RESUMO
The pathophysiological mechanisms associated with the effects of red blood cell (RBC) transfusion on cardiopulmonary function and inflammation are unclear. We developed an experimental model of homologous 14-days stored RBC transfusion in hypovolemic swine to evaluate the short-term effects of transfusion on cardiopulmonary system and inflammation. Sixteen healthy male anesthetized swine (68±3.3 kg) were submitted to controlled hemorrhage (25% of blood volume). Two units of non-filtered RBC from each animal were stored under blood bank conditions for 14 days. After 30 min of hypovolemia, the control group (n=8) received an infusion of lactated Ringer's solution (three times the removed volume). The transfusion group (n=8) received two units of homologous 14-days stored RBC and lactated Ringer's solution in a volume that was three times the difference between blood removed and blood transfusion infused. Both groups were followed up for 6 h after resuscitation with collection of hemodynamic and respiratory data. Cytokines and RNA expression were measured in plasma and lung tissue. Stored RBC transfusion significantly increased mixed oxygen venous saturation and arterial oxygen content. Transfusion was not associated with alterations on pulmonary function. Pulmonary concentrations of cytokines were not different between groups. Gene expression for lung cytokines demonstrated a 2-fold increase in mRNA level for inducible nitric oxide synthase and a 0.5-fold decrease in mRNA content for IL-21 in the transfused group. Thus, stored homologous RBC transfusion in a hypovolemia model improved cardiovascular parameters but did not induce significant effects on microcirculation, pulmonary inflammation and respiratory function up to 6 h after transfusion.
Assuntos
Animais , Masculino , Pneumonia/fisiopatologia , Fenômenos Fisiológicos Respiratórios , Preservação de Sangue/métodos , Fenômenos Fisiológicos Cardiovasculares , Transfusão de Eritrócitos/métodos , Hipovolemia/terapia , Suínos , Preservação de Sangue/efeitos adversos , Ensaio de Imunoadsorção Enzimática , Citocinas/sangue , Resultado do Tratamento , Transfusão de Eritrócitos/efeitos adversos , Modelos Animais de Doenças , HemodinâmicaRESUMO
The pathophysiological mechanisms associated with the effects of red blood cell (RBC) transfusion on cardiopulmonary function and inflammation are unclear. We developed an experimental model of homologous 14-days stored RBC transfusion in hypovolemic swine to evaluate the short-term effects of transfusion on cardiopulmonary system and inflammation. Sixteen healthy male anesthetized swine (68±3.3 kg) were submitted to controlled hemorrhage (25% of blood volume). Two units of non-filtered RBC from each animal were stored under blood bank conditions for 14 days. After 30 min of hypovolemia, the control group (n=8) received an infusion of lactated Ringer's solution (three times the removed volume). The transfusion group (n=8) received two units of homologous 14-days stored RBC and lactated Ringer's solution in a volume that was three times the difference between blood removed and blood transfusion infused. Both groups were followed up for 6 h after resuscitation with collection of hemodynamic and respiratory data. Cytokines and RNA expression were measured in plasma and lung tissue. Stored RBC transfusion significantly increased mixed oxygen venous saturation and arterial oxygen content. Transfusion was not associated with alterations on pulmonary function. Pulmonary concentrations of cytokines were not different between groups. Gene expression for lung cytokines demonstrated a 2-fold increase in mRNA level for inducible nitric oxide synthase and a 0.5-fold decrease in mRNA content for IL-21 in the transfused group. Thus, stored homologous RBC transfusion in a hypovolemia model improved cardiovascular parameters but did not induce significant effects on microcirculation, pulmonary inflammation and respiratory function up to 6 h after transfusion.
