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Apêndice Apêndice – Protocolo publicado na Cochrane Library Non-invasive positive pressure ventilation (CPAP or BiPAP) in cardiogenic pulmonary oedema [Protocol] FMR Vital, A Sen, AN Atallah, MTT Ladeira, BGDO Soares, KEA Burns, C Hawkes The Cochrane Database of Systematic Reviews 2005, Issue 4 Copyright © 2005 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd. DOI : 10.1002/14651858.CD005351 This version first published online: 20 July 2005 in Issue 3, 2005 Date of Most Recent Substantive Amendment: 09 May 2005 This record should be cited as: Vital FMR, Sen A, Atallah AN, Ladeira MTT, Soares BGDO, Burns KEA, Hawkes C. Non-invasive positive pressure ventilation (CPAP or BiPAP) in cardiogenic pulmonary oedema. The Cochrane Database of Systematic Reviews 2005, Issue 3. Art. No.: CD005351. DOI: 10.1002/14651858.CD005351. Abstract This is the protocol for a review and there is no abstract. The objectives are as follows: The objective of this review is to determine the effectiveness and safety of NPPV compared to standard medical therapy in adult patients with acute, or acute on chronic, cardiogenic pulmonary oedema with respect to mortality. As a secondary objective we will look at tracheal intubation rates, changes in blood gases and vital signs, hospital and intensive care unit (ICU) length of stay, effect of positive end-expiratory pressure (PEEP) levels, and bilevel NPPV vs CPAP, duration of therapy, treatment failure, complications, increase in frequence of acute myocardial infarction, compliance of patients in accepting the NPPV. Background Acute heart failure (AHF) is defined as the rapid onset of signs and symptoms secondary to abnormal cardiac function. Cardiac dysfunction can be related to systolic or diastolic dysfunction, to abnormalities in cardiac rhythm, or to pre-load and after-load mismatch. It is often life threatening and requires urgent treatment. AHF may occur with or without previous cardiac disease and can culminate in acute cardiogenic pulmonary oedema (ACPO), that is accompanied by severe respiratory distress, with crackles over the lung on ascultation, orthopnoea and O 2 saturation usually at
Apêndice failure of the cardiac pump causes increased back pressure on the pulmonary circulation leading to the extravasation of fluid. This fluid fills the alveoli, dilutes surfactant and neutralises its lubricating properties. The lungs become stiff and expansion difficult, compliance is decreased and the work of breathing is dramatically increased (Chadda 2002; Martínez 1995; Meyer 1998; Park 2001). As gravity causes most of the oedema fluid to collect at the lung bases in the upright patient, there is intrapulmonary shunting and ventilation-perfusion (V-Q) mismatching in these areas. This causes the typical radiological appearance of upper lobe blood diversion. The clinical effects of this are: hypoxaemia, increased work of breathing, anxiety and the concurrent sympathetic nervous system response - tachycardia, hypertension, peripheral vasoconstriction and diaphoresis (Allison 1991). The most common causes of ACPO are acute coronary syndromes (60-70% of patients with AHF), hypertensive crisis, dilated cardiomyopathy, acute arrhythmia, valvular regurgitation, severe aortic valve stenosis, acute severe myocarditis, cardiac tamponade and aortic dissection (ACC/AHA 1995; Gibelin 2002; Nieminen 2005; SBC 2004). Most patients with ACPO can be treated with oxygen, diuretics, nitroglycerin, morphine sulfate, nitroprusside, dobutamine, dopamine, thrombolytic or urgent surgery (ACC/AHA 1995). However, some patients require endotracheal intubation and mechanical ventilation to survive. The object of mechanical ventilation is to increases pulmonary compliance and improve oxygenation by recruiting previously collapsed alveoli (ACC/AHA 1995; Levitt 2001). However, while lifesaving, invasive ventilation may lead to complications such as infection or injury to the trachea (Keenan 1997). Additionally, endotracheal intubation and mechanical ventilation may prolong intensive care unit or hospital stay because additional time may be necessary for weaning or for managing the complications of intubation (traumatic injury to the upper and lower airway and an increased risk of ventilator associated nosocomial infections) (Pang 1998). However today it is known the same objectives can be obtained in selected patients with the use of noninvasive positive pressure ventilation (NPPV). Systematic review about NPPV in patients with chronic obstructive pulmonary disease (COPD) showed significant decreases in mortality, intubation rates, complications associated with treatment and treatment failure. It also demonstrated a rapid improvement, within the first hour, in pH, PaCO 2 and respiratory rate and a reduction in length of hospital stay (Ram 2004). There are two main forms of NPPV: continuous positive airway pressure CPAP) and bi-level positive pressure ventilation ( Bi-level or BiPAP®- Respironics, Inc, Murrysville, PA). CPAP maintains positive pressure throughout the whole respiratory cycle preventing alveoli from collapsing at the end of expiration. Thus, less energy is used re-opening stiff alveoli. This leads to an increase in lung compliance, a decrease in threshold work, a decrease in preload and afterload (Allison 1991; Bersten 1991; Martínez 1995; Rasanen 1985). CPAP improves arterial blood oxygenation (PaO 2 ) by increasing the functional residual capacity of the lungs, improving gas exchange and reducing intrapulmonary shunt. By preserving spontaneous respiratory effort, high mean airway pressures are avoided and a lower mean intrathoracic pressure develops during inspiration. This prevents the adverse cardiovascular effects associated with high intrathoracic pressures; any secondary reduction in venous return is minimised and the risk of barotrauma is potentially removed (Covelli 1982; Kelly 1997). Relief of respiratory distress with CPAP has been associated with significant haemodynamic improvement and reversal of hypertension and tachycardia (Väisänen 1987). The Bi-level combines
