The initial manifestation of severe pneumonia in COVID-19 is hypoxemic respiratory failure

followed by a rapid increase in heart rate. However, our patient had a poor compensatory increase in
his heart rate, despite changes in his clinical status. The hypothesis that most closely matches the
manifestation of sinus bradycardia in patients with COVID-19 is the release of inflammatory
cytokines that act directly on the sinoatrial node. Our patient had an acute respiratory failure with
elevated C-reactive protein and D-Dimer inflammatory markers. Other mechanism that possibly
contributes to the episode of bradycardia in these patients is the medication that received during
treatment, such as azithromycin, dexamethasone, Angiotensin II Receptor Blockers (ARBs), and
lorazepamThe initial manifestation of severe pneumonia in COVID-19 is hypoxemic respiratory
failure followed by a rapid increase in heart rate. However, our patient had a poor compensatory
increase in his heart rate, despite changes in his clinical status. The hypothesis that most closely
matches the manifestation of sinus bradycardia in patients with COVID-19 is the release of
inflammatory cytokines that act directly on the sinoatrial node. Our patient had an acute respiratory
failure with elevated C-reactive protein and D-Dimer inflammatory markers. Other mechanism that
possibly contributes to the episode of bradycardia in these patients is the medication that received
during treatment, such as azithromycin, dexamethasone, Angiotensin II Receptor Blockers (ARBs),
and lorazepamThe initial manifestation of severe pneumonia in COVID-19 is hypoxemic respiratory
failure followed by a rapid increase in heart rate. However, our patient had a poor compensatory
increase in his heart rate, despite changes in his clinical status. The hypothesis that most closely
matches the manifestation of sinus bradycardia in patients with COVID-19 is the release of
inflammatory cytokines that act directly on the sinoatrial node. Our patient had an acute respiratory
failure with elevated C-reactive protein and D-Dimer inflammatory markers. Other mechanism that
possibly contributes to the episode of bradycardia in these patients is the medication that received
during treatment, such as azithromycin, dexamethasone, Angiotensin II Receptor Blockers (ARBs),
and lorazepam