PubMed Health⌕ Search

PubMed · 9921427

Cyclopropane. 1963.

Abstract

Special precautions are stressed for cyclopropane, not because they are uniquely required for this drug, but because failure to observe them is apt to result in the more rapid occurrence of disaster for the patient. Strict attention to every minute detail is absolutely essential for good, safe cyclopropane anesthesia. Most important of all is adequate ventilation. Practically, this means assisting or controlling the ventilation at all times. Constant monitoring of the precordial heart tones is also mandatory. The blood pressure must be checked frequently, especially when the level of anesthesia is being deepened. In addition to all the required antiexplosion precautions required in operating rooms, we also recommend the use of a wet towel grounding as an added precaution. The anesthesiologist should further protect himself and the patient by keeping everything around the head of the table at the same electrical potential by frequently touching the various items. He should maintain constant contact with the patient whenever possible. The anesthesiologist should train himself to take these precautions automatically, so that they will not be omitted during trying circumstances. Our experience has been that residents trained to administer good, safe cyclopropane anesthesia according to the principles enunciated usually are much more attentive to details with other techniques. Constant observation of the patient and the progress of the surgery is also necessary, if good cyclopropane anesthesia is to result. Finally, there are some guiding principles that I believe are essential for the conduct of good, safe cyclopropane anesthesia. 1. Be thoroughly familiar with the pharmacological actions of the drug. 2. Maintain a healthy respect for the potency of the drug, but no fear. 3. Be especially sure to maintain adequate ventilation through a patent airway. 4. Remember the drug is explosive. 5. Be eternally vigilant to the minute details of the conduct of the anesthesia. 6. This drug is for the real "pro," not the amateur. It is to be handled with the finesse of the violinist, not with the banging of the cymbal player. 7. Answer for yourself the question, "If this drug is so frequently selected for the very poor risk patient, wouldn't it be equally good or better for the healthy patient?".

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J S Denson. 1998. Cyclopropane. 1963.. https://doi.org/10.1097/00004311-199803640-00008

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Diabetic patients have an impaired cerebral vasodilatory response to hypercapnia under propofol anesthesia.

BACKGROUND AND PURPOSE: The purpose of this study was to examine the effects of diabetes mellitus and its severity on the cerebral vasodilatory response to hypercapnia. METHODS: Thirty diabetic patients consecutively scheduled for elective major surgery were studied. After induction of anesthesia, a 2.5-MHz pulsed transcranial Doppler probe was attached to the patient's head at the right temporal window, and mean blood flow velocity of the middle cerebral artery (Vmca) was measured continuously. After the baseline Vmca, arterial blood gases, and cardiovascular hemodynamic values were measured, end-tidal CO2 was increased by reducing ventilatory frequency by 2 to 5 breaths per minute. Measurements were repeated when end-tidal CO2 increased and remained stable for 5 to 10 minutes. RESULTS: Significant differences were observed in absolute and relative CO2 reactivity between the diabetes and control groups (absolute CO2 reactivity: control, 2.8+/-0.7; diabetes mellitus, 2.1+/-1.3; P<0.01; relative CO2 reactivity: control, 6.3+/-1.4; diabetes mellitus, 4.5+/-2.7; P<0.01, Mann-Whitney U test). Significant differences were also found between diabetic patients with retinopathy and those without retinopathy in absolute (P=0.002) and relative (P=0.002) CO2 reactivity, glycosylated hemoglobin (P=0.0034), and fasting blood sugar (P=0.01) (Scheffé's test, Mann-Whitney U test). There was an inverse correlation between absolute CO2 reactivity and glycosylated hemoglobin (r=0.69, P<0.001). CONCLUSIONS: Insulin-dependent diabetic patients have an impaired vasodilatory response to hypercapnia compared with that of the control group, and the present findings suggest that their degree of impairment is related to the severity of diabetes mellitus.

Anesthesia↗

Investigation of the effects of naratriptan, rizatriptan, and sumatriptan on jugular venous oxygen saturation in anesthetized pigs: implications for their mechanism of acute antimigraine action.

The effects of naratriptan, rizatriptan, and sumatriptan on arteriovenous oxygen saturation difference and carotid hemodynamics were compared in the anesthetized pig. Oxygen and carbon dioxide partial pressures in systemic arterial and jugular venous blood as well as hemoglobin oxygen saturation were determined by conventional blood gas analysis. Vehicle (n = 19) or naratriptan, rizatriptan, or sumatriptan (0.63, 2.5, 10, 40, 160, 630, and 2,500 microg/kg i.v.; n = 7/group) were infused cumulatively. In naratriptan-, rizatriptan-, and sumatriptan-treated animals, jugular venous oxygen saturation decreased dose dependently (geometric mean ED50 values of 3.1, 17.9, and 16.0 microg/kg, respectively) concomitantly with increases in carotid vascular resistance. Rizatriptan significantly and dose dependently, from 160 microg/kg, increased PvCO2 (P < 0.05 versus vehicle). Naratriptan and sumatriptan also tended to increase PvCO2 albeit nonstatistically significantly. All three triptans consistently evoked quantitatively similar carotid vasoconstriction, whereas decreases in jugular venous oxygen saturation (VOS) and increases in PvCO2 had different magnitudes and occurred only in around one-half of the animals studied. Maximal variations in PvCO2 were found to correlate highly with those in PvO2 (P = 0.002), but maximal variations in carotid resistance failed to correlate with those in PvCO2 (P = 0.76) or PvO2 (P = 0.28). The results demonstrate that the triptans investigated robustly produced carotid vasoconstriction, but elicited less consistent decreases in VOS and increases in jugular PvCO2, possibly suggestive of distinct mechanisms. Collectively, the data suggest that triptan-induced increases in arteriovenous oxygen saturation difference and carbon dioxide partial pressure in venous blood draining the head are class effects.

Anesthesia↗

Dynamic receptive fields of reconstructed pyramidal cells in layers 3 and 2 of rat somatosensory barrel cortex.

Whole-cell voltage recordings were made in vivo from subsequently reconstructed pyramidal neurons (n = 30) in layer 3 (L3) and layer 2 (L2) of the barrel cortex of urethane-anaesthetised rats. Average resting membrane potentials were well below (15-40 mV) action potential (AP) initiation threshold. The average spontaneous AP activity (0.068 +/- 0.22 APs s-1) was low. Principal whisker (PW) deflections evoked postsynaptic potentials (PSPs) in almost all cells of a PW column but evoked AP activity (0.031 +/- 0.056 APs per PW stimulus 6 deg deflection) was low indicating 'sparse' coding by APs. Barrel-related cells (n = 16) have their soma located above a barrel and project their main axon through the barrel whereas septum-related cells (n = 8) are located above and project their main axon through the septum between barrels. Both classes of cell had broad subthreshold receptive fields (RFs) which comprised a PW and several (> 8) surround whiskers (SuW). Barrel-related cells had shorter PSP onset latencies (9.6 +/- 4.6 ms) and larger amplitude PW stimulus responses (9.1 +/- 4.5 mV) than septum-related cells (23.3 +/- 16.5 ms and 5.0 +/- 2.8 mV, respectively). The dendritic fields of barrel-related cells were restricted, in the horizontal plane, to the PW column width. Their axonal arbors projected horizontally into several SuW columns, preferentially those representing whiskers of the same row, suggesting that they are the major anatomical substrate for the broad subthreshold RFs. In barrel-related cells the response time course varied with whisker position and subthreshold RFs were highly dynamic, expanding in size from narrow single-whisker to broad multi-whisker RFs, elongated along rows within 10-150 ms following a deflection. The response time course in septum-related cells was much longer and almost independent of whisker position. Their broad subthreshold RF suggests that L2/3 cells integrate PSPs from several barrel columns. We conclude that the lemniscal (barrel-related) and paralemniscal (septum-related) afferent inputs remain anatomically and functionally segregated in L2/3.

Anesthesia↗