Assuntos
Preservação de Sangue/métodos , Fenômenos Fisiológicos Cardiovasculares , Transfusão de Eritrócitos/métodos , Hipovolemia/terapia , Pneumonia/fisiopatologia , Fenômenos Fisiológicos Respiratórios , Animais , Preservação de Sangue/efeitos adversos , Citocinas/sangue , Modelos Animais de Doenças , Ensaio de Imunoadsorção Enzimática , Transfusão de Eritrócitos/efeitos adversos , Hemodinâmica , Masculino , Oxigênio/metabolismo , Reprodutibilidade dos Testes , Ressuscitação/métodos , Suínos , Fatores de Tempo , Resultado do TratamentoRESUMO
BACKGROUND: The functional haemodynamic variables pulse pressure variation (PPV), stroke volume variation (SVV), and systolic pressure variation (SPV) are widely used to assess haemodynamic status. However, it is not known how these perform during acute lung injury (ALI). This study evaluated the effects of different ventilatory strategies on haemodynamic parameters in pigs with ALI during normovolaemia and hypovolaemia. METHODS: Eight anaesthetized Agroceres pigs [40 (1.9) kg] were instrumented with pulmonary artery, PiCCO, and arterial catheters and ventilated. Three ventilatory settings were randomly assigned for 10 min each: tidal volume (VT) 15 ml kg(-1) and PEEP 5 cm H(2)O, VT 8 ml kg(-1) and PEEP 13 cm H(2)O, or VT 6 ml kg(-1) and PEEP 13 cm H(2)O. Data were collected at each setting at baseline, after ALI (lung lavage+Tween 1.5%), and ALI with hypovolaemia (haemorrhage to 30% of estimated blood volume). RESULTS: At baseline, high VT increased PPV, SVV, and SPV (P<0.05 for all). During ALI, high VT significantly increased PPV and SVV [(P = 0.002 and P = 0.008) respectively.]. After ALI with hypovolaemia, ventilation at VT 6 ml kg(-1) and PEEP 13 cm H(2)O decreased the accuracy of functional haemodynamic variables to predict hypovolaemia, with the exception of PPV (area under the curve 0.875). The parameters obtained by PiCCO were less influenced by ventilatory changes. CONCLUSIONS: VT is the ventilatory parameter which influences functional haemodynamics the most. During ventilation with low VT and high PEEP, most functional variables are less able to accurately predict hypovolaemia secondary to haemorrhage, with the exception of PPV.
Assuntos
Lesão Pulmonar Aguda/fisiopatologia , Hipovolemia/fisiopatologia , Respiração com Pressão Positiva/métodos , Animais , Modelos Animais de Doenças , Hemodinâmica/fisiologia , Hemorragia/complicações , Hipovolemia/diagnóstico , Hipovolemia/etiologia , Monitorização Fisiológica/métodos , Sus scrofa , Volume de Ventilação Pulmonar/fisiologiaRESUMO
BACKGROUND: Patients with idiopathic pulmonary fibrosis (IPF) present an important ventilatory limitation reducing their exercise capacity. Non-invasive ventilatory support has been shown to improve exercise capacity in patients with obstructive diseases; however, its effect on IPF patients remains unknown. OBJECTIVE: The present study assessed the effect of ventilatory support using proportional assist ventilation (PAV) on exercise capacity in patients with IPF. METHODS: Ten patients (61.2+/-9.2 year-old) were submitted to a cardiopulmonary exercise testing, plethysmography and three submaximal exercise tests (60% of maximum load): without ventilatory support, with continuous positive airway pressure (CPAP) and PAV. Submaximal tests were performed randomly and exercise capacity, cardiovascular and ventilatory response as well as breathlessness subjective perception were evaluated. Lactate plasmatic levels were obtained before and after submaximal exercise. RESULTS: Our data show that patients presented a limited exercise capacity (9.7+/-3.8 mL O(2)/kg/min). Submaximal test was increased in patients with PAV compared with CPAP and without ventilatory support (respectively, 11.1+/-8.8 min, 5.6+/-4.7 and 4.5+/-3.8 min; p<0.05). An improved arterial oxygenation and lower subjective perception to effort was also observed in patients with IPF when exercise was performed with PAV (p<0.05). IPF patients performing submaximal exercise with PAV also presented a lower heart rate during exercise, although systolic and diastolic pressures were not different among submaximal tests. Our results suggest that PAV can increase exercise tolerance and decrease dyspnoea and cardiac effort in patients with idiopathic pulmonary fibrosis.
