In this swine model of out-of-hospital cardiac arrest, our group observed that following the induction of VF, all animals continued breathing for about one minute at a mean frequency of 10 breaths per minute (Figure 1). The continued breathing was then followed by the crescendo-decrescendo pattern of gasping that has previously been described  (Figure 1). The recorded air flow pattern during the first minutes following the onset of ventricular fibrillation was similar to that of regular spontaneous breathing of an anesthetized animal and was different from the air flow pattern typical for gasping or agonal ventilation that occurred during minutes 2 to 5 (Figure 2). This continued breathing pattern was also clearly different from the pattern of assisted mechanical ventilation (Figure 3). The finding of continued breathing for the first minute following VF cardiac arrest, if confirmed in humans, is of clinical relevance. The failure to recognize spontaneous breathing and gasping following cardiac arrest potentially delays the recognition of the arrest and, thus, the early initiation of resuscitation efforts.
The explanation for the observation of continued breathing during the first minute following VF cardiac arrest might well be related to carotid artery and cerebral blood flow patterns immediately following untreated VF cardiac arrest. Frenneaux and Steen [17, 18] reported that carotid artery blood flow was relatively well maintained for the first minute following untreated VF cardiac arrest, before rapidly and markedly decreasing during the second minute and remaining marginal but still present for up to four minutes. Ristagno and colleagues  also found that there was substantial cerebral cortical microvascular flow after the onset of VF that rapidly decreased during the first three minutes of untreated VF cardiac arrest in swine. Cerebral blood flow differs from coronary artery blood flow, which ceases almost immediately after VF cardiac arrest .
Our observation of normal breathing during the first minute of VF was followed by a slower rate of spontaneous ventilation during minutes 2 to 5, which was typical of gasping or agonal respiration. As shown in Figure 2, gasping has a ventilatory flow pattern distinctly different from normal breathing or mechanical ventilation and typically exhibits a crescendo-decrescendo frequency pattern. After the fifth minute of untreated VF, gasping was not observed.
Gasping following cardiac arrest has been previously reported in human [1–3] as well as in animal models. In 1988 study in rats, von Planta and colleagues  reported that "gasping typically began 1 min after the induction of VF". In a swine model of VF cardiac arrest, Srinivasan  found that the time to the first gasp was 1.5 ± 0.5 min and that gasping ended on average 4.7 min after the onset of VF cardiac arrest. Ristagno and colleagues  also reported on the frequency of gasping during minutes 2 to 5 after onset of VF cardiac arrest. In their swine model, Frenneaux and Steen  found that gasping typically began weakly, increased to a maximum and generally ceased entirely by about 5 minutes post VF induction. These reports do not comment on spontaneous ventilatory activity during the first minute of VF cardiac arrest.
Menegazzi et al.  reported in a study of 12 swine that were sedated with ketamine/xylazine, and anesthetized with alpha-chloralose that all had agonal respirations through the first 2 minutes of arrest. The number of swine presenting spontaneous respiratory activity decreased to 11 (92%) at minute 3, five (42%) at minute 4, and two (17%) at minute 7. Mean respiratory rates ranged from 6 to 11 breaths/min. This report did not analyze the air the air flow pattern or the wave form of the end-tidal CO2 curves and invariably refers to post arrest ventilations as agonal respirations, whereas our findings suggest two different types of agonal respirations; initially continued breathing followed by typical agonal or gasping ventilations.
We believe that this is the first published report showing two different spontaneous air flow patterns during the early phase following VF cardiac arrest. However, based upon the references cited we wonder whether this has been a present but unrecognized phenomenon.
The pattern of continued spontaneous breathing for the first minute of VF cardiac arrest may be explained by continued perfusion through the carotid artery (and presumably continued cerebral blood flow), as reported by Frenneaux and Steen  following the induction of VF. Breathing no doubt stops in response to inadequate cerebral blood flow. Gasping, produced by a more primitive ventilatory center located in the brain stem is then activated [11–14]. Gasping is initiated during the second minute of VF cardiac arrest and increases during the third minute, but as the gasping center in the brain stem becomes more ischemic, the frequency of gasping decreases and eventually stops. This is a plausible explanation for the classically described crescendo-decrescendo pattern of gasping following untreated cardiac arrest .
There are limitations to this study that must be considered. This study is observational only and was not designed to determine the mechanisms of spontaneous breathing and gasping. Gasping is markedly more pronounced in immature animals [11–13]. Although the young swine used in this study were not immature, they might have exhibited a higher relative frequency of gasping compared with aged animals. The phenomenon of gasping is also related to the type and duration of anesthesia the animals are subjected to before the induction VF and the presence or absence of paralysis. The swine in this study were not paralyzed and were maintained on a relatively low concentration of isoflurane, which is less likely to suppress gasping relative to some other commonly used anesthetics, but might reduce the respiratory stimulation due to increasing pCO2 . In our experience, high doses of isoflurane will also suppress gasping.