Cardiology - Capsule Cases Flashcards
A 46-year-old man develops cardiogenic shock 48 hours after admission with an anterior myocardial infarction. He had intermittent chest pain symptoms for 3 days prior to admission. On admission, he underwent coronary angiography and percutaneous coronary intervention – a stent was inserted in to the left anterior descending artery. His ECG improved but there were anterior Q-waves and a degree of residual ST elevation. A loud pan systolic murmur is heard which is new.
Once the patient improved from this acute episode, right and left heart catheterisation were performed. The pressure and oxygen saturation data obtained are shown below. Oxygen Sats Pressure (mmHg): Superior vena cava = 74% Right atrium (mean) = 75%, 7mmHg Right ventricle = 87%, 50/12mmHg Pulmonary capillary wedge = 16mmHg Left ventricle = 96%, 140/12mmHg Aorta = 97%, 110/60mmHg What do these figures reveal as the diagnosis?
There is a step up in oxygen saturation between RA & RV. This can only occur when there is an abnormal connection between these two chambers i.e. via a VSD. This is confirmed by raised right ventricular pressures.
You are called to see a 46-year-old patient on the medical assessment unit who has been admitted with a 2-hour history of central chest discomfort. He has also noted severe pain in the left side of his jaw and has felt sweaty. He is not short of breath but does feel nauseated although he has not vomited. He has not experienced these symptoms before and has no previous medical history of note. He smokes 10 cigarettes a day and has done so since his teens. He drinks alcohol in moderation and is on no medication. He is married with two children.
On examination, he is a little clammy, pulse 95bpm and regular, blood pressure 140/85 mmHg and apyrexial. His heart sounds are normal and his lungs are clear. Physical examination is otherwise unremarkable.
Which three further investigations would you arrange immediately?
ECG
Cardiac Enzymes
Chest radiograph
In addition to routine blood tests (FBC, U&Es, glucose, troponin etc.), pulse oximetry and cardiac monitoring are also indicated.
Formal blood gases are not necessarily needed at this stage in the absence of shortness of breath.
You are called to see a 46-year-old patient on the medical assessment unit who has been admitted with a 2-hour history of central chest discomfort. He has also noted severe pain in the left side of his jaw and has felt sweaty. He is not short of breath but does feel nauseated although he has not vomited. He has not experienced these symptoms before and has no previous medical history of note. He smokes 10 cigarettes a day and has done so since his teens. He drinks alcohol in moderation and is on no medication. He is married with two children.
On examination, he is a little clammy, pulse 95bpm and regular, blood pressure 140/85 mmHg and apyrexial. His heart sounds are normal and his lungs are clear. Physical examination is otherwise unremarkable.
Anteroseptal MI
There is ST elevation in the anterolateral leads V1-V4. To confirm that this is an acute STEMI there should be reciprocal changes on the opposite wall: there is T wave inversion in the inferior leads 3 and AVF.
Left Ventricular aneurysms can present with ST elevation together with Q waves alone but without the reciprocal changes.
This patient has had myocardial infarction. He was treated with thrombolysis with rapid resolution of ST elevation. On day 3 post-MI, he complained of severe dyspnoea and orthopnoea. On clinical examination, a loud, pan-systolic murmur was audible and he was cold, clammy and tachycardic, BP 80/50mmHg. Which is the most likely diagnosis?
Ventricular septal defect post MI
This patient has developed a post-MI VSD as demonstrated by shock and a new systolic murmur. Post-MI, acutely, the myocardium may rupture with profound shock and rapid demise. Papillary muscle rupture may also occur, most often of the mitral valve, with development of mitral regurgitation and cardiac failure. Post-MI deaths have decreased in hospitals due to increasing use of percutaneous coronary intervention (PCI), thrombolysis and coronary artery bypass grafting (CABG).
This patient has had myocardial infarction. He was treated with thrombolysis with rapid resolution of ST elevation. On day 3 post-MI, he complained of severe dyspnoea and orthopnoea. On clinical examination, a loud, pan-systolic murmur was audible and he was cold, clammy and tachycardic, BP 80/50mmHg. This is their subsequent Echo, label the following arrows
This patient has sustained a post-MI ventricular septal defect (VSD). How would you manage this patient?
