Printer Friendly

Anaesthesia for implantation of the Jarvik 2000 Flowmaker[R] LVAD.

SUMMARY

The Jarvik 2000 Flowmaker[R] is an intraventricular continuous axial flow left ventricular assist device. We describe the anaesthetic management and considerations for five patients with end-stage heart failure who underwent implantation of the Jarvik 2000 Flowmaker[R] as a bridge to transplantation or as destination therapy.

Key Words: anaesthesia, Jarvik 2000 Flowmaker[R], ventricular assist device

**********

The Jarvik 2000 Flowmaker[R] (Jarvik Heart, Inc., New York, NY, U.S.A.) is an implantable left ventricular assist device (LOAD) that produces continuous non-pulsatile axial flow by means of a single rotating vaned impeller, rotating at 8000-12000 rpm (1). It is unique amongst currently available LUADs in that its small size (90 g, 2.5 cm by 5.5 cm) allows it to be implanted directly into the apex of the left ventricle without an inflow cannula. The outflow is attached to the aorta via a Dacron graft. A percutaneous driveline connects the device to a control and battery. The rate of flow can be adjusted on a scale of 1 to 5. Since 2000, it has been used as bridge to cardiac transplantation in the United States and Europe, as well as a form of destination therapy in Europe for patients with end-stage cardiac failures (1-3). As of September 2005, the longest the implant had been used without replacement or repair is 5.2 years (personal communication).

The surgical approach is through a median sternotomy or left thoracotomy and the device can be inserted with or without cardiopulmonary bypass (CPB) (4). The anaesthetic management of the Jarvik 2000 FlowMaker[R] inserted into fibrillating hearts whilst on CPB has been previously discussed (5). We present our experience with the anaesthetic management for the first five insertions of the Jarvik 2000 Flowmaker[R] in Australasia.

CASE HISTORIES

All patients suffered from end-stage, New York Heart Association Class 4 cardiac failure, with previous hospital admissions requiring intravenous inotropes. The first four had been placed on the cardiac transplant register for end-stage cardiac failure. Extensive investigations carried out as part of their assessment for transplant eligibility included echocardiography, oxygen consumption testing, right heart haemodynamic studies and coronary angiography. Patient 5 was ineligible for transplantation and had the device inserted as destination therapy. The aetiology of cardiac failure and other patient characteristics can be found in Table 1.

An illustrative case--Patient 1

Patient 1 was a 34-year-old male, suffering from anthracycline-induced cardiomyopathy.

One week before implantation he had been admitted for decompensated heart failure and treated with maximal medical therapy, including levosimendan, followed by a milrinone infusion started the day before surgery. A pulmonary artery flow-directed continuous cardiac output catheter had been inserted preoperatively.

Premedication consisted of oral lorazepam and intramuscular morphine. Upon arrival in the operating theatre a large peripheral intravenous cannula and a radial arterial line were inserted in the right upper limb. Anaesthesia was induced with fentanyl 12 [mu]g/kg, sevoflurane and pancuronium 8 mg and thereafter maintained with up to sevoflurane 2% in oxygen and air and a morphine infusion, with the aid of a BIS[R] (Aspect Medical Systems, Inc, Newton, MA, U.S.A.) monitor. Antibiotic prophylaxis with vancomycin and gentamicin was given according to institutional practice. A39 Fr left-sided double-lumen tube was used to achieve lung isolation and, at the end of surgery, was exchanged for a single-lumen endotracheal tube prior to transfer to the intensive care unit (ICU).

A multi-lumen central venous catheter was inserted in the left subclavian vein and a large-bore double-lumen venous catheter was placed in the left internal jugularvein. High dose aprotinin (Trasylol[R], Bayer AG, Germany) and an autologous blood salvage system (Cell Saver 5[R], Haemonetics, Braintree, MA, U.S.A.) were used. A transoesophageal echocardiography (TOE) probe was inserted and external defibrillator pads were placed prior to surgery.

He was positioned in a partial right lateral position and following full anticoagulation with heparin, cannulae were inserted into the left femoral vessels and connected to the CPB circuit.

The details of the surgical implantation have been previously described (6). In summary for this case, the aortic graft was sewn onto the descending aorta and the power cable was brought through the abdominal wall in the right hypochondrium. A silicone/polyester sewing cuff was then sewn onto the apex of the left ventricle and an incision made in the ventricular wall within the ring. A coring device was inserted to make a clean circular cut and upon its removal, the LVAD was immediately placed in the apex. All this was performed with the heart still beating. Titrated doses of esmolol (100 mg in total) were given to reduce the heart rate, aiming for a target of less than 50 beats per minute. The device was then connected to the power supply and tested through its range of speeds from 1 to 5. It was left to run at the speed that allowed for intermittent aortic valve opening, which for this patient was speed 2.

Protamine was administered to reverse heparinization and fresh frozen plasma, platelets and washed blood from the blood salvage system were given as required.

Vasoactive drugs used included glyceryltrinitrate (GTN), noradrenaline and milrinone, guided by haemodynamic data from invasive pressures, cardiac output monitoring and TOE.

The patient was transferred to the ICU for postoperative management. His and the other patients' courses in the ICU and subsequently in the ward are summarized in Table 2. Postoperative pain management included intercostal nerve blocks placed by the surgeon towards the end of surgery and intravenous opioids as continuous infusions or patient controlled analgesia.

Unlike Patient 1, the other four patients were not on intravenous inotropes just prior to surgery and had pulmonary artery catheters with continuous cardiac output monitoring placed after induction of anaesthesia. Their anaesthetic management was otherwise similar to Patient 1 except where described in the brief summaries to follow. Other than Patient 1 and 2, the other patients did not receive any esmolol at time of implantation. Mean surgical time was 225 min (SD 45 min) (Table 2).

Patient 2

The planned surgical approach, because of surgical preference, for Patient 2 was via a median sternotomy. He had a pre-existing internal bi-ventricular pacing cardiodefibrillator (ICD) which was switched off just prior to surgery. Following sternotomy he was cannulated via the ascending aorta and right atrium in the event CPB would be necessary. The outflow graft was anastomosed onto the ascending aorta. Esmolol 40 mg was given and, as the device was inserted into the left ventricle and started, the cardiac output and blood pressure fell precipitously. He required cardiopulmonary bypass for 28 minutes while awaiting cardiac function and LOAD function to stabilize. He was the only patient to require cardiopulmonary bypass and was easily weaned from bypass and transferred to ICU. The immediate postoperative period was complicated by ongoing bleeding despite attempts to correct the coagulopathy with infusion of blood products. This required four further operations in the first 72 hours to secure haemostasis and eventually close the sternum. As a result of this, his extubation was delayed until the third postoperative day.

[FIGURE 1 OMITTED]

The rest of his postoperative course was relatively uneventful and he was discharged home on day 21 and readmitted 66 days post-LOAD insertion for cardiac transplantation. A left ventricular thrombus was seen at the base of the explanted device (Figure 1).

Patient 3

Anaesthesia for this patient with Becker's muscular dystrophy was maintained with total intravenous anaesthesia using a target controlled infusion of propofol, fentanyl and morphine without neuromuscular blockade.

Patient 4

Patient 4 underwent percutaneous closure of a patent foramen ovale with an Amplatzer[R] device (AGA Medical Corporation, Golden Valley, MN, U.S.A.) 13 days prior to insertion of the LVAD. While the preoperative echocardiogram showed normal right ventricular function, he developed right heart failure with pulmonary hypertension after insertion of the device. Inhaled nitric oxide was used to reduce pulmonary vascular resistance and manage his right heart failure.

Patient 5

Patient 5 was ineligible for cardiac transplantation due to other co-morbidities including end-stage renal failure. A Jarvik 2000 FlowMaker[R] was inserted as destination therapy. As his femoral and aortic vessels were heavily calcified, surgery was performed without femoral or central cannulation. Interestingly, he had pre-existing severe pulmonary hypertension with a raised transpulmonary gradient of 26 mmHg, in the absence of significant respiratory disease. This resulted in worsening right heart failure while on one-lung ventilation with increasing central venous pressure and falling cardiac output. He required high doses of adrenaline (up to 1 [mu]g/kg/min), noradrenaline (up to 1.2 leg/kg/min), vasopressin (up to 8 IU/h), inhaled nitric oxide (up to 60 ppm) and return to two-lung ventilation to maintain adequate blood pressure prior to device insertion. Vasopressin was weaned off once the LVAD was inserted. He was discharged, but died during a subsequent admission (Figure 2).

[FIGURE 2 OMITTED]

DISCUSSION

The Jarvik 2000 FlowMaker[R] functions as a true ventricular assist device, with the flow rate depending on the pump speed and the pressure differential between the left ventricle and the aorta (7). The presence of native ventricular function generates pulsatility across the pump as the pump speed is reduced. When blood begins to flow across the aortic valve, a dicrotic notch appears on the arterial wave form. The latest generation pumps are controlled by the ILS-Flow controller (Intermittent Low Speed) where the speed of rotation falls for 8 seconds during each 64 second cycle. This reduces stasis in the aortic root and ventricular apex. A pulse is easily discernable during this period. As the pump is particularly afterload sensitive, haemodynamic goals include a low normal mean arterial pressure of 70-80 mmHg.

Potential advantages of the Jarvik 2000 FlowMaker[R] are related to its small size and intraventricular position. It can be used for smaller patients and children where other larger LVADs are relatively contraindicated. Lack of an abdominal pocket also simplifies the surgical procedure and eliminates the risk of pocket infection. Intra-device thrombosis may be reduced by the continuous flow and the absence of an inflow cannula (1). However, a thrombus may still form in low flow areas in the left ventricle, as in Patient 2 (8). As an alternative to an abdominal driveline, a post-auricular skull-mounted power delivery system has been used for patients receiving the device as destination therapy and may potentially reduce the incidence of driveline infection. It has been suggested that the device is associated with a lower incidence of infection and haemolysis (8,9).

The anaesthetic management of patients undergoing insertion of the Jarvik 2000 FlowMaker[R] presents several challenges to the anaesthetist including the patients' underlying medical condition, the surgical procedure and potential complications.

In a patient with end-stage cardiac failure, cardiac output is relatively fixed and dependent on adequate preload and heart rate (10). Increases in afterload may reduce cardiac output. Patients are also prone to malignant ventricular arrhythmias, requiring prior insertion of ICDs and placement of external defibrillator pads at the start of the procedure. Biventricular pacing ICDs may have been placed to resynchronise atrio-ventricular contraction and improve cardiac output.

Many patients, particularly those with idiopathic cardiomyopathies, have pre-existing right ventricular failure. Flow-directed pulmonary artery catheters with mixed venous oxygen saturation monitoring and TOE are used to guide fluid and drug therapy to optimize haemodynamic status perioperatively. Haemodynamic goals include maintenance of adequate left ventricular filling and heart rate, reducing afterload and provision of right ventricular support.

The left ventricle is offloaded once the pump is started. Failure to maintain adequate left ventricular preload in the presence of a working pump can cause subatmospheric pressures to develop in the ventricle with entrainment of air through fresh suture lines causing systemic air embolism. Left ventricular filling also requires adequate right ventricular function. Right ventricular dysfunction may be pre-existing and can be worsened by rapid infusion of fluids, blood transfusion, pre-existing pulmonary hypertension, hypoxic vasoconstriction from lung isolation and right ventricular dilatation with a shift of the interventricular septum to the left (11). Increasing the pump speed under these circumstances may be detrimental. Frusemide may be used to maintain fluid balance during transfusion of blood products. Insertion of another Jarvik device into the right ventricle to serve as a right ventricular assist device is being investigated (12).

Before insertion of the device a complete TOE examination is performed, in particular to exclude a patent foramen ovale and to assess for aortic regurgitation (10,11). TOE is used to monitor cardiac filling and function, confirm the device's intraventricular position and orientation towards the mitral inflow, ensure adequate removal of air, assess right heart function, and flow across the aortic valve. It is important to exclude a patent foramen ovale again after device insertion as it may be unmasked with a fall in left atrial pressures. Identification of the site of insertion of the aortic graft and measurements of velocity through it allows for calculation of the flow generated by the pump.

Vasoactive drugs are often required as vasodilation is common due to anaesthetic agents, angiotensin converting enzyme inhibitors, milrinone and the inflammatory response to surgery and cardiopulmonary bypass, if used. Vasopressors used intraoperatively in our patients included phenylephrine, noradrenaline, adrenaline and vasopressin. However, vasoconstrictor use must be judicious as the flow rate across the device is impeded by high afterload. Milrinone with its inodilator properties is particularly useful in supporting right ventricular function while reducing pulmonary vascular resistance. GTN infusions and inhaled nitric oxide are used to manage pulmonary hypertension.

Use of a left thoracotomy approach brings with it the usual considerations relating to lung isolation, positioning and vascular access. Arterial lines are set preferentially in the radial arteries as brachial lines may be kinked during positioning. For patients without significant lung disease, such as Patients 1, 3 and 5, maintenance of oxygenation during one-lung ventilation may require high inspired oxygen concentration, continuous positive airway pressure to the left lung, positive end-expiratory pressure to the right lung and/or intermittent two-lung ventilation. Patient 5 had significant pulmonary hypertension, which presented significant problems with right heart failure during one-lung ventilation. The left thoracotomy approach carries advantages for patients with prior median sternotomies, such as Patient 4, and simplifies the surgical approach for future cardiac transplantation.

The anaesthetic technique of high-dose opioid, inhalational anaesthetic and muscle relaxant we used for four of our patients is similar to that generally used for critically ill patients undergoing cardiac surgery (5,10). We chose a total intravenous anaesthetic technique for Patient 3 in view of his muscular dystrophy. A BIS[R] monitor was used to guide doses of anaesthetic agents to maintain adequate anaesthesia while minimizing haemodynamic instability.

The Jarvik 2000 FlowMaker[R] may be inserted in fibrillating hearts, with and without CPB, or beating hearts slowed down by adenosine or esmolol without CPB (4). A reduction in heart rate may improve surgical conditions, and reduce both blood loss and entrainment of air during the exchange of the coring device for the LVAD. Insertion of the LVAD on a beating heart may avoid the many complications associated with CPB and potentially shorten surgical time. Prophylactic cannulation and connection to the bypass machine was carried out for four of our patients. Only one patient required CPB. Possible reasons for that include the use of esmolol in the presence of poor cardiac function and sudden offloading of the left ventricle with worsening of right ventricular function. Esmolol was used in two of our patients, and may have contributed to the haemodynamic problems during insertion of the device for Patient 2. The remaining three patients did not develop any complications despite not receiving esmolol. Previously reported surgical time for cases performed with partial CPB was a mean of 6 h (SD 1.0 h) (5). The shorter time seen in our patients is likely to be due to the modified surgical technique to allow for off-pump insertion of the pump, but may also be a result of learning experience. At present there is little data comparing the outcomes of on-pump and off-pump insertion of the Jarvik 2000 FlowMaker[R].

Patients undergoing LVAD insertions are at high risk of excessive perioperative bleeding and coagulopathy (13). Large-bore venous access is essential. Blood loss with insertion of the Jarvik 2000 FlowMaker[R] may be less compared with other LVADs as there is no need to create an abdominal pocket, the device's minimal 'dead space', and the possibility of avoiding CPB during insertion. Our patients received aprotinin, an antifibrinolytic agent, which has been shown to reduce blood loss and transfusion requirements during LVAD insertions (14). We also routinely use an autologous blood recovery unit to reduce allogeneic red cell transfusion. Fresh whole blood, fresh frozen plasma and platelets were infused as necessary for each patient once the device was inserted to reduce the risk of excessive bleeding.

In conclusion, with an increasing number of patients with end-stage cardiac failure and a lack of organ donors, LVADs such as the Jarvik 2000 FlowMaker[R] offer a viable and attractive treatment option for these patients, either as a bridge to transplantation or as destination therapy. Knowledge of the unique properties and function of the Jarvik 2000 FlowMaker[R] and close cooperation between the anaesthetist and surgeon are essential to ensure an optimal surgical and anaesthetic course for the patient. We believe that the potential to avoid CPB for device insertion is a significant advance in LVAD technology.

ACKNOWLEDGEMENTS

The authors thank Dr David Perlman (Consultant Anaesthetist) and Dr Donald Stewart (Consultant Anaesthetist), Department of Anaesthesia and Pain Medicine, Royal Perth Hospital for their contributions to the work on which this paper is based.

Accepted for publication on August 15, 2006.

REFERENCES

(1.) Frazier OH, Myers TJ, Gregoric ID et al. Initial clinical experience with the Jarvik 2000 implantable axial-flow left ventricular assist system. Circulation 2002; 105:2855-2860.

(2.) Westaby S, Banning AP, Saito S et al. Circulatory support for long-term treatment of heart failure: experience with an intraventricular continuous flow pump. Circulation 2002; 105:2588-2591.

