case study of respiratory failure

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Reviewed By Behavioral Science Assembly

Submitted by

Lokesh Venkateshaiah, MD

Division of Pulmonary, Critical Care and Sleep Medicine

The MetroHealth System, Case Western Reserve University

Cleveland, Ohio

Bruce Arthur, MD

J. Daryl Thornton, MD, MPH

Assistant Professor

Division of Pulmonary, Critical Care and Sleep Medicine, Center for Reducing Health Disparities

Submit your comments to the author(s).

A 60-year-old man presented to the emergency department complaining of persistent right-sided chest pain and cough. The chest pain was pleuritic in nature and had been present for the last month. The associated cough was productive of yellow sputum without hemoptysis. He had unintentionally lost approximately 30 pounds over the last 6 months and had nightly sweats. He had denied fevers, chills, myalgias or vomiting. He also denied sick contacts or a recent travel history. He recalled childhood exposures to persons afflicted with tuberculosis. 

The patient smoked one pack of cigarettes daily for the past 50 years and denied recreational drug use. He reported ingesting twelve beers daily and had had delirium tremens, remote right-sided rib fractures and a wrist fracture as a result of alcohol consumption. He had worked in the steel mills but had discontinued a few years previously. He collected coins and cleaned them with mercury. 

The patient’s past medical history was remarkable for chronic “shakes” of the upper extremities for which he had not sought medical attention. Other than daily multivitamin tablets, he took no regular medications. 

Hospital course  He was initially admitted to the general medical floor for treatment of community-acquired pneumonia (see Figure 1) and for the prevention of delirium tremens. He was initiated on ceftriaxone, azithromycin, thiamine and folic acid. Diazepam was initiated and titrated using the Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWAS-Ar), a measure of withdrawal severity (1).  By hospital day 5, his respiratory status continued to worsen, requiring transfer to the intensive care unit (ICU) for hypoxemic respiratory failure. His neurologic status had also significantly deteriorated with worsening confusion, memory loss, drowsiness, visual hallucinations (patient started seeing worms) and worsening upper extremity tremors without generalized tremulousness despite receiving increased doses of benzodiazepines.

Physical Exam

White blood cell count was 11,000/mm 3 with 38% neutrophils, 8% lymphocytes, 18 % monocytes and 35% bands

Hematocrit 33%

Platelet count was 187,000/mm 3

Serum sodium was 125 mmol/L, potassium 3 mmol/L, chloride 91 mmol/L, bicarbonate 21 mmol/L, blood urea nitrogen 14 mg /dl, serum creatinine  0.6 mg/dl and anion gap of 14.

Urine sodium <10 mmol/L, urine osmolality 630 mosm/kg

Liver function tests revealed albumin 2.1 with total protein 4.6, normal total bilirubin, aspartate transaminase (AST) 49, Alanine transaminase (ALT) 19 and alkaline phosphatase 47.

Three sputum samples were negative for acid-fast bacilli (AFB).

Bronchoalveolar lavage (BAL) white blood cell count 28 cells/µl, red blood cell count 51 cells/µl, negative for AFB and negative Legionella culture.  BAL gram stain was without organisms or polymorphonuclear leukocytes.

Blood cultures were negative for growth.

Sputum cultures showed moderate growth of Pasteurella multocida.

2D transthoracic ECHO of the heart showed normal valves and an ejection fraction of 65% with a normal left ventricular end-diastolic pressure and normal left atrial size.  No vegetations were noted.

Purified protein derivative (PPD) administered via Mantoux testing was 8 mm in size at 72 hr after placement.

Human immunodeficiency virus (HIV) serology was negative. 

Arterial blood gas (ABG) analysis performed on room air on presentation to the ICU: pH 7.49, PaCO 2 29 mm Hg, PaO 2 49 mm Hg.

case study of respiratory failure

After admission to the ICU, the patient was noted to be in acute lung injury (ALI), a subset of acute respiratory distress syndrome (ARDS). The diagnosis of ALI requires all three of the following:  (a) bilateral pulmonary infiltrates, (b) a PaO 2 :FiO 2 ratio of ≤ 300 and (c) echocardiographic evidence of normal left atrial pressure or pulmonary-artery wedge pressure of ≤ 18 mm Hg (2). 

While patients with ALI and ARDS can be maintained with pressure-limited or volume-limited modes of ventilation, only volume assist-control ventilation was utilized in the ARDS Network multicenter randomized controlled trial that demonstrated a mortality benefit.

Noninvasive ventilation has not been demonstrated to be superior to endotracheal intubation in the treatment of ARDS or ALI and is not currently recommended (4).

This is a case of heavy metal poisoning with mercury.  The patient used mercury to clean coins.  Family members who had visited his house while he was hospitalized found several jars of mercury throughout his home.  The Environmental Protection Agency (EPA) was notified and visited the home.  They found aerosolized mercury levels of > 50,000 PPM and had the home immediately demolished. 

Alcoholic hallucinosis is a rare disorder occurring in 0.4 - 0.7% of alcohol-dependent inpatients (5).  Affected persons experience predominantly auditory but occasionally visual hallucinations.  Delusions of persecution may also occur.  However, in contrast to alcohol delirium, other alcohol withdrawal symptoms are not present and the sensorium is generally unaffected.

Delerium tremens (DT) occurs in approximately 5% of patients who withdraw from alcohol and is associated with a 5% mortality rate. DT typically occurs between 48 and 96 hr following the last drink and lasts 1-5 days.  DT is manifested by generalized alteration of the sensorium with vital sign abnormalities.  Death often results from arrhythmias, pneumonia, pancreatitis or failure to identify another underlying problem (6).  While DT certainly could have coexisted in this patient, an important initial step in the management of DT is to identify and treat alternative diagnoses.

Delirium is frequent among older patients in the ICU (7), and may be complicated by pneumonia and sepsis.  However, pneumonia and sepsis as causes for delirium are diagnoses of exclusion and should only be attributed after other possibilities have been ruled out. 

Frontal lobe stroke is unlikely, given the absence of other findings in the history or physical examination present to suggest an acute cerebrovascular event. 

In 1818, Dr. John Pearson coined the term erethism for the characteristic personality changes attributed to mercury poisoning (8).  Erethism is classically the first symptom in chronic mercury poisoning (9).  It is a peculiar form of timidity most evident in the presence of strangers and closely resembles an induced paranoid state.  In the past, when mercury was used in making top hats, the term “mad as a hatter” was used to describe the psychiatric manifestations of mercury intoxication.  Other neurologic manifestations include tremors, especially in patients with a history of alcoholism, memory loss, drowsiness and lethargy.  All of these were present in this patient. 

Acute respiratory failure (ALI/ARDS) can occur following exposure to inhalation of mercury fumes (10). Mercury poisoning has also been associated with acute kidney injury (11). 

Although all of the options mentioned above could possibly contribute to the development of delirium, only mercury poisoning would explain the constellation of findings of confusion, upper extremity tremors, visual hallucinations, somnolence and acute respiratory failure (ALI/ARDS).

Knowledge of the form of mercury absorbed is helpful in the management of such patients, as each has its own distinct characteristics and toxicity. There are three types of mercury: elemental, organic and inorganic. This patient had exposure to elemental mercury from broken thermometers. 

Elemental mercury is one of only two known metals that are liquid at room temperature and has been referred to as quicksilver (12). It is commonly found in thermometers, sphygmomanometers, barometers, electronics, latex paint, light bulbs and batteries (13).  Although exposure can occur transcutaneously or by ingestion, inhalation is the major route of toxicity.  Ingested elemental mercury is poorly absorbed and typically leaves the body unchanged without consequence (bioavailability 0.01% [13]). However, inhaled fumes are rapidly absorbed through the pulmonary circulation allowing distribution throughout the major organ systems.  Clinical manifestations vary based on the chronicity of the exposure (14).  Mercury readily crosses the blood-brain barrier and concentrates in the neuronal lysosomal dense bodies. This interferes with major cell processes such as protein and nucleic acid synthesis, calcium homeostasis and protein phosphorylation.  Acute exposure symptoms manifest within hours as gastrointestinal upset, chills, weakness, cough and dyspnea.

Inorganic mercury salts are earthly-appearing, red ore found historically in cosmetics and skin treatments.  Currently, most exposures in the United States occur from exposure through germicides or pesticides (15).  In contrast to elemental mercury, inorganic mercury is readily absorbed through multiple routes including the gastrointestinal tract.  It is severely corrosive to gastrointestinal mucosa (16).  Signs and symptoms include profuse vomiting and often-bloody diarrhea, followed by hypovolemic shock, oliguric renal failure and possibly death (12).

Organic mercury, of which methylmercury is an example, has garnered significant attention recently following several large outbreaks as a result of environmental contamination in Japan in 1956 (17) and grain contamination in Iraq in 1972 (18).  Organic mercury is well absorbed in the GI tract and collects in the brain, reaching three to six times the blood concentration (19).  Symptoms may manifest up to a month after exposure as bilateral visual field constriction, paresthesias of the extremities and mouth, ataxia, tremor and auditory impairments (12).  Organic mercury is also present in a teratogenic agent leading to development of a syndrome similar to cerebral palsy termed "congenital Minamata disease" (20).

The appropriate test depends upon the type of mercury to which a patient has been exposed.  After exposure to elemental or inorganic mercury, the gold standard test is a 24-hr urine specimen for mercury.  Spot urine samples are unreliable.  Urine concentrations of greater than 50 μg in a 24-hr period are abnormal (21).  This patient’s 24-hr urine level was noted to be 90 μg.  Elemental and inorganic mercury have a very short half-life in the blood.

Exposure to organic mercury requires testing hair or whole blood.  In the blood, 90% of methyl mercury is bound to hemoglobin within the RBCs.  Normal values of whole blood organic mercury are typically < 6 μg/L. This patient’s whole blood level was noted to be 26 μg/L.  This likely reflects the large concentration of elemental mercury the patient inhaled and the substantial amount that subsequently entered the blood.

Mercury levels can be reduced with chelating agents such as succimer, dimercaprol (also known as British anti-Lewisite (BAL)) and D-penicillamine, but their effect on long-term outcomes is unclear (22-25).

