Pulmonary injury follows systemic inflammatory reaction in infrarenal aortic surgery*

Adembri, Chiara; Kastamoniti, Eleni; Bertolozzi, Iacopo; Vanni, Simone; Dorigo, Walter; Coppo, Mirella; Pratesi, Carlo; Gaudio, Angelo Raffaele De; Gensini, Gian Franco; Modesti, Pietro Amedeo

doi:10.1097/01.ccm.0000124875.98492.11

Cited by 74 publications

(69 citation statements)

References 27 publications

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“…Such disasters are typically attributed to the supposedly unpredictable efects of opioids, while the occult role of hyperventilation escapes notice because the victims appear to have completely recovered from anesthesia [3,4] . The resulting fear of opioids discourages their use, which indirectly exaggerates stress related postoperative problems including fever, tachycardia, hypertension, dysrhythmias, laryngospasm, dementia, bowel ileus, myocardial infarction, stroke, exaggerated pain, nausea, vomiting, atelectasis, systemic inlammation, Adult Respiratory Distress Syndrome (ARDS), Systemic Inlammatory Response Syndrome (SIRS) and death [46,99] . There are also substantial increases in cancer and heart disease in the distant aftermath of surgery [48] .…”

Section: ]Llmentioning

confidence: 99%

“…Opioid analgesia inhibits surgical nociception and improves surgical outcome [43][44][45] , but its beneits often escape the notice of anesthesia practitioners because the surgical stress reaction does not reach peak intensity until 48 hours after surgery [46,47] . The increased morbidity and mortality persists in the distant aftermath of surgery, mostly in the form of heart disease and cancer [48] .…”

Section: Hypoventilation Hyperventilation Opioids and Anesthesiamentioning

confidence: 99%

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Four Forgotten Giants of Anesthesia History

Coleman¹,

Internationals²

2016

JAS

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Introduction Does wisdom perhaps appear on the earth as a raven, which is inspired by the smell of carrion? --Friedrich NietzschePast is prologue. Carbon dioxide confusion has played a pivotal role in the evolution of modern anesthesia. Professional anesthesiology organizations have persistently neglected CO 2 management standards in favor of lesser issues [1][2][3][4] , so that the anesthesiology profession remains mired at the crossroads of revolutionary advance and ongoing self-destruction that can only be understood in historical context. Dr. Ralph Waters founded the profession on the basis of a practical new technique that introduced elective intubation and hyperventilation to abolish CO 2 toxicity disasters, but the harmful habit of hyperventilation has distorted anesthesia beliefs, habits, and practices; derailed research; halted professional advance; discouraged opioid treatment; abolished the therapeutic beneits of CO 2 ; exaggerated morbidity and mortality; and introduced a host of vexing clinical problems. It has indirectly fostered the iction that further improvements in anesthesia safety are impossible, which has undermined reimbursement, emasculated staf privileges, devastated morale, discouraged professional membership A , and rationalized the replacement of anesthesiologists by nurses.Meanwhile, the confusing chemistry, physiology, and pathology of carbon dioxide have yielded their secrets, modern anesthesia machines have eliminated the toxicity problem, modern agents have eliminated explosions, and modern monitoring AbstractThe anesthesiology profession may one day serve as a cautionary tale of how power, politics and privilege can perturb science and progress. Previous anesthesia practitioners possessed a superior understanding of physiology and pharmacology, but overenthusiastic CO 2 supplementation with inadequate monitors and machines caused asphyxiation disasters that were improperly attributed to CO 2 toxicity. Dr. Ralph Waters founded the anesthesiology profession on the basis of a practical new anesthetic technique that introduced elective intubation and hyperventilation to eliminate CO 2 toxicity, but mechanical hyperventilation dangerously depletes CO 2 tissue reserves and exaggerates morbidity and mortality. The beneits of CO 2 supplementation were forgotten, and consequent CO 2 confusion has derailed research, discouraged opioid treatment, damaged patient safety, and disrupted professional progress. Anesthesiologists can no longer claim to provide superior service, and hospital administrators are replacing them with nurses. Professional membership is in decline, and professional survival is in question. Modern machines have eliminated asphyxiation, and modern monitoring enables safe and beneicial hypercarbia that complements opioid treatment and minimizes surgical morbidity and mortality. CO 2 reform promises revolutionary advance but faces formidable opposition. [5] . The restoration of past principles using modern capnography, pulse oximetry, synthetic opioids, and improved inha...