- Analgesia as needed
- Consider Coronary angiography
- Arrange urgent transfer to cardiothoracic unit
- Consider intra-aortic balloon pump
- Consider positive pressure ventilation
- Consider Swann-Ganz pulmonary artery catheter - passing of a catheter into the right side of the heart and the pulomary arteries. It is done to monitor the heart’s function and blood flow and pressures in and around the heart.
- Ionotropic support
A 67-year-old male smoker is brought to the ED via blue light ambulance with severe central chest pain radiating to his neck and left arm. He had been admitted with unstable angina previously but had been asymptomatic since. He had no other significant past medical history.
On examination, he is in pain, is sweaty with a pulse of 100bpm, blood pressure 170/100 mmHg and respiratory rate of 30/min. Heart sounds are normal, JVP is not elevated and the chest is clear.
What would be your initial management in the ED?
The immediate management should be ECG, Aspirin 300mg, and oxygen saturation monitoring.
Mnemonic MONA= morphine, oxygen, nitrates and asprin.
Subsequently, a portable CXR is indicated (the patient should be kept in the resuscitation area and mobile film performed), oxygen saturations can be quickly performed with observations, the patient should be sat up and given oxygen via a face mask if oxygen saturation are less than 90%.
Diamorphine is correct but should be titrated to pain (20mg is too high initial dose).
A 67-year-old male smoker is brought to the ED via blue light ambulance with severe central chest pain radiating to his neck and left arm. He had been admitted with unstable angina previously but had been asymptomatic since. He had no other significant past medical history.
On examination, he is in pain, is sweaty with a pulse of 100bpm, blood pressure 170/100 mmHg and respiratory rate of 30/min. Heart sounds are normal, JVP is not elevated and the chest is clear.
The following ECG is obtained (image below). What does the ECG show?
ST elevation primarily in the anterior leads = acute anterolateral myocardial infarction.
There is ST elevation most pronounced in V2-V5, but also to a lesser extent in the lateral leads I and aVL. Note that there is ‘reciprocal’ ST depression in leads III and aVF.
What is your immediate management priority once diagnosis of acute anterior myocardial infarction has been made?
Salvaging any threatened myocardium is time sensitive. Thrombolysis or primary angioplasty are appropriate. Anticoagulation is not routinely indicated in patients with acute myocardial infarctions. All patients will have cardiac monitoring
A 67-year-old male smoker is brought to the ED via blue light ambulance with severe central chest pain radiating to his neck and left arm. He had been admitted with unstable angina previously but had been asymptomatic since. He had no other significant past medical history.
On examination, he is in pain, is sweaty with a pulse of 100bpm, blood pressure 170/100 mmHg and respiratory rate of 30/min. Heart sounds are normal, JVP is not elevated and the chest is clear.
The patient received primary angioplasty and recovers on the coronary care unit. Over the next few hours, the patient becomes increasingly short of breath and the following chest x-ray is performed (image below).
The patients blood pressure is now recorded at 75/50 mmHG. What is the next step in the management of this patient?
CPAP
Treatment options limited due to low blood pressure and cardiogenic shock. The only management step here should be to initiate CPAP (continuous positive airway pressure). This method of non invasive ventilation will allow the lung fluid to effectively pushed under pressure back into the vasculature to improve blood pressure. This will then permit drugs such as IV diuretics to be given without risk of further hypotension. Adrenaline and salbutamol are not indicated here. Oxygen alone would not result in resolution of the pulmonary oedema. IV fluids would be dangerous and risky to to this patient who has intravascular fluid in the wrong compartment (lungs).
A 67-year-old male smoker is brought to the ED via blue light ambulance with severe central chest pain radiating to his neck and left arm. He had been admitted with unstable angina previously but had been asymptomatic since. He had no other significant past medical history.
On examination, he is in pain, is sweaty with a pulse of 100bpm, blood pressure 170/100 mmHg and respiratory rate of 30/min. Heart sounds are normal, JVP is not elevated and the chest is clear.
The patient received primary angioplasty and recovers on the coronary care unit. Over the next few hours, the patient becomes increasingly short of breath and the following chest x-ray is performed (image below).
The patients blood pressure is now recorded at 75/50 mmHG.
What three invesitigations would you consider to determine the cause for this deterioration
Renal Function
Echocardiogram
ECG
The majority of patients returning to coronary care after a primary PCI will be fine but you need to be aware of some complications, pulmonary oedema being one of them. It is important to consider the cause for the acute left ventricular failure (LVF). Another ECG to see if arrhythmia such as AF. VT. Also to consider whether the stent has occluded already (malpositioned) so ST elevation may be still present. Normally these patient still have ongoing chest pain. Rarely the patient may have pre-existing unknown renal failure and the amount of contrast given during the procedure tips them into acute LVF. Thus routine bloods are important such as renal function. A full blood count may also give some indication of blood loss such as from the arterial puncture site that can be masked in the retroperitoneal space (femoral access less used currently for access and most patients will have radial artery access). Next an echocardiogram would be very helpful to diagnose left ventricular function and if any rupture, valve dysfunction or development of septal VSD (may be early to see this in time frame of presentation).
A 54-year-old man presents to the emergency department with a 3-hour history of sudden onset, severe crushing central chest pain associated with sweating, shortness of breath and nausea. He had previously been well, although had suffered with what he called ‘indigestion’ and ‘heart burn’ for many years for which he regularly took Gaviscon. He had been recently diagnosed with hypertension by his GP who had treated him with Bendroflumethiazide 2.5mg OD. He smoked 20 cigarettes per day and had done so for over 30 years. His mother had suffered with angina in her 70’s and later died age 75 from a stroke.
On examination, he appeared unwell, was cold and clammy, HR 72 bpm, BP 147/91 mmHg, saturation 95% on room air. His JVP was not elevated, heart sounds were normal and chest clear to auscultation.
Look at the ECG recorded on admission (figure 1). What is the most likely diagnosis? Whcih artery coronary artery is most likely affected?
ECG findings: ST segment elevation leads V2, V3 and leads I and aVL, reciprocal ST segment depression in leads, II, III and aVF. Diagnosis: acute anterior myocardial infarction with lateral extension (acute anterolateral MI).
The anterior/anterolateral wall is supplied by the left anterior descending artery.
A 54-year-old man presents to the emergency department with a 3-hour history of sudden onset, severe crushing central chest pain associated with sweating, shortness of breath and nausea. He had previously been well, although had suffered with what he called ‘indigestion’ and ‘heart burn’ for many years for which he regularly took Gaviscon. He had been recently diagnosed with hypertension by his GP who had treated him with Bendroflumethiazide 2.5mg OD. He smoked 20 cigarettes per day and had done so for over 30 years. His mother had suffered with angina in her 70’s and later died age 75 from a stroke.
On examination, he appeared unwell, was cold and clammy, HR 72 bpm, BP 147/91 mmHg, saturation 95% on room air. His JVP was not elevated, heart sounds were normal and chest clear to auscultation.
Look at the ECG recorded on admission (figure 1). The patient is transferred to CCU, attached to a cardiac monitor and an IV cannula inserted. What would be your initial managment?
Intravenous opiates (morphine or diamorphine), high flow oxygen only if saturations are below the expected range, oral Aspirin 300mg and sublingual GTN are the immediate management of the patient. Intravenous Metoclopramide 10mg is also given to counteract the emetic effects of the opiates.
The mnemonic: MONA can be used to help remember the immediate management of patients:
M – morphine
O – oxygen
N – nitrogycerin
A – aspirin
A patient suffers an anterolateral MI. They are treated with a PCI. What five medications should they be prescribed on discharge?