  • Sullivan JT, Sykora K, Schneiderman J, et al. Assessment of alcohol withdrawal: the revised clinical institute withdrawal assessment for alcohol scale (CIWA-Ar). Br J Addict 1989;84:1353-1357.
  • Bernard GR, Artigas A, Brigham KL, et al. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 1994;149:818-824.
  • The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000;342:1301-1308.
  • Agarwal R, Reddy C, Aggarwal AN, et al. Is there a role for noninvasive ventilation in acute respiratory distress syndrome? A meta-analysis. Respir Med 2006;100:2235-2238.
  • Soyka M. Prevalence of alcohol-induced psychotic disorders. Eur Arch Psychiatry Clin Neurosci 2008;258:317-318.
  • Tavel ME, Davidson W, Batterton TD. A critical analysis of mortality associated with delirium tremens. Review of 39 fatalities in a 9-year period. Am J Med Sci 1961;242:18-29.
  • McNicoll L, Pisani MA, Zhang Y, et al. Delirium in the intensive care unit: occurrence and clinical course in older patients. J Am Geriatr Soc 2003;51:591-598.
  • Bateman T. Notes of a case of mercurial erethism. Medico-Chirurgical Transactions 1818;9:220-233.
  • Buckell M, Hunter D, Milton R, et al. Chronic mercury poisoning. 1946. Br J Ind Med 1993;50:97-106.
  • Rowens B, Guerrero-Betancourt D, et al. Respiratory failure and death following acute inhalation of mercury vapor. A clinical and histologic perspective. Chest 1991;99:185-190.
  • Aguado S, de Quiros IF, Marin R, et al. Acute mercury vapour intoxication: report of six cases. Nephrol Dial Transplant 1989;4:133-136.
  • Ibrahim D, Froberg B, Wolf A, et al. Heavy metal poisoning: clinical presentations and pathophysiology. Clin Lab Med 2006;26:67-97, viii.
  • A fact sheet for health professionals - elemental mercury. Available from: http://www.idph.state.il.us/envhealth/factsheets/mercuryhlthprof.htm
  • Clarkson TW, Magos L, Myers GJ. The toxicology of mercury - current exposures and clinical manifestations. N Engl J Med 2003;349:1731-1737.
  • Boyd AS, Seger D, Vannucci S, et al. Mercury exposure and cutaneous disease. J Am Acad Dermatol 2000;43:81-90.
  • Dargan PI, Giles LJ, Wallace CI, et al. Case report: severe mercuric sulphate poisoning treated with 2,3-dimercaptopropane-1-sulphonate and haemodiafiltration. Crit Care 2003;7:R1-6.
  • Eto K. Minamata disease. Neuropathology 2000;20:S14-9.
  • Bakir F, Damluji SF, Amin-Zaki L, et al. Methylmercury poisoning in Iraq. Science 1973;181:230-241.
  • Berlin M, Carlson J, Norseth T. Dose-dependence of methylmercury metabolism. A study of distribution: biotransformation and excretion in the squirrel monkey. Arch Environ Health 1975;30:307-313.
  • Harada M. Congenital Minamata disease: intrauterine methylmercury poisoning. Teratology 1978;18:285-288.
  • Graeme KA, Pollack CVJ. Heavy metal toxicity Part I: Arsenic and mercury. J Emerg Med 1998;16:45-56.
  • Aaseth J, Frieheim EA. Treatment of methylmercury poisoning in mice with 2,3-dimercaptosuccinic acid and other complexing thiols. Acta Pharmacol Toxicol (Copenh) 1978;42:248-252.
  • Archbold GP, McGuckin RM, Campbell NA. Dimercaptosuccinic acid loading test for assessing mercury burden in healthy individuals. Ann Clin Biochem 2004;41:233-236.
  • Kosnett MJ. Unanswered questions in metal chelation. J Toxicol Clin Toxicol 1992;30:529-547.
  • Zimmer LJ, Carter DE. The efficacy of 2,3-dimercaptopropanol and D-penicillamine on methyl mercury induced neurological signs and weight loss. Life Sci 1978;23:1025-1034.

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case study of respiratory failure

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BEEM Cases 3 – Acute Respiratory Failure: NIPPV & POCUS

acute respiratory failure

BEEM Cases 3 on EM Cases – Acute Respiratory Failure. BEEM Cases  is a collaboration between Andrew Worster of Best Evidence in Emergency Medicine (BEEM) and Emergency Medicine Cases’ Anton Helman, Rory Spiegel and Justin Morgenstern.

Written by Justin Morgenstern (@First10EM), edited by Anton Helman (@EMCases), September 2016

Dypnea & Acute Respiratory Failure: Sometimes the Cause is Not So Obvious

The case….

A 73-year-old woman presents to the emergency department via EMS with increasing shortness of breath and cough over the past day. She has a history of COPD, CHF, hypertension, and hyperlipidemia. On arrival, she is breathing rapidly at 34 breaths a minute and is using all her accessory muscles. Her heart rate is 115, BP 155/95, Temp 37.5 and oxygen saturation 89% on 4L via nasal cannula. You perform a rapid physical exam, but you still aren’t sure exactly what is causing her dyspnea. Your RT turns to you and asks what you’d like to do.

Shortness of breath is a very common chief complaint in the emergency department, but despite our familiarity with this symptom, management is not always straightforward. The differential diagnosis is extensive, including the common cardiorespiratory conditions, but extending to toxicologic, hematologic, neuromuscular, metabolic, and psychiatric causes. Over the past decade, we have seen the widespread adoption of new technologies to help us manage these patients. This post will look at some new evidence on two of those technologies: noninvasive positive pressure ventilation (NIPPV) and ultrasound (POCUS). We will answer 3 questions based on 3 systematic reviews using the BEEM critical appraisal framework:

Question #1

Does noninvasive positive pressure ventilation (NIPPV) reduce mortality in acute respiratory failure?

Jump to Question 1 Discussion

Question #2

Does prehospital CPAP or BiPAP improve clinical outcomes for patients in acute respiratory failure?

Jump to Question 2 Discussion

Question #3

What is the sensitivity and specificity of POCUS using B-lines in diagnosing acute cardiogenic pulmonary edema in patients presenting to the ED with acute dyspnea?

Jump to Question 3 Discussion

Question #1 Does noninvasive positive pressure ventilation (NIPPV) reduce mortality in acute respiratory failure?

Cabrini L, Landoni G, Oriani A. Noninvasive ventilation and survival in acute care settings: a comprehensive systematic review and metaanalysis of randomized controlled trials. Critical care medicine. 43(4):880-8. 2015.

Study details (PICO)

Systematic review and meta-analysis

Key results

This meta-analysis found 78 trials that fit the inclusion criteria, with a total of 7365 patients. For the primary outcome of mortality, they found that noninvasive positive pressure ventilation decreased overall mortality (RR=0.73 [95% CI: 0.66, 0.81]) with a NNT=19.

BE EM   critique

This is the largest review of NIPPV to date and its primary outcome is mortality, the ultimate clinical outcome. Although 60% of the data is from the ICU setting, the results are probably still applicable to the ED and provide convincing evidence that patients with acute respiratory distress (except asthma) should be considered for NIPPV as a first line therapy. The suggestion that early NIPPV is better than late requires further study.

Key EBM point : Heterogeneity. The trials included in this meta-analysis displayed high heterogeneity. This simply means that the trials were different from each other in some way. There are two key types of heterogeneity. Clinical heterogeneity occurs when there is variability in key clinical aspects of trials. For example, two trials may look at different populations of patients or measure different outcomes. Statistical heterogeneity refers to the likelihood that the variability among the different results (one trial might report a 2% benefit whereas another reports a 18% benefit) is due to chance alone. Heterogeneity matters because if trials are too dissimilar it may not be appropriate to combine them into a single statistical analysis.

Case continued…

You start the patient on BiPAP and within 10 minutes her numbers have improved and she looks a lot better. One of the paramedics who brought her in is surprised by the rapid improvement and asks you if they should be starting some kind of non-invasive ventilation in the ambulance before arriving at the emergency department.

Question #2 Does NIPPV improve clinical outcomes in acute respiratory failure?

Goodacre S, Stevens JW, Pandor A. Prehospital noninvasive ventilation for acute respiratory failure: systematic review, network meta-analysis, and individual patient data meta-analysis. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 21(9):960-70. 2014.

Primary outcome (mortality): Key results

  • CPAP reduced morality (OR=0.41; 95% credible interval [Crl] 0.20 to 0.77)
  • The effect of BiPAP on mortality was unclear (OR=1.94; 95% Crl = 0.65 to 6.14)

Secondary outcome (intubation):

  • CPAP reduced intubations (OR=0.32; 95% Crl 0.17 to 0.62)
  • The effect of BiPAP on intubation was unclear (OR=0.40; 95% Crl = 0.14 to 1.16)

The benefits of NIPPV for patients in acute respiratory failure are well documented. Also, NIPPV is likely to be most effective when introduced early. The evidence supporting at least CPAP from this study is encouraging but differences in outcomes between CPAP and BiPAP reflects more upon the lack of large RCTs rather than the actual clinical difference between them. Regardless, the cost of equipping ambulances with NIPPV gear has to be taken into consideration when assessing its effectiveness in the prehospital setting.

The patient is improving, but you still aren’t sure about the diagnosis. There might have been an elevated JVP, but her neck isn’t easy to examine. The lungs sound a little wheezy, but there were probably some fine crackles there as well. You are resigned on waiting for the chest x-ray, when your resident asks if lung ultrasound might help diagnose pulmonary edema.

Question #3 Accuracy of POCUS for Diagnosing Acute Heart Failure

What is the sensitivity and specificity of point of care ultrasound (POCUS) using B-lines in diagnosing acute cardiogenic pulmonary edema in patients presenting to the ED with acute dyspnea?

Al Deeb M, Barbic S, Featherstone R, Dankoff J, Barbic D. Point-of-care ultrasonography for the diagnosis of acute cardiogenic pulmonary edema in patients presenting with acute dyspnea: a systematic review and meta-analysis. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 21(8):843-52. 2014.

They identified 7 studies that included a total of 1075 patients. Two of the studies were ED studies. The other 5 took place in the ICU, hospital wards, or prehospital environment.

Diagnostic characteristics:

  • Sensitivity of B lines of POCUS to diagnose acute pulmonary edema: 94% [95% CI: 81.3%, 98.3%]
  • Specificity of B lines of POCUS to diagnose acute pulmonary edema: 92% [95% CI: 84.2%, 96.4%]
  • Positive likelihood ratio 12.4 [95% CI: 5.7, 26.8]
  • Negative likelihood ratio 0.06 [95% CI: 0.02, 0.22]

The question asked in this review is relevant but as the authors admit, there is no standardized threshold for the diagnosis of acute cardiac pulmonary edema (ACPE) and no definitive gold standard. Like the first study reviewed in this BEEM Cases, this one was too heterogeneous. While this study was exhaustive in searching for ultrasound diagnostics performed at the bedside it was not restrictive in settings, patient demographics, or ultrasound training of provider and this would lead to heterogeneity. Another issue that contributes to the heterogeneity and challenges the validity of the results is the lack of standardization of the ultrasound exam: The identification of ACPE using B-lines via the Volpicelli method is dependent upon patient position as well as position duration.

The conclusion that B-line on ultrasound can confirm the diagnosis when the pretest probability of disease is high or low has little utility. Diagnostic tests are valuable when they can confirm or refute a diagnosis when the pretest probability is indeterminate.

Case Resolution…

The patient rapidly improves after being placed on BiPAP. Your bedside ultrasound was consistent with CHF, but understanding the limitations of the test you also ordered your traditional work-up including blood work, ECG, and chest x-ray. Within a few hours in the department, after treatment with nitroglycerin and furosemide, you are able to titrate down and then discontinue the positive pressure ventilation. On a repeat bedside ultrasound, the b-lines have disappeared. Combining the ultrasound findings with the remainder of your tests, and most importantly your clinical judgement and frequent reassessments of the patient, you diagnose her with an exacerbation of CHF and admit her to the medical team for monitoring and adjustment of her medications.

