The blood gas monitoring systems devised in the 1950s, could not be used to continuously monitor respiratory gases in the body. In the 1970s, Huch, Lubbers and Severinghaus developed transcutaneous oximetry to provide a nearly-continuous monitor of arterial oxygen [40–42]. In the late 1970s and early 1980s, Beran et al. and Severinghaus added transcutaneous analysis of carbon dioxide [43,44]. The device heated the skin under the electrode, increasing cutaneous blood flow, thereby arterializing cutaneous gases and minimizing diffusion distances of oxygen and carbon dioxide to the electrode surface. Monitoring of both gases was found to accurately reflect arterial blood gas values in infants, and transcutaneous oximetry continues to be used for this purpose in neonatal ICUs. In older children and adults, measurement of transcutaneous oxygen partial pressures is less accurate, particularly at high PO₂ values. Transcutaneous oximetry did find new life, however, in the 1980s, when surgeons Hauser and Shoemaker demonstrated that transcutaneous oximetry could be used to quantify skin oxygen levels in ischemic limbs [45]. Transcutaneous oximetry is now used routinely in wound clinics to determine a patient’s capacity to heal. Anesthesiologists have contributed to this field [46,47].

The involvement of anesthesiologists in on-site management of victims of major disasters came to the fore in the Moorgate Tube Train accident, in London in 1975. 43 people died and 72 required treatment in hospital. Prior planning, good communication, and the need for mobile medical teams to have emergency management experience, were all identified as key factors in the successful management of disaster victims. Anesthesiologists around the world subsequently became core members of local and national disaster planning processes.

In 1977, The Association of Anaesthetists of Great Britain and Ireland established the Pask Certificate of Honour. Named after Edgar Pask, anaesthetist and experimental physiologist in the Royal Air Force, the award honors the gallantry of a registrar anaesthetist in the Moorgate disaster. In 2010, the award was made to 113 anaesthetists who had served in the Armed Forces in Iraq from 2003 to 2009.

Successful completion of Fellowship training of anesthesiologists in Australia and New Zealand now requires accreditation in one of the following courses: Emergency Management of Severe Trauma (EMST), Advanced Trauma Life Support (ATLS) or Effective Management of Anaesthetic Crises (EMAC).

Small studies are of limited or no use if they do not uncover a significant effect (they may be too small to reveal a significant difference). They are only useful if they reveal significant differences. For example, in 1976, Johnston et al. reported on the arrhythmias in 48 patients having transphenoidal removal of pituitary tumors after receiving submucosal injections of epinephrine in saline to minimize bleeding [48]. Of patients anesthetized with halothane, 50% developed three or more premature ventricular contractions at a dose of 2.1 mg/kg epinephrine, a dose significantly less than the 6.7 mg/kg dose of epinephrine required to produce the same rate of PVCs during anesthesia with isoflurane. This small study in humans showed that the alkane, halothane, predisposed to ventricular arrhythmias far more than did the ether, isoflurane.

In the 1980s, inhaled anesthetics were shown to have pre-conditioning effects mimicking ischemic preconditioning (a brief period of myocardial ischemia preceding a more prolonged period will protect the human heart from subsequent periods of ischemia [49] thereby reducing the impact of myocardial ischemia [50].) The protection was found to be long lasting (days) [51,52], a change persisting in the absence of anesthesia, indicating that volatile anesthetics (all of them) can up-regulate and down-regulate genes. Perhaps this explains other phenomena such as the long-term remedy supplied by anesthesia to treat severe mental depression (see below).

Studies examining survival of the heart in the face of stresses such as hypoxia make use of a now-ubiquitous device, trans-esophageal echocardiography. This noninvasive approach to evaluating the heart broke onto the scene in the early 1980s. Anesthesiologist Michael Cahalan was a leader of the evaluation and use of this device. His 1987 review article noted that echocardiography could be used to support the clinician (including the surgeon) and to further research [53].

In the 1980s and early 1990s, Hunt’s group examined the effect of hypovolemia on wounds, and found evidence for the benefit of generous fluid administration. Michael Hartmann, an anesthesiologist in Malmo, Sweden, demonstrated in 1992, that giving more fluid in response to low wound oxygen levels increased healing capacity (collagen deposition) in colon surgery patients [54]. This area of investigation was challenging. First, patients in the 1980s and 1990s were generally hypothermic. Hypothermia induced peripheral vasoconstriction and diuresis, thereby decreasing total blood volume by about 20% and limiting venous acceptance of additional fluid. A cold hypovolemic patient who received a fluid bolus might develop pulmonary edema, despite a low total blood volume. Second, heart rate, blood pressure, and urine output frequently remained normal despite up to a 20% volume loss.

