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through a mask interface &#40;IPAP 12 cmH<span class="elsevierStyleInf">2</span>O&#44; EPAP 10 cmH<span class="elsevierStyleInf">2</span>O&#44; FiO<span class="elsevierStyleInf">2</span> started at 100&#37; and titrated to SpO<span class="elsevierStyleInf">2</span>&#41;&#46; Initially&#44; while on NIV&#44; she maintained SpO<span class="elsevierStyleInf">2</span> &#62; 90&#37;&#44; with FiO<span class="elsevierStyleInf">2</span> of 60-80&#37;&#44; whereas saturations would drop within minutes while on a non-rebreather mask &#40;15L &#47; min&#41;&#44; during attempted breaks from NIV&#46; We did not offer high-flow nasal cannula &#40;HFNC&#41; oxygen therapy&#44; partially because of its excessively high oxygen consumption&#44; which presented logistical barriers in our resource-limited setting during a pandemic&#46; Furthermore&#44; we expected &#8220;true&#8221; positive pressure ventilation to have more beneficial effects on obesity-related&#44; position-dependent atelectasis&#44; and on a potentially present obstructive sleep apnea&#46; Over the first week of admission&#44; she developed progressive hypoxaemia&#44; while denying dyspnoea&#46; Our patient repeatedly refused intubation and invasive ventilation&#44; citing a lack of symptoms&#44; and a fear for a worse outcome with mechanical ventilation&#46; On day three&#44; the patient desaturated to S<span class="elsevierStyleInf">p</span>O<span class="elsevierStyleInf">2</span> of about 50&#37; &#40;despite FiO<span class="elsevierStyleInf">2</span>100&#37;&#41;&#44; while denying dyspnoea&#44; and without exhibiting tachypnea&#46; Following prone positioning&#44; saturations recovered to above 90&#37;&#46; Intermittent awake proning was&#44; from that moment on&#44; continued three times daily&#46; On day seven&#44; S<span class="elsevierStyleInf">p</span>O<span class="elsevierStyleInf">2</span> again dropped to 30-55&#37;&#44; from then on never exceeding 60&#37;&#44; and at times reaching levels as low as 21&#37;&#44; with no further response to prone positioning&#46; Changes in ventilatory settings &#40;EPAP as low as 6 and up to 14cmH<span class="elsevierStyleInf">2</span>O&#59; as CPAP&#44; or with pressure support of up to 6 cmH<span class="elsevierStyleInf">2</span>O&#59; FiO<span class="elsevierStyleInf">2</span> from here on never below 100&#37;&#41; yielded no improvement in respiratory parameters&#46; An arterial line was placed in the left brachial artery&#44; to allow for regular blood sampling&#46; Arterial blood was extremely dark &#40;<a class="elsevierStyleCrossRef" href="#fig0001">Fig&#46; 1</a>B&#41;&#44; with a P<span class="elsevierStyleInf">a</span>O<span class="elsevierStyleInf">2</span> of 28mmHg&#46; Accidental venous sampling was excluded with an adequate arterial blood pressure waveform&#46; There was no methemoglobinaemia&#46; Meanwhile&#44; our patient was able to speak coherent&#44; full sentences&#44; and denied having any sensation of dyspnoea&#44; although she was at times tachypneic&#46; She remained firm in her view&#44; and persistently refused endotracheal intubation&#46; After enduring extreme hypoxaemia for about two days in a seemingly stable condition&#44; she suddenly developed ventricular fibrillation&#44; rapidly followed by asystole and death&#46; Resuscitative efforts were not successful&#46;</p><elsevierMultimedia ident="fig0001"></elsevierMultimedia><p id="para0002" class="elsevierStylePara elsevierViewall">Silent&#44; or &#8220;happy&#8221; hypoxaemia is a well-known phenomenon in COVID-19&#46;<a class="elsevierStyleCrossRef" href="#bib0001"><span class="elsevierStyleSup">1</span></a><span class="elsevierStyleSup">&#44;</span><a class="elsevierStyleCrossRef" href="#bib0002"><span class="elsevierStyleSup">2</span></a> Several theories have been proposed for its