- Clopidogrel 75mg OD (could also be ticagrelor 90 mg bd or prasugrel 10 mg od which are stronger antiplatelets),
- Bisoprolol up to 10 mg OD,
- Ramipril up to 10mg OD,
- Aspirin 75mg OD,
- Atorvastatin 80mg OD are correct.
The NICE guidelines for the secondary prevention of MI recommend that all patients should be offered an ACEi, dual antiplatelet therapy, a beta-blocker and a statin.
A 75-year-old male patient with known coronary artery disease, is referred by his General Practitioner with increasing frequency of chest pains for the past 2 weeks. Eight years previously he suffered an acute anterior myocardial infarction for which he was thrombolysed. Coronary angiogram at the time demonstrated a 90% stenosis of the LAD artery and he underwent percutaneous coronary intervention. He is an ex-smoker. No other relevant past medical history.
His medications are as follows:
Aspirin 75mg OD
Atenolol 25mg BD
Ramipril 5mg BD
Simvastatin 40mg OD
Glyceryl tri-nitrate (GTN) spray PRN
He has had occasional exertional angina for the past year, but this had become frequent in the past two weeks although they generally lasted less than 20 minutes. He had had episodes at rest today although these were relieved with sublingual GTN spray.
On examination, the pulse was slow rising, 80bpm and regular, blood pressure 100/80 mmHg and respiratory rate 16/min. The apex beat was non-displaced, but heaving. Heart sounds demonstrated a grade 2 ejection systolic murmur at the right sternal edge which radiated to the neck. The lungs were clear.
What is the cause of the murmur?
Aortic stenosis
Many cardinal features of aortic stenosis are present in this patient with a slow rising pulse, narrow pulse pressure, and ejection systolic murmur radiating to the neck.
Mitral regurgitation typically produces a pansystolic murmur, which does not radiate to the neck.
A 75-year-old male patient with known coronary artery disease, is referred by his General Practitioner with increasing frequency of chest pains for the past 2 weeks. Eight years previously he suffered an acute anterior myocardial infarction for which he was thrombolysed. Coronary angiogram at the time demonstrated a 90% stenosis of the LAD artery and he underwent percutaneous coronary intervention. He is an ex-smoker. No other relevant past medical history.
His medications are as follows:
Aspirin 75mg OD
Atenolol 25mg BD
Ramipril 5mg BD
Simvastatin 40mg OD
Glyceryl tri-nitrate (GTN) spray PRN
He has had occasional exertional angina for the past year, but this had become frequent in the past two weeks although they generally lasted less than 20 minutes. He had had episodes at rest today although these were relieved with sublingual GTN spray.
On examination, the pulse was slow rising, 80bpm and regular, blood pressure 100/80 mmHg and respiratory rate 16/min. The apex beat was non-displaced, but heaving. Heart sounds demonstrated a grade 2 ejection systolic murmur at the right sternal edge which radiated to the neck. The lungs were clear.
Which four investigations would you request in the ED?
Chest Xray
Full blood count
ECG
Troponin levels
ECG will be important to rule out other cardiac causes of chest pain.
Baseline bloods will be required for this patient, including troponin levels to rule out myocardial infarction.
CXR is needed to assess the size of the heart and the lung fields (indicating heart failure).
A 75-year-old male patient with known coronary artery disease, is referred by his General Practitioner with increasing frequency of chest pains for the past 2 weeks. Eight years previously he suffered an acute anterior myocardial infarction for which he was thrombolysed. Coronary angiogram at the time demonstrated a 90% stenosis of the LAD artery and he underwent percutaneous coronary intervention. He is an ex-smoker. No other relevant past medical history.
His medications are as follows:
Aspirin 75mg OD
Atenolol 25mg BD
Ramipril 5mg BD
Simvastatin 40mg OD
Glyceryl tri-nitrate (GTN) spray PRN
He has had occasional exertional angina for the past year, but this had become frequent in the past two weeks although they generally lasted less than 20 minutes. He had had episodes at rest today although these were relieved with sublingual GTN spray.
On examination, the pulse was slow rising, 80bpm and regular, blood pressure 100/80 mmHg and respiratory rate 16/min. The apex beat was non-displaced, but heaving. Heart sounds demonstrated a grade 2 ejection systolic murmur at the right sternal edge which radiated to the neck. The lungs were clear.
What does his ECG show?
The ECG demonstrates left bundle branch block – prolongation of all QRS complexes. There is also some evidence of left ventricular hypertrophy in the anterolateral leads: the depth of the S wave in V2 + height R wave in V5 > 30mm (although, note that further interpretation of the ECG is difficult in the setting of left bundle branch block).
Which three of the following statements regarding imaging of aortic stenosis are correct?
- Catheter coronary angiogram is not usually performed in patients prior to undergoing aortic valve replacement
- CT coronary angiogram is the diagnostic investigation of choice
- Echo is the diagnostic imaging modality of choice
- Left ventricular hypertrophy is usually seen with severe aortic stenosis
- The CXR in severe cases may still appear normal
- Echo is the diagnostic imaging modality of choice
- Left ventricular hypertrophy is usually seen with severe aortic stenosis
- The CXR in severe cases may still appear normal
Which two of the following are true in patients with symptomatic aortic stenosis?
- Exercise testing is routinely indicated to assess the severity of stenosis
- It is usually inherited in an autosomal dominant mode of transmission
- The majority of patients present under the age of 40 years
- The most common cause under 60 years is a bicuspid aortic valve
- Valvular replacement is the treatment of choice
- The most common cause under 60 years is a bicuspid aortic valve
- Valvular replacement is the treatment of choice
What does this chest xray show?
Pulmonary oedema
Acute pulmonary oedema signs on CXR – cardiomegaly, prominent upper lobe veins, diffuse interstitial shadowing, classic perihilar ‘bat wings’ shadowing.
What does this ECG show?
Anterior myocardial infarction
The ECG shows evidence of an anterior ST-elevation myocardial infarction with Q-waves. There are also reciprocal changes in the inferior leads (III and avF)
A 70-year-old man presents to the ED with a six-hour history of central chest pain and shortness of breath. The pain does not radiate but he feels sick and sweaty. Six days previously he had experienced an episode of severe chest pain which radiated to his left shoulder. The pain had lasted about an hour and settled with indigestion treatment. The patient did not seek medical help as he did not want to disturb the doctor. He is normally in good health. He has hypertension and takes amlodipine 5mg od. He is a current smoker with a 40 pack per year history.
On examination, he is cold and clammy and short of breath at rest. His pulse is 80 bpm, BP 150/60 mmHg, respiratory rate 25 breaths per minute and O2 saturation is 90% breathing air. A systolic murmur is present at the left lower sternal border. His JVP is raised and there are revealed bilateral coarse crackles to the mid-zones on chest auscultation. Abdominal and neurological examination is normal.
Chest Xray shows pulonary oedema
Which 5 of the following treatments would you inititate?
- Aspirin
- Beta-blocker
- Calcium channel blocker
- Diamorpine IV
- Furosemide
- Oxygen therapy
- Primary percutaneous angioplasty
Aspirin
Diamorpine IV
Furosemide
Oxygen therapy
Primary percutaneous angioplasty
This patient has evidence of acute myocardial infarction and heart failure. He requires oxygen therapy as his O2 saturation is currently 90% breathing air. He also needs aspirin immediately and long-term for secondary prevention of further ischaemic events. Unless there is a significant contra-indication, this patient will require dual anti-platelet therapy. He also needs intravenous furosemide is indicated for his pulmonary oedema. He is a candidate for urgent primary percutaneous angioplasty and needs urgent referral to cardiology for possible intervention.
Beta-blockers should not be started while the patient has acute pulmonary oedema (but will be started once his fluid overload has been treated). Calcium channel blockers have a negative inotropic effect and should be avoided if possible, particularly in the acute setting.
Which three are the clinical features of mitral regurgitation?
