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Heart failure (HF) manifests primarily as dyspnea, fatigue, and fluid retention, resulting in peripheral and pulmonary edema. Symptoms may vary depending on which ventricle is more affected, left or right.Left-Sided Heart FailureAlso known as left ventricular failure, this condition results from the left ventricle's inability to fill or eject sufficient blood into the systemic circulation. It leads to pulmonary congestion, which occurs when the left ventricle fails to eject blood effectively...
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Acute respiratory failure is a condition characterized by the inability of the lungs to perform their primary function: gas exchange. This failure leads to insufficient oxygen levels (hypoxemia) in the blood, elevated carbon dioxide levels (hypercapnia), or both, causing critical impairment in organ function.
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Updated: Dec 7, 2025

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Syncope at SARS-CoV-2 onset.

Ciro Canetta1, Silvia Accordino1, Elisabetta Buscarini2

  • 1Emergency Medicine Unit, Ospedale Maggiore di Crema, Crema, Italy.

Autonomic Neuroscience : Basic & Clinical
|September 25, 2020
PubMed
Summary
This summary is machine-generated.

Syncope, or fainting, in COVID-19 patients may be linked to a reduced heart rate response during hypocapnic hypoxemia. This impaired response could stem from SARS-CoV-2 affecting the brainstem

Keywords:
Angiotensin-converting enzyme-2 (ACE2) receptorBaroreceptor reflexCentral chemoreceptorsHypocapnic hypoxemiaSARS-CoV-2Syncope

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Area of Science:

  • Neurology
  • Infectious Diseases
  • Cardiology

Background:

  • Syncope (fainting) can occur at the onset of SARS-CoV-2 infection.
  • The underlying mechanisms for syncope in COVID-19 patients are not fully understood.
  • Understanding these mechanisms is crucial for managing neurological and cardiovascular complications of COVID-19.

Purpose of the Study:

  • To investigate the clinical and laboratory findings in SARS-CoV-2 positive patients experiencing syncope.
  • To explore the potential link between syncope, heart rate response, and hypocapnic hypoxemia in COVID-19.
  • To hypothesize the molecular mechanisms by which SARS-CoV-2 might cause syncope.

Main Methods:

  • Retrospective analysis of 35 SARS-CoV-2 positive patients with syncope at disease onset.
  • Clinical examinations (neurologic, cardiologic), electrocardiography, chest CT, and arterial blood gas analysis were performed.
  • Comparison of heart rate between syncope patients and 68 SARS-CoV-2 positive patients without syncope.

Main Results:

  • All patients tested positive for SARS-CoV-2 via RT-PCR.
  • Clinical, neurologic, cardiologic, and ECG findings were normal; chest CT showed interstitial pneumonia.
  • Syncope patients exhibited significantly lower heart rates during hypocapnic hypoxemia compared to non-syncope patients.

Conclusions:

  • Impaired compensatory heart rate increase during acute hypocapnic hypoxemia may lead to syncope in susceptible COVID-19 patients.
  • SARS-CoV-2 may impair baroreflex and chemoreceptor function by affecting ACE2 receptors in the brainstem.
  • This dysfunction could inhibit the necessary tachycardia, predisposing patients to syncope.