Clinical Integration: Medicine

By Manda Raz

Clinical Cases Explained! - ideal for Problem-Based Learning courses

Clinical Integration: Medicine features 100 clinical cases, with detailed explanations and notes, to help medical students and junior doctors link basic medical science with clinical context and build an appreciation of how pathophysiology manifests as recognisable clues.

The book shows readers the logical connections between patient history, examination findings, investigation results, management rationale and their underlying mechanisms. Readers learn to understand the “why and how” behind the diagnosis, investigation and management of common clinical problems.

The book uses a system-based approach to cover 100 clinical cases, from aortic dissection to urinary tract infections, via dementia and pneumothorax. Every case uses a consistent format to:

• highlight the key elements of the history, examination, investigation and treatment phases of medical practice
• provide rapid access to important facts
• explore the links between pathophysiology and clinical clues that underpin common medical conditions

• Language: English
• Publisher: Scion Publishing
• Release date: Aug 21, 2021
• ISBN: 9781911510758

Book preview

1

CARDIOLOGY

CASE 1: Aortic dissection

History

•A 47-year-old ¹ male presents with sudden onset severe tearing central chest ² pain radiating to his back ³ . He reports it started thirty minutes after he had a tablet of cocaine .

•He reports a history of poorly treated hypertension ⁴ for which he has never taken medications.

•The patient states his father was a tall man like himself ⁵ with some issues with his heart valves ⁵ , but was unable to provide further detail.

•However, he has never been tested ⁶ since he is estranged from his family and doesn’t like visiting doctors ⁶ .

•He has never had similar chest pain ⁷ to this previously.

•He is a current smoker ⁸ with a 40 pack year history but reports nil illicit drug use ⁸ .

•He has no history of previous cardiac surgery or chest trauma ⁹ .

•He is previously opioid naive and has already received 10mg morphine and 50mcg of fentanyl ¹⁰ by the ambulance officers.

•The patient reports feeling light-headed ¹¹ in the last few minutes and appears to be becoming increasingly unwell ¹¹ .

1 Typically advanced age is a risk factor for Stanford classification type B aortic dissection with other associated risk factors such as hypertension. A young or middle-aged patient presenting with features of aortic dissection is epidemiologically more likely to be presenting with type A aortic dissection.

2 Central chest pain with radiation to the back is the most common symptom occurring in over 90% of patients presenting with aortic dissection. Pain described as ‘tearing, sharp or ripping’ in nature is particularly concerning for dissection. Abrupt onset thoracic or abdominal chest pain with a tearing quality forms one of the clinical features in the triad suggestive of aortic dissection. Furthermore, pain predominantly located in the chest, more so than the back or abdomen, is suggestive of ascending aorta involvement.

3 Typically in descending aortic dissections, the pain is located primarily in the posterior chest/upper back. However, as most type A aortic dissections also include a distal extent of dissection, descending aortic manifestations may be present as well. This suggests that the aortic dissection likely extends beyond the aortic arch into the descending aorta.

4 Systemic hypertension is one of the most important predisposing factors of acute aortic dissection. Hypertension is more common in type B aortic dissection but nonetheless is also associated with type A dissection. Untreated hypertension in a patient presenting with sudden onset tearing chest pain is concerning for aortic dissection.

5 Aortic dissection is associated with genetically mediated collagen disorders such as Marfan syndrome and Ehlers–Danlos syndrome. The patient’s family history is concerning for a genetic collagen disorder that is likely Marfan syndrome. Marfan syndrome is typically present in up to 50% of those presenting with aortic dissection below the age of 40. Most patients with Marfan syndrome and aortic dissection have a family history of aortic dissection or aortic root dilation. Marfan syndrome follows an autosomal dominant inheritance pattern.

6 This patient could have had aortic root dilation since birth which has not been monitored or treated with beta blockers to attenuate aortic root dilation. Additionally, with poorly controlled hypertension his risk for type A aortic dissection is high. Risk of cardiovascular death is very high in such individuals and they require close monitoring and optimisation.

7 The chest pain is new; having never experienced such pain before excludes other differentials including gastritis and angina. The quality and intensity of the chest pain associated with aortic dissection is typically unlike any previous chest pain experienced by the patient.

8 Smoking is another risk factor associated with aortic dissection as it can cause weakening of aortic walls. Cocaine use is also associated with aortic dissection as it produces an abrupt severe increase in blood pressure (BP) due to catecholamine release.

9 Previous cardiac surgery or catheterisation for coronary or valvular disease can be complicated by aortic dissection. While trauma rarely leads to classic aortic dissection, it can result in a localised tear in the aortic isthmus. Motor vehicle related chest trauma can, however, result in aortic rupture or transection.

10 The patient has received significant amounts of opioid analgesia and still remains in pain. In a patient that is previously opioid naive, high amounts of analgesia is concerning for the severity of the underlying aetiology causing the pain. Such a patient should warrant thorough investigation even if the aetiology isn’t apparent initially.

11 Light-headedness in this presentation is suggestive of the patient becoming increasingly haemodynamically unstable. It warrants urgent stabilisation of the patient and identification of the aetiology, in order that appropriate therapy can be provided to prevent multi-organ failure and death.

Examination

•On examination the patient appears pale ¹ and presyncopal ¹ .

•He is a tall man ² with a bulging chest ² .

•He is still speaking in full sentences ³ but can be seen holding his central chest and epigastric region.

•Resting rate (RR) is 22 ⁴ , he is saturating at 94% on air and is afebrile ⁵ .

•There is also a 30mmHg difference in systolic blood pressure between both arms ⁶ , with the right arm blood pressure measurement reading of 60/45 and left arm 90/55.

•Pulse is 125bpm and regular ⁷ .

•When assessing radial pulses, he is noted to have a weak right radial pulse ⁸ compared to his left.

•Jugular venous pressure (JVP) is elevated to 4–5cm ⁹ with the patient positioned at 45 degrees.

•Upon auscultation of the heart, an early diastolic murmur ¹⁰ is appreciated at left upper sternal border.

•Auscultation of the lungs was unremarkable ¹¹ .

•Nil neurological deficits ¹² such as hemiplegia, dysphasia, dysarthria or sensory loss are observed.

1 The patient appearing pale and presyncopal on general examination is concerning for insufficient cardiac output and a reduced mean arterial pressure. These features are once again suggestive of haemodynamic instability in this patient.

2 A bulging chest appearance is concerning for pectus carinatum, which is often a phenotypic characteristic of Marfan syndrome. Furthermore, individuals with Marfan syndrome are usually tall. These features are consistent with the patient having an underlying genetic predisposition. Other physical features include pectus excavatum, increased arm span to height ratio, scoliosis, elbow extension greater than 170 degrees/joint hypermobility, high arched palate, flattened cornea/displacement of the ocular lens and pes planus.

3 Given that the patient is still speaking in full sentences, at this point the patient is still maintaining his airway. Throughout this initial assessment period, the airway, breathing and circulation need to be monitored very closely and managed as appropriate if any issues are identified. The patient appears to be in peri-arrest and is deteriorating in the setting of the likely type A aortic dissection.