Assuntos
Tolerância ao Exercício/fisiologia , Fibrose Pulmonar Idiopática/fisiopatologia , Ventilação Pulmonar/fisiologia , Idoso , Antropometria , Teste de Esforço , Feminino , Humanos , Fibrose Pulmonar Idiopática/reabilitação , Masculino , Pessoa de Meia-Idade , Consumo de OxigênioRESUMO
We evaluated the recovery of cardiovascular function after transient cardiogenic shock. Cardiac tamponade was performed for 1 h and post-shock data were collected in 5 domestic large white female pigs (43 +/- 5 kg) for 6 h. The control group (N = 5) was observed for 6 h after 1 h of resting. During 1 h of cardiac tamponade, experimental animals evolved a low perfusion status with a higher lactate level (8.0 +/- 2.2 vs 1.9 +/- 0.9 mEq/L), lower standard base excess (-7.3 +/- 3.3 vs 2.0 +/- 0.9 mEq/L), lower urinary output (0.9 +/- 0.9 vs 3.0 +/- 1.4 mL x kg(-1) x h(-1)), lower mixed venous saturation, higher ileum partial pressure of CO2-end tidal CO2 (EtCO2) gap and a lower cardiac index than the control group. Throughout the 6-h recovery phase after cardiac tamponade, tamponade animals developed significant tachycardia with preserved cardiac index, resulting in a lower left ventricular stroke work, suggesting possible myocardial dysfunction. Vascular dysfunction was present with persistent systemic hypotension as well as persistent pulmonary hypertension. In contrast, oliguria, hyperlactatemia and metabolic acidosis were corrected by the 6th hour. The inflammatory characteristics were an elevated core temperature and increased plasma levels of interleukin-6 in the tamponade group compared to the control group. We conclude that cardiovascular recovery after a transient and severe low flow systemic state was incomplete. Vascular dysfunction persisted up to 6 h after release of tamponade. These inflammatory characteristics may also indicate that inflammatory activation is a possible pathway involved in the pathogenesis of cardiogenic shock.
Assuntos
Tamponamento Cardíaco/fisiopatologia , Hipotensão/fisiopatologia , Choque Cardiogênico/fisiopatologia , Síndrome de Resposta Inflamatória Sistêmica/fisiopatologia , Animais , Tamponamento Cardíaco/sangue , Feminino , Hipotensão/etiologia , Recuperação de Função Fisiológica , Choque Cardiogênico/sangue , Suínos , Síndrome de Resposta Inflamatória Sistêmica/etiologia , Fatores de TempoRESUMO
We evaluated the recovery of cardiovascular function after transient cardiogenic shock. Cardiac tamponade was performed for 1 h and post-shock data were collected in 5 domestic large white female pigs (43 ± 5 kg) for 6 h. The control group (N = 5) was observed for 6 h after 1 h of resting. During 1 h of cardiac tamponade, experimental animals evolved a low perfusion status with a higher lactate level (8.0 ± 2.2 vs 1.9 ± 0.9 mEq/L), lower standard base excess (-7.3 ± 3.3 vs 2.0 ± 0.9 mEq/L), lower urinary output (0.9 ± 0.9 vs 3.0 ± 1.4 mL·kg-1·h-1), lower mixed venous saturation, higher ileum partial pressure of CO2-end tidal CO2 (EtCO2) gap and a lower cardiac index than the control group. Throughout the 6-h recovery phase after cardiac tamponade, tamponade animals developed significant tachycardia with preserved cardiac index, resulting in a lower left ventricular stroke work, suggesting possible myocardial dysfunction. Vascular dysfunction was present with persistent systemic hypotension as well as persistent pulmonary hypertension. In contrast, oliguria, hyperlactatemia and metabolic acidosis were corrected by the 6th hour. The inflammatory characteristics were an elevated core temperature and increased plasma levels of interleukin-6 in the tamponade group compared to the control group. We conclude that cardiovascular recovery after a transient and severe low flow systemic state was incomplete. Vascular dysfunction persisted up to 6 h after release of tamponade. These inflammatory characteristics may also indicate that inflammatory activation is a possible pathway involved in the pathogenesis of cardiogenic shock.
