Correspondence
633
Making up inotrope solutions Rooney proposed a formula to minimise drug wastage when delivering inotropes via a syringe pump (Anaesthesia 1992; 47: 83). His formula gives a final volume of solution from a known drug dose and patient body weight, which will then deliver the drug at a concentration such that 1 pg.kg-'.min-l = 1 m1.h-'. I would like to suggest a much simpler solution. This gives final volume (ml) = 0.25 x drug dose (mg). Body weight is excluded. This simple equation can be used for all adults, although 1 m1.h-I will deliver precisely 1 pg.kg-l.rnin-l for a 66.7 kg patient. However, inotropes are not strictly administered as predetermined doses according to precise body weights, but are instead titrated to the clinical response. The requirements of dobutamine or dopamine in adult patients
usually range from 2-15 pg.kg-'.min-l, and this delivery range of 2-15 ml.h-' allows easy adjustments. Also, since most patients who require inotropes are not weighed daily (or perhaps even at all), body weight equations are imprecise anyway. The above simple equation will also work quickly 'in reverse' i.e. derive the dose needed to make up a solution of required final volume, since the ratio of final volume (in ml) to dose (in mg) is always a simple 1 to 4. Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong.
T.E. OH
Change to the TVX transducer cartridge
I would like to report a change that Ohmeda have agreed to make to the black adaptor that is supplied with the TVX Transducer Cartridge for use with Excel ventilators. The cartridge is supplied with a small black adaptor to fit to the 15 mm connection of a tracheal tube, as shown in Fig. 1. A problem is caused by the fact that this black adaptor had a 22 mm knurled outer rim, that will fit tightly into a 22 mm female connection, as shown erroneously fitted into a catheter mount in Fig. 2. However, because of the knurled edge, a leak is inevitable, which is not audible above other noises, but is apparent when inspired and
Fig. 2. TVX Transducer Cartridge with black adaptor wrongly fitted into 22 mm female connector.
expired volumes are compared; this emphasises the value of always measuring the expired volume. The adaptor will, in future, be made with an outside diameter greater than 22 mm and the knurled portion will incorporate small thumb grips for fitting and removing. In the meantime I would suggest care in ensuring that the present adaptor is not fitted into 22 mm connections. Fig. 1. TVX Transducer Cartridge with black adaptor correctly fitted to 15 mm tracheal tube connector.
Maelor Hospital, Wrexham, CIwyd
G. ARTHURS
A difficult airway managed by computer?
The introduction of a computerised infusion system to deliver propofol [ I ] has allowed anaesthetists to alter the depth of anaesthesia in a simple and controlled manner. We would like to report a case where we used this system to manage a patient with a difficult airway. A 24-year-old female presented as an emergency for exploration of a blocked ventriculo-peritonea1 shunt. She had signs of raised intracranial pressure. Pre-operative examination revealed an obese women of below average intelligence, with spina bifida, hydrocephalus, and a fixed
flexion deformity of her cervical spine. Her old notes were not available. We therefore treated her as a potentially difficult tracheal intubation. Venous access was established and 100% oxygen administered via a Bain system. Continuous monitoring of heart rate, blood pressure and oxygen saturation was instituted. Anaesthesia was induced with propofol over a 10 min period using the computerised system by increasing the target concentration in 0.5 pg.ml-l increments. A laryngeal mask was inserted without difficulty a t a target concentration of 4.5 pg.ml-'
634
Correspondence
and anaesthesia maintained by the propofol infusion (6.0-3.0 pg.ml-') with the patient breathing oxygenenriched air. This was supplemented by the surgeon using local anaesthetic infiltration. Exploration of the distal end of the shunt was not required and the operation lasted 30 min. Oxygen saturation remained about 95% throughout and the highest recorded end-tidal CO, was 6.5 kPa. The patient made a swift and uneventful recovery. We would like to recommend this technique of controlled intravenous induction and maintenance of anaesthesia as a possible alternative in patients with
difficult airways in whom the use of a volatile agent is contraindicated. Institute of Neurological Sciences, Clasgow C51 4TF
R.E. MACKENZIE W.A. MCFADZEAN
Reference [ I ] WHITEM, KENNYGNS. Intravenous propofol anaesthesia using a computerised infusion system. Anaesthesia 1990; 4 5 204-9.
Can calcium channel blockers prior to tracheal intubation prevent myocardial ischaemia?
I read with interest the article by Omote et al. (Anaesthesia 1992; 47: 24-7). I would like to make a few comments regarding the clinical implications derived from their investigation. Their article demonstrated that nicardipine 20-30 pg.kg-' prevented effectively the increases in blood pressure and rate-pressure product associated with laryngoscopy and tracheal intubation in hypertensive patients, although they observed no significant difference in heart rate responses to tracheal intubation among the patients with and without nicardipine pretreatment. These results are consistent with previous investigations [ 1,2] showing how little vasodilators affected heart rate increases following tracheal intubation. Based on their present results and other reports regarding the effects of nicardipine on myocardial metabolism and coronary haemodynamics [3,4], they have assumed that nicardipine seems to be an appropriate agent for attenuation of haemodynamic alterations associated with laryngoscopy and tracheal intubation in patients with cardiovascular disease. However, they have shown no data demonstrating a lower incidence of myocardial ischaemia in the patients receiving nicardipine pretreatment. It is generally supposed that patients with ischaemic heart disease can tolerate hypertension better, and conversely can only tolerate poorly hypotension and tachycardia. Therefore, it seems unlikely that calcium channel blockers are of value in patients with ischaemic heart disease, because their administration prior to laryngoscopy and tracheal intubation may elicit profound hypotension which comprises coronary blood flow with a risk of developing myocardial ischaemia [2]. In addition, Lieberman et al. [S] have noted that myocardial ischaemia occurred with significant increases in heart rate, and with significant decreases in blood pressure
and coronary perfusion pressure in patients undergoing holothane anaesthesia for coronary artery revascularisation. They concluded that rate-pressure product was not a useful determinant for predicting myocardial ischaemia. Nevertheless, I believe that further clinical studies should be performed to evaluate whether calcium channel entry blockers could ameliorate myocardial ischaemia in patients with ischaemic heart disease undergoing laryngoscopy and tracheal intubation.
.
Department of Anaesthesiology Institute of Clinical Medicine. University of Tsukuba, Tsukuba City, Ibaraki 305, Japan
T. NISHIKAWA
References [I] STOELTING RK. Attenuation of blood pressure response to laryngoscopy and tracheal intubation with sodium nitroprusside. Anesthesia and Analgesia 1979; 58: I 16-9. T, NAMIKI A. Attenuation of the pressor response [2] NISHIKAWA to laryngoscopy and tracheal intubation with intravenous verapamil. Acta Anaesthesiologica Scandinavica 1989; 3 3 232-5. [3] HANETC, ROUSEAUMF, VINCENT M-F, POULEUR H. Effects of nicardipine on mycardial metabolism and coronary haemodynamics: a review. British Journal of Clinical Pharmacology 1986; 2 2 2 15s-29. [4] THOMASSEN A, BAGGERJP, NIELSENTT, HENNINGSEN P. Metabolic and hemodynamic effects of nicardipine during pacing-induced angina pectoris. American Journal of Cardiology 1987; 5 9 219-24. [5] LIEBERMAN RW, ORKINFK, JOBES DR, SCHWARTZAJ. Hemodynamic predictors of myocardial ischemia during halothane anesthesia for coronary-artery revascularization. Anesthesiology 1983; 5 9 36-41,
Blease Manley 4 ventilator and PEEP
I would like to bring to your attention a possible pitfall which may have serious sequelae if unrecognised. It concerns the Blease Manley 4 ventilator which may be used in a semi-closed mode and which allows ventilation via either a Bain system or a circle absorber. Using this mode of ventilation, respiratory frequency is controlled by a separate rate control knob on the top of the ventilator which is ungraduated and if inadvertently turned fully clockwise may stop the ventilator. This, of course, will normally not go unrecognised and will be promptly corrected with no harm to the patient. However, I have recently discovered that if the ventilation is so turned off one of two possible sequelae may ensue, depending upon the phase of respiration. Firstly, if ventilation is on the expiratory phase of the cycle the fresh anaesthetic gas will be spilled in the normal fashion with no deleterious effect to
the patient. The second possibility is that the ventilator is turned off during the inspiratory phase of the cycle. If this occurs, there is not only a maintenance of the PEEP which is applied directly to the patient's airway, but the PEEP will rise pari-passu with the fresh gas flow to the circle absorber. This pressure will rise to a maximum of around 70 cmH,O, at which point a pressure relief valve inside the ventilator is activated. One can easily imagine therefore the potential horrendous respiratory and cardiovascular consequences which can ensue in only a matter of seconds if the correct circumstances combine. Nowadays one would anticipate that most modern operating theatres are equipped with ventilation pressure alarms which can alert one to unexpected changes in airway pressure, but unfortunately these are not always in routine use and I would therefore suggest that extreme
633
Making up inotrope solutions Rooney proposed a formula to minimise drug wastage when delivering inotropes via a syringe pump (Anaesthesia 1992; 47: 83). His formula gives a final volume of solution from a known drug dose and patient body weight, which will then deliver the drug at a concentration such that 1 pg.kg-'.min-l = 1 m1.h-'. I would like to suggest a much simpler solution. This gives final volume (ml) = 0.25 x drug dose (mg). Body weight is excluded. This simple equation can be used for all adults, although 1 m1.h-I will deliver precisely 1 pg.kg-l.rnin-l for a 66.7 kg patient. However, inotropes are not strictly administered as predetermined doses according to precise body weights, but are instead titrated to the clinical response. The requirements of dobutamine or dopamine in adult patients
usually range from 2-15 pg.kg-'.min-l, and this delivery range of 2-15 ml.h-' allows easy adjustments. Also, since most patients who require inotropes are not weighed daily (or perhaps even at all), body weight equations are imprecise anyway. The above simple equation will also work quickly 'in reverse' i.e. derive the dose needed to make up a solution of required final volume, since the ratio of final volume (in ml) to dose (in mg) is always a simple 1 to 4. Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong.
T.E. OH
Change to the TVX transducer cartridge
I would like to report a change that Ohmeda have agreed to make to the black adaptor that is supplied with the TVX Transducer Cartridge for use with Excel ventilators. The cartridge is supplied with a small black adaptor to fit to the 15 mm connection of a tracheal tube, as shown in Fig. 1. A problem is caused by the fact that this black adaptor had a 22 mm knurled outer rim, that will fit tightly into a 22 mm female connection, as shown erroneously fitted into a catheter mount in Fig. 2. However, because of the knurled edge, a leak is inevitable, which is not audible above other noises, but is apparent when inspired and
Fig. 2. TVX Transducer Cartridge with black adaptor wrongly fitted into 22 mm female connector.
expired volumes are compared; this emphasises the value of always measuring the expired volume. The adaptor will, in future, be made with an outside diameter greater than 22 mm and the knurled portion will incorporate small thumb grips for fitting and removing. In the meantime I would suggest care in ensuring that the present adaptor is not fitted into 22 mm connections. Fig. 1. TVX Transducer Cartridge with black adaptor correctly fitted to 15 mm tracheal tube connector.
Maelor Hospital, Wrexham, CIwyd
G. ARTHURS
A difficult airway managed by computer?
The introduction of a computerised infusion system to deliver propofol [ I ] has allowed anaesthetists to alter the depth of anaesthesia in a simple and controlled manner. We would like to report a case where we used this system to manage a patient with a difficult airway. A 24-year-old female presented as an emergency for exploration of a blocked ventriculo-peritonea1 shunt. She had signs of raised intracranial pressure. Pre-operative examination revealed an obese women of below average intelligence, with spina bifida, hydrocephalus, and a fixed
flexion deformity of her cervical spine. Her old notes were not available. We therefore treated her as a potentially difficult tracheal intubation. Venous access was established and 100% oxygen administered via a Bain system. Continuous monitoring of heart rate, blood pressure and oxygen saturation was instituted. Anaesthesia was induced with propofol over a 10 min period using the computerised system by increasing the target concentration in 0.5 pg.ml-l increments. A laryngeal mask was inserted without difficulty a t a target concentration of 4.5 pg.ml-'
634
Correspondence
and anaesthesia maintained by the propofol infusion (6.0-3.0 pg.ml-') with the patient breathing oxygenenriched air. This was supplemented by the surgeon using local anaesthetic infiltration. Exploration of the distal end of the shunt was not required and the operation lasted 30 min. Oxygen saturation remained about 95% throughout and the highest recorded end-tidal CO, was 6.5 kPa. The patient made a swift and uneventful recovery. We would like to recommend this technique of controlled intravenous induction and maintenance of anaesthesia as a possible alternative in patients with
difficult airways in whom the use of a volatile agent is contraindicated. Institute of Neurological Sciences, Clasgow C51 4TF
R.E. MACKENZIE W.A. MCFADZEAN
Reference [ I ] WHITEM, KENNYGNS. Intravenous propofol anaesthesia using a computerised infusion system. Anaesthesia 1990; 4 5 204-9.
Can calcium channel blockers prior to tracheal intubation prevent myocardial ischaemia?
I read with interest the article by Omote et al. (Anaesthesia 1992; 47: 24-7). I would like to make a few comments regarding the clinical implications derived from their investigation. Their article demonstrated that nicardipine 20-30 pg.kg-' prevented effectively the increases in blood pressure and rate-pressure product associated with laryngoscopy and tracheal intubation in hypertensive patients, although they observed no significant difference in heart rate responses to tracheal intubation among the patients with and without nicardipine pretreatment. These results are consistent with previous investigations [ 1,2] showing how little vasodilators affected heart rate increases following tracheal intubation. Based on their present results and other reports regarding the effects of nicardipine on myocardial metabolism and coronary haemodynamics [3,4], they have assumed that nicardipine seems to be an appropriate agent for attenuation of haemodynamic alterations associated with laryngoscopy and tracheal intubation in patients with cardiovascular disease. However, they have shown no data demonstrating a lower incidence of myocardial ischaemia in the patients receiving nicardipine pretreatment. It is generally supposed that patients with ischaemic heart disease can tolerate hypertension better, and conversely can only tolerate poorly hypotension and tachycardia. Therefore, it seems unlikely that calcium channel blockers are of value in patients with ischaemic heart disease, because their administration prior to laryngoscopy and tracheal intubation may elicit profound hypotension which comprises coronary blood flow with a risk of developing myocardial ischaemia [2]. In addition, Lieberman et al. [S] have noted that myocardial ischaemia occurred with significant increases in heart rate, and with significant decreases in blood pressure
and coronary perfusion pressure in patients undergoing holothane anaesthesia for coronary artery revascularisation. They concluded that rate-pressure product was not a useful determinant for predicting myocardial ischaemia. Nevertheless, I believe that further clinical studies should be performed to evaluate whether calcium channel entry blockers could ameliorate myocardial ischaemia in patients with ischaemic heart disease undergoing laryngoscopy and tracheal intubation.
.
Department of Anaesthesiology Institute of Clinical Medicine. University of Tsukuba, Tsukuba City, Ibaraki 305, Japan
T. NISHIKAWA
References [I] STOELTING RK. Attenuation of blood pressure response to laryngoscopy and tracheal intubation with sodium nitroprusside. Anesthesia and Analgesia 1979; 58: I 16-9. T, NAMIKI A. Attenuation of the pressor response [2] NISHIKAWA to laryngoscopy and tracheal intubation with intravenous verapamil. Acta Anaesthesiologica Scandinavica 1989; 3 3 232-5. [3] HANETC, ROUSEAUMF, VINCENT M-F, POULEUR H. Effects of nicardipine on mycardial metabolism and coronary haemodynamics: a review. British Journal of Clinical Pharmacology 1986; 2 2 2 15s-29. [4] THOMASSEN A, BAGGERJP, NIELSENTT, HENNINGSEN P. Metabolic and hemodynamic effects of nicardipine during pacing-induced angina pectoris. American Journal of Cardiology 1987; 5 9 219-24. [5] LIEBERMAN RW, ORKINFK, JOBES DR, SCHWARTZAJ. Hemodynamic predictors of myocardial ischemia during halothane anesthesia for coronary-artery revascularization. Anesthesiology 1983; 5 9 36-41,
Blease Manley 4 ventilator and PEEP
I would like to bring to your attention a possible pitfall which may have serious sequelae if unrecognised. It concerns the Blease Manley 4 ventilator which may be used in a semi-closed mode and which allows ventilation via either a Bain system or a circle absorber. Using this mode of ventilation, respiratory frequency is controlled by a separate rate control knob on the top of the ventilator which is ungraduated and if inadvertently turned fully clockwise may stop the ventilator. This, of course, will normally not go unrecognised and will be promptly corrected with no harm to the patient. However, I have recently discovered that if the ventilation is so turned off one of two possible sequelae may ensue, depending upon the phase of respiration. Firstly, if ventilation is on the expiratory phase of the cycle the fresh anaesthetic gas will be spilled in the normal fashion with no deleterious effect to
the patient. The second possibility is that the ventilator is turned off during the inspiratory phase of the cycle. If this occurs, there is not only a maintenance of the PEEP which is applied directly to the patient's airway, but the PEEP will rise pari-passu with the fresh gas flow to the circle absorber. This pressure will rise to a maximum of around 70 cmH,O, at which point a pressure relief valve inside the ventilator is activated. One can easily imagine therefore the potential horrendous respiratory and cardiovascular consequences which can ensue in only a matter of seconds if the correct circumstances combine. Nowadays one would anticipate that most modern operating theatres are equipped with ventilation pressure alarms which can alert one to unexpected changes in airway pressure, but unfortunately these are not always in routine use and I would therefore suggest that extreme
