Day 2 A&E Flashcards
A 35-year-old patient on the Acute Medical Unit (AMU) has a blood pressure of 92/60 mmHg and a heart rate of 120 bpm.
The patient has warm peripheries, normal skin turgor, moist mucous membranes and a normal jugular venous pressure (JVP).
Based on the clinical findings, which of the following is a potential cause of this patient’s low blood pressure?
- Cardiac tamponade
- Dehydration
- Acute myocardial infarction (MI)
- Sepsis
- Occult haemorrhage
Sepsis
This patient is in shock which can be defined as low blood pressure that leads to cellular hypoperfusion.
In addition to low blood pressure, other signs of shock include tachypnoea, tachycardia, oliguria and altered mental status.
Of the four major types of shock (hypovolaemic, obstructive, cardiogenic and distributive), the only one that causes warm peripheries is distributive shock. This is because, in distributive shock, it is a drop in systemic vascular resistance (SVR) that leads to low blood pressure as opposed to a drop in cardiac output (CO) - note that blood pressure = CO x SVR. Vasodilation cause a decrease in SVR and warm peripheries. In other forms of shock, the SVR increases to compensate for the low cardiac output and hence the peripheries will feel cold.
The two most common causes of distributive shock are sepsis and anaphylaxis. In distributive shock, patients are usually euvolaemic.
A 27 year old teaching assistant is brought into A&E following a paracetamol overdose.
He is reluctant to talk to members of staff and you are unable to ascertain when he took the overdose.
Which of the following is the correct management of this patient?
Start N-Acetylcysteine regardless of plasma paracetamol concentration
If the time of overdose is uncertain, N-Acetylcysteine therapy should be initiated regardless of plasma paracetamol concentration.
The therapy is considered safe and it would be more harmful to leave the patient untreated.
Pathophysiology of paracetamol overdose
(4)
When taken as an overdose, the metabolism of paracetamol results in a buildup of a toxic substance called NAPQI (N-acetyl-p-benzoquinone-imine).
NAPQI is inactivated by glutathione.
In an overdose, glutathione stores are rapidly depleted, and NAPQI is left un-metabolised.
It can cause liver and kidney damage.
The medical foundation doctor is called to review an 87 year old lady who has fallen on a medical ward.
The exact mechanism, or injuries sustained from the fall, is currently unclear as the fall was not witnessed and the patient is confused.
The patient’s airway is patent, on assessment of breathing there is reduced left-sided chest expansion, and this side is hyper-resonant to percussion with significantly diminished breath sounds.
- oxygen saturations of 92% on 15L/min facemask oxygen
- heart rate of 108
- respiratory rate of 26
- blood pressure of 88/64
The patient has IV access.
What is the diagnosis?
What is the single best treatment? (2)
Needle thoracocentesis on the left side
This patient has a left-sided tension pneumothorax as evidenced by the
- reduced expansion
- breath sounds
- hyper-resonance
- associated with shock (hypotension, tachycardia, hypoxia)
The immediate treatment required is needle decompression by inserting a wide-bore cannula into the affected side of the chest in the second intercostal space mid-clavicular line.
A 16 year old male is brought into the emergency department with severe difficulty in breathing, a rash and tongue swelling.
His heart rate is 135 and his blood pressure is 113/87.
Which of the following blood tests is most likely to reveal the diagnosis in this patient?
When should samples be taken? (3)
Mast cell tryptase
This patient is suffering from anaphylaxis, and this would be supported by a rise in the mast cell tryptase during and after the reaction.
Samples should be taken during, 4h and 12h post reaction.
A 55-year-old man presents to the Emergency Department with a 1 day history of palpitations.
He has a past medical history of childhood asthma and schizophrenia.
He was started on a new antipsychotic yesterday.
