Intravenous Administration Of Sodium Bicarbonate Research Articles

End-tidal carbon dioxide after sodium bicarbonate infusion during mechanical ventilation or ongoing cardiopulmonary resuscitation

PurposeEnd-tidal CO2 is used to monitor the ventilation status or hemodynamic efficacy during mechanical ventilation or cardiopulmonary resuscitation (CPR), and it may be affected by various factors including sodium bicarbonate administration. This study investigated changes in end-tidal CO2 after sodium bicarbonate administration. Materials and methodsThis single-center, prospective observational study included adult patients who received sodium bicarbonate during mechanical ventilation or CPR. End-tidal CO2 elevation was defined as an increase of ≥20% from the baseline end-tidal CO2 value. The time to initial increase (lag time, Tlag), time to peak (Tpeak), and duration of the end-tidal CO2 rise (Tduration) were compared between the patients with spontaneous circulation (SC group) and those with ongoing resuscitation (CPR group). ResultsThirty-three patients, (SC group, n = 25; CPR group, n = 8), were included. Compared with the baseline value, the median values of peak end-tidal CO2 after sodium bicarbonate injection increased by 100% (from 21 to 41 mmHg) in all patients, 89.5% (from 21 to 39 mmHg) in the SC group, and 160.2% (from 15 to 41 mmHg) in the CPR group. The median Tlag was 17 s (IQR: 12–21) and the median Tpeak was 35 s (IQR: 27–52). The median Tduration was 420 s (IQR: 90–639). The median Tlag, Tpeak, and Tduration were not significantly different between the groups. Tduration was associated with the amount of sodium bicarbonate for SC group (correlation coefficient: 0.531, p = 0.006). ConclusionThe administration of sodium bicarbonate may lead to a substantial increase in end-tidal CO2 for several minutes in patients with spontaneous circulation and in patients with ongoing CPR. After intravenous administration of sodium bicarbonate, the use of end-tidal CO2 pressure as a physiological indicator may be limited.

Concentration of 2,3 bisphosphoglycerate in cattle affected with acute ruminal acidosis.

The main objective of the study conducted here was to estimate the concentration of 2,3‐Bisphosphoglycerate (2,3‐BPG), 1,3‐Bisphosphoglycerate (1,3‐BPG), bisphospho‐glycerate mutase (BPGM) and 3‐phosphoglycerate (3PG) in cattle clinically diagnosed with acute ruminal acidosis. A secondary objective was to examine the physical and chemical characteristics of the ruminal fluid in affected cattle. A total of 20 cattle clinically diagnosed with acute ruminal acidosis and eight clinically normal cattle were included in this study. The results showed that decrease of ruminal pH changed the ruminal fluid colour, odour and consistency, as well as decreased the sedimentation time, increased the methylene blue reduction time, and decreased ruminal microflora motility. The study indicated that the concentration of 2,3‐BPG, BPGM and BPGP decreased with the decrease of ruminal pH, while 3‐PG concentration was not affected with the decrease of ruminal pH. In conclusion, 2,3‐BPG could play a role in the pathogenesis of ruminal acidosis, and thus, the intravenous administration of sodium bicarbonate is important, particularly in severe cases, to correct any systemic acidosis that can decrease 2,3‐BPG concentration and results in tissue hypoxia.

A Systematic Review of Aluminium Phosphide Poisoning

Every year, about 300,000 people die because of pesticide poisoning worldwide. The most common pesticide agents are organophosphates and phosphides, aluminium phosphide (AlP) in particular. AlP is known as a suicide poison that can easily be bought and has no effective antidote. Its toxicity results from the release of phosphine gas as the tablet gets into contact with moisture. Phosphine gas primarily affects the heart, lungs, gastrointestinal tract, and kidneys. Poisoning signs and symptoms include nausea, vomiting, restlessness, abdominal pain, palpitation, refractory shock, cardiac arrhythmias, pulmonary oedema, dyspnoea, cyanosis, and sensory alterations. Diagnosis is based on clinical suspicion, positive silver nitrate paper test to phosphine, and gastric aspirate and viscera biochemistry. Treatment includes early gastric lavage with potassium permanganate or a combination with coconut oil and sodium bicarbonate, administration of charcoal, and palliative care. Specific therapy includes intravenous magnesium sulphate and oral coconut oil. Moreover, acidosis can be treated with early intravenous administration of sodium bicarbonate, cardiogenic shock with fluid, vasopresor, and refractory cardiogenic shock with intra-aortic baloon pump or digoxin. Trimetazidine may also have a useful role in the treatment, because it can stop ventricular ectopic beats and bigeminy and preserve oxidative metabolism. This article reviews the epidemiological, toxicological, and clinical/pathological aspects of AlP poisoning and its management.

Non-Cardiogenic Pulmonary Edema in Salicylate Posioning

Salicylate-induced pulmonary edema (SIPE) can occur in both acute and chronic users of aspirin or salicylate products. The medical history, especially when it reveals the use of salicylates, is critical when considering this diagnosis. Unfortunately, the neurologic and systemic effects of salicylate toxicity may hinder the ability to obtain a reliable medical history. SIPE should be considered in patients who present with pulmonary edema and neurological changes, anion-gap metabolic acidosis, or possible sepsis. Some patients may be treated for “pseudosepsis” or other conditions, thereby delaying the diagnosis of salicylate intoxication. Misdiagnosis and possibly delayed diagnosis of SIPE can lead to a significant increase in morbidity and mortality. Serum and urine alkalinization by administration of intravenous sodium bicarbonate are commonly utilized therapeutic strategies. Finally, hemodialysis is a therapy, which should be considered early in the course of treatment. The objective of this case report and review is to emphasize the importance of rapid diagnosis and appropriate treatment in patients with SIPE, and summarize the current literature as it relates to the adult population.

Current Management of Salicylate-Induced Pulmonary Edema

Salicylate-induced pulmonary edema (SIPE) can occur in both acute and chronic users of aspirin or salicylate products. The medical history, especially when it reveals the use of salicylates, is critical when considering this diagnosis. Unfortunately, the neurologic and systemic effects of salicylate toxicity may hinder the ability to obtain a reliable medical history. SIPE should be considered in patients who present with pulmonary edema and neurological changes, anion-gap metabolic acidosis, or possible sepsis. Some patients may be treated for "pseudosepsis" or other conditions, thereby delaying the diagnosis of salicylate intoxication. Misdiagnosis and possibly delayed diagnosis of SIPE can lead to a significant increase in morbidity and mortality. Serum and urine alkalinization by administration of intravenous sodium bicarbonate are commonly utilized therapeutic strategies. Finally, hemodialysis is a therapy which should be considered early in the course of treatment. The objective of this review was to emphasize the importance of rapid diagnosis and appropriate treatment in patients with SIPE, and summarize the current literature as it relates to the adult population.

Dogma Disputed

Sodium bicarbonate is an ideal buffer for the treatment of metabolic acidosis if the following conditions are present: 1) the desired pH is close to 6.1, 2) the recipient has the ability to excrete instantly any additional carbon dioxide generated, and 3) the additional osmoles do not shift the pKa of all buffers downward. Unfortunately, none of these three conditions are met. Intravenous sodium bicarbonate might provide a benefit if the patient who has metabolic acidosis needs more extracellular fluid volume (eg, those who have lactic acidosis). However, in trials comparing the effect of sodium bicarbonate with sodium chloride or albumin, sodium bicarbonate was not superior. Consequently, the intravenous administration of sodium bicarbonate is not recommended for the treatment of newborns who have metabolic acidosis.

Efficacy of Single-Bolus Administration of Sodium Bicarbonate to Prevent Contrast-Induced Nephropathy in Patients With Mild Renal Insufficiency Undergoing an Elective Coronary Procedure

We sought to clarify whether a single-bolus intravenous administration of sodium bicarbonate in addition to hydration with sodium chloride prevents contrast-induced nephropathy (CIN). One hundred forty-four patients with mild renal insufficiency (serum creatinine >1.1 to <2.0 mg/dl) undergoing an elective coronary procedure were randomly assigned to the following 2 groups: standard hydration with sodium chloride plus single-bolus intravenous administration of sodium bicarbonate (20 mEq) immediately before contrast exposure (group A, n = 72) and standard hydration alone (group B, n = 72). The primary end point was development of CIN, defined as an increase >25% or >0.5 mg/dl in serum creatinine within 3 days after the procedure. Incidence of the primary end point was lower in group A than in group B (1.4% vs 12.5%, p = 0.017). Incidence of adverse clinical events (acute pulmonary edema, acute renal failure requiring dialysis, and death within 7 days of procedure) did not differ between the 2 groups (0% vs 1.4%). In conclusion, single-bolus intravenous administration of sodium bicarbonate in addition to standard hydration can more effectively prevent CIN than standard hydration alone in patients with mild renal insufficiency undergoing an elective coronary procedure.

Sodium bicarbonate for prevention of contrast-induced acute kidney injury: a systematic review and meta-analysis

There have been conflicting reports on the use of intravenous administration of sodium bicarbonate for prevention of contrast-induced acute kidney injury (CI-AKI). The aim of this study was to evaluate the use of sodium bicarbonate for prevention of CI-AKI. This is a symptomatic review and meta-analysis of prospectively randomized studies, abstracts and manuscripts, published from 1950 to 20 February 2009. Of 192 identified publications, 18 studies (n = 3055) were included. Nine studies were only published as an abstract. CI-AKI occurred in 11.6%. Six prospective studies demonstrated that intervention with sodium bicarbonate resulted in a decreased risk of CI-AKI. The aggregate result of the prospective trials also demonstrated a benefit favouring sodium bicarbonate (RR = 0.66, 95% CI = 0.45-0.95). This effect was most prominent in coronary procedures and in patients with chronic kidney disease. There was no effect on need for renal replacement therapy (RRT) and mortality. Published manuscripts demonstrated a beneficial effect, while abstracts could not. Also, funnel plot analysis suggested a publication bias. In addition, we found significant clinical and statistical heterogeneity between studies. Finally, the quality of the individual studies was limited. The incidence of CI-AKI was higher than recently reported, and varied among study cohorts. We found a preventive effect of the use of sodium bicarbonate on the risk for CI-AKI, however, with borderline statistical significance. There was no effect on need for RRT or mortality. The relative low quality of the individual studies, heterogeneity and possible publication bias means that only a limited recommendation can be made in favour of the use of sodium bicarbonate.

Life-Threatening Flecainide Intoxication in a Young Child Secondary to Medication Error

To describe a case of life-threatening flecainide intoxication in a toddler, secondary to accidental reversal of syringes used for oral administration. A 2-year-old male with a history of a persistent junctional reciprocating tachycardia had been receiving flecainide 4.8 mg/kg/day (1 mL 3 times daily) and nadolol 2 mg/kg/day (5 mL once daily) for 10 months. One morning, 3 hours after the drugs were administered, he became bradycardic (heart rate 50 beats/min) and then presented to the emergency department with vital signs absent. After initial cardiopulmonary resuscitation and epinephrine, he was bradycardic; this was followed by wide-complex tachycardia that converted rapidly to narrow-complex tachycardia after bolus administration of intravenous sodium bicarbonate for suspected flecainide intoxication. Following resuscitation, he remained hemodynamically stable and was discharged in normal sinus rhythm without neurologic sequelae. Drug concentrations obtained at the time of presentation showed a serum concentration of flecainide of 0.668 microg/mL. Drug formulations were also analyzed and found to contain the expected concentration of flecainide. Literature regarding adverse drug events in the pediatric outpatient population is reviewed, as well as how these risks apply to flecainide, a medication with a low margin of safety. Pediatric experience with flecainide intoxication and sodium bicarbonate administration as an antidote is reviewed. Analysis of the serum drug concentrations demonstrated blood concentrations consistent with syringe reversal, which would have produced a 5-fold flecainide overdose. The Naranjo probability scale indicated a highly probable relationship between flecainide ingestion and the life-threatening event in this case. This case of life-threatening flecainide intoxication in a young child, secondary to accidental reversal of medication syringes, underscores the importance of providing parents with accurate dispensing information and labeling medication bottles and syringes in an unambiguous manner.

Abstract 2017: A Single Bolus Intravenous Administration of Sodium Bicarbonate is Effective in the Prevention of Contrast-Induced Nephropathy in Patients with Renal Insufficiency Undergoing Diagnostic Coronary Arteriography or Elective Percutaneous Coronary Intervention

BACKGROUND: Recent prospective studies have demonstrated that intravenous hydration with sodium bicarbonate (SB) is effective in the prevention of contrast-induced nephropathy (CIN). However, it has not yet been invetigated whether a single bolus intravenous administration of SB immediately before exposure to contrast media can prevent CIN. Accordingly, this prospective, controlled, randomized trial was designed to examine the efficacy of a single bolus administration of SB in the prevention of CIN in patients with renal insufficiency undergoing diagnostic coronary arteriography (CAG) or elective percutaneous coronary intervention (PCI). METHODS: A total of 144 patients with a serum creatinine level of &gt;1.1 mg/dl and &lt;2.0 mg/dl scheduled for diagnostic CAG or elective PCI were enrolled in this study. The patients were randomly assigned to the following 2 groups: standard intravenous hydration with sodium chloride plus a single bolus intravenous administration of SB (20 ml = 20 mEq) 5 min before exposure of contrast media (group A, n = 72) and standard intravenous hydration with sodium chloride alone (group B, n = 72). The primary end point was the development of CIN, defined as an increase of ≥25% or ≥0.5mg in serum creatinine level within 3 days after the procedure. We also evaluated the incidence of adverse clinical events, including acute pulmonary edema, acute renal failure requiring dialysis, and death within the first 7 days after the procedure. RESULTS: There were no significant group differences in age, gender, the frequencies of diabetes mellitus and PCI, serum creatinine at baseline, the volume of contrast media, and drugs administered. The single bolus intravenous administration of SB led to a significant increase in arterial blood pH (7.41 ± 0.04 to 7.43 ± 0.03, p &lt;0.001). The incidence of primary end point was significantly lower in group A than in group B (1.4% vs 12.5%, p = 0.017). The incidence of adverse clinical events did not differ significantly between the 2 groups (0% vs 1.4%). CONCLUSIONS: A single bolus intravenous administration of SB before contrast injection is effective in the prevention of CIN in patients with renal insufficiency undergoing diagnostic CAG or elective PCI.

Unintentional poisoning by phosphine released from aluminum phosphide

Aluminum phosphide as a releaser of phosphine gas is used as a grain preservative. In this case report, we describe an accidental severe poisoning in a 35-year-old woman, her 18-year-old daughter, and 6-year-old son caused by inhalation of phosphine gas released from 20 tablets of aluminum phosphide stored in 15 rice bags. The boy died 2 days after exposure before admission to hospital and any special treatment, but the others were admitted 48 h after exposure. They had signs and symptoms of severe toxicity, and their clinical course included metabolic acidosis, electrocardiographic changes, and hypotension. They were treated by intravenous administration of sodium bicarbonate, magnesium sulfate, and calcium gluconate. The patients were discharged after 3 days and followed up for 1 week after discharge. Rapid absorption of phosphine by inhalation, induction of hyperglycemia, and surviving of patients are interesting issues of this case report.

Comment on Point:Counterpoint “In health and in a normoxic environment, V̇o2 maxis/is not limited primarily by cardiac output and locomotor muscle blood flow”

Comment on Point:Counterpoint “In health and in a normoxic environment, V̇<scp>o</scp>_{2 max}is/is not limited primarily by cardiac output and locomotor muscle blood flow”

Successful treatment of acute aluminium phosphide poisoning: possible benefit of coconut oil

Aluminium phosphide is used to control rodents and pests in grain storage facilities. It produces phosphine gas, which is a mitochondrial poison. Unfortunately, there is no known antidote for aluminium phosphide intoxication, but our recent experience with a case showed that rapid prevention of absorption by coconut oil might be helpful. In the present case, we used the same protocol in a 28-year-old man who had ingested a lethal amount (12 g) of aluminium phosphide with suicidal intent and was admitted to hospital approximately 6 hours postingestion. The patient had signs and symptoms of severe toxicity, and his clinical course included metabolic acidosis and liver dysfunction. Treatment consisted of gastric lavage with potassium permanganate solution, oral administration of charcoal and sorbitol suspension, intravenous administration of sodium bicarbonate, magnesium sulphate and calcium gluconate, and oral administration of sodium bicarbonate and coconut oil. Conservative and supportive therapy in the Intensive Care Unit was also provided. The patient survived following rapid treatment and supportive care. It is concluded that coconut oil has a positive clinical significance and can be added to the treatment protocol of acute aluminium phosphide poisoning in humans.

Management of the Cardiovascular Complications of Tricyclic Antidepressant Poisoning

Experimental studies suggest that both alkalinisation and sodium loading are effective in reducing cardiotoxicity independently. Species and experimental differences may explain why sodium bicarbonate appears to work by sodium loading in some studies and by a pH change in others. In the only case series, the administration of intravenous sodium bicarbonate to achieve a systemic pH of 7.5-7.55 reduced QRS prolongation, reversed hypotension (although colloid was also given) and improved mental status in patients with moderate to severe tricyclic antidepressant poisoning. This clinical study supports the use of sodium bicarbonate in the management of the cardiovascular complications of tricyclic antidepressant poisoning. However, the clinical indications and dosing recommendations remain to be clarified. Hypotension should be managed initially by administration of colloid or crystalloid solutions, guided by central venous pressure monitoring. Based on experimental and clinical studies, sodium bicarbonate should then be administered. If hypotension persists despite adequate filling pressure and sodium bicarbonate administration, inotropic support should be initiated. In a non-randomised controlled trial in rats, epinephrine resulted in a higher survival rate and was superior to norepinephrine both when the drugs were used alone or when epinephrine was used in combination with sodium bicarbonate. Sodium bicarbonate alone resulted in a modest increase in survival rate but this increased markedly when sodium bicarbonate was used with epinephrine or norepinephrine. Clinical studies suggest benefit from norepinephrine and dopamine; in an uncontrolled study the former appeared more effective. Glucagon has also been of benefit. Experimental studies suggest extracorporeal circulation membrane oxygenation is also of potential value. The immediate treatment of arrhythmias involves correcting hypoxia, electrolyte abnormalities, hypotension and acidosis. Administration of sodium bicarbonate may resolve arrhythmias even in the absence of acidosis and, only if this therapy fails, should conventional antiarrhythmic drugs be used. The class 1b agent phenytoin may reverse conduction defects and may be used for resistant ventricular tachycardia. There is also limited evidence for benefit from magnesium infusion. However, class 1a and 1c antiarrhythmic drugs should be avoided since they worsen sodium channel blockade, further slow conduction velocity and depress contractility. Class II agents (beta-blockers) may also precipitate hypotension and cardiac arrest.

Sodium bicarbonate-augmented stress thallium myocardial scintigraphy

It is well known that sodium bicarbonate in pharmacological doses induces transient alkalosis, causing intracellular transport of serum potassium. The aims of this study were (a) to investigate whether, in humans, myocardial thallium-201 uptake can be augmented by pretreatment with a single bolus of sodium bicarbonate at a pharmacological dose, (b) to verify general safety aspects of the intervention and (c) to evaluate the clinical implications of augmentation of (201)Tl uptake, if any. Routine exercise myocardial scintigraphy was performed twice in eight adult volunteers (five normal and three abnormal), once without intervention and the second time (within a week) following intravenous administration of sodium bicarbonate (88 mEq in 50 ml) as a slow bolus 1 h prior to the injection of (201)Tl. Conventional myocardial thallium study was compared with sodium bicarbonate interventional myocardial scintigraphy with respect to myocardial uptake (counts per minute per mCi injected dose), washout patterns in normal and abnormal myocardial segments, and overall clinical interpretation based on planar and single-photon emission tomographic (SPET) images. All patients remained asymptomatic after the intervention. A mean increase of 53% in myocardial uptake of thallium was noted in post-exercise acquisitions after the intervention, confirming uptake of the tracer via the potassium-hydrogen pump and its augmentation by transient alkalosis. The washout pattern remained unchanged. The visual quality of planar and SPET images improved significantly after the intervention. Out of the five abnormal myocardial segments identified in three cases, four showed significant filling-in after the intervention, causing the diagnosis to be upgraded from "partial scar" to "ischaemia", or from "ischaemia" to "normal". The overall scan impression changed in two out of three such cases. Sodium bicarbonate augmentation may have significant implications for stress-thallium scintigraphy and may be a new parameter for defining myocardial viability.

Does urine alkalinization increase salicylate elimination? If so, why?

Urine alkalinization is a treatment regimen that increases poison elimination by the administration of intravenous sodium bicarbonate to produce urine with a pH > or = 7.5. Experimental and clinical studies confirm that urinary alkalinization increases salicylate elimination, although the mechanisms by which this occurs have not been elucidated. The conventional view is that ionisation of a weak acid, such as salicylic acid, is increased in an alkaline environment. Since the ionisation constant (pKa) is a logarithmic function then, theoretically, a small change in urine pH will have a disproportionately larger effect on salicylate clearance. Hence, elimination of salicylic acid by the kidneys is increased substantially in alkaline urine. However, as salicylic acid is almost completely ionised within physiological pH limits, alkalinization of the urine could not, therefore, significantly increase the extent of ionisation further and the conventional view of the mechanism by which alkalinization is effective is patently impossible. Further experimental studies are required to clarify the mechanisms by which urine alkalinization enhances salicylate elimination.

ナリジクス酸により重篤な代謝性アシドーシスと意識障害を来した１例

We treated a case of metabolic acidosis and delirium induced by 4g of nalidixic acid ingestion. A 32-year-old previously healthy woman suffering from dyspnea was brought to our emergency treatment center delirious, screaming continuously, and hyperventilating. Arterial blood gas analysis revealed acidemia with metabolic acidosis and compensatory respiratory alkalosis. Intravenous administration of sodium bicarbonate, gastric lavage, and activated charcoal administration through a gastric tube restored her orientation after receiving sodium bicarbonate, which suggested acidemia affected her consciousness. She was lucid and had fully recovered 12 hours after drug ingestion. One hour after drug ingestion, serum nalidixic acid concentration was 155.16μg/ml, 68.80μglml 3 hours after, and 0.065μg/ml 14 hours after.

Overdoses of tricyclic antidepressants: grandchildren and grandparents

TCAs are an extremely toxic source of poisoning in young children. Overdoses of TCAs can cause coma, seizures, hypotension, cardiac arrhythmias, and cardiac arrest. Treatment is directed at rapid assessment, monitoring, support of vital functions, halting drug absorption, and treating CNS and cardiac toxic effects. All children should be monitored for a minimum of 6 hours, and many require admission to a critical care unit. The mainstay of therapy is alkalinization. Intravenous administration of sodium bicarbonate is the preferred treatment for hypotension, shock, and arrhythmias. Blood pH should be monitored and should be maintained between 7.45 and 7.55. More specific drug therapy, cardioversion, or artificial pacing may be required for refractory arrhythmias. Before the child is discharged from the hospital, strategies to reduce the risk of future poisonings should be discussed with the child's family.

Changes in end-tidal carbon dioxide tension following sodium bicarbonate administration: correlation with cardiac output and haemoglobin concentration.

An intravenous administration of sodium bicarbonate (NaHCO3) forms excess CO2, resulting in an immediate increase in end-tidal carbon dioxide tension (PETCO2). We hypothesized that the time until PETCO2 reached a maximum, and the magnitude of the increase in PETCO2 are influenced by cardiac output and haemoglobin concentration, respectively. To test this hypothesis, we examined changes in PETCO2 following an intravenous administration of NaHCO3 at different levels of cardiac output and haemoglobin concentration. We administered 0.2 mmol.kg-1 of 8.4% NaHCO3 into the vena cava in 15 anesthetized dogs under mechanical ventilation of 20 breaths per min. Cardiac output was increased by dopamine infusion, and decreased by blood withdrawal under halothane anaesthesia. Haemoglobin concentrations were changed by haemodilution with hydroxyethyl starch. When control measurements were taken, time-max (the time until the increase in PETCO2 reached a maximum) was 4 +/- 0.2 breaths-time, and delta CO2-max (the magnitude of the increase in PETCO2) was 0.90 +/- 0.04 kPa (6.6 +/- 0.3 mmHg). Cardiac output was inversely correlated with time-max (r = 0.94, P < 0.0001), while it revealed a poor correlation with delta CO2-max. Haemoglobin concentration showed a significant correlation with delta CO2-max (r = 0.736, P < 0.005), but not with time-max. We concluded that the time course and the magnitude of changes in PETCO2 following intravenous administration of NaHCO3 reflect changes in cardiac output and haemoglobin concentration, respectively.

Capture and transportation of Elasmobranchs, with emphasis on the Grey Nurse Shark (Carcharias taurus)

Physiological changes manifest during the capture and transportation of elasmobranchs are discussed. Reference is made to the general adaptation syndrome and to mechanisms of change in concentrations of blood glucose, blood acid and serum electrolyte. Methods of alleviating these profound changes are suggested, with emphasis on the capture and transportation of the grey nurse shark (Carcharias taurus). The hoop method is shown to be a convenient technique for capturing wild grey nurse sharks, and a combination of ketamine hydrochloride and xylazine hydrochloride, with antagonism by yohimbine hydrochloride, is found to provide an acceptable regime of transportation anaesthesia. Intravenous administration of sodium bicarbonate and glucose as well as oxygenation of water in the life-support system are shown to be valuable methods of alleviating stress-induced blood acidosis.