- Atrial fibrillation
- Dyspnoea
- Pansystolic Murmur radiating to the axilla
- Pink cheeks
- Slow rising pulse
- Atrial fibrillation
- Dyspnoea
- Pansystolic Murmur radiating to the axilla
Mitral regurgitation – often presents with dyspnoea, fatigue, palpitations. Signs – atrial fibrillation, displaced hyperdynamic apex, pansystolic murmur at the apex radiating to the axilla. The more severe the larger the ventricle.
The cardinal symptoms of mitral stenosis are also fatigue and dyspnoea. Pink cheeks (mitral facies) are a sign associated with mitral stenosis, not regurgitation.
Which 3 of the following drugs are likely to increase the risk of myopathy when given with simvastatin?
Paroxetine
Simvastatin
Erythromycin
Ramipril
Bezafibrate
Simvastatin
Erythromycin
Bezafibrate
Amiodarone is an inhibitor of various CYP450 enzymes. There is some evidence of a high incidence of myopathy when amiodarone is given with high dose simvastatin. Whether amiodarone inhibits the metabolism of simvastatin and increases the risk of muscle toxicity is not known. The interaction is not established but caution should be taken when prescribing both drugs concurrently. Amiodarone alone can cause myopathy. Erythromycin is an inhibitor of CYP450 enzymes and raises the levels of drugs metabolised by these enzymes such as statins. Both statins and fibrates can cause myopathy and concurrent use may increase the risk. There is also an increased risk of myopathy also when simvastatin is given with other inhibitors of the CYP450 enzyme system in the liver such as grapefruit juice, ciclosporin and ketoconazole.
There are no clinical interactions between simvastatin and paroxetine or ramipril.
You have been called to the Coronary Care Unit to review a 55-year-old male recently admitted and treated following a myocardial infarction. He has developed a marked sinus bradycardia (38 bpm) and his blood pressure is 90/50 mmHg. He is responsive but feels unwell. He is not complaining of chest pain or dyspnoea.
What would be your next intervention?
As he is conscious and not complaining of a chest pain, no intervention is needed
Administer adenosine bolus IV 6mg
Administer amiodarone bolus IV 100mg
Administer lidocaine bolus 100mg
Administer atropine IV 500 micrograms
Administer atropine IV 500 micrograms
Sinus bradycardia post-MI, particularly if the patient is hypotensive, is an indication for the anticholinergic/antimuscarinic agent, atropine. This is given IV 500micrograms, repeated every 3-5 minutes to a maximum dose of 3mg. Do call for help if unsure, or if the patient fails to respond promptly. Adenosine is used to treat supraventricular tachycardias. Amiodarone and lidocaine are negatively inotropic and used to treat a variety of tachyarrhythmias. Amiodarone is contraindicated in sinus bradycardia.
A 75-year-old man with a history of ischaemic heart disease and COPD is admitted with an infective exacerbation of his COPD. The patient is penicillin allergic and takes the following medication:
Isosorbide mononitrate M/R 60mg OD
Amlodipine 5mg OD
Aspirin 75mg OD
Simvastatin 20mg ON
Seretide 125 inhaler 2 puffs BD
Tiotropium 18 microgram inhaler 1 puff OD
Salbutamol 100 microgram inhaler 2 puffs PRN
Next morning on the post take ward round it is noted that the patient is in a new atrial fibrillation with a pulse rate of 120bpm and a BP of 110/60mmHg. The consultant wants the patient to be treated with the antiarrhythmic drug amiodarone.
Too high a dose during maintenance therapy can lead to side effects. Which of the following are common side effects of amiodarone therapy?
Corneal microdeposits
Hyperthroidism
Slate-grey or bluish pigmentation of light exposed skin
Pneumonitis
Alopecia
bilateral pedal oedema
muscle cramps
Corneal microdeposits
Hyperthroidism
Slate-grey or bluish pigmentation of light exposed skin
Pneumonitis
Most patients taking amiodarone develop corneal microdeposits which are reversible on withdrawal of treatment. These rarely interfere with vision. If vision is impaired amiodarone must be stopped and expert advice sought. Amiodarone contains iodine and can cause disorders of the thyroid function; both hypo- and hyperthyroidism may occur. Since there is a possibility of phototoxic reactions, patients should be advised to shield the skin from light during treatment with amiodarone and for several months after discontinuing treatment. A wide spectrum sunscreen to protect against long wave ultra-violet and visible light should be used. Pneumonitis should always be suspected if new or progressive shortness of breath or cough develops in a patient taking amiodarone. Alopecia may be a very rare side effect of amiodarone.
