Category Archives: Resus

Life-saving medicine

Why I don't give vasopressors in sepsis

It’s become popular to use the term ‘vasopressors’ or just ‘pressors’ when noradrenaline/norepinephrine or even (in some places still) dopamine are given. I have resisted this trend and continue to use the term ‘vasoactive’ drugs, on the basis that the effects they produce (and that we may desire) are not limited to a pure alpha adrenergic effect on vascular tone, but they have effects on heart rate and contractility too (as well as preload through venous effects). If you don’t believe me about noradrenaline/norepinephrine, then check out one of my favourite critical care papers of all time: the CAT study.
There are of course real pressors out there – phenylephrine acts on alpha receptors, as does methoxamine. Metaraminol predominantly acts on alpha receptors but does also cause some release of noradrenaline/norepinephrine.
Why is this important? All these drugs will fix hypotension, right? Yes, they should. However should blood pressure be our main treatment goal? What we’re really interested in is organ perfusion, which depends on regional blood flow to vital organs. It’s possible that a drug could fix the measured blood pressure and give a nice ‘macroscopic’ number, while at the same time reducing cardiac output and adversely affecting regional blood flow to organs through local vasoconstrictive effects. My view is that this is more likely with pure ‘pressors’ (like phenylephrine), which is why I avoid them in septic shock and opt for catecholamine infusions (noradrenaline/norepinephrine).
This is important in my practice setting of retrieval medicine, where, prior to interfacility transport, physicians might sometimes be tempted to ‘push pressors’ peripherally rather than insert a central venous catheter and commence a catecholamine infusion. While the former approach might be more expeditious and make the vital signs chart look pretty, one wonders about what effect this is having on tissue oxygen delivery.
A fascinating review of papers on pressor physiology1 suggests these agents have the following effects:

  • conflicting data on changes in myocardial perfusion
  • increase both left and right heart afterload
  • decrease venous compliance with the potential to increase venous return although the impact of this on cardiac output is controversial
  • controversial effect on cerebral bloodflow
  • decrease bloodflow to the kidneys
  • adverse affects on gastrointestinal tract bloodflow


abstract1
Phenylephrine and methoxamine are direct-acting, predominantly α(1) adrenergic receptor (AR) agonists. To better understand their physiologic effects, we screened 463 articles on the basis of PubMed searches of “methoxamine” and “phenylephrine” (limited to human, randomized studies published in English), as well as citations found therein. Relevant articles, as well as those discovered in the peer-review process, were incorporated into this review. Both methoxamine and phenylephrine increase cardiac afterload via several mechanisms, including increased vascular resistance, decreased vascular compliance, and disadvantageous alterations in the pressure waveforms produced by the pulsatile heart. Although pure α(1) agonists increase arterial blood pressure, neither animal nor human studies have ever shown pure α(1)-agonism to produce a favorable change in myocardial energetics because of the resultant increase in myocardial workload. Furthermore, the cost of increased blood pressure after pure α(1)-agonism is almost invariably decreased cardiac output, likely due to increases in venous resistance. The venous system contains α(1) ARs, and though stimulation of α(1) ARs decreases capacitance and may transiently increase venous return, this gain may be offset by changes in afterload, venous compliance, and venous resistance. Data on the effects of α(1) stimulation in the central nervous system show conflicting changes, while experimental animal data suggest that renal blood flow is reduced by α(1)-agonists, and both animal and human data suggest that gastrointestinal perfusion may be reduced by α(1) tone.

A review of clinical articles2 reveals few evidence-based indications for true pressors. Possible situations where they may be of benefit include intraoperative hypotension, aortic stenosis, during cyanotic episodes in Tetralogy of Fallot, and some obstetric situations. In the setting of sepis, phenylephrine has been compared with noradrenaline in which an initial pilot study found a statistically significant reduction in creatinine clearance and increase in arterial lactate after initiating the phenylephrine infusion. However a subsequent randomised controlled comparison of phenylephrine with noradrenaline/norepinephrine did not show differences in cardiopulmonary performance, global oxygen transport, or regional hemodynamics, although there were only 16 patients in each group3.


abstract2
Phenylephrine is a direct-acting, predominantly α(1) adrenergic receptor agonist used by anesthesiologists and intensivists to treat hypotension. A variety of physiologic studies suggest that α-agonists increase cardiac afterload, reduce venous compliance, and reduce renal bloodflow. The effects on gastrointestinal and cerebral perfusion are controversial. To better understand the effects of phenylephrine in a variety of clinical settings, we screened 463 articles on the basis of PubMed searches of “methoxamine,” a long-acting α agonist, and “phenylephrine” (limited to human, randomized studies published in English), as well as citations found therein. Relevant articles, as well as those discovered in the peer-review process, were incorporated into this review. Phenylephrine has been studied as an antihypotensive drug in patients with severe aortic stenosis, as a treatment for decompensated tetralogy of Fallot and hypoxemia during 1-lung ventilation, as well as for the treatment of septic shock, traumatic brain injury, vasospasm status-postsubarachnoid hemorrhage, and hypotension during cesarean delivery. In specific instances (critical aortic stenosis, tetralogy of Fallot, hypotension during cesarean delivery) in which the regional effects of phenylephrine (e.g., decreased heart rate, favorable alterations in Q(p):Q(s) ratio, improved fetal oxygen supply:demand ratio) outweigh its global effects (e.g., decreased cardiac output), phenylephrine may be a rational pharmacologic choice. In pathophysiologic states in which no regional advantages are gained by using an α(1) agonist, alternative vasopressors should be sought.

These review articles reinforce my own bias against the use of pure pressors in septic shock, although clearly more clinical research is needed. I am inclined to agree with the reviewers’ concluding statement:
…in all clinical settings, phenylephrine reduces cardiac output, and in most clinical settings has been shown to significantly increase LV afterload. Thus, only in instances in which its regional effects are thought to outweigh its global effects should phenylephrine be used for the treatment of hypotension.
1. The physiologic implications of isolated alpha(1) adrenergic stimulation
Anesth Analg. 2011 Aug;113(2):284-96
2. The clinical implications of isolated alpha(1) adrenergic stimulation
Anesth Analg. 2011 Aug;113(2):297-304
3. Phenylephrine versus norepinephrine for initial hemodynamic support of patients with septic shock: a randomized, controlled trial
Crit Care. 2008;12(6):R143
Full Text available here

Pre-hospital CPAP for pulmonary oedema

The physician-staffed mobile intensive care units of SAMU (Service d’Aide Médicale Urgente) in France provided the location for this randomised controlled trial of CPAP for acute cardiogenic pulmonary oedema.


STUDY OBJECTIVE: The purpose of this randomized controlled trial was to determine the immediate and delayed effects of noninvasive ventilation for patients in acute cardiogenic pulmonary edema (ACPE) in addition to aggressive usual care in a medical prehospital setting.

METHODS: Out-of-hospital patients in severe ACPE were eligible for the study. Patients were randomized to receive either usual care, including conventional optimal treatment with furosemide, oxygen, and high-dose boluses of isosorbide dinitrate plus oxygen, or conventional medications plus out-of-hospital continuous positive airway pressure (CPAP). The primary outcome was the treatment success defined as all of respiratory rate less than 25 breaths per minute and oxygen saturation of greater than 90% at the end of 1-hour study. Secondary end points included death during 30 days after inclusion. Lengths of intensive care unit and hospital stays were also recorded.

RESULTS: In total, 124 patients were enrolled into the study. The 2 groups had similar baseline characteristics. For the primary outcome analysis, 22 (35.5%) of 62 patients were considered as experiencing a treatment success in the usual care group vs 19 (31.7%) of 60 in the CPAP group (P = .65). Seven patients died within 30 days in the usual care group vs 6 in the CPAP group (P = .52). There were no statistically significant differences between the treatment groups for length of stay either in hospital or in the intensive care unit.

CONCLUSION: In the prehospital setting, in spite of its potential advantages for patients in ACPE, CPAP may not be preferred to a strict optimal intravenous treatment.

Continuous positive airway pressure for cardiogenic pulmonary edema: a randomized study
Am J Emerg Med. 2011 Sep;29(7):775-81

Prehospital Spine Immobilisation for Penetrating Trauma

The Executive Committee of Prehospital Trauma Life Support, comprised of surgeons, emergency physicians, and paramedics, has reviewed the literature and produced the following recommendations on Prehospital Spine Immobilisation for Penetrating Trauma:


PHTLS Recommendations

  • There are no data to support routine spine immobilization in patients with penetrating trauma to the neck or torso.
  • There are no data to support routine spine immobilization in patients with isolated penetrating trauma to the cranium.
  • Spine immobilization should never be done at the expense of accurate physical examination or identification and correction of life-threatening conditions in patients with penetrating trauma.
  • Spinal immobilization may be performed after penetrating injury when a focal neurologic deficit is noted on physical examination although there is little evidence of benefit even in these cases.

Prehospital Spine Immobilization for Penetrating Trauma—Review and Recommendations From the Prehospital Trauma Life Support Executive Committee
Journal of Trauma-Injury Infection & Critical Care September 2011;71(3):763-770

Pre-hospital thoracotomy

The London Helicopter Emergency Medical Service provides a physician / paramedic team to victims of trauma. One of the interventions performed by their physicians is pre-hospital resuscitative thoracotomy to patients with cardiac arrest due to penetrating thoracic trauma. They have published the outcomes from this procedure over a 15 year period which show an 18% survival to discharge rate, with a high rate of neurologically intact survivors1.
The article was submitted for publication on February 1, 2010, and in the discussion mentions a further two survivors from the procedure performed after conducting the study. It is likely therefore in the year and a half since submission still more patients have been saved. It will be interesting to read future reports from this team as the numbers accumulate; penetrating trauma missions are sadly increasing in frequency.
Having worked for these guys and performed this procedure in the field a few times myself, I can attest to the training and governance surrounding this system. The technique of clamshell thoracotomy is well described 2 and one I would recommend for the non-surgeon.

BACKGROUND: Prehospital cardiac arrest associated with trauma almost always results in death. A case of survival after prehospital thoracotomy was published in 1994 and several others have followed. This article describes the result of prehospital thoracotomy in a physician-led system for patients with stab wounds to the chest who suffered cardiac arrest on scene.
METHODS: A 15-year retrospective prehospital trauma database review identified victims of stab wounds to the chest who suffered cardiac arrest on scene and had thoracotomy performed according to local standard operating procedures.
RESULTS: Overall, 71 patients met inclusion criteria. Thirteen patients (18%) survived to hospital discharge. Neurologic outcome was good in 11 patients and poor in 2. Presenting cardiac rhythm was asystole in four patients, pulseless electrical activity in five, and unrecorded in the remaining four. All survivors had cardiac tamponade. The medical team was present at the time of cardiac arrest for six survivors (good neurologic outcome): arrived in the first 5 minutes after arrest in three patients (all good neurologic outcome), arrived 5 minutes to 10 minutes after arrest in two patients (one poor neurologic outcome), and in one patient (poor neurologic outcome) the period was unknown. Of the survivors, seven thoracotomies were performed by emergency physicians and six by anesthesiologists.
CONCLUSIONS: Prehospital thoracotomy is a well-established procedure in this physician-led prehospital service. Results from this and other similar systems suggest that when performed for the subgroup of patients described, significant numbers of survivors with good neurologic outcome can be expected.

1. Thirteen Survivors of Prehospital Thoracotomy for Penetrating Trauma: A Prehospital Physician-Performed Resuscitation Procedure That Can Yield Good Results
J Trauma. 2011 May;70(5):E75-8
2. Emergency thoracotomy: “how to do it”
Emerg Med J. 2005 January; 22(1):22–24
Full text available here

Exsanguinating cardiac arrest not always fatal

The British Military has developed a reputation for aggressive pre-hospital critical care including (but not limited to) the use of blood products and tourniquets, and coordinated field hospital trauma care. They now report the outcomes for patients with traumatic cardiac arrest, mainly from improvised explosive devices. Of 52 patients, 14 (27%) demonstrated return of spontaneous circulation (ROSC), of whom four (8%) survived to hospital discharge with a neurologically good recovery. Resuscitative thoracotomy (RT) was performed on 12 patients (8 in the ED), including all four survivors. RT enabled open-chest CPR, release of pericardial tamponade, lung resection and compression of the descending thoracic aorta for haemorrhage control.
No patients who arrested in the field survived, although one of the neurologically well-recovered survivors arrested during transport to hospital and was in cardiac arrest for 24 minutes. The authors propose this individual’s survival was in part due to ‘the high level of care that he received during retrieval, including haemorrhage control, tracheal intubation and transfusion of blood products‘.
Asystole was universally associated with death but agonal / bradycardic rhythms were not. In keeping with other studies, cardiac activity on ultrasound was associated with ROSC.


