Lung auscultation was clear and respiratory rate was 20 respirations per minute. Jugular venous pressure was not elevated and there was no pedal oedema or calf tenderness. Cardiovascular examination revealed dual heart sounds with ejection systolic murmur at the aortic region radiating to the carotids. Her Glasgow coma scale was 15/15 and she was alert and orientated. Her temperature was 36.3☌, oxygen saturation was 97% at room air and her random blood sugar was 6.2 mmol/L. On examination her blood pressure was 155/85 mmHg when lying down and 175/90mmHg when standing, and heart rate was 73 beats per minute. It is unlikely that the dizziness is due to vestibular dysfunction and is more likely to be due to a cardiac arrhythmia such as bradyarrythmia. It is worrisome that the dizziness was always followed by syncopal episodes that increased in frequency over a period of 24 hours. There was no history of bleeding or volume depletion. The additional information above confirms that the dizziness was not associated with head movement and was not postural in nature. This time she was referred to hospital for further assessment. Again, there was no precipitant or sudden change in posture or emotion prior to the dizziness. These episodes were also followed by syncopal episodes lasting between a few seconds to 2 minutes. She had been well over the next 8 months but 18 hours before her current presentation to the emergency department, she experienced five separate but similar episodes of dizziness while lying in bed. No further investigation was done at that stage but she was advised to go to hospital if the dizziness recurred. An ECG revealed normal sinus rhythm at 80 beats per minute (Figure 1). She immediately presented to her GP and her antihypertensive medication was adjusted. She described a prodrome of hot sensation and diaphoresis prior to loss of consciousness. 3 Lastly, the combination of a calcium channel blocker and an angiotensin receptor blocker may cause postural hypotension.Įight months before her current presentation to the emergency department, while sitting and having lunch, she had two episodes of sudden dizziness followed by syncope lasting for 1–2 minutes. A history of gastroesophageal reflux raises the possibility of peptic ulcer development, which may cause anaemia or volume depletion, contributing to her dizziness. However, in this case, the patient’s euthyroid status rules out these possibilities. On the other hand, hypothyroidism may cause hypotension and bradycardia, which also lead to dizziness. 5,6 Similarly, over-replacement of thyroxine can lead to a hyperthyroid state, which, in turn, can lead to atrial tachyarrythmias presenting with palpitations and dizziness. 4–6 The accumulation of iron in the myocardium can lead to severe left ventricular diastolic dysfunction that ultimately leads to heart failure and cardiac arrhythmias. 3 Haemachromatosis can contribute to the development of cardiomyopathy. Chronic hypertension may cause left ventricular diastolic dysfunction, leading to low cardiac output, which may lead to cardiac arrhythmias. The additional information produces a list of differential diagnoses. Her medications include lercanidipine 20 mg daily, irbesartan 150 mg daily and omeprazole 20 mg daily. She is a lifelong non-smoker and drinks three glasses of wine each day with dinner. She had a history of hypertension, stable familial haemochromatosis, gastroesophageal reflux disease and hypothyroidism, which was treated with thyroxine but treatment was ceased due to euthyroid status. = sensation of disconnection from the environment Four categories causing a sensation of dizziness 1,2 Categories In the case study described in this article, the patient presented with dizziness followed by fainting episodes, indicating presyncope rather than vertigo. 1,2 Unfortunately, patients tend to use the term dizziness loosely. 1 When a patient describes dizziness, it can reflect one of four conditions ( Table 1). Dizziness is a common presentation that accounts for about 5% of primary care visits.
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