Mark A Rodrigues and Emily R McCall-Smith
Station 2.1: Acute pericarditis
You are an emergency department junior doctor. Your next patient is Jason Anderson (DOB 22/03/85), a 29-year-old man who has come in with chest pain. He says he has felt generally unwell over the last few days with a fever, muscle ache and a sore throat. Today he developed sharp retrosternal chest pain radiating to his neck. The pain is worsened by movement and breathing. Please assess Mr Anderson and instigate appropriate management.
‘The patient is maintaining a patent airway.’
No additional airway support required.
‘Respiration rate (RR) 12/min, oxygen saturations are 97% on air. No chest wall tenderness. The chest is resonant throughout. Good air entry is heard bilaterally with no wheeze or crackles.’
No respiratory support required.
‘Heart rate (HR) 78 bpm regular, blood pressure (BP) 128/64 mmHg, capillary refill time (CRT)<2 seconds. The JVP is not elevated. Cardiovascular (CV) exam shows normal heart sounds (HS), with a pericardial friction rub. No murmurs.’
Obtain intravenous (IV) access and send off bloods.
‘The patient is alert. Blood sugar 6.9 mmol/L.’
‘Temperature is 37.2°C. There is mild erythema in his throat, with some palpable cervical lymph nodes. The rest of the examination is normal.’
Bloods: FBC, U&Es, ESR, CRP. Look for evidence of inflammation. Troponin is used as a marker of myocardial damage (elevated in ≈50% with pericarditis) but may also help differentiate from acute coronary syndrome. U&Es will show elevated urea in uraemic pericarditis
ECG: Classical finding is widespread ‘saddle-shaped’ ST elevation with upwards concavity in I, II, aVF, aVL and V3–6. PR depression is virtually diagnostic of pericarditis. Helps distinguish from myocardial infarction
Echo: Will show pericardial effusions (present in 10% of cases of pericarditis) and tamponade if present–though tamponade should be diagnosed clinically. It will also demonstrate concomitant heart disease, such as left ventricular wall motion abnormalities seen post-myocardial infarction
|Parameter||Value||Normal range (units)|
|Haemoglobin||140 g/L||Men: 135–180 (g/L)|
Women: 115–160 (g/L)
|ESR||48 mm/h||Men: (Age in years)/2 (mm/h)|
Women: (Age in years+10)/2 (mm/h)
|CRP||63 mg/L||0–10 (mg/L)|
|Urea||6 mmol/L||2.5–6.7 (mmol/L)|
|Creatinine||80 μmol/L||70–130 (μmol/L)|
|eGFR||>60 mL/min||>60 (mL/min)|
|Sodium||140 mmol/L||135–145 (mmol/L)|
|Potassium||4 mmol/L||3.5–5.0 (mmol/L)|
|Troponin||0.01 μg/L||0–0.1 (μg/L)|
‘Bloods show an elevated WCC (18×109/L), ESR (48 mm/h) and CRP (63 mg/L). Troponin and U&Es are normal. ECG shows widespread concave ST elevation and PR depression. CXR shows mild cardiomegaly, with clear lungs and no pneumothorax. The ECHO shows a small pericardial effusion.’
Initial Management 
‘Mr Anderson looks more comfortable. He still has chest pain but it is not as severe. His observations remain stable and his clinical examination is unchanged.’
Pericardiocentesis: Mandatory in patients with cardiac tamponade (hypotension, raised JVP, muffled heart sounds and pulsus paradoxus). It should be considered in patients with possible bacterial or neoplasic pericarditis. It is optional in patients with large or recurrent pericardial effusions or patients with small pericardial effusions in whom the other tests have been inconclusive (allows identification of underlying aetiology of the effusion).
Handing over the Patient
‘Mr Anderson is a 29-year-old man with acute viral pericarditis. He presented with sharp chest pain on a background of an upper respiratory tract infection. He is haemodynamically stable. Investigations are in keeping with viral pericarditis and a small pericardial effusion, confirmed on echo. He has commenced ibuprofen, co-codamol and gastric protection.
He has been reviewed by the cardiology registrar and will be admitted to the cardiology ward overnight for observations with a view to discharge tomorrow and a repeat echocardiogram in a couple of days to ensure the pericardial effusion is not enlarging. He requires a pain review later this evening.’
Station 2.2: Acute left ventricular failure
You are the junior doctor on the hospital-at-night team. One of the nurses fast-bleeps you to see an 84-year-old lady, Mrs Margaret Jenkins (DOB 20/08/30), who has become acutely breathless and is coughing up pink frothy sputum. She was admitted last night, and has been given 4 litres of fluid in the last 12 hours following an episode of diarrhoea where she had become clinically dehydrated.
