A quantitative evaluation of aerosol generation during cardiopulmonary resuscitation

Abstract

It is unclear if cardiopulmonary resuscitation is an aerosol-generating procedure and whether this poses a risk of airborne disease transmission to healthcare workers and bystanders. Use of airborne transmission precautions during cardiopulmonary resuscitation may confer rescuer protection but risks patient harm due to delays in commencing treatment. To quantify the risk of respiratory aerosol generation during cardiopulmonary resuscitation in humans, we conducted an aerosol monitoring study during out-of-hospital cardiac arrests. Exhaled aerosol was recorded using an optical particle sizer spectrometer connected to the breathing system. Aerosol produced during resuscitation was compared with that produced by control participants under general anaesthesia ventilated with an equivalent respiratory pattern to cardiopulmonary resuscitation. A porcine cardiac arrest model was used to determine the independent contributions of ventilatory breaths, chest compressions and external cardiac defibrillation to aerosol generation. Time-series analysis of participants with cardiac arrest (n = 18) demonstrated a repeating waveform of respiratory aerosol that mapped to specific components of resuscitation. Very high peak aerosol concentrations were generated during ventilation of participants with cardiac arrest with median (IQR [range]) 17,926 (5546-59,209 [1523-242,648]) particles.l^-1 , which were 24-fold greater than in control participants under general anaesthesia (744 (309-2106 [23-9099]) particles.l^-1 , p < 0.001, n = 16). A substantial rise in aerosol also occurred with cardiac defibrillation and chest compressions. In a complimentary porcine model of cardiac arrest, aerosol recordings showed a strikingly similar profile to the human data. Time-averaged aerosol concentrations during ventilation were approximately 270-fold higher than before cardiac arrest (19,410 (2307-41,017 [104-136,025]) vs. 72 (41-136 [23-268]) particles.l^-1 , p = 0.008). The porcine model also confirmed that both defibrillation and chest compressions generate high concentrations of aerosol independent of, but synergistic with, ventilation. In conclusion, multiple components of cardiopulmonary resuscitation generate high concentrations of respiratory aerosol. We recommend that airborne transmission precautions are warranted in the setting of high-risk pathogens, until the airway is secured with an airway device and breathing system with a filter.

Keywords: CPR; aerosol-generating procedure; cardiopulmonary resuscitation; out-of-hospital cardiac arrest.

Figure 1

Breathing system with aerosol sampling used for all studies. HME, heat and moisture exchange filter.

Figure 2

Comparison of timelines demonstrating aerosol concentrations and their association with exhaled carbon dioxide recorded during sampling. Blue, aerosol concentration; red, ETCO₂; red arrows, ventilatory breaths. Note same y‐axis for comparison. (a) Representative timeline for a participant with cardiac arrest during CPR (30:2 compressions to breaths). This shows the repeating pattern of aerosol peaks associated with ventilatory breaths (seen also on corresponding ETCO₂ trace). Note the prolonged aerosol plateau associated with the second breath and chest compressions; (b) aerosol concentrations generated by an equivalent pattern of ventilation in a participant under general anaesthesia and not in cardiac arrest, receiving two ventilatory breaths and no chest compressions. CC, chest compressions; RC, rhythm check.

Figure 3

Timelines demonstrating aerosol concentrations and exhaled carbon dioxide values associated with chest compressions and defibrillation in human participants. Blue, aerosol concentration; red, ETCO₂; red arrows, breaths. (a) Aerosol concentrations during a period of chest compressions following a 5 s rhythm check dissociating it from ventilatory breaths; (b) aerosol generation associated with external cardiac defibrillation during CPR (black arrow, external cardiac defibrillation shock). (Data shown in (a) and (b) are from two different participants in cardiac arrest).

Figure 4

Average aerosol concentrations associated with isolated ventilatory breaths (breath 1 of the breath couplets). Bold line, median; boxplots show IQR; circles, individual data points; whiskers, range; grey, participants under general anaesthesia (n = 16); orange, participants in cardiac arrest (n = 18); blue, porcine cardiac arrest model (n = 8). ns = p > 0.05; **p < 0.01; ****p < 0.001.

Figure 5

Representative respiratory aerosol concentration and ETCO₂ during components of resuscitation in the porcine cardiac arrest model. Blue, aerosol concentration; red, ETCO₂; red arrows, breaths; CC, chest compressions; shock, external cardiac defibrillation shock. (a) Aerosol recorded during ventilation of an anaesthetised pig before termination and starting CPR; (b) aerosol generation during: compression only CPR; compressions followed by external defibrillation; and isolated defibrillation shocks; (c) aerosol generated by sequences of two ventilatory breaths followed by a 20‐s pause (x 3) without any chest compressions. This is followed by 30 x chest compressions and a 20‐s pause; followed by an isolated defibrillation shock; (d) aerosol generated during cycles of two ventilatory breaths followed by 30 x chest compressions. Note the similar aerosol and ETCO₂ profile to the human data in Fig. 2a; (e) comparison of the particle size distribution, during 60 s of ventilation of the anaesthetised animal vs. 60 s of ventilation following cardiac arrest. Aerosol concentrations normalised to dN/dlogD_p to account for the lognormal size distribution, n = 8. Blue line, pre‐arrest median; black line, post‐arrest median; (f) data in (e) normalised to the maximum value per animal. Blue line, normalised pre‐arrest median; black line, normalised post‐arrest median; shaded area, IQR. Note changes of y‐axis aerosol scale between (a–d) to best represent the data graphically.