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FLÁVIA MARIA RIBEIRO VITAL EFETIVI
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Vital, Flávia Maria Ribeiro Efetiv
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UNIVERSIDADE FEDERAL DE SÃO PAULO
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DEDICATÓRIA A Deus, dádiva de viv
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EPÍGRAFE “A vida é curta, A art
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4.6.3 Incidência de IAM durante a
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LISTA DE FIGURAS Figura 1. Fluxogra
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Figura 25. Gráfico de metanálise
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LISTA DE ABREVIATURAS BiPAP - Bi-le
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RESUMO
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Resumo com pressão positiva não-i
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Introdução 2 Insuficiência card
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Introdução 4 respiratório, além
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Objetivos 7 2.1 Objetivos primário
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Métodos 9 3.1 Modelo de estudo Rev
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Métodos 11 3.3.4.2 Desfechos secun
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Métodos 13 or #24 or #25 ) or #35
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Métodos 15 grupo intervenção ant
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Métodos 17 publicação (Egger et
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Resultados 19 4.1 Busca dos estudos
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Resultados 21 4.2 Desenho dos estud
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Resultados 23 QUADRO 1. CARACTERÍS
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Resultados 25 Takeda et al, 1998; S
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Resultados 27 Ao realizarmos a aná
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Resultados 29 dados, aos excluirmos
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Resultados 31 Figura 8. Gráfico de
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Resultados 33 Figura 11. Gráfico d
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Resultados 35 4.6.2.3 NPPV bi-level
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Resultados 39 4.6.3.4 CPAP versus N
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Resultados 41 2001), num total de 1
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Resultados 43 4. 6.5.3 NPPV bi-leve
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Resultados 45 Figura 29. Riscos rel
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Resultados 47 4. 6.6.1.5 Distensão
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Resultados 51 Não houve diferença
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Resultados 53 4. 6.6.2.13 Convulsã
Page 80 and 81: Resultados 55 4. 6.6.3.5 Vômito Do
Page 82 and 83: Resultados 57 de 266 pacientes. Nã
Page 84 and 85: Resultados 59 4. 6.8.3 NPPV bi-leve
Page 86 and 87: Resultados 61 4.6.9.2 CPAP versus T
Page 88 and 89: Resultados 63 variação de normali
Page 90 and 91: Resultados 65 entre os grupos em re
Page 92 and 93: Resultados 67 Figura 51. Gráfico d
Page 94 and 95: Resultados 69 relação a PAS após
Page 96 and 97: Resultados 71 heterogeneidade, uma
Page 102 and 103: Resultados 77 4.7 Pesquisa de viés
Page 104 and 105: Discussão 79 Os resultados dos 21
Page 106 and 107: Discussão 81 reforça a idéia de
Page 108 and 109: Discussão 83 Nosso estudo não apr
Page 110 and 111: Discussão 85 que apresentavam indi
Page 112 and 113: Discussão 87 Figura 72. Gráfico d
Page 114 and 115: Discussão 89 da heterogeneidade, a
Page 120 and 121: Discussão 95 ventilados mecanicame
Page 122 and 123: Conclusões 97 6.1 Implicações pa
Page 124 and 125: Anexos 97 Anexo 1 - Ficha para cole
Page 126 and 127: Anexos 99 Anexo 2 - Característica
Page 128 and 129: Anexos 101 Niranjan 1998 Panacek 20
Page 132 and 133: Apêndice pressure support on inspi
Page 134 and 135: Apêndice • Length of Intensive C
Page 136 and 137: Apêndice Selection of studies and
Page 138 and 139: Apêndice • Department of Interna
Page 140 and 141: Apêndice Covelli 1982 Covelli HD,
Page 142 and 143: Apêndice http://publicacoes.cardio
Page 144 and 145: Referências Bibliográficas 116 1.
Page 146 and 147: Referências Bibliográficas 118 pr
Page 148 and 149: Referências Bibliográficas 120 44
Page 150 and 151: Referências Bibliográficas 122 65
Page 152 and 153: ABSTRACT
Page 154 and 155: BIBLIOGRAFIA CONSULTADA
Page 156 and 157: Biliografia Consultada 11. Brochard
Page 158 and 159: Biliografia Consultada 33. Jackson
Page 160 and 161: Biliografia Consultada 55. Mollica
Page 162: Biliografia Consultada 76. Salvucci
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