Survival rates after cardiac arrest are depressingly low and have only marginally improved, if at all, since the fifties. It is not all gloom though. A study in Resuscitation 83 (2012) is testament to how there is some thinking going on outside the box.
Reading current CPR research and writing is frustrating and tedious. Take for example all effort that goes into proving any benefit or harm from adrenaline in cardiac arrest. All those studies, all those patients, all that talk and all that controversy tell me one thing:
Whatever the result, the benefit, or harm, is going to be marginal at best. It will not be the quantum leap we should aim for.
Good thing there are researchers who are thinking outside the box and explore concepts like ECMO in cardiac arrest and SNPeCPR
SNPeCPR and other concepts
SNPeCPR, sodium nitroprusside enhanced CPR, is a novel take on CPR. The way it is described in the article it is a combination of three novel concepts in CPR that have shown promise. ACD-CPR with ITD, sodium nitroprusside and lower abdominal binding.
ACD-CPR with ITD means active compression decompression CPR with an impedance threshold device.
ACD-devices basically means giving compressions using a device with a suction cup it. The suction cup allows for active re-expanding of the chest generating more negative intrathoracic pressure in the chest, theoretically increasing venous return.
ITD, impendance treshold device, is a device that prevents air from flowing freely into the lungs in the recoil phase of a compression. Theoretically it should augment the active decompression described above.
Abdominal binding simply means compressing the aortic blood flow into the lower extremities. By doing that we minimise the vessel volume that needs to be perfused, redistributing the blood flow from the lower extremities to the parts that matter, the thorax and the brain.
Sodium nitroprusside. Instead of infusing adrenaline we infuse sodium nitroprusside. Instead of increasing vascular resistance and whipping an already ischaemic heart with adrenaline, we administer an agent that opens up the vessels for blood flow and oxygen delivery.
15 pigs were anesthesized and had ventricular fibrillation induced by delivering an electric current through a pacing wire and were left in V-fib for 6 minutes.
Eight pigs received standard CPR for fifteen minutes before they were shocked. The other seven progressed through three phases making up the SNPeCPR arm. First five minutes of standard CPR with only compression and no active decompressions. Then five minutes of ACD-ITD CPR and finally ACD-ITD with abdominal binding. Two minutes into each of the three phases the subjects were injected with 1mg of sodium nitroprusside.
Primary endpoints were carotid blood flow and ROSC.
Results – Carotid Blood Flow
Carotid blood flow (CBF) results are in the diagram. Standard CPR achieves CBF that is approximately a third of normal baseline CBF.
After five minutes CBF is somewhat better in the SNP subjects.
After ten minutes CBF is significantly better in SNPeCPR subjects who are now being resuscitated with ACD-ITD.
CBF is almost back to normal after 15 minutes when the subjects are being resuscitated ACD-ITD and abdominal binding.
Results – ROSC after defibrillation
All animals on the ACD-ITD and abdominal binding protocol were shocked to ROSC after only one shock. Only two out of eight animals in the standard-CPR group had ROSC. Both required 4 defib shocks.
This is a tiny animal study performed in a controlled lab environment. Still, something worked. All animals in the ACT-ITD-abdominal binding sequence had ROSC after one defib shock.
It´s hard to say which of the components worked. I’m betting on the abdominal aortic occlusion. The increase in blood flow after abdominal binding is striking.
But who knows…I guess there could be a delayed SNP effect, from the poor perfusion in the earlier stages?
Study lives here.