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1.
Harefuah ; 151(2): 86-9, 128, 127, 2012 Feb.
Artigo em Hebraico | MEDLINE | ID: mdl-22741208

RESUMO

INTRODUCTION: Periodic breathing (PB) is evident during exercise in some patients with chronic heart failure (CHF) and is accompanied by hyperventilation. AIM: To determine whether the presence of PB predicts excessive reduced exercise capacity in patients with severe CHF relative to patient with CHF of similar severity but with no PB. METHODS: Sixty-one CHF patients underwent cardiopulmonary exercise from 2009 to 2011 as part of their evaluation for cardiac transplantation. From this data, we selected patients in which the term "periodic breathing" appeared in their report. Matching patients with CHF without PB were identified from the same pool. RESULTS: Fifteen CHF patients with PB and 18 patients with CHF with similar ejection fraction but without PB (control) were identified from the pool of 61 patients. The PB group had a lower peak oxygen uptake related to body weight (VO2/ kg] and anaerobic threshold [AT) than the control group, by 30 +/- 11 and 39 +/- 4%, respectively (p < 0.05). The ventilatory equivalent for CO2 production (VE/VCO2) at the AT was higher and the end tidal pressure of CO2 (PETCO2) was lower in the control group as compared with the PB group (p < 0.05]. VE/ VCO2 at the AT was inversely correlated with peak VO2/kg [r = -0.45, p < 0.05]. DISCUSSION: PB in patients with severe CHF is associated with excessively reduced exercise capacity. Increased ventilatory requirement may enhance dyspnea and may add to exercise limitation in these patients. CONCLUSION: Periodic breathing reflects the severity of CHF and is associated with excessively reduced exercise tolerance in patients with CHF.


Assuntos
Respiração de Cheyne-Stokes/etiologia , Tolerância ao Exercício , Insuficiência Cardíaca/fisiopatologia , Adulto , Limiar Anaeróbio , Dióxido de Carbono/metabolismo , Doença Crônica , Dispneia/etiologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Consumo de Oxigênio , Índice de Gravidade de Doença
2.
Pediatr Pulmonol ; 46(2): 193-8, 2011 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-21259450

RESUMO

BACKGROUND: Prone sleeping position, use of soft mattresses and head covering by bedclothes are known risk factors for sudden infant death syndrome (SIDS). Rebreathing carbon dioxide (CO(2) ) may be a possible mechanism or a confounding factor of SIDS. OBJECTIVE: To compare the aeration properties of a new concept of infant sleeping surface (Net) to three commercial mattresses advertised to improve aeration and to two standard infant mattresses. DESIGN: Two experiments were performed: (I) A container (head box), filled with 7% CO(2) mixture, was opened to the mattress to allow gas mixture to passively diffuse outside and equilibrate with the surrounding room air. (II) Simulation of normal breathing of an infant, using a unidirectional reciprocal syringe, to determine CO(2) accumulation within the head box. METHODS: CO(2) concentrations in the head box were continuously measured until CO(2) levels fell below 1% or for 5 min (experiment I), or until CO(2) accumulation levels plateaued or for 6 min (experiment II). RESULTS: The Net had a significantly faster rate of CO(2) elimination (88.5 ± 4.6 and 91.9 ± 0.9 sec, Net alone and when covered with a sheet, respectively) compared to 238.3 ± 14.2 sec to 387.8 ± 7.9 sec for the other mattresses (P < 0.001). Only the Net was able to prevent CO(2) accumulation with maximal CO(2) levels (0.56 ± 0.03% and 1.16 ± 0.05%; Net alone and when covered with a sheet, respectively) significantly lower than the range of 4.6-6.3% for the other mattresses (P < 0.001). CONCLUSIONS: The new sleeping surface exhibited significantly better aeration properties in dispersing CO(2) and in preventing its accumulation.


Assuntos
Leitos , Respiração , Sono/fisiologia , Dióxido de Carbono/análise , Humanos , Lactente , Recém-Nascido , Morte Súbita do Lactente/prevenção & controle
3.
Arch Phys Med Rehabil ; 90(8): 1414-7, 2009 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-19651277