His basic observations are as follows:
- HR 100
- RR 25
- BP 125/80
- T 37.3
- SO2 96% RA
On examination;
- JVP is not visible and there was no peripheral oedema
- Auscultation of his heart and lungs were normal
- A portion of his ECG is shows torsades
What is the most appropriate management for this patient? (1)
What was the cause of his TDP? (1)
IV Magnesium Sulphate
IV Magnesium Sulphate is the most appropriate treatment for Torsades De Pointes, which is what this patient has on ECG.
Antipsychotics can cause a prolonged QT interval, which can develop into TDP.
A 30-year-old gentleman is brought into the A&E Department by ambulance.
His wife had called the ambulance after witnessing him collapse at home about 20 minutes ago.
She describes witnessing jerking movements of his legs after he had collapsed.
There was no urinary or faecal incontinence and no biting of the tongue.
He was unconscious for about 5 minutes.
This was the first time something like that had happened.
Apart from a recent chest infection a week ago which he saw his GP for and is on antibiotics for, there is no significant past medical or medication history.
On examination, he appeared sleepy and difficult to rouse.
Cardiac, respiratory and abdominal examinations were normal.
There was no obvious bruising or bleeding.
His basic observations are as follows:
HR 98, RR 11, BP 140/90, T 37.3, SO2 96%
Which investigations should be ordered for this patient in A&E to determine the underlying cause of his presentation? (8)
- CT head
- FBC
- U&Es
- Serum calcium
- LFTs
- ABG
- Blood glucose
- Urine tox screen
The clinical presentation in this scenario is consistent with that of a seizure.
A relatively long period of unconsciousness and a significant post-ictal state (difficult to rouse) point to the fact that a seizure has occurred.
This is the best set of investigations that should be ordered in the Emergency setting to look for an underlying cause of the seizure.
A CT head is indicated to look for intracranial pathology such as space occupying lesions.
Infections, electrolyte abnormalities, hepatic encephalopathy, hypoglycaemia and hypoxia can all cause seizures.
Drug intoxication or withdrawal can also cause seizures and that can be investigated with a urine toxicology screen.
Inverstigations for patient with a seizure
(8)
- CT head
- FBC
- U&Es
- Serum calcium
- LFTs
- ABG
- Blood glucose
- Urine tox screen
A 69 year old female presents with a three day history of severe burning chest pain while eating.
She has recently been treated in the community for a mild pneumonia.
What is the most likely cause of her symptoms?
How can she avoid this in future?
Doxycycline
Doxycycline is an antibiotic used in the treatment of pneumonia that is also associated with the development of oesophagitis due to its direct chemical irritant effect on the mucosa.
Patients should be advised to take Doxycycline with a large glass of water whilst in an upright position.
A 59 year old male presents to the emergency department complaining of palpitations.
There is no abnormality on assessment of his airway and breathing, and the patient is not complaining of any pain.
On assessment of circulation, the patient appears pale and sweaty, a radial pulse is palpable with a rate of ~200, blood pressure is 86/48, and the cardiac monitor shows a broad-complex tachycardia.
What is the single best definitive treatment for this patient?
Why does the treatment need to be so specific?
If the treatment is ineffective, what should be given?
Synchronised DC cardioversion
This patient having an unstable ventricular tachycardia (unstable as evidenced by systolic blood pressure <90).
The definitive treatment in this case is to cardiovert the patient using electricity (i.e. a shock), this should be synchronised to avoid causing a R on T phenomenon, which would put the patient into ventricular fibrillation.
If initial shocks are un-successful, the energy can be increased and after three attempts IV amiodarone is given before subsequent shocks
Definition of Ventricular Tachycardia
(2)
Ventricular Tachycardia (VT) is a type of broad complex tachycardia characterised by;
- heart rate of more than 100 bpm
- QRS width of more than 120 ms.
Other types of broad complex tachycardias include Torsades de Pointes (TdP) and Supraventricular tachycardia (SVT) with aberrant conduction.