About the Author: Anton Helman

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Hi Anton, great post! Q # 1 – The majority of trials are on patients with either COPD exacerbation or ACPE. For these 2 categories, NPPV efficacy in terms of ETI reduction and mortality are okay. Bottom line 1: NPPV is first choice in ACPE or COPDex – Acute hypoxemic respiratory failure (except ACPE) is still controversial. Few positive RCTs on pneumonia (Confalonieri M goo.gl/K4EHZV, Brambilla AM goo.gl/uKKDpx, Cosentini R goo.gl/rReh7f), one recent positive RCT on ARDS (Patel BK oo.gl/lKNqkv). Bottom line2: NPPV for pneumonia –> 1. okay in the immunocompromised population, 2. In the immunocompetent population: early application, that is patient selection is the key (and short trial) – ARDS. Patient selection seems the key, however needs further confirmation – Asthma. Primum non nocere!

Q # 2 Pre-hospital NPPV modality of choice might be CPAP. 1.The majority of patients have AHF/ACPE, 2. easier to learn and carry, 3. cheaper

Q # 3 LUS is already in every acute dyspnoea algorythm (Lichtenstein blue protocol goo.gl/yEy6ug) When in doubt (pretest probability indeterminate) more useful if negative (SNOUT) than positive (SPIN), since interstitial syndrome might be due to other causes (pneumonia, ARDS, fibrosis)

Thanks again for your work Roberto

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Thanks for the excellent comment Roberto.

With regards to question one, I think you hit on the key issue. Acute respiratory failure is not a single condition, but actually a collection of many different conditions, and NIPPV might (and probably does) have different effects on different conditions. This is a large part of the BEEM focus on the heterogeneity of the underlying trials. Although not the focus of the paper, NIPPV clearly has an indication in COPD and CHF (as well as ARDS and post-extubation, but those are less relevant in the emergency department). There aren’t great studies in asthma, but I think the evidence favours NIPPV. I definitely use NIPPV early in severe asthma. I would not use NIPPV long term in pneumonia. However, I think the key take home for the emergency department, where we have undifferentiated patients, is that NIPPV seems to lower mortality overall, and should be started early while we work on determining the underlying cause of this patient’s respiratory distress.

With regards to pre-hospital NIPPV, ease of use and cost are definitely important issues. (I would also like to see more compatibility between prehospital equipment and inhospital equipment, both for cost and ease of patient care.) Unless we see large advantages to BiPAP, and I agree that CPAP probably makes the most sense for EMS. However, all of the questions are relatively complex. EMS agencies with longer transport time might benefit from BiPAP – although that assumption currently doesn’t have any evidence to back it up.

In terms of lung ultrasound, I will tell you I use it every shift. However, the widespread use of ultrasound and adoption into protocols does not mean that we are practicing evidenced based medicine. I think the numbers here (which are pretty consistent with all the studies I have seen, including that Lichtenstein paper) show that lung ultrasound is about as accurate for ruling in as it is for ruling out (sensitivity and specificity are both in the low to mid 90s). However, the studies that give us those number have a number of issues that could be inflating the accuracy. The diagnosis in many patients is obvious without ultrasound, and the patients who are less obvious clinically are also less obvious on ultrasound. I love ultrasound an will continue to use it, with the caveat that in the initially undifferentiated patient (pretrest probability of 50%), the numbers reported for ultrasound don’t get be above a 95% post test probability if positive, nor do they get me under a 5% post test probability if negative, so I am am constantly aware that my ultrasound diagnosis might be wrong.

Cheers Justin

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  • Open access
  • Published: 10 March 2023

Guideline-based management of acute respiratory failure and acute respiratory distress syndrome

  • Seitaro Fujishima   ORCID: orcid.org/0000-0001-8823-8440 1  

Journal of Intensive Care volume  11 , Article number:  10 ( 2023 ) Cite this article

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Acute respiratory failure (ARF) is defined by acute and progressive hypoxemia caused by various cardiorespiratory or systemic diseases in previously healthy patients. Among ARF, acute respiratory distress syndrome (ARDS) is a serious condition with bilateral lung infiltration, which develops secondary to a variety of underlying conditions, diseases, or injuries. This review summarizes the current standard of care for ARF and ARDS based on current major guidelines in this field. When administering fluid in patients with ARF, particularly ARDS, restrictive strategies need to be considered in patients without shock or multiple organ dysfunction. Regarding oxygenation targets, avoiding excessive hyperoxemia and hypoxemia is probably a reasonable choice. As a result of the rapid spread and accumulation of evidence for high-flow nasal cannula oxygenation, it is now weakly recommended for the respiratory management of ARF in general and even for initial management of ARDS. Noninvasive positive pressure ventilation is also weakly recommended for the management of certain ARF conditions and as initial management of ARDS. Low tidal volume ventilation is now weakly recommended for all patients with ARF and strongly recommended for patients with ARDS. Limiting plateau pressure and high-level PEEP are weakly recommended for moderate-to-severe ARDS. Prone position ventilation with prolonged hours is weakly to strongly recommended for moderate-to-severe ARDS. In patients with COVID-19, ventilatory management is essentially the same as for ARF and ARDS, but awake prone positioning may be considered. In addition to standard care, treatment optimization and individualization, as well as the introduction of exploratory treatment, should be considered as appropriate. As a single pathogen, such as SARS-CoV-2, exhibits a wide variety of pathologies and lung dysfunction, ventilatory management for ARF and ARDS may be better tailored according to the respiratory physiologic status of individual patients rather than the causal or underlying diseases and conditions.

Introduction

Acute respiratory failure (ARF) is defined as acute and progressive hypoxemia developing within hours, days, or up to a month caused by various respiratory, cardiovascular, or systemic disease in previously healthy patients. ARF is distinguished from chronic respiratory failure and acute exacerbations of underlying respiratory disease.

Among ARF, acute respiratory distress syndrome (ARDS) is a serious condition associated with bilateral lung infiltration. ARDS may develop secondary to a variety of underlying conditions, diseases, or injuries (Table 1 ) [ 1 ]. Neutrophil-dominant acute inflammation and diffuse alveolar damage (DAD) with the presence of hyaline membranes are observed on histological examination of lung tissues from patients with ARDS. The pathophysiology of ARDS includes an increase in pulmonary microvascular permeability with resultant pulmonary edema due to tissue injury and disruption of vascular regulatory mechanisms. ARDS was initially described as a single organ dysfunction, but is now recognized as one component of multiple organ dysfunction syndrome.

Currently available guidelines for ARF and ARDS

To date, there are currently no guidelines which cover all aspects of ARF. However, several guidelines for airway and ventilatory management are available and are referred in the following sections. In addition, the Japanese clinical practice guidelines for management of sepsis and septic shock 2020 (J-SSCG 2020) includes several clinical questions and recommendations which can be extrapolated to ARF in general [ 2 ].

With regard to ARDS, the American Thoracic Society (ATS), European Society of Intensive Care Medicine (ESICM), and Society of Critical Care Medicine (SCCM) have published a joint guideline on mechanical ventilation in adult patients with ARDS. In addition, guidelines for ARDS have been published by the Faculty of Intensive Care Medicine (FICM) and Intensive Care Society (ICS) of United Kingdom (jointly as guidelines on the management of acute respiratory distress syndrome: FICM/ICS-ARDS-GL2018), Société de Réanimation de Langue Française (SRLF) of France (management of acute respiratory distress syndrome: SRLF-ARDS-GL2019), Scandinavian Society of Anaesthesiology and Intensive Care Medicine (SSAI; Scandinavian clinical practice guideline on mechanical ventilation in adults with the acute respiratory distress syndrome: SSAI-ARDS-GL2016), and Korean Society of Critical Care Medicine (KSCCM) and Korean Academy of Tuberculosis and Lung Diseases (KATRD) of South Korea (jointly as the clinical practice guideline of acute respiratory distress syndrome: KSCCM/KATRD-ARDS-GL2016) [ 3 , 4 , 5 , 6 , 7 , 8 ]. In Japan, an initial guideline was developed in 2005 by the Japanese Respiratory Society (JRS), with the latest version jointly published in 2022 by the JRS, Japanese Society of Intensive Care Medicine (JSICM), and Japanese Society of Respiratory Care Medicine (JSRCM) as the ARDS clinical practice guideline 2021 (Japanese ARDS-GL2021) [ 9 ]. In addition, the Surviving Sepsis Campaign Guidelines (international guidelines for management of sepsis and septic shock 2021; SSCG2021) also include clinical questions regarding ventilatory management.

Since early 2020, novel coronavirus-induced disease 2019 (COVID-19) has become a major cause of ARF and ARDS. The large number of cases caused by a single microorganism is unprecedented in modern times. The above-mentioned guidelines are generally applicable to ARF and ARDS caused by COVID-19. However, specific guidelines for the management of COVID-19 should also be consulted as many international and regional guidelines for COVID-19 have now been published [ 10 ] based on evidence specific to COVID-19.

Diagnosing ARF and ARDS

ARF is typically diagnosed according to a PaO 2  ≤ 60 Torr at room air or PaO 2 /FIO 2 ratio ≤ 300. ARF can be caused by a range of lung, heart, or other systemic diseases and conditions. American College of Physicians has developed a guideline for the appropriate use of point-of-care ultrasonography in patients with acute dyspnea, and weakly recommends its use in addition to the standard diagnostic pathway when there is diagnostic uncertainty [ 11 ].

The clinical diagnosis of ARDS is currently based on the Berlin definition: (1) PaO 2 /FIO 2 ratio ≤ 300 under positive end-expiratory pressure (PEEP)/continuous positive airway pressure (CPAP) ≥ 5 cmHO 2 ; (2) acute onset within a week; (3) bilateral shadows in the lung fields, and (4) respiratory failure that cannot be explained by cardiac failure or excess fluid alone [ 12 ]. Recently, high-flow nasal cannula oxygenation (HFNC, also called high-flow nasal oxygen therapy: HFNO or nasal high flow therapy: NHFT) and noninvasive positive pressure ventilation (NPPV, also called NIV) have become widely used, with an SpO 2 /FIO 2 ratio ≤ 315 irrespective of PEEP proposed as an alternative criterion of ARDS [ 13 ].

Fluid balance assessments, levels of plasma brain natriuretic peptide (BNP) or serum NT-proBNP, and echocardiographic evaluation are clinically used in differentiating ARDS from hydrostatic pulmonary edema. In JRS/JSICM/JSRCM-GL2021, a systematic review reported a sensitivity of 0.77 and specificity of 0.62 for a cutoff value of 400–500 pg/mL for BNP, sensitivity of 0.50 and specificity of 0.82 for a cutoff value of 1000 pg/mL, and sensitivity of 0.71 and specificity of 0.89 for a cutoff value of 4000 pg/mL for NT-proBNP when differentiating ARDS from hydrostatic pulmonary edema. According to these results, the use of serum BNP or NT-proBNP levels is weakly recommended [ 9 ]. In patients with severe ARDS, measurement of extravascular lung water using transpulmonary thermodilution should be considered. Measurement of pulmonary artery wedge pressure by invasive right heart catheterization is now rarely performed.

After clinical exclusion of hydrostatic pulmonary edema, the diagnosis of ARDS is made according to the aforementioned diagnostic criteria. However, it is still necessary to rule out ARDS mimics, particularly those with established treatments (Table 2 ) [ 1 , 14 ]. Bronchoalveolar lavage is particularly useful in differentiating various respiratory infections, acute eosinophilic pneumonia, cryptogenic organizing pneumonia, interstitial pneumonia, hypersensitivity pneumonitis, alveolar hemorrhage, and drug-induced lung injury.

Management of ARF and ARDS

In this section, the current standard approach to the management of ARF and ARDS is presented based on recent guidelines. Recommendations for ARF are given in SSCG2021, J-SSCG2020, and SRLF-GL2019, and are summarized in Table 3 . For ARDS, recommendations for ventilatory management are summarized in Table 4 , and those for adjunctive therapies are presented in Table 5 . Key topics in the above-mentioned guidelines are discussed below with reference to recent evidence.

  • Oxygenation targets

The traditional treatment strategy regarding oxygenation in ARF is to maintain adequate oxygenation to avoid the risk of hypoxemia. On the other hand, it has been customary to aim for an FIO 2  ≤ 60% to avoid hyperoxic lung injury in ventilated patients. However, a recent systematic review and cohort study reported a positive association between hyperoxemia and poor survival. As a result, optimal oxygenation targets have again become a topic of discussion [ 15 , 16 ]. After 2016, six RCTs comparing groups with lower and higher oxygen targets were published, with none reporting a significant difference in primary outcomes between the two groups [ 17 , 18 , 19 , 20 , 21 ]. In these studies, the actual difference between study groups was 15–28 mmHg in PaO 2 or 1–4% in SaO 2 , and PaO 2 was maintained between 70 and 110 mmHg in both groups in all studies. These situations have resulted in inconsistent recommendations between SSCG2021, J-SCG2020, and JRS/JSICM/JSRCM-GL2021 as shown in Tables 3 and 4 . As a recent network meta-analysis demonstrated decreased survival in patients with a PaO 2 target of 55–75 mmHg and patients with a PaO 2  ≥ 150 mmHg, it seems appropriate to follow the traditional oxygenation strategy that avoids excess hypoxemia and hyperoxemia [ 22 ]. In patients with acute exacerbation of chronic obstructive pulmonary disease (COPD), an SaO 2 of 88% to 92% is considered an adequate oxygenation target, as suggested by a recent observational study [ 23 ].

Ventilatory management

In ARF, the choice between the use of nasal cannula, HFNC, NPPV, or invasive positive pressure ventilation (IPPV) is based on the presence of underlying disease and severity of hypoxemia. In the HFNC guidelines by the American College of Physicians, HFNC was weakly recommended for ARF over NPPV due to a systematic review reporting that HFNC for ARF is associated with lower mortality and a lower intubation rate compared to NPPV [ 24 ]. For patients with ARF post-extubation, a separate systematic review suggested that HFNC may reduce the reintubation rate and improve patient comfort compared with conventional oxygen therapy, and thus was also weakly recommended. The European Respiratory Society (ERS)/ATS guidelines recommend bilevel positive airway pressure (bilevel-PAP) for patients with acute exacerbation of COPD accompanied by acute hypercarbia, CPAP for cardiogenic pulmonary edema, and NPPV for post-operative setting and early ARF in immunosuppressed patients [ 25 ]. Regarding ARDS, IPPV has been the gold standard; however, HFNC and NPPV are weakly recommended as alternative options to initial management in JRS/JSICM/JSRCM-GL2021.

The benefit of low tidal volume ventilation with IPPV has been demonstrated not only in ARDS, but also in ARF. Low tidal volume ventilation is weakly recommended for ARF in SSCG2021 and SRLF-GL2019, and strongly recommended for ARDS in JRS/JSICM/JSRCM-GL2021, SSCG2021, SRLF-GL2019 and FICM/ICS-GL2018. In J-SSCG2020, lung protective ventilation is weakly recommended for ARF.

Limiting plateau pressure and high-level PEEP is recommended weakly to strongly in all guidelines, although the most recent Cochrane analysis did not find a survival benefit for high-level PEEP [ 26 ]. Prone position ventilation with prolonged hours is weakly to strongly recommended for moderate-to-severe ARDS in all guidelines. Regarding recruitment maneuvers, JRS/JSICM/JSRCM-GL2021 recommends against their routine use while the SSCG 2021 weakly recommends the traditional recruitment maneuver of applying an airway pressure of 30–40 cm H 2 O for 30–40 s [ 9 , 27 , 28 ]. Early and limited use of muscle relaxants are weakly to strongly recommended for patients with moderate to severe ARDS. There are weak-to-strong recommendations against the use of high-frequency oscillatory ventilation (HFOV).

Fluid management

There are currently no standardized guidelines for fluid management in ARF; however, daily fluid balance assessments are fundamentally important in reducing the risk of iatrogenic pulmonary edema. Even mild fluid overload may worsen pulmonary edema and thereby exacerbate hypoxemia in patients with ARDS due to an increase in pulmonary microvascular permeability. A recent systematic review reported that restrictive fluid management improves oxygenation and prolongs ventilator-free days, but does not improve mortality in patients with sepsis or ARDS [ 29 ]. Based on this evidence, the JRS/JSICM/JSRCM-GL2021 and FICM/ICS-GL 2018 weakly recommend restrictive fluid management [ 4 , 9 ].

On the other hand, stabilization of vital signs with fluid resuscitation is essential in sepsis and septic shock, which is a major cause of ARDS. Accordingly, an appropriate fluid management strategy should be selected in patients with ARDS depending on the presence of other organ dysfunction or hemodynamic shock [ 30 ]. In the most recent RCT for patients with septic shock, a trend toward increased survival was observed in a subgroup with respiratory support, although restrictive fluid management did not show overall survival benefit [ 31 ], supporting the use of the above strategy. In severe cases, echocardiography and measurement of central venous pressure should be performed to monitor fluid responses and inform fluid administration.

Pharmacotherapy

In ARF, pharmacotherapy should be focused on the underlying disease or diseases that are causing hypoxemia. For ARDS, corticosteroids are often administered worldwide including Japan [ 32 ]. However, the results of RCTs for pharmacological treatment of ARDS have been mixed due to diversity in the causes and severity of ARDS and the effects of the type, timing of administration, dosage, and duration of administration of corticosteroids. Accordingly, corticosteroid administration is considered both a standard and exploratory treatment for ARDS. The latest RCT “DEXA-ARDS” included 277 patients with a PaO 2 /FIO 2  ≤ 200 mmHg under PEEP ≥ 10 cmHO 2 and a FIO 2  ≥ 0.5 at 17 Spanish intensive care units. Patients in the dexamethasone group were treated with 20 mg intravenous dexamethasone (methylprednisolone equivalent 100–120 mg) daily for five days and 10 mg for additional five days [ 33 ]. A recent systematic review that included 18 RCTs also demonstrated a net survival benefit for corticosteroids in patients with ARDS of any cause [ 34 ]. Based on these findings, it can be suggested that although older versions such as SSAI-ARDS-GL2016 and KSCCM/KATRD-ARDS-GL2016 are against the use of corticosteroids, their use is weakly to strongly recommended in the more recent JRS/JSICM/JSRCM-GL2021 and FICM/ICS-GL2018. Guidelines for the diagnosis and management of critical illness-related corticosteroid insufficiency (CIRCI) include ARDS and weakly recommend the use of corticosteroids [ 35 ].

A specific neutrophil elastase inhibitor, sivelestat, was developed and approved for the treatment of acute lung injury associated with systemic inflammatory response syndrome in Japan. In the Japanese ARDS guidelines 2016, a systematic review was performed including data from the Japanese phase III trial and the international phase III STRIVE study, with no difference in survival or ventilator-free days observed [ 1 ]. Based on these findings, the latest JRS/JSICM/JSRCM-GL2021 also weakly recommends against the routine use of sivelestat.

In situations where respiratory infections cannot be ruled out, the use of broad-spectrum antibiotic regimens including a macrolide or new quinolone is often considered. Antimicrobial therapy against methicillin-resistant Staphylococcus aureus , Pneumocystis jirovecii , fungi, Mycobacterium tuberculosis , viruses, and SARS-CoV-2 may also be considered as appropriate.

Extracorporeal membrane oxygenation

The benefit of extracorporeal membrane oxygenation (ECMO) has been clarified in recent studies, with ECMO now weakly recommended for severe ARDS in most guidelines. The systematic review of the newest JRS/JSICM/JSRCM-GL2021 included two RCTs (CESAR and EOLIA studies) and found a significant decrease in 60-day and 90-day mortalities but no increase in the incidence of stroke [ 9 ].

However, it is important to recognize and follow the accepted indications and contraindications for ECMO to obtain improved implementation results. In the latest ELSO guidelines, common indications for veno-venous ECMO are: (1) hypoxemic respiratory failure (PaO 2 /FiO 2  < 80 mmHg) after optimal medical management including, in the absence of contraindications, a trial of prone positioning; (2) hypercapnic respiratory failure (pH < 7.25) despite optimal conventional mechanical ventilation (respiratory rate 35 breaths per minute and plateau pressure [Pplat] ≤ 30 cm H 2 O); and (3) ventilatory support as a bridge to lung transplantation or primary graft dysfunction following lung transplantation [ 36 ]. Central nervous system hemorrhage, significant central nervous system injury, irreversible and incapacitating central nervous system pathology, systemic bleeding, contraindications to anticoagulation, immunosuppression, older age (increasing risk of death with increasing age but no threshold is established), and mechanical ventilation for more than seven days with a Pplat > 30 cm H 2 O and an FiO 2  > 90% are listed as relative contraindications to ECMO.

A certain proportion of patients with COVID-19 develop ARF and ARDS depending on patient age, comorbidities, immune status, and SARS-CoV-2 virus genotype among other factors. Although there are rare cases with a rapidly progressive course, the progression of the disease is typically slow and the number of days from the onset of symptoms to the start of artificial ventilation is as high as 3–4 days for the original variant of SARS-CoV-2 [ 37 ]. The rate of severe illness is lower in Omicron variants of SARS-CoV-2 compared to Delta variants; however, the mortality of the patients once admitted to ICU does not differ between Omicron and Delta variants [ 38 ].

In the chaotic early stages of the COVID-19 pandemic, a specific phenotype of COVID-19-induced ARDS with higher lung compliance was proposed and discussed [ 39 ]. However, after the accumulation of numerous cases worldwide over more than two years, a recent systematic review did not find evidence of a specific phenotype of ARDS related to COVID-19 [ 40 ]. These findings indicate that the management of ARF and ARDS in patients with COVID-19 should be the same as for other causes. However, parameters of mechanical ventilation, including PEEP, should be individualized based on the ventilatory and systemic condition of individual patients [ 41 ]. Pharmacological therapies, including corticosteroids, should be administered according to the guidelines and statements specific to COVID-19.

In addition to standard ventilatory management, the benefits of awake prone positioning for non-intubated patients have been posited and examined. Although the results of RCTs are conflicting, a recent systematic review demonstrated a reduced risk of endotracheal intubation with awake prone positioning [ 42 ].

The criteria for the introduction of ECMO and the survival rate in COVID-19 are similar to those in other diseases; however, the duration of ECMO use tends to be longer in patients with COVID-19 [ 43 ]. In a recent systematic review, increased mortality was reported to be associated with older age, male sex, chronic lung disease, longer duration of symptoms, longer duration of invasive mechanical ventilation, higher PaCO 2 , higher driving pressure, and less previous experience with ECMO [ 44 ].