Which three of the following are suitable pharmacological treatments to restore sinus rhythm in the acute management of paroxysmal atrial fibrillation?
Amiodarone
Flecanide
Digoxin
Amlodopine
Sotalol
Amiodarone
Flecanide
Sotalol
Digoxin is usually effective for controlling the ventricular rate at rest. Amlodipine is a dihydropyridine calcium channel blocker which does not have any negative chronotropic effects and is therefore not indicated for use in arrhythmias. The other three drugs are all suitable for treatment of paroxysmal atrial fibrillation. Normally drugs with additional class of antiarrhythmic activity such as class 1 and 3 are most effective.
Amiodarone used with which of the following drugs may result in toxicity of that drug?
Digoxin
Digitoxin
Theophylline
Warfarin
Phenytoin
Digoxin
Digitoxin
Warfarin
Phenytoin
Amiodarone effectively doubles serum digoxin and digitoxin levels. It reduces both renal and non-renal excretion of digoxin. It also inhibits hepatic metabolism of digitoxin. The maintenance dose of digoxin and digitoxin should, therefore, be halved. Amiodarone inhibits the metabolism of warfarin through the CYP450 enzymes and therefore increases the anticoagulant effect of warfarin and the likelihood of toxicity. Amiodarone inhibits the metabolism of phenytoin and increases plasma concentration. Amiodarone does not interact with theophylline however it does cause thyroid dysfunction which may affect theophylline requirements so it may be good practice to ensure theophylline levels are therapeutic when amiodarone is used.
What is the correct loading regime for amiodarone?
Amiodarone 200mg TDS
Amiodarone 200mg TDS 1/52, 200mg BD 1/52 then 200mg OD
Amiodarone 200mg TDS 2/52, 200mg BD 2/52 then 200mg OD
Amiodarone 100mg TDS 2/52, 200mg TDS 2/52 then 200mg OD
Amiodarone 200mg TDS 2/52, 200mg BD 4/52 then 200mg OD
Amiodarone 200mg TDS 1/52, 200mg BD 1/52 then 200mg OD
It should be prescribed as 200mg TDS for one week, then 200mg BD for one week then 200mg OD thereafter.
A 64-year-old man presents acutely to ED with progressively worsening severe headache. Whilst waiting to be seen he has a seizure, which is witnessed by one of the nursing staff and described as tonic-clonic. His seizure settles spontaneously. He has no past medical history and is not on any medication.
His observations following the seizure are: temperature is 36.9°C, heart rate 80 bpm, BP 240/150mmHg, and oxygen saturation 98% breathing air. GCS Score is 15/15. On examination, there is left ventricular apical heave, normal heart and breath sounds. Neurological examination is normal except for fundoscopy which shows flame shaped haemorrhages on a background of dot and blot haemorrhages.
His ECG shows left axis deviation with left ventricular hypertrophy.
Blood results:
Hb 140135-180 g/L
WCC 54-11 x109/L
Plt 160150-450 x109/L
MCV 8076-100 fL
Na+ 135136-145 mM
K+ 4.23.5-5.1 mM
Ur 81.7-8.3 mM
Cr 19062-106 µM
CRP 30-5 mg/L
Glucose 5.34-6 mM
What is the most likely diagnosis?
- Epilepsy
- Hypertensive emergency
- Brain tumour
- MDMA (‘Ectasy’) intoxication
- Sepsis
Hypertensive emergency
The most likely diagnosis is a hypertensive emergency. This refers to severe systemic hypertension: systolic >200mmHg and diastolic >130mmHg with associated end organ damage.
A diagnosis of epilepsy can not be made following a single seizure. Investigation for an underlying cause must also be undertaken. Brain tumours, both primary and malignant, may present with seizures. However, there are no other findings to support this diagnosis.