Assuntos
Animais , Feminino , Tamponamento Cardíaco/fisiopatologia , Hipotensão/fisiopatologia , Choque Cardiogênico/fisiopatologia , Síndrome de Resposta Inflamatória Sistêmica/fisiopatologia , Tamponamento Cardíaco/sangue , Hipotensão/etiologia , Recuperação de Função Fisiológica , Suínos , Choque Cardiogênico/sangue , Síndrome de Resposta Inflamatória Sistêmica/etiologia , Fatores de TempoRESUMO
The mortality rate of severe sepsis is still high (20 to 65%) despite the advances in critical care. The most important determinant of the prognosis in this condition is the occurrence of multiple organ dysfunction syndrome (MODS). The lung is the most frequently identified organ to fail in sepsis and is also the most frequent primary site of infection. The development of acute respiratory distress syndrome (ARDS) is common in those cases. The current understanding of the pathogenesis of ARDS suggests that the degree of inflammatory response and its sustained leukocyte activation may determine the clinical evolution of ARDS. The way that mechanical ventilation is delivered is responsible for the start and/or the perpetuation of a pro-inflammatory cascade activation that, due to the loss of the alveolar compartmentalization in ARDS, can reach the bloodstream and induce MODS. On the other hand, during sepsis, the alveolar compartmentalization is lost, allowing the passage of cytokines, released to the bloodstream by any other organ, to the pulmonary endothelium. These cytokines, especially IL-1, TNF-alpha and IL-8, have important roles in the lung dysfunction. Experimental and clinical studies have been demonstrated that ventilation strategies using low tidal volumes and limitation of airway pressures can block cytokines and reduce mortality of patients with respiratory failure. The studies are still insufficient to determine the role of pharmacological therapies in those patients.
Assuntos
Síndrome do Desconforto Respiratório/microbiologia , Sepse/microbiologia , Animais , Humanos , Pulmão/microbiologia , Síndrome do Desconforto Respiratório/sangue , Síndrome do Desconforto Respiratório/imunologia , Sepse/sangue , Sepse/imunologiaRESUMO
OBJECTIVE: To study the mask mechanics and air leak dynamics during noninvasive pressure support ventilation. SETTING: Laboratory of a university hospital. DESIGN: A facial mask was connected to a mannequin head that was part of a mechanical respiratory system model. The mask fit pressure (P(mask-fit)) measured inside the mask's pneumatic cushion was adjusted to 25 cmH(2)O using elastic straps. Pressure support (PS) was set to ensure a maximal tidal volume distal to the mask (VT(distal)) but avoiding failure to cycle to exhalation. MEASUREMENTS: Airway pressure (P(aw)), P(mask-fit), mask occlusion pressure (P(mask-occl)=P(mask-fit)-P(aw)), VT proximal (VT(prox)), distal to the mask (VT(distal)), air leak volume ( Leak=VT(prox)-VT(distal)), and inspiratory air leak flow rate (difference between inspiratory flow proximal and distal to the mask) were recorded. RESULTS: PS 15 cmH(2)O was the highest level that could be used without failure to cycle to exhalation (VT(distal) of 585+/-4 ml, leak of 32+/-1 ml or 5.2+/-0.2% of VT(prox), and a minimum P(mask-occl) of 1.7+/-0.1 cmH(2)O). During PS 16 cmH(2)O the P(mask-occl) dropped to 1.1+/-0.1 cmH(2)O, and at this point all flow delivered by the ventilator leaked around the mask, preventing the inspiratory flow delivered by the ventilator from reaching the expiratory trigger threshold. CONCLUSION: P(mask-fit) and P(mask-occl) can be easily measured in pneumatic cushioned masks and the data obtained may be useful to guide mask fit and inspiratory pressure set during noninvasive positive pressure ventilation.