Concluding remarks

ARF and ARDS develop secondary to a wide variety of diseases and conditions, and the mechanisms of hypoxemia are varied. This review summarized the current standard of care for ARF and ARDS based on major guidelines in this field. As has been repeatedly mentioned, “standard” care needs to be continually updated considering new evidence. In addition to standard care, treatment optimization and individualization as well as the introduction of exploratory treatment should be considered appropriate. In light of the fact that even a single pathogen, such as SARS-CoV-2, exhibits a wide variety of pathologies and lung dysfunction, ventilatory management for ARF and ARDS may be suitably tailored according to the respiratory physiologic status of individual patients rather than the causal or underlying diseases and conditions.

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Abbreviations

  • Acute respiratory distress syndrome
  • Acute respiratory failure

American Thoracic Society

Bilevel positive airway pressure

  • Brain natriuretic peptide

Critical illness-related corticosteroid insufficiency

Chronic obstructive pulmonary disease

Coronavirus-induced disease 2019

Continuous positive airway pressure

Diffuse alveolar damage

Extracorporeal Life Support Organization

European Society of Intensive Care Medicine

Faculty of Intensive Care Medicine

High-flow nasal cannula

High-flow nasal oxygen therapy

High-frequency oscillatory ventilation

Intensive Care Society

Invasive positive pressure ventilation

Japanese Respiratory Society

Japanese clinical practice guidelines for management of sepsis and septic shock 2020

Japanese Society of Intensive Care Medicine

Japanese Society of Respiratory Care Medicine

Korean Academy of Tuberculosis and Lung Diseases

Korean Society of Critical Care Medicine

Noninvasive ventilation

Nasal high-flow therapy

  • Noninvasive positive pressure ventilation

Positive end-expiratory pressure

Severe acute respiratory syndrome coronavirus 2

Society of Critical Care Medicine

Société de Réanimation de Langue Française

Scandinavian Society of Anaesthesiology and Intensive Care Medicine

Surviving Sepsis Campaign Guidelines

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Center for General Medicine Education, Keio University School of Medicine, 35 Shinanomachi, Shinjyuku-Ku, Tokyo, 160-8582, Japan

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Fujishima, S. Guideline-based management of acute respiratory failure and acute respiratory distress syndrome. j intensive care 11 , 10 (2023). https://doi.org/10.1186/s40560-023-00658-3

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The condition, patient course, lessons for the clinician, suggested readings, case 6: acute-onset respiratory failure in a 4-month-old girl.

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Dr Harper has disclosed no financial relationships relevant to this article. This commentary does not contain a discussion of an unapproved/investigative use of a commercial product/device.

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Beth D. Harper; Case 6: Acute-onset Respiratory Failure in a 4-month-old Girl. Pediatr Rev July 2017; 38 (7): 338–339. https://doi.org/10.1542/pir.2016-0093

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A 4-month-old girl presents with a 1-week history of a temperature to 102°F (38.9°C), congestion, rhinorrhea, and cough. She has had fatigue and diaphoresis with feedings over the last week, although this did not occur before this time. She was born at term following normal findings on prenatal ultrasonography. Initially, she had difficulty gaining weight, but she is now growing along the 10th percentile. She had 1 overnight hospitalization for bronchiolitis at age 2 months and was treated with albuterol for a total of 1 week. Her mother has a history of asthma in childhood.

On physical examination, the girl is febrile and has a heart rate of 150 beats/min, respiratory rate of 46 breaths/min, and intercostal and subcostal retractions. Chest auscultation reveals bilateral coarse breath sounds. A rapid respiratory syncytial virus (RSV) antigen test is positive, and she is admitted to the inpatient ward. She remains tachycardic, with an increased heart rate to 170 beats/min. Following administration of a 20-mL/kg normal saline bolus, her respiratory distress acutely worsens. Her respiratory rate increases to 70 breaths/min and she exhibits head bobbing with ongoing retractions. Re-examination reveals a new S3 gallop on auscultation, and a liver edge is now palpable. Chest radiography shows haziness in both lung fields, small pleural effusions bilaterally, and an enlarged cardiac silhouette ( Fig 1 ). Additional studies reveal the diagnosis.

Figure 1. Chest radiograph shows haziness in both lung fields, small pleural effusions bilaterally, and an enlarged cardiac silhouette.

Chest radiograph shows haziness in both lung fields, small pleural effusions bilaterally, and an enlarged cardiac silhouette.

The girl’s initial presentation was concerning for bronchiolitis, and she had an RSV infection confirmed. Other primary respiratory causes, including pneumonia and reactive airway disease, were also considered. However, cardiac dysfunction was suspected because of the development of gallop and a palpable liver edge after fluid administration. Electrocardiography showed left ventricular hypertrophy and deep Q waves in the inferior leads ( Fig 2 ). Infectious myocarditis and cardiomyopathies were considered. Her troponin T concentration was elevated at 0.03 ng/mL (0.3 μg/L). Echocardiography showed severe left ventricular dysfunction and a probable anomalous left coronary artery from the pulmonary artery (ALCAPA). At cardiac catheterization, the diagnosis of ALCAPA was confirmed.

Figure 2. Electrocardiography shows evidence of left ventricular hypertrophy (tall S waves in V1 and tall R waves in V6) and deep Q waves in the inferior leads.

Electrocardiography shows evidence of left ventricular hypertrophy (tall S waves in V1 and tall R waves in V6) and deep Q waves in the inferior leads.

ALCAPA, previously known as Bland-White-Garland syndrome, is a rare form of congenital heart disease. As the name implies, the left coronary artery originates from the pulmonary artery rather than branching from the aorta. At birth, the condition is often asymptomatic and unrecognized because physiologically elevated pulmonary artery pressure allows sufficient anterograde flow through the left coronary artery. With decreasing pulmonary pressures after birth, blood may not flow from the pulmonary artery into the aberrant coronary, resulting in the development of myocardial ischemia and necrosis in the first few postnatal months. In some affected infants, ischemia may be subclinical due to collateral coronary vessels originating from the right coronary artery. This may delay the development of symptoms and, therefore, the diagnosis.

ALCAPA is often diagnosed in the first few months after birth in infants presenting with cardiac dysfunction. Infants may present with myocardial ischemia, cardiac dysfunction, elevated cardiac enzymes, or cardiac failure and cardiogenic shock. Reported symptoms include failure to thrive, poor feeding, fatigue, and diaphoresis. It can also present with acute respiratory failure and sudden cardiac death and may mimic myocarditis. Although some of these clinical manifestations are due to changing infant cardiac physiology, a concurrent illness that adds stress to the cardiopulmonary system may also precipitate heart failure. However, there are cases of patients surviving into adulthood with undetected ALCAPA.

Chest radiography usually demonstrates cardiomegaly. Electrocardiography may reveal ischemia or infarction, particularly in the anterior leads. Echocardiography can often identify the anomalous origin of the left coronary artery. In some cases where there is low flow in the coronary artery, visualization on echocardiography may be difficult, and cardiac catheterization with direct angiography may be necessary to confirm the diagnosis and for preoperative planning. Without repair, the prognosis of ALCAPA is poor.

Treatment of ALCAPA is surgical correction. Such correction is often accomplished with a coronary transfer procedure in which the left main coronary artery is reimplanted into the aorta, although other operative procedures do exist. Mitral valve repair may also be indicated at the time of surgery. Myocardial function improves postoperatively, even in cases with prior ischemia. Prognosis is excellent following repair, with long-term follow-up studies demonstrating greater than 98% survival at 20 years and low rates of repeat surgery. Results of echocardiography, electrocardiography, and chest radiography also normalize.

The girl was intubated and started on inotropic support. She underwent cardiac surgery 1 day after admission, recovered well, and was discharged 2 weeks later.

Heart failure should be considered in cases of respiratory failure that are not responsive to supportive care or that worsen with fluid administration.

Fluid boluses should be administered with caution in the setting of suspected heart failure.

Anomalous left coronary artery from the pulmonary artery (ALCAPA) can cause myocardial ischemia in infancy, and its acute presentation may mimic myocarditis.

The prognosis for ALCAPA is excellent with timely diagnosis and surgical repair.

AAP Textbook of Pediatric Care, 2nd Edition

Appendix A: Pediatric Cardiopulmonary Resuscitation - https://pediatriccare.solutions.aap.org/chapter.aspx?sectionId=138300647&bookId=1626&resultClick=1#160132374

For a comprehensive library of AAP parent handouts, please go to the Pediatric Patient Education site at http://patiented.aap.org .

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COVID patients at higher risk for respiratory complications well after infection, study finds

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The risks of  respiratory complications were eightfold and nearly twofold greater in COVID-19 patients in South Korea and Japan during and after infection, respectively, than in the general population, suggests a study published yesterday in Nature Communications .

Led by researchers at Kyung Hee University College of Medicine in Seoul, the study assessed the  risk of acute or post-acute respiratory complications after COVID-19 infection among a main cohort of 2,312,748 Koreans and a Japanese replication cohort of 3,115,606. The average age of the Korean cohort was 47.2 years, 48% were women, and 17.1% had tested positive for COVID-19.

Much higher risk compared to flu

The risk of respiratory complications among COVID-19 patients in the main Korean cohort was significantly higher than that among the general population during (hazard ratio [HR], 8.06) and after (HR, 1.68) infection. A similar trend was noted in the Japanese replication cohort (respective HRs, 4.17 and 3.32). 

The risk of developing post-acute respiratory conditions was highest in the first 3 months after COVID-19 infection (main HR, 2.51; replication HR, 4.40) but was still elevated after 6 months (main HR, 1.10; replication HR, 2.67).

Relative to the risk of acute respiratory complications in influenza patients, SARS-CoV-2 infection was significantly tied to an increased risk (main cohort HR, 4.32; replication cohort HR, 6.51). 

Relative to the general population, COVID patients were at a significantly higher risk for several types of post-acute respiratory condition, including chronic respiratory failure (main cohort HR, 8.92; replication HR, 7.55) and chronic obstructive pulmonary disease (COPD), emphysema, asthma, pulmonary sarcoidosis, and interstitial lung disease (main HR, 10.38; replication HR, 4.75). 

The risk of acute respiratory complications, including aspergillosis pneumonia (main HR, 6.85; replication HR, 4.97) and pneumothorax, acute respiratory failure (main HR, 112.04; replication HR, 6.49) rose in COVID-19 patients compared with the general population. This tendency held true in comparison with flu patients.

Vaccination greatly reduced the risk

The risk of acute respiratory complications declined with increasing number of COVID-19 vaccine doses (HR after one dose, 0.51; HR after two or more (HR, 0.24). The lowest risk of post-acute respiratory complications was seen among recipients of mixed types of vaccines (HR, 0.18).

Post-recovery from COVID-19, the immune system undergoes reconstruction.

The risks of respiratory complications during infection were higher in patients with moderate or severe COVID-19 symptoms (HR, 39.54). Both the wild-type SARS-CoV-2 strain and the Delta variant were linked to a higher risk of acute respiratory complications (wild-type HR, 9.21; Delta HR, 7.44). The risk of post-acute respiratory conditions showed a similar trend.

"Post-recovery from COVID-19, the immune system undergoes reconstruction," the study authors wrote. "However, the elevated interferon responsive genes in monocytes can still be found after 4 months since the infection, which implies that the immune system is not fully recovered after 4 months, and constant attention must be paid to the patients."

The researchers added that the findings underscore the need for better healthcare policies to manage social health. " To minimize adverse respiratory outcomes after being infected with SARS-CoV-2, the government should make policies to mix and match the vaccine types to individuals," they wrote. "Individuals should be investigated even after full recovery from COVID-19 to resolve post-acute COVID-19 conditions."

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  • Published: 20 May 2024

Continuous estimation of respiratory system compliance and airway resistance during pressure-controlled ventilation without end-inspiration occlusion

  • Yuqing Chen 1 ,
  • Yueyang Yuan 2 ,
  • Qing Chang 1 ,
  • Hai Zhang 1 ,
  • Feng Li 1 &
  • Zhaohui Chen 3  

BMC Pulmonary Medicine volume  24 , Article number:  249 ( 2024 ) Cite this article

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Assessing mechanical properties of the respiratory system (C st ) during mechanical ventilation necessitates an end-inspiration flow of zero, which requires an end-inspiratory occlusion maneuver. This lung model study aimed to observe the effect of airflow obstruction on the accuracy of respiratory mechanical properties during pressure-controlled ventilation (PCV) by analyzing dynamic signals.

A Hamilton C3 ventilator was attached to a lung simulator that mimics lung mechanics in healthy, acute respiratory distress syndrome (ARDS) and chronic obstructive pulmonary disease (COPD) models. PCV and volume-controlled ventilation (VCV) were applied with tidal volume (V T ) values of 5.0, 7.0, and 10.0 ml/kg. Performance characteristics and respiratory mechanics were assessed and were calibrated by virtual extrapolation using expiratory time constant (RC exp ).

During PCV ventilation, drive pressure (DP) was significantly increased in the ARDS model. Peak inspiratory flow (PIF) and peak expiratory flow (PEF) gradually declined with increasing severity of airflow obstruction, while DP, end-inspiration flow (EIF), and inspiratory cycling ratio (EIF/PIF%) increased. Similar estimated values of C rs and airway resistance (R aw ) during PCV and VCV ventilation were obtained in healthy adult and mild obstructive models, and the calculated errors did not exceed 5%. An underestimation of C rs and an overestimation of R aw were observed in the severe obstruction model.

Using the modified dynamic signal analysis approach, respiratory system properties (C rs and R aw ) could be accurately estimated in patients with non-severe airflow obstruction in the PCV mode.

Peer Review reports

Mechanical ventilation is an important lifesaving procedure with wide clinical applications for various critical conditions. The adequate setting of ventilator parameters should be based on the patient’s condition for optimal patient outcomes and to minimize ventilator-associated injury and complications [ 1 , 2 ]. Pressure-controlled ventilation (PCV) is broadly used for cases of severe respiratory failure. PCV improves arterial oxygenation and decreases peak airway pressure because it decelerates inspiratory low. However, PCV has some limitations, including insufficient ventilation and excessive ventilation [ 3 , 4 , 5 , 6 , 7 , 8 ].

Currently, the dynamic properties of the respiratory system and engineering models for various diseases are exploited in the diagnosis and treatment of pulmonary disorders [ 9 , 10 ]. However, mechanical features cannot be assessed directly during mechanical ventilation and are commonly presented as lumped indicators, including airway resistance (R aw ) and compliance (C rs ) [ 11 , 12 ]. Static compliance (C st ) is an important physiological index for evaluating the elastic properties of the overall respiratory system in invasive cases and is calculated by the ratio of the tidal volume to driving pressure [ 13 ]. C st can be monitored by setting an end-inspiratory occlusion in the volume-controlled ventilation (VCV) mode. During PCV, an appropriate inspiratory time should be preset to acquire the approximate plateau pressure (P plat ). Nevertheless, setting an appropriate inspiratory time may be challenging because the patient’s condition may change quickly. In addition, end-inspiration occlusion necessitates ventilation to be discontinued. Furthermore, this maneuver can be influenced by strong, spontaneous breathing. Therefore, other methods that do not require end-inspiratory occlusion need to be developed [ 14 , 15 ].

Recently, methods have been proposed for the assessment of respiratory system properties without end-inspiration occlusion. Multiple linear regression (MLR), considering the least-squares fitting (LSF) technique, constitutes the most applied tool in recent years. It approximates C st and R aw with high accuracy in case of negligible spontaneous breathing effort [ 16 , 17 , 18 ]. Further tools encompass the constrained optimization strategy [ 19 ], electrical impedance tomography (EIT) monitoring, linear fitting of the flow velocity waveform, short expiratory occlusions, repeated changes in pressure support level, and artificial neural networks [ 20 , 21 , 22 , 23 ]. Still, the above techniques have some limitations: some do not adapt to spontaneous breathing conditions [ 16 , 17 , 18 ], while others apply sophisticated medical information or specific manual maneuvers, and others use empirical parameters [ 20 , 22 ]. More importantly, most of them have more accurate measurements during VCV with constant inspiratory flow, with reduced accuracy when inspiratory flow is variable, such as in the PCV and PSV modes or spontaneous breathing effort. Secondly, the noise interference of ventilation waveforms exists in the real clinical setting, and noises encompass spontaneous breathing efforts, suctions, and coughing. Selecting adequate breaths that are less affected by noise might enhance accuracy in C st and R aw estimations.

In mechanically ventilated cases, expiration is a passive process depending on the expiratory time constant (RC exp ) of the respiratory system. RC exp reflects the mechanical features of the respiratory system [elastance and resistance (RC exp = R aw ×C rs )] and reveals the changes in the features of the pneumatic respiratory system [ 24 ]. C rs and R aw might be obtained from the passive deflation of lungs by using RC exp and specific equations. In a previous bench study by the authors, the C rs value was generally overestimated in the active breathing patient and underestimated in severe obstructive conditions, and the estimated error of R aw by the RC exp technique was minimal during passive breathing [ 15 ]. Recently, respiratory mechanics were estimated by modifying ventilation waveforms in the PCV mode to assess C st and R aw obtained by the end-inspiratory occlusion maneuver in the VCV mode. The continuous ventilation waveforms were examined, and an extra virtual tidal volume (V T ) was calculated using RC exp and an appropriate equation. Then, respiratory mechanics were estimated by analyzing the dynamic signals, which considerably improved static measurements. Such an approach improves estimation precision in respiratory system mechanics via real-time collection of respiratory data from the inspiration and expiration phases by applying specific Eqs. [ 25 , 26 ]. C st and R aw measurements based on the end-inspiratory occlusion maneuver in the real clinical setting were considered the gold standard for the validation of the proposed approach. The present study aimed to assess the accuracy of respiratory mechanical properties by the extra virtual V T in the PCV mode.

Lung models

The ASL 5000 Breathing Simulator (IngMar Medical, Pittsburg, PA, USA) features a computerized lung simulator with a piston that moves in a cylinder. This simulator was set to a single compartment based on a work by Beloncle et al. and previous bench studies by the authors [ 15 , 27 ]. The applied respiratory mechanics parameters simulated an adult patient (65 to 70 kg body weight) placed in the semi-recumbent position. Six clinical scenarios with/without expiratory flow limitation (EFL) were constructed as follows [ 10 , 28 , 29 ]: healthy adult [inspiratory resistance (R insp ) and expiratory resistance (R exp ) of 5.0 cmH 2 O/L/s], mildly, moderate-to-severe obstruction [R insp =R exp =10.0, 15.0, and 20.0 cmH 2 O/L/s], severe obstruction with EFL [R insp =10.0 cmH 2 O/(L/s), R exp =20.0 cmH 2 O/L/s], and ARDS [R insp =R exp =10 cmH 2 O/L/s]. C st was set at 30 (ARDS) and 60 (COPD) mL/cmH 2 O, and inspiratory time at 0.8 s (ARDS) and 1.6 s (COPD). Inspired oxygen fraction (F I O 2 ) was 0.21 for all measurements.

Ventilator settings

A dry circuit was used for the bench work, simulating a passive condition with both breathing frequency and P mus of zero. A Hamilton C3 ventilator (Hamilton Medical AG, Bonaduz, Switzerland) was attached to the lung simulator calibrated by the end-inspiratory occlusion maneuver in the VCV mode utilizing a constant flow. The Hamilton C3 device was used in the VCV mode. Positive end-expiratory pressure (PEEP) was 5.0 cmH 2 O, and the backup breathing rate was 10 breaths/min. During VCV and PCV, respiratory mechanics setting was performed to maintain the output tidal volume (V T ) at 5.0, 7.0, and 10.0 ml/kg. A reduced inspiratory rise time was applied to prevent overshooting in the PCV mode.

Data collection

After baseline pressure stabilization, typical breaths were selected and recorded at 1-min intervals. Data were obtained for a total of six times after inspiratory pressure levels were adjusted in each lung model. All breaths were assessed offline using the ASL 5000 breathing simulator software.

Peak inspiratory flow (PIF), end-inspiratory flow (EIF), end-inspiratory pressure (EIP), and actual inspiratory time (T I ) were determined using the simulator. Expiratory V T was also evaluated. Peak expiratory flow (PEF) and total PEEP were collected in the expiration phase (Figure S1 ).

Respiratory mechanics indexes were considered the main determinants of the interaction between the patient and the ventilator. During PCV, the quasi-static two-point compliance of the respiratory system (C rs ) was determined as V T by driving pressure (DP). DP was the difference between EIP and total PEEP obtained at end-inspiration and end-expiration, respectively. RC exp was the V T /flow ratio at 75% of expiratory V T [ 30 ]. The equations representing these relationships are:

Extra virtual tidal volume:

Inspiratory resistance (R insp ) was derived from the following equations considering dynamic signals:

Expiratory resistance (R exp ) was assessed with Eqs.  5 and 6 :

The percentages of measurement errors for compliance or resistance (%error C rs and %error R aw ) were calculated as follows [ 27 ]:

Statistical analysis

All analyses were performed using SPSS 19.0 (IBM, Armonk, NY, USA). Data were shown as means ± standard deviations (SDs). The Shapiro-Wilk test was used for normality assessment. One-way ANOVA was used for comparisons in different settings. C rs , R insp , and R exp were calculated in the VCV mode using the end-inspiration occlusion approach and the dynamic signal analysis method with extra virtual V T in the PCV mode, with a two-tailed t -test for comparisons. Absolute differences between the extra virtual V T and occlusion methods were determined, and P  < 0.01 indicated statistical significance. Differences between PCV and VCV were determined as absolute percentages of values measured in the VCV mode.

EIF and extra virtual V T in the PCV mode under passive breathing

In PCV, EIF/PIF% was not above 5% in the non-severe obstructive lung models [R aw ≤10.0 cmH 2 O/L/s] and close to 0 in the ARDS lung model. EIF/PIF% was increased with the aggravation of airflow obstruction, i.e., about 10% at a R aw of 20.0 cmH 2 O/L/s ( P  < 0.001). Extra virtual V T and the percentage of extra virtual V T and V TE (ΔV T %) were also increased (all P  < 0.05). Compared with the normal adult lung model, there were significant differences in EIF/PIF% and ΔV T % under moderate to severe obstructive conditions (Table  1 ).

