On the 8th of May we are changing our current troponin test to a HS-Trop (high sensitivity troponin). This will allow us to exclude ACS earlier in the patient journey, however it does mean getting used to new numbers and a new protocol. Read more
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
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.
- 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
- 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
- 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.
- Defintion:Transient Loss of Consciousness (TLOC) due to cerebral hypoperfusion, characterised by a rapid onset, short duration, and spontaneous complete recovery.
- Common ED Complaint: 1.7% of all attendances
- Difficult Diagnosis: less than 50% get a diagnosis in ED
- Mortality & Serious Outcome: 0.8% mortality & 10.3% serious outcome @ 30 days
Ask 3 Questions!
- Is this Syncope?
- What is the underlying cause?
- What is the best Follow-Up for this patient?
- Cardiac: Heart Block, Myocardial infarction, Myocarditis
- Metabolic: Hypothermia, Hyperkalaemia, Hypokalaemia, Hypothyroid, Hypoxia
- Toxin: digoxin, B-blocker
For ALL conditions leading to bradycardia treating the underlying condition is the most appropriate treatment and for some the only thing that will work (i.e. severe hypothermia) Read more
PPCI (Leeds PPCI Pathway)
- Target: Door to balloon 90min
- Time: Chest pain within 12hrs (or worsened within 12hrs)
- ECG: ST elevation MI (1mm Limb or 2mm Chest leads) OR New LBBB. (Posterior MI do posterior leads and discuss with LGI)
- Contact PPCI team @ LGI (Mobile No. up in Resus)
- Arrange blue light (P1) ambulance to LGI
- Ticagrelor 180mg and Aspirin 300mg (if anti-coagulated Discuss with PCI team)
- Intubated patient: Often LGI would accept but need to arrange Cardiac ICU. If no bed patient could go for PCI to return locally immediately after PCI to our ICU’S?
- LGI Full: Occasionally the cath lab is full and can’t accept your patient
- Calling Manchester and Sheffield: It’s worth a go but they don’t have agreements with us so having your patient accepted can be difficult
- Don’t Forget Thrombolyisis: We need to open up the patients artery, if there is no quick decision to go for PPCI – Consider Thrombolysis
Aortic Dissection (AD), is uncommon (1 AD:200 ACS) but is…Rapidly FATAL! Unfortunately recognising aortic dissection is difficult with a clinician pickup rate of 15-43%. Read more
For many conditions the patient should be informed to stop driving and inform the DVLA of their condition. It is the patients responsibility to inform the DVLA, and we should encourage them to do so.
[There is a £1000 fine AND the risk of prosecution] Read more
- Cardiac arrhythmias are relatively common presentations to ED.
- There are many causes, some more sinister than others.
- If your patient is not acutely unwell then expert advice may be required.
- Whats the cause? – treating the precipitant often sorts the AF (adding B-Blockers to Sepsis can make things worse)
- Stable or Unstable? – Electricity vs. Drugs
- less than 48hrs? – Rhythm vs. Rate control
- CHADS-VASC vs. HASBLED – Anticoagulation
- Arrhythmia Clinic – referral form attached tho the PDF
PDF: Patient Info