Category: Cardiac

Malignant/Accelerated Hypertension

There are several terms commonly used “Accelerated Hypertension”, “Hypertensive Emergency”, “Malignant Hypertension”. They all have a very similar definition (ESC/ESH, NICE, ACEP)

Patient has both:

  1. Blood pressure: Systolic ≥180mmHg OR Diastolic ≥110mmHg (often >220/120mmHg)
  2. End-Organ Damage: Retinal Changes, Encephalopathy, Heart Failure, Acute Kidney Injury, etc.

Mortality has improved in recent years with 5yr survival of 80% if treated. However, untreated average life expectancy is 24 months.

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Acute Heart Failure (AHF) – ESC

Patients presenting with AHF have a high mortality 4-10% in-hospital and 25-30% at 1yr, and 45% if re-admitted. So rapid diagnosis a treat is essential.

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

ESC Guide – 2021 Heart Failure

Presentations

Decompensated Heart Failure

Isolated Right Vent-Failure

Pulmonary Oedema

Cardiogenic Shock

Managment

Treatment – Time Matters!!!

  • Mortality increased by 1%/hour IV treatment not started

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)

Oxygen
  • Not all patients should be given Oxygen ESC suggest maintain SaO2 >90%
  • Early NIV is suggested if any of:
    • RR >25bpm or SaO2 <90% despit oxygen
    • Signs type 2 respiratory failure

Metanalysis suggests early NIV may reduce need for intubation and improve mortality

NIV Guide-HERE

Diuretic

Vasodilator

Inotropes

Hypomagnesaemia

Classification

  • Normal: 1.1-0.7
  • Mild: 0.69-0.5 – No symptoms or non-specific symptoms, such as lethargy, muscle cramps, or muscle weakness
  • Severe: <0.5 – Severe neurologic symptoms such as nystagmus, tetany, seizures, and cardiac arrhythmias

Signs/Symps (normally <0.5)

  • MSK: Muscle Twitch, Tremor, Tetany, Cramps
  • CNS: Apathy, Depression, Hallucination, Agitation, Confusion, Seizure
  • CVS: Tachycardia, Hypertension, Arrhythmia, Digoxin Toxicity
  • BioChem: Hypokalaemia, Hypocalcaemia, Hypophosphataemia, Hyponatraemia

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Syncope – ESC 2018

  • 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!

  1. Is this Syncope?
  2. What is the underlying cause?
  3. What is the best Follow-Up for this patient?

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Myocardial Infarction (MI) – PPCI/Thrombolysis

PPCI (Leeds PPCI Pathway)

  • Target: Door to balloon 90min
  • Criteria:
    • 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)
  • Actions:
    • Resuscitate
    • Contact PPCI team @ LGI (Mobile No. up in Resus)
    • Arrange blue light (P1) ambulance to LGI
    • Prasagrel 60mg if no previous CVA or Ticagrelor 180mg if previous CVA and Aspirin 300mg (if anti-coagulated Discuss with PCI team)
  • Problems: 
    • 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

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ACS Pathway 2022

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 

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
  • Plus Either:
    • Ticagrelor 180mg stat (Hx of CVA)
    • Prasugrel 60mg stat (NO 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. 

NB: 2nd Trop should be done >8hr after chest pain (this may be <6hrs from the initial Trop)

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).