An Introduction to Critical Care Technology

Who is a Critical Care Technologist?

Critical care technologists (CCTs) are professionals who specialise in medical physics and clinical engineering. They are an integral part of the Critical Care team and make sure that the equipments and technology needed to support organ function and maintain life are working and being used properly.

Critical care technicians often arrive on the scene to assist during health emergencies. These professionals can treat a variety of injuries or physical ailments, as well as transport patients to a hospital for extended treatment.

Job Description and Duties

Critical care technician’s are trained to provide high-quality out-of-hospital care to patients in emergency situations. They may encounter various situations like cardiac arrest, respiratory distress, choking, fractures, childbirth, road traffic accidents etc. When entering an accident scene, a critical care technician quickly assesses the problems and begins implementing medical aid. Their primary duty is to provide medical care and get patients to a medical facility where they can receive extended treatment. Critical care technicians also work in medical facilities where they assist the critical care team. Additional job duties are based on the amount of training and experience of the technician. For example, critical care technicians with paramedic training can perform procedures like endotracheal intubations, as well as use complex equipment like electrocardiograms.

According to the U.S. Bureau of Labor Statistics (BLS), emergency medical workers, including critical care technicians, can work over 40 hours a week and sometimes at odd or irregular hours (www.bls.gov).

Critical care technicians can also be exposed to harmful diseases, violence from patients, stress, and injuries. Some of the work may involve handling of hazardous chemicals and substances. So, protective overalls, gloves, glasses, mask etc may have to be worn according to the demand of the situation.

A critical care technician works alongside doctors, nurses and other medical staff like physiotherapists, dietitians and pharmacists. So he/she should be able to work in a team. There is possibility of frequent contact with very sick patients and distressed relatives, so the work can be stressful and emotionally challenging at times.​​​

Routine work usually includes the following duties:

• setting up equipment, connecting it to patients and monitoring the machinery as it is being used
• carrying out regular maintenance checks and cleaning of intensive care equipment and bedside technical support
• decontaminating machinery when it needs to be sent for repair
• working with other healthcare professionals during life threatening events, trained at providing CPR

Some of the equipments commonly used include (but are not limited to):

• Blood analysers (ABG machine)
• Dialysis machines
• Mechanical Ventilators
• Defibrillators
• Multichannel monitors – both invasive and non-invasive monitoring devices
• Infusion pumps
• 12 lead ECG
• Portable X-ray
• USG
• Glucometers
• Computer

​

Qualities

To become a critical care technologist, you will need:

• an interest in technology, science and medicine
• the ability to work accurately, precisely
• good problem solving and decision making skills
• the ability to empathise with patients, and put them at ease
• good communication skills
• the ability to cope with distressing situations
• Physical strength
• Ability to work under stress

Training and development

Skills and knowledge should be kept up-to-date through the career by continuing professional development activities (CPD).

Opportunities

Job opportunities may be found within larger Govt. hospitals as well as in private set-ups like ICU, Dialysis unit etc.

With experience, one may be able to progress in his/her career from CCT to Lead CCT. Alternatively, one can move into a specialist field of critical care such as the liver and transplant work, cardiology, neurophysiology, burns, premature baby units, and respiratory physiology.

Pros and Cons of a Critical Care Technician

Pros of Being a Critical Care Technician

Faster-than-average job growth (expected 23% growth between 2012 and 2022)*

Satisfaction of helping others*

May be responsible for saving lives*

Does not require years of formal training*

Cons of Being a Critical Care Technician

May be required to work nights or weekends*

Must pass licensure exam to work*

Work may be physically strenuous and stressful*

May be exposed to contagious diseases*

Sources:*U.S. Bureau of Labor Statistics

Job Prospects 

Current statistics from Indian perspective was not available during write-up of the article. The U.S. Bureau of Labor Statistics (BLS) predicted that EMTs may see an employment growth of 33% from 2010-2020. Predicted contributory factors include an increase in the number of natural disasters, car accidents and violence. With an increase in life expectancy there has been a steady increase in the elderly population. This has led to an increase in the incidence of age-related health emergencies, which also puts these workers in demand. 

New Drug of Abuse: Gabapentin

Gabapentin is increasingly being used by patients in methadone maintenance programs to get a high.

Increasing availability, infrequent drug testing, and potentiation of euphoria when combined with opioids have likely all contributed to gabapentin misuse.

• Drug Abuse Warning Network (DAWN) data show that ED visits involving the nonmedical use of gabapentin have increased by 90% in the United States since 2008. 
• DAWN data also suggest that 20% of patients in treatment may misuse or abuse gabapentin.

Meanwhile, there has been a rise in gabapentin prescribing.

Current advice on prescribing Gabapentin: use caution. Don't necessarily avoid prescribing it, but be careful and prescribe it from visit to visit. Don't just give somebody six refills and say you will see them in 6 months.

source: http://www.medscape.com/viewarticle/855819?nlid=93367_2982, (Medscape Medical News from the American Academy of Addiction Psychiatry (AAAP) 26th Annual Meeting)

Laparoscopy in COPD: Management of Anaesthesia

anesthesia exposed infants express significantly more anxious behavior which persists for at least five months suggesting long-term effects

Multiple Exposures To Post-Natal Anesthesia Leave A Long-Term Effect On Behavior Of The ChildA

Researchers from the Mount Sinai University and Yerkes National Primate Research Center, Emory University studied the effect of repeated postnatal anesthesia exposure on a rhesus monkey model that was translationally equivalent and had similar neurodevelopmental stages corresponding to human. 

Experiment

• Ten non-human primates (rhesus monkeys) were exposed to a common pediatric anesthetic called Sevoflurane for a comparable length of time required for a significant surgical procedure in humans (four hours)
• They were exposed to the anesthetic at postnatal day seven and then again two and four weeks later
• Socioemotional behavior of exposed subjects compared with that of healthy controls at six months of age using a mild social stressor such as exposure to an unfamiliar human

Observation

• They found the anesthesia-exposed infants expressed significantly more anxious behaviors overall compared with controls
• The study results also demonstrate that alterations in emotional behavior persist at least five months after anesthesia exposure, suggesting long-term effects

Inference

• Repeated exposure to anesthesia early in life causes alterations in emotional behavior that may persist long-term
• Future studies using this primate model can be carried out to develop a new anesthetic agent or prophylactic treatment to reduce the harmful impact of anesthesia on behavior in children
• Studies on the mechanism how it affects the central nervous system is needed

The article was published in Anesthesiology Journal, Issue: November 2015 

Note: The current article was sourced from: docplexus

A brief literature review on hemodynamic responses to laryngoscopy and intubation and the role of LMA

Awake Intubation (procedure in brief)

Burstein et al (1950) induced anaesthesia with various combinations of cyclopropane, ether, N₂O, Pentothal sodium and cocaine in a study of 106 cases. They found substantial increase in pulse rate during laryngoscopy and endotracheal intubation in most of the cases. A deepening of plane of anaesthesia reduced the magnitude of this response (1).

King BD et al (1951) observed the cardiovascular changes with laryngoscopy and tracheal intubation in 46 patients who required GA for surgical procedures. Laryngoscopy was usually completed in 15 seconds. The average rise of systolic blood pressure, diastolic blood pressure and heart rate (HR) after laryngoscopy and tracheal intubation were 53 mm Hg, 34 mm Hg and 23 bpm respectively. They returned to pre-laryngoscopic level within 5 mins. With deepening of anaesthesia to 2^nd or 3^rd plane, intubation induced average rise in systolic blood pressure, diastolic blood pressure and heart rate were 16 mm Hg, 10 mm Hg and 13 bpm respectively.

They concluded that during light GA, direct laryngoscopy and endotracheal intubation is capable of producing circulatory effects characterized by a rise in BP and HR. These changes initiated by the laryngoscope passing on the base of tongue or lifting the epiglottis are independent of the type of laryngoscope blade used. Deeper anaesthesia abolishes these phenomena (2).

Prys-Roberts C et al (1971) studied the electrocardiographic and haemodynamic responses during the induction of anaesthesia followed by laryngoscopy and tracheal intubation in a group of 16 untreated hypertensive patients and in a group of 20 patients receiving antihypertensive therapy upto and including the day of surgery. They compared five different induction agents – thiopentone, methohexitone, propanidid, diazepam and neurolept analgesia induced by combination of phenoperidine and droperidol.

They came to the conclusion that prophylactic blockage of β-adrenergic receptors was necessary to prevent hypertensive crisis during laryngoscopy and tracheal intubation in both treated and untreated hypertensive patients (3).

Kautto UM (1982) studied the effects of fentanyl on arterial pressure and heart rate during laryngoscopy and intubation in 45 normotensive, surgical patients, who were randomly allocated to three groups receiving 2 or 6 micrograms/kg of fentanyl or saline in a double-blind fashion before anaesthetic induction with thiopental.

The result showed that fentanyl supplementation with 2 micrograms/kg significantly attenuated the arterial pressure and heart rate increases during laryngoscopy and intubation, and fentanyl, 6 micrograms/kg, completely abolished these responses (4).

Derbyshire DR et al (1983) measured plasma adrenaline and noradrenaline concentrations in 24 patients during the induction of anaesthesia and the subsequent tracheal intubation. The patients received either suxamethonium 1 mg/kg or pancuronium 0.1 mg/kg to facilitate tracheal intubation.  Mean arterial pressure (MAP) increased in both groups following laryngoscopy and tracheal intubation and there were concomitant increases in the plasma catecholamine concentrations, the changes being more marked in the suxamethonium group.

There was a significant correlation between MAP and plasma catecholamine concentrations in the suxamethonium group. Measurement of plasma catecholamine concentrations in samples obtained simultaneously from central venous, peripheral venous and arterial sites were in broad agreement; the greatest changes occurred in central venous samples (5).

Shribman AJ et al (1987) compared the catecholamine and cardiovascular responses to laryngoscopy alone with those following laryngoscopy and intubation in 24 patients allocated randomly to each group. Following induction with fentanyl and thiopentone, atracurium was administered and artificial ventilation undertaken via a facemask for 2 min with 67% nitrous oxide in oxygen. Following laryngoscopy, the vocal cords were visualized for 10 s. In one group of patients, ventilation was then re-instituted via a facemask, while in the second group the trachea was intubated during the 10-s period and ventilation of the lungs maintained. Arterial pressure, heart rate and plasma noradrenaline and adrenaline concentrations were measured before and after induction and at 1, 3 and 5 min after laryngoscopy.

There were significant and similar increases in arterial pressure and circulating catecholamine concentrations following laryngoscopy with or without intubation. Intubation, however, was associated with significant increases in heart rate, which did not occur, in the laryngoscopy-only group (6).

Braude N et al (1989) compared the pressor response of tracheal intubation with that of laryngeal mask insertion in two groups of 24 and 23 healthy patients respectively. All patients were anaesthetized with thiopentone, nitrous oxide, enflurane and paralysed with atracurium.

They showed a similar, but attenuated pattern of response associated with Laryngeal mask insertion in comparison with laryngoscopy and intubation; significant differences between the groups were evident in arterial diastolic blood pressure immediately after insertion and again 2 minutes later.  They concluded that use of the laryngeal mask may offer some limited advantages over tracheal intubation in the anaesthetic management of patients where the avoidance of the pressor response is of particular concern (7).

Hickey S et al (1990) investigated the cardiovascular effects related to insertion of the Brain laryngeal mask airway and compared these effects with those after insertion of a Guedel oral airway. Arterial pressure and heart rate in 100 patients were measured using an Ohmeda 2300 Finapres arterial pressure monitor. Arterial pressure decreased significantly (P<0.001) and heart rate increased significantly (P<0.001) after induction of anaesthesia with 2.5 mg/kg of propofol. A significant increase in arterial pressure (P<0.02) and in heart rate (P<0.001) followed insertion of the laryngeal mask and the Guedel airway, with no difference between the two groups at any time. The changes in arterial pressure and heart rate returned to 'at insertion' levels within 60 seconds of the stimulus (8).

Hassan HG et al (1991) studied the relationship between the intensity of the stimulus exerted against the base of the tongue during direct laryngoscopy and the magnitude of associated hemodynamic and catecholamine responses in 40 ASA I or II patients. Laryngoscopy lasting 40 s was performed with a size 3 Macintosh blade connected to a force-displacement transducer. The intensity of the stimulus exerted during laryngoscopy was expressed by the product of its average force (N) and duration (s) and given as impulse in Ns. Highly significant relationships were found between the impulse during laryngoscopy and the maximal hemodynamic and catecholamine responses. Also, when laryngoscopy was followed by orotracheal intubation, significant relationships were found with steeper slopes of the regression lines for systolic blood pressure, heart rate and plasma epinephrine concentrations. A more rapid regression of hemodynamic data was seen in intubated patients, whereas their plasma catecholamine concentrations regressed more slowly. The mechanisms of the responses to laryngoscopy and orotracheal intubation were proposed to be by somato-visceral reflexes. Stimulation of proprioceptors at the base of the tongue during laryngoscopy induced impulse-dependent increases of systemic blood pressure, heart rate and plasma catecholamine concentrations. Subsequent orotracheal intubation recruited additional receptors that elicit augmented hemodynamic and epinephrine responses as well as some vagal inhibition of the heart (9).

Wilson IG et al (1992) compared the cardiovascular responses induced by laryngoscopy and intubation with those produced by insertion of a laryngeal mask in 40 healthy patients. Anaesthesia was induced with thiopentone and maintained with enflurane and nitrous oxide in oxygen. Vecuronium was used for muscle relaxation. Arterial pressure was measured with a Finapres monitor. The mean maximum increase in systolic arterial pressure after laryngoscopy and tracheal intubation was 51.3% compared with 22.9% for laryngeal mask insertion (p less than 0.01). Increases in maximum heart rate were similar, (26.6% v 25.7%) although heart rate remained elevated for longer after tracheal intubation. They concluded that insertion of the laryngeal mask airway was accompanied by smaller cardiovascular responses than those after laryngoscopy and intubation and that its use may be indicated in those patients in whom a marked pressor response would be deleterious (10).

Brimacombe J (1995) performed a meta-analysis on randomized prospective trials comparing the laryngeal mask airway (LMA) with other forms of airway management to determine if the LMA offered any advantages over the tracheal tube (TT) or facemask (FM). Of the 858 LMA publications identified to December 1994, 52 met the criteria for the analysis. Thirty-two different issues were tested using Fisher's method for combining the P values. The LMA has 13 advantages over the TT and four over the FM. The LMA had two disadvantages over the TT and one over the FM. There were 12 issues where neither device had an advantage.

Advantages over the TT included: increased speed and ease of placement by inexperienced personnel; increased speed of placement by anaesthetists; improved haemodynamic stability at induction and during emergence; minimal increase in intraocular pressure following insertion; reduced anaesthetic requirements for airway tolerance; lower frequency of coughing during emergence; improved oxygen saturation during emergence; and lower incidence of sore throat in adults.

Advantages over the FM included: easier placement by inexperienced personnel; improved oxygen saturation; less hand fatigue; and improved operating conditions during minor paediatric otological surgery.

Disadvantages over the TT were lower seal pressures and a higher frequency of gastric insufflation. The only disadvantage compared with the FM was that oesophageal reflux was more likely (11).

Fujii Y et al (1995) studied the effects of laryngeal mask airway (LMA) insertion and tracheal intubation on circulatory responses in normotensive (n = 24) and hypertensive (n = 22) patients. In a randomized, double-blind manner, LMA insertion or tracheal intubation was performed after induction of anaesthesia with thiopentone and muscle relaxation with succinylcholine. In both normotensive and hypertensive patients, heart rate (HR), mean arterial pressure (MAP) and rate-pressure product increased after tracheal intubation or LMA insertion compared with baseline (P < 0.05).

The haemodynamic changes were greater after intubation than after LMA insertion (P < 0.05). Following intubation of the trachea or insertion of the LMA, HR increased more markedly in hypertensive patients than in normotensive patients (P < 0.05). Plasma adrenaline and noradrenaline concentrations after tracheal intubation or LMA insertion increased compared with baseline values (P < 0.05) in normotensive and hypertensive patients. The increase in noradrenaline concentration after tracheal intubation was greater than that after LMA insertion (P < 0.05). No patient revealed ECG evidence of myocardial ischaemia. They concluded that insertion of LMA is associated with less circulatory responses than tