Why COVID-19 Silent Hypoxemia Is Baffling to Physicians

Abstract

Patients with coronavirus disease (COVID-19) are described as exhibiting oxygen levels incompatible with life without dyspnea. The pairing-dubbed happy hypoxia but more precisely termed silent hypoxemia-is especially bewildering to physicians and is considered as defying basic biology. This combination has attracted extensive coverage in media but has not been discussed in medical journals. It is possible that coronavirus has an idiosyncratic action on receptors involved in chemosensitivity to oxygen, but well-established pathophysiological mechanisms can account for most, if not all, cases of silent hypoxemia. These mechanisms include the way dyspnea and the respiratory centers respond to low levels of oxygen, the way the prevailing carbon dioxide tension (Pa CO 2) blunts the brain's response to hypoxia, effects of disease and age on control of breathing, inaccuracy of pulse oximetry at low oxygen saturations, and temperature-induced shifts in the oxygen dissociation curve. Without knowledge of these mechanisms, physicians caring for patients with hypoxemia free of dyspnea are operating in the dark, placing vulnerable patients with COVID-19 at considerable risk. In conclusion, features of COVID-19 that physicians find baffling become less strange when viewed in light of long-established principles of respiratory physiology; an understanding of these mechanisms will enhance patient care if the much-anticipated second wave emerges.

Possible silent hypoxemia in a COVID-19 patient: a case report

“…Hypoxemia occurs when PaO2 is less than 80 mmHg, and severe hypoxemia is when it is less than 60 mmHg. There are four main factors that can impair pulmonary gas exchange and cause hypoxemia when breathing room water is at sea level: hypoventilation, diffusion limitation, shunt, and ventilation-perfusion mismatch [7][8][9]. This unusual 'silent hypoxemia' phenomenon showed it is possible that the virus has an idiosyncratic effect on the respiratory control system.…”

“…Since carbon dioxide removal is still effective, patients do not feel shortness of breath [15]. Risk factors for silent hypoxemia are old age and having diabetes [9]. Therefore, early detection of silent hypoxemia such as using prehospital pulse oximetry [5], or radiology imaging [16,17] might be used as a red ag sign of impending danger of eminent cardiac arrest or sudden respiratory failure.…”

Methylene Blue Inhibits In Vitro the SARS-CoV-2 Spike – ACE2 Protein-Protein Interaction – A Mechanism That Can Contribute to Its Antiviral Activity Against COVID-19

“…This increases the oxygen-binding capacity of hemoglobin and, thus, oxygen delivery to tissues -an important benefit for COVID-19 patients. COVID-19 patients often exhibiting low oxygen levels, typically incompatible with life without dyspnea -a phenomenon termed silent hypoxemia (or happy hypoxia in public media) (Tobin et al, 2020). Possibly relevant to this, MeBlu was found to improve hypoxemia and hyperdynamic circulation in patients with liver cirrhosis and severe hepatopulmonary syndrome (Schenk et al, 2000).…”

Continuous assessment of neuro-ventilatory drive during 12 hours of pressure support ventilation in critically ill patients

“…As reviewed elsewhere [8,11,25], the neuro-ventilatory drive originates from the respiratory centers, a network of interconnected neurons in the pons and medulla, modulated by gas exchange, physical exercise, sleep, emotional and behavioral inputs, pain, discomfort, sedation and analgesia. In pathological conditions, air trapping, decreased lung and/or chest wall compliance, increased airway resistance and/or respiratory muscle weakness may alter the coupling between patient's effort and diaphragmatic excursion (neuro-ventilatory coupling) increasing the neuro-ventilatory drive [16,[44][45][46].…”

“…Theoretically, PSV should support the respiratory muscles allowing spontaneous breathing with a "normal" neuro-ventilatory drive [6][7][8]. Over-assistance would result in low neuro-ventilatory drive putting the patient at risk of diaphragmatic atrophy [9,10] while, on the other hand, under-assistance would result in high neuro-ventilatory drive, dyspnea [11], diaphragmatic fatigue and patient self-in icted lung injury (P-SILI) [12]. Assessing the neuro-ventilatory drive would be pivotal to set and monitor PSV, but, unfortunately, is di cult to realize in clinical practice [13].…”