ip inoculum is a good model for the induction of lung dysfunction in sepsis, and suitable for studies of therapeutic interventions.

Pretreatment with N-nitro-L-arginine Methyl Ester Improved Oxygenation After Inhalation of Nitric Oxide in Newborn Piglets with Escherichia coli Pneumonia and Sepsis

We evaluated the effects of a combined therapy of pre-blockade endogenous nitric oxide synthase (NOS) with N-nitro-L-arginine methyl ester (L-NAME) and continuous inhaled NO (iNO) on the gas exchange and hemodynamics of Escherichia coli pneumonia and sepsis in newborn piglets. Seven to ten day old ventilated newborn piglets were randomized into 5 groups: control, E. coli pneumonia control, pneumonia with iNO 10 ppm, pneumonia pre-treated with L-NAME 10 mg/kg, and pneumonia with the combined therapy of L-NAME pretreatment and iNO. E. coli pneumonia was induced via intratracheal instillation of Escherichia coli, which resulted in progressively decreased cardiac index and oxygen tension; increased pulmonary vascular resistance index (PVRI), intrapulmonary shunting, and developed septicemia at the end of 6 hr experiment. iNO ameliorated the progressive hypoxemia and intrapulmonary shunting without affecting the PVRI. Only two of 8 animals with L-NAMEpretreated pneumonia survived. Whereas when iNO was added to infected animals with L-NAME pretreatment, the progressive hypoxemia was abolished as a result of a decrease in intrapulmonary shunting without reverse of the high PVRI and systemic vascular resistance index induced by the L-NAME injection. This result suggests that a NOS blockade may be a possible supportive option for oxygenation by iNO treatment in neonatal Gram-negative bacterial pneumonia and sepsis.

Pretreatment with N-nitro-L-arginine Methyl Ester Improved Oxygenation After Inhalation of Nitric Oxide in Newborn Piglets with Escherichia coli Pneumonia and Sepsis

We evaluated the effects of a combined therapy of pre-blockade endogenous nitric oxide synthase (NOS) with N-nitro-L-arginine methyl ester (L-NAME) and continuous inhaled NO (iNO) on the gas exchange and hemodynamics of Escherichia coli pneumonia and sepsis in newborn piglets. Seven to ten day old ventilated newborn piglets were randomized into 5 groups: control, E. coli pneumonia control, pneumonia with iNO 10 ppm, pneumonia pre-treated with L-NAME 10 mg/kg, and pneumonia with the combined therapy of L-NAME pretreatment and iNO. E. coli pneumonia was induced via intratracheal instillation of Escherichia coli, which resulted in progressively decreased cardiac index and oxygen tension; increased pulmonary vascular resistance index (PVRI), intrapulmonary shunting, and developed septicemia at the end of 6 hr experiment. iNO ameliorated the progressive hypoxemia and intrapulmonary shunting without affecting the PVRI. Only two of 8 animals with L-NAMEpretreated pneumonia survived. Whereas when iNO was added to infected animals with L-NAME pretreatment, the progressive hypoxemia was abolished as a result of a decrease in intrapulmonary shunting without reverse of the high PVRI and systemic vascular resistance index induced by the L-NAME injection. This result suggests that a NOS blockade may be a possible supportive option for oxygenation by iNO treatment in neonatal Gram-negative bacterial pneumonia and sepsis.

Different doses of exogenous surfactant for treatment of meconium aspiration syndrome in newborn rabbits

OBJETIVO: Avaliar os efeitos de duas diferentes doses de surfactante exógeno sobre a mecânica pulmonar e sobre a regularidade da expansão do parênquima pulmonar em coelhos recém-nascidos. MÉTODO: Coelhos recém-nascidos foram traqueostomizados e randomizados em quatro grupos de estudo: grupo-Controle, sem aspiração de mecônio; grupo MEC, com aspiração de mecônio e sem tratamento com surfactante exógeno; grupos S100 e S200, ambos com aspiração de mecônio e tratados respectivamente com 100 e 200 mg/kg de surfactante exógeno (produzido e fornecido pelo Instituto Butantan). Os animais dos 4 grupos foram ventilados por 25 minutos. A mecânica pulmonar foi avaliada a partir dos valores de complacência dinâmica, pressão ventilatória, volume-corrente e volume pulmonar máximo (curva P-V). A análise histológica foi feita calculando-se o diâmetro alveolar médio (Lm) e o índice de distorção através do desvio padrão do Lm. Utilizou-se ANOVA One Way com a = 0,05. RESULTADOS: Após 25 minutos de ventilação, os valores de complacência dinâmica (ml/cm H2O.kg) foram: 0,87± 0,07 (Controle); 0,49±0,04 (MEC*); 0,67±0,06 (S100) e 0,67±0,08 (S200) e de pressão ventilatória (cm H2O): 9,0± 0,9 (Controle); 16,5±1,7 (MEC*); 12,4±1,1 (S100) e 12,1±1,5 (S200). Ambos os grupos tratados tiveram padrão de expansão do parênquima mais homogêneo em relação aos animais não tratados: índice de distorção de 7,5± 1,9 (Controle); 11,3±2,5 (MEC*); 5,8±1,9 (S100) e 6,7±1,7 (S200) (*p < 0,05 vs outros grupos). CONCLUSÕES: Animais tratados com surfactante mostraram melhora significativa da mecânica pulmonar e maior homogeneidade do padrão de expansão pulmonar comparados ao grupo não tratado. Não houve influência das doses de surfactante utilizadas.

