Are we Placing mCPR Devices too Early?

First, there are two proposed mechanisms of CPR, brilliantly summarized in this paper:

Cardiac Pump Mechanism:

“blood is squeezed from the heart into the arterial and pulmonary circulations, with closure of the mitral and tricuspid valves, preventing retrograde blood flow, and opening of the aortic and pulmonary valves in response to forward blood flow. Air is thought to move freely in and out of the lungs, so that the intrathoracic pressures do not significantly rise and the pulmonary circulation is not adversely affected by chest compressions. With the relaxation of chest compression, the heart fills with blood and air passively returns to the lungs.”

Thoracic Pump Mechanism:

“With each chest compression the intrathoracic pressure rises because of the collapse of the airways; the thoracic pump theory. This theory presumes that the rise in the intrathoracic pressures results in collapse of the pulmonary airways, thereby reducing the movement of air out of the lungs and reducing the size of the intrathoracic structures, but not necessary equally. The collapse of venous structures at the thoracic inlet was postulated to prevent retrograde venous blood flow and with each relaxation of chest compressions, the intrathoracic pressure falls with return of venous blood.”

It is likely that both mechanisms are at play:

…In patients with an average chest configuration and those with so‐called “barrel chests,” secondary to emphysema or other causes, the lateral chest roentgenogram often shows a significant distance between the anterior chest‐wall and the heart. In such patients it is nearly inconceivable that sternal compressions of the chest during CPR could result in cardiac compression. Rather, the mechanism of blood flow from chest compressions is probably secondary to the rhythmic alterations of the intrathoracic pressure and releases, for example, the “thoracic pump” theory.

Is there any evidence that M-CPR Devices improve outcomes – since they’re marketed as “life saving devices”?

A Meta Analysis from Gates et. al. concluded:

Existing studies do not suggest that mechanical chest compression devices are superior to manual chest compression, when used during resuscitation after out of hospital cardiac arrest.

However, if there’s no difference in survival, and it’s not WORSE than manual CPR, why not use it to cognitively offload tasks? Because, it may be worse.

Gonzales et. al. compared “pit crew” resuscitation with “scripted” mCPR implementation and found:

In this EMS system with a standardized, “pit crew” approach to OHCA that prioritized initial high-quality initial resuscitative efforts and scripted the sequence for initiating mechanical CPR, use of mechanical CPR was associated with decreased ROSC and decreased survival to discharge.

Why might this be the case?

We know based off work by Hwang et. al. who showed that standard CPR (inter-nipple line) often results in compression or narrowing of the LVOT or the aortic root. In this study, the area of maximal compression was over the aorta in 59% of patients!

In another study, anderson et. al. used transthoractic echo to mark the location of the aortic root and the left ventricle of animals, and randomized them to receive CPR at one of the two locations. As you can probably guess, aortic systolic and diastolic pressures as well as ETCO2 were higher in the LV group, and 9 of the LV group (69%) achieved ROSC and survived at least 60 minutes compared to none who received chest compressions over the aortic root. 

All of these studies and more are explained in a wonderful video created by Felipe Teran:

The folks at The Ultrasound Podcast also discuss using TEE to guide hand or device palcement for CPR:

TEE to save lives, guide compressions, and guide interventions Pt 1. #FOAMED.  p.s. – checkout cabofest2018.com  But, how do we do we know that we’re compressing the LV without TEE?

Well, we don’t exactly. However, Qvigstad E et. al. published a study in Resuscitation titled “Clinical pilot study of different hand positions during manual chest compressions monitored with capnography.”

They compared how hand positioning at the inter-nipple line (INL), 2 cm below the INL, 2 cm below and to the left, and 2 cm below and to the right affect ETCO2.

They found that there’s not “one superior hand position”, and that optimal positioning varies:

How does this explain when we should place mCPR?

It doesn’t really, but one argument against mCPR, specifically one based off of the cardiac pump mechanism, is that the device is consistent and doesn’t fatigue, yet this might be it’s downfall. It’s postulated, and demonstrated in the above videos that it may just be consistently compressing the aortic outflow tract, and not the left ventricle. 

Are we applying mCPR too early?

Poole et. al discuss this in a paper titled: Mechanical CPR: Who? When? How?

In their paper they discuss how the device is frequently deployed early, even before defibrillating the patient. Others

In clinical practice, published literature reports marked variability in the hands-off time during device deployment, with pauses in excess of 1 minute being reported. In the LINC trial, the median reported chest compression pause associated with device deployment was 36.0 s (IQR 19.5, 45.5)

The authors continue and note that…

subsequent improvement in flow-fraction following device deployment meant that the median flow-fraction over the first 10 minutes of the cardiac arrest was higher in the mechanical CPR arm (mechanical 0.84 (IQR 0.78, 0.91) vs manual 0.79 (IQR 0.70, 0.86), p < 0.001). A similar pattern was observed in the CIRC trial.

So it seems that it takes longer to place the device than most think, but once it’s placed the “flow-fraction” is higher with mCPR. Therefore, the reason outcomes are not better with mCPR compared to manual CPR is that the first few minutes matter the most, and we’re stopping CPR to apply the device during the period in which we’re most likely to obtain ROSC.