She was diagnosed with moderate left ventricular systolic dysfunction 2 weeks ago after an episode of collapse. At this point she was started on an ACE inhibitor, a beta-blocker, and furosemide: all of which have not been prescribed on this admission due to the dehydration.
‘There are a large amount of frothy pink secretions coming from the patient’s mouth, and you hear a strange choking noise.’
You clear the patient’s airway using suction, and the airway noises clear.
‘RR is 34/min, oxygen saturations are 82% on room air. There is no history of COPD. Mrs Jenkins is using her accessory muscles. There are coarse bibasal crackles.’
Start the patient on 15 L oxygen via a non-rebreather mask. Perform an ABG and request an urgent portable CXR.
Perform a cardiovascular exam, looking at the JVP, listening to the heart for murmurs, e.g. VSD or mitral regurgitation, and additional heart sounds. Feel for hepatomegaly or ascites, and check for peripheral oedema in the ankles, or over the sacrum in bed-bound patients.
‘The patient is tachycardic at 150 bpm, with a BP of 152/90 mmHg and CRT of 3 seconds. She looks distressed and is sweating profusely. The JVP is raised–so much so that you see the earlobe ‘wiggling’. You hear a third heart sound on auscultation. Mrs Jenkins has pitting oedema of both legs to the knees.’
Stop IV fluids, and treat for pulmonary oedema (furosemide, glyceryl trinitrate, morphine (with metoclopramide)). Perform an ECG looking for any precipitating causes for the LVF, e.g. arrhythmias, LVH (secondary to hypertension) or ischaemia. Obtain IV access and take bloods. Insert a urinary catheter if not already in place, to allow accurate assessment of fluid balance.
‘The patient is GCS 14 (E4, M6, V4). Blood sugar is 4.0 mmol/L.’
CXR: Look for the typical features of LVF, although the radiographic changes can lag behind the clinical picture. Features of pulmonary oedema on chest X-ray are bat’s wing shadowing, pleural effusions, Kerley-B lines, cardiomegaly and upper lobe diversion. Look for other causes of acute dyspnoea, such as consolidation or pneumothorax
ABG: This will likely show hypoxia. Initially the PaCO2 might be low due to hyperventilation, but may rise later due to reduced gas exchange. Look to see if the patient is acidotic, as this is important in determining whether CPAP (type 1 respiratory failure) or BiPAP (type 2 respiratory failure) is required. Remember patients with renal failure may already have a metabolic acidosis, and therefore could be acidotic with a normal PaCO2 as well as with type 2 respiratory failure. Indeed a metabolic and respiratory acidosis might exist together
Echo: An important investigation to be performed early. This may demonstrate the cause of heart failure, e.g. left ventricular systolic dysfunction or aortic stenosis, which guides decision about treatment later on, e.g. ACE inhibitor/beta-blocker for LVSD, surgery for AS
Bloods: FBC, U&Es, LFTs, TFTs, CRP. Look for evidence of infection by doing an FBC and CRP. Look for anaemia as this may exacerbate heart failure. Check U&Es as you will be treating the patient with diuretics and an ACE inhibitor, and look at the LFTs–which may be deranged if there is hepatic congestion in right heart failure. Check blood glucose for diabetes. Troponin may be high if an MI has precipitated the LVF; however, it may be difficult to interpret as it can be raised by LVF itself. Thyroid function tests should be done, as thyroid disease can aggravate or mimic heart failure
|Parameter||Value||Normal range (units)|
|Haemoglobin||150 g/L||Men: 135–180 (g/L)|
Women: 115–160 (g/L)
|CRP||4 mg/L||0–10 (mg/L)|
|Urea||6.8 mmol/L||2.5–6.7 (mmol/L)|
|Creatinine||156 μmol/L||70–130 (μmol/L)|
|eGFR||58 mL/min||>60 (mL/min)|
|Sodium||140 mmol/L||135–145 (mmol/L)|
|Potassium||4.2 mmol/L||3.5–5.0 (mmol/L)|
|Bilirubin||5 μmol/L||3–17 (μmol/L)|
|ALT||20 IU/L||5–35 (IU/L)|
|ALP||57 IU/L||30–300 (IU/L)|
|PaO2||8 kPa on air||>10 (kPa) on air|
|PaCO2||4.9 kPa||4.7–6.0 (kPa)|
|HCO3||24 mmol/L||22–26 (mmol/L)|
‘CXR shows cardiomegaly, upper lobe venous diversion, pleural effusions, with fluid in the horizontal fissure, and Kerley-B lines. ECG shows sinus tachycardia. Bloods show a normal FBC, urea 6.8 mmol/L, creatinine 156 µmol/L, eGFR 58 mL/min, Na 140 mmol/L, K 4.2 mmol/L. TFTs are in progress. LFTs are normal. ABG on air shows type 1 respiratory failure, with a PaO28 kPa, PaCO24.9 kPa, pH 7.35, HCO324 mmol/L.’
