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In the UK in 2018, 30,829 patients were treated during an out of hospital cardiac arrest (OOHCA), with 29.4% admitted to hospital with a return of spontaneous circulation (ROSC) and 9.3% surviving to discharge (Out-of-Hospital Cardiac Arrest Outcomes Registry Epidemiology Report, 2018 p.18). The current RCUK guidance state Provide artificial ventilation as soon as possible in any patient in whom spontaneous ventilation is inadequate or absent(Resuscitation Council UK ,2015 p.7) but it has been said that the standard Airway Breathing Circulation should be replaced with Circulation Airway Breathing (Henlin et al., 2014). This essay aims to critically analyse the use of positive pressure ventilation and explore the idea that passive ventilation may provide a superior prognosis for patients in cardiac arrest.
Cardiopulmonary resuscitation (CPR)interruptions can be a major contributor to the consistently poor outcome seen in OOHCA as it results in no circulatory support (Valenzuela et al., 2005) and therefore interruptions to CPR due to advanced airway placement should be avoided (Resuscitation Council UK, 2015). Shekerdemian and Bohn (1999) supports positive pressure ventilation by stating that respiratory support is fundamental to maintaining cardiopulmonary function and that the heart and lungs have a close relationship in providing tissue perfusion. Bobrow et al. (2009) found that passive insufflation was superior to positive pressure ventilation in OOHCA patients with an initial ventricular tachycardia or ventricular fibrillation rhythm. This observational study has a degree of bias as it focusses purely on potential cardiac causes of cardiac arrest and dismisses any non-shockable rhythms. However, it could be argued that benefits of passive insufflation or positive pressure ventilation could be more obvious in patients with a potentially cardiac cause of arrest due to the close relationship between the heart and lungs. Bobrow et al. (2018) discuss the result of Miminally Interrupted Cardiac Resuscitation (MICR) training, arguing that a 100% non-rebreather mask and good quality chest compressions was sufficient in providing adequate tissue perfusion. It was found that there was a survival-to-hospital discharge increase from 1.8% to 5.4%. However, due to the change of not using a bag-valve-mask (BVM) during CPR, paramedics involved in the study were permitted to continue using a BVM at a rate of 8 breaths per minute, which threatens this studys validity. Witnessed cardiac arrests by emergency medical staff were also excluded but witnessed cardiac arrests are more likely to survive when Basic Life Support is administered by paramedics (Vukmir 2004). With this study being conducted in urban Arizona, it lacks external validity and consequently, it is challenging to apply it to paramedic practice in the UK; as per Ambulance Quality Indictators: Clinical Outcomes 2018 London Ambulance Service had a rate of 8% survival-to-discharge as opposed to the much more rural South East Coast Ambulance Service of 5.7% (NHS England 2018).
NHS Pathways accurately identifies 75.9% of adult cardiac arrests and as a result, call handlers are able to facilitate bystander CPR (Deakin, England and Diffey 2017). Chest compression only CPR is now an integral part of initial by-stander CPR protocol (Cabrini et al. 2010). There is an increased survival rate of patients receiving chest compression only CPR as opposed to standard CPR, consisting of compressions and ventilations, or no bystander CPR at all (Bobrow et al. 2010, Svensson et al. 2010). However, this may be due to members of the public being more willing to start CPR if it involves chest compressions only. Some bystanders admit their reluctance to start standard CPR is due to the concern of contracting disease from mouth-to-mouth contact (Kern et al., 1998). Svensson et al., found no significant difference in survival rates past 30 days between compression only CPR and standardised CPR. It can be inferred that positive pressure ventilation is not paramount to patient survival and that passive insufflation may be sufficient.
Several clinical studies of ventilation&during a cardiac arrest have demonstrated respiratory rates far in excess of the 10 per minute recommended by the ERC (ONeill and Deakin, 2007 p.82). Delayed ventilation and the use of passive oxygenation may decrease the risk of hyperventilation during cardiopulmonary resuscitation as it allows less time for the patient to be hyperventilated. Pitts and Kellerman (2004) discovered that paramedics were ventilating at approximately 37 breaths per minute. Ventilations that were supplied at the recommended 12 breaths per minute were more likely to be successfully resuscitated. Ventilations in excess of 20 per minute produced significantly higher mean thoracic pressures and lower coronary perfusion pressures and could be detrimental against patient survival (Pitts and Kellerman 2004, ONeill and Deakin 2007). While there are ethical implications of using a human sample, the pigs that Pitts et al. use in their study cannot represent the human population due to, while similar, different pulmonary anatomy. Porcine tracheas are longer than humans and more cartilaginous, as well as smaller in diameter (Judge et al. 2014). It can thus be argued that these anatomical differences would have an effect on the sample numbers that survived. Despite further training, paramedics of the Milwaukee Emergency Medical Services were still hyperventilating their patients at 22 breaths per minute (Pitts and Kellerman 2004). Human factors regarding excessive positive pressure ventilation must be acknowledged. The prevalence of hyperventilation during CPR is a consequence of many factors including&the stress and excitement of responding to a cardiac arrest (Graham et al., 2015). Heart rate among ambulance staff was found to consistently increase with each emergency call, significantly so when called to acutely unwell children (Karlsson, Niemala and Jonsson 2011). Positive pressure ventilation has an impact on the preload and afterload of the heart and therefore impacting circulation (Lansdorp et al. 2014). Increased intrathoracic pressure and the consequential decrease in blood flow to the right side of the heart reduce cardiac output despite effective chest compressions (Pitts and Kellerman 2004). Pitts and Kellerman (2004) suggest that the increased intrathoracic pressure and the resulting decrease in blood flow to the right atrium was the cause of the failure to achieve ROSC. However, the Resuscitation Council UK (2015) state hyperventilation-induced vasoconstriction may worsen cerebral oxygen delivery (Resuscitation Council UK, 2015 p.6). This is paradoxical to Sigurdsson et al. (2003) who consider that ventilation is paramount to refilling the cardiac ventricles and increasing cardiac preload.