existence&#44; most revolving around intrapulmonary shunting as the primary driver of hypoxaemia&#44; with relative preservation of lung compliance in the early stages of the disease&#44;<a class="elsevierStyleCrossRef" href="#bib0003"><span class="elsevierStyleSup">3</span></a> and resultant normocarbia or even hypocarbia&#44;<a class="elsevierStyleCrossRef" href="#bib0004"><span class="elsevierStyleSup">4</span></a> although a neural factor has also been proposed&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">5</span></a> In our case&#44; we think a certain level of hypoxaemia at baseline associated with previously undiagnosed&#44; but potentially present obesity hypoventilation syndrome may have contributed to our patient&#39;s tolerance of extremely low arterial oxygen levels&#46;</p><p id="para0003" class="elsevierStylePara elsevierViewall">The optimal timing of intubation in severe COVID-19 remains controversial&#46; Early on in the pandemic&#44; prominent authors urged clinicians to intubate early&#44; in order to prevent patient self-induced lung injury &#40;P-SILI&#41;&#44; which was hypothesised to result from excessive respiratory effort&#46;<a class="elsevierStyleCrossRef" href="#bib0006"><span class="elsevierStyleSup">6</span></a> Furthermore&#44; non-invasive respiratory support was feared to lead to droplet formation&#44; putting health-care workers at risk&#46;<a class="elsevierStyleCrossRef" href="#bib0007"><span class="elsevierStyleSup">7</span></a> Conversely&#44; it has been argued that early&#44; potentially unnecessary intubation may increase mortality by exposing patients to the risks of sedation and invasive ventilation&#46;<a class="elsevierStyleCrossRef" href="#bib0008"><span class="elsevierStyleSup">8</span></a> As the pandemic progressed&#44; many clinicians adopted a &#8220;wait-and-see&#8221; strategy&#44; where patients are initially managed with non-invasive ventilatory support &#40;including NIV and HFNC&#41;&#44; and are intubated only upon failure of such therapies&#46;<a class="elsevierStyleCrossRef" href="#bib0009"><span class="elsevierStyleSup">9</span></a> More recent studies yield conflicting results&#44; and although non-invasive respiratory support appears safe&#44; and has been shown to reduce the need for invasive ventilation&#44; the optimum timing of intubation in COVID-19 is as of yet still unknown&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">10</span></a> It may be reasonable to use a step-up approach&#44; starting HFNC in patients who fail conventional oxygen therapy&#44; failure of which could be followed by a trial of CPAP&#44; and eventually&#44; if indicated&#44; intubation&#46;<a class="elsevierStyleCrossRef" href="#bib0011"><span class="elsevierStyleSup">11</span></a></p><p id="para0004" class="elsevierStylePara elsevierViewall">To aid in deciding whom to intubate&#44; authors have proposed using the ROX index&#44;<a class="elsevierStyleCrossRef" href="#bib0012"><span class="elsevierStyleSup">12</span></a> which&#44; in several retrospective series&#44; has been reported to predict failure of non-invasive respiratory support in COVID-19&#46;<a class="elsevierStyleCrossRef" href="#bib0012"><span class="elsevierStyleSup">12</span></a><span class="elsevierStyleSup">&#44;</span><a class="elsevierStyleCrossRef" href="#bib0013"><span class="elsevierStyleSup">13</span></a> While most studies were performed in cohorts treated with HFNC&#44; the ROX index has been reported to correlate with outcomes after CPAP as well&#46;<a class="elsevierStyleCrossRef" href="#bib0014"><span class="elsevierStyleSup">14</span></a> It should be noted that different studies report different cut-offs &#40;such as &#60;3&#46;85<a class="elsevierStyleCrossRef" href="#bib0012"><span class="elsevierStyleSup">12</span></a> and &#60;5&#46;99<a class="elsevierStyleCrossRef" href="#bib0013"><span