Assuntos
Máscaras , Respiração com Pressão Positiva/instrumentação , Análise de Falha de Equipamento , Humanos , Manequins , Mecânica RespiratóriaRESUMO
A insuficiência cardíaca congestiva leva a aumento na água extravascular pulmonar, redução do volume e da complacência pulmonar e aumento da resistência de vias aéreas, resultando em aumento do trabalho respiratório, aumento do consumo de oxigênio e aumento da sobrecarga ventricular esquerda. A utilização de pressão positiva contínua nesses pacientes melhora a oxigenação, diminui o trabalho respiratório, melhora a mecânica pulmonar, reduz a pressão transmural sobre o ventrículo esquerdo e diminui o retorno venoso, contribuindo para maior desempenho cardíaco. O uso de pressão positiva contínua diminui a necessidade de ventilação mecânica no edema agudo de pulmão e reduz o tempo de internação na unidade de terapia intensiva. A utilização de pressão positiva contínua noturna em cardiopatas crônicos demonstrou melhora significativa da fração de ejeção durante o dia, em associação com melhora da classe funcional, após o tratamento por um mês em pacientes com cardiomiopatia dilatada e apnéia obstrutiva do sono concomitante. O uso de pressão positiva contínua deve ser entendido não só como o primeiro suporte ventilatório no edema agudo dos pulmöes, como também um tratamento não-farmacológico que tem o potencial de melhorar a função cardíaca nos pacientes clinicamente estáveis, porém com insuficiência cardíaca grave.
Assuntos
Humanos , Cardiopatias , Insuficiência Cardíaca , Respiração com Pressão Positiva , Edema Pulmonar , Insuficiência RespiratóriaRESUMO
BACKGROUND: In patients with the acute respiratory distress syndrome, massive alveolar collapse and cyclic lung reopening and overdistention during mechanical ventilation may perpetuate alveolar injury. We determined whether a ventilatory strategy designed to minimize such lung injuries could reduce not only pulmonary complications but also mortality at 28 days in patients with the acute respiratory distress syndrome. METHODS: We randomly assigned 53 patients with early acute respiratory distress syndrome (including 28 described previously), all of whom were receiving identical hemodynamic and general support, to conventional or protective mechanical ventilation. Conventional ventilation was based on the strategy of maintaining the lowest positive end-expiratory pressure (PEEP) for acceptable oxygenation, with a tidal volume of 12 ml per kilogram of body weight and normal arterial carbon dioxide levels (35 to 38 mm Hg). Protective ventilation involved end-expiratory pressures above the lower inflection point on the static pressure-volume curve, a tidal volume of less than 6 ml per kilogram, driving pressures of less than 20 cm of water above the PEEP value, permissive hypercapnia, and preferential use of pressure-limited ventilatory modes. RESULTS: After 28 days, 11 of 29 patients (38 percent) in the protective-ventilation group had died, as compared with 17 of 24 (71 percent) in the conventional-ventilation group (P<0.001). The rates of weaning from mechanical ventilation were 66 percent in the protective-ventilation group and 29 percent in the conventional-ventilation group (P=0.005): the rates of clinical barotrauma were 7 percent and 42 percent, respectively (P=0.02), despite the use of higher PEEP and mean airway pressures in the protective-ventilation group. The difference in survival to hospital discharge was not significant; 13 of 29 patients (45 percent) in the protective-ventilation group died in the hospital, as compared with 17 of 24 in the conventional-ventilation group (71 percent, P=0.37). CONCLUSIONS: As compared with conventional ventilation, the protective strategy was associated with improved survival at 28 days, a higher rate of weaning from mechanical ventilation, and a lower rate of barotrauma in patients with the acute respiratory distress syndrome. Protective ventilation was not associated with a higher rate of survival to hospital discharge.