Partial liquid ventilation with perfluorocarbon improves gas exchange and decreases inflammatory response in oleic acid-induced lung injury in beagles

The aim of this study was to determine the effect of partial liquid ventilation (PLV) using a perfluorocarbon (PFC) on gas exchange and lung inflammatory response in a canine acute lung injury model. After inducing severe lung injury by oleic acid infusion, beagle dogs were randomized to receive either gas ventilation only (control group, n = 6) or PLV (PLV group, n = 7) by sequential instillation of 10 mL/kg of perfluorodecalin (PFC) at 30 min intervals till functional residual capacity was attained. Measurements were made every 30 min till 210 min. Then the lungs were removed and bronchoalveolar lavage (BAL) (35 mL/kg) was performed on the right lung and the left lung was submitted for histologic analysis. There was significant improvement in PaO2 and PaCO2 in the PLV group compared to the control group (p < 0.05) which was associated with a significant decrease in shunt (p < 0.05). There was no significant difference in parameters of lung mechanics and hemodynamics. There was a significant decrease in cell count and neutrophil percentage in BAL fluid and significantly less inflammation and exudate scores in histology in the PLV group (p < 0.05). We conclude that PLV with perfluorodecalin improves gas exchange and decreases inflammatory response in the acutely-injured lung.

Tratamiento de la fibrosis pulmonar idiopática con colchicina / Treatment of idiopathic pulmonary fibrosis with colchicine

Background: Experimental and clinical evidences suggest that colchicine can be effective in the treatment of patients with idiopathic pulmonary fibrosis. Aim: To assess the effect of colchicine in the treatment of idiopathic pulmonary fibrosis. Patients and methods: Patients with clinically diagnosed idiopathic pulmonary fibrosis were treated with colchicine in doses of 0.5 to 1 mg/day, according to tolerance and followed for periods ranging from 7 to 40 months. The clinical and radiological score reported by Watters et al was used for the longitudinal assessment of patients. Maintenance or improvement in forced vital capacity and maintenance or decrease in alveolar arterial O2 gradient during follow up, were considered as positive therapeutic responses. Results: Seventeen patients (10 male, aged 61 to 81 years old) were studied. Their basal score for dyspnea was 5.8 (over 20), for the chest X ray examination was 2.4 (over 3) and for CT scan was 2.8 (over 3). Basal FVC was 77 percent of predicted value (range 51-108 percent), basal FEV, was 82 percent (range 59-117 percent) and FEV1/FVC was 0.82 (range 0.68-0.95). PaO2 at rest was 78 mm Hg (ranges 63-97). Alveolar-arterial PO2 gradient was 16 mm Hg (range 5-31.6) at rest and 31 mm Hg (range 5.7-51.4) after exercise. Six patients (35 percent) had a positive response to therapy. Conclusions: The response rates of these patients to colchicine are at least similar to those obtained with steroids, but with less side effects

Uso del óxido nítrico en la valoración de la hipertensión arterial pulmonar / Nitric oxide in the evaluation of pulmonary hypertension

Hemos empleado el óxido nítrico en un paciente pediátrico con cardiopatía congénita de tipo canal atrio-ventricular completo con hipertensión arterial pulmonar severa, cianosis y desnutrición avanzada. Este ha sido llevado al laboratorio de cateterismo cardiaco para valorar el estado de los vasos pulmonares y precisar el daño vascular pulmonar, por lo cual se realizan pruebas farmacológicas con aire ambiente, oxígeno al 100 por ciento y óxido nítrico. En el estudio se demuestra el efecto vasodilatador importante del óxido nítrico: la presión de arteria pulmonar y resistencias arteriolares pulmonares descienden en forma notable de 8.75 U Wood/m² a 1.32 U Wood/m², el gasto pulmonar total aumenta, y el gradiente entre la presión en cuña y la del atrio izquierdo desparece. Por eso la hipertensión arterial pulmonar severa es reversible si el defecto congénito es corregido quirúrgicamente

Rendimiento del atleta que hace ejercicio en aire contaminado con ozono / Performance of athletes exercising in ozone polluted air

