Mr Clarkson Cardiac Risk Factors E C G Basics S T Elevation E C G Leads Renin Angiotensin System Jugular Venous Pressure Blood Coagulation Differential Diagnosis Of Chest Pain Cardiac Markers Of Infarction Cardiac Action Potentials Cardiovascular Reflexes Cardiovascular Pharmacology

It was a busy afternoon in the Emergency Department with what seemed to be a constant stream of patients coming through the door. I picked up the triage notes for my next patient – a 63 year old gentleman who had walked into the department with chest pain. ^{Differential Diagnosis Of Chest Pain}

Mr Clarkson had been triaged to the ‘majors’ area. His initial observations had been in normal range aside from a slightly elevated blood pressure, but repeat observations showed he had now developed a slight tachycardia (heart rate 109bpm). His oxygen saturations were 98% on room air. At first glance, Mr Clarkson appeared sweaty and in discomfort. I knew it was crucial to perform an ECG as soon as possible to see if he was having a heart attack and one of the nurses offered to fetch the ECG machine immediately. ^{E C G Basics ◦ Cardiac Action Potentials}

I took a focussed history from Mr Clarkson and discovered that although this was the first time he had experienced severe chest pain, he had had some mild discomfort in the chest over the past few weeks when he had ‘overdone it’. He described the pain as a ‘crushing’ pain in the centre of his chest which had started half an hour ago whilst he had been shopping with his wife and was getting progressively worse. He was also feeling breathless and had developed a slight discomfort in his left arm. His wife was extremely worried as Mr Clarkson’s father had died in his 60s from a heart attack, so she had driven him straight to A&E.

Noting his family history of cardiac disease, I proceeded to ask Mr Clarkson about any other cardiac risk factors. He reported he was on tablets from his GP for blood pressure and had recently started a statin for high cholesterol. He worked as a van driver and admitted to having rather a sedentary lifestyle. Although he tried to give up smoking a couple of years ago, he had restarted and now smoked a pack of cigarettes per day.^{Cardiac Risk Factors}

I performed a cardio-respiratory examination; his heart sounds were normal and his chest sounded clear bilaterally. I looked for any signs of heart failure such as a raised JVP or peripheral oedema but these were not present. I noted his raised BMI – another risk factor for cardiac disease. The ECG machine arrived, so I asked the nurse to attach the leads whilst I continued asking Mr Clarkson about his medication history and allergy status.^{J V P}

The nurse looked worried as she printed the ECG and handed it to me for review:

I immediately looked for any ischaemic changes and noticed significant ST elevation in leads 2, 3 and aVF with reciprocal ST depression in lead 1 and aVL – Mr Clarkson was indeed having a heart attack. I asked the nurse to transfer him to the resuscitation area, attach cardiac monitoring and repeat the 12-lead ECG in 15 minutes. I inserted a cannula and took bloods, including a troponin and creatinine kinase which would indicate damage to the heart. ^{E C G Leads ◦ S T Elevation ◦ Cardiac Markers Of Infarction}

I took the ECG to discuss with my A&E Registrar who agreed that we should commence treatment for an inferior ST-elevation myocardial infarction (STEMI) immediately and call the Cardiology Registrar. I bleeped Cardiology and fortunately the Registrar was in A&E having just reviewed another patient. He came to review Mr Clarkson immediately and confirmed that the he needed to be transferred to the Cardiac Catheterisation Lab immediately for Primary Percutaneous Intervention. He prescribed aspirin and ticagrelor to be given stat according to the hospital guidelines. He also asked me to give Mr Clarkson morphine for analgesia. I asked about oxygen therapy as I had read a recent guideline stating that supplementary oxygen was only recommended during a STEMI if the saturations were less than 94%. He agreed that Mr Clarkson did not require oxygen at present, but asked me to request a chest x-ray.

Mr Clarkson was transferred to Cardiac Catheterisation Lab immediately and later in the day I checked his troponin which had come back highly elevated as expected (12684), indicating that myocardial ischaemia had occurred. I followed up his case and discovered that he had undergone primary percutaneous coronary intervention (Primary PCI) and had had a drug-eluting stent inserted into his right coronary artery. Following the Primary PCI, Mr Clarkson had been prescribed fondaparinux subcutaneously for three days. He was also commenced on regular secondary preventative medications including aspirin, ticagrelor, ramipril, metoprolol and atorvastatin, and referred to a cardiac rehabilitation programme. ^{Blood Coagulation ◦ Cardiovascular Reflexes ◦ Renin Angiotensin System}