Causes of Ventricular Tachycardia
(4)
Causes of Ventricular Tachycardia
Electrolyte abnormalities such as hypokalaemia and hypomagnesaemia
Structural heart disease including Myocardial infarction and HOCM
Drugs that cause QT prolongation e.g. clarithromycin, erythromycin
Inherited channelopathies e.g. Romano-Ward syndrome, Brugada syndrome
Management of Ventricular Tachycardia
(2)
Patients with adverse features should be offered synchronised DC shock.
The main medical treatment option for stable patients with a regular broad complex tachycardia is IV Amiodarone.
A 30 year old gentleman is being treated for pneumonia in the A&E department. He was started on IV antibiotics as per hospital guidelines. 10 minutes later, he complains of difficulty breathing.
His observations are as follows:
T: 37.3, HR: 110; RR: 26, O2: 98%, BP: 116/70
On examination, you notice his lips are swollen and he appears flushed. He is in respiratory distress. He has developed an urticarial rash over his torso. On auscultation, his chest is clear.
What is the most appropriate management for this patient?
(3)
Stop intravenous antibiotics immediately
administer IM Adrenaline 1:1000 0.5ml
IV 0.9% NaCl 500ml
According to the UK resuscitation council guidelines, this is the most appropriate management of anaphylaxis at the ideal doses and routes of administration.
Note that although anti-histamine and steroids are still in the treatment guidelines, they SHOULD NOT be given in the initial ABCDE assessment. Instead, they should be administered when the patient is stablised.
A 29 year old female who lives alone presents with a headache, nausea and feeling generally unwell.
She has recently moved into a new house.
On examination, she is drowsy with a GCS of 14, has saturations of 100% and is noted to have bright red lips.
What is the diagnosis?
What is the most appropriate initial treatment for this patient?
Why is her saturation at 100%?
15L high flow oxygen with a non-rebreathe mask
- The history of this patient suggests carbon monoxide poisoning, having moved into a new house, suggesting a gas leak.
- Cherry red lips are typical in these patients, and they will have high oxygen saturations as the pulse oximeter cannot recognise the difference between oxyhaemaglobin and carboxyhaemaglobin.
A 68-year old woman is an inpatient at the cardiac care unit (CCU).
She is fluid overloaded, the doctors put her on 1L fluid restriction and prescribed her furosemide 40mg IV once daily to off-load her.
However, she is still positive 2 L fluid balance after one day, and has produced minimal amounts urine.
On reviewing her renal function it is noticed that her eGFR is 26 ml/min/1.73m^2.
What is the most appropriate course of action regarding her diuretic therapy?
Increase furosemide to 80 mg intravenously
This question tests the knowledge of the mode of action of furosemide, a commonly prescribed diuretic.
Furosemide is a loop diuretic which works on the thick ascending loop of Henle, targeting the NaKCl cotransporter on the apical membrane.
This means that it must be first filtered into the tubules by the glomerulus to have a diuretic action.
Therefore, in patients with poor renal function, the dose of furosemide must be increased so that an increased concentration reaches the glomerulus and tubules to achieve the desired effect.
Presentation of pulmonary oedema
(4)
Patients with acute pulmonary oedema can present with;
- extreme dyspnea
- restlessness
- anxiety
- frothy sputum
Presentation of fluid overload
(4)
- bilateral reduced air entry
- inspiratory crepitations
- raised JVP
- S3 gallop peripheral oedema.
A 91 year old man present to A&E severely short of breath.
He was recently discharged 5 days ago from an admission due to confusion.
Today, his legs are very swollen, with pitting oedema beyond the knees. His JVP is raised.
Listening to the lungs there are bilateral basal end-inspiratory crackles.
A murmur is heard when listening to the heart.
He has a past medical history of mitral regurgitation, type 2 diabetes, and heart failure.
Blood results compared to the previous admission show he is in AKI stage 1.
What is the most appropriate management?
IV furosemide
Patients who are severely fluid overloaded, especially with pulmonary congestion, require diuresis for fluid removal independent of any changes in their eGFR.
When there is elevated central venous pressure, the renal function may recover with the aid of diuresis.
A 23-year-old male is brought to A&E unresponsive. His ECG is shown below:
What does the ECG show?
What is the next best step in management?
Start CPR and deliver an unsynchronised DC cardioversion
This ECG shows ventricular fibrillation.
This is a rhythm that cannot sustain cardiac output.
This patient needs immediate CPR and the delivery of an unsynchronised shock
A 30-year-old woman presents to the Emergency Department with palpitations for the past few hours. She was recently started on haloperidol for acute psychosis.
Her ECG shows Torsades de pointes.
What is the definition of Torsades de pointed? (2)
What is the first-line management for this patient? (1)
Magnesium sulphate
Torsades de pointes is a rare, polymorphic ventricular tachycardia where the QRS axis is constantly shifting.
Patients typically have a prolonged QTc interval on ECG (>0.45s).
This patient is at risk of prolonged QTc due to the recent administration of haloperidol.
Patients should receive cardiac monitoring and IV Magnesium.
A 65 year-old man presents to the emergency department with chest pain.
This came on suddenly whilst he was watching television and radiates to his back, between his shoulder blades.
It was 10/10 in severity initially, but has lessened in intensity since and has spread gradually down his back.
He has a past medical history of hypertension.
On examination, cardiovascular and respiratory examination are unremarkable. Observations show hypertension and tachycardia.
Give the most likely diagnosis.
Which bedside test is the single most specific in aiding diagnosis?
Bilateral blood pressure measurements
A blood pressure difference of >20mmHg in the context of this history is highly suggestive of aortic dissection.
Pulse differences in the lower limbs may also be found.
Presentation of Type B dissections:
(3)
Presentation of Type B dissections:
Interscapular pain (thoracic descending aorta)
Abdominal pain (abdominal descending aortic; mesenteric arteries)
Flank pain (renal arteries)
Presentation of Type A aortic dissection (5)
Type A dissections (ascending aorta and aortic arch):
Central chest pain (coronary ostia –> MI)
Dyspnoea (ascending aorta –> aortic regurgitation –>CCF)
Neck/jaw pain (aortic arch)
Horner’s (cervical sympathetic ganglia)
Symptoms of stroke (carotid arteries)
Type A vs Type B aortic dissection management
Type A
- surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention
Type B
- conservative management
- bed rest
- reduce blood pressure IV labetalol to prevent progression
Investigations for aortic dissection
(3)
Chest x-ray
- widened mediastinum
CT angiography of the chest, abdomen and pelvis is the investigation of choice
- suitable for stable patients and for planning surgery
- a false lumen is a key finding in diagnosing aortic dissection
Transoesophageal echocardiography (TOE)
- more suitable for unstable patients who are too risky to take to CT scanner
A 19-year old male is admitted to the Emergency Department following a night out with his friends.
He presents with rigidity, disorientation and a temperature of 39.2.
He states he had taken some pills during the night out. It is suspected he has taken ecstasy.
His observations are stable.
He is normally fit and well.
Which of the following is the most likely diagnosis?
Serotonin syndrome
Correct. Serotonin syndrome is most commonly associated with SSRI and MAOI antidepressants but can also be caused by ecstasy and amphetamines.
It is a potentially life-threatening drug-induced condition caused by too much serotonin in the synapses of the brain.
It has an onset within hours and presents with combination of neuromuscular, autonomic and mental state symptoms.
Clinical features of Serotonin Syndrome
(3)
It is characterised by a triad of:
- Mental status changes
- Autonomic hyperactivity
- Neuromuscular abnormalities.
It commonly presents within the first couple of months of starting an SSRI or when there are drug interactions, particularly between tramadolol and sertraline.
A 22-year old gentleman presents to the A&E Department with an 8 hour history of diffuse abdominal pain and vomiting. He is breathing heavily and appears quite drowsy.
