Undifferentiated Palpitations — DCE Clinical Case

Long case

Patient scenario

Mrs JM is a 68-year-old retired nurse who presents with a 6-month history of intermittent palpitations, described as a fast and irregular sensation in the chest, lasting from 30 minutes to several hours, occurring three to four times per week. The episodes are associated with progressive exertional dyspnoea — she now becomes breathless walking up a single flight of stairs, when previously she walked two flights without difficulty. She has had no syncope, but one episode of near-syncope on standing rapidly. She has had no chest pain. She has noticed a 4-kilogram weight loss over the three months, increased sweating, and intermittent loose stools, which she attributes to the stress of the palpitations. [1]

Her past medical history includes the hypertension (diagnosed 15 years ago), the type 2 diabetes (diagnosed 8 years ago), and the stage 3 chronic kidney disease (the eGFR of 45 mL per minute per 1.73 square metres). She had a cholecystectomy 10 years ago. She has no history of the ischaemic heart disease, the stroke, or the heart failure. [1]

Her medications are the perindopril 5 mg daily, the amlodipine 10 mg daily, the metformin 1000 mg twice daily, and the aspirin 100 mg daily. She has no drug allergies. She does not smoke, she drinks 2 to 3 standard drinks of alcohol per week, and she drinks 2 cups of coffee per day. She lives with her husband and is independent in the activities of the daily living. [1]

Her family history: her father had the hypertension and the type 2 diabetes; her mother had the atrial fibrillation and the stroke at the age of 72; her brother is well at 65. There is no family history of the sudden cardiac death under the age of 40 or the inherited cardiac conditions. [1]

Examination findings

The patient is comfortable at rest, afebrile, and normotensive. The pulse is irregularly irregular at 95 beats per minute, with an apex rate of 110 — the apex-radial deficit is consistent with atrial fibrillation. The blood pressure is 150 over 88. The respiratory rate is 18. The oxygen saturation is 97 per cent on room air. [1]

The jugular venous pressure is not elevated. The apex beat is not displaced and is of normal character. The first and second heart sounds are normal, with no added sounds and no murmurs. [1]

The thyroid examination reveals a smooth, firm, non-tender goitre of approximately 40 grams, with a soft bruit over the right lobe. There is no exophthalmos, no lid retraction, and no lid lag. [1]

The chest is clear to auscultation. There is no peripheral oedema. There is a fine tremor of the outstretched hands. The reflexes are present and symmetric. [1]

Candidate's opening statement (SASPOP)

"Doctor, my patient is Mrs JM, a 68-year-old retired nurse who presents with a 6-month history of intermittent palpitations and progressive exertional dyspnoea, who works in the home and is independent in her activities. She has coexisting hypertension, type 2 diabetes, and stage 3 chronic kidney disease. The examination reveals the atrial fibrillation with the apex-radial deficit, a smooth goitre with a bruit, and a fine tremor — the findings are consistent with the thyrotoxic atrial fibrillation from the suspected Graves disease. Her problems are: paroxysmal or persistent atrial fibrillation with a rapid ventricular response; thyrotoxicosis from the suspected Graves disease; hypertension; type 2 diabetes; stage 3 chronic kidney disease (the eGFR of 45); exertional dyspnoea; and a high stroke risk with the CHA2DS2-VASc score of 4 (the age 65 to 74, the hypertension, the diabetes, the female sex)." [1]

Problem list

1. Paroxysmal or persistent atrial fibrillation with a rapid ventricular response — the likely thyrotoxic in origin.
2. Thyrotoxicosis from the suspected Graves disease — the smooth goitre with the bruit, the weight loss, the tremor, the sweating, the loose stools.
3. Hypertension — diagnosed 15 years ago, on the perindopril and the amlodipine.
4. Type 2 diabetes — diagnosed 8 years ago, on the metformin.
5. Stage 3 chronic kidney disease — the eGFR of 45, affecting the drug dosing.
6. Exertional dyspnoea — the functional limitation from the AF with the rapid ventricular response and possibly the rate-related cardiomyopathy.
7. High stroke risk — the CHA2DS2-VASc of 4, requiring the oral anticoagulation. [1]

Integrated management plan

Investigations. I would order the full blood count (the anaemia), the thyroid function with the TSH and the free T4 and the thyroid peroxidase antibodies (the suspected thyrotoxicosis — the suppressed TSH and the elevated free T4 with the positive TPO antibodies support the Graves disease), the urea and electrolytes with the eGFR (the baseline and the monitoring of the chronic kidney disease), the HbA1c (the diabetes control), the lipid profile and the liver function tests. I would order the 12-lead ECG to confirm the AF and to look for the ischaemia, the LVH, or the other abnormalities. I would order the transthoracic echocardiogram to assess the left atrial size (the marker of the chronicity and the recurrence risk), the left ventricular size and the systolic function (the tachycardiomyopathy from the uncontrolled rate), the valve structure and the function (the exclusion of the valvular AF, which would affect the anticoagulation choice), and the pulmonary artery pressure. I would consider the thyroid ultrasound and the thyroid uptake scan to characterise the goitre and to confirm the Graves disease (the diffuse increased uptake). [1]