Marcy (1993) observes that hyperinflation can cause alveolar rupture, pneumothoraces and other lung trauma. Schulman, Beilin and Olshwang (1987) reveal that intrapleural pressures were twice as high with the use of simultaneous chest compressions and ventilations. Dogs resuscitated using this method were all found to have barotrauma at autopsy. Unfortunately, the CPR techniques in this study are outdated and are not in line with current resuscitation guidelines but the pathophysiology of hyperinflation would not change. Dogs are likely to tolerate different peak inspiratory airway pressures and it can be claimed that they are more susceptible to barotrauma. Despite the high intrathoracic pressures involved in positive pressure ventilation, cases of pulmonary barotrauma are relatively few (Hillman and Albin 1986).
A further by-product of positive pressure ventilation is air entering the stomach, causing gastric distension and increasing the risk of a soiled airway through regurgitation. It can be argued that tracheal intubation avoids gastric insufflation and protects against aspiration (Newell, Grier and Soar, 2018). However, there are concerns regardless of airway device of the risk of aspiration with positive pressure ventilation (Bernardini and Natalini, 2009). Kahzin et al. (2008) discovered that during their randomised study, the frequency of gastric regurgitation was similar in all airway devices using positive pressure ventilation. Therefore, it could be poignant to investigate the use of passive insufflation in current paramedic practice instead. A key component that these scholars fail to acknowledge is the use of oesophageal tubes to relieve the building pressure inside the stomach and prevent gastric regurgitation.
There is a high failure rate amongst paramedics when intubating a patient (Fullerton, Roberts and Wyse, 2009), resulting in delays in chest compressions, which can be seen as a major contributing factor to the continuing high mortality rates in OOHCA (Valenzuela et al. 2005). While these patients are still being ventilated via a BVM, Fullerton, Roberts and Wyse (2009) state that there were failure rates of 15-30% in cardiac arrests where a paramedic attempted to intubate; furthermore, there were no significant differences in failure rates between paramedic and doctor led intubations in OOHCA and therefore the skill level demonstrated in this study is irrelevant when applied to delays in chest compressions due to intubation attempts. Fullerton, Roberts and Wyse (2009) fail to account for human factors such as stress, hierarchy etc. as to why intubation was unsuccessful and chest compressions delay as a result. Seligman et al. (2017) state that loss of airway is a common cause of death among patients, highlighting the importance of having an established airway and therefore, one could argue that it is important to insert an airway as soon as possible. Conversely, both Fullerton Roberts and Wyse and Seligman et al. fail to recognise that each OOHCA job is unique and no other causes of difficult intubation or loss of airway are highlighted. While, passive insufflation removes the need or stress in attempting to insert an advanced airway, alternative methods of advanced airway such as Supra-glottic airways and I Gels, remove the interruption in chest compressions and still provide positive pressure ventilation. Also, inserting an endotracheal tube with continued chest compressions had a minor influence on their effectiveness, and therefore it can be inferred that chest compressions do not need to be stopped in order to intubate (Gatward et al. 2008).
The purpose of positive pressure ventilation is to prevent hypoxia and hypercapnia (Kill et al., 2013). Hypercapnia is associated with higher rates of mortality (del Castillo et al., 2012) and thus ventilation is associated with improved rate of return of spontaneous circulation compared with non-ventilated animals (Idris et al., 1995 p.3063). Idris et al. (1995) used a laboratory model of cardiac arrest to look at the effects hypercapnia in pigs. While this is a laboratory model and so is difficult to apply to out of hospital, adequate positive pressure ventilation was fundamental for successful resuscitation. It is a common finding in post-ROSC patients that they are acidotic (Chazan, Stenson and Kurland, 1968) whether it is due to respiratory acidosis or metabolic acidosis caused by a myocardial infarction. Post-ROSC, ineffective ventilation will result in hypercapnia which may have cerebral vasodilation consequences and prevent the patient returning to neurological normality (Newell, Grier and Soar, 2018), the main objective when resuscitating a patient. Thus, it can be inferred that by using passive insufflation as oppose to positive pressure ventilation, there would be a significant increase of hypercapnic patients post-ROSC. Del Castillo et al. (2012) found that in a study of 223 children, mortality rate for patients with hypercapnia was 59%. While this is a noteworthy figure, the results are not only limited due to sample size but the distinct physiological differences between children and adults.
In conclusion, there are findings that support passive insufflation as an intervention that is easy to teach and removes the adverse effects of positive pressure ventilation. However, these studies are observational and to progress further, randomised controlled trials should be conducted as there is very little evidence of the adverse effects of passive insufflation. Furthermore, the majority of trials that have been done are completed in a laboratory setting and samples have been primarily swine. It is clear that positive pressure ventilation has been a part of CPR guidelines due to its ability to maintain tissues perfusion and its effect on cardiac output, but while the likelihood of surviving an out of hospital cardiac arrest is higher than it used to be, the general likelihood of survival-to-hospital-discharge is still low. The only way to improve this prognosis is to explore ways in which to adapt our current guidelines.
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