Estimation of C rs in various models in the VCV and PCV modes

Inspiratory V T in the PCV mode was corrected by RC exp and EIF. The estimated value of C rs was larger than the value without extra virtual V T calibration and close to the value obtained in the VCV mode with end-inspiratory occlusion. The estimated C rs decreased significantly with increasing severity of airflow obstruction in either ventilatory mode, and uncalibrated C rs values were only 49.28 ± 0.34 mL/cmH 2 O (PCV mode) and 57.38 ± 1.00 mL/cmH 2 O (VCV mode) ( P  < 0.01) in the severe obstructive lung model [R aw =20.0 cmH 2 O/L/s]. After the correction of extra virtual V T , the calculated errors were < 5% in all four lung models [R aw ≤15.0 cmH 2 O/L/s], which showed no significant differences compared with estimated values in the VCV mode (Table  2 ; Fig.  1 A).

figure 1

(A) Errors of system compliance (Crs) in various lung models during PC ventilation. (B) Errors of Rinsp in different lung models during PC ventilation. (C) Errors of Rexp in different lung models during PC ventilation. Data are shown as mean ± SD

Estimation of R aw in various models in the VCV and PCV modes

There were similar estimated R insp and R exp in the PCV and VCV modes with R aw ≤10.0 cmH 2 O/L/s, and calculated errors were ≤ 10.0%. After V T calibration, the estimated errors of R insp and R exp were reduced to < 5%. In severe obstructive and obstructive with EFL models, the estimated errors of R insp and R exp were significantly reduced and were below 10% after V T calibration (Tables  3 and 4 ; Fig.  1 B and C).

Bland-Altman analysis of differences between the PCV and VCV modes

In all five lung profiles with normal system compliance (60.0 mL/cmH 2 O), the difference in C rs between the V T calibration and end-inspiration occlusion approaches was 1.82  ±  1.43 mL/cmH 2 O; the weighted correlation coefficient of C rs equaled 0.549 after V T calibration ( P  < 0.001). The differences of R insp and R exp values in all lung models were 0.79 ± 1.96 × 0.89 and 0.38 ± 1.96 × 0.69 cmH 2 O/L/s, and the weighted correlation coefficients of R insp and R exp were equal to 0.954 and 0.969, respectively (all P  < 0.001) (Figs.  2 and 3 ).

figure 2

Bland-Altman plots depicting system compliance ( A ), inspiratory resistance ( B ) and expiratory resistance ( C ) by the V T calibration and end-inspiration occlusion approaches. Data from 5 (C rs ) and 6 (R aw ) lung models, in totally 168 breaths. Each circle reflects one breath for a given model. Dashed lines in the middle depict mean differences between the V T calibration and end-inspiration occlusion approaches. The remaining two dashed lines are mean ± 1.96*SD

figure 3

Associations of estimated C rs ( A ), R insp ( B ) and R exp ( C ) with gold standard obtained by the end-inspiration occlusion approach. Data from 5 (C rs ) and 6 (R aw ) lung models, totally 168 breaths were examined. Each circle reflects one breath for a given model

This bench study mostly revealed the following. (1) During PCV under the passive breathing condition, the estimated error was affected by the severity of airway obstruction, significantly underestimated in C rs , and significantly overestimated in R aw without V T calibration. (2) In the non-severe obstructive condition [R aw ≤ 10.0 cmH 2 O/L/s], estimated errors were ≤ 10% in calculated C rs and R aw . (3) The estimated accuracies of C rs , R insp , and R exp were improved by V T calibration with extra virtual inspiratory volume.

During mechanical ventilation, assessing the respiratory mechanics by end-inspiratory occlusion with a constant inspiratory flow is a classic measurement method. However, the occlusion technique may be performed with no gas flow and fixed tidal volume. It is important for the patient to make no efforts during static measurements, whether related to disease, sedation, or paralysis, and special ventilatory settings are also required (such as constant inspiratory flow and end-inspiration pause) [ 31 , 32 , 33 ]. The most important concern is that measurement data are reflected by mechanical properties under static or quasi-static conditions. The occlusion method could neither be adapted to the PCV mode since inspiratory flow is always variable nor be used in assisted ventilation in which the spontaneous effort is always present and variable. Recently, several continuous respiratory mechanics measurement techniques, including LSF and expiratory time constant method (RC exp ), have been developed. These newer approaches not only have good adaptability and anti-noise-interference performance but also could be applied during assisted mechanical ventilation with spontaneous breathing [ 34 ].

Volta et al. found that EFL substantially reduces the accuracy of resistance and compliance assessed by the LSF method; the determination of respiratory indexes during inspiration helps evaluate respiratory mechanics in flow-limited COPD cases, and the LSF technique could detect PEEPi dyn only using inspiratory data [ 18 ]. However, the estimated error of LSF was affected by the spontaneous breathing effort, and Raw underestimation and C rs overestimation were observed in the PSV mode [ 16 , 35 ]. The other approaches have certain limitations. Some could not deal with significant spontaneous breathing, while others are based on sophisticated medical equipment or manual maneuvers, preventing their routine clinical use [ 18 , 19 , 20 , 21 , 22 ]. Recently, Pan et al. proposed a tool measuring quasi-static respiratory system compliance (C q−stat ) in the PCV mode without the need for the end-inspiratory occlusion maneuver, with a virtual assessment of flow-time waveforms with end-inspiration flow not equaling zero, to allow for C q−stat determination [ 14 ]. In this bench study, the dynamic signal analysis approach was used to collect and calculate gas flow, airway pressure, and volume data at different time points during mechanical ventilation, and the estimated C rs , R insp , and R exp were calibrated by virtual extrapolation of V T when end-inspiration flow was not zero. Dynamic signal analysis does not require special maneuvers such as long-time pauses at the inspiration or expiration phase [ 26 ]. In healthy adults and mild obstruction lung models, no significant differences were found in estimated C rs and R aw (R insp and R exp ) between the PCV and VCV modes with EIF < 2.0 L/min and EIF/PIF% < 5.0%. The calculated error was increased when EIF/PIF% was above 5% in the PCV mode. Due to the exacerbation of airflow obstruction, PIF was decreased, and EIF did not drop to zero at the end of inspiration. EIF/PIF% was increased to about 10%, resulting in V T decrease, C rs underestimation, and R aw overestimation. After V T calibration with RC exp and EIF, the accuracy of the estimation was improved significantly, and the values obtained were similar to those estimated in the VCV mode by the occlusion method.

In the classic system compliance (C rs ) calculation equation, C rs is the ratio of the monitored tidal volume (V T ) to the driving pressure (DP) of the airway. The tidal volume is the sum of the gas output capacity of the ventilator during the inhalation phase. In the classic calculation scheme, the tidal volume is the gas output capacity value measured after the end-inspiratory flow rate reaches 0. On the other hand, in this study, due to the special nature of the PCV mode, the end-inspiratory flow rate does not always decrease to 0. Therefore, an additional parameter (i.e., the extra virtual tidal volume) was designed to simulate the gas capacity generated after the flow rate continued to decrease to 0. It was found that the addition of the extra virtual tidal volume was of great significance for calculating C rs under the PCV ventilation state.

One of the limitations of the present bench study is the standardization of simulation indexes for the respiratory system’s mechanics in the lung model. Although the mechanical lung simulator cannot completely replace animal experiments and real clinical practice, the ASL 5000 mechanical lung simulator also has its unique advantages. Firstly, it can simulate simple single-chamber linear models and complex lung mechanics models with dual-chamber nonlinearity. In this study, we attempted to explore a new respiratory mechanics calculation scheme that can be applied to non-interrupted breathing and non-constant inspiratory flow mechanical ventilation conditions and can accurately calculate the respiratory mechanics characteristics of patients with different respiratory system diseases. Therefore, a mechanical lung simulator was first used for the experiment because its output data is relatively stable, and this lung simulator is also often selected in many mechanical simulation experiments. Further animal experiments will be conducted in the future [ 36 ]. Secondly, the passive breathing condition was simulated during PCV since spontaneous breathing effort might affect V T and C rs . It is not clear whether this scheme could be applied to other assisted ventilatory modes such as PSV. Thirdly, airway resistance varies with gas flow through the trachea and bronchus. Therefore, the above data reflect maximal resistance in a patient during breathing, and whether they can be translated in the clinical setting is unknown. Therefore, further clinical trials are warranted.

Using the modified dynamic signal analysis approach, respiratory system properties (C rs and R aw ) could be accurately estimated in patients with non-severe airflow obstruction in the PCV mode. Compared with the VCV mode with constant flow, inspiratory flow decreased exponentially in the PCV mode. PIF and the deceleration rate of inspiratory flow were dependent upon the mechanical characteristics of the respiratory system, especially airflow obstruction.

Data availability

All data generated or analyzed during this study are included in this article.

Abbreviations

  • Pressure-controlled ventilation
  • Chronic obstructive pulmonary disease

Volume-controlled ventilation

Tidal volume

Drive pressure

Peak inspiratory flow

Peak expiratory flow

End-inspiration flow

Inspiratory cycling ratio

  • Airway resistance

Static compliance

Plateau pressure

Multiple linear regression

Least-squares fitting

Electrical impedance tomography

Expiratory time constant

Expiratory flow limitation

Positive end-expiratory pressure

End-inspiration pressure

Inspiratory time

Respiratory system compliance

Driving pressure

Standard deviation

Quasi-static respiratory system compliance

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Acknowledgements

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This study was supported by the “Star of Jiaotong University” program of Shanghai Jiao Tong University Medical and the Industrial Cross Research Fund Project (grant no YG2019ZDB08) to Yuqing Chen.

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Yueyang Yuan

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Yuqing Chen and Feng Li contributed to the concept and drafted the manuscript or substantively revised it. Yueyang Yuan contributed to the manuscript design. Qing Chang, Hai Zhang, and Zhaohui Chen contributed to data acquisition and analysis. FL contributed to the interpretation of the data. All authors read and approved the final manuscript.

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Chen, Y., Yuan, Y., Chang, Q. et al. Continuous estimation of respiratory system compliance and airway resistance during pressure-controlled ventilation without end-inspiration occlusion. BMC Pulm Med 24 , 249 (2024). https://doi.org/10.1186/s12890-024-03061-2

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Case Report

Acute respiratory failure in a 35-year-old woman following preterm vaginal delivery, h m bhandari.

1 University Hospitals of Coventry and Warwickshire NHS Trust, Coventry, UK

2 Warwick Medical School, The University of Warwick, Coventry, UK

A 35-year-old woman, a non-smoker with a normal body mass index, ‘felt wheezy’ and developed profound hypoxia 30 min after preterm vaginal delivery at 24+ weeks of gestation. She denied other symptoms, had no fever but was tachycardic and tachypnoeic with normal blood pressure. Pulmonary embolism, amniotic fluid embolism, cardiomyopathy, arrhythmias, sepsis and non-cardiogenic pulmonary oedema were considered as differential diagnoses. Chest X-ray showed an increased pulmonary vasculature, but the blood tests, ECG, echocardiogram and CT pulmonary angiogram were essentially normal. She was managed on a high dependency area with high-flow oxygen and intravenous antibiotics. She improved dramatically and the oxygen requirements dropped to 2 L over the next 4 h. It is plausible that this woman had acute non-cardiogenic pulmonary oedema secondary to a combination of risk factors. This case highlights the importance of a methodical and multidisciplinary approach for a prompt diagnosis and successful treatment of an acutely ill parturient.