Conclusion Consider applying your mCPR device later in the arrest, rather than sooner When performing manual chest compressions, monitoring ETCO2 can help ensure proper hand positioning Perform post event reviews using manufacturer software to measure CPR fraction and pauses associated with mCPR application

First, there are two proposed mechanisms of CPR, brilliantly summarized in this paper:

Cardiac Pump Mechanism:

“blood is squeezed from the heart into the arterial and pulmonary circulations, with closure of the mitral and tricuspid valves, preventing retrograde blood flow, and opening of the aortic and pulmonary valves in response to forward blood flow. Air is thought to move freely in and out of the lungs, so that the intrathoracic pressures do not significantly rise and the pulmonary circulation is not adversely affected by chest compressions. With the relaxation of chest compression, the heart fills with blood and air passively returns to the lungs.”

Thoracic Pump Mechanism:

“With each chest compression the intrathoracic pressure rises because of the collapse of the airways; the thoracic pump theory. This theory presumes that the rise in the intrathoracic pressures results in collapse of the pulmonary airways, thereby reducing the movement of air out of the lungs and reducing the size of the intrathoracic structures, but not necessary equally. The collapse of venous structures at the thoracic inlet was postulated to prevent retrograde venous blood flow and with each relaxation of chest compressions, the intrathoracic pressure falls with return of venous blood.”

It is likely that both mechanisms are at play:

…In patients with an average chest configuration and those with so‐called “barrel chests,” secondary to emphysema or other causes, the lateral chest roentgenogram often shows a significant distance between the anterior chest‐wall and the heart. In such patients it is nearly inconceivable that sternal compressions of the chest during CPR could result in cardiac compression. Rather, the mechanism of blood flow from chest compressions is probably secondary to the rhythmic alterations of the intrathoracic pressure and releases, for example, the “thoracic pump” theory.

Is there any evidence that M-CPR Devices improve outcomes – since they’re marketed as “life saving devices”?

A Meta Analysis from Gates et. al. concluded:

Existing studies do not suggest that mechanical chest compression devices are superior to manual chest compression, when used during resuscitation after out of hospital cardiac arrest.

However, if there’s no difference in survival, and it’s not WORSE than manual CPR, why not use it to cognitively offload tasks? Because, it may be worse.

Gonzales et. al. compared “pit crew” resuscitation with “scripted” mCPR implementation and found:

In this EMS system with a standardized, “pit crew” approach to OHCA that prioritized initial high-quality initial resuscitative efforts and scripted the sequence for initiating mechanical CPR, use of mechanical CPR was associated with decreased ROSC and decreased survival to discharge.

Why might this be the case?

We know based off work by Hwang et. al. who showed that standard CPR (inter-nipple line) often results in compression or narrowing of the LVOT or the aortic root. In this study, the area of maximal compression was over the aorta in 59% of patients!

In another study, anderson et. al. used transthoractic echo to mark the location of the aortic root and the left ventricle of animals, and randomized them to receive CPR at one of the two locations. As you can probably guess, aortic systolic and diastolic pressures as well as ETCO2 were higher in the LV group, and 9 of the LV group (69%) achieved ROSC and survived at least 60 minutes compared to none who received chest compressions over the aortic root. 

All of these studies and more are explained in a wonderful video created by Felipe Teran:

The folks at The Ultrasound Podcast also discuss using TEE to guide hand or device palcement for CPR:

TEE to save lives, guide compressions, and guide interventions Pt 1. #FOAMED.  p.s. – checkout cabofest2018.com  But, how do we do we know that we’re compressing the LV without TEE?

Well, we don’t exactly. However, Qvigstad E et. al. published a study in Resuscitation titled “Clinical pilot study of different hand positions during manual chest compressions monitored with capnography.”

They compared how hand positioning at the inter-nipple line (INL), 2 cm below the INL, 2 cm below and to the left, and 2 cm below and to the right affect ETCO2.

They found that there’s not “one superior hand position”, and that optimal positioning varies:

How does this explain when we should place mCPR?

It doesn’t really, but one argument against mCPR, specifically one based off of the cardiac pump mechanism, is that the device is consistent and doesn’t fatigue, yet this might be it’s downfall. It’s postulated, and demonstrated in the above videos that it may just be consistently compressing the aortic outflow tract, and not the left ventricle. 

Are we applying mCPR too early?

Poole et. al discuss this in a paper titled: Mechanical CPR: Who? When? How?

In their paper they discuss how the device is frequently deployed early, even before defibrillating the patient. Others

In clinical practice, published literature reports marked variability in the hands-off time during device deployment, with pauses in excess of 1 minute being reported. In the LINC trial, the median reported chest compression pause associated with device deployment was 36.0 s (IQR 19.5, 45.5)

The authors continue and note that…

subsequent improvement in flow-fraction following device deployment meant that the median flow-fraction over the first 10 minutes of the cardiac arrest was higher in the mechanical CPR arm (mechanical 0.84 (IQR 0.78, 0.91) vs manual 0.79 (IQR 0.70, 0.86), p