class="elsevierStyleSup">13</span></a>&#41;&#46; Our patient had ROX-indexes as low as 1&#46;12&#44; clearly indicating a high risk of treatment failure&#46;</p><p id="para0005" class="elsevierStylePara elsevierViewall">The phenomenon of seemingly well-tolerated hypoxaemia in COVID-19 has led to further controversy&#44; as it seems counter-intuitive to intubate a patient who&#44; despite having low oxygen saturations&#44; is feeling well&#46; This discrepancy between subjective and objective findings has led some authors to argue that such patients should not be intubated&#44; as long as they remain asymptomatic&#44; and do not exhibit increased work of breathing&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">15</span></a> Even though we are inclined to agree with this concept in general&#44; as long as hypoxaemia is mild to moderate&#44; we believe our case demonstrates the dangers when such an approach is taken to the extreme&#46; There is a point where hypoxaemia can lead to rapid cardiovascular decompensation&#44;<a class="elsevierStyleCrossRef" href="#bib0002"><span class="elsevierStyleSup">2</span></a> where &#8220;happy&#8221; hypoxaemia can show its unfriendly side&#58; sudden cardiac death&#46;</p><span id="sec0002" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cesectitle0003">Funding</span><p id="para0006" class="elsevierStylePara elsevierViewall">The authors declare that no external funding was received for the conduct of this study and&#47;or the preparation of this manuscript&#46;</p></span></span>"
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Letter to the Editor
The unfriendly side of “happy hypoxaemia”: Sudden cardiac death
C.M.C. Serbanescu-Kele Apor de Zalána,b,
Corresponding author
cserbanescu@viecuri.nl

Corresponding author.
, R.P. Banwariea,c, K.D. Banwaria, B.A. Pankaa,c
a Department of Internal Medicine and Intensive Care, s Lands Hospitaal, Paramaribo, Suriname
b Department of Intensive Care, VieCuri Medical Center, Venlo, 5900 BX Venlo, the Netherlands
c Department of Intensive Care, Academic Hospital Paramaribo, Paramaribo, Suriname
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through a mask interface &#40;IPAP 12 cmH<span class="elsevierStyleInf">2</span>O&#44; EPAP 10 cmH<span class="elsevierStyleInf">2</span>O&#44; FiO<span class="elsevierStyleInf">2</span> started at 100&#37; and titrated to SpO<span class="elsevierStyleInf">2</span>&#41;&#46; Initially&#44; while on NIV&#44; she maintained SpO<span class="elsevierStyleInf">2</span> &#62; 90&#37;&#44; with FiO<span class="elsevierStyleInf">2</span> of 60-80&#37;&#44; whereas saturations would drop within minutes while on a non-rebreather mask &#40;15L &#47; min&#41;&#44; during attempted breaks from NIV&#46; We did not offer high-flow nasal cannula &#40;HFNC&#41; oxygen therapy&#44; partially because of its excessively high oxygen consumption&#44; which presented logistical barriers in our resource-limited setting during a pandemic&#46; Furthermore&#44; we expected &#8220;true&#8221; positive pressure ventilation to have more beneficial effects on obesity-related&#44; position-dependent atelectasis&#44; and on a potentially present obstructive sleep apnea&#46; Over the first week of admission&#44; she developed progressive hypoxaemia&#44; while denying dyspnoea&#46; Our patient repeatedly refused intubation and invasive ventilation&#44; citing a lack of symptoms&#44; and a fear for a worse outcome with mechanical ventilation&#46; On day three&#44; the patient desaturated to S<span class="elsevierStyleInf">p</span>O<span class="elsevierStyleInf">2</span> of about 50&#37; &#40;despite FiO<span class="elsevierStyleInf">2</span>100&#37;&#41;&#44; while denying dyspnoea&#44; and without exhibiting tachypnea&#46; Following prone positioning&#44; saturations recovered to above 90&#37;&#46; Intermittent awake proning