Must have done at least 6 months of anaesthetics/ICU
Must have at least 3 staff members – someone to perform sedation, someone to perform procedure, someone to monitor the patient
Department must be safe – Senior ED clinician in department has final say over if it is appropriate to perform at any given time.
Where should it be performed?
Full monitoring – 3 lead ECG, sats probe, BP cuff, CO2 monitoring
Levels of Sedation
Analgesia: Relief of pain without intentionally producing a sedated state. Altered mental status may occur as a secondary effect of medications administered for analgesia.
Minimal sedation (anxiolysis): The patient responds normally to verbal commands. Cognitive function and coordination may be impaired, but ventilatory and cardiovascular functions are unaffected.
Moderate sedation and analgesia: The patient responds purposefully to verbal commands alone or when accompanied by light touch. Protective airway reflexes and adequate ventilation are maintained without intervention. Cardiovascular function remains stable.
Deep sedation and analgesia: The patient cannot be easily aroused but responds purposefully to noxious stimulation. Assistance may be needed to ensure the airway is protected and adequate ventilation maintained. Cardiovascular function is usually stable.
General anaesthesia: The patient cannot be aroused and often requires assistance to protect the airway and maintain ventilation. Cardiovascular function may be impaired.
Dissociative sedation: Dissociative sedation is a trance-like cataleptic state in which the patient experiences profound analgesia and amnesia, but retains airway protective reflexes, spontaneous respirations, and cardiopulmonary stability. Ketamine is the pharmacologic agent used for procedural sedation that produces this state
Any procedure that may cause pain and anxiety
Most commonly bone/joint manipulations
Patient is clinically unwell/unstable – anaesthetic assistance should be sought
Patient is assessed to have a potentially ‘difficult airway’ – anaesthetic assistance should be sought and procedure reconsidered – may be more appropriate to be done in theatre
For an emergency procedure in a patient who has not fasted, balance the risks and benefits of the decision to proceed with sedation before fasting criteria are achieved, on the urgency of the procedure and the target depth of sedation..
If safe and appropriate to wait until fully fasted, wait:
2 hours for clear fluids
6 hours for solids
Patient MUST be consented appropriately
Risks and benefits along with potential side effects should be explained
The ACS pathway is for patients where coronary ischemia is in your differential. It is not a blanket pathway for chest pain of unknown cause.
Patients presenting >8hrs post chest pain *NEW*
If an initial trop is taken >8 hours post chest pain, and patients have no new ECG ischaemia, and no history of unstable angina, there is no compulsion to repeat a second troponin.
ACS Treatment(Not STEMI going for PPCI)
Aspirin 300mg stat
Ticagrelor 180mg stat
Fondaparinux 2.5mg sc stat.
Anticoagulated with a NOAC, or with Warfarin (with a therapeutic INR),
Aspirin 300mg stat
Clopidogrel 300mg stat
Treatment STEMI going for PPCI
Aspirin 300mg stat
Ticagrelor 180mg stat (NO Hx of CVA)
Prasugrel 60mg stat (Hx of CVA)
Direct admissions to CCU
Patients with ST Elevation (if not accepted for primary PCI) or those with CP + new ST Depression should be discussed with a local Cardiologist and come directly to CCU.
As it is difficult to be prescriptive for every other circumstance, a discussion with a senior / cardiologist may be worthwhile in order to best place your patient within the hospital. Factors that should make you think about a senior discussion are included on the pathway.
Patients where MI is excluded
If patients do exit the pathway (no new symptoms, no new ECG ischemia and troponins that meet the exit criteria to exclude an MI), two other important possibilities still require consideration:
Is the history in keeping with unstable angina? (This is still an ACS). If so the patient will require an acute inpatient admission with telemetry and IP cardiology review.
Is the chest pain due to a significant alternative diagnosis? If so this still needs to be actively considered/ investigated/ treated.
Patients on Warfarin/DOAC : Use Asprin and Clopidogrel
When do we take the blood samples? – The initial troponin must be taken at least 2hrs after chest pain, a second trop may be required 6hrs after the 1st (AAU/CDU)
Do we need to do a HEART score? – No, evidence shows the use of risk stratification in these pathways doesn’t increase safety but only increases admissions
Can we rule out ACS after the first trop?[Symptoms of Unstable Angina require admission]
Troponin <5ng and the ecg is normal we can rule out ACS.
Troponin <39ng(female)/58ng(male) and >8hrs from onset of chest pain [this is a pragmatic decision agreed locally by EM/AM?cardiology]
Why does it have different cut offs for male/female? – It is known women have significantly lower troponin to men, ESC recommends using the different cut offs
How should we treat transgender/intersex patients – There is no good evidence I can find (I would suggest using the female cut off – as patients who have transitioned to male are probably not going to have as high a troponin, and those who have transitioned to females may have reduced their baseline troponin with hormone therapy) – Be aware the lab can only report against the one registered sex for the patient.
Doesn’t highSTEACS have a 3hr Trop too? – Yes it does and in time we will be aiming to utilise this too. However, this relies on using Delta’s (i.e. the change in troponin), and it is felt that it is worth delaying introduction of this until we have got used to the new pathway.
Why are the numbers on the official highSTEACS pathway different? – This is because it uses the Abbott test. the highSTEACS pathway has been also validated on the Siemens assay we will be using. As to why the Abbot and Siemens cut-offs are so different, this is due to the way the assays amplify the troponin present (its not as simple as a U&E that just measures what is there).
We now have no excuse for loosing ECGs and not sending them to the wards with patients!
Please ensure you put an operator ID in as well as all the patient information to ensure the ECG transmits to EPR – if you are having problems look at the troubleshooting guide on the side of the machine.
Ensure a doctor/ACP signs all ECGs using EPR – just like when they were paper!
The presentation of AHF can vary but tends to fall in to the following 4 categories, which can be determined clinically and can help guide your approach to treatment; warm-dry, warm-wet, cold-dry, cold-wet.
It is worth noting that the vast majority of patients will be norm-hypertensive. However, 5-8% are Hypertensive this confers a very poor prognosis.
ECG: Rarely normal (High NPV), and may identify underlying cause
CXR: Pulmonary congestion, Effusion, Cardiomegaly (20% will have an almost “Normal” CXR)
BNP: Can be helpful (we have it)
>845 show increased mortality
<100 AHF is unlikely
BNP is not a specific test and will elevate for many reasons
POCUS: This can be very useful in identifying cases but training is required [Bilat B lines in 2 zones each side]
Condition specific tests: Try to identify the underlying trigger dependent on history and exam (e.g. ABG, Trop, U&E, TFT, LFT, CTPA)
ECHO: this is important but not necessary in the ED phase (unless the patient has haemodynamic instability i.e. cardiogenic shock)
Treatment – Time Matters!!!
Mortality increased by 1%/hour IV treatment not started
Treatment after 12hrs from onset makes little difference
Treat The Cause!: If you can identify the trigger treat it it will in turn improve the AHF. (e.g. AMI, Arrythmia(Tachy/Brady), Massive PE)
Vasodilator: has 2 effects reducing vascular resistance and thus increasing stroke volume [NOT to be used if sBP<90mmHg]