AIM: To determine the characteristics of military traumatic cardiorespiratory arrest (TCRA), and to identify factors associated with successful resuscitation.

METHODS: Data was collected prospectively for adult casualties suffering TCRA presenting to a military field hospital in Helmand Province, Afghanistan between 29 November 2009 and 13 June 2010.

RESULTS: Data was available for 52 patients meeting the inclusion criteria. The mean age (range) was 25 (18-36) years. The principal mechanism of injury was improvised explosive device (IED) explosion, the lower limbs were the most common sites of injury and exsanguination was the most common cause of arrest. Fourteen (27%) patients exhibited ROSC and four (8%) survived to discharge. All survivors achieved a good neurological recovery by Glasgow Outcome Scale. Three survivors had arrested due to exsanguination and one had arrested due to pericardial tamponade. All survivors had arrested after commencing transport to hospital and the longest duration of arrest associated with survival was 24min. All survivors demonstrated PEA rhythms on ECG during arrest. When performed, 6/24 patients had ultrasound evidence of cardiac activity during arrest; all six with cardiac activity subsequently exhibited ROSC and two survived to hospital discharge.

CONCLUSION: Overall rates of survival from military TCRA were similar to published civilian data, despite military TCRA victims presenting with high Injury Severity Scores and exsanguination due to blast and fragmentation injuries. Factors associated with successful resuscitation included arrest beginning after transport to hospital, the presence of electrical activity on ECG, and the presence of cardiac movement on ultrasound examination.

Outcomes following military traumatic cardiorespiratory arrest: A prospective observational study
Resuscitation. 2011 Sep;82(9):1194-7

Trauma mortality and systolic BP

Here’s some further evidence that a ‘lowish’ – as opposed to a low – systolic blood pressure is a reason to be vigilant in trauma. In this study, it was BP measurement in the ED (rather than pre-hospital) that was assessed:


Introduction: Non-invasive systolic blood pressure (SBP) measurement is often used in triaging trauma patients. Traditionally, SBP < 90 mmHg has represented the threshold for hypotension, but recent studies have suggested redefining hypotension as SBP < 110 mmHg. This study aims to examine the association of SBP with mortality in blunt trauma patients.
Methods: This is an analysis of prospectively recorded data from adult (≥16 years) blunt trauma patients. Included patients presented to hospitals belonging to the Trauma Audit and Research Network (TARN) between 2000 and 2009. The primary outcome was the association of SBP and mortality rates at 30 days. Multivariate logistic regression models were used to adjust for the influence of age, gender, Injury Severity Score (ISS) and Glasgow Coma Score (GCS) on mortality.

Results: 47,927 eligible patients presented to TARN hospitals during the study period. Sample demographics were: median age: 51.1 years (IQR=32.8–67.4); male 60% (n=28,694); median ISS 9 (IQR = 8–10); median GCS 15 (IQR = 15–15); and median SBP 135 mmHg (IQR = 120–152). We identified SBP < 110 mmHg as a cut off for hypotension, where a significant increase in mortality was observed. Mor- tality rates doubled at <100 mmHg, tripled at <90 mmHg and were 5- to 6-fold at <70 mmHg, irrespective of age.
Conclusion: We recommend triaging adult blunt trauma patients with a SBP < 110 mmHg to resuscitation areas within dedicated trauma units for close monitoring and appropriate management.

Systolic blood pressure below 110mmHg is associated with increased mortality in blunt major trauma patients: Multicentre cohort study
Resuscitation. 2011 Sep;82(9):1202-7

Score to predict traumatic coagulopathy

Acute traumatic coagulopathy (ATC) is present in up to 25% of major trauma patients by the time they arrive in hospital. A predictive tool called the coagulopathy of severe trauma (COAST) score was retrospectively derived and then prospectively validated in major trauma patients in the state of Victoria, Australia. The definition of ATC was INR > 1.5 (1.0–1.3) or aPTT of > 60 s (25–38 s) on hospital presentation.
The study claims that a subgroup of patients with acute traumatic coagulopathy can be accurately identified based on simple observations in the pre-hospital phase or immediately on presentation to the ED, and that this could improve the feasibility of prospective interventional studies. Perhaps this will lead on to evaluation of pre-hospital tranexamic acid or even blood products?
At the cutoff score of ≥3, 40 coagulopathic patients would have been missed with 60 patients correctly predicted. The authors argue that while the low sensitivity of the score missed these coagulopathic patients, they had significantly better outcomes (and contained a significantly higher proportion of patients with isolated severe head injury).