The physiological changes during pregnancy and in the puerperium cause an increase in oxygen demand. Acute hypoxia during this period is uncommon due to maternal compensation, but undiagnosed pathological causes can be life-threatening.

Owing to its multifactorial aetiology, diagnosis of pathological hypoxia can be a challenge, but with a methodical history, focused examination, appropriate investigations and multidisciplinary involvement, most causes of obstetric hypoxia can be diagnosed and successfully treated.

We report an unusual case of acute respiratory failure following immediate preterm vaginal delivery, which spontaneously resolved a few hours later with no conclusive identifiable cause.

Case presentation

A 35-year-old woman with a history of mid-trimester miscarriage at 15 weeks was seen in the antenatal clinic at 16 weeks’ gestation in her second pregnancy. She had a booking body mass index of 24 and was a non-smoker. Her medical history included treatment for symptomatic anaemia and an open abdominal myomectomy within the past year. She was not on any medications and had no allergies.

During this pregnancy, she was admitted at 24 weeks’ gestation with a history of abdominal pain with backache and incidentally found to be in threatened preterm labour. She was given antenatal corticosteroids for fetal lung maturity and magnesium sulfate for fetal neuroprotection, but was not given any other tocolytics. The woman was allowed to drink and encouraged to keep well hydrated and intravenous fluids were not necessary. The contractions settled with magnesium sulfate and 28 h after magnesium therapy, her membranes ruptured spontaneously draining clear liquor and 18 h later she delivered a live infant vaginally.

Within 30 min of delivery, she ‘felt wheezy’ and was found to be profoundly hypoxic. On further questioning she denied any other symptoms, and on examination she was alert and orientated, without fever, tachycardic with a pulse rate of 120 bpm, urine dipstick negative, blood pressure of 120/70 mm Hg, tachypnoeic at 24 breaths/minute, normal jugular venous pressure, auscultation of her heart showed normal heart sounds and her chest revealed fine bibasal crepitations.

Investigations

The arterial blood gas analysis was suggestive of hypoxia (saturations of 88% on room air with a partial pressure of oxygen of 6.8 kPa). A chest X-ray ( figure 1 ) showed increased pulmonary vasculature and an ECG showed a sinus tachycardia. A CT pulmonary angiogram (CTPA; figure 2 ) showed no evidence of pulmonary embolism (PE) but dependent air space opacities consistent with acute respiratory distress syndrome or non-cardiogenic pulmonary oedema. An echocardiogram showed normal valve morphology and good biventricular function. Blood tests were requested (including full blood count, urea and electrolytes, C reactive protein, liver function test and clotting profile), which were all normal. The placental histology subsequently showed chorioamnionitis with early funisitis.

An external file that holds a picture, illustration, etc.
Object name is bcr2014203676f01.jpg

Anteroposterior chest X-ray immediately after the onset of acute respiratory failure.

An external file that holds a picture, illustration, etc.
Object name is bcr2014203676f02.jpg

CT pulmonary angiogram showing no evidence of pulmonary embolism but dependent air space opacity consistent with acute respiratory distress syndrome or non-cardiogenic pulmonary oedema.

Differential diagnosis

A 35-year-old woman developing acute hypoxia in the immediate postnatal period following a few days of relative immobilisation and a preterm delivery may have PE, amniotic fluid embolism, cardiomyopathy, arrhythmias, sepsis or a non-cardiogenic pulmonary oedema ( table 1 ). She had no chest pain or shortness of breath and the CTPA ruled out the possibility of a PE. ECG ruled out arrhythmias and echocardiogram ruled out any other cardiac causes. Absence of chest pain and shortness of breath, hypotension, normal coagulation profile and a spontaneous resolution were against amniotic fluid embolism.

Table 1

Common causes of postpartum hypoxia

In our case, it is plausible that the most likely explanation suggests acute non-cardiogenic pulmonary oedema secondary to a combination of suggested aggravating factors. These factors include spontaneous preterm labour, magnesium sulfate and corticosteroid administration and chorioamnionitis (see the Discussion section).

She was managed on a high dependency area and was treated with 60% humidified high-flow oxygen. She was started on intravenous antibiotics as sepsis was one of the differential diagnoses. Over the next 4 h, she subsequently improved dramatically and oxygen requirements dropped to 2 L on nasal specs (with saturations of >95%).

Outcome and follow-up

The patient subsequently made a full recovery and a repeat chest X-ray ( figure 3 ) 40 h following this acute episode was clear. She had a postnatal follow-up at 6 weeks and had no residual symptoms.

An external file that holds a picture, illustration, etc.
Object name is bcr2014203676f03.jpg

Anteroposterior chest X-ray taken 40 h after excludes any other pulmonary pathology.

Pulmonary oedema complicates 0.08–0.5% of pregnancies, 1 2 but can occur in up to 7% of cases following spontaneous preterm delivery between 24 and 33 weeks. 3 According to the Scottish Confidential Audit of Severe Maternal Morbidity Report 2008, pulmonary oedema is the fourth most common cause of severe maternal morbidity in pregnant women. 4

A retrospective case–control study conducted by Ogunyemi 3 identified spontaneous preterm labour (OR 10.9), antenatal corticosteroids (OR 2.3) and magnesium sulfate (OR 5.3) administration as independent risk factors for increasing the risk of developing acute pulmonary oedema. A recent systematic review and meta-analysis, though, did not find any significant increase in the risk of pulmonary oedema and respiratory distress with magnesium sulfate prophylaxis for neuroprotection in preterm labour. 5 Samol and Lambers 6 elegantly demonstrated that the mean length of duration from the beginning of magnesium sulfate treatment to identification of pulmonary oedema was found to be 1.96 days, and in this case it was 70 h. They also demonstrated that women who received larger amounts of fluids at the onset of magnesium sulfate therapy and those who had a more positive balance on day one were significantly more at risk of pulmonary oedema.

Any disruption of Starling's forces (hydrostatic pressure, oncotic pressure and capillary permeability) surrounding fluid movement across capillary membranes will influence the development of pulmonary oedema (reviewed in ref. 7 ). Wilkens et al 8 discovered that magnesium sulfate and β-sympathomimetic tocolytic agents, when administered simultaneously, increased the risk of pulmonary oedema. It is suggested that these agents increase hydrostatic pressure within the pulmonary vasculature, subsequently resulting in the passage of fluid within the interstitium. 6

Yeast et al 9 demonstrated that intravenous magnesium sulfate for preterm labour or pre-eclampsia caused a decreased colloid osmotic pressure and increased the risk of pulmonary oedema. Also, women with clinical chorioamnionitis are found to be at a three times higher risk of pulmonary oedema. This finding underpins the possible mechanism of increased capillary permeability secondary to underlying infection. 3

Learning points

  • Although pulmonary embolism, cardiac failure and lower respiratory tract infection are more common causes of acute respiratory failure in the postnatal period, other possible causes should be sought and ruled out.
  • Pulmonary oedema is common after spontaneous preterm delivery, particularly in women who have received antenatal corticosteroids and magnesium sulfate.
  • This case highlights the importance of a methodical and multidisciplinary approach for a prompt diagnosis and successful treatment of a medical condition in the acutely ill parturient.

Contributors: HMB conceived the idea and drafted the manuscript. MG contributed extensively to the idea and the drafting of the manuscript. JW was involved in overall supervision and advised on the drafting of the manuscript and critical appraisal.

Competing interests: None.

Patient consent: Obtained.

Provenance and peer review: Not commissioned; externally peer reviewed.

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    Abstract. This case study explores the management of an unusually complicated case of acute respiratory distress syndrome (ARDS) extending over 52 days of hospitalization. Despite the utilization of conventional medical treatments and optimum respiratory support modalities, the patient's condition worsened and death was imminent without salvage ...

  17. A Case Report of Neonatal Acute Respiratory Failure Due to Severe Acute

    Overall, this case represents a unique presentation of respiratory failure due to SARS-CoV-2 in a neonatal patient and expands the clinical spectrum of pediatric COVID-19. CONCLUSIONS More extensive studies are needed to better understand the pediatric disease spectrum and clinical outcomes of COVID-19, particularly in newborns and children ...

  18. A 45-Year-Old Man With Severe Respiratory Failure After Cardiac ...

    Additional information: To analyze this case with the videos, see the online article. References 1. Sekiguchi H, Schenck LA, Horie R, et al. Critical care ultrasonography differentiates ARDS, pulmonary edema, and other causes in the early course of acute hypoxemic respiratory failure. Chest. 2015;148(4):912-918. 2.

  19. Case 18-2020: A 73-Year-Old Man with Hypoxemic Respiratory Failure and

    Presentation of Case Dr. Lila M. Martin: A 73-year-old man was transferred to the intensive care unit (ICU) of an academic health center in Boston for acute hypoxemic respiratory failure

  20. Clinical Management of Respiratory Failure & ARDS: Case Study

    GMED3009 Respiratory Failure and ARDS Case Study 24 1 .pdf... Case study John Low a 67-year-old male presented to Emergency department with 4 days worsening dyspnoea, shortness of breath preceding coryzal illness. The patient denies any chest pain or palpitations and nil peripheral oedema. The patient had a set of vital signs and blood taken.

  21. Case 6: Acute-onset Respiratory Failure in a 4-month-old Girl

    A 4-month-old girl presents with a 1-week history of a temperature to 102°F (38.9°C), congestion, rhinorrhea, and cough. She has had fatigue and diaphoresis with feedings over the last week, although this did not occur before this time. She was born at term following normal findings on prenatal ultrasonography. Initially, she had difficulty gaining weight, but she is now growing along the ...

  22. Case 32-2015

    A 57-year-old man was admitted to the intensive care unit in the winter because of severe pneumonia and acute hypoxemic respiratory failure. One month earlier, he had returned from a trip to Southe...

  23. A case of hypercapnic respiratory failure

    This case illustrates a stepwise approach towards patients with chronic hypercapnic respiratory failure. Asking the patient about sleep-related symptoms, breathing sounds and medication use is essential. Evaluation of the flow-volume curve shape is key as it can reveal important information about the airways.

  24. COVID patients at higher risk for respiratory complications ...

    The risks of respiratory complications were eightfold and nearly twofold greater in COVID-19 patients in South Korea and Japan during and after infection, respectively, than in the general population, suggests a study published yesterday in Nature Communications.. Led by researchers at Kyung Hee University College of Medicine in Seoul, the study assessed the risk of acute or post-acute ...

  25. Continuous estimation of respiratory system compliance and airway

    Background Assessing mechanical properties of the respiratory system (Cst) during mechanical ventilation necessitates an end-inspiration flow of zero, which requires an end-inspiratory occlusion maneuver. This lung model study aimed to observe the effect of airflow obstruction on the accuracy of respiratory mechanical properties during pressure-controlled ventilation (PCV) by analyzing dynamic ...

  26. Case Report: Acute respiratory failure in a 35-year-old woman following

    A retrospective case-control study conducted by Ogunyemi 3 identified spontaneous preterm labour (OR 10.9), antenatal corticosteroids (OR 2.3) and magnesium sulfate ... Although pulmonary embolism, cardiac failure and lower respiratory tract infection are more common causes of acute respiratory failure in the postnatal period, other possible ...