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Conventional CPR is inherently inefficient at supplying proper blood flow and cardiac output to patients.  During CPR, we rely on negative pressure, or the formation of a vacuum, to refill the heart during chest recoil.  But, during chest recoil, air rushes in through the open airway and can almost completely wipe out the vacuum needed to return blood to the heart.  Then you compress again, but very little blood gets circulated because of that.  It’s a vicious cycle that can happen during CPR.
Enter the ResQPOD….
How does a ResQPOD work?
First, remember that the ResQPOD works to enhance CIRCULATION.  It works during CHEST WALL RECOIL, not during ventilations; therefore it’s primarily a circulation device, not a ventilation device!
So, during the chest wall recoil phase, the ResQPOD prevents air from rushing into the chest, enhancing the vacuum in the chest.  It’s seriously as simple as that…

Enhanced vacuum results in greater preload of the heart (increased venous return) and more blood flow to the heart muscle itself.  The vacuum created can also lower intracranial pressure.
Increased preload = increased cardiac output.
Increased cardiac output = increased blood flow to the vital organs.
Because the impedance happens when a negative pressure is applied on the patient side of the ResQPOD, it is extremely difficult for patients to take a breath through it.  Keep in mind that once a spontaneous pulse has returned and you are no longer performing CPR, the ResQPOD should be removed. 


  • If the ResQPOD becomes clogged or has secretions in it, it needs to be removed.
  • Once spontaneous circulation has returned, ResQPOD needs to be removed.


  • PEEP should be off (or at least minimal) while using the ResQPOD.



Up-To-Date (10-13-2015)
INSPIRATORY IMPEDANCE THRESHOLD DEVICES — An inspiratory impedance threshold device (ITD) is designed to modulate intrathoracic pressures during passive inspiration after positive pressure ventilation in order to enhance return of blood to the heart during cardiopulmonary resuscitation (CPR). The device is a plastic appliance with a silicone diaphragm placed between the airway and the bag ventilator.
The generation of negative intrathoracic pressure during passive or active decompression of the chest wall during chest compressions increases venous return to the heart (ie, preload). Without an ITD, passive airflow into the patient's airways during either active or passive decompression of the chest wall during CPR mitigates the generation of negative intrathoracic pressures, resulting in decreased venous return (preload) [6,7]. Decreased venous return results in lower systolic blood pressures generated with active chest compressions.
The ITD permits positive pressure ventilation and exhalation but prevents the flow of air into the patient's airway during chest wall relaxation. Employing an ITD during active or passive decompression of the chest with CPR augments negative intrathoracic pressures and improves both preload and myocardial perfusion.
Most studies of ITDs have been done with active compression-decompression CPR and therefore cannot be directly extrapolated to all types of CPR [8,9]. Nevertheless, ITDs are likely to augment all types of CPR and should not affect standard CPR guidelines, such as the compression to ventilation ratio (30 to 2).
The ITD is effective at enhancing the generation of negative intrathoracic pressures in patients ventilated using a bag-mask, but correlation with improved clinical outcomes in these patients remains unproven [10]. When the ITD is used as part of bag-mask ventilation, it is crucial to maintain a good mask seal, and for this reason a two-person ventilation technique is recommended. (See "Basic airway management in adults".)
Clinical trials of ITDs have reported mixed results:
●In a multicenter trial in which 400 out-of-hospital cardiac arrest patients received treatment with active compression-decompression CPR and were randomly assigned to ventilation incorporating either an active ITD or a sham device, survival at 24 hours (primary endpoint) was achieved in 32 percent of patients in the ITD group and 22 percent in the sham group (odds ratio [OR] 1.64; 95% CI 1.07-2.6) [11]. Among patients who survived to hospital discharge, 6 of 10 in the ITD group had normal neurologic function compared with 1 of 8 in the sham group, but this outcome did not reach statistical significance.
●In a study of 230 cardiac arrest patients, 25 percent of those randomly assigned to resuscitation incorporating an ITD survived to ICU admission versus 17 percent of patients whose treatment involved a sham device [12]. Planned post-hoc analyses based on arrhythmias found that among patients with pulseless electrical activity (PEA) at any time during resuscitation, those treated with an ITD had higher ICU admission and 24 hour survival rates (41 and 27 percent) compared with patients not treated with an ITD (20 and 11 percent) (OR for ICU admission 2.82; 95% CI 1.19-6.67) (OR for 24 hour survival 3.01; 95% CI 1.07-8.96).
●Conversely, in a multicenter prospective trial of 8718 cardiac arrest patients given CPR and randomly assigned to treatment with an ITD or a sham device, no significant difference was found in neurologically satisfactory (modified Rankin score <3) survival (254 [5.8 percent] survivors in the active ITD group versus 260 [6 percent] survivors in the sham ITD group) [13]. In addition, there was no difference between groups in adverse events or in secondary outcomes, including return of spontaneous circulation on arrival or survival to hospital discharge.
Recommendations — The 2010 ACLS Guidelines state that ITDs may be used by trained personnel in adult cardiac arrest. However, these Guidelines were published prior to the publication of the large negative trial described above [13]. It remains to be determined whether ITDs may benefit particular subgroups of cardiac arrest patients (eg, those treated with active compression-decompression CPR) and therefore further research with ITDs is justified.