(3.) Siegenthaler MP, Martin J, Van de Loo A, Doenst T, Bothe W, Beyersdorf E Implantation of the permanent Jarvik-2000 left ventricular assist device. J Am Coll Cardiol 2002; 39:1764-1772.

(4.) Frazier OH. Implantatation of the Jarvik 2000 left ventricular assist device without the use of cardiopulmonary bypass. Ann Thorac Surg 2003; 75:1337-1340.

(5.) Nussmeier NA, Probert CB, Hirsch D et al. Anesthetic management for implantation of the Jarvik 2000[TM] left ventricular assist system. Anesth Analg 2003; 97:964-971.

(6.) Westaby S, Frazier OH, Pigott DW, Saito S, Jarvik RK. Implant technique for the Jarvik 2000 Heart. Ann Thorac Surg 2002; 73:1337-1340.

(7.) Frazier OH, Myers TJ, Westaby S, Gregoric ID. Clinical experience with an implantable, intracardiac, continuous flow circulatory support device: physiologic implications and their relationship to patient selection. Ann Thorac Surg 2004; 77:133-142.

(8.) Myers TJ, Robertson K, Pool T, Shah N, Gregoric I, Frazier OH. Continuous flow pumps and total artificial hearts: management issues. Ann Thorac Surg 2003; 75:579-85.

(9.) Siegenthaler MP, Martin J, Pernice K et al. The Jarvik 2000 is associated with less infections than the HeartMate left ventricular assist device. Eur J Cardiothoracic Surg 2003; 23:748-755.

(10.) Mets B. Anesthesia for left ventricular assist device placement. J Cardiothor Vase Anesth 2000; 14:316-326.

(11.) Hirsch DJ, Cooper JR. Cardiac Failure and left ventricular assist devices. Anesthesiol Clin Nth Am 2003; 21:625-638.

(12.) Radovancevic B, Gregoric ID, Tamez D et al. Biventricular support with the Jarvik 2000 axial flow pump: a feasibility study. ASAIO J 2003; 49:604-607.

(13.) Goldstein DJ, Mehmet CO, Rose EA. Implantable left ventricular assist devices. N Engl J M 1998; 339:1522-1533.

(14.) Goldstein D, Seldomridge J, Chen J et al. Use of aprotinin in LVAD recipients reduces blood loss, blood use and periopoerative mortality. Ann Thorac Surg 1995; 59:1063-1067.

L. H. TAN *, C. COKIS ([dagger])

Department of Anaesthesia and Pain Medicine, Royal Perth Hospital, Perth, Western Australia, Australia

* M.B., B.S., M. Med (Anaesthesiology), Clinical Assistant, Department of Anaesthesia and Pain Medicine, Royal Perth Hospital and Associate Consultant, Department of Anaesthesia and Surgical Intensive Care, Changi General Hospital, Singapore. ([dagger]) M.B.B.S., F.A.N.Z.C.A., Consultant Anaesthetist.

Address for reprints: Dr C. Colds, Department of Anaesthesia and Pain Medicine, Royal Perth Hospital, Wellington Street, Perth, WA. 6000.
TABLE 1
Patient characteristics

Patient number 1 2

Age (y) 34 35

Gender male male

BSA ([m.sup.2]) 2.10 1.94

Aetiology of anthracycline-induced familial,
cardiomyopathy possibly viral
 trigger

Other co-morbidities non Hodgkin's B cell hereditary
 lymphoma, spherocytosis,
 childhood epilepsy. renal impairment,
 chronic atrial
 fibrillation,
 Grave's disease,
 ICD in situ.

Duration of 4 60
symptoms (mo)

Last day of most milrinone, 0 levosimendan, 23
recent IV inotrope (still using on day
use (Drug, days of surgery)
before surgery) 4.7 (with milrinone 2

Cardiac index infusion)
([1.min.sup.-1][.m.sup.-2)] 1.9 (without IV
 inotropes)

Patient number 3 4

Age (y) 29 59

Gender male male

BSA ([m.sup.2]) 1.70 1.97

Aetiology of Becker muscular ischaemic
cardiomyopathy dystrophy related

Other co-morbidities Becker muscular IHD with MI and
 dystrophy, OPCAB 22 months
 scoliosis, earlier, patent
 ICD in situ. foramen ovale closed
 percutaneously,
 anticoagulated for
 left atria] thrombus,
 atrial fibrillation,
 diabetes mellitus,
 hypertension.

Duration of 10 6
symptoms (mo)

Last day of most milrinone, 3 levosimendan, 12
recent IV inotrope levosimendan, 9
use (Drug, days
before surgery) 2.47 2.00

Cardiac index
([1.min.sup.-1][.m.sup.-2)]

Patient number 5

Age (y) 70

Gender male

BSA ([m.sup.2]) 1.81

Aetiology of ischaemic
cardiomyopathy

Other co-morbidities IHD, MI 11 days
 before surgery,
 end-stage renal
 failure on
 haemodialysis,
 peripheral vascular
 disease with previous
 abdominal aortic
 aneurysm repair,
 ICD in situ.

Duration of 24
symptoms (mo)

Last day of most dopamine, 7
recent IV inotrope
use (Drug, days
before surgery) 3.92 (with dopamine

Cardiac index infusion)
([1.min.sup.-1][.m.sup.-2)]

BSA: body surface area, ICD: internal cardio-defibrillator, IHD:
ischaemic heart disease, MI: myocardial infarction, OPCAB: off-pump
cardiac bypass surgery, IV. intravenous.

TABLE 2
Intra- and postoperative course

Patient number 1 2

Surgical approach left thoracotomy median sternotomy

Surgical time (min) 300 180

Blood products used
intraoperatively

Washed red cells (ml) 1225 1288

Fresh whole
blood (units) - -

Packed red
cells (units) - -

Fresh frozen
plasma (units) 4 2

Single donor
platelets (units) 1 2

Duration of
ventilation
post-op (h) 3.50 69

Vasoactive drugs noradrenaline noradrenaline
used in ICU GTN adrenaline
 milrinone GTN
 milrinone
Duration of vasoactive
drug use post-op (h) 43 66

Complications in ICU nil ongoing bleeding,
 decreased urine
 output

Duration of
ICU stay (h) 24 168

Complications post ICU haemothorax, sinusitis,
 hypotension mild epistaxis

Duration of hospital
stay post-op (days) 19 21

Duration of
support (days) 146 66 - transplanted

Patient number 3 4

Surgical approach left thoracotomy left thoracotomy

Surgical time (min) 228 210

Blood products used
intraoperatively

Washed red cells (ml) - -

Fresh whole
blood (units) 2 2

Packed red
cells (units) - -

Fresh frozen
plasma (units) 4 4

Single donor
platelets (units) 1 2

Duration of
ventilation
post-op (h) 9 15

Vasoactive drugs noradrenaline noradrenaline
used in ICU adrenaline adrenaline
 milrinone dobutamine
 milrinone
 inhaled NO

Duration of vasoactive
drug use post-op (h) 18 29

Complications in ICU nil nil

Duration of
ICU stay (h) 21 23

Complications post ICU anaemia. gout,
 pneumonia,
 intestinal
 bleeding

Duration of hospital
stay post-op (days) 15 77

Duration of
support (days) 132 118

Patient number 5

Surgical approach left thoracotomy

Surgical time (min) 210

Blood products used
intraoperatively

Washed red cells (ml) 590

Fresh whole
blood (units) -

Packed red
cells (units) 1

Fresh frozen
plasma (units) 2

Single donor
platelets (units) 2

Duration of
ventilation
post-op (h) 15

Vasoactive drugs noradrenaline
used in ICU adrenaline
 GTN
 inhaled NO

Duration of vasoactive
drug use post-op (h) 72

Complications in ICU nil
Duration of

ICU stay (h) 68
Complications post ICU hypotension with
 haemodialysis

Duration of hospital
stay post-op (days) 21
Duration of

support (days) 37 - died

ICU: intensive care unit, GTN: glyceryltrinitrate,
post-op: postoperative, NO: nitric oxide.
COPYRIGHT 2006 Australian Society of Anaesthetists
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2006 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Tan, L.H.; Cokis, C.
Publication:Anaesthesia and Intensive Care
Date:Dec 1, 2006
Words:4013
Previous Article:Continuing medical education: a needs analysis of anaesthetists.
Next Article:Increasing the use of an existing medical emergency team in a teaching hospital.

Terms of use | Privacy policy | Copyright © 2019 Farlex, Inc. | Feedback | For webmasters