Category: Cardiac

ECG placement & mis-LEADing ECG’s

  • V1: 4th intercostal space (ICS), RIGHT margin of the sternum
  • V2: 4th ICS along the LEFT margin of the sternum
  • V4: 5th ICS, mid-clavicular line
  • V3: midway between V2 and V4
  • V5: 5th ICS, anterior axillary line (same level as V4)
  • V7: Left posterior axillary line, in the same horizontal plane as V6.
  • V8: Tip of the left scapula, in the same horizontal plane as V6.
  • V9: Left paraspinal region, in the same horizontal plane as V6.

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Adult Sedation

This guideline is a brief summary of the RCEM 2012 Safe sedation in the ED and RCEM – Pharmacological Agents for Procedural Sedation and Analgesia in the Emergency Department – March 2019. Please read these documents in full or participate in RCEM learning elearning for further information.

 

Who can perform it?

  • Senior medical staff (ST3+)
  • 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?

  • ED resus
  • 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

Indications

  • Any procedure that may cause pain and anxiety
    • Most commonly bone/joint manipulations
    • DC cardioversion

Contraindications

Fasting

  • 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

Consent

Medications

DRUGROLEROUTEINITIAL DOSE (elderly)REPEAT DOSE (elderly)INITIAL DOSE (adult)REPEAT DOSE (adult)ONSET (min)PEAK EFFECT (min)
PropofolSedation/AmnesiaIV10-20mg (slowly)10-20mg (slowly)0.5-1mg/kg0.5mg/kg every 3-5min0.5-11-2
MidazolamSedation/AmnesiaIV (over 1-2 min)0.5mg0.5mg1-2mg (max 2.5mg as single dose)After 2-5min1-23-4
KetamineSedation/Amnesia/AnalgesiaIV (give over 30-60sec)10-30mg1mg/kg0.25-0.5mg/kg every 5-10 min0.5-11-2
KetamineSedation/Amnesia/AnalgesiaIM4-5mg/kg2-2.5mg/kg every 5-10min0.5-11-2
KetamineAnalgesia (sub-dissociative)IV0.3mg/kg0.5-11-2
FentanylAnalgesia (with other sedation)IVup to 0.5µg/kgup to 0.5µg/kg (every 2min)1-23-5
FentanylSedation/AmnesiaIVup to 0.5-1.0µg/kg up to 0.5-1.0µg/kg (every 2min)1-23-5
KetofolSedation/Amnesia/AnalgesiaIV0.5-0.75mg/kg (of both agents)0.5-11-2

RCEM – Pharmacological Agents for Procedural Sedation and Analgesia in the Emergency Department – March 2019 – see this document for the references numbered in the table. Only use medications that you are familiar with unless supervised by an experienced colleague.

Post sedation care

  • Patient must be observed in a safe place until:
    • Observations returned to normal
    • The patient is fully awake with intact airway reflexes
    • Nausea, vomiting and pain have been fully addressed
  • Patient must be advised not to drive for 24 hours.
  • Advice leaflet should be given. – HERE
  • Fill in adhoc form on EPR – this covers pre sedation airway assessment, drugs given and any complications
  • Ensure any drugs used are prescribed and signed for. Controlled drugs should also be signed in the CD book by whoever administered them.

Pulmonary Embolism in Pregnancy

Unfortunately the the normal pathway for investigation of PE performs poorly in pregnancy RCOG have the following pathway

1. Investigation – of suspected PE

  • Clinical assessment – its all on the history and exam scoring doesn’t work
  • Perform the following tests:
    • CXR – sheilding can protect the baby and may avoid further radiation
    • ECG
    • Bloods: FBC, U&E, LFTs
  • Commence Dalteparin (unless treatment is contraindicated) – Trust Guide
  • Arrange admission to AAU/AMU (>20/40  AMU @CRH and inform Obstetrics) – if admission not agreed refer to advice below

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ACS (HS-Trop) Pathway

When is the ACS pathway used? 

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: 

  1.  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. 
  2.  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

PDF: Full Guidance

FAQ’s

  • highSTEACS pathway developed in scotland. 
  • 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).

 

Digital ECG

Digital ECG has now gone live on both sites.

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!

Quick Reference and Trouble Shooting Guide are available here  Digital ECG Quick reference guide

The SOP for reviewing and signing ECGs is available here Digital ECG SOP

 

Acute Heart Failure (AHF) – ESC 2016

 

AHF Triggers

there are many triggers for AHF, which if recognized and treated with help improve outcomes

  • Cardiac: ACS, Arrhythmia, Aortic Dissection, Acute Valve Incompetence, VSD, Malignant Hypertension
  • Respiratory: PE, COPD
  • Infection: Pneumonia, Sepsis, Infective endocarditis
  • Toxins/Drugs: Alcohol, Recreational drugs, NSAIDs, Steroids, Cardiotoxic meds
  • Increased Sympathetic Drive: Stress
  • Metabolic: DKA, Thyroid dysfunction, Pregnancy, Adrenal Dysfunction
  • Cerebrovascular Insult

Presentation & Clinical Classification

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.

Investigations

  • 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] 
  • Diuretic: commonly we use frurosemide 20-40mg IV, however, depending on the patient higher doses can be used. [Doses over 160mg has been shown to increase mortality!]
  • Oxygen: maintain SaO2 of 95% OR 88-92% if at risk of hypercapnic coma [Avoid hyperoxia]
  • NIV: recommended in respiratory distress (RR >25bpm, SpO2 <90%) & start ASAP, this can reduce intubations and make the patient feel more comfortable. However, doesn’t increase survival NIV Guide-HERE
  • SHOCK!!!: there is no agreement on the best treatment, ICU & Medical/Cardiology input is vital, as inotropes & vasporessors (Noradrenaline recommended) will need to be considered.

ESC Guide – 2016 Heart Failure