I would like to thank Ross Armstrong RRT for submitting this presentation:

Extracorporeal Membrane Oxygenation:  ECMO

Extracorporeal Membrane Oxygenation (ECMO) is a form of cardiopulmonary life-support which has widespread use in the neonatal and pediatric population of patients suffering from cardiac failure and/or refractory respiratory failure.  Even with the widespread use with neonates and pediatrics, the adult population has been slow to adapt the use of cardiopulmonary bypass or ECMO outside of the CVOR.
Recent (past 5 years or so) advances in technology and reports from studies of ECMO use on adult patients suffering from refractory respiratory failure, has been leading to steadily increasing use of ECMO in the adult population. We’ve seen a slight uptick in the amount of ECMO use here in the Treasure Valley recently. Keep in mind that all the information I’m summing up and attempting to explain deals with the adult population…
ECMO is essentially a modification to the cardiopulmonary bypass circuit used in CVOR, and many may have heard it referred to as a Left Ventricular Assist Device or ‘LVAD’ if a patient is brought back to the room after surgery on it.  This is meant to be a temporary support treatment while waiting for the heart/organs recover or for the surgery team to get an actual LVAD implanted in the patient.

Configurations of ECMO:
There are two configurations to how ECMO can be run.  Veno-arterial (VA) and Veno-Venous (VV).  VA is essentially cardiopulmonary bypass, the heart does not beat so the body has no circulation support and the ECMO machine does 100% of the patient’s blood flow responsibilities.  Blood is drained from a central vein to the ECMO machine and then returned to the arterial system (generally the femoral artery).  VA is the preferred method for recovery of the heart after surgery and provides both cardiac and respiratory support.
VV works by draining the blood from the venous system and returning it back to the venous system.

This configuration only provides respiratory support and relies on the heart for systemic circulation.  By providing adequate gas exchange there is no real compromise of cardiac function.   This is the preferred method for patients who require ECMO because all other conventional therapies have failed.  VV ECMO augments gas exchange so potentially dangerous ventilator settings can be avoided.  VV ECMO doesn’t cure any underlying disease processes that caused the respiratory failure, it merely just allows the lungs to ‘rest’ while attempting to fix the root cause and recover pulmonary function.

How ECMO works: Picture form!

Take a look at the picture below… Notice how the double lumen catheter sits.  Now, here’s my best explanation of how VV ECMO works:

  1. Oxygenated blood from the ECMO gets delivered in the right atrium at the tricuspid valve.
  2. The oxygenated blood then gets pumped into the right ventricle.
  3. From the right ventricle it gets pumped through the pulmonary valve through the pulmonary arteries into the lungs.
  4. From the lungs, the blood moves through the pulmonary veins to the left atrium.
  5. Blood is then pumped through the mitral valve to the left ventricle.
  6. From the left ventricle, blood is pumped through the aortic valve into the aorta where it is then moved systemically to perfuse all the other organs and tissues.
  7. Deoxygenated blood is then removed back to the ECMO machine from ports on the tube in the inferior and superior vena cava.


Weaning from ECMO:
While the patient is on VV ECMO, the vent settings are used minimally to protect the lungs and keep them patent.  To wean from VV ECMO, the perfusionist will slowly decrease the amount of ‘work’ the ECMO is doing for the patient.  At their sickest point, the VV ECMO could be doing essentially 100% of the gas exchange for the patient.  As the lungs recover and the root of the problem is getting fixed, the VV ECMO support is decreased slowly, while the ventilator is manipulated, for the patient’s lungs to assist more and more in the gas exchange process. 

Final Thoughts:
I wouldn’t be surprised if ECMO pops up more and more in the future here in the Treasure Valley.  As I understand it right now, it’s a very expensive venture to go on.  Boise probably isn’t large enough of a population to have more than one unit at different hospitals for patients requiring ECMO, but that doesn’t mean we don’t have some docs that won’t try to…  The advancements being made with ECMO are pretty astounding, I mean, cripes! Look at these two: