Alpha-2 agonists for sedation


A 66 year old woman was admitted to the ICU with acute type II respiratory failure secondary to a community acquired pneumonia (CURB-65 score 4) complicating severe COPD (FEV1 40% predicted). Collateral history revealed many concerning features; the patient had a poor exercise tolerance (mMRC dyspnoea scale score 3, exercise tolerance <100m), was alcohol dependent (drinking 120 units per week) and previously had been admitted to hospital with an exacerbation of COPD requiring NIV, and treatment for acute alcohol withdrawal.


Mechanical ventilation was commenced using a lung-protective strategy with permissive hypercapnia. Sedation was achieved using remifentanil and propofol, targeting a Richmond Agitation Scale Score (RASS) of -2 to 0. A noradrenaline infusion was commenced to maintain a mean arterial pressure of ≥65mmHg. A neutral cumulative fluid balance was targeted. Broad-spectrum antimicrobial therapy was continued as per local antimicrobial guidelines. Intravenous B vitamins were administered and enteral feeding was established via a nasogastric tube.

In view of the patient’s comparatively poor pre-morbid function and high risk of delirium, early extubation to NIV was identified as the preferred strategy. By day 3 the patient had improved such that this became a realistic goal. In order to prevent acute alcohol withdrawal, yet use benzodiazepines sparingly to avoid associated respiratory depression, remifentanil-propofol sedation was substituted for a clonidine infusion, which was continued following extubation. Low doses of chlordiazepoxide were used as rescue therapy in accordance with Clinical Institute Withdrawal Assessment for Alcohol scale (CIWA-Ar) scoring.

The patient progressed well, was weaned from both NIV and clonidine and was discharged from HDU to a respiratory ward on day 8. She survived to hospital discharge.


What role do Alpha-2 Agonists have for sedation in critical care?Read More »


Extracorporeal CO2 removal

A 42 year old man presented with a week-long history of increasing shortness of breath, cough  (productive of purulent sputum) and fevers on a background of significant chronic lung disease. He had a ten year history of interstitial lung disease and was on the waiting list for a lung transplant. He used oxygen at a rate of 2 litres per minute at home, 24 hours a day. His usual exercise tolerance of 200 metres had been significantly reduced for the past week. His regular medications included seretide and salbutamol inhalers, lansoprazole, azathioprine, prednisolone alendronate.

On arrival in hospital, he was alert and orientated. He had a patent airway, but was tachypnoeic (rate of 50/minute) using his respiratory accessory muscles and a tracheal tug was evident. An arterial blood gas revealed type two respiratory failure (pH 7.26; pO2 8.14, pCO2 7.52 on 15 liters/min of face mask oxygen). He was hypotensive (80/40mmHg) and tachycardic (130/minute, sinus rhythm). A pyrexia of 39.2°C was recorded. Blood results showed normal renal function, a slightly elevated white cell count of 14.

The patient was admitted to the high dependency for close monitoring in view of his history and presentation. He was commenced on treatment for a presumed infection (viral or bacterial) with oseltamivir, co-amoxiclav and clarithromycin and given three “pulsed” doses (750mg) of methylprednisolone. He remained stable for the next twelve hours.

Early the next morning, he became very hypoxic (oxygen saturations less than 50%), bradycardic (<35 beats per minute) and had a brief hypoxic respiratory arrest. He received 1 cycle of cardiopulmonary resuscitation and was intubated. There was subsequently a return of spontaneous circulation.

The next 24 hours involved a period of difficulty with ventilation. His peak airway pressures were very high, despite being paralysed and a low volume/high respiratory rate strategy being employed. He was discussed with a tertiary respiratory centre and it was decided that he should be transferred for insertion of a pumpless arteriovenous interventional lung assist (for extracorporeal carbon dioxide removal) as a bridge prior to lung transplantation. He had formal ultrasound measurement of his femoral arteries. His left common femoral artery was widely patent (AP and transverse diameter of 8-9mm throughout), but the right was only 4-5mm throughout.

In the meantime, his peak airway pressures were consistently between 35 and 40cmH2O, despite tidal volumes of 230ml, 3.8ml/kg). With a rate of 32-35 breaths per minute, his pH was  initially maintained above 7.2, with a pCO2 of 9-11kPa. Over the course of the next few hours, this became increasingly difficult to achieve. His oxygen requirements did not escalate (an FiO2 of 0.6 provided a pO2 of 8-9kPa). When his pCO2 increased to 15.4kPa and his pH dropped to 7.17, further adjustments were made and the PEEP decreased to 5cmH2O from 10cmH2O. His noradrenaline requirements were increasing and with the aid of the cardiac output monitoring, he was cautiously given fluid with a good response.

He was transferred to the centre in which a lung transplant could be performed within hours of the referral. A Novalung device was inserted and he underwent a bilateral lobar lung transplant several days later. He was in hospital for 6 weeks and made a very good long-term recovery. At six months, he was extremely well and was undertaking his activities of daily living completely normally with stable lung function. He even managed to complete an eight mile bike ride.

What is the rationale for extracorporeal lung assist?
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Diagnosing Ventilator Associated Pneumonia

A 64 year old lady who had been admitted with acute pancreatitis due to gallstones. She was initially admitted to the intensive care unit for cardiovascular management and management of her electrolyte imbalance. After a few days she was intubated for hypoxia.

She developed pancreatic necrosis and pseudocyst formation. These were drained by percutaneous drains whereby she showed some improvement with more stability in her cardiovascular system. She had two failed extubations and then had a tracheostomy placed. She was weaned from the ventilator but then remained on 40-45% of oxygen for a number of weeks. Serial scans showed a static nature to her pseudocysts. Her inflammatory markers remained static at a moderate level over this time. It was felt that she had a ventilator associated pneumonia and was started on antibtiotics. She then showed improvement a number of days later. She was further weaned from the ventilator and decannulated. She needed recannulation later and suffered another episode of ventilator associated pneumonia which was treated. Eventually a number of months later she was discharged to the ward and then home.

How can we diagnose ventilator associated pneumonia?

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Mechanical Ventilation of Chronic Obstructive Airways Disease

A 68-year-old went into respiratory arrest on the chest ward. He had been admitted 2 weeks previously for an exacerbation of chronic obstructive airways disease (COAD). He has had two previous episodes of reduced conscious level due to hypercapnoea, which resolved with non-invasive ventilation and oxygen titration.

He was immediately intubated on the ward and transferred to the intensive care unit for ventilation. Hypoxia was corrected to a PaO2 >8.0kPa with a moderate FiO2. However he remained very difficult to ventilate and maintained a persistently high PaCO2. The highest level was 21kPa. He was treated with B2 agonist nebulisers, anti-muscarinic nebulisers, systemic steroids, aminophylline infusions, magnesium infusions and a ketamine infusion. He also needed vasopressor support and for a period of time continuous renal replacement therapy. After a week when his ventilator pressures reduced he had an uneventful percutaneous tracheostomy. Sedation was then reduced and he was awake and spontaneously breathing but with a high level of support. He was recurrently troubled by episodes of bronchospasm and air trapping. The lowest settings for inspiratory pressure were 14 cmH2O. He deteriorated a number of times before care was withdrawn and he died 20 days later.

Can we predict which COAD patients will benefit from mechanical ventilation?

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Predicting Weaning from Mechanical Ventilation

A 60 year old man was electively admitted to the intensive care unit following a combined kidney pancreas transplant. Diabetes mellitus was the cause for his end stage renal failure. He was admitted for overnight HDU care, and was discharged the following day. He had delayed graft function thought to be related to a prolonged cold ischaemic time of the kidney. He would need dialysis until the function of the transplanted kidney improved. Four days later whilst on the ward he became hypotensive, became unconscious and suffered a cardiac arrest. He was successfully resuscitated and was readmitted to ICU.

In the ICU he required a blood transfusion as his haemoglobin level had dropped. He was taken to theatre for a re-laparotomy and a graft pancreatectomy was performed and all bleeding was stopped.

He continued to suffer from delayed kidney graft function and needed intermittent dialysis. After two days he was on minimal respiratory support and on sedation hold was deemed ready for extubation. He was extubated successfully and remained so for the next 12 hours. He then had an episode of bradycardia and had a markedly reduced cardiac output. He was re-intubated and stabilised. A temporary pacing wire was inserted to control potential episodes of bradycardia.

His condition remained stable over the next day and was again extubated. His oxygenation needs increased over the next 12 hours and was placed on non- invasive ventilation. This stabilised him over the next 12 hours but he suffered from retained secretions and was re-intubated. He then suffered with an ileus and had abdominal distension which complicated his respiratory function. He had a tracheostomy placed and remained on mechanical ventilation for 2 weeks. He was difficult to wean as he suffered set backs related to acute sputum retention and a ventilator associated pneumonia.

This patient had been extubated twice with some degree of morbidity associated with it as he had to be reintubated. It would also be reasonable to assume that this increased his length of stay on the ICU slowed down his ICU discharge. Deciding when to extubate a patient seems to be still a difficult decision to make in some cases and the experience of senior clinicians remains an important role.

For those who have not accumulated this level of clinical experience are there tools available to help them in deciding when and who could be weaned and extubated from mechanical ventilation?Read More »

Arthrogryposis & Paediatric Difficult Airway


A 4 month old infant with arthropgryposis multiplex congenital was admitted to the paediatric assessment unit. The infant had been acutely unwell over the preceding 12 hours with respiratory compromise and a productive cough with green sputum. He had signs of respiratory distress with a RR of 40, pulse oximetry showed SpO2 of 85% on air and only 90% with a facemask, reservoir bag and high flow oxygen. It was felt that the infant would need to be intubated and ventilated. Two months before the infant had had a respiratory arrest on the neonatal ward and was unable to be intubated. That situation was resolved by mask ventilation and rescue with an LMA. There were obvious concerns that direct laryngoscopy would be unsuccessful and may precipitate a terminal decline in the patient’s condition.

The infant’s breathing was supported by bag/mask ventilation whilst he was transferred to an ENT theatre. Further anaesthetic support and an ENT surgeon were sought. I.v. access was established through a scalp vein. Ventilation was switched to an Ayres T piece with Jackson-Rees modification. Induction of anaesthesia was initiated with sevoflurane and oxygen. Direct laryngoscopy showed a Lehane and Cormack grade 4 view.

A rigid bronchoscope with video camera monitor was used by the ENT surgeon to obtain a view of the glottis. An epidural catheter was placed down the side port of the bronchoscope and was directed through the vocal cords. The bronchoscope was removed and a fine bore suction catheter was railroaded over the epidural catheter to give more stiffness. The positions of the end of the catheters were checked with the bronchoscope. A size 3.0cm uncuffed endotracheal tube was then railroaded over the catheters into trachea. Position and length were confirmed with the bronchoscope and ventilation was continued. The arrangement is shown in Figure 1.

The child was then transferred to the adult ICU where a retrieval team arrived to transfer the patient to a PICU.

What is arthrogryposis? Describe some methods for achieving control of the difficult paediatric airway.Read More »

Management of Inhalational Injury

A 30-year-old man with no significant past medical history was admitted to ED from a house fire started by a piece of faulty electrical equipment. There were superficial skin burns only but some evidence of a possible inhalation injury with singed nasal hairs and a hoarse voice. Coughing resulted in expectoration of carbonaceous sputum with some haemoptysis. Arterial blood gas analysis revealed a PaO2 of 10.4 kPa on 40% oxygen a carboxyhaemoglobin level of 18%.