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Section: ]Llmentioning

confidence: 99%

Section: Hypoventilation Hyperventilation Opioids and Anesthesiamentioning

confidence: 99%

Four Forgotten Giants of Anesthesia History

Coleman¹,

Internationals²

2016

JAS

View full text Add to dashboard Cite

show abstract

“…This increases the risk of infarction and metastasis. Brain, nerve, retina, ovary, placenta, lung, artery, and cervix tissues are rich in tissue factor and therefore especially vulnerable to both primary malignancy and metastasis [210,552,556,557,[598][599][600]. SRM activity thus explains the close association of malignancy with chronic disease, environmental stress, inflammation, elevated Factor VII and Factor VIII activity, increased blood viscosity and coagulability, accelerated atherosclerosis, and seemingly unrelated forms of malignancy [556][557][558]566,[601][602][603][604][605].…”

Section: Inflammation Apoptosis and Malignancymentioning

confidence: 99%

“…Unfortunately, these conventional cancer treatments are harmful and unreliable. Surgery, radiation, and toxic chemicals all increase SRM activity, which explains why conventional treatments are accompanied by increased risk of cancer and cardiovascular disease [552,556,557,[598][599][600]. They are plagued by toxic side effects and physical disfiguration, bedeviled by the subsequent appearance of other, seemingly unrelated, forms of cancer, and they increase morbidity and mortality from atherosclerosis, infarction, and pulmonary embolus [582].…”

Section: Inflammation Apoptosis and Malignancymentioning

confidence: 99%

Stress repair mechanism activity explains inflammation and apoptosis

Coleman¹

2012

ABB

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“…However, few studies have evaluated the impact of fluid infusion on pulmonary gas exchange. Furthermore, among the possible complications, the pulmonary ones have high incidence and mortality rate, which is mostly a consequence of pulmonary edema caused by ischemia and reperfusion of the aorta (16)(17)(18)(19)(20)(21)(22).…”

Section: Introductionmentioning

confidence: 99%

Effect of saline infusion for the maintenance of blood volume on pulmonary gas exchange during temporary abdominal aortic occlusion

Amorim¹,

Pinheiro²,

Beppu³

et al. 2007

Braz J Med Biol Res

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We analyzed the effects of saline infusion for the maintenance of blood volume on pulmonary gas exchange in ischemia-reperfusion syndrome during temporary abdominal aortic occlusion in dogs. We studied 20 adult mongrel dogs weighing 12 to 23 kg divided into two groups: ischemia-reperfusion group (IRG, N = 10) and IRG submitted to saline infusion for the maintenance of mean pulmonary arterial wedge pressure between 10 and 20 mmHg (IRG-SS, N = 10). All animals were anesthetized and maintained on spontaneous ventilation. After obtaining baseline measurements, occlusion of the supraceliac aorta was performed by the inflation of a Fogarty catheter. After 60 min of ischemia, the balloon was deflated and the animals were observed for another 60 min of reperfusion. The measurements were made at 10 and 45 min of ischemia, and 5, 30, and 60 min of reperfusion. Pulmonary gas exchange was impaired in the IRG-SS group as demonstrated by the increase of the alveolar-arterial oxygen difference (21 ± 14 in IRG-SS vs 11 ± 8 in IRG after 60 min of reperfusion, P = 0.004 in IRG-SS in relation to baseline values) and the decrease of oxygen partial pressure in arterial blood (58 ± 15 in IRG-SS vs 76 ± 15 in IRG after 60 min of reperfusion, P = 0.001 in IRG-SS in relation to baseline values), which was correlated with the highest degree of pulmonary edema in morphometric analysis (0.16 ± 0.06 in IRG-SS vs 0.09 ± 0.04 in IRG, P = 0.03 between groups). There was also a smaller ventilatory compensation of metabolic acidosis after the reperfusion. We conclude that infusion of normal saline worsened the gas exchange induced by pulmonary reperfusion injury in this experimental model. Correspondence

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Pulmonary injury follows systemic inflammatory reaction in infrarenal aortic surgery*

Cited by 74 publications

References 27 publications

Four Forgotten Giants of Anesthesia History

Four Forgotten Giants of Anesthesia History

Stress repair mechanism activity explains inflammation and apoptosis

Effect of saline infusion for the maintenance of blood volume on pulmonary gas exchange during temporary abdominal aortic occlusion

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