A 2-year-old boy is seen by the general practitioner as his parents are concerned that he is struggling to gain weight and is excessively short of breath on exertion. He was previously diagnosed with congenital pulmonary stenosis which was managed conservatively however the parents are now questioning whether surgical intervention may be required.
What murmur is likely to be heard on examination?
Ejection systolic, louder on expiration
Ejection systolic, louder on inspiration
Holo-systolic, louder on expiration
Holo-systolic, louder on inspiration
Late systolic
In pulmonary stenosis, ejection systolic is heard and is louder on inspiration
Ejection systolic murmurs that are louder on inspriration diseases
pulmonary stenosis
atrial septal defect
Ejection systolic murmurs that are louder on expiration diseases
aortic stenosis
hypertrophic obstructive cardiomyopathy
Mnemonic for murmurs based on inspiration and expiration
RILE
Right-sided murmur → heard best on Inspiration
Left-sided murmur → heard best on Expiration
Ejection systolic murmur causes
- Aortic stenosis
- HOCM
- Pulmonary stenosis
- Atrial septal defect
- Tetralogy of Fallot
What can murmurs be divided into
- Ejection systolic
- Holosystolic (pansytolic)
- Late systolic
- Early diastolic
- Mid-late diastolic
- Continuous machine like murmur
Causes of holosystolic murmurs
- mitral/tricuspid regurgitation (high-pitched and ‘blowing’ in character)
tricuspid regurgitation becomes louder during inspiration, unlike mitral reguritation. During inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole - ventricular septal defect (‘harsh’ in character)
Causes of late systolic murmurs
- mitral valve prolapse
- coarctation of aorta
Causes of early diastolic murmurs
- aortic regurgitation (high-pitched and ‘blowing’ in character)
- Graham-Steel murmur (pulmonary regurgitation, again high-pitched and ‘blowing’ in character)
Causes of mid-late diastolic murmurs
- mitral stenosis (‘rumbling’ in character)
- Austin-Flint murmur (severe aortic regurgitation, again is ‘rumbling’ in character)
Causes of continuous machine like murmur
patent ductus arteriosus
Draw diagram of murmurs in cardiac cycle including aortic stenosis, mitral rugrgitation, patent ductus arteriosum, aortic regurgitation, mitral stenosis
A 50-year-old man is admitted to Resus with a suspected anterior myocardial infarction. An ECG on arrival confirms the diagnosis and thrombolysis is prepared. The patient is stable and his pain is well controlled with intravenous morphine. Clinical examination shows a blood pressure of 140/84 mmHg, pulse 90 bpm and oxygen saturations on room air of 97%. What is the most appropriate management with regards to oxygen therapy?
2-4 l/min via nasal cannulae
No oxygen therapy
15 l/min via reservoir mask
28% via Venturi mask
35% via Venturi mask
No oxygen therapy
According to UK guidelines, oxygen should only be administered to patients with suspected acute myocardial infarction if they are hypoxaemic (SpO2 <94%). In this case, the patient has oxygen saturations of 97% on room air, which is within the normal range. Unnecessary oxygen administration in normoxaemic patients with acute myocardial infarction may be harmful as it can increase coronary vascular resistance and reduce coronary blood flow.
A 36-year-old man presents to the Emergency Department with chest pain. This started around 2 hours ago and is described as severe. The pain is central, with no radiation. It is not worse on deep inspiration.
He smokes 10 cigarettes/day but is otherwise fit and well. His father had a myocardial infarction at the age of 61 years. Examination of the cardiovascular system is unremarkable with a blood pressure of 136/84 mmHg, pulse 96/min, respiratory rate 14/min and saturations 98% on room air.
An ECG is taken:
What is the most likely diagnosis?
Pulmonary embolism
Anterior myocardial infarction
Acute pericarditis
Hypertrophic obstructive cardiomyopathy
Brugada syndrome
Acute pericarditis
The ECG shows widespread ST elevation but the most diagnostic feature of the ECG is the PR depression - this is very specific for pericarditis and makes the diagnosis clear.