The patient is apyrexial with normal heart rate making a diagnosis of sepsis or MDMA toxicity very unlikely. The CRP would also be expected to be elevated with sepsis.
A patient is presenting as a hypertensive emergency with evidence of end-organ damage. Which four of the following should be carried out as part of his management?
- Reduce blood pressure to 110mmHg over a 24-hour period
- Admit to a monitored bed
- Commence IV sodium nitroprusside
- Administer SL nifedipine
- Request a CT scan of his head
- Reduce blood pressure to 110mmHg over a 24-hour period
- Admit to a monitored bed
- Commence IV sodium nitroprusside
- Request a CT scan of his head
Sub-lingual nifedipine is fast acting and may precipitate a sudden drop in blood pressure leading to a stroke. The aim is for a gradual decrease in blood pressure to prevent cerebral hypoperfusion.
Most patients do not need to be admitted and can be treated with oral medication, except in certain circumstances such as encephalopathy. This patient requires admission and monitoring and treatment with IV sodium nitroprusside may be commenced. A CT scan of the head to exclude an intracerebral bleed is necessary in this patient and echocardiography for assessment of left ventricular function may need to be considered. Other investigations to look for an underlying will also need to be performed.
Can you identify the three prescribing errors in the drug chart medications?
- The dose of bendroflumethiazide should be 50mg
- The dose of digoxin should be 125 micrograms
- Digoxin is usually given three times a day
- Bendroflumethiazide is usually given once a day
- The dose of nifedipine should be 10mg
- Erythromycin is usually given twice a day
- Bendroflumethiazide is usually prescribed in the evening
- The usual dose of erythromycin is 5mg
- The dose of digoxin should be 125 micrograms
- Bendroflumethiazide is usually given once a day
- The dose of nifedipine should be 10mg
Be careful with digoxin doses – common doses are 62.5 or 125 micrograms.
Digoxin is usually given once a day in the morning.
Bendroflumethiazide is given in the morning – it is a diuretic and should not be given at night, or patients will need the toilet and will not sleep. Common doses are 2.5/5mg.
Nifedipine SR typical dose is 10mg.
Erythromycin used at 250/500mg four times a day.
Aspirin 75mg is the correct dose for TIA’s.
A 28-year-old male army recruit collapsed and died suddenly while on a 5-mile run during basic training. His initial medical examination had not noted any medical abnormality and, in particular, his blood pressure had been normal and auscultation of the heart had not detected any cardiac murmurs. He had no previous medical history.
What is the most likely diagnosis?
Hypertrophic cardiomyopathy
The marked hypertrophy of the left ventricle in the absence of an identifiable cause (e.g. hypertension, or valvular disease) along with the disorganised arrangement of the hypertrophied cardiac muscle fibres is typical of hypertrophic cardiomyopathy (HCM) which is also called hypertrophic obstructive cardiomyopathy (HOCM). The LV hypertrophy can be asymmetric (e.g. more thickening in the septum than the free wall) but it is more usually symmetric (concentric) evenly affecting the full circumference of the left ventricle. The history of sudden death in a young person during exercise, whilst not specific for this condition, is fairly typical.
A 28-year-old male army recruit collapsed and died suddenly while on a 5-mile run during basic training. His initial medical examination had not noted any medical abnormality and, in particular, his blood pressure had been normal and auscultation of the heart had not detected any cardiac murmurs. He had no previous medical history.
What is the most likely mechanism of death?
Arrhythmia
The suddenness of death indicates that it was due to a cardiac arrhythmia and this is the usual mode of death in hypertrophic cardiomyopathy. Arrhythmias occur in this condition because the severe thickening of the left ventricle increases the metabolic demand of the muscle whilst moving the subendocardial region further away from the coronary arterial blood supply on the epicardial surface of the heart. There is often also obstruction to aortic outflow by the thickened ventricular septum. The subendocardial region being at the “end of the line” of the blood supply becomes prone to ischaemia.