Rate control. The immediate priority is the rate control to relieve the symptoms and to prevent the tachycardiomyopathy. The beta-blocker is the preferred agent in the thyrotoxic AF — it controls the rate and the adrenergic symptoms. The propranolol is the traditional choice (it partially inhibits the peripheral T4-to-T3 conversion), but the metoprolol or the bisoprolol are the alternatives. The calcium channel blocker (the diltiazem) is the alternative if the beta-blocker is contraindicated. The digoxin is less effective in the thyrotoxic AF (the increased clearance and the sympathetic tone overcome the vagal effect). The target ventricular rate is less than 110 at rest for the initial control, with the tighter control (60 to 100) if the symptoms persist. [1]

Anticoagulation. The CHA2DS2-VASc score is 4 (the age 65 to 74, the hypertension, the diabetes, the female sex), which indicates an annual stroke risk of approximately 4 to 5 per cent without the anticoagulation. The oral anticoagulation is indicated. The apixaban 5 mg twice daily is the preferred agent for the non-valvular AF (the dose is reduced to 2.5 mg twice daily if two of the three are met: the age 80 or more, the weight 60 kg or less, the creatinine 133 micromoles per litre or more — this patient does not meet the reduction criteria at present, but the renal function must be monitored). The aspirin is stopped, as it is not effective for the AF stroke prevention. The HAS-BLED score should be calculated (the uncontrolled hypertension, the abnormal renal function — the two factors that are present), but a high bleeding score does not preclude the anticoagulation — it prompts the correction of the modifiable factors (the blood pressure control). [1]

Treatment of the underlying thyrotoxicosis. The carbimazole (the starting dose of 10 to 40 mg daily, depending on the severity) to block the thyroid hormone synthesis. The beta-blocker for the symptom control. The consideration of the definitive treatment with the radioactive iodine (the I-131 — the preferred definitive treatment for the Graves disease in the older patient, with the awareness that the AF may worsen transiently during the early post-treatment period from the release of the stored thyroid hormone) or the surgery (the total thyroidectomy, if there is a large goitre with the compressive symptoms or the suspicion of the malignancy). The Graves disease is the likely diagnosis (the diffuse goitre with the bruit, the positive TPO antibodies), but the diagnosis should be confirmed with the TSH receptor antibodies (the TRAb — the specific marker of the Graves disease) [3].

Comorbidity management. The hypertension (the continuation of the perindopril and the amlodipine, with the target of 130 over 80 in the diabetic; the beta-blocker will contribute to the blood pressure control). The diabetes (the metformin continuation, the consideration of the SGLT2 inhibitor for the renal and the cardiovascular protection). The chronic kidney disease (the renoprotective measures, the dose adjustment of the renally cleared drugs, the avoidance of the nephrotoxins — the NSAIDs, the contrast without the prophylaxis). The lifestyle (the weight management, the alcohol reduction, the sleep apnoea screen — the sleep apnoea is a treatable driver of the AF and the hypertension). [1]

Rhythm control. The restoration of the sinus rhythm may be considered after the euthyroid state is achieved, as the AF in the thyrotoxicosis often reverts to the sinus rhythm with the treatment of the underlying cause. If the AF persists after the euthyroid state is restored, the rhythm control with the electrical cardioversion or the catheter ablation may be considered, especially in the symptomatic patient or the patient with the tachycardiomyopathy. The anticoagulation must be continued for at least 4 weeks after the successful cardioversion, regardless of the CHA2DS2-VASc score, because of the stunning of the atrial mechanical function and the thromboembolic risk [3].

