OSCE 3

You are looking after a 81 year old gentleman with a background history of COPD who is day 4 after an Ivor-Lewis oesophagectomy, on the background of prolonged malnutrition. His other background history consists of ischaemic heart disease, hypertension, previous TIA and  Type 2 diabetes.

You are asked to review his ECG after he has become tachycardic.

Interpret this ECG and describe how you would assess the patient.

The original CICM text for this OSCE was unhelpful:

ECGs:  Candidates were asked to list abnormalities and potential aetiologies, and provide suggestions regarding management. Examples included myocardial infarction, AV nodal re- entrant tachycardia, atrial flutter with bifascicular block, and hyperkalemia. 
Eleven out of twenty-eight candidates passed this section.

So, I had to make something up.

That ECG is from my private collection of arrhythmias. It is AF.

Assessment should probably consist of 

• History
  • Duration of arrhthmia
  • Antecedent events, eg. line insertion
  • Chest pain
  • Shortness of breath
  • Palpitations
  • Dizzyness/nausea
• Examination
  • Respiratory compromise, i.e. APO
  • Haemodynamic stability
  • Features of sepsis
  • Drain output, i.e. is there a leak?
• Investigations
  • ABG
  • Electrolytes (EUC, CMP)
  • CXR
  • Cardiac enzymes
  • Inflammatory markers
  • TTE

What are the possible causes?

This table is probably applicable:

Causes of Atrial Fibrillation Organised by System

Vascular: Myocardial infarction Pulmonary embolism Pulmonary hypertension Subarachnoid haemorrhage Infectious: Sepsis Myocarditis Pericarditis Infective endocarditis Neoplastic: Cardiac mass, eg. myxoma Drug-induced: Catecholamines Alcohol Caffeine Idiopathic: Infiltrative disease, eg. amyloidosis Age-related fibrotic changes

Idiopathic: Infiltrative disease, eg. amyloidosis Age-related fibrotic changes Congenitial: Atrial septal defect Familial AF Autoimmune: Autoimmune myocarditis Traumatic: Cardiac contusion Cardiac surgery Endocrine/environmental: Hypothermia Hyperthyroidism Haemochromatosis/iron overload Phaeochromocytoma Electrolyte derangement

The patient has no symptoms, and the following findings:

• RR 24
• SpO2 94% on 35% via Venturi Mask
• BP 110/54 (MAP 73)
• Creps in both lung bases
• Unchanged drain output

What are the goals of your management?

Well; rate control or rhythm control are really the goals. in this haemodynamically stable patient, rate control would be a reasonable option. Addressing the causes would also be good. So:

• Attention to airway, breathing and circulation.
• Identify and rectify reversible factors as above
• Fluid bolus if hypovolaemic
• Correct electrolyte abnormalities
• Treat pain
• Consider MgSO_4​, 10-20mmol
• If that does not work, antiarrhythmics (more on that later)

What evidence is there to guide a decision regarding rate vs. rhythm control?

• Four studies (AFFIRM, RACE, STAF and PIAF) in support of rate control instead of rhythm control. They were published between 2000 and 2003.  
• Meta-analysis (Caldeira et al, 2012) identified four more (a total of eight) suitably high-quality studies, featuring data from 7499 patients.
• "No clear survival benefit is apparent"
•  Rate control was found to be superior only in terms of the composite endpoint (death, stroke and recurrent hospitalisation).
• Theoretically, rhythm control should actualy be better (particularly in the absence of significant structural heart disease) because it may prevent myocardial remodelling.

Why is any management necessary? What are the consequences of this rhythm?

• Adverse haemodynamic effects due to the following factors:
  • loss of atrial systole (the "kick")
  • Decreased diastolic filling time during rapid AF
  • "Tachycardiomyopathy" - a global cardiompyopathy associated with the rapid rate
• Pulmonary oedema
• Patient discomfort due to palpitations
• Cardiac ischaemia
• Systemic embolism and strok

What pharmacological options for rate control are available?

The 2014 AHA statement gives the following recommendations:

• β-blocker or calcium channel blocker for paroxysmal AF, which can be given IV if they are haemodynamically stable (CCBs are favoured in COPD patients)
• IV amiodarone for critically ill patients
• If the patient has some sort of pre-excitation problem, these AV node blockers are not recommended (cardioversion is the better choice; the AHA also recommend procainamide for stable patients but this is not available in Australia)
• If the patient is in decompensated heart failure, calcium channel blockers are not recommended (use digoxin or amiodarone instead). In the long term these people seem to benefit from a combination of digoxin and a β-blocker

In short, this guy could have amiodarone or verapimil. 

What rate would you aim for?

The 2014 AHA statement  recommends a rate of 80 or so as the endpoint to aim for, but give a slightly weaker recommendation in favour of a more "lenient" rate (~110) provided the LV function is well-preserved. 

With amiodarone infusion, the rate returns to ~ 80, but remains irregular. What are the risks of embolic stroke in this patient? How would you assess this risk?

The CHA₂DS₂-VASc scoring system is the recommended method of determining the risk of stroke. In essence it comes down to three main categories: score 0, score 1 and any score of 2 or more.

C	Congestive heart failure (or Left ventricular systolic dysfunction)	1
H	Hypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication)	1
A2	Age ≥75 years	2
D	Diabetes Mellitus	1
S2	Prior Stroke or TIA or thromboembolism	2
V	Vascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)	1
A	Age 65–74 years	1
Sc	Sex category (i.e. female sex)	1

• A score of 0 is hard to get, but confers a virtually negligible risk of stroke (~ 0%).
• A score of 1 equates to a risk of 1.3% and a score of 2 puts you in a high risk category (2.2%).
• The maximum score is 9, with an associated stroke risk of 15.2%.
• The guy in this Viva scores a 7.

Mind you, these are annual risks. What's the daily risk in ICU patients? Nobody knows. 

When and how would you anticoagulate this patient?

The options are:

• Warfarin: relative risk reduction for stroke 62%; absolute risk reduction 2.8% per year
• Aspirin: relative risk reduction for stroke 22%; absolute risk reduction 1.5% per year
• Warfarin plus aspirin: no additional benefit over warfarin alone
• Dabigatran: 35% reduction in stroke compared to warfarin

The 2014 AHA statement recommends:

• No anticoagulation is a reasonable choice if the AF is within 48 hours and the CHA₂DS₂-VAScscore is 0; the risk of stroke is 0.2%.
• If the AF is within 48 hours and the score is anything but 0, IV heparin is recommended.
• If the AF has been going on for longer than 48 hours (or, god knows how long) - IV heparin should be used.
• If you are going to anticoagulate, anticoagulation with something should continue for at least 3 weeks before and 4 weeks after their TOE-cardioversion.
• Aspirin is an alternative if the score is 1
• Warfarin or similar if the score is 2 or greater
  • Essentially this means that if you're over 75 you automatically score some warfarin because that age bracket immediately gets you a score of 2 from the CHA₂DS₂-VASc scoring system.

Disclaimer: the viva stem above may be an original CICM stem, acquired from their publicly available past papers. Or, perhaps it is a slightly altered version of the original CICM stem. Or, it is a completely original viva stem, concocted by the monstrously amoral author of Deranged Physiology for nothing more than his own personal amusement. In either case, because the college do not make the main viva text or marking criteria available, almost everything here has been confabulated. It might sound like a plausible viva and it could be used for the purpose of practice, but all should be aware that it does not represent the "true" canonical CICM viva station.