Semi-elective endotracheal intubation was performed using an uncut orotracheal tube. Ventilatory parameters were adjusted to give a tidal volume of 6-8 ml/kg and plateau pressure of less than 30 cmH20. Recruitment manouveres were performed to give an optimum compliance in the region of 40-50 ml/cmH20 with a positive end-expiratory pressure of 8 H20. The inspired fraction of oxygen was kept high (i.e. greater than 60%) until there was a fall of the carboxyhaemoglobin level to less than 5% at which point downwards titration was performed as guided by a target SpO2 of 94%.

Fibreoptic bronchoscopy was performed approximately six hours after admission to intensive care which demonstrated carbonaceous colonisation of the lower respiratory tract and areas of erythematous and denuded epithelium. Within 12 hours of intubation significant oedema of the face and upper airway had developed. A restrictive fluid regimen was instituted and there was gradual resolution of this swelling over the next 3 days. At this time, gas exchange was satisfactory and the patient was successfully extubated before being discharged to the high-dependency unit.

How is inhalational injury managed on the ICU?Read More »

Invasive Ventilation of Life-Threatening Asthma

Invasive Ventilation in Life-Threatening Asthma

An 18-year-old known asthmatic presented with a two-day history of increasing shortness of breath on a background of a recent coryzal illness. She had a background of reasonably poor control and had been admitted to the intensive care unit for mechanical ventilation twice as a child. Her current medication included regular inhaled serotide 250, montelukast 10mg and theophylline MR 450mg BD. At presentation she was in extremis; pulse rate was 65 per minute, blood pressure 75/54 mmHg and respiratory rate 14 per minute. Arterial blood gas analysis demonstrated a PaCO2 of 11 kPa and PaO2 of 7.6 kPa with associated respiratory acidosis. Nebulised salbutamol and intravenous magnesium sulphate therapy was administered. along with 200mg of intravenous hydrocortisone. On arrival of the intensive care team, the patient’s respiratory rate deteriorated to a rate of 4 per minute. Assisted ventilation with a self-inflating bag and 100% oxygen was performed; rapid-sequence intubation was performed using ketamine and rocuronium.

Following intubation, immediate difficulties were experienced with mechanical ventilation. High airway pressures in excess of 40 cmH2O with tidal volumes of less than 200 ml were observed. Immediate chest radiography confirmed correct positioning of the endotracheal tube and excluded a pneumothorax. Adequate sedation and neuromuscular blockade were confirmed. Auscultation confirmed severe, widespread wheeze with limited air entry. Further nebulised salbutamol was administered and an aminophylline infusion initiated. The patient was transferred to the intensive care unit where magnesium, ketamine and vecuronium by infusion were added. Various modes of mechanical ventilation were tried including volume and pressure triggered with varying success; this included lengthening the I:E ratio, frequent disconnections to allow deflation and adjustment of PEEP to maximum compliance. Continuous salbutamol was administered via an ultrasonic nebuliser. Airway pressures remained high and there was little improvement in her acidosis. 2 hours after admission the patient suffered a PEA cardiac arrest from which she could not be resuscitated.

What are the difficulties in ventilating severe asthmatics, and what strategies can we use to overcome them?

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High Frequency Oscillatory Ventilation in ARDS

High Frequency Oscillatory Ventilation in ARDS

A 45 year old female presented to A&E with a 5 day history of worsening SOB, cough productive of green sputum, lethargy, anorexia, fever and rigors. She had no co- morbidities and was active and independent with a good exercise tolerance. On examination she looked unwell, clammy and drowsy. Her respiratory rate was 35 breaths per minute and SpO2 of 84% on 15 Litres of oxygen via a non-rebreathing mask. Her blood pressure was 88/40 mmHg with a heart rate of 140 per minute despite having received 3 litres of fluid. Arterial blood gas showed PaO2 6.0kPa, pH 7.28, PaCO2 7.1 kPa, Bicarbonate 14 mmol/l, BE -11 and Lactate 8.6 mmol/l. Chest radiograph demonstrated significant bilateral consolidation with infiltrates consistent with ARDS. PaO2:FiO2 was calculated as 15 indicating severe ARDS presumed secondary to CAP.

