A 41-year-old G3P0+2 woman presents to her general practitioner for a routine antenatal check at 14 weeks gestation. She has a past medical history of treatment-resistant schizophrenia, epilepsy, hypertension, antiphospholipid syndrome, and dyslipidemia.
Her regular medications include lamotrigine, labetalol, atorvastatin, low molecular weight heparin, and clozapine. She has recently begun a course of nitrofurantoin for a urinary tract infection.
What medication is contraindicated in this woman?
Atorvastatin
Clozapine
Lamotrigine
Low-molecular-weight-heparin
Nitrofurantoin
Atorvastatin: Pregnancy is a contraindication to statin therapy
A 38-year-old homeless man is brought to the emergency department after being found unresponsive in a local park. On admission, his temperature is 30.2 ºC and an ECG shows a broad complex polymorphic tachycardia. The patient is diagnosed with torsades de pointes.
What is the most appropriate treatment?
Adenosine
Amiodarone
Atropine
Calcium gluconate
Magnesium sulphate
Magnesium sulphate
What is torsades de pointes?
Torsades de pointes (‘twisting of the points’) is a form of polymorphic ventricular tachycardia associated with a long QT interval
A 72-year-old man presents to the emergency department with feeling generally unwell and lethargic for the past 2 weeks. His only other symptom is a yellow-green tinge to his vision.
He has a past medical history significant for atrial fibrillation, depression and a myocardial infarction 3 years ago. He takes numerous tablets that come in a blister pack and he doesn’t know the names of them.
A blood test taken shows the following:
Digoxin concentration 3 mcg/l (<1 mcg/l)
What drug may have precipitated this clinical picture and why?
Bendroflumethiazide
Citalopram
Isosorbide mononitrate
Ramipril
Simvastatin
Bendroflumethiazide is a drug that can precipitate digoxin toxicity. It causes hypokalaemia, and since potassium is a competitive inhibitor of digoxin, less potassium means digoxin can have more of an effect on Na+/K+ ATPase.
Indication for digoxin
Mainly used for rate control in the management of atrial fibrillation. As it has positive inotropic properties it is sometimes used for improving symptoms (but not mortality) in patients with heart failure.
What is digoxin?
cardiac glycoside
Mechanism of action of digoxin
- Decreases conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter
- Increases the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump. Also stimulates vagus nerve
Digoxin monitoring and when should levels be taken
- Narrow therapeutic index
- Digoxin level is not monitored routinely, except in suspected toxicity
- if toxicity is suspected, digoxin concentrations should be measured within 8 to 12 hours of the last dose
At what concentration does digoxin toxicity occur?
- Plasma concentration alone does not determine whether a patient has developed digoxin toxicity.
- Toxicity may occur even when the concentration is within the therapeutic range
- The BNF advises that the likelihood of toxicity increases progressively from 1.5 to 3 mcg/l.
Features of digoxin toxicity
- generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
- arrhythmias (e.g. AV block, bradycardia)
- gynaecomastia
Precipitating factors for digoxin toxicity
- classically: hypokalaemia
digoxin normally binds to the ATPase pump on the same site as potassium. Hypokalaemia → digoxin more easily bind to the ATPase pump → increased inhibitory effects - increasing age
- renal failure
- myocardial ischaemia
- hypomagnesaemia hypercalcaemia, hypernatraemia,
- acidosis
- hypoalbuminaemia
- hypothermia
- hypothyroidism
- drugs
Drugs that may precipitate digoxin toxicity
- amiodarone, quinidine, verapamil, diltiazem, spironolactone (competes for secretion in distal convoluted tubule therefore reduce excretion), ciclosporin
- Also drugs which cause hypokalaemia e.g. thiazides and loop diuretics
Management of digoxin toxicity
- Digibind (Digoxin antibodies)
- correct arrhythmias
- monitor potassium
A 22-year-old male presents for a pre-participation sports medical. He is an amateur triathlete and reports no symptoms. Examination is unremarkable. His ECG shows sinus bradycardia with a PR interval of 220 ms, but is otherwise normal. He has no family history of sudden cardiac death or syncope.
What is the most appropriate next step in his management?
- Reassure and allow to continue sports
- Refer for electrophysiology study
- Advise 24-hour Holter monitoring
- Start beta-blocker therapy
- Arrange echocardiogram
- Reassure and allow to continue sports is correct because first-degree heart block (prolonged PR interval) is a recognised benign finding in well-trained athletes, especially when asymptomatic, with no concerning features on history or examination. According to UK guidelines, this does not require intervention or further investigation if there are no symptoms or family history of cardiac disease. Athletes commonly exhibit such ECG changes due to increased vagal tone; it resolves with detraining and poses no risk.
