To our knowledge, this is the first study to report changes in peripheral arterial pressure due to aortic occlusion in humans suffering from OHCA. Our findings demonstrate that aortic occlusion during ACLS increases peripheral arterial pressure. The REBOA catheter in use is not approved to perform aortic pressure recordings, hence we were not able to measure the central aortic blood pressure. However, we find it likely that an increase in the radial or brachial arterial pressures during CPR also indicate an increase in central aortic blood pressure.
During spontaneous circulation, the blood pressure is amplified and augmented from the aorta to the peripheral arteries, where the systolic pressures increase and the diastolic pressure and mean pressures may decline (17–19). The ventricular systole creates a forward pressure wave that is transmitted along the elastic aorta. The wave hits zones of impedance mismatch, e.g. arterial bifurcations, arterial tapering, changes in arterial stiffness and impedance (17, 20) and is reflected retrograde towards the heart. It then meets the forward pressure wave, and creates an augmented and amplified pressure wave (17).
During cardiac arrest, the scenario is different. Chest compressions pump the blood through the aorta, mimicking the ventricular systole. It was initially proposed as a result of the direct compression of the heart between the sternum and the vertebrae, “the cardiac pump” theory (21). A later explanation is that an increase in intra-thoracic pressure beyond the extra-thoracic pressure is the cause of blood flow during CPR (9, 22), “the thoracic pump” theory. Another possible mechanism is the “respiratory pump” theory (23) where the negative intrathoracic pressure during the relaxation phase (the “diastole”) cause improved return of blood to the heart (e.g. impedance threshold device). It is however possible that it is the sum of different simultaneous mechanisms that produces the forward blood flow (24, 25).
Few studies describe simultaneous radial arterial and central aortic pressures during CPR. One human study (10) demonstrated that the radial arterial pressure correlated with the aortic pressure during CPR. During the compression phase the radial arterial pressure was significantly lower than the aortic pressure, both at baseline and after epinephrine was administered. During the relaxation phase the radial arterial pressure was significantly higher than aortic pressure and the femoral arterial pressure was comparable to the aortic pressure. Another study (9) found that the peak compression phase right atrial pressure (RAP) was slightly higher than the radial arterial pressure, and the relaxation phase gradient between the radial artery and right atria was found to be approximately 11 mmHg. In two case reports the radial arterial compression phase, relaxation phase and mean pressures increased after aortic occlusion (4). In these, RAP was measured simultaneously, and the coronary perfusion pressure increased from − 2 to 8 mmHg and 15 to 18 mm Hg, respectively. These studies indicate first that changes in radial arterial pressures may indicate changes in central aortic pressures, and second that aortic occlusion may increase aortic pressure and subsequently the CPP.
Systolic blood pressure can differ significantly between the central and peripheral arteries (17). The radial or brachial arterial pressure is commonly measured in patients and the mean arterial pressure is used as a substitute to tissue perfusion (26). This may create erroneous assumption of the patient’s central aortic blood pressure. Few studies, and with small sample sizes, report intra-arterial systolic blood pressure differences between the brachial and radial artery (27). One study demonstrated that on average, radial arterial systolic pressure was 5.5 mmHg higher than brachial arterial systolic pressure. Most patients had systolic radial arterial BP > 5 mmHg higher than brachial and as much as 14% of the patients had radial arterial systolic BP > 15 mmHg higher than brachial. This so-called “Popeye phenomenon” (27) clearly demonstrates that there is not equivalence between brachial and radial arterial pressure. Further, it is shown that brachial cuff BP measurements systematically underestimate the true intra-arterial brachial pressure by 5.7 mmHg (28). Combined with the difference of > 15 mmHg from brachial to radial arterial pressure as shown (27), the difference from brachial cuff-measured systolic pressure and invasive radial pressure may be above 20 mmHg. How, and where, arterial pressure is measured are therefore important to consider in clinical practice.
If spontaneous circulation is achieved, it is not known how the lumen-occluding balloon will affect the forward wave or the subsequent reflection wave. One may speculate that a stunned heart would deteriorate under the afterload created by the inflated balloon. However, it may also be that a potential increase in aortic pressure will contribute to improved myocardial perfusion and subsequent improvement of contractility (29). This may possibly be mediated through the Greggs phenomena (30), where improved coronary perfusion results in increased oxygen uptake followed by increased cardiac strength. The cause of this is not clear, but may involve restoration of adequate subendocardial oxygen supply (ischemia effect) (31) or “the garden-hose effect”, where the increased blood flow through coronary vasculature stretches the surrounding myocardium (sarcomere stretch), with an increased left ventricular contractility due to the Frank-Starling mechanism (32, 33). It is also not known if, and by how much, the Anrep effect (34) contribute to the haemodynamic situation after ROSC. The Anrep effect is a positive inotropic effect after a sudden increase in systolic pressure. This enhancement in left ventricular function may contribute to improved post ROSC circulation, even after the deflation of the REBOA balloon. If this effect, or Greggs phenomena, is at all valid during CPR, is unknown.
First, the small number of patients cause the data to be regarded as preliminary findings. Second, it was a single-centre study, with few physicians and paramedics involved. Third, all the physicians were board-certified anaesthesiologist with considerable experience with the use of ultrasound and Seldinger technique, and the results may not be relevant to other settings where cardiac arrest patients are treated. Fourth, the arterial pressures are measured with one-minute sampling rate. The blood pressure may vary during this time interval, hence further studies may benefit from the use of higher sampling rate, or continuous sampling. Finally, this study primarily increase knowledge on the hemodynamic changes caused by REBOA during CPR and cannot conclude about the potential clinical benefit from a REBOA intervention.