You are unable to take a proper history from him. His mother, who came along with him mentioned that has been a healthy boy since young, with no significant past medical history. He went out with his friends the night before and had a few pints of beer. There was no mention of any trauma.
His observations are as follows:
T: 37.3, HR: 105, RR: 25, O2: 97%, BP: 100/70
You quickly do an ABG and it shows the following:
pH: 7.2 (7.35 - 7.45)
PO2: 11.5 kPa (10 - 15)
PCO2: 4.3 kPa (4.5 - 6)
HCO3: 15 mmol/l (22 - 26)
PO4: 2.8 (2.5 - 4.5)
Cl: 105 (95 - 105)
Na: 133 mmol/l (135 - 145)
K: 5.4 mmol/l (3.5 - 5)
Lac: 2.6 mmol/l (0.5 - 1.0)
Glucose: 19 mmol/l
Albumin: 40 g/L (35 - 50)
Anion Gap: 18.4 (normal = <12)
What is the most likely diagnosis?
Which appropriate investigation can confirm the underlying diagnosis?
Blood Ketones
Ketones should be measured if DKA is suspected.
The high anion gap metabolic acidosis and hyperglycaemia in the setting of an acute abdomen can point to DKA.
Lactate may be slightly raised in DKA.
Hyponatraemia can occur as a pseudo-hyponatraemia due to the large amounts of glucose.
What is a synacthen test?
A synacthen test is ordered if an Addisonian crisis is suspected as the underlying diagnosis.
A patient with Addison’s can present with features including hypotension, hypoglycaemia, hyperkalaemia and hyponatraemia.
This is not sufficiently demonstrated in this scenario and hence is not the best answer.
Addisonian crisis presentation:
(4)
A patient with Addison’s can present with features including:
- hypotension
- hypoglycaemia
- hyperkalaemia
- hyponatraemia
A 77 year old female present to hospital with left leg redness and pain.
She is diagnosed with cellulitis and given intravenous fluids and oral flucloxacillin.
She has a background of asthma, ischaemic heart disease, and heart failure.
The next day she complains of feeling short of breath.
On auscultation there are bilateral crackles heard.
Observations show she is tachycardic and saturating 92% on room air.
What is the most appropriate management plan?
Intravenous furosemide
This patient has a background of heart failure and this presentation is likely due to decompensated heart failure as a result of iatrogenic fluid overload.
The symptoms and signs are suggestive of pulmonary oedema. The fluid needs to be off-loaded using furosemide.
A 20-year-old gentleman is brought into the A&E Department. He is a known epileptic and is taking valproate regularly. He started seizing about 5 minutes ago and is still currently jerking uncontrollably.
His basic observations are as follows:
HR 100, RR 12, BP 140/90, T 35.8, SO2 92%
He is immediately put in the recovery position, started on high-flow oxygen and an oropharyngeal airway adjunct is inserted. His blood glucose level is 6.2 mmol/L.
After about 15 minutes, he is still seizing. 2 doses of IV Lorazepam 4mg had been administered but it did not seem to help. His SO2 has improved to 98% on room air.
What is next most appropriate treatment option for this patient?
IV infusion of Phenytoin
This patient is in status epilepticus that has persisted for 15 minutes and failed to improve on 2 doses of IV Lorazepam.
A second, more longer-acting anti-convulsant is needed at this stage, and guidelines recommend an infusion of Phenytoin.
Emergency Management of Status Epilepticus
(9)
1. ABCDE approach
2. Oxygen
3. Ensure IV access
4. Arterial Blood gas
5. FBC/UE/CRP/glucose/Calcium/Phosphate/Magnesium
6. Anaesthetic review to ensure the airway is managed
7. IV lorazepam 4mg
- A second dose of lorazepam should be given if no response
- In the absence of IV access, PR diazepam or buccal midazolam can be administered.
8. If the initial benzodiazepine fails, further anti-convulsants can be used:
- Leviteracetam
- Phenytoin
- Valproate
9. If seizures continue to persist, intubation and general anaesthesia is necessary.
A 62 year old male patient presents to the emergency department with a 20 minute history of shortness of breath, dizziness, and severe malaise.