was&#44; from that moment on&#44; continued three times daily&#46; On day seven&#44; S<span class="elsevierStyleInf">p</span>O<span class="elsevierStyleInf">2</span> again dropped to 30-55&#37;&#44; from then on never exceeding 60&#37;&#44; and at times reaching levels as low as 21&#37;&#44; with no further response to prone positioning&#46; Changes in ventilatory settings &#40;EPAP as low as 6 and up to 14cmH<span class="elsevierStyleInf">2</span>O&#59; as CPAP&#44; or with pressure support of up to 6 cmH<span class="elsevierStyleInf">2</span>O&#59; FiO<span class="elsevierStyleInf">2</span> from here on never below 100&#37;&#41; yielded no improvement in respiratory parameters&#46; An arterial line was placed in the left brachial artery&#44; to allow for regular blood sampling&#46; Arterial blood was extremely dark &#40;<a class="elsevierStyleCrossRef" href="#fig0001">Fig&#46; 1</a>B&#41;&#44; with a P<span class="elsevierStyleInf">a</span>O<span class="elsevierStyleInf">2</span> of 28mmHg&#46; Accidental venous sampling was excluded with an adequate arterial blood pressure waveform&#46; There was no methemoglobinaemia&#46; Meanwhile&#44; our patient was able to speak coherent&#44; full sentences&#44; and denied having any sensation of dyspnoea&#44; although she was at times tachypneic&#46; She remained firm in her view&#44; and persistently refused endotracheal intubation&#46; After enduring extreme hypoxaemia for about two days in a seemingly stable condition&#44; she suddenly developed ventricular fibrillation&#44; rapidly followed by asystole and death&#46; Resuscitative efforts were not successful&#46;</p><elsevierMultimedia ident="fig0001"></elsevierMultimedia><p id="para0002" class="elsevierStylePara elsevierViewall">Silent&#44; or &#8220;happy&#8221; hypoxaemia is a well-known phenomenon in COVID-19&#46;<a class="elsevierStyleCrossRef" href="#bib0001"><span class="elsevierStyleSup">1</span></a><span class="elsevierStyleSup">&#44;</span><a class="elsevierStyleCrossRef" href="#bib0002"><span class="elsevierStyleSup">2</span></a> Several theories have been proposed for its existence&#44; most revolving around intrapulmonary shunting as the primary driver of hypoxaemia&#44; with relative preservation of lung compliance in the early stages of the disease&#44;<a class="elsevierStyleCrossRef" href="#bib0003"><span class="elsevierStyleSup">3</span></a> and resultant normocarbia or even hypocarbia&#44;<a class="elsevierStyleCrossRef" href="#bib0004"><span class="elsevierStyleSup">4</span></a> although a neural factor has also been proposed&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">5</span></a> In our case&#44; we think a certain level of hypoxaemia at baseline associated with previously undiagnosed&#44; but potentially present obesity hypoventilation syndrome may have contributed to our patient&#39;s tolerance of extremely low arterial oxygen levels&#46;</p><p id="para0003" class="elsevierStylePara elsevierViewall">The optimal timing of intubation in severe COVID-19 remains controversial&#46; Early on in the pandemic&#44; prominent authors urged clinicians to intubate early&#44; in order to prevent patient self-induced lung injury &#40;P-SILI&#41;&#44; which was hypothesised to result from excessive respiratory effort&#46;<a class="elsevierStyleCrossRef" href="#bib0006"><span class="elsevierStyleSup">6</span></a> Furthermore&#44; non-invasive respiratory support was feared to lead to droplet formation&#44; putting health-care workers at risk&#46;<a class="elsevierStyleCrossRef" href="#bib0007"><span class="elsevierStyleSup">7</span></a> Conversely&#44; it has been argued that early&#44; potentially unnecessary intubation may increase mortality by exposing patients to the risks of sedation and invasive ventilation&#46;<a class="elsevierStyleCrossRef" href="#bib0008"><span class="elsevierStyleSup">8</span></a> As