The prompt treatment of pain and the control of seizures are essential parts of paramedic practice. This has resulted in paramedics, in many parts of the world, being empowered to administer opiate analgesia and benzodiazepines. These drugs are increasingly being supplemented by Ketamine—both as an analgesic agent, as well as for its sedatory properties.
While these drugs are deemed to be safe for pre-hospital administration, their use does represent a risk of drug-induced respiratory depression. This has resulted in a number of ambulance services also providing reversal agents such as Naloxone (primarily provided for reversal of recreational over-dose) and Flumazenil for use in iatrogenic-induced respiratory depression. However, these drugs are not without side-effects—most notably, the reversal of the analgesic effects of opiates and blocking the anti-convulsion properties of benzodiazepines. Regardless of whether reversal agents are required, their use would still require that the paramedic can accurately identify that respiratory depression has occurred.
So what is the answer to the safe administration of these drugs within the cramped, often poorly-lit and moving ambulance? The answer is essentially prompt recognition through the use of effective monitoring to identify impending respiratory depression before it happens. This is because interventions such as gentle stimulus can instigate effective breathing. Hamad Medical Corporation Ambulance Service (HMC AS) mandates continuous monitoring of nasal EtC02, Sp02, four-lead ECG and non-invasive blood pressure (NiBP) in all patients who receive Fentanyl, Midazolam or Ketamine, supported by supplementary nasal oxygen, at 2–4 litres/minute (lpm), reflecting published best practice guidelines (Academy of Medical Royal Colleges, 2013).
For many critical care paramedics, this represented a significant change in clinical practice, as they have traditionally relied solely upon Sp02 monitoring. So why is EtC02 such an essential element of safe patient monitoring? The short answer is: why wait for hypoxia and/or apnoea to develop before identifying respiratory depression? Especially when continuous nasal EtC02 monitoring will detect the development of hypoventilation much earlier than can be detected by a drop in Sp02 monitoring (Miner et al, 2002; Burton et al, 2006), which may only occur post apnoea. Burton et al noted that in patients undergoing procedural sedation, one-third experienced hypoventilation and/or apnoea which was detected by EtCO2 in 70% of patients up to 4 minutes before a drop in SpO2 was detected. Similar results have been noted by Miner et al. There is a marked time lag between hypoventilation and/or apnoea developing and a drop in Sp02 being noted (Miner et al, 2002). While the use of supplementary oxygen can safely prolong any apnoeic period, it is not a replacement for effective monitoring.
The ability to provide effective analgesia is the hallmark of an effective healthcare system. However, this must be done safely to minimise the risk to patients when potent medications are used. The availability of simple-to-use and reliable EtC02 monitoring is an essential part of pre-hospital monitoring.