Optimum fluid volume management to prevent complications remains controversial [55]. Brandstrup’s group in Copenhagen, demonstrated that giving about 2700 ml of colloid (large molecule) containing fluids improved wound outcomes more than giving 5000 ml of crystalloid (salt water). But Kabon and colleagues showed that giving high volumes of crystalloid intraoperatively led to higher wound oxygen levels than giving standard volumes (near the Brandstrup crystalloid value). Anesthesiologists, including TJ Gan, Markus Rehm, and Matthias Jacob, in addition to those already mentioned, continue this debate over fluid management. Current research is focused on so-called goal-directed therapy, in which transesophageal echocardiography, non-invasive cardiac output monitors, and other approaches are used to guide fluid therapy. Goal-directed therapy is promising, although formulation of guidelines must await completion of the large randomized trials that will provide the evidence.

In 2000 [56], anesthesiologists Greif and colleagues demonstrated that patients having colon surgery had less SSI (and an increase in wound oxygen) when given 80% oxygen during surgery. Several subsequent studies found similar results, but two found no benefit, leaving us with uncertainty about the value of high-inspired oxygen. Most agree that breathing high concentrations of oxygen for a few hours in the perioperative period is safe. A 2012 report by Meyhoff and colleagues found that mortality is not decreased by greater concentrations of oxygen for a subset of patients (those with cancer), and post-hoc analysis suggested the need to evaluate potential adverse effects of increased concentrations in patients undergoing surgery for cancer [57]. Ensuring the adequacy of perfusion by preventing activation of the SNS, appears to be a major determinant of success.

Could volatile anesthetics be used to treat mental depression? Electro-convulsive therapy (ECT) (administered along with short acting hypnotics) is frequently and successfully used to treat major depression, but it is associated with prolonged memory loss. In 1985, psychiatrist Langer and anesthesia colleagues in Vienna reasoned that perhaps the therapeutic benefit of the convulsions might be associated with the electrical silence that follows seizures rather than the convulsion, itself. If so, perhaps the use of inhaled anesthetics to achieve electrical silence in such patients might be advantageous because there would not be a prolonged effect on memory. They demonstrated that deep anesthesia with isoflurane, inducing a period of ‘electrocerebral silence,’ reduced depression in 9 of 11 subjects [58]. These results were confirmed in 1995 [59].

In 1993, a separate group from Wurzburg also demonstrated that burst-suppression associated with a deep level of isoflurane anesthesia was as effective as ECT [60]. They noted that anesthesia required more time and monitoring than ECT, and therefore suggested it as a second level intervention. Use of isoflurane did not become routine, probably because psychiatrists make treatment decisions and the support for treatment with isoflurane came from small studies, only some of which were randomized and controlled.

Scott Tadler from the Dept. of Anesthesiology at the University of Utah revived the idea of treating depression in patients with concentrations of isoflurane sufficient to briefly cause burst suppression. First, using animal models of learned helplessness, he and colleagues demonstrated that isoflurane has an antidepressant-like effect (SC Tadler, A Light, R Hughen. (2009). Isoflurane Demonstrates Antidepressant-like Activity in a Mouse Model of Depression [Abstract].Anesthesia and Analgesia,108(S), 212.). The effect was comparable to that of desipramine, using the forced swim test in mice. Paul Shepard, a psychiatrist at the University of Maryland, picked up on these results and demonstrated an antidepressant like effect in rats for isoflurane, but not for halothane. These results imply antidepressant effects unique to isoflurane and perhaps a result of medication-induced cerebral isoelectricity (achieved by isoflurane but not halothane) These data suggest the need to explore the effects of other medications that cause isoelectricity. Next, in an open label pilot study, Tadler, Weeks and colleagues found that isoflurane effectively treated depression and caused less memory loss than traditional electroconvulsive therapy [61,62]. Finally, preliminary results from a 2011 study indicate that ketamine acutely diminished depression in patients not responsive to ECT [63]. Whether this positive result would be sustained for more than a few hours is unknown but worth pursuing.

Anesthesia profoundly affects the central nervous system, but we assume that the alterations are transient, disappearing when anesthetic administration ceases. After all, the patient does awaken. Or are there persistent subtle effects that vex’or help’us? In the 1990s, Olney’s group found that halothane could prevent MK-801 (a drug with properties similar to ketamine) from inducing neurotoxicity [64], later adding isoflurane and propofol [65]. However, in 2003, Olney’s group suggested that midazolam, nitrous oxide and isoflurane given to the developing brain of rats caused cerebral apoptotic degeneration [66]. Injury to neurons in adult rat brains might be produced by nitrous oxide, with isoflurane acting to protect the brain [67].

Could similar effects produce postoperative cognitive dysfunction (POCD) in humans? In 1998, anesthesiologists Moller et al reported that patients older than 60 years were more likely to have POCD than unoperated peers, with operated patients still differing from controls 3 months after surgery [68]. But is this a consequence of the surgery, the anesthetic, being in a strange (hospital) environment or all of the above? In 2003, anesthesiologists Rasmussen et al. found that, yes, POCD occurred after surgery in patients aged 60 or greater, but that the extent of dysfunction after 3 months did not differ between patients given general versus regional anesthesia [69].

Finally, are children, particularly younger children, at risk of POCD? Considerable laboratory and epidemiological data have been gathered, with inconclusive evidence prompting concern. In 2011, this concern resulted in a presently ongoing multidisciplinary effort to determine whether such effects exist [70].

Renal transplantation and the AIDS epidemic transformed transfusion medicine, leading anesthesiologists to re-evaluate the management of anemia, blood loss, and transfusion. LT Goodnough championed approaches to reduce blood transfusion, acceptance of a lower transfusion threshold (7 g/dL hemoglobin rather than 10), and investigated the potential value of pre-donation of autologous blood and use of erythropoietin to increase red cell mass in patients scheduled for surgery potentially producing large blood loss. In the late 1990s, anesthesiologist Richard Weiskopf and his colleagues at UCSF, defined the physiologic responses to acute severe anemia in unanesthetized fit volunteers. Their findings supported the concept of a transfusion target of 7 g/dL [71].

Sessler, at UCSF, defined how anesthesia leads routinely to hypothermia. In 1988, he and his colleagues found that anesthesia broadens the threshold to the body’s response to hypothermia [72]. In the mid-1980s, Scott Augustine (a Navy anesthesiologist in San Diego) developed the forced air warmer (Bair Hugger), the first effective means of maintaining normal core temperature during anesthesia (aside from keeping the operating room too warm for the surgeons) [73]. Thus, by 1990, anesthesiologists were poised to examine whether preventing SNS activation by keeping patients warm during surgery would reduce SSI.

Based on Hunt and colleagues’ demonstration that SNS-induced peripheral vasoconstriction caused wound hypoxia; on Sessler and his colleagues’ demonstration of the mechanisms of anesthesia-induced hypothermia; and on Augustine’s development of a successful method for preventing anesthesia-induced hypothermia (the forced air warming blanket), maintenance of intraoperative normothermia was investigated as a means of improving wound outcomes. The outcome trial that resulted was published in 1996 [74]. It demonstrated that maintaining normal core temperature (36.6°C) while aggressively providing fluids and pain control reduced SSI by 67% in colon surgery patients, compared with a control group allowed to cool to 34.7°C (the routine in clinical practice at the time). Schmied et al. in Sessler’s group added further to the importance of maintaining normothermia [75]. They found that mild hypothermia (only a 1.6°C decrease) increased intra-and postoperative blood loss.

The effect of these studies on practice was rapid and widespread. By 1999, Center for Disease Control (CDC) infection control guidelines incorporated maintenance of normal core temperature for patients undergoing colon surgery. Numerous devices are presently marketed to safely prevent and treat anesthesia-related hypothermia, including forced air warmers, resistive warmers, and conductive warmers. Of note, pre-warming the patient prevents much intraoperative hypothermia and should be considered for most patients [76].

Venous thrombo-embolism significantly increases morbidity and mortality in patients undergoing surgery, and anesthesiologists have, along with surgeons, played a major role in instituting preventive measures. Pulmonary embolism is the third most common cause of preventable hospital related death, and commonly follows DVT in the lower limbs [77,78]. Surgical patients are at significant risk of developing DVT, due to intraoperative venous stasis and changes in fibrinolytic activity, as well as low postoperative mobility. The simple technique of ensuring that occlusion of calf blood vessels is avoided during surgery, is the responsibility of the anesthesia care team. Additional measures have included intermittent calf compression with sequential compression devices, and the intra-operative use of low molecular weight dextrans [79]. Rapid post-operative mobilization is also a feature of modern surgery, and anesthesiologists have played a role by adopting drugs that are rapidly eliminated.

Inhaled anesthetics can affect the environment in two ways. One is by depletion of the ozone layer. As proposed by chemists Frank Rowland and Mario Molina in 1973, breakdown of anesthetics containing bromine (halothane) or chlorine (chloroform, halothane, enflurane, isoflurane), releases the atomic halogen which, in turn, breaks down ozone [80]. Since ozone absorbs ultraviolet light, its loss would permit more ultraviolet light to reach the surface of the earth with potentially devastating effects. Rowland and Molina won the 1995 Nobel Prize for their work. The Montreal Protocol on Substances That Deplete the Ozone Layer was an international agreement limiting the release of such halogenated compounds into the environment and came into effect in the late 1980s [80], with subsequent improvement in the ozone layer. Release of inhaled anesthetics appears not to have been included in the Protocol. The anesthetics desflurane and sevoflurane in the 1990s, displaced the earlier chlorine- and bromine-containing anesthetics, and neither desflurane nor sevoflurane contain these halogens, being halogenated solely with fluorine (harmless to the ozone layer) [81].

However, inhaled anesthetics can affect the environment in a second way. All absorb infrared light. In 1937, Luft made use of this in his design of the infrared analyzer [82]. In 1991, Norwegian anesthesiologists noted the ability of nitrous oxide to act as a greenhouse gas and suggested use of lower inflow rates to minimize release into the atmosphere [83]. In 2010, anesthesiologist Susan Ryan, working with basic scientists, demonstrated that inhaled anesthetics are greenhouse gases, opening a new avenue for arguing about optimal anesthetic technique [84]. Not all anesthetics provided equal concern, desflurane having a several-fold greater potential environmental impact. However, “the overall contribution of inhalation anesthetics to greenhouse gas emission is miniscule…”, [85] “approximately 0.01% of that of the CO₂ released from global fossil fuel combustion.” [86] Even so, the anesthesia department at the University of Utah saved the equivalent greenhouse gas potential of driving 5.4 million miles over one year, by converting much of their anesthetic vapor use at their hospitals from desflurane to isoflurane. Ryan and Jodi Sherman from Yale addressed the wide range of environmental issues in anesthesia: [87] supply chain waste and contamination; disposal of unused drugs; entry of metabolized drugs into the water supply; greenhouse gas production; and disposable waste generation. The Stockholm County Council (http://​www.​janusinfo.​se/​In-English/​) has compiled data that allows comparison of the environmental impact of various drugs based on persistence, bioaccumulation, toxicity, and expected concentration in the environment. Few anesthetic drugs have been classified in this way, but such data may ultimately guide anesthesiologists interested in providing the best anesthetic care with the lowest ecological footprint. For now, regional anesthesia appears to have the smallest footprint.

A 2003 meta-analysis by anesthesiologists Petrucci and Iacovelli, found that using smaller tidal volumes in patients suffering from acute respiratory distress syndrome (ARDS) or acute lung injury (ALI) might decrease mortality [88]. In 2007, anesthesiologists Mascia et al. found that large tidal volumes per se produced lung injury in patients with severe brain injury [89]. In 2008, internists Meade et al. disputed the survival value of smaller tidal volumes in patients with ARDS or ALI [90]. However, Lellouche et al. reported in 2012 that large tidal volumes lead to organ failure and prolonged ICU stay in cardiac surgical patients [91].

From 2009 to 2012, three anesthesiologists (Scott Reuben, Joachim Boldt, and Yoshitaka Fujii) and a cardiologist (Don Poldermans) engaged in anesthesia related research, admitted to research misconduct, ranging from ethics violations to fabrication of data. This worldwide misconduct, from the US to Europe to Japan, led to retraction of more than 100 articles, with at least 200 more in jeopardy. All four individuals were publishing research germane to the topic of this chapter; that is, in areas independent of producing anesthesia.

Does working outside the mainstream of traditional anesthesia related research make it easier to commit fraud? Is this a reflection of the degree to which anesthesia related research has come to be increasingly focused on topics outside of producing anesthesia? Are journals just getting better at identifying misconduct? Regardless, this is a concerning development!

Should anesthetists participate in the intravenous delivery of drugs deliberately intended to kill those sentenced to death? In 2012, the American Board of Anesthesiologists said no, indicating that they would revoke the certification of any anesthesiologist participating in such lethal injection, defending their action by pointing to the Hippocratic injunction that physicians do no harm. Those supporting lethal injection argued that anesthesiologists are best equipped to supply such injections humanely.