the pandemic progressed&#44; many clinicians adopted a &#8220;wait-and-see&#8221; strategy&#44; where patients are initially managed with non-invasive ventilatory support &#40;including NIV and HFNC&#41;&#44; and are intubated only upon failure of such therapies&#46;<a class="elsevierStyleCrossRef" href="#bib0009"><span class="elsevierStyleSup">9</span></a> More recent studies yield conflicting results&#44; and although non-invasive respiratory support appears safe&#44; and has been shown to reduce the need for invasive ventilation&#44; the optimum timing of intubation in COVID-19 is as of yet still unknown&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">10</span></a> It may be reasonable to use a step-up approach&#44; starting HFNC in patients who fail conventional oxygen therapy&#44; failure of which could be followed by a trial of CPAP&#44; and eventually&#44; if indicated&#44; intubation&#46;<a class="elsevierStyleCrossRef" href="#bib0011"><span class="elsevierStyleSup">11</span></a></p><p id="para0004" class="elsevierStylePara elsevierViewall">To aid in deciding whom to intubate&#44; authors have proposed using the ROX index&#44;<a class="elsevierStyleCrossRef" href="#bib0012"><span class="elsevierStyleSup">12</span></a> which&#44; in several retrospective series&#44; has been reported to predict failure of non-invasive respiratory support in COVID-19&#46;<a class="elsevierStyleCrossRef" href="#bib0012"><span class="elsevierStyleSup">12</span></a><span class="elsevierStyleSup">&#44;</span><a class="elsevierStyleCrossRef" href="#bib0013"><span class="elsevierStyleSup">13</span></a> While most studies were performed in cohorts treated with HFNC&#44; the ROX index has been reported to correlate with outcomes after CPAP as well&#46;<a class="elsevierStyleCrossRef" href="#bib0014"><span class="elsevierStyleSup">14</span></a> It should be noted that different studies report different cut-offs &#40;such as &#60;3&#46;85<a class="elsevierStyleCrossRef" href="#bib0012"><span class="elsevierStyleSup">12</span></a> and &#60;5&#46;99<a class="elsevierStyleCrossRef" href="#bib0013"><span class="elsevierStyleSup">13</span></a>&#41;&#46; Our patient had ROX-indexes as low as 1&#46;12&#44; clearly indicating a high risk of treatment failure&#46;</p><p id="para0005" class="elsevierStylePara elsevierViewall">The phenomenon of seemingly well-tolerated hypoxaemia in COVID-19 has led to further controversy&#44; as it seems counter-intuitive to intubate a patient who&#44; despite having low oxygen saturations&#44; is feeling well&#46; This discrepancy between subjective and objective findings has led some authors to argue that such patients should not be intubated&#44; as long as they remain asymptomatic&#44; and do not exhibit increased work of breathing&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">15</span></a> Even though we are inclined to agree with this concept in general&#44; as long as hypoxaemia is mild to moderate&#44; we believe our case demonstrates the dangers when such an approach is taken to the extreme&#46; There is a point where hypoxaemia can lead to rapid cardiovascular decompensation&#44;<a class="elsevierStyleCrossRef" href="#bib0002"><span class="elsevierStyleSup">2</span></a> where &#8220;happy&#8221; hypoxaemia can show its unfriendly side&#58; sudden cardiac death&#46;</p><span id="sec0002" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cesectitle0003">Funding</span><p id="para0006" class="elsevierStylePara elsevierViewall">The authors declare that no external funding was received for the conduct of this study and&#47;or the preparation of this manuscript&#46;</p></span></span>"
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ISSN: 25310437
Original language: English
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Pulmonology

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