Initial Management 
Loop diuretic: Treat with furosemide. If the patient is diuretic naïve and has normal renal function, then 40 mg IV is adequate. If the patient is already on diuretics or has renal failure, then higher doses may be needed, e.g. 50–100 mg IV. Doses above 50mg must be given by IV infusion, and at a rate no faster than 4 mg/min. Elderly people, especially if they have a low body weight, will also require a dose reduction. Diuretics will cause immediate vasodilation as well as the delayed diuresis
Morphine Sulfate: Titrate 1–10 mg in 1 mg increments according to response. It will reduce anxiety and pain, as well as causing vasodilation which will reduce preload on the heart. Reduce the dose if the patient is elderly, frail or has a history of respiratory disease. Don’t forget to prescribe a prophylactic antiemetic with it, for example, metoclopramide 10 mg IV. Monitor respiratory rate while giving morphine
Nitrates: Give 800 micrograms (2 sprays) of sublingual glyceryl trinitrate immediately providing the systolic BP is>100 mmHg. Common side effects are headache and hypotension. For patients with severe LVF, or patients who haven’t responded to SL glyceryl trinatrate+morphine, consider a nitrate infusion (if BP still>100 mmHg). The starting dose depends on baseline BP, usual dose is 0.3 mg/h–1 mg/h. This will reduce the cardiac preload
Oxygen: Should be given to treat hypoxaemia when oxygen saturation is<90%, which is associated with an increased short-term mortality. Oxygen shouldn’t be given routinely, as it can cause vasoconstriction and reduced cardiac output. Consider CPAP for early refractory hypoxia
‘Mrs Jenkins does not appear to be much better. She is still producing secretions and is now requiring airway support with an NP tube. RR is now 36/min. Oxygen saturations are 93% on 15 L oxygen. There are still loud bibasal crackles. HR is 125 bpm and BP is 98/66 mmHg. Peripheries are clammy with a CRT of 3 seconds. Cardiac examination is unchanged. Mrs Jenkins has passed approximately 10 mL of urine over the last 45 minutes. The nurse is worried about managing her on the ward as they have other patients who require their attention.’
You need to speak with ITU urgently. The patient has had a poor response to the initial treatment. In severe or resistant cases, patients may require support with an intra-aortic balloon pump. Invasive monitoring and inotropes may be required, particularly as she is now hypotensive. Obviously this is something that a junior doctor will not be required to deal with, but it is useful to know what further treatment may be available.
Handing over the Patient to ITU
‘My name is Emma Smith and I’m the FY1 covering the wards tonight. I’d like to discuss a patient with you, whom I’d like you to review please.
The patient is Mrs Jenkins, an 84-year-old lady, who has developed acute pulmonary oedema this evening, after treatment with IV fluids for the last 2 days. She is known to have a history of moderate LVSD, but has no other significant medical history.
She has failed to improve significantly despite high-flow oxygen, morphine, furosemide and glyceryl trinitrate spray. Her current observations are oxygen sats 93% on 15 L oxygen, RR is 36/min, HR 125 bpm, BP 98/66 mmHg. She has a markedly elevated JVP, coarse bibasal crackles and bilateral pitting oedema. She has only passed 10 mL of urine in the last 45 minutes.
She was previously independent and had a good quality of life, and we feel that she would be a candidate for escalation of her care. I’m just about to repeat her ABG, but please could you review her urgently.’
‘After 24 hours in ITU, Mrs Jenkins has improved, and she is transferred to the ward for ongoing care.’
ACE inhibitors–(or ARB if ACE inhibitor not tolerated) recommended in all patients with an ejection fraction≤40%. This reduces the risk of future heart failure-related hospitalizations and premature death. Start at a low dose and titrate up, monitoring U&Es after each increment
Beta-blockers–once the episode of acute left ventricular failure has been stabilized. They are recommended for all patients with an ejection fraction≤40% to reduce the risk of future heart failure-related hospitalizations and premature death. Titrate dose up, monitoring HR and BP after each increment
Mineralocorticoid (aldosterone) receptor antagonists, e.g. spironolactone or eplerenone–recommended for patients in class II–IV heart failure and an ejection fraction of≤35% despite the above treatment, as it again, reduces the risk of future heart failure-related hospitalizations and premature death
Digoxin–used in patients with reduced ejection fraction and coexisting AF. Can also be used in patients with severe and resistant LVSD to reduce symptoms and reduce heart failure-related hospitalization