Introduction: The inability to accurately predict acute traumatic coagulopathy (ATC) has been a key factor in the low level of evidence guiding its management. The aim of this study was to develop a tool to accurately identify patients with ATC using pre-hospital variables without the use of pathology or radiological testing.

Methods: Retrospective data from the trauma registry on major trauma patients were used to identify vari- ables independently associated with coagulopathy. These variables were clinically evaluated to develop a scoring system to predict ATC, which was prospectively validated in the same setting.

Results: There were 1680 major trauma patients in the derivation dataset, with 151 patients being coagulopathic. Pre-hospital variables independently associated with ATC were entrapment (OR 1.85; 95% CI: 1.12–3.06), temperature (OR 0.60; 95% CI: 0.60–0.72), systolic blood pressure (OR 0.99; 95% CI: 0.98–0.99), abdominal or pelvic content injury (OR 2.0; 95% CI: 1.27–3.12) and pre-hospital chest decompression (OR 4.99; 2.77–8.99). The COAST score was developed, scoring points for entrapment, temperature <35 ◦ C, systolic blood pressure <100 mm Hg, abdominal or pelvic content injury and chest decompression. Prospectively validated using 1225 major trauma patients, a COAST score of ≥3 had a specificity of 96.4% with a sensitivity of 60.0%, with an area under the receiver operating characteristic curve of 0.83 (0.78–0.88).
Conclusions: The COAST score accurately identified a group of patients with ATC using pre-hospital obser- vations. This predictive tool can be used to select patients for inclusion into prospective studies examining management options for ATC. Mortality in these patients is high, potentially improving feasibility of outcome studies.

Still no cardiac arrest survival benefit from epinephrine?

A double blind randomised controlled trial showed significantly better rates of return of spontaneous circulation and hospital admission with the use of adrenaline (epinephrine) compared with placebo. This effect was observed with both shockable and non-shockable initial cardiac arrest rhythms. There was no statistically significant difference in the primary outcome of survival to hospital discharge.
Interesting but unfortunate political factors appear to have prevented recruitment to the required numbers of patients for this study so it is underpowered for its primary outcome of survival to hospital discharge, which in the adrenaline group was double that in the placebo group, although this did not reach statistical significance. What was supposed to be a multi-centre study became a single centre one and it was not possible to continue as the study drugs reached their expiry date and no additional funding was available.
So do ROSC and survival to admission matter? The authors make the following point:


While not the primary outcome of our study, ROSC is an increasingly important clinical endpoint as the influence of post resuscitation care interventions (i.e.: therapeutic hypothermia, managing underlying cause, organ perfusion and oxygenation) on survival to hospital discharge are recognised.

Optimum dose and timing of adrenaline remain unknown, along with whether it impacts on long-term outcomes.


BACKGROUND: There is little evidence from clinical trials that the use of adrenaline (epinephrine) in treating cardiac arrest improves survival, despite adrenaline being considered standard of care for many decades. The aim of our study was to determine the effect of adrenaline on patient survival to hospital discharge in out of hospital cardiac arrest.

METHODS: We conducted a double blind randomised placebo-controlled trial of adrenaline in out-of-hospital cardiac arrest. Identical study vials containing either adrenaline 1:1000 or placebo (sodium chloride 0.9%) were prepared. Patients were randomly allocated to receive 1ml aliquots of the trial drug according to current advanced life support guidelines. Outcomes assessed included survival to hospital discharge (primary outcome), pre-hospital return of spontaneous circulation (ROSC) and neurological outcome (Cerebral Performance Category Score – CPC).

RESULTS: A total of 4103 cardiac arrests were screened during the study period of which 601 underwent randomisation. Documentation was available for a total of 534 patients: 262 in the placebo group and 272 in the adrenaline group. Groups were well matched for baseline characteristics including age, gender and receiving bystander CPR. ROSC occurred in 22 (8.4%) of patients receiving placebo and 64 (23.5%) who received adrenaline (OR=3.4; 95% CI 2.0-5.6). Survival to hospital discharge occurred in 5 (1.9%) and 11 (4.0%) patients receiving placebo or adrenaline respectively (OR=2.2; 95% CI 0.7-6.3). All but two patients (both in the adrenaline group) had a CPC score of 1-2.