Communication. I would explain the diagnosis to the patient in the plain language: "Your thyroid gland is overactive, producing too much thyroid hormone, which is causing the palpitations and the irregular heart rhythm. We will treat the thyroid condition with the medication, control the heart rate with a beta-blocker, and start a blood thinner to prevent the stroke, which is the most important complication of the irregular rhythm. Once your thyroid is treated, the heart rhythm may return to normal, and we will reassess the need for the ongoing treatment." I would discuss the anticoagulation decision (the benefits versus the bleeding risk), the medication side effects (the carbimazole — the agranulocytosis, the patient must report the sore throat and the fever immediately; the apixaban — the bleeding, the patient must report the unusual bruising or the bleeding), and the follow-up plan (the thyroid function tests every 4 to 6 weeks during the carbimazole titration, the renal function every 3 to 6 months, the cardiology and the endocrinology referral). [1]

Discussion questions

Examiner: "How would the management differ if the AF were valvular rather than non-valvular?" [1]

"The key difference is the anticoagulation. For the valvular AF — defined as the AF in the presence of the moderate-to-severe mitral stenosis or a mechanical prosthetic heart valve — the warfarin is the mandatory agent, with the target INR of 2.0 to 3.0 (or higher, depending on the valve type and the position). The direct oral anticoagulants (the apixaban, the rivaroxaban, the dabigatran) are contraindicated in the valvular AF, based on the RE-ALIGN trial that showed the harm of the dabigatran in the mechanical valve patients. For the non-valvular AF, the DOACs are preferred over the warfarin, with the lower risk of the intracranial haemorrhage and the comparable or superior efficacy. The echocardiogram is therefore essential in the new AF — to distinguish the valvular from the non-valvular, and to guide the anticoagulation choice [3]."

Examiner: "What is the risk of the carbimazole, and how do you counsel the patient?" [1]

"The most important adverse effect of the carbimazole is the agranulocytosis — the neutrophil count drops, and the patient develops the severe infection. The incidence is approximately 0.3 per cent. The patient must be counselled to stop the carbimazole immediately and to present to the emergency department if they develop the sore throat, the fever, or the mouth ulcers — the symptoms of the neutropenic sepsis. A full blood count is checked urgently, and the carbimazole is withheld if the neutrophil count is low. The other adverse effects include the rash (common, usually mild, managed with the antihistamines or the switch to the propylthiouracil), the hepatitis (rare, monitor the liver function), and the vasculitis (rare, the drug-induced ANCA-positive vasculitis). The propylthiouracil is the alternative, but it carries the higher risk of the hepatotoxicity (the acute liver failure) and is reserved for the first trimester of the pregnancy, the thyroid storm, and the carbimazole intolerance." [1]

Examiner: "When would you consider the catheter ablation for this patient's AF?" [1]

"The catheter ablation (the pulmonary vein isolation) is considered for the symptomatic paroxysmal or the persistent AF that is refractory to the medication, or the patient who does not tolerate the medication. In this patient, the immediate priority is the treatment of the underlying thyrotoxicosis, as the AF in the thyrotoxicosis often reverts to the sinus rhythm with the euthyroid state. If the AF persists after the euthyroid state is achieved and the symptoms are refractory to the rate control, the rhythm control with the electrical cardioversion or the ablation may be considered. The ablation is more effective for the paroxysmal AF than the persistent AF, and the success rate is lower in the patients with the structural heart disease (the left atrial dilatation, the left ventricular dysfunction). The patient's preferences, the procedural risks, and the expected benefit should guide the decision." [1]

Short case — focused cardiovascular examination

Instruction

"Examine this patient's cardiovascular system." [1]

Systematic examination routine

1. General inspection. Confirm the patient is comfortable, assess for the distress, the pallor, the flushing, the thyroid signs.
2. The hands and the pulse. Examine the hands (the nail-bed pallor, the fine tremor of the thyrotoxicosis, the thyroid acropachy). Assess the pulse — the rate, the rhythm (the regular or the irregular), the character (the collapsing water-hammer of the aortic regurgitation), the volume. Confirm the pulse at the radial and the apex for the apex-radial deficit.
3. The blood pressure. Measure the blood pressure, noting the systolic, the diastolic, and the pulse pressure.
4. The face and the neck. Examine the face (the malar flush of the mitral stenosis, the anxious facies). Examine the eyes (the conjunctival pallor, the exophthalmos, the lid retraction, the lid lag — the thyroid signs). Examine the jugular venous pressure (the elevation of the heart failure, the prominent a wave of the pulmonary hypertension, the cannon a waves of the complete heart block). Examine the carotid pulse (the character, the volume).
5. The praecordium. Inspect for the deformities and the scars. Palpate the apex beat (the location, the character — the displaced, the thrusting, the sustained, the double impulse), the right ventricular heave, and the thrills.
6. Auscultation. Auscultate the heart sounds (the first, the second — the splitting), the added sounds (the third, the fourth, the clicks, the snaps, the rubs), and the murmurs (the systolic — the ejection, the pansystolic, the late; the diastolic — the early, the mid). Use the dynamic manoeuvres (the inspiration, the expiration, the Valsalva, the squat-to-stand) to characterise the murmurs.
7. The back and the chest. Listen to the lung bases (the crackles of the heart failure). Examine the sacral oedema.
8. The abdomen and the periphery. Palpate for the hepatomegaly, the ascites, the pulsatile liver of the tricuspid regurgitation. Examine the femoral pulses, the peripheral pulses, the peripheral oedema, the peripheral stigmata of the endocarditis (the splinter haemorrhages, the Osler nodes, the Janeway lesions).
9. The thyroid. Inspect the neck, palpate the thyroid (the size, the consistency, the nodules, the tenderness), listen for the bruit. [1]