RESUMO

OBJECTIVE: To study the effect of posture on the hypercapnic ventilatory responses (HCVR). DESIGN: Nonrandomized controlled study. SETTING: Rehabilitation hospital and a pulmonary institute. PARTICIPANTS: Patients with neurologically stable C(5-8) tetraplegia (n=12) and healthy control subjects (n=7). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Supine and seated forced vital capacity (FVC) and HCVR, and supine and erect blood pressure. RESULTS: FVC in the sitting position was reduced in patients with tetraplegia (52+/-13% predicted); supine FVC was 21% higher (P=.0005). In the sitting position, HCVR was lower in patients than in controls (0.8+/-0.4 vs 2.46+/-0.3 L/min/mmHg, P<.001). Supine HCVR was not significantly different between the groups. When HCVR was normalized to FVC, there was still a significant difference between patients and controls in the sitting position. Patients with tetraplegia were orthostatic (mean supine blood pressure 91+/-13 mmHg vs mean erect blood pressure 61+/-13 mmHg, respectively, P<.0001). The magnitude of the orthostatism correlated with that of the postural change in HCVR (r=.93, P<.0001). CONCLUSIONS: Respiratory muscle weakness may contribute to the attenuated HCVR in tetraplegia. However, the observation that supine HCVR is still low even when normalized to FVC suggests a central posture-dependent effect on the HCVR, which may be linked to the postural effect on arterial blood pressure.


Assuntos
Hipercapnia/fisiopatologia , Postura/fisiologia , Quadriplegia/fisiopatologia , Traumatismos da Medula Espinal/complicações , Adolescente , Adulto , Análise de Variância , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Quadriplegia/etiologia , Estatísticas não Paramétricas , Decúbito Dorsal , Capacidade Vital
4.
Arch Phys Med Rehabil ; 88(2): 262-4, 2007 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-17270528

RESUMO

OBJECTIVE: To test whether pharmacologic angiotensin-converting enzyme (ACE) inhibition in carriers of the ACE DD or DI (D, deletion; I, insertion of 287 base pairs) genotypes can simulate the genetic advantage of the II genotype and thereby enhance the conditioning effects of aerobic exercise. DESIGN: Nonrandomized controlled trial. SETTING: Pulmonary institute. PARTICIPANTS: Twelve sedentary men with controlled hypertension (5 with DD genotype, 7 with DI genotype; age, 53+/-7y) treated by ACE inhibitors (study group) and 10 patients (8 men, 2 women; 2 with DD genotype, 8 with DI genotype; age, 54+/-10y) who were treated by other antihypertensive drugs (controls). INTERVENTION: Exercise training. MAIN OUTCOME MEASURES: Training effect was measured by maximal oxygen uptake (Vo(2)max) anaerobic threshold (Vo(2AT)), and the corresponding work rates (WR) (in watts)-WRmax and WR(AT)-before and after 10 weeks of training. RESULTS: Vo(2)max increased by a mean of 10% (200mL/min) and WRmax by 14% (25W) in each group (P<.001). Vo(2AT) and WR(AT) tended to increase more in the study group (Vo(2AT): 10% [186+/-35mL/min] vs 5% [100+/-1mL/min]; P<.006; WR(AT): 19% [19+/-2W] vs 12% [11+/-3W]; P<.03; respectively). CONCLUSIONS: This study did not show an enhancement of exercise-related conditioning by pharmacologic ACE inhibition among hypertensive patients with ACE DD and DI genotypes, comparable to the advantage conferred by the II genotype.


Assuntos
Inibidores da Enzima Conversora de Angiotensina/uso terapêutico , Exercício Físico , Hipertensão/genética , Hipertensão/reabilitação , Peptidil Dipeptidase A/genética , Limiar Anaeróbio/fisiologia , Tolerância ao Exercício/fisiologia , Feminino , Deleção de Genes , Genótipo , Humanos , Hipertensão/fisiopatologia , Masculino , Pessoa de Meia-Idade , Consumo de Oxigênio/fisiologia
5.
Respiration ; 74(4): 406-10, 2007.
Artigo em Inglês | MEDLINE | ID: mdl-16679754

RESUMO

BACKGROUND: Uncertainty arises when physiological findings indicate a cardiovascular limitation but the limiting constituents within the cardiovascular system cannot be identified. OBJECTIVES: It was the aim of this study to investigate the value of two-modality exercise testing to assess effort intolerance when the cause remains obscure despite standard exercise testing. METHODS: A second modality maximal exercise test to fatigue, using either upper extremity or supine exercise, was performed following a nonconclusive standard sitting ergometry. Six patients (4 males) with a mean age of 56 +/- 22 years with severe exercise intolerance were enrolled in the study. RESULTS: In 4 of the patients, arm exercise capacity exceeded leg capacity, indicating peripheral limitation. In 1 of these patients, hemoglobin saturation decreased markedly only during sitting exercise while it remained normal during arm exercise, indicating a unique, iatrogenic abnormality. In another patient, supine leg exercise capacity exceeded sitting capacity, indicating peripheral venous limitation, and in an additional patient, leg capacity exceeded arm capacity pointing towards a central abnormality. In all 6 patients, the second modality test highlighted the correct diagnosis. CONCLUSIONS: Arm exercise that is added to a standard leg exercise may distinguish between central circulatory and peripheral vascular lower extremity limitation. Supine posture augments venous return to the heart and is useful when preload may be limiting. These modes of exercise may be added to a standard sitting or upright test in order to differentiate between central cardiovascular versus peripheral vascular (arterial or venous) causes of exercise limitation.


