I have a question on the August talk on intubation of asthmatic patients. I don't quite understand how physiologically going from bi-level positive pressure to intubating would be that much worse for preload. I see that an ET tube adds all its negative effects of infection time on vent.... I do not understand how the BIPAP 12/6 with a good mask seal is not going to affect the preload and hemodynamics? If we are not using as high of a driving pressure to get the breath in the I time should be fairly short and a lower peep with a long expiration should allow more venous return in a non air trapping asthmatic? Pleas help me understand this better.
William: You are correct in that there are similarities with BiPAP and Endotracheal intubation. Both use external pressure to assist inspiration and have a pressure against which the patient exhales. The big difference though is that with BiPAP the patient still uses his or her own muscles to initiate and create a negative pressure for inspiration. The IPAP only assists with this action whereas with an intubated patient there is no negative intra-thoracic component to breathing and the breath is entirely driven by positive pressure. For exhalation, the EPAP creates a resistance against the expired breath, but the patient's chest muscles still actively force air out of the lungs. In intubated patients, especially those who are paralyzed, it is only elastic recoil the produces exhalation. It is exhalation that is the problem with these patients and the loss of active contraction of the chest wall leads to air trapping in a paralyzed asthmatic. This is why you may see clinicians squeeze the chest wall of an intubated asthmatic.
In addition the loss of negative intrathoracic pressure during inspiration coupled with it's replacement with only positive airway pressure leads to a much greater decreased venous return. As a result, blood pressures can drop quickly in intubated asthmatic children, especially if they are dehydrated from their tachypnea and lack of oral intake.
Bottom line both BiPAP and ETI screw up cardiopulmonary physiology, but BiPAP just does it to a lesser degree.
Thanks for you thoughts.
Al
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William K. - August 31, 2022 5:58 PM
I have a question on the August talk on intubation of asthmatic patients. I don't quite understand how physiologically going from bi-level positive pressure to intubating would be that much worse for preload. I see that an ET tube adds all its negative effects of infection time on vent.... I do not understand how the BIPAP 12/6 with a good mask seal is not going to affect the preload and hemodynamics? If we are not using as high of a driving pressure to get the breath in the I time should be fairly short and a lower peep with a long expiration should allow more venous return in a non air trapping asthmatic? Pleas help me understand this better.
Alfred S. - September 2, 2022 5:21 PM
William: You are correct in that there are similarities with BiPAP and Endotracheal intubation. Both use external pressure to assist inspiration and have a pressure against which the patient exhales. The big difference though is that with BiPAP the patient still uses his or her own muscles to initiate and create a negative pressure for inspiration. The IPAP only assists with this action whereas with an intubated patient there is no negative intra-thoracic component to breathing and the breath is entirely driven by positive pressure. For exhalation, the EPAP creates a resistance against the expired breath, but the patient's chest muscles still actively force air out of the lungs. In intubated patients, especially those who are paralyzed, it is only elastic recoil the produces exhalation. It is exhalation that is the problem with these patients and the loss of active contraction of the chest wall leads to air trapping in a paralyzed asthmatic. This is why you may see clinicians squeeze the chest wall of an intubated asthmatic.
In addition the loss of negative intrathoracic pressure during inspiration coupled with it's replacement with only positive airway pressure leads to a much greater decreased venous return. As a result, blood pressures can drop quickly in intubated asthmatic children, especially if they are dehydrated from their tachypnea and lack of oral intake.
Bottom line both BiPAP and ETI screw up cardiopulmonary physiology, but BiPAP just does it to a lesser degree.
Thanks for you thoughts.
Al