Key signs this patient demonstrates

• An irregularly irregular pulse at 95 beats per minute, with an apex rate of 110 — the apex-radial deficit consistent with atrial fibrillation.
• A blood pressure of 150 over 88 — the hypertension.
• A normal apex beat and normal heart sounds, with no murmurs — no structural valve disease to explain the AF.
• A smooth, firm, non-tender goitre with a soft bruit over the right lobe — the Graves disease.
• A fine tremor of the outstretched hands — the thyrotoxicosis. [1]

Presentation template

"I introduced myself to the patient, explained the examination, and obtained consent. On general inspection, the patient is comfortable at rest, with no pallor, no flushing, and no distress. [1]

The hands show a fine tremor of the outstretched fingers. The pulse is irregularly irregular at 95 beats per minute, with an apex rate of 110 — the apex-radial deficit is consistent with atrial fibrillation. The blood pressure is 150 over 88. The jugular venous pressure is not elevated. The carotid pulse is normal in character and volume. [1]

On examination of the face, there is no exophthalmos, no lid retraction, and no lid lag. The eyes show no conjunctival pallor. The thyroid examination reveals a smooth, firm, non-tender goitre of approximately 40 grams, with a soft bruit over the right lobe. [1]

The apex beat is not displaced and is of normal character. There is no right ventricular heave. The first and second heart sounds are normal, with no added sounds and no murmurs. The chest is clear. There is no peripheral oedema. [1]

In summary, this patient has atrial fibrillation with an underlying smooth goitre and a thyroid bruit, and a fine tremor — the findings are consistent with the thyrotoxic atrial fibrillation from the suspected Graves disease. I would like to check the full blood count, the thyroid function with the TSH and the free T4 and the thyroid antibodies, the urea and electrolytes, and I would organise an echocardiogram. I would assess the stroke risk with the CHA2DS2-VASc score and the bleeding risk with the HAS-BLED score, and I would initiate the appropriate management — the rate control with the beta-blocker, the anticoagulation, and the treatment of the underlying thyrotoxicosis." [1]

Discussion — the broad-complex tachycardia branch point

Examiner: "How would your management change if the patient presented with a broad-complex tachycardia rather than the narrow-complex AF?" [1]

"The broad-complex tachycardia changes the management entirely. The principle is that the broad-complex tachycardia is the ventricular tachycardia until proven otherwise, especially in the patient with the structural heart disease (the prior infarction, the cardiomyopathy). If the patient is haemodynamically unstable — the hypotension, the shock, the altered mental state, the cardiac arrest — the management is the immediate synchronised DC cardioversion (the 200 joules biphasic, escalating). If the patient is haemodynamically stable, the management is the intravenous amiodarone (300 mg over 20 to 60 minutes, then the infusion) or the intravenous procainamide or the lignocaine, with the synchronised DC cardioversion if the pharmacological conversion fails or the haemodynamics deteriorate. The AV nodal blockers (the adenosine, the verapamil, the beta-blocker, the digoxin) are contraindicated — they do not terminate the VT and may precipitate the haemodynamic collapse. The critical error is the assumption of the SVT with aberrancy and the administration of the verapamil or the adenosine, which can be fatal in the VT patient." [1]

Examiner: "How would you distinguish the WPW-related pre-excited AF from the VT, and why does the distinction matter?" [1]

"The pre-excited AF in the WPW syndrome presents as the irregularly irregular broad-complex tachycardia — the conduction down the accessory pathway produces the broad QRS, and the variable conduction produces the irregularity. The VT, in contrast, is typically the regular broad-complex tachycardia. The irregularity is the key discriminator. The distinction matters because the management is opposite: the pre-excited AF requires the avoidance of the AV nodal blockers (they accelerate the accessory pathway conduction and increase the VF risk) and the treatment with the synchronised DC cardioversion (if unstable) or the intravenous procainamide or the amiodarone (if stable). The AV nodal blockers (the verapamil, the adenosine, the beta-blocker, the digoxin) are contraindicated in the pre-excited AF. The administration of the verapamil to the pre-excited AF is a life-threatening error. The history of the WPW pattern on the prior ECG, or the recognition of the delta wave on the baseline ECG, supports the diagnosis of the pre-excited AF." [1]