Assuntos
Braço/fisiologia , Fenômenos Fisiológicos Cardiovasculares , Teste de Esforço , Tolerância ao Exercício/fisiologia , Hemoglobinas/metabolismo , Perna (Membro)/fisiologia , Doenças Vasculares Periféricas/diagnóstico , Adolescente , Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Reprodutibilidade dos Testes , Testes de Função Respiratória
6.
Isr Med Assoc J ; 7(3): 151-5, 2005 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-15792258

RESUMO

BACKGROUND: One mechanism that may limit training effect in chronic obstructive pulmonary disease is the ventilatory limitation and associated dyspnea. OBJECTIVES: To minimize ventilatory limitation during training of patients with severe COPD by applying bi-level positive pressure ventilation during training in order to augment training intensity (and effect). METHODS: The study group comprised 19 patients (18 males, 1 female) with a mean age of 64 +/- 9 years. Mean forced expiratory volume in 1 second was 32 +/- 4% of predicted, and all were ventilatory-limited (exercise breathing reserve 3 +/- 9 L/min, normal > 15 L/min). The patients were randomized: 9 were assigned to training with BiPAP and 10 to standard training. All were trained on a treadmill for 2 months, twice a week, 45 minutes each time, at maximal tolerated load. Incremental maximal unsupported exercise test was performed before and at the end of the training period. RESULTS: BiPAP resulted in an increment of 94 +/- 53% in training speed during these 2 months, as compared to 41 +/- 19% increment in the control group (P < 0.005). Training with BiPAP yielded an average increase in maximal oxygen uptake of 23 +/- 16% (P < 0.005), anaerobic threshold of 11 +/- 12% (P < 0.05) and peak O2 pulse of 20 +/- 19% (P < 0.05), while peak exercise lactate concentration was not higher after training. Interestingly, in the BiPAP group, peak exercise ventilation was also 17 +/- 20% higher after training (P < 0.05). Furthermore, contrary to our expectation, at any given work rate, ventilation (and tidal volume) in the BiPAP group was higher in the post-training test as compared to the pre-training test, and the end tidal partial pressure of CO2 at 55 watts was lower, 40 +/- 4 and 38 +/- 4 mmHg respectively (P < 0.05). No improvement in exercise capacity was observed after this short training period in the control group. CONCLUSION: Pressure-supported ventilation during training is feasible in patients with severe COPD and it augments the training effect. The improved exercise tolerance was associated with higher ventilatory response and therefore lower P(ET)CO2 at equal work rates after training.


Assuntos
Terapia por Exercício , Doença Pulmonar Obstrutiva Crônica/reabilitação , Respiração Artificial , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Índice de Gravidade de Doença
7.
Clin Endocrinol (Oxf) ; 59(6): 763-7, 2003 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-14974919

RESUMO

OBJECTIVE: Primary IGF-I deficiency (Laron syndrome, LS) may decrease exercise capacity as a result of a lack of an IGF-I effect on heart, peripheral muscle or lung structure and/or function. METHODS: Eight patients (six females) who had never received treatment with IGF-I, with mean age of 36 +/- 10 (SD) years (range 21-48), weight 47 +/- 9 kg (31-61), height 126 +/- 12 cm (112-140) and body mass index of 29 +/- 4 kg/m2 (24-34), and 12 age-matched controls, underwent lung function tests and incremental cycling to the limit of tolerance (CPX, MedGraphics). Predicted values for the patients were derived from adult equations based on height. RESULTS: In LS patients, lung function was near normal; vital capacity was 84 +/- 11% of expected (66-103). Peak exercise O2-uptake and the anaerobic threshold were reduced, 57 +/- 20% of predicted and 33 +/- 9% of predicted peak (P = 0.005 vs. controls), despite normal mean exercise breathing reserve. All parameters were normal in the controls. CONCLUSION: Exercise capacity in untreated adults with LS is significantly reduced. The limitation for most patients was not ventilatory but resulted either from low cardiac output and/or from dysfunction of the peripheral muscles. However, the relative contribution of each of these elements and/or the role of poor fitness needs further study.


Assuntos
Tolerância ao Exercício , Hormônio do Crescimento/metabolismo , Fator de Crescimento Insulin-Like I/deficiência , Adulto , Estudos de Casos e Controles , Criança , Teste de Esforço , Feminino , Frequência Cardíaca , Humanos , Masculino , Pessoa de Meia-Idade , Oxigênio/sangue , Testes de Função Respiratória , Síndrome
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