Tag: Chest Compressions

Cerebral blood flow during and after cardiac arrest

As discussed in a previous post, perfusion of the brain following long-term (>5 min) ischemia has been shown to be significantly compromised, particularly in subcortical regions. An interesting recent article by Ristagno, et. al in Resuscitation (May 2008) has added new data to the equation, using some of the most advanced technologies available for measuring cerebral microvascular blood flow.

To briefly summarize the experiment, pigs were subjected to 3 minutes of untreated ventricular fibrillation followed by 4 minutes of cardiopulmonary resuscitation and subsequent defibrillation. Blood flow in large (>20 micrometers) and small (<20 micrometers) cerebral vessels was measured during and after CPR by direct visualization using orthogonal polarization spectral imaging (OPS) together with cortical-tissue partial pressure of carbon dioxide.

Though prior studies implied a dissociation between microcirculatory flow and macrocirculation during CPR, Ristagno, et. al found “a close relationship between microvascular flows and the macrocirculation during cardiac arrest, during CPR and following return of spontaneous circulation (ROSC).” Interestingly, they also noted that cerebral blood flow was reduced, but did not stop, for more than 2 minutes after cardiac arrest, most likely due to residual compliance in the arterial circuit. After ROSC, flow progressively increased back to normal (pre-arrest) values within 3 minutes.

Importantly, the researchers also noted that cerebral cortical-tissue partial pressure of carbon dioxide (a measure of the severity of cerebral ischemia) increased progressively througout CPR, providing evidence for the fact that the pressure and flow generated during chest compressions “may minimise but do not reverse the magnitude of the brain ischaemia which preceded the start of CPR.”

Though many investigations, such as the previously reported study by Fischer & Ames reported no-reflow or hypoperfusion following ischemia, these authors observed no such phenomena, possibly because of the short duration of cardiac arrest. Indeed, they ultimately conclude that “a 3-min interval of ischaemia was therefore probably not long enough to induce alterations in blood flow during reperfusion.” Also of importance is the fact that OPS technology limits visualization of microvessels to within 1mm of the cortical surface. However, this paper still gives us better insight into the immediate effects of cardiac arrest, cardiopulmonary resuscitation, and reperfusion on microcirculatory flow in the brain.

Load distributing band CPS

The Autopulse presents an alternative to the (high impulse) active compression-decompression devices that cryonics organizations currently employ to provide cardiopulmonary support (CPS) during stabilization. The Autopulse uses batteries instead of compressed oxygen and is easy to set up and operate. Disadvantages include its cost, limited patient size range, and the modifications that cryonics organizations must make to protect it from water during operation in a portable ice bath. But perhaps the most serious concern that has been expressed about the Autopulse (or any other mechanical CPR devices without active decompression) is that it may be less effective for patients with flail chest during extended CPS times.

The most fundamental question, however, is whether load distributing band CPR (LDB-CPR) is superior to high impulse active compression-decompression CPR (HI-ACD CPR). Some studies report impressive performance of the Autopulse in animal models but a recent randomized trial found worse neurological outcomes versus manual CPR. An editoral discussing these apparently contradictory results contains an interesting observation:

“Standard, manual CPR may be better than is generally recognized. Preclinical investigations of the LDB-CPR device typically compared it with the only commercially available mechanical CPR device, a gas drive piston-cylinder. This device compresses the sternum 1.5 to 2 inches, presumably causing cardiac compression, the other mechanism of blood flow during CPR. In preclinical comparisons, the pistoncylinder device appears to have been adjusted to produce 20% anterior-posterior sternal displacement, similar to that produced by LDB-CPR and likely to be less than an inch in 20-kg swine. This 20% value may represent the optimal performance characteristics for LDB-CPR in small swine but may have reduced the performance of the older pistoncylinder device. A comparison of LDB-CPR to “good” manual CPR in a laboratory model could prove to be revealing.”

To our knowledge, realistic head-to-head comparisons between good mechanical HI-ACD CPR and LDS-CPR, including the use of an inspiratory impedance threshold device, such as the ResQPOD, have not been published so far.