Age: 47 years
Gender: Female
Occupation: Social worker
Working diagnosis: Childhood murmur
HISTORY
The patient had been followed for a murmur noted in childhood. After reaching adult life no further follow-up had been recommended. She felt well.
In her mid-40s, she visited her family doctor with episodes of palpitations and one syncopal episode, but no workup was ensued. Previously, she had had a hysterectomy for fibroids, but no other medical history. She did not smoke or drink. She had no other health problems, though recalled a tender swelling in her neck around a year ago that resolved spontaneously.
Over the preceding 6 months she complained of increasing frequency of syncopal episodes that seemed to be precipitated by exertion. Flecainide was prescribed empirically with little effect. She had increasing exertional breathlessness and fatigue, and was barely able to walk 100 m without stopping. She had had to quit work a month earlier and had not left the house for 2 weeks.
Comments: Innocent murmurs in childhood are common; echocardiography was not available in the 1960s and, thus, was not employed in our patient for evaluation of the murmur as is usually done today. As decades pass from a childhood diagnosis, patients are often understandably ill informed of an anatomical diagnosis or its pathological significance.
Unless the cause of syncope can be clearly established on clinical grounds, such as vasovagal syncope, a cardiac workup is indicated.
Empiric antiarrhythmic therapy is not recommended prior to the nature of arrhythmia or the cause of syncope being fully assessed and identified.
CURRENT SYMPTOMS
The patient mainly complained of increasing breathlessness with exertion. She had syncopal episodes after mild exertion. She complained of swollen ankles and had gained 20 kg in weight over the last year. She had general constitutional upset, with malaise, fatigue, nausea, and vomiting.
NYHA class: III
Comments: In this context, a cardiac cause of syncope should be the primary concern. Syncope can occur due to supraventricular or ventricular tachycardia, or with episodes of bradycardia or heart block. Syncope on exertion may also suggest a structural cardiac cause such as aortic stenosis or hypertrophic obstructive cardiomyopathy.
PHYSICAL EXAMINATION
BP 100/60 mm Hg, HR 108, afebrile, oxygen saturation 94% on room air
Height 170 cm, weight 104 kg, BSA 2.22 m 2
Surgical scars: Hysterectomy scar was present, but no others.
Neck veins: Visible 3 cm above the sternal angle, with occasional cannon A-waves
Lungs/chest: Normal vesicular breath sounds throughout both lung fields
Heart: The rhythm was irregular. There was no right ventricular heave. There were no added heart sounds or murmurs. Both heart sounds were normal.
Abdomen: The patient was obese. The abdomen was not tender, and no organomegaly was noted.
Extremities: Mild bilateral pedal edema. Peripheral pulses were all palpable with normal pulse volume.
PERTINENT NEGATIVES
There was no cyanosis or clubbing, and no splinter hemorrhages or any stigmata of endocarditis.
Comments: The patient has an irregular tachycardia and is mildly hypoxic.
The absence of a murmur limits the differential diagnosis, though severe regurgitant or even stenotic lesions can be inaudible.
LABORATORY DATA
| Hemoglobin | 14.0 g/dL (11.5–15.0) |
| Hematocrit/PCV | 41% (36–46) |
| MCV | 92 fL (83–99) |
| Platelet count | 268 × 10 9 /L (150–400) |
| Sodium | 135 mmol/L (134–145) |
| Potassium | 4.5 mmol/L (3.5–5.2) |
| Creatinine | 1.2 mg/dL (0.6–1.2) |
| Blood urea nitrogen | 7.3 mmol/L (2.5–6.5) |
| Magnesium | 0.92 mmol/L (0.7–1.0) |
OTHER RELEVANT LAB RESULTS
| TSH | >100 pmol/L (0.5–5) |
| Free T4 | 3.3 pmol/L (7.5–21.0) |
| Thyroid peroxidase (Other autoantibodies all negative) | 1136 IU/mL (<60) |
| Alanine transferase | 106 IU/L (8–40) |
| Alkaline phosphatase | 148 U/L (38–126) |
| Bilirubin | 2.4 μmol/dL (3–24) |
| Albumin | 4.3 g/dL (37–53) |
Comments: The weight gain, fatigue, and malaise seemed likely to be a mixed picture of cardiac failure (although the normal JVP shows there is no right heart decompensation at present), rhythm disturbance, and hypothyroidism. The episode of tender neck swelling in the past suggests the patient may have subacute thyroiditis.
Hypothyroidism can occur in conjunction with Addison’s disease as part of an organ-specific autoimmune disease (notably polyglandular autoimmune syndrome type II, which is hypoadrenalism with either hypothyroidism and/or type I diabetes). Thyroxine replacement in an Addisonian state can precipitate Addisonian crisis. With the borderline low random cortisol level (which is difficult to interpret), a cortisol stimulation test was needed to rule out adrenal insufficiency, and in this case was normal. A raised alkaline phosphatase and other liver dysfunction are often present in hypothyroidism.
ELECTROCARDIOGRAM
FINDINGS
Heart rate: 117 bpm
QRS axis: −38°
QRS duration: 206 msec
There is an irregular, wide complex tachycardia, with widespread ST–T-wave abnormalities.
Comments: The very broad QRS complex is suggestive of possible metabolic toxicity. Though the irregularity is very suspicious for atrial fibrillation, it can be difficult to distinguish whether a broad complex tachycardia is a ventricular or supraventricular tachycardia with a ventricular conduction defect.
Hypothyroidism can cause bradycardia and a prolonged QT interval and, if severe, can cause variable degree of AV block and bundle branch block. Rapid atrial fibrillation is more common with hyperthyroidism.
CHEST X-RAY
FINDINGS
Cardiomegaly with a cardiothoracic ratio of 60% and a straight left heart border.
Comments: The opacity adjacent to the lower right heart border is more lucent than the adjacent cardiac tissue and likely represents a fat pad. One cannot exclude a pericardial effusion, as can be seen in hypothyroidism. Otherwise, the CXR and physical examination indicate that hypothyroidism is not the only cause of the patient’s symptoms.
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