Abstract
Objective: The relationship between COVID-19 and blood pressure (BP) has raised great concern since the discovery of Angiotensin Convertase Enzyme 2 (ACE 2) – mediated mechanism of action for Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-COV2). Hypertension (HTN) itself proved to be a risk factor for more severe Coronavirus Disease 19 (COVID -19). However less studies focus on the trend of blood BP for patients with COVID-19 during the initial phase of disease. Design and method: We present the case of a 71 years old woman with grade 2 HTN previously controlled with diuretic and betablocker therapy that came to our hospital with dyspnea, cough and debilitating fatigue progressively worsened in the last 10 days. The patient also related the first episode of syncope in her life the night before the presentation. Results: The clinical evaluation revealed a conscious, euvolemic, with polypnea and a peripheral saturation in oxygen of 86%, corrected to 95% with 9 liters oxygen/minute via simple face mask and a BP of 110/70 mmHg with a ventricular rate of 45 beats per minute in supine position. The assessment of BP values while standing showed a value of 78/60 mmHg after 1 minute and 58/40 mmHg after 3 minutes, while the ventricular rate increased overall to 65 beats per minute. ECG was remarkable only for mild bradycardia and computed tomography pulmonary angiogram excluded pulmonary embolism. The patient was admitted with severe COVID-19 accompanied by severe orthostatic hypotension and bradycardia. Continuous telemonitoring showed only mild bradycardia. Under standard COVID 19 treatment, after 10 days, her symptoms had resolved with no residual orthostatic hypotension or bradycardia. Conclusions: In conclusion this case reflects the life-threatening dysautonomia caused by SARS-COV 2 infection. More concern should be placed on this type of fragile patients, taking into account both the macroscopic implications of being confined to bed for a long period of time and the microscopic butterfly effect caused by the binding of the virus on the widespread ACE 2 in the lungs, heart, kidneys and digestive tract.
Published Version
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