CONCLUSION: Patients receiving adrenaline during cardiac arrest had no statistically significant improvement in the primary outcome of survival to hospital discharge although there was a significantly improved likelihood of achieving ROSC.

Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
Resuscitation. 2011 Sep;82(9):1138-43

Pre-hospital ECMO

Two cases are reported of the pre-hospital institution of venoarterial extracorporeal membrane oxygenation (ECMO) for patients in cardiac arrest. One was from France and the other from Germany – both countries with mature physician-staffed pre-hospital systems. The two cases were a 9 yr old drowning victim1 and a 48 year old marathon runner2. They each received BLS then ACLS then ECMO, and both went from asystole to sinus rhythm after the institution of ECMO. Sadly both failed to neurologically recover and died in hospital.
If irreversible anoxic encephalopathy could be detected in the field, patients could be better selected for this intervention. An editorialist3 states:


Until we have a hand held device which can measure neuronal integrity on a cellular level in the field we must use our best judgement, and in many cases give the patient the benefit of the doubt by cannulating them, cooling for 24 h and then making a neurological assessment and withdrawing ECLS if necessary.

Other issues to consider are:

  • Can society afford this level of intervention?
  • Could this intervention, when associated with brain death, result in sufficiently recovered organs for transplantation?
  • How can the infrastructure be created to enable rapid institution of pre-hospital ECMO?

I suspect as the equipment becomes even more portable and self-maintaining, pre-hospital / retrieval physicians already expert in critical care interventions such as seldinger-guided vascular access will be the ones instituting this therapy. In the meantime, we await evidence of outcome benefit and some objective means of case selection.
1. Out-of-hospital extracorporeal life support for cardiac arrest—A case report
Resuscitation. 2011 Sep;82(9):1243-5
2. Out-of-hospital extra-corporeal life support implantation during refractory cardiac arrest in a half-marathon runner
Resuscitation. 2011 Sep;82(9):1239-42
3. Community extracorporeal life support for cardiac arrest – When should it be used?
Resuscitation. 2011 Sep;82(9):1117

Mouth-to-nose breathing

Interesting – mouth to nose breathing was more effective than mouth-to-mouth in simulated resuscitations using anaesthetised, apnoeic patients:


BACKGROUND: The authors hypothesized that mouth ventilation by a resuscitator via the nasal route ensures a more patent airway and more effective ventilation than does ventilation via the oral route and therefore would be the optimal manner to ventilate adult patients in emergencies, such as during cardiopulmonary resuscitation. They tested the hypothesis by comparing the effectiveness of mouth-to-nose breathing (MNB) and mouth-to-mouth breathing (MMB) in anesthetized, apneic, adult subjects without muscle paralysis.

METHODS: Twenty subjects under general anesthesia randomly received MMB and MNB with their heads placed first in a neutral position and then an extended position. A single operator performed MNB and MMB at the target breathing rate of 10 breaths/min, inspiratory:expiratory ratio 1:2 and peak inspiratory airway pressure 24 cm H₂O. A plethysmograph was used to measure the amplitude change during MMB and MNB. The inspiratory and expiratory tidal volumes during MMB and MNB were calculated retrospectively using the calibration curve.

RESULTS: All data are presented as medians (interquartile ranges). The rates of effective ventilation (expired volume > estimated anatomic dead space) during MNB and MMB were 91.1% (42.4-100%) and 43.1% (42.5-100%) (P < 0.001), and expired tidal volume with MMB 130.5 ml (44.0-372.8 ml) was significantly lower than with MNB 324.5 ml (140.8-509.0 ml), regardless of the head position (P < 0.001).
CONCLUSIONS: Direct mouth ventilation delivered exclusively via the nose is significantly more effective than that delivered via the mouth in anesthetized, apneic adult subjects without muscle paralysis. Additional studies are needed to establish whether using this breathing technique during emergency situations will improve patient outcomes.

Effectiveness of breathing through nasal and oral routes in unconscious apneic adult human subjects: a prospective randomized crossover trial
Anesthesiology. 2011 Jul;115(1):129-35