She was managed as per sepsis guidelines. Oxygen therapy was continued and CPAP was initiated due to the hypoxia whilst an ICU bed was being prepared for admission. Noradrenaline was commenced at 0.2mcg/kg/min which continued to increase. Repeat arterial blood gases confirmed worsening type 2 respiratory failure and the patient was clinically exhausted. A modified rapid sequence induction was performed and IPPV commenced. Her oxygenation remained a problem and despite a FiO2 of 1.0 and PEEP of 20 his SpO2 remained 85% and PaO2 6kPa. The patients’ sedation was deepened and muscle relaxant administered. Lung protective ventilation was continued however arterial blood gases continued to worsen. The decision was made to convert the patient from conventional ventilation (CV) to High-Frequency Oscillator Ventilation (HFOV). The initial ABGs after an hour of HFOV showed an improvement as did subsequent numbers. This mode of ventilation was continued for a further 48 hours and then converted to CV. Gas exchange continued to improve. Over the course of the following 4 weeks the patient had a tracheostomy performed to aid weaning. She subsequently developed a Ventilator Associated Pneumonia and worsening ARDS required a further period of HFOV. Improvement continued and the patient was successfully decannulated and discharged from ICU.

What is the evidence base for high frequency oscillatory ventilation in ARDS?

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Obesity Hypoventilation Syndrome

Obesity Hypoventilation Syndrome

 A 66 year old man was brought by ambulance to ED after becoming acutely dyspnoeic at home, and his wife had struggled to wake him after an afternoon sleep. He had a moderate smoking history of 20 pack years and quit 20 years ago, and drank approximately 20 units of alcohol as beer per week. There were no preceding prodromal respiratory or infective symptoms reported. On examination, he was obese with a weight of 120 kg. He was snoring, which eased with a chin-lift or jaw thrust, but he would not tolerate an airway adjunct. His respiratory rate was 8 and shallow, producing SpO2 84% on high flow oxygen. He was flushed and veno-dilated peripherally, with a tachycardia of 110 bpm sinus rhythm. Most notably, he was difficult to rouse, with a GCS of 9 (E2 M5 V2). Arterial blood sampling revealed a profound hypercapnoeic respiratory acidosis with no degree of compensation. Chest X-ray showed poorly expanded lungs with bilateral basal atelectasis and prominent pulmonary vasculature. Empiric naloxone was ineffective and he was commenced on non-invasive ventilation (NIV). The working diagnosis was an acute non-infective exacerbation of previously undiagnosed chronic obstructive pulmonary disease (COPD). Treatment involved bronchodilators, steroids and bilevel pressure support non- invasive ventilation.
One hour after NIV had been established, the patient’s respiratory acidosis was worse and his clinical picture was unchanged. He was intubated then transferred to Intensive Care. CTPA ruled out significant pulmonary emboli but was suggestive of pulmonary hypertension. Ventilation was not difficult, with near normal inspiratory pressures, and his minimal wheeze resolved quickly. As his respiratory acidosis normalised, his GCS rapidly improved to the point of safe extubation after just 48 hours. Given his obesity he was extubated to non-invasive pressure support ventilation immediately. After a further 24 hours, his gas exchange began to deteriorate again. Increasing inspiratory pressure improved his tidal volumes but his intrinsic rate of breathing slowed such that his minute ventilation remained static. He eventually found a stable equilibrium using nocturnal bilevel pressure support with a high mandatory backup rate (pressure control), which maintained a normal minute ventilation. Although he developed hypercapnoea each night, this was mild and eventually compensated. With the NIV, he did not obstruct, have hypopnoeic events or desaturated overnight, which markedly improved his daytime somnolence and effort of breathing.

What are the clinical features and approaches to management of obesity hypoventilation syndrome?

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