Prove it: Can a vacuum device during CPR improve cardiac output?

Although it resulted in greater blood flow back to the heart, a small sample size was just one of the study's limitations

Rescue 36 and Engine 47 respond to a report of an unconscious person. The engine crew arrives to find a 68-year-old male who collapsed while mowing the grass. The firefighters confirm he has no pulse, begin CPR, and attach the AED. 

After a short analysis period, the AED recommends a shock. One of the firefighters delivers the shock and the rest of the team resumes CPR.

The medics arrive, place the patient on a cardiac monitor; he has no pulse and slow electrical activity. Medic Williams inserts a supraglottic airway and verifies placement with waveform capnography. Medic Sandoval inserts an intraosseous line in the patient's right tibia and quickly administers 1 milligram of epinephrine.

Williams notes that capnography values remain steady at about 13 mmHg for the first 10 minutes of the resuscitation attempt. At the 20-minute mark, the ECG displays asystole, despite the cumulative dose of 4 milligrams of epinephrine. 

The capnography value is now 8 mmHg. Williams confirms the chest compressors are meeting the depth requirements, yet the capnography value does not rise.

Sandoval contacts a medical control physician to request authorization to terminate the resuscitation attempt. The physician agrees the team provided all recommended interventions and the patient meets the criteria for termination of resuscitation efforts.

Intrathoracic pressure regulation

Researchers in Minnesota tested a novel device that improves the efficiency of the recoil phase of CPR. It is called the intrathoracic pressure regulation (ITPR) device and it fits into the ventilation circuit. In between assisted breaths delivered by the medics during CPR, the ITPR device creates a vacuum that sucks air out the patient's chest, thus lowering intrathoracic pressure. [1]

Reducing intrathoracic pressure should result in greater blood flow back to the heart. Researchers hoped to demonstrate in a small group of patients that the device would increase cardiac output during the compression phase of CPR before undertaking a larger more definitive study.

The population for this investigation included adult patients who suffered a non-traumatic out-of-hospital cardiac arrest. First-arriving BLS rescuers initiated CPR, which included the use of an impedance threshold device (ITD).

Once advanced life support personnel arrived, they initiated advanced care consistent with the 2005 guideline recommendations by the American Heart Association.

Supervisor's role

Researchers placed the ITPR device on supervisor's vehicles rather than on first-response ambulances. Once on scene, paramedic supervisors removed the ITD from the ventilatory circuit and inserted the ITPR device between the patient and the ventilation source, which was usually a bag-valve mask. 

Medics then connected the ITPR to a manometer and a vacuum source, such as a portable suction machine. After delivering an assisted breath, a switch within the ITPR device closed the ventilation port.

This allowed the continuously running vacuum pump to suction air out of the patient's airway and lungs rather than passively allowing air to flow out, as is the case with conventional CPR. 

Once the device was in place and functioning properly, the supervisor was responsible for ensuring the device was appropriately used throughout the remainder of the resuscitation attempt.

Because the ITPR device only works with an advanced airway, the researchers could only enroll patients who were intubated with an endotracheal tube or a laryngeal tube, which was the alternative airway used in the EMS system.

Preliminary evaluation

The primary evaluation endpoint for this investigation was end-tidal carbon dioxide (ETCO2) readings. It is often very difficult to directly measure circulation during a resuscitation attempt. Therefore, many researchers use ETCO2 measurement as a surrogate marker for circulation. 

Improving the quality of chest compressions improves blood flow to the lungs and other organs, and therefore increases ETCO2 readings. Researchers compared ETCO2 readings measured just before ITPR device placement to the highest ETCO2 readings measured during CPR after ITPR device placement. 

Additionally the researchers compared the mean average ETCO2 readings of the patients who received CPR with the ITPR device in place to the mean ETCO2 readings in a group who received CPR without the ITPR device applied.

The results

As expected, there was no significant increase in ETCO2 values during the traditional resuscitation attempt for the 74 patients who did not receive ITPR treatment.

On the other hand, for the 11 patients who did receive treatment with the ITPR device, ETCO2 values increased from 21 mmHg in the period just before ITPR device placement to an average of 32 mmHg during the post placement period, with a maximum post placement recorded value of 45 mmHg.

Two circulatory phases occur during standard closed chest CPR. The compression phase increases intrathoracic pressure. This pressure forces blood out of the heart chambers toward the brain and extrathoracic vital organs.

On the other hand, the chest recoil phase decreases intrathoracic pressure, which draws blood back into the chest. 

In order to push out an adequate amount of blood to keep the brain functioning, there must be enough blood return to the heart to fill the chambers. In theory, any intervention that creates a greater vacuum during the recoil phase should improve blood return to the heart and greater cardiac output during chest compression.

Negative pressure

Achieving and maintaining a longer period of negative intrathoracic pressure results in higher coronary perfusion pressure (CPP).[2] Failure to achieve CPP of at least 15 mmHg is correlated with a failure to achieve ROSC during a resuscitation attempt.[3]

Animal models of ventricular fibrillation cardiac arrest demonstrated that use of the ITPR device resulted in CPP greater than 25 mmHg with 100 percent one-hour survival.[4] Despite the fact that the ITPR device fits into the ventilatory circuit, proper use does not appear to impede effective oxygenation.[5]

In addition to the improved CPP, the ITPR device may also improve blood flow to the brain. The vacuum created by the ITPR device may draw cerebrospinal fluid down the vertebral canal into the thoracic cavity. This lowers the volume of cerebrospinal fluid within the cranial vault, which reduces intracranial pressure. 

In order to reach the brain, the pressure within the carotid arteries must overcome intracranial pressure. Therefore, lowering intracranial pressure makes it possible to achieve adequate cerebral perfusion even during CPR when pressure in the carotid arteries is less than normal.

One animal study demonstrated that CPR augmented by the use of the ITPR device could almost double carotid blood flow and cerebral perfusion pressure.[5]


Although the results from this investigation are encouraging, we must be careful not to ascribe greater meaning than actually exists. This paper reports the findings from a feasibility study, not a randomized controlled trial.

Think of a feasibility study as a rehearsal for a larger and more comprehensive investigation that examines an idea to see if the definitions and data collection methods will actually work. This allows researchers to refine the process before committing the resources to a more labor-intensive and costly endeavor.

It is possible that other unmeasured variables produced the observed increase in carbon dioxide levels. In both the treatment and control groups, rescuers used an impedance threshold device (ITD) early in the resuscitation attempt. The ITD improves blood return to the heart and will increase ETCO2 readings.

Pre-ITPR device use of the ITD may have influenced the post-ITPR device carbon dioxide measurements. Since there were so few subjects in the treatment group, this influence could have made the difference between treatment and control groups appear greater than it actually was.

Long-term changes

Although the research team observed an increase in ROSC rates from 46 percent in the control group to 73 percent in the treatment group, there is no data on what long-term changes the device may provide.

ROSC only means that someone thought the patient regained a pulse during the resuscitation attempt. It does not mean that the pulse lasted until the patient arrived in the emergency department. It is one thing to get return of spontaneous circulation, but having that patient leave the hospital and return to a normal life is something altogether different.

Rescue teams in this study also knew which patients received ITPR therapy and which ones did not. This information could have caused rescue teams to inadvertently treat one group differently than the other.

For example, it is natural to believe that scientific advancements will improve health care. Seeing the ITPR device in place and understanding it is supposed to improve survival might cause a medic to believe a pulse is present when it really is not. 

To minimize this potential confounder, future investigations will have to involve an ITPR device that looks like a functional device but does not create the vacuum.

This study suggests but does not prove that adding an ITPR device to the ventilatory circuit during the attempted resuscitation from out-of-hospital cardiac arrest may improve blood flow to the brain and vital organs. 

A larger more controlled trial is necessary to determine if the ITPR is actually both producing these observed effects and improving long-term survival.


  1. Segal, N., Parquette, B., Ziehr, J., Yannopoulos, D., & Lindstrom, D. (2013). Intrathoracic pressure regulation during cardiopulmonary resuscitation: A feasibility case-series. Resuscitation, 84(4), 450-453. doi:10.1016/j.resuscitation.2012.07.036
  2. Yannopoulos, D., Sigurdsson, G., McKnite, S., Benditt, D., & Lurie, K. G. (2004). Reducing ventilation frequency combined with an inspiratory impedance device improves CPR efficiency in swine model of cardiac arrest. Resuscitation, 61(1), 75– 82. doi:10.1016/j.resuscitation.2003.12.006
  3. Paradis, N. A., Martin, G. B., Rivers, E. P., Goetting, M. G., Appleton, T. J., Feingold, M., & Nowak, R. M. (1990). Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation. Journal of the American Medical Association, 263(8), 1106 –1113. doi:10.1001/jama.1990.03440080084029
  4. Yannopoulos, D., Aufderheide, T. P., McKnite, S., Kotsifas, K., Charris, R., Nadkarni, V., Lurie, K. G. (2006). Hemodynamic and respiratory effects of negative tracheal pressure during CPR in pigs. Resuscitation, 69(3), 487-494. doi:10.1016/j.resuscitation.2005.11.005
  5. Yannopoulos, D., Nadkarni, V. M., McKnite, S. H., Rao, A., Kruger, K., Metzger, A., Benditt, D. G., Lurie, K. G. (2005). Intrathoracic pressure regulator during continuous-chest-compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest. Circulation, 112(6), 803-811. doi: 10.1161/​CIRCULATIONAHA.105.541508

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