Se examinó la literatura sobre le rendimiento del que se ejercita en aire con ozono. La acción de ozono está mediada por receptores muscarinicos y otros de naturaleza desconocida lcalizados, aparentemente, sobre el epitelio respiratorio de transporte gaseoso. Por su acción sobre dichos receptores se reduce la fase inspiratoria de la ventilación pulmonar en un efecto asociado con la aparición de dolor y aumenta la resistencia al paso del aire. Si el ejercicio eleva la ventilación a 90 o más litros por minuto, la concentración efectiva de ozono aumenta hasta potenciar su efecto en la inspiración y la resistencia. La reducción potenciada de la fase inspiratoria y el dolor asociado con ella (a) antagonizan fuertemente el esfuerzo ventilatorio del que se ejercita y (b) reducen la capacidad de responder al aumento en resistencia con inspiraciones aumentadas. De este modo aparece una caída importante en el remdimeinto

Efeitos do captopril na hemodinâmica, nas trocas gasosas e na capacidade de exercício em portadores de hipertensäo pulmonar secundária a doença pulmonar obstrutiva crônica / Effects of captopril on hemodinamics, gas exchange and exercise tolerance in patients with pulmonary hypertension secondary to chronic obstructive lung disease

Captopril, um potente inibidor da enzima conversora da angiotensina, foi utilizado em pacientes com doença pulmonar obstrutiva crônica (DPOC) (média dos volumes expiratórios forçados no 1§ segundo - VEFl = 0,73 L) e hipertensäo pulmonar (média de pressäo de artéria pulmonar - PAP = 41,3 mmHg). Na primeira fase da investigaçäo, realizou-se teste de esforço por incrementos de carga, em clicoergômetro, até o limite de tolerância dos pacientes. Este estudo foi caracterizado como duplo-cego, cruzado e aleatório, onde os indivíduos receberam por via oral, placebo (Pl) ou captopril (Cp) 25 mg, em dias diferentes. Na segunda fase, os pacientes foram submetidos a estudo hemodinâmico e gasimétrico (arterial e venoso misto) na posiçäo supina, antes, 60 min após administraçäo de placebo e imediatamente após o exercício (movimentos de pedalar com os membros inferiores). Após 30 min de descanso, o mesmo protocolo foi repetido substituindo-se o placebo por captopril 25 mg. Na avaliaçäo metabólica (cicloergométrica), o captopril aumentou significativamente o consumo máximo de oxigênio (média do consumo de O2 no exercício máximo-VO2 max, Cp = 0,81 l/min vs. Pl = 0,73 l/min) e isto esteve associado a uma menor freqüência cardíaca e maior pulso de O2 no exercício máximo. No estudo hemodinâmico, os valores médios da PAP e RVP no repouso e com captopril foram similares aos obtidos com placebo, porém no exercício, estes valores foram significativamente menores quando os pacientes receberam captopril...

Lack of effect of nifedipine and pulmonary hypertension in a group of COPD decompensated patients

Se estudió el efecto del oxígeno y de la nifedipina (NFD) en la hemodinamia y el intercambio gaseoso en un grupo de 20 pacientes con enfermedad pulmonar obstructiva crónica. Los pacientes se encontraban respirando espontáneamente y fueron estudiados antes y después de recibir 30mg de NFD sublingual respirando aire u oxígeno (FIO20,40). No se encontraron cambios significativos de la presión media de la arteria pulmonar (PAP) con O2 o NFD. La resistencia vascular pulmonar (PVR) disminuyó solamente después de la administración de NFD. La presión wedge (PAPWd) y la presión auricular derecha (RAP) aumentaron con la NFD. La NFD produjo una pequeña pero significativa disminución de la PaO2 y aumento del Qva/Qt. Se encontraron correlaciones significativas entre los valores basales de PVR vs PaO2 y PvO2 (r=-0,51, p<0,02 y r=-0,63, p<0,01, respectivamente); Q vs Qva/Qt con aire o con O2 (r=0,58, p<0,01 y 0,48, p< 0,05, respectivamente); valores basales de saturación arterial de oxígeno vs cambio de la PVR producido por la NFD (r=0,65, p<0,01); Qva/Qt basal vs cambio del Qva/Qt luego de la NFD (deltaQva/Qt%) (r=0,78,p<0,01). En este grupo de pacientes la NFD no cambió la PAP, disminuyendo la PVR. La presion auricular derecha aumentó ligeramente y el trabajo ventricular derecho no cambió con la administración de NFD. Nosotros pensamos que estos dos hallazgos no son positivos en el manejo de pacientes con insuficiencia ventricular derecha. Por otro lado a NFD desmejoró ligeramente el intercambio gaseoso. Teniendo en cuenta que la NFD inhibe la vasoconstricción pulmonar hipóxica (HPV), la relación encontrada entre los valores de Qva/Qt basales y el deltaQva/Qt% producido por la NFD, demostraría que la HPV es más fuerte en aquelles pacientes descompensados que mantienen mejor intercambio gaseoso, y más débil en los que tienen peor intercambio gaseoso