On physical examination you note a recent midline sternotomy scar.
Electrocardiogram (ECG) reveals regular monomorphic broad QRS complexes at a rate of 140bpm and absent P waves.
During the assessment in the emergency department the patient collapses and there is no palpable pulse.
CPR is commenced and has been carried out for 2 minutes.
What is the next most appropriate management step? (2)
What is the most likely diagnosis?
- Emergency unsynchronised direct current (DC) cardioversion
- Pulseless VT is a shockable rhythm so the patient requires defibrillation
The patient presents with sustained ventricular tachycardia causing haemodynamic instability.
A 76 year old male has been admitted to the intensive care unit for treatment of a community acquired pneumonia.
He has a background of hypertension and ischaemic heart disease, and takes aspirin, amlodipine and ramipril.
Three days after starting IV antibiotics, he complains of chest pain and palpitations.
His ECG shows a polymorphic ventricular tachycardia.
Which of the following is the most likely cause of his arrhythmia?
Which interval does it lengthen?
- Co-amoxiclav
- Clarithromycin
- Gentamicin
- Tazocin
- Amoxicillin
Clarithromycin
Clarithromycin can cause prolongation of the QT interval, which can lead to a polymorphic VT, otherwise known as torsades de points.
Cause of Torsades De Pointes
(6)
Causes of a long QT interval which may predispose a patient to developing TDP include the following.
This can be remembered by a useful mnemonic - TIMMES:
Toxins: drugs including anti-arrhythmics, anti-psychotics and tricyclic antidepressants
Inherited: congenital long QT syndromes such as Romano-Ward and Jervell and Lange-Nielson syndromes.
Ischaemia
Myocarditis
Mitral valve prolapse
Electrolyte abnormalities, such as hypokalaemia and hypocalcaemia
Subarachnoid Haemorrhage
Management of Torsades De Pointes
In unstable patients with haemodynamic compromise, DC cardioversion can be done.
In stable patients, the choice of treatment is IV Magnesium Sulphate 2g over 1 to 2 minutes.
A 33-year-old gentleman with no significant past medical history is involved in a road traffic accident and was rushed into the Emergency Department.
His basic observations are as follows: HR 110, RR 35, BP 70/50, SO2 88% RA.
He is in severe respiratory distress.
After a quick initial assessment, the consultant decides to perform an immediate needle decompression with a large-bore needle inserted into his right 2nd intercostal space midclavicular line.
Give the underlying diagnosis (1)
Which examination findings would the consultant most likely have elicited? (4)
- Tracheal deviation to the left
- reduced chest expansion
- hyperresonant percussion on the right
- decreased vocal resonance on the right
This option describes the typical examination findings in a patient with a tension pneumothorax.
A tension pneumothorax may be large enough to shift the trachea to the opposite side.
Due to the collection of air in the pleural space, percussion will appear hyperresonant and vocal resonance will be decreased on the same side as the pneumothorax.
Other findings may include signs of haemodynamic instability and crepitus over the skin from surgical emphysema
What is meant by Hemodynamic instability?
Hemodynamic instability occurs when there’s abnormal or unstable blood pressure, which can cause inadequate blood flow to the organs
Towards vs Away
A 65-year-old woman presents to the Emergency Department with a 2 hour history of chest discomfort and difficult breathing.
She has a past medical history of poorly controlled SLE.
Her basic observations are as follows: HR 110, RR 25, BP 80/60, SO2 92% RA.
On examination, she appears very anxious and has some difficulty breathing.
Her JVP is raised and there is some pedal oedema.
On auscultation, heart sounds are difficult to hear.
You notice that when she breathes in, her JVP rises and her systolic blood pressure drops.
Given the underlying diagnosis, what is the most appropriate management?
Pericardiocentesis
Pericardiocentesis involves the insertion of a needle into the pericardial sac to relieve over-accumulation of fluid.
