Presenting the European perspective, Scogvoll and coworkers [14
] reported that the annual incidence of attempted CPR ranged from 33 to 71 per 100,000 inhabitants. Sudden cardiac death accounts for approximately 1000 lives per day in the USA [5
]. In the majority of cases, CPR and other treatment efforts are unsuccessful, and the patient was eventually pronounced dead. A number of clinical indicators can be used to determine when those efforts should be terminated [15
]. Morrison and colleagues [12
] described a clinical decision rule for termination of resuscitation (TOR), which was designed to help emergency medical services to determine whether to terminate resuscitative efforts in the setting of out-of-hospital cardiac arrest. In that Canadian study, the investigators sought to validate their previously proposed prediction rule, namely that TOR should be considered if spontaneous circulation does not return before transport is initiated, if no automatic external defibrillator (AED) shocks are given before transport is initiated, and if arrest was not witnessed by emergency personnel. This simple prediction rule has 99.5% PPV and a specificity of 90.2%, and may be useful for providing supplementary guidance in the field [17
]. However, a rule cannot determine, for example, how long to continue resuscitation efforts before declaring 'no ROSC'. Decisions about TOR continue to cause difficulties for health care professionals. Current guidelines provide some information on underlying principles, but they do not include a objective, clear and numerical decision rule regarding TOR.
Several animal and clinical studies suggest that the PetCO2
can be used to determine when resuscitation should be ceased. Investigators have suggested that there is a close correlation between PetCO2
and cardiac output, stroke volume, and coronary and cerebral perfusion pressure during CPR. Kalenda [19
] first reported a decrease in PetCO2
in patients who could not be resuscitated, and a significant rise in PetCO2
in those patients in whom ROSC could be achieved.
Falk and coworkers [20
] found that PetCO2
decreased from mean of 1.4% before arrest to 0.4% after the onset of cardiac arrest. It then increased with CPR and ROSC. Sanders and colleagues [21
] found that the end-tidal carbon dioxide level predicted successful resuscitation after in hospital and out-of-hospital cardiac arrest. The average, initial, final, maximum and minimum values of PetCO2
were all higher in resuscitated patients. No patient with an average PetCO2
value of less than 1.33 kPa (10 mmHg) was resuscitated.
Callaham and Barton [22
] found that the four patients who had initial and later PetCO2
values of less than 1.33 kPa (10 mmHg) were all resuscitated. These data and similar reports of ROSC after prolonged resuscitative attempts [23
] with low PetCO2
values may account for the reluctance of the scientific community to incorporate PetCO2
in Utstein-style reports and resuscitation algorithms. In a landmark prospective study, Levine and colleagues [8
] observed 150 patients suffering cardiac arrest and measured PetCO2
using a mainstream capnometer. They compared 20-minute PetCO2
and initial values and concluded that initial values are unreliable in predicting mortality. The 20-minute values of PetCO2
were promising and more reliable in predicting mortality. Values less then 1.33 kPa (10 mmHg) after 20 minutes of CPR were incompatible with survival, and the authors are of the opinion that this could be helpful in deciding when to stop resuscitation efforts. We established the relationship between PetCO2
and prognosis in prehospital CPR in our previous studies [5
]. In the second study [24
], we confirmed that PetCO2
and mean arterial pressure values are prognostic for the outcome of out-of-hospital cardiac arrest. During a cardiac arrest, PetCO2
can be considered an indirect parameter for the evaluation of cardiac output in the prehospital setting, together with mean arterial pressure, when spontaneous circulation is restored.
Our study is the largest prospective study of the predictive value of PetCO2 measurement for ROSC and survival, and includes 737 victims of out-of-hospital sudden cardiac arrest. We confirmed that bystander CPR, witnessed arrest, shockable initial rhythm, initial, average, 10-minute, 15-minute, 20-minute, maximum and final values of PetCO2 and arrival time were all associated with improved ROSC and survival.
We found that PetCO2 values above 1.9 kPa (14.3 mmHg) measured after 20 minutes of resuscitation identified patients with ROSC with 100% sensitivity, specificity, PPV and NPV. No patients with initial, average, final and maximum PetCO2 values of less than 1.33 kPa (10 mmHg) was resuscitated. With a cut-off point of 20-minute PetCO2 value at 1.5 kPa (13.5 mmHg) in patients with shockable initial rhythm and a cut-off point at 2.1 kPa (15.8 mmHg) in patients with nonshockable initial rhythm, sensitivity and NPV were 100% in predicting discharge from hospital.
In nonshockable rhythm we found higher initial values and lower values after 1 minute of CPR. In our previous study [25
] we confirmed PetCO2
to be markedly elevated during the first minute of CPR in asphyxial cardiac arrest. This study therefore confirmed the findings of studies that used animal models in which cardiopulmonary arrest was induced by asphyxia. In this study the PetCO2
values during CPR were initially high, then decreasing to subnormal levels and then increasing again to near-normal levels in patients with ROSC. This pattern of PetCO2
change is different from the pattern observed in cardiac arrest caused by venticular fibrillation, because cardiac arrest from venticular fibrillation results in an abrupt cessation of cardiac output and pulmonary blood flow. We concluded that, during the period of asphyxia, continued cardiac output before cardiac arrest permits continued delivery of carbon dioxide to the lungs, which (in the absence of exhalation) results in higher alveolar carbon dioxide levels. This is reflected in increased PetCO2
when ventilation is resumed.
Our findings in patients with shockable initial rhythm confirmed the view of Levine and coworkers [8
] that the data from their study (PetCO2
in patients with pulseless electrical activity) can be extended to all types of cardiac arrest. Sehra and coworkers [26
], in a human model of ventricular fibrillation, confirmed that PetCO2
can predict severity of ventricular fibrillation cardiac arrest and efficacy of CPR in this type of cardiac arrest. Our findings in shockable group possible indirectly confirm the three-phase, time-dependent concept of cardiac arrest due to ventricular fibrillation [26
values under 1.5 kPa (11.3 mmHg) after 20 minutes of CPR (or less that 1.8 kPa [13.5 mmHg] after 15 minutes of CPR) are incompatible with ROSC. This is time of the end of haemodynamic phase of CPR. Possibly, these values represent irreversible hemodynamic collapse, with inadequate coronary or myocardial perfusion pressure, or they may represent perfusion pressures supplied too late (after the haemodynamic phase), with consequent irreversible tissue damage [27
Our prehospital data, combined with the findings of other investigators, provide strong support for a resuscitation thresholds of PetCO2 1.33 kPa (10 mmHg) initially and 1.9 kPa (14.3 mmHg) after 20 minutes of CPR in the field. The initial values of PetCO2 are not influenced by medications used during CPR, and values at 20 minutes reflect the patient's 'response' to resuscitation efforts. We recommend initial and 20-minute (final PetCO2) to be ranked in Utstein-style reports. The objectives of this approach are to assess the initial condition of the patient in the setting of nontraumatic normothermic cardiac arrest, and to optimize the reliability of PetCO2 in predicting survival in such patients.
Our finding are potentially important, especially in emergency medical system that do not include physicians. The results of the study confirm that PetCO2
can play a pivotal role in the multifactorial decision-making process of whether to discontinue resuscitative efforts. Application of our findings could improve clinical prediction rules for TOR in the field and reduce the number of patients with cardiac arrest who undergo prolonged, futile resuscitation efforts; furthermore, they may reduce transportation of patients with refractory cardiac arrest to the hospital. For the health care system, there is less cost involved in TOR in the field than in the transfer of the patient to the hospital [12