In the discussion sections, given ST elevations, cardiac history in family, one should initially treat as ACS until proven otherwise
A 68-year-old man presents to his GP with ongoing chest pain. He describes a central, tight chest pain on exertion that resolves with rest. He has a past medical history of hypertension and hypercholesterolaemia. He is currently taking aspirin 75mg OD, atorvastatin 40mg OD, bisoprolol 10mg OD and GTN spray PRN. Despite maximum tolerated dose of bisoprolol, he still experiences chest pain on moderate exertion.
What is the most appropriate next step in management?
Add amlodipine
Add isosorbide mononitrate
Add ivabradine
Add nicorandil
Refer for coronary angiography
Add amlodipine
If angina is not controlled with a beta-blocker, a longer-acting dihydropyridine calcium channel blocker should be added
A 19-year-old man has a medical examination before joining the army. He denies any symptoms and has no family history of note. The ECG shows the following:
© Image used on license from Dr Smith, University of Minnesota
Based on the ECG, what is the most likely diagnosis?
-Trifascicular block
- Hypertrophic obstructive cardiomyopathy
- Long QT syndrome
- Arrhythmogenic right ventricular cardiomyopathy
- Dextrocardia
Hypertrophic obstructive cardiomyopathy
Note the left ventricular hypertrophy and deep ST depression and T-wave inversions consistent with hypertrophic obstructive cardiomyopathy.
A 35-year-old man presents to the emergency department following an episode of syncope.
An ECG is performed, which demonstrates sinus rhythm at rate 85 bpm. The QRS duration is 110 ms, PR interval is 180ms and corrected QT interval is 500ms.
Of the following, what is the cause for the abnormality seen on the ECG?
Cyclizine
Hypercalcaemia
Hypokalaemia
Pyrexia
Subdural haemorrhage
Hypokalaemia
Types of long QT and what are they associated with
- Long QT1 - usually associated with exertional syncope, often swimming
- Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli
- Long QT3 - events often occur at night or at rest
A 45-year-old woman presents to the Emergency Department with shortness of breath, chest pain, and dry cough. She denies any symptoms in her calves. Her medical history includes breast cancer.
Observations:
Blood pressure: 128/82 mmHg
Pulse: 80 bpm
Respiratory rate: 20/min
Oxygen saturation: 97% on room air
Temperature: 38.1ºC
Suspecting a pulmonary embolism, a D-dimer test has been performed, with the following result:
D-Dimer 350 ng/mL (< 400)
What is the most appropriate next step in management?
Repeat D-dimer
Request CT pulmonary angiogram (CTPA)
Start apixaban
Start treatment dose tinzaparin
Stop investigating for a pulmonary embolism
Stop investigating for a pulmonary embolism (calculate wells score)
What is the triad of PE symptoms?
pleuritic chest pain, dyspnoea and haemoptysis
How many patients present with classical triad for PE?
We know from experience that few patients (around 10%) present with the textbook triad of pleuritic chest pain, dyspnoea and haemoptysis
Symptom frequency in PE
The PIOPED study1 in 2007 looked at the frequency of different symptoms and signs in patients who were diagnosed with pulmonary embolism.
The relative frequency of common clinical signs is shown below:
- Tachypnea (respiratory rate >20/min) - 96%
- Crackles - 58%
- Tachycardia (heart rate >100/min) - 44%
- Fever (temperature >37.8°C) - 43%
Updates on the guidelines for PE
NICE updated their guidelines on the investigation and management of venous thromboembolism (VTE) in 2020. One of the key changes was the use of the pulmonary embolism rule-out criteria (the PERC rule):
- a copy of criteria can be found in the image below
- all the criteria must be absent to have negative PERC result, i.e. rule-out PE
- this should be done when you think there is a low pre-test probability of PE, but want more reassurance that it isn’t the diagnosis. this low probability is defined as < 15% (this is based on clinical reasoning), although it is clearly difficult to quantify such judgements
- a negative PERC reduces the probability of PE to < 2%
- if your suspicion of PE is greater than this then you should move straight to the 2-level PE Wells score, without doing a PERC
Wells scoring for PE