A needle is usually inserted just left to the xiphoid process, aiming towards her left shoulder.
This can be done to treat cardiac tamponade, which is what this lady has. SLE is a risk factor for the development of cardiac tamponade.
This lady also displays Beck’s triad - the combination of raised JVP, hypotension and muffled heart sounds, a feature of cardiac tamponade.
She has Kussmaul’s sign (rise in JVP with inspiration) and pulsus paradoxus (drop in systolic blood pressure of about 15 mmHg with inspiration), which are also features of cardiac tamponade.
Causes of metabolic alkalosis
(8)
Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly to problems of the kidney or gastrointestinal tract
- Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis, nasogastric suction)
- Diuretics
- Liquorice, carbenoxolone
- Hypokalaemia
- Primary hyperaldosteronism
- Cushing’s syndrome
- Bartter’s syndrome
- Congenital adrenal hyperplasia
Causes of metabolic acidosis
(3)
COPD
Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary oedema
Sedative drugs: benzodiazepines, opiate overdose
Mechanism of metabolic alkalosis (3)
Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule
extracellular fluid depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised aldosterone levels
In hypokalaemia, K+ shift from cells → extracellular fluid, alkalosis is caused by shift of H+ into cells to maintain neutrality
What is a metabolic alkalosis? (3)
Metabolic alkalosis
Usually caused by a rise in plasma bicarbonate levels.
Rise of bicarbonate above 24 mmol/L will typically result in renal excretion of excess bicarbonate.
Caused by a loss of hydrogen ions or a gain of bicarbonate.
It is due mainly to problems of the kidney or gastrointestinal tract
A 19 year old female presents to the emergency department complaining of palpitations. The patient has had similar episodes in the past, but has not previously attended hospital, and she has no other past medical history.
On examination, the patient is alert and orientated, heart and breath sounds are normal, the radial pulse is regular and the rate is 190, blood pressure is 102/57, oxygen saturations are 98% on air, and respiratory rate is 19.
IV access is in situ.
A 12-lead ECG is done.
What is the diagnosis?
What is the treatment?
This patient is having a stable supraventricular tachycardia (in this case an atrioventricular nodal re-entrant tachycardia).
The treatment of choice in this case would be to try vagal manoeuvres (ask the patient to blow into a 20ml syringe with the plunger down), if these are un-successful then medical therapy may be required, or if the patient becomes unstable DC cardioversion would be the treatment of choice.
A 55-year-old lady comes into the Emergency Department complaining of palpitations and difficulty breathing.
She has had past medical history of COPD, DM and OA. Her regular medications include Metformin, Paracetamol, Seretide and Salbutamol inhalers.
Her basic observations are as follows: HR 145, RR 29, BP 70/60, T 37.3, SO2 92% RA.
Her ECG shows the following rhythm:
What is the diagnosis from the ECG?
What is the most appropriate treatment for this patient?
This patient has a narrow complex tachycardia or supraventricular tachycardia (SVT) on her ECG.
In patients who have features of:
- heart failure
- ischaemia
- syncope or hypotension
synchronised cardioversion should be performed.
As this patient is hypotensive with a BP of 70/60, she should be offered synchronised DC.
A 75-year old male presents to the Emergency Department with palpitations that started an hour ago.
His observations include a heart rate of 230bpm which is regular, blood pressure 168/74mmHg and Sp02 95% (on room air).
An ECG is performed which shows no P-waves and narrow QRS complexes.
What is the most likely diagnosis?
What is the first-line treatment?
What is the second-line treatment?
Atrio-ventricular node re-entry tachycardia (AVNRT)
AVN re-entry tachycardias occur when there are two pathways within the AVN.
AVNRT is the most common type of supraventricular tachycardia (SVT).
As the patient is stable and the rhythm is regular, vagal manoeuvres should be attempted first.
If this fails, IV Adenosine can be used.