4 The patient is only mildly tachypnoeic which is likely in keeping with the shock presentation. However, underlying causes of respiratory distress should be excluded, such as haemothorax resulting from the aortic dissection.

5 Absence of hypoxia and the patient being afebrile reduces the likelihood of an infective process and septic shock precipitating the presentation. Moreover, the absence of hypoxia also makes primary respiratory complications or a primary respiratory aetiology less likely.

6 A difference in blood pressure between arms is a very concerning feature suggesting type A aortic dissection with involvement of the aortic arch. With a reduced blood pressure in the right arm, the concern is that the dissection of aorta is causing impaired blood flow into the brachiocephalic artery. The brachiocephalic artery provides circulation to the right upper limb through the right subclavian artery.

7 Tachycardia is an indicator of the patient’s state of likely hypovolaemic shock; currently the patient is trying to compensate for hypotension by increasing the heart rate. Regularity of the pulse is indicative that the patient isn’t in atrial fibrillation.

8 A weak right radial pulse is another sign for extension of the aortic dissection to at least the arch of the aorta. This is a marker of severity in type A aortic dissection and is associated with increased mortality. Variation of pulse and/or variation of blood pressure between limbs is another high risk feature that is part of the clinical triad suggesting acute aortic dissection.

9 An elevated JVP is often a marker of either hypervolaemia or right heart dysfunction. In this scenario, it is unlikely that the patient is clinically overloaded, given the blood pressure and overall clinical scenario. However, an elevated JVP can also suggest the presence of a large pericardial effusion, preventing right heart filling, that causes distension of neck veins. Pericardial effusion leading to cardiac tamponade is a common consequence of this presentation.

10 An early diastolic murmur at the left sternal border is consistent with aortic regurgitation. This may be pre-existing in a patient with likely an underlying genetic predisposition to aortic root dilation. However, acute dissection into the aortic valvular annulus leading to severe aortic regurgitation is a known complication.

11 Lungs being clear on auscultation is further reassuring that the aortic dissection hasn’t ruptured or leaked into the pleural space. Typically you will hear left basal dullness of auscultation if an effusion has accumulated due to acute aortic dissection.

12 Neurological deficits can result from aortic dissection due to carotid artery dissection or compression, which can produce a hemiplegia along with other neurological features. Additionally, spinal occlusion due to dissection may produce paraplegia with sensory loss.

Investigations

•A 12-lead ECG reveals non-specific anterior-lateral T wave inversion and ST depression ¹ .

•Chest X-ray demonstrates normal lung fields ² but an abnormally large cardiac silhouette ³ as well as mediastinal widening ⁴ .

•An urgent bedside transthoracic echocardiogram (TTE) ⁵ is completed which reveals a large pericardial effusion ⁶ with moderate ventricular compression and interdependence ⁶ .

•A dilated aortic root with dissection flap prolapse and evidence of severe aortic regurgitation is visualised ⁷ .

•Furthermore, on imaging of the aorta a linear echodensity ⁸ is visualised with false lumen flow ⁸ to at least the mid-distal ascending aorta on TTE ⁹ .

•Urgent bloods are completed including X-match and group and hold of 10 units of packed red blood cells (PRBC) ¹⁰ .

•The patient’s haemoglobin was 115g/L ¹¹ with a normal renal function ( estimated glomerular filtration rate (eGFR) >90ml/min/1.73m ² ) ¹¹ and normal coagulation profile.

1 Non-specific ischaemic electrocardiogram (ECG) changes are suggestive of insufficient blood flow through the coronary arteries. A potential differential remains an acute myocardial infarction and this should be excluded appropriate with investigations. However, aortic dissection can also produce non-specific ECG changes if it leads to coronary ischaemia through involvement of the coronary arteries.

2 A normal lung field is reassuring, as this implies that the patient is not having a large tension pneumothorax, which could also cause the patient to develop life-threatening shock. Additionally, the absence of pleural effusions is reassuring that the dissection hasn’t ruptured or leaked into the pleural cavity.

3 A large cardiac silhouette is a non-specific sign which could represent underlying cardiomegaly due to dilated cardiomyopathy. However, in this presentation it further raises questions regarding the possibility of an underlying pericardial effusion.

4 Mediastinal widening is in keeping with the diagnosis of acute aortic dissection. Mediastinal widening and/or aortic widening is the third feature in the clinical triad for acute aortic dissection, especially type A.

5 In a haemodynamically unstable patient, the ideal modality of investigation is transoesophageal echocardiography as it is a portable procedure that can yield the diagnosis within minutes and is easily performed in the emergency cubicle. However, it is a procedure that can only be performed by senior members of the cardiology team. In contrast, a transthoracic echocardiogram is even more readily available and most emergency physicians and cardiology trainees can perform this imaging modality. It is particularly good at identifying ascending aortic dissection and coexistent aortic valve disruption, and providing assessment of pericardial effusions.

6 The large pericardial effusion is likely contributing to the patient’s shock and hypotension. The presence of ventricular compression and interdependence is suggestive of tamponade physiology resulting from this effusion. This patient requires urgent intervention given these findings.

7 The presence of a dissection flap prolapse leading to aortic regurgitation is suggestive of acute aortic regurgitation resulting from aortic dissection. Given that the patient likely has Marfan syndrome, it is unlikely that he will have an intrinsically normal valve. In such scenarios, aortic valve replacement is warranted. In people with intrinsically normal valves who have aortic regurgitation due to a correctable aortic valve complication, repair is feasible.

8 A linear echodensity in the ascending aorta likely represents the dissection flap. False lumen blood flow is further suggestive of the presence of type A acute aortic dissection on the TTE.

9 A major limitation in TTE imaging of the aorta is the inability to adequately visualise past the mid-distal ascending aorta. The transverse and descending aorta are typically not visualised through this imaging modality. While TTE certainly provides the diagnosis, the extent of the dissection is not known exactly in this patient.

10 Given the imaging findings and haemodynamic instability, this patient requires urgent surgical intervention. He will most definitely require significant blood products, given the significant blood loss that has already occurred and will occur intra-operatively. Preoperative bloods are warranted as well and should be sent off now.

11 The patient is mildly anaemic, likely secondary to extensive intrathoracic bleeding. Because the baseline haemoglobin is not available it is hard to quantify how much blood has been lost based on this result. Normal renal function and clotting factors are reassuring and positive prognostic factors suggesting the absence of involvement of other systems at this stage.

Management

Immediate

The patient must be transferred to a resuscitation cubicle ¹ in the emergency department as this is a medical emergency. With any medical emergency it is essential to ensure the airway, breathing and circulation (ABC) ² is optimised first. Two large-bore intravenous cannulas (IVCs) ³ should be inserted immediately. An arterial line ⁴ can also be considered. Given hypotension secondary to hypovolaemia from intrathoracic bleeding, intravenous fluid ⁵ should be given to the patient as a bolus. Providing blood pressure support through vasoactive agents such as metaraminol, adrenaline or noradrenaline ⁶ should be avoided. PRBC should be available urgently due to ongoing blood loss. Once the patient is optimised with regard to the ABCs, definitive treatment can be provided.

Surgical management

This patient is not a candidate for sole medical management ⁷ of his aortic dissection. Acute type A aortic dissection is a surgical emergency ⁸. The absence of significant comorbidities and neurological symptoms ⁹ suggestive of stroke are positive prognostic factors. The patient appears to be a suitable surgical candidate hence urgent cardiothoracic referral and transfer to the operating theatre should be arranged.

An open repair of the dissection ¹⁰ with aortic valve replacement and drainage of the large pericardial effusion is required and would provide definitive management.

Long-term

There are three main long-term management strategies in patients who survive the initial dissection and in this case operative repair:

Anti-impulse therapy

Aggressive antihypertensive therapy is required longterm to reduce systemic blood pressure and the rate of rise in systolic blood pressure ¹¹. Patient education regarding this is imperative ¹².

Identification of associated genetic conditions

Formal screening for underlying genetic conditions ¹³ should be completed in this patient. Screening first-degree family members ¹⁴ with TTE can also be considered.

Surveillance imaging

Baseline computed tomographic (CT) angiography ¹⁵ or thoracic magnetic resonance (MR) should be performed prior to discharge. Follow-up imaging with either modality at 3, 6 and 12 months, and annually thereafter is suggested, even if the patient remains asymptomatic ¹⁶.

1 Transfer to a resuscitation cubicle is required as the patient is very unwell and can deteriorate very rapidly. Hence, full resuscitation facilities should be available. If they are not available, urgent transfer is required.

2 Ensure the patient is maintaining their airway; if there are concerns, endotracheal intubation or airway adjuncts should be implemented. Since the patient is still speaking, this is not required at this point. Continue to monitor saturations and respiratory rate as a measure of breathing. Finally, circulation support is likely needed in this individual, given the hypovolaemic state.

3 Given the poor circulatory state, two large IVCs are required in order to support the circulation. These can be used to provide fluids, blood and medications in order to stabilise the patient haemodynamically.

4 An arterial line will be useful for continual blood pressure monitoring and frequent blood sampling in this patient.

5 Intravenous fluid therapy will replace some of the lost intravascular volume and support the blood pressure and circulation.

6 These are vasoactive agents and inotropes that can be used in the acute setting to support blood pressure in most instances. However, they should be avoided in acute aortic dissection to prevent hypertension. Metaraminol causes peripheral vasoconstriction through its α1-adrenergic agonist action, consequently increasing systolic blood pressure. Noradrenaline also stimulates α1 and α2 adrenergic receptors to increase peripheral vascular resistance and hence blood pressure. Adrenaline primarily has β1 agonistic actions that increase heart rate and contractility. Adrenaline also has adrenergic actions to a lesser extent, while noradrenaline has β-agonist actions to a lesser extent.

7 Indicators for medical management of aortic dissection are uncomplicated type B dissection, stable isolated arch dissection or chronic stable type B dissection. This patient does not meet any of these criteria. When medically managing a patient, the aim is reduce the systemic blood pressure and myocardial contractility in order to prevent further spread of intramural haematoma and rupture.

8 Time is very important in type A aortic dissections, with the rate of mortality increasing with every hour without surgical intervention. Surgery is the only definitive management, especially in a patient with apparent complications from the acute aortic dissection such as aortic regurgitation and the development of a large pericardial effusion with tamponade physiology. There is also likely involvement of the coronary arteries given the non-specific anterior–lateral ECG changes.

9 The absence of other medical comorbidities, such as advanced age, malignancy and dementia, that may limit survival of the patient to less than one year makes the patient an appropriate surgical candidate. Haemorrhagic stroke is also a relative contraindication to surgical intervention due to intraoperative heparinisation for induction onto coronary artery bypass. The absence of any neurology is reassuring in this patient.

10 An open repair will involve evacuation of the pericardial effusion, excision of the intimal tear, reconstitution of the aorta with a synthetic graft followed by replacement of the aortic valve with either bio-prosthetic or metallic valve. A metallic valve in this patient, although it provides superior longevity, would consign the patient to lifelong warfarin therapy, which may not be suitable due to previous compliance issues.

11 Aggressive blood pressure control will reduce aortic wall stress and prevent further dissections in the long term. Beta blockers are typically first-line agents but other antihypertensive agents will usually be required to achieve sufficient blood pressure control. The target blood pressure should be less than 120/80.

12 Patient education is very important in all patients especially if there is a history of poor medical attendance and adherence. Close follow-up with multiple members of the medical profession and family education can assist in improving long-term management.

13 It is highly likely this patient has Marfan syndrome that has predisposed this presentation. Screening for this needs to occur so relevant investigations and treatments can be provided regarding any associated genetic conditions. As a general rule, patients with Marfan syndrome should only participate in low to moderate intensity exercise. They should avoid exercising to exhaustion and especially activities which involve the Valsalva manoeuvre.

14 Given the likely genetic predisposition, TTE of firstdegree relatives to assess for aortic aneurysm, dilated aortic root or bicuspid aortic valve is reasonable.

15 CT angiography of the aorta is more readily available but it does expose the patient to considerable ionising radiation which should be avoided if possible. CT angiography also requires iodine-based contrast which can cause nephrotoxicity. Ideally, MR angiography should be used in young patients but understandably this is not always feasible.

16 Serial imaging aims to detect the following abnormalities: recurrence of the dissection, aneurysm formation or leakage at the surgical anastomosis. In the early stages, the patient will often be asymptomatic despite the presence of these abnormalities on imaging.

CASE 2: Aortic stenosis

History

•A 67-year-old ¹ female presents to her general practitioner (GP) with 5 months of dyspnoea ² .

•She originally ascribed this to just getting older, but now she becomes dyspnoeic when mobilising around the shops ³ and is unable to walk the dogs without stopping frequently. This was never an issue before ⁴ .

•When inquiring about syncope, she reports not having any syncopal events but on one hot day, she felt like she was going to faint ⁵ when she was cleaning the house and had to sit down.

•She also recalls feeling dyspnoeic with only mild exertion when she had a viral chest infection ⁶ a few months ago but did not seek medical attention as the dyspnoea resolved with the resolution of the infection.

•She reports no associated chest pain or palpitations ⁷ .

•She reports no orthopnoea, paroxysmal nocturnal dyspnoea or peripheral oedema ⁸ .

•She is an ex-smoker of 30 pack years ⁹ , but quit 10 years ago.

•Otherwise her past medical history ¹⁰ and family history are unremarkable.

1 The two most common valvular pathologies (myxomatous mitral regurgitation and calcific aortic stenosis) are degenerative in their pathophysiology and thus their incidence increases with age. 10% of people older than 85 years will have aortic stenosis.

2 This patient has presented with chronic, progressive dyspnoea. The differentials for this presentation include more than just cardiological diagnoses. One should also think of respiratory system disorders such as chronic obstructive pulmonary disease and interstitial lung disease.

3 When someone presents with dyspnoea, it is useful to identify their current exercise tolerance. Mobilising around the shops would most likely be less than a kilometre’s worth of walking. This information is also useful as it identifies that this dyspnoea is limiting the patient’s usual activities of daily living.

4 Her current exercise tolerance is significantly decreased compared to her premorbid exercise tolerance. It’s important to compare baselines. You wouldn’t know unless you remembered to ask!

5 The classical triad of symptoms in aortic stenosis is syncope, angina and dyspnoea, remembered by the mnemonic SAD . These three symptoms should always be attained and quantified on history as their presence carries prognostic significance. Patients presenting with angina have a 5-year mean survival. Patients presenting with syncope have a 3-year mean survival and patients with dyspnoea from congestive heart failure have a 2-year mean survival. This patient has not had syncope, but has had an episode of presyncope. Aortic stenosis results in a fixed cardiac output state and in periods of stress or hypovolaemia, patients may experience presyncope or syncope. In this case it was dehydration on a hot day that resulted in the presyncopal episode.

6 Here is another clue. Degenerative calcific aortic stenosis is asymptomatic for a long period of time; approximately 10 years. In periods of physiological stress, however, the symptoms may become apparent.

7 Patients with aortic stenosis may present with angina. Around half of the patients would have concomitant coronary artery disease and the other half have angina due to increased oxygen demand in the hypertrophied myocardium and altered coronary flow.

8 The patient does not have any other signs of left heart failure apart from exertional dyspnoea.

9 Smoking is an independent risk factor that increases the progression of aortic stenosis. Calcific aortic stenosis occurs from a combination of degenerative and inflammatory processes. Smoking causes an inflammatory state, promoting calcium deposition which in turn stiffens the leaflets and reduces the valve area.

10 Complete your cardiovascular history by ascertaining all traditional risk factors for ischaemic heart disease such as hypertension, dyslipidaemia, diabetes and family history of ischaemic heart disease. Additionally, it is worthwhile asking for a past history of rheumatic fever. Prior to the advent of antibiotics, rheumatic fever was the most common cause of aortic stenosis. It causes commissural fusion, fibrosis and stiffening of the aortic cusps, resulting in a stenotic valve.

Examination

•The patient appears well with no signs of increased work of breathing ¹ . She is not obese.

•Her heart rate is 70bpm and is regular. Her blood pressure is 150/95mmHg. Her respiratory rate is 16 and her saturations are 97% on air. She is

afebrile.

•Examination of the hands revealed no clubbing or nicotine stains ² .

•There was an anacrotic carotid pulse ³ . The JVP is not elevated.

•The apex beat is displaced to the 6 th intercostal space, just lateral to the mid-clavicular line and is pressure loaded ⁴ .

•Auscultation of the chest reveals a harsh crescendo–decrescendo ejection systolic murmur loudest in the right upper sternal edge ⁵ , with the murmur radiating to the carotids ⁶ .

•This murmur is accentuated with the patient breathing out, leaning forward and squatting ⁷ .

•The murmur did not change in intensity with Valsalva manoeuvre ⁸ .

•Auscultation of the lungs reveal clear air entry ⁹ , with no dullness to percussion.

•She does not have any peripheral stigmata of infective endocarditis ¹⁰ such as Janeway lesions, Osler nodes or splinter haemorrhages.

•There was no peripheral oedema ¹¹ .

1 As always, the initial assessment of patient is the observation. Here she looks well, which largely rules out an acute pathology. No increased work of breathing shows that there is no respiratory compromise at rest.

2 The patient presents with dyspnoea, which should indicate to the doctor to look for peripheral signs of respiratory disease as well as cardiovascular disease. Clubbing would indicate interstitial lung disease, and nicotine stains would indicate chronic obstructive pulmonary disease.

3 Characterising the pulse helps in differentiating between aortic stenosis and regurgitation. This is best done at the carotid or brachial artery. The radial pulse is weak and not the best for characterisation. If the stenosis is severe, there may be a slow upstroke (anacrotic pulse), or the peak of the pulse may be late ( tardus ) or have decreased amplitude ( parvus ). If the pulse has a delayed peak and a small volume it is called pulsus parvus et tardus .

4 The apex beat is displaced inferolaterally from its original position at the 5th intercostal space, mid-axillary line due to left ventricular hypertrophy. The apex beat can be characterised as pressure loaded if it is sustained or forceful. This occurs in concentric hypertrophy. In eccentric hypertrophy you may have a volume loaded apex beat which is diffuse and non-sustained.

5 The classical description of the murmur of aortic stenosis is a crescendo–decrescendo mid-systolic ejection murmur best heard at the right upper sternal border (aortic region) that radiates to the carotids. It is a mid-systolic murmur as the left ventricular pressure only exceeds the systemic pressure and the pressure gradient of the aortic valve during mid-systole. A2 may also be softened or absent due to an immobile aortic valve. As the severity of the aortic stenosis worsens, the murmur also changes. A2 becomes delayed, which may merge with P2, resulting in a single S2. If A2 becomes even more delayed you may have paradoxical splitting, where the aortic valve closes later than the pulmonic valve. Additionally, for patients with a congenital bicuspid valve, there may be an ejection systolic click early after S1; and for patients who have developed a stiff and non-compliant left ventricle, an S4 may be heard.

6 Radiation of the murmur to the carotids excludes pulmonic stenosis, aortic sclerosis and hypertrophic obstructive cardiomyopathy as the cause of the ejection systolic murmur.

7 Dynamic manoeuvres are performed to confirm your suspicion of aortic stenosis compared to other valvular pathologies. First step is to differentiate between left-sided murmurs and right-sided murmurs by listening to the murmur in both expiration and inspiration. Expiration promotes venous return from the pulmonary veins into the left side of the heart, thereby increasing left ventricular end diastolic volume. This corresponds to more stroke volume (as per Frank Starling’s Law), which in turn results in an increased turbulent flow across the mitral and aortic valves. Conversely, inspiration decreases the intrathoracic pressure, which increases venous return to the right side of the heart. This then increases the right ventricular end diastolic volume, the right ventricular stroke volume and the turbulent flow across the tricuspid and pulmonary valves. Once the murmur has been localised to a left-sided lesion best heard in the aortic region, you can accentuate the murmur by having the patient lean forward. This brings the aortic valve closer to the chest wall so that it is heard more easily. Then you can differentiate between aortic stenosis and hypertrophic obstructive cardiomyopathy (HOCM) with further manoeuvres. The murmur of aortic stenosis will increase with manoeuvres that increase preload, such as squatting and passive leg raising. These same manoeuvres decrease the murmur of HOCM, as increased preload improves the left ventricular outflow tract (LVOT) obstruction. Manoeuvres that will increase the murmur of HOCM are the Valsalva manoeuvre and isometric handgrip, as it increases the afterload and worsens the LVOT obstruction.

8 Valsalva is a forced expiration against a closed glottis. This increases the intrathoracic pressure, which dramatically reduces the venous return to the left side of the heart. The decreased left ventricular end diastolic volume results in worsened LVOT obstruction in HOCM and thus the murmur is worse. This is pathognomonic of HOCM.

9 Clear air entry leans against interstitial lung disease, where you would expect to hear fine inspiratory bibasal crepitations, and chronic obstructive airways disease where you have a prolonged expiratory phase and expiratory wheeze.

10 Infective endocarditis is a common differential when patients present with valvular abnormalities. Bear in mind, it is more common to cause aortic regurgitation than stenosis. Peripheral stigmata of infective endocarditis include splinter haemorrhages, Osler nodes (erythematous tender nodules on fingers or toes), Janeway lesions (non-tender erythematous maculopapular lesions in palms of hands or soles of feet) or Roth spots (retinal haemorrhages with clear centres).

11 The lack of peripheral oedema demonstrates that there is no biventricular failure from the aortic stenosis.

Investigations

•Her 12-lead ECG shows sinus rhythm with a heart rate of 74 beats per minute (bpm), marked left axis deviation ¹ and severe left ventricular hypertrophy ² with the sum of the S wave in V1 and R wave in V6 being 40mm.

•There is also a mildly prolonged QRS complex ³ with a duration of 0.1 seconds and T-wave inversion and concave 2mm (0.2mV) ST segment depression in the lateral leads ⁴ .

•Chest X-ray demonstrates a normal cardiac silhouette ⁵ but post-stenotic dilatation of the aorta ⁶ .

•Basic serology is unremarkable ⁷ .

•Transthoracic echocardiogram was performed as an outpatient and showed severe aortic stenosis ⁸ with a mean pressure gradient of 60mmHg and an aortic valve area of 0.7cm ² .

•There was also moderate left ventricular concentric hypertrophy ⁹ .

•The left ventricular ejection fraction (LVEF) was 45%. She also underwent cardiac angiography ¹⁰ to rule out concomitant coronary artery disease.

1 The mean electrical axis of the heart has shifted to the left, indicating left-sided predominance of myocardium; this may indicate a degree of left ventricular hypertrophy.

2 Left ventricular hypertrophy is the most common ECG finding in aortic stenosis. The heart has adapted to the pathological stress placed upon it from aortic stenosis. The fact that the heart has had time to remodel shows that this process has been occurring for a long time. Concentric left ventricular remodelling occurs from sarcomeres being laid down in parallel, which aids the left ventricle in ejecting against a higher pressure load. This also increases myocardial oxygen demand and makes the heart more susceptible to ischaemia.

3 Aortic stenosis can affect the conductive system of the heart. When extensive, the calcification of the aortic valve can also extend into the conduction system into the atrioventricular node, causing AV nodal block or even intraventricular block. Here, the patient has slightly delayed intraventricular conduction, as described by the mildly prolonged QRS.

4 These ECG findings indicate an LV strain pattern that is common in hypertensive heart disease or aortic stenosis. Classically the lateral leads have T wave inversion and concaved ST segment depression. This is differentiated from an ischaemic change as there is usually horizontal ST segment depression or elevation in NSTEMIs or STEMIs.

5 Despite the concentric hypertrophy, you can have a normal cardiac silhouette on chest X-ray. There may be rounding of the LV border and apex if there is severe concentric hypertrophy.

6 Post-stenotic dilatation of aorta is the most common X-ray finding in aortic stenosis. In a lateral view, you may see aortic valve calcification, but it is not always present.

7 Serology is commonly unremarkable in aortic stenosis.

8 Transthoracic echocardiogram is the investigation of choice in diagnosis of aortic stenosis. It provides information about the leaflet morphology and can also grade the severity of the stenosis. It can also assess for the sequelae of aortic stenosis such as degree of hypertrophy, any concomitant functional mitral regurgitation and increased pulmonary artery pressures. Leaflet morphology helps distinguish the cause of aortic stenosis. If there are two leaflets, then congenital bicuspid aortic stenosis is diagnosed. Bicuspid valves are unequal in size and progressively thicken and calcify, usually necessitating replacement earlier on in life. Patients become symptomatic in middle age. Aortic stenosis is graded with three parameters: jet velocity, pressure gradient and valve area. For reference, the normal aortic valve area is 2–4cm ² .

iMild aortic stenosis has a jet velocity of <3 metres/second, a pressure gradient of <25mmHg and an aortic valve area of >1.5cm ²

ii Moderate aortic stenosis has a jet velocity of 3–4 metres/second, a pressure gradient of 25–40mmHg and an aortic valve area of 1–1.5cm ²

iii Severe aortic stenosis has a jet velocity of >4 metres/second, a pressure gradient of >40mmHg and an aortic valve area of <1cm ² .

9 ECG findings of left ventricular hypertrophy may not all correlate to echocardiographic findings of hypertrophy. In this case there is a slight discrepancy between the ECG and echocardiographic severity of left ventricular hypertrophy.

10 Cardiac angiography serves multiple purposes. It serves to determine the peri-operative risk for an aortic valve replacement and if severe coronary lesions are present, it can determine if any bypass grafting needs to be done at the time of the aortic valve replacement. Furthermore, in the case where the patient presents with angina, it can delineate whether or not the angina is from myocardial oxygen demand or from coronary disease. Finally, it can accurately measure the degree of stenosis in patients who have discrepant clinical and echocardiographic findings.

Management

Acute

It is uncommon for patients with aortic stenosis to have emergency presentations ¹ and they can usually be managed on an outpatient basis. Those with acute symptoms can present with angina pectoris, cardiogenic syncope or acute pulmonary oedema. The specific management of these patients is outlined in Cases 9, 6 and 4, respectively. This patient presented with progressive dyspnoea without signs of decompensation and thus she would be suitable for an urgent referral to a cardiothoracic clinic for consideration of surgical aortic valve repair.

Monitoring

Patients who do not meet criteria for surgery ² require regular surveillance ³ with serial echocardiograms. The aortic valve area on average decreases by around 0.1cm² per year, which increases the pressure gradient to around 7mmHg per year. Therefore even if patients do not require an aortic valve replacement, they will require intervention later.

Medical treatment

Medical treatment in patients with aortic stenosis is limited, as no medications are known to have prognostic benefit or delay disease progression. Medical treatment, when indicated, is for symptom management:

1. For angina, beta blockers ⁴ can be used.

2. For heart failure, loop diuretics ⁵ are used.

3. Digoxin ⁶ could also be used for patients in heart failure.

Intervention

The choice of intervention depends on the age, level of function and the patient’s comorbidities. For children, very young adults with congenital aortic stenosis or those who are unfit for surgical replacement, balloon valvuloplasty can be considered. For others who are elderly (>75 years old) with inoperable aortic stenosis, transcatheter aortic valve replacement can be an option. Otherwise, surgical aortic valve replacement is the surgery of choice.

Surgical aortic valve replacement

Surgical replacement would be the recommended treatment ⁷ for this patient, as she presented with symptomatic aortic stenosis and is fit enough to undergo the surgery. It is the only definitive treatment for severe aortic stenosis. Aortic valve replacement requires median sternotomy and all of its associated morbidities ⁸. Bioprosthetic valves do not last as long as mechanical valves ⁹, but also do not carry with them the systemic thromboembolic risk that mechanical valves do. Patients require follow-up ¹⁰ on discharge to assess for late complications and valve function.

Transcatheter aortic valve replacement (TAVR)

This is a relatively new non-surgical intervention where a bioprosthetic valve is implanted within the native aortic valve. This is done mostly via femoral arterial access ¹¹, but in patients with difficult anatomy, a direct transaortic or transapical approach may be required. It improves effective aortic valve orifice area and haemodynamics; and has better survival rates than medical management. The evidence for this procedure is emerging ¹², but it is a good alternative for patients who are deemed too high risk for surgical aortic valve replacement.

Percutaneous balloon aortic valvuloplasty

This is a non-surgical, palliative treatment ¹³ option for patients with aortic stenosis. It has a percutaneous approach, where a catheter with a balloon is threaded through the aortic valve and inflated, opening the stenotic valve. It does not alter prognosis and there is a high rate of restenosis ¹⁴.

1 Aortic stenosis is usually picked up incidentally via auscultation. When it isn’t, it can present with either of the triad of symptoms. Thankfully, most patients have not acutely decompensated and can be referred to the cardiothoracic surgeon and cardiologist in a timely matter.

2 Indications for surgery include symptomatic patients with severe aortic stenosis. For those who are asymptomatic, surgery is indicated if their LVEF is <50%, they have severe hypertrophy (>15mm wall thickness) or have significant ventricular arrhythmias. Patients should be under the age of 75 and be fit to undergo major cardiovascular surgery.

3 Regular surveillance is most commonly for patients who are asymptomatic with mild to moderate aortic stenosis. These patients are re-evaluated every 6 months as their aortic stenosis will continue to progress and patients may develop symptoms, worsening exercise tolerance or LV systolic dysfunction.

4 Beta blockers slow the heart and decrease the overall oxygen use. They are only used if angina is the predominant symptom.

5 Loop diuretics decrease the preload to prevent exacerbation of heart failure that develops in aortic stenosis. This needs to be balanced with the risk of hypovolaemia, as patients can tip into hypotension and develop syncope.

6 Digoxin can help with dyspnoea in patients with heart failure.

7 Surgical replacement is the only definitive therapy and it is recommended for all patients with severe aortic stenosis who can safely undergo surgery. Timing is important to maximise the benefit and minimise the risk for the patient. Patients who may not be deemed suitable for surgery include the elderly (>75 years), those who are frail (poor functional status) and medically comorbid.

8 Aortic valve replacement requires median sternotomy, cardiopulmonary bypass, aortic cannulation and a post-operative ICU stay. This is safe for many patients, but patients need to be well selected for the procedure and complications should be prevented vigilantly to ensure an uncomplicated postoperative course.

9 Choice of valve depends on the expected lifespan for the patient. Bioprosthetic valves are not as durable but have less systemic thromboembolic risk and do not need lifelong anticoagulation (they do, however, need 3–6 months of anticoagulation postoperatively). Mechanical valves are much more durable, but patients need to remain on warfarin with an international normalised ratio (INR) of 2.5–3.5 due to high risk of systemic thromboembolic events.

10 Patients should be routinely followed up post-surgery to ensure adequate valvular function and to assess for complications such as prosthetic valve thrombosis, conduction disorders and paravalvular leaks.

11 Femoral arterial access is needed so that a catheter can be placed up into the aorta and through the aortic valve to ensure appropriate implantation of the aortic valve. Specific complications associated with femoral arterial access are noted in Case 8 .

12 Current evidence demonstrates that it improves the prognosis for patients who traditionally have no treatment options for their inoperable severe aortic stenosis. In high risk patients, survival rates are similar with transcatheter aortic valve replacements (TAVRs) and surgical aortic valve replacements. There are some important differences in periprocedural risks. TAVR patients were demonstrated to have more major vascular complications and strokes. Patients undergoing surgical aortic valve replacement were demonstrated to have more major bleeding complications and new-onset atrial fibrillation.

13 Balloon valvuloplasty does not change the disease process and therefore does not change the disease progression. It is used only to improve the symptoms of aortic stenosis or as a bridging therapy to transcatheter aortic valve replacement or surgical aortic valve replacement.

14 Restenosis of aortic valve and clinical deterioration usually occur within 6–12 months and long-term outcomes mimic those of untreated aortic stenosis. It is worth noting that quality of life was noted to have improved in patients with balloon valvuloplasty vs. no treatment at short term (30 days and 6 months) but not at 12 months.

CASE 3: Atrial fibrillation

History

•A 61-year-old man ¹ presents to the Emergency Department (ED) because of palpitations.

•The palpitations began 2 hours ago ² while watching television.

•He describes the palpitations as uncomfortable and fast ³ .

•He says he may have had similar episodes in the past ⁴ but they never lasted this long.

•He has no chest pain ⁵ or dyspnoea ⁶ at the time of presentation.

•He has an exercise tolerance in excess of 3km ⁷ .

•He reports no orthopnoea or paroxysmal nocturnal dyspnoea ⁸ .

•He has otherwise been well over the past few days and reports no infective symptoms ⁹ .

•He has a background of alcohol abuse ¹⁰ and can drink up to 14 units of alcohol per night.

•He also has a history of type 2 diabetes mellitus ¹¹ , hypertension ¹² , asthma ¹³ and obesity ¹⁴ .

1 The incidence of atrial fibrillation (AF) increases with age. A patient in their 30s presenting with palpitations is far more likely to have some other type of supraventricular tachycardia. The risk of AF also increases with the presence of other medical comorbidities such as diabetes, heart failure, coronary artery disease, hypertension, chronic kidney disease, etc.

2 This patient has a clear onset of symptoms that is likely to coincide with the commencement of a possible arrhythmia. AF is usually asymptomatic and can present with a wide spectrum of symptoms; these may be cardiac.

3 Palpitations are a common complaint in symptomatic AF. The fact that the patient describes them as fast raises the concern that the patient is also tachycardic, likely with rapid ventricular rate.

4 Intermittent episodes of palpitations in the past are consistent with arrhythmias. In the case of AF, it is likely to be paroxysmal rather than permanent. It may be helpful to get the patient to tap out the palpitations to establish whether the rhythm is irregular, regular, fast or slow. If the patient reports the ability to self-terminate the palpitations, then this would be suggest of supraventricular tachycardia such as atrioventricular nodal tachycardia.

5 Coronary artery disease is not very commonly associated with AF. AF can occur transiently in 6–21% patients presenting an acute myocardial infarction and hence the presence of chest pain must be explored. It is postulated that atrial ischaemia due to the myocardial infarction leads to AF.

6 AF and heart failure commonly occur together. Often an acute exacerbation of heart failure can precipitate AF. Each of them can predispose to each other and must be screened for in the history. Heart failure can lead to atrial stretching that predisposes to AF (which is often quite difficult to treat in the setting of underlying structural changes). AF causes a reduction in cardiac output, which may result in hypotension and acute heart failure.

7 The patient has reasonable exercise tolerance, suggesting that overall cardiac function is not greatly impaired. It is important to get an understanding of current exercise tolerance in all patients presenting with cardiac symptoms. Exercise tolerance is also a significant prognostic factor.

8 These are signs of pulmonary congestion and left-sided cardiac failure, which is common in patients presenting with palpitations.

9 Infection is known to cause acute presentations of heart failure or any arrhythmia such as AF. The risk of AF increases after infection with the influenza virus and pneumonia, hence it is important to screen for infection in patients presenting with palpitations and suspected AF.

10 Alcohol consumption is a significant risk factor for developing AF. AF occurs in around 60% of heavy drinkers with or without an underlying alcoholic cardiomyopathy. Often, episodes of AF occur post periods of increased alcohol intake such as weekends or holidays.

11 Hypoglycaemia in the setting of diabetes can also predispose patients to palpitations. It is important to take a detailed medication history and check blood glucose levels (BGLs). Diabetes is also associated with the development of AF; it is postulated that increased left ventricular mass and arterial stiffness may be mechanisms for the development of AF in diabetic patients.

12 Hypertension is also associated with an increased risk of AF. If hypertension is aggressively treated, patients might be tachycardic and have palpitations (which can mimic atrial fibrillation) to compensate for hypotension.

13 Chronic airways disease can predispose patients to developing pulmonary hypertension which may lead to remodelling of the heart. This remodelling can be linked to the presence of arrhythmias.

14 Obesity is also linked with complications such as obstructive sleep apnoea and right-sided heart failure. Once again the remodelling of the heart can lead to disruption of conduction pathways and arrhythmias. Furthermore, obesity is linked with an increased size of the left atrium, increased left atrial pressure and diastolic dysfunction, which increases the risk of developing AF.

Examination

•On examination the patient appears mildly uncomfortable but is otherwise alert ¹ .

•He smells strongly of alcohol ² .

•There is no evidence of diaphoresis and he appears well perfused ³ .

•His blood pressure is currently 120/75mmHg ⁴ ; his heart rate is 155bpm and is irregularly irregular ⁵ .

•He is not febrile or hypoxic , and has normal respiratory rate ⁶ .

•His jugular venous pressure is not elevated ⁷ but on close inspection A waves are absent ⁸ .

•There is an appreciable apical–radial pulse deficit ⁹ .

•Heart sounds are dual ¹⁰ with no added sounds ¹¹ .

•Breath sounds are normal ¹² with no added sounds.

•There is no hemiplegia, weakness, speech disturbances ¹³ , nystagmus or vertigo ¹⁴ .

1 The patient is likely distressed by the palpitations but appears to be otherwise well. In patients presenting with more acutely life-threatening arrhythmias such as ventricular tachycardia, cardiac output is commonly compromised leading to haemodynamic instability.

2 Alcohol is strongly associated with AF. This suggests a significant history of alcohol abuse and poor self-care. The patient must be assessed for signs and symptoms of alcoholic cardiomyopathy.

3 Diaphoresis may be a sign of acute haemodynamic instability in the setting of underlying myocardial ischaemia or life-threatening arrhythmia. Assessment of haemodynamic stability is paramount regardless of the underlying arrhythmia, as it will guide management.

4 Most of the medications used in AF will also cause hypotension and hence it is very important to monitor this. AF reduces cardiac output due to impaired diastolic filling, leading to a reduction in stroke volume. This leads to some degree of hypotension in the patient. Nonetheless, this patient appears haemodynamically stable and normotensive at this stage.

5 This is highly suggestive of AF with rapid ventricular rate. It is due to rapid and irregular beating of the atria, typically coming from ectopic foci outside of the sinus node. These impulses are conducted irregularly, leading to this rhythm.

6 The patient is not in any respiratory distress. Patients presenting with heart failure or a lower respiratory tract infection may trigger AF in a patient with an underlying predisposition for AF. There does not seem to be any respiratory decompensation in this patient.

7 Elevated JVP is a sign for right heart failure or tricuspid regurgitation; both can be mechanisms that predispose to arrhythmias such as AF. Fluid status is very important in the assessment of a patient presenting with AF with rapid ventricular rate. If the patient is also in acute heart failure then the treatment will need to be tailored accordingly and beta blockers should be avoided.

8 Since atrial contraction is lost in AF, A waves in the JVP are no longer visualised. This is a very difficult sign to appreciate but is nearly always pathognomonic with AF.

9 The apex beat can be difficult to palpate, especially in obese patients. An apical radial pulse deficit is seen in AF where the radial heart rate is less than the apical heart rate. Since the heart rate is irregular, some contraction will occur with insufficient filling of the left ventricle and results in beats with insufficient stroke volume to transmit the pressure wave to the arm.

10 The presence of an S3 heart sound may be a sign of systolic heart failure in the setting of an overly compliant myocardium (because S3 is produced when a large amount of blood strikes a ‘stretchable’ left ventricle), whereas an S4 heart sound can be a sign of diastolic heart failure or active ischaemia. The absence of both is reassuring.

11 Valvular heart disease, particularly mitral regurgitation, can lead to myocardial remodelling, left atrial enlargement and hence AF. It is especially important to exclude a mitral stenosis murmur (mid-diastolic rumble at the apex with presystolic accentuation). AF with moderate to severe mitral stenosis is considered valvular AF and is very high risk for thromboembolic complications, particularly stroke.

12 The patient has no signs of acute pulmonary congestion which might be a sign of acute heart failure. Auscultation of the chest forms a significant part of the patient’s volume assessment. This patient appears to be relatively euvolaemic. There are also no apparent unilateral crepitations or wheeze that may be concerning for infection.

13 Often patients presenting with signs of acute ischaemic stroke may be found to be in AF. Weakness, speech disturbances and hemiplegia are some of the many features of anterior circulation stroke.

14 Nystagmus and vertigo are signs of a posterior circulation stroke. In an embolic stroke secondary to AF, patients can have multi-territory deficits. AF is a major risk factor for future ischaemic strokes and hence clinicians must make sure to exclude stroke in these patients.

Investigations

•A 12-lead ECG reveals an irregularly irregular rhythm with an absence of P waves ¹ .

•It is a narrow complex tachycardia ² with a rate of around 150bpm ³ . Bloods are performed which reveal a potassium of 3.5mmol/L ⁴ but normal full blood examination, renal function ⁵ and thyroid function ⁶ .

•The chest X-ray shows normal cardiac silhouette ⁷ and nil overt signs of fluid overload ⁸ .

•A bedside echocardiogram reveals a left ventricular ejection fraction of 55% with mild hypertrophic changes ⁹ and normal valvular function ¹⁰ .

•There is bilateral mild–moderate atrial enlargement ¹¹ .

•No thrombus is seen in the left atrium ¹² on transthoracic echocardiogram (TTE).

1 This is in keeping with AF on ECG and represents irregular beating of the atria. Sometimes fibrillation waves can also be seen along the baseline of the ECG, which is further suggestive of AF. Be mindful, however, that fibrillatory waves may mimic P waves and lead to misdiagnosis. Other features of AF include an absence of an isoelectric baseline.

2 Typically, the ECG in AF will be narrow complex unless there is an underlying bundle branch block, accessory pathway or rate-related aberrant conduction.

3 This is suggestive of AF with rapid ventricular rate; the irregular atrial beats from ectopic foci are being conducted and leading to frequent ventricular contraction. This is leading to regular contractions without sufficient filling time and reduced cardiac output.

4 Hypokalaemia increases the risk of AF compared to normokalaemia. Any patients with low potassium should be treated with IV or oral treatment to replete serum potassium.

5 Renal function and full blood exam should be done with all patients. Renal failure and infection can be identified on these investigations. Furthermore, these bloods provide a baseline for the patient at admission.

6 Clinical or subclinical hyperthyroidism is present in less than 5% of patients with AF. Thyroid function tests should be obtained in all patients with first episode AF or those with frequent exacerbation, as this might be an exacerbating cause.

7 Cardiomegaly is a sign of heart failure or cardiomyopathy which may be seen in AF. Flattening of the left atrial border can also be seen on chest X-ray in patients with severe left atrial dilatation.

8 The absence of pulmonary congestion and pleural effusions on chest X-ray further confirms the euvolaemic status of this patient. If this patient were overloaded and given beta blockers acutely, it could send them into acute cardiogenic shock.

9 This patient has normal left ventricular ejection fraction, hence systolic function is maintained. In patients with reduced ejection fraction, cardioselective beta blockers would be indicated. Systolic dysfunction on echocardiogram independently predicts an increased risk of stroke in patients with AF. The presence of underlying conditions such as left ventricular hypertrophy and focal wall motion abnormalities may also be found through this. An echocardiogram can also be used when the patient is in sinus rhythm to evaluate the relative atrial contribution to left ventricular filling.

10 This is significant as occult mitral stenosis may present with AF. The absence of mitral valve pathology influences the risk of thrombus formation. Long-term sinus rhythm is often very difficult in patients with mitral stenosis unless they have procedural repair.

11 Normal left atrial dimension is less than 4cm and enlargement is common in AF. Hypertension and mitral valve disease are common causes for left atrial dilatation. Left atrial enlargement is prognostically important and decreases the probability of long-term maintenance of sinus rhythm.

12 While TTE can be used to identify left atrial thrombus, it has poor sensitivity. It is unable to sufficiently visualise the left atrial appendage, a common side for thrombi. Ideally, a transoesophageal echocardiogram should be used if thrombus needs to be excluded with greater accuracy.

Management

Acute

In patients with new onset AF with a rapid ventricular rate, an assessment needs to be made regarding the need for urgent cardioversion ¹. If the patient does not require cardioversion, rate control is recommended ² to improve symptoms and reduce the risk of tachycardia-mediated cardiomyopathy ³. Patients with heart failure with reduced ejection fraction can be difficult to rate control ⁴.

Given that this patient has had symptoms for <48 hours, they should be considered for cardioversion ⁵ to revert back to sinus rhythm. These patients do not require maintenance antiarrhythmics ⁶. In patients in AF for > 48 hours ⁷, cardioversion cannot be done acutely without a transoesophageal echocardiogram to exclude atrial thrombi.

Anticoagulation

All patients with non-valvular atrial fibrillation ⁸ should be assessed for stroke risk using the CHA2DS2-VASc risk tool ⁹. Bleeding risk ¹⁰ should also be assessed in these patients. Patients with valvular AF ¹¹ should be anticoagulated with warfarin regardless of their other comorbidities.

Long-term

Long-term management revolves around managing the underlying aetiology ¹². Furthermore, adequate long-term rate and rhythm control ¹³ needs to evaluated. If AF is recurrent, catheter ablation can be explored ¹⁴ to ensure better long-term maintenance of sinus rhythm. In patients with heart failure with reduced ejection fraction, AF ablation is associated with a significant benefit ¹⁵.

1 Urgent cardioversion is indicated in patients presenting with acute ischaemia, significant hypotension such that they won’t tolerate pharmacological treatment, severe heart failure or the presence of a pre-excitation syndrome leading to rapid conduction, classically through an accessory pathway. Urgent cardioversion can only be considered when the onset of atrial fibrillation appears to clearly be within the last 48 hours.

2 First-line rate control agents include beta blockers or centrally acting calcium channel blockers. A goal acutely of ≤100bpm is sufficient for a patient who is otherwise asymptomatic and has normal systolic function. Digoxin is typically avoided in patients for rate control.

3 Chronic tachycardia leads to significant structural changes in the heart such as ventricular dilatation. Often the tachycardia cardiomyopathy predisposes to further arrhythmias of the heart.

4 Patients with acutely decompensated heart failure and reduced ejection fraction should be treated with IV amiodarone or digoxin to acutely control heart rate. Beta blocker therapy should only be commenced or increased once the patient has been stabilised from the heart failure perspective. It is rare to need cardioversion for acute heart failure unless they are becoming haemodynamically unstable. The mainstay for treatment is managing fluid overload with diuretics and vasodilators. Initial attempts of rate reduction should be to achieve a rate <120bpm in this setting.

5 The decision to offer patients cardioversion if they are otherwise haemodynamically stable is dependent on multiple factors. Cardioversion in very elderly patients or patients with large left atrial dimensions above 5cm are normally excluded; if needed, cardioversion is carefully considered on a case-by-case basis. Patients with a reversible underlying disorder such as thyroid disease, pericarditis and postoperative AF should be offered cardioversion. These patients should ideally be young (<65 years) and have normal left ventricular systolic function. The absence of hypertension is also preferred. Patients with acute heart failure presenting with new onset AF can be offered cardioversion as it will improve the cardiac output. Finally, patients who have only developed atrial fibrillation recently and where it appears to be early in its natural history should ideally be offered cardioversion.

6 Patients with first presentation AF who have been cardioverted do not require antiarrhythmics such as amiodarone, flecainide or sotalol, in the first instance at least.

7 For patients with AF >48 hours in duration, 4 weeks of anticoagulation prior to cardioversion and another 4 weeks post cardioversion is required. This is to prevent any atrial thrombi causing acute stroke from embolisation. Transoesophageal echocardiography can be used to screen patients for the presence of thrombus if cardioversion is required before 4 weeks. Long-term anticoagulation following the completion of 4 weeks post cardioversion is dependent on the patient’s thromboembolic risk profile.

8 Please note that CHA 2 DS 2 -VASc is only valid in patients with non-valvular AF.

9 The CHA 2 DS 2 -VASc risk tool stands for the following:

C – congestive heart failure (1 point)

H – hypertension (1 point)

A2 – age ≥75 (2 points)

D – diabetes (1 point)

S2 – history of stroke, TIA or thromboembolism (2 points)

V – vascular disease: history of MI, peripheral arterial disease, aortic atherosclerosis (1 point)

A – age between 65 and 74 (1 point)

Sc – sex category; i.e. female sex (1 point).

A patient with non-valvular AF and a score of ≥2 should be anticoagulated from a stroke prevention perspective. A CHA2DS2-VASc score of 2 represents an approximate 2% annual risk of stroke, and a score of 6 represents a 10% stroke risk. Patients with a score of 1 are borderline and should be anticoagulated on clinical judgement. The current recommendation is for the use of direct oral anticoagulants (DOACs)