Management of Massive Grain Aspiration

Slinger, Peter; Blundell, Peter E.; Metcalf, Ian

doi:10.1097/00000542-199710000-00039

Cited by 29 publications

(20 citation statements)

References 4 publications

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“…Indeed, the advent of clinical blood gas analysis in the 1950s revealed surprisingly profound hypercapnia (PaCO 2 > 150 mmHg, pH <7.0) without negative consequence in thoracic surgical cases involving one-lung ventilation [ 9 ]. A PaCO 2 of 501 mmHg from massive grain aspiration in a healthy farmer with complete recovery has been reported [ 135 ]. The concept of permissive hypercapnia -purposefully limiting tidal volume and pressure and accepting subsequent hypercapnic acidosis in status asthmaticus was fi rst studied and gained credence in the mid 1980s.…”

Section: Hypoxia and Respiratory Acidosis In Critical Illnessmentioning

confidence: 99%

Hypoxia and Its Acid–Base Consequences: From Mountains to Malignancy

Swenson

2016

Advances in Experimental Medicine and Biology

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Hypoxia, depending upon its magnitude and circumstances, evokes a spectrum of mild to severe acid-base changes ranging from alkalosis to acidosis, which can alter many responses to hypoxia at both non-genomic and genomic levels, in part via altered hypoxia-inducible factor (HIF) metabolism. Healthy people at high altitude and persons hyperventilating to non-hypoxic stimuli can become alkalotic and alkalemic with arterial pH acutely rising as high as 7.7. Hypoxia-mediated respiratory alkalosis reduces sympathetic tone, blunts hypoxic pulmonary vasoconstriction and hypoxic cerebral vasodilation, and increases hemoglobin oxygen affinity. These effects and others can be salutary or counterproductive to tissue oxygen delivery and utilization, based upon magnitude of each effect and summation. With severe hypoxia either in the setting of profound arterial hemoglobin desaturation and reduced O2 content or poor perfusion (ischemia) at the global or local level, metabolic and hypercapnic acidosis develop along with considerable lactate formation and pH falling to below 6.8. Although conventionally considered to be injurious and deleterious to cell function and survival, both acidoses may be cytoprotective by various anti-inflammatory, antioxidant, and anti-apoptotic mechanisms which limit total hypoxic or ischemic-reperfusion injury. Attempts to correct acidosis by giving bicarbonate or other alkaline agents under these circumstances ahead of or concurrent with reoxygenation efforts may be ill advised. Better understanding of this so-called "pH paradox" or permissive acidosis may offer therapeutic possibilities. Rapidly growing cancers often outstrip their vascular supply compromising both oxygen and nutrient delivery and metabolic waste disposal, thus limiting their growth and metastatic potential. However, their excessive glycolysis and lactate formation may not necessarily represent oxygen insufficiency, but rather the Warburg effect-an attempt to provide a large amount of small carbon intermediates to supply the many synthetic pathways of proliferative cell growth. In either case, there is expression and upregulation of many genes involved in acid-base homeostasis, in part by HIF-1 signaling. These include a unique isoform of carbonic anhydrase (CA-IX) and numerous membrane acid-base transporters engaged to maintain an optimal intracellular and extracellular pH for maximal growth. Inhibition of these proteins or gene suppression may have important therapeutic application in cancer chemotherapy.

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Section: Hypoxia and Respiratory Acidosis In Critical Illnessmentioning

confidence: 99%

Hypoxia and Its Acid–Base Consequences: From Mountains to Malignancy

Swenson

2016

Advances in Experimental Medicine and Biology

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“…Remarkably, in the vast majority of cases, even in two cases with extremely high arterial pCO 2 tensions of 375 and 501 mm Hg, respectively, and in cases of prolonged hypercapnia lasting for several hours, the patients have shown a full recovery and had no residual neurological impairment (2,19,22). Only a few cases report permanent damage after CO 2 narcosis.…”

Section: Outcome Of Hypercapnic Comamentioning

confidence: 99%

Hypercapnic Coma Due to Spontaneous Pneumothorax: Case Report and Review of the Literature

Otten

Schwarte

Oosterhuis

et al. 2012

The Journal of Emergency Medicine

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“…Reassuringly, there is overwhelming evidence that, with few exceptions, marked levels of hypercapnia are very well tolerated in mechanically ventilated patients [6,7]. In the context of the evidence from our work and that of others, we have proposed that hypercapnia may be beneficial in the context of organ injury [5].…”

Section: Introductionmentioning

confidence: 59%

“…In addition, adverse effects may develop at much lower levels in vulnerable patients (elevated intracranial pressure; inability to buffer CO 2 adequately in the context of renal failure or parenteral nutrition), or in specific organ systems. We do know that humans ± and experimental animals ± can tolerate exceptional levels of CO 2 , and when adequately ventilated, can recover rapidly and completely [6,7]. Yet, while more (high doses) may well be tolerated in the critically ill, dose-response data have not been adequately characterized, and, while effects in a single organ system may be beneficial, concomitant, and late, effect in all physiological systems need to be addressed.…”

Section: Discussionmentioning

confidence: 99%