A 55 year old lady comes into the A&E Department complaining of palpitations and difficulty breathing.
She has a past medical history of COPD, DM and OA.
Her regular medications include Metformin, Paracetamol, Seretide and Salbutamol inhalers.
Her basic observations are as follows:
HR 145, RR 29, BP: 70/60, T 37.3, SO2: 92%
Her ECG shows the following rhythm:
What is the most appropriate treatment for her?
DC cardioversion
This patient has a narrow complex tachycardia or supraventricular tachycardia (SVT) on her ECG.
In patients who have features of;
- heart failure
- ischaemia
- syncope
- hypotension
synchronised cardioversion should be performed.
As this patient is hypotensive with a BP of 70/60, she should be offered synchronised DC cardioversion.
A 24-year-old lady is brought into the Emergency Department (ED) with palpitations that occurred suddenly earlier that day.
On assessment, she reports no other symptoms and a past medical history of poorly controlled asthma.
An ECG shows a heart rate of 150 bpm and a regular narrow complex tachycardia.
Which of the following is the next best step in management?
Valsalva manoeuvre
This patient’s ECG findings are characteristic of supraventricular tachycardia (SVT).
In the absence of adverse features (myocardial ischaemia, heart failure, syncope or shock), the first-line management of an SVT is vagal manoeuvres.
These aim to stimulate the vagus nerve in order to slow down the heart rate.
The Valsalva manoeuvre is commonly performed by asking the patient to blow through an occluded syringe for about 15 seconds.
Alternative vagal manoeuvres include carotid sinus massage and applying a cold stimulus to the face.
A 2 year old boy is brought to AE after behaving strangely.
On triage, his heart rate is noted to be above 250 beat per minute.
His ECG is shown below.
What is the diagnosis?
What is the most appropriate treatment?
The boy has SVT
- ice water submersion to trigger the mammalian diver reflex to slow the heart rate down - submerge their face for 5 seconds
- if that was ineffective, then IV adenosine
Adenosine essentially resets the cardiac cycle by causing a block to the AV NODE
A 60-year-old woman is brought into the emergency department by ambulance due to severe chest pain which started 30 minutes ago.
This came on whilst she was watching television, and is accompanied by nausea, sweating and dyspnoea.
She has a past medical history of hypertension, type 2 diabetes and hypercholesterolaemia.
She is a heavy smoker with a 20 pack-year history.
Her ECG shows T wave inversion in leads II, III and aVF.
Troponin T (at admission): 9 ng/L (normal <14 ng/L)
Troponin (repeated at 4 hours): 45 ng/L
What is the single most likely diagnosis?
NSTEMI
The clinical picture combined with the rise in troponin and ECG findings make this the most likely diagnosis.
In NSTEMI and STEMI, the initial troponin may be ‘normal’ as it can take several hours (depending on the assay and the degree of myocardial damage) for the cardiac biomarkers to become detectable.
Hyperacute T waves (HATW)
Broad, asymmetrically peaked or ‘hyperacute’ T-waves (HATW) are seen in the early stages of ST-elevation MI (STEMI), and often precede the appearance of ST elevation and Q waves.
Particular attention should be paid to their size in relation to the preceding QRS complex, as HATW may appear ‘normal’ in size if the preceding QRS complex is of a small amplitude.
A 56 year old gentleman presents with a 3 day history of nausea, anorexia, weakness and dizziness.
He reports that he had been suffering from a flu-like illness in the preceding week.
His past medical history includes hypertension, vasculitis and osteoarthritis.
His medications include ramipril, prednisolone and ibruprofen.
On examination he is mildly hypotensive with a significant postural drop.
Bloods show a mild hyponatreamia and hyperkalaemia.
What is the most appropriate initial management of this patient?
IV hydrocortisone
This presentation of Addisonian crisis is in somebody on long-term steroids who has undergone an additional stress (i.e. viral illness).
The most important management here is to provide extra glucocorticoid to cover for the increased demand caused by the illness.
