Day 2 felt a lot easier than Day 1. I knew which platform the train left from. I knew that my team were a friendly and forgiving lot. Most reassuringly, I knew that I didn’t have much to live up to (the previous F1 hadn’t turned up for about 3 months).
I clerked more new patients in at AMU. At 3pm, a 68 year old woman was referred from her GP for two reasons: 1) atypical chest pain for the last month and 2) a pulse of 48.
This is a woman who had a known background of angina for the past few months, but was adamant that this pain was different. She described 5-10 minute episodes of poorly localised non pleuritic pain in the front of the chest radiating down the left arm and to the jaw. It was like “being wound up” and she made Levine’s sign (a clenched fist over the chest as she described the pain). It was relived by her GTN spray. What then was different to her normal anginal pain? Two things: 1) it was much worse than normal (8/10 severity, compared to 5/10 normally) and 2) it occurred almost exclusively in the morning, and was definitely not related to exertion, nor relieved by rest.
This was odd. A cardiac systems review also showed that her shoes were not fitting her properly for the last month because of bilateral leg swelling. In addition, she was getting short of breath on walking 20 yards, whereas a month ago she went for long leisurely walks.
Palpitations? “Yes doctor. Lasts for maybe 30 seconds, happens anytime, maybe once a day.” *Taps out slow regular beat*
CV risk factor wise, she had hypertension, hypercholesterolemia, a father who died of an MI at 58, an ex smoker for 10 years with a 45 pack year history and no known diabetes. She also had a diagnosis of angina.
Her previous medical history was also relevant for a recent diagnosis of COPD, made 2 weeks ago in the GP by spirometry, as well as rheumatic fever 40 years ago and CKD stage 3.
Her medications included atenolol 25mg BD, aspirin 75mg OD, GTN PRN, alendronic acid 70mg once weekly, bendroflumethiazide 2.5mg OD, losartan 50mg OD, omeprazole 10mg OD as well as a Combivent inhaler.
She lived alone in a bungalow and was fully independent. She wasn’t particularly worried and only came here because her GP told her to.
On examination, she looked comfortable at rest. HS I was quiet and II was very loud. There was also a 2/6 probably pansystolic murmur which was heard throughout the precordium with no radiation to the carotids or axilla.
Her JVP was not raised at 3cm. There was bilateral pitting oedema to the lower third of the shin, with no tenderness or erythema.
The lungs were clear, including the bases.
ECG showed sinus bradycardia (48) with a borderline first degree heart block.
My impression at this stage was that this was weird. Whatever else was going on, there was probably some fluid overload. Given the worsening shortness of breath, and her established ischaemic heart disease, this was probably heart failure, although a worsening of her kidney disease was possible. There were no signs or symptoms of liver disease, which I thought would be the next most likely cause.
The question is why would her heart failure deteriorate over the last month, and also cause ischaemic pain in the mornings. I figured that the ischaemia could occur when the heart failure is at its worst i.e. on lying flat for prolonged periods, as would be the case in the mornings. This could also explain why her idea of ‘rest’ (lying flat) did not help, and exertion (i.e. getting upright) may not be so bad for her. I thought of the causes of heart failure, which could be split into intrinsic problems with the heart (supply) and increased demand on the heart.
Intrinsic problems of the heart include ischaemia (ACS is the main concern), arrhythmia (this patient was in sinus bradycardia) and valvulopathy (this patient had a pansystolic murmur and a history of rheumatic fever).
Increased demand could be due to anaemia, thyrotoxicosis or sepsis.
In this patient, I thought that the most likely cause would be the bradycardia as a result of the beta blocker. You would expect most of the other causes to lead to a tachycardia as a response to an inadequate cardiac output. This would also be consistent with the mild AV block developing, although we had no old ECGs to compare to. The consultant agreed with this 🙂
I suggested the following investigations in the plan:
U&E (renal function)
WCC differential (any infection leading to increased cardiac output demanded)
Continuous Telemetry ECG
Echo (LVEF and valve assessment)
With the following immediate management:
Stop beta blocker
Furusemide 40mg PO
Salbutamol nebulised 5mg
The consultant added a respiratory nurse review and a heart failure nurse review. He added LFTs to look for another potential cause of fluid overload. He also reminded me that I forgot the chest xray in all the excitement.
I noticed that the AMU nurses did an ECG and CXR on most patients. I will now think of AMU clerkings as history, examination, impression, ?CXR, ?ECG, investigations and management. It’s pretty easy to get so focused on the differential and immediate management that the basics can get forgotten.