- Refer for electrophysiology study would be indicated if there were concerning symptoms (e.g., syncope), high-grade AV block, or suspicion of underlying conduction system disease. In this scenario, the patient is asymptomatic with only first-degree heart block on ECG—making this option unnecessary and invasive.
- Advise 24-hour Holter monitoring might be considered if there were intermittent symptoms suggestive of arrhythmia (such as palpitations, syncope, dizziness) or more advanced conduction abnormalities seen on resting ECG. Here, the absence of symptoms and isolated first-degree AV block make ambulatory monitoring unwarranted
- Start beta-blocker therapy would not be appropriate as beta-blockers can worsen bradycardia and AV conduction delays. There is also no indication for pharmacological intervention in an asymptomatic athlete with benign ECG findings.
- Arange echocardiogram could be justified if there was suspicion of structural heart disease (murmur on exam, abnormal cardiac silhouette on CXR) or additional abnormal ECG findings pointing towards cardiomyopathy. This athlete’s examination and history are entirely normal; thus echo adds little value.
ECG changes that are considered normal variants in an athlete
- sinus bradycardia
- junctional rhythm
- first degree heart block
- Mobitz type 1 (Wenckebach phenomenon)
A 60-year-old man is admitted with severe central chest pain to the resus department. The admission ECG shows ST elevation in leads V1-V4 with reciprocal changes in the inferior leads. Which one of the following is most likely to account for these findings?
75% occlusion of the left anterior descending artery
75% occlusion of the left circumflex artery
75% occlusion of the right coronary artery
100% occlusion of the left circumflex artery
100% occlusion of the left anterior descending artery
Widepread ST elevation in this territory implies a complete occlusion of the left anterior descending artery.
Causes of ST elevation on ECG
- myocardial infarction
- pericarditis/myocarditis
- normal variant - ‘high take-off’
- left ventricular aneurysm
- Prinzmetal’s angina (coronary artery spasm)
- Takotsubo cardiomyopathy
- Severe hyperkalemia
- rare: subarachnoid haemorrhage
A 62-year-old woman is brought in by ambulance to the emergency department. She reports worsening shortness of breath and palpitations. ECG shows atrial fibrillation with a fast ventricular response, with a heart rate of 157 bpm. On examination, she has bilateral crepitations on auscultation of the lungs and bilateral ankle oedema. Chest x-ray shows pulmonary oedema. Blood results are shown below.
Troponin 21 ng/L (<14)
What is the next most appropriate management step?
Adenosine
Amiodarone
Intravenous metoprolol
Synchronised DC cardioversion
Unsynchronised DC cardioversion
Synchronised DC cardioversion
An 83-year-old female presents to the cardiology clinic with persistent shortness of breath which is limiting her activities of daily living. She has a history of dilated cardiomyopathy, for which she currently takes candesartan, bisoprolol and furosemide. An echocardiogram shows a left ventricular ejection fraction of 40%.
Which of the following would be the most appropriate additional long-term therapy for improving this patients prognosis?
Bendroflumethiazide
Diltiazem
Dobutamine
Ramipril
Spironolactone
Offer a mineralcorticoid receptor antagonist, in addition to an ACE inhibitor (or ARB) and beta-blocker, to people who have heart failure with reduced ejection fraction if they continue to have symptoms of heart failure
Chronic heart failure drug management
- Depends if preserved vs reduced ejection fraction
- For reduced ejection fraction, The first-line treatment for all patients is both an ACE-inhibitor and a beta-blocker:
- generally, one drug should be started at a time. NICE advise that clinical judgement is used when determining which one to start first
- The standard second-line treatment if symptoms continue is an aldosterone antagonist (e.g. spironolactone and eplerenone). There is an increasing role for SGLT-2 inhibitors in the management of heart failure with a reduced ejection fraction
- Third-line treatment should be initiated by a specialist.
- Other treatments include offering annual influenza vaccine and one-off pneumococcal vaccine.
Do ACE inhibitors and beta blockers have a mortality effect on heart failure
- They improve mortality in heart failure with reduced ejection fraction
- ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with preserved ejection fraction
Which beta blockers are licensed in the UK to treat heart failure?
bisoprolol, carvedilol, and nebivolol
Evidence for use of SGLT 2 inhibitors in heart failure
- the evidence base shows SGLT-2 inhibitors reduced hospitalisation secondary to heart failure and cardiovascular death
- international guidelines widely recommend their usage. In terms of NICE, a technology appraisal from 2021 support the use of dapagliflozin as an add-on to optimised standard care
What should be monitored in second line therapy for chronic heart failure?
it should be remembered that both ACE inhibitors (which the patient is likely to already be on) and aldosterone antagonists both cause hyperkalaemia - therefore potassium should be monitored
