The first time I performed cardiopulmonary resuscitation [CPR] on a patient was in the emergency department of Sunnybrook Hospital in Toronto, Canada; it was certainly an indelible moment in my training. As an intern, and especially as medical consult at Bellevue Hospital in New York City, I was involved in the resuscitative efforts of countless patients and this continued during my fellowship at Stanford. Throughout these years I’ve found that the physiological nuances of CPR are important for all resuscitationists to recognize in an effort to improve care of the pulseless patient.
The cardiac & the thoracic pumps during CPR
“External cardiac massage” as we know it today was introduced in 1960 . As initially described, the goal of CPR was to compress and release the ventricles between the sternum and thoracic spine. Classically this mechanistic explanation of CPR is termed the ‘cardiac pump’ theory . It posits that during chest compression the heart is compressed, intraventricular pressure gradients are generated – thereby closing the atrioventricular valves and opening the semilunar valves – and blood is expelled into the great arteries. During chest decompression, the pressure drop within the ventricles opens the atrioventricular valves and ‘sucks’ blood into the ventricles, much like heart function in vivo.
This explanation was quickly challenged, however, based on both canine and human data. In the former, CPR was marked by nearly identical pressures in all heart chambers and esophageal pressure – a surrogate for intrathoracic pressure [ITP] – during chest compression [3, 4]. In other words, no pressure gradient formed between heart chambers as would be predicted by the cardiac pump theory. Further, the rise in pressure within all chambers of the heart mirrored the rise in ITP. Nevertheless, during chest compression, ITP rises relative to extrathoracic pressure and this gradient determines blood flow under the banner of the ‘thoracic pump’ theory. Early data supporting the thoracic pump theory in humans arose from the description of ‘cough CPR’ whereby consciousness could be maintained in a patient with ventricular fibrillation as long as cough was continued . Clearly during cough there is minimal cardiac compression, but a large intrathoracic to extrathoracic pressure gradient.
The mechanism of blood flow described by the thoracic pump theory is less intuitive but posits that chest compression raises intrathoracic aortic pressure relative to extrathoracic aortic pressure and this drives blood out of the chest . Importantly, intrathoracic venous pressure is also raised relative to extrathoracic venous pressure, however, pressure within the extrathoracic venous system does not increase on account of venous valves and the relatively high compliance of the lumped venous system . That is, because the lumped arterial compliance is 30 times lower than the venous system , if an equivalent parcel of blood is delivered out of the thorax and into the great vessels during chest compression, the pressure within the extrathoracic arteries is expected to increase 30 times more than within the extrathoracic veins.
And the winner is …
Determination of which of the aforementioned models drives blood flow during CPR is readily investigated with ultrasonography. Nevertheless, the use of both transthoracic and transesophageal ultrasound during human CPR, like the methods used to study CPR before them, have yielded mixed results with respect to the dominant mechanism of blood flow [7-9]. Some studies have revealed little ventricular compression and no valve closure during hemodynamically successful CPR, while others have provided evidence supporting the cardiac pump theory . The reason that both mechanisms have been supported is likely that both are functioning simultaneously during CPR – the thoracic and cardiac pump theories are not mutually exclusive. Differences in compression location, force, chest wall characteristics and volume-status all likely account for disparate experimental results [11-13].
Despite both mechanisms being important during CPR, many adjuncts have been developed based on optimizing the thoracic pump. Ostensibly, maximizing and minimizing ITP during chest compression and decompression, respectively, will maximize blood flow – treating the thorax, essentially, as a billows. ITP is augmented by simultaneous ventilation-compression CPR, vest CPR and abdominal compression [14-16]. The latter two effectively reduce chest wall compliance akin to obesity and a stiff chest wall raises ITP. Further, abdominal compression may raise afterload, facilitate aortic back pressure and coronary perfusion . These methods have improved hemodynamics in animal models but have been lackluster in human trials . By contrast, active compression-decompression CPR minimizes ITP during decompression. It does so by actively recoiling the chest using a plunger-like mechanism affixed to the chest wall . Similarly, an inspiratory-threshold device placed via a facemask or in-line with an endotracheal tube selectively raises inspiratory resistance. Resultantly, a partial vacuum is created during chest recoil . Purportedly, active decompression and inspiratory threshold mechanisms facilitate venous return during chest wall recoil. While these devices had initial success in human trials, subsequent studies have been mixed .
A unique approach to optimizing the thoracic pump is the application of interspersed abdominal compression . This technique involves compressing the abdomen during chest wall decompression. Putatively, abdominal compression raises mean circulatory pressure – the pressure head for venous return . If this occurs while right atrial pressure is falling, i.e. during chest wall recoil, the gradient for venous return is magnified; however, there are important caveats. Firstly, abdominal compression will only raise venous return when the venous vasculature is relatively full . If the patient is hypovolemic, force applied to the abdomen may raise the resistance to venous return and diminish great vein blood flow . This underscores some success during CPR while applying volume infusion or passive leg raise . Additionally, reducing ITP will only favor venous return in the absence of great vein collapse at the thoracic inlet. In a patient without end-expiratory pressure, venous return is limited at roughly atmospheric pressure by great vein collapse . If a patient has a low right atrial pressure to begin with  and/or if the patient is hypovolemic with high resistance to venous return, reducing ITP will not augment blood flow as great vein Starling Resistors become limiting .
Time on chest
Ultimately, the disappointment of some of the CPR adjuncts in humans may simply be a function of time. Delaying the initiation of adequate CPR from 6 to 12 minutes significantly raised the requirement for coronary perfusion pressure and diminished likelihood of the return of spontaneous circulation . Simply, the longer the heart itself is starved of perfusion, the greater the degree of myocardial tetany and irreversible structural damage. Thus the emphasis on good quality CPR with minimal interruption .
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