I have read some postings with regards to this vent, which i have no experience in using. Is it a beneficial vent to have in your arsenal? Would you purchase one if you didn't currently have one? Is there any comparison to using an IPV with the CMV vent adaptors? I would like to hear about your thoughts and experiences? Also, Can an IPV with adaptors be used in conjunction with the Drager XL.
Chris Hanson RN, RRT-NPS, CPFT, AE-C
ER Registered Nurse
Grand Junction, Colorado
The vdr is a great vent to have in you bag. especially if you have a trauma and or burn center. The are wonderfull to recruit the atelectatic patient, secretion removal issue patient, and even pulmonary hypertension patient. They require alot of education on how the machine works as well as great understanding of effects of Raw and Cs on ventilation. This is one of my favorite vents to use on the right patients. I wish Iworked more often so that I could use it even more.
asfar as IPV with the XL, they work fine together. Best way is too turn flowmonitoring off, ATC off and change the patient to PCV+assist. You will then need to closely monitor patient while IPV is inline (about 20 min)Other possibilities is to get a IPV 2C that allows for CPAP to be added and then just attach the ETT or Trach to the tube itself.
I'm not sure about the Drager, but not too long ago we used IPV in-line with the ServoI (PCV) on a patient with RUL Cocci pneumonia and it worked great.
We used the cone adaptor at the ET Tube and ran it continuous for 12hr and couldn't keep up with the secretions it was mobilizing...the ET tube ended up occluding, the stuff was so thick. It was the only intervention that improved the X-ray including bronchoscopy.
It was labeled, "Poorman's VDR4". LOL!
The December supplement of Critical Care Medicine is all about new stuff in CPR. It is a fascinating issue---stuff on the impedance monitor, down-regulating the mitochondria to reduce repefusion injury (some studies have shown that FIO2/PaO2 reduction does the same---I guess it's either supply or demand side reduction of oxygen radicals and what can make the most money gets the prime time..or what is feasible)...anyway
One of the subjects...
"Endothelium and cardiopulmonary resuscitation.
Critical Care Medicine. Eighth Wolf Creek Conference on CPR: Addressing the Scientific Basis of Reanimation. 34(12) Suppl:S458-S465, December 2006.
Adams, Jose A. MD
The endothelium is a viable target for injury, repair and cellular modulation. Because of its vast extension and active metabolic status of producing mediators for vasomotor tone, coagulation, and inflammation, it is a key target for therapy during ischemia/reperfusion injury. Cardiopulmonary resuscitation is a model of whole-body ischemia/reperfusion injury. It has become apparent that the endothelium participates in a host of responses elicited by ischemia/reperfusion. This review examines the role of the endothelium during and after ischemia/reperfusion and the participation by its mediators and evidence for endothelial involvement during and after cardiopulmonary resuscitation. The strategic location of the endothelium makes it an excellent signal transduction mechanism for a host of disease processes. In addition to biochemical stimuli, mechanical stimulation of the endothelium elicits production of several mediators, including endothelium-derived nitric oxide, prostaglandins, and antithrombotics and anticoagulants. Whole-body, periodic acceleration is a novel method of stimulating the endothelium via pulsatile shear stress. Periodic acceleration has been shown to be an effective experimental method of cardiopulmonary resuscitation, with evidence of postresuscitation cardioprotective effects. This review indicates that understanding endothelial modulation during and after ischemia/reperfusion will significantly improve therapeutic choices."
OK guys "whole body periodic acceleration" as a therapeutic option isn't just a come on line. (But why not keep it in mind for that special pitch?).... The article describes ..
"Mechanical Method to Stimulate the Endothelium TOP
Our laboratory has pioneered the use of a noninvasive method to stimulate the endothelium via pulsatile shear stress. Whole-body, periodic acceleration (pGz) is the motion of the supine body back and forth (headward to footward), similar to that which occurs when a mother pushes a carriage back and forth. In addition to the native heart rate, pGz increases vascular pulsations in both animal models and humans. In a cardiac arrest animal model, pGz produces sufficient forward blood flow to meet critical organ blood flow needs and to maintain ventilation. The mechanical mechanisms by which movement of blood and ventilation occur using pGz have been previously reported (100-104). Our laboratory has studied some of the biochemical effects produced by pGz in animal models, isolated vessels, and humans (87, 104-107). Application of pGz to healthy animals for 1 hr induces production of NO, prostacyclin, prostaglandin E2 and tissue plasminogen activator antigen (t-PAag) and its measured activity (Fig. 4). These changes take place without change in endothelin 1 or increase in procoagulant activity (105). In both isolated perfused vessels, and human volunteers, pGz also increased eNO (105, 106)."
I wonder if IPV and the VDR confer such a benefit, even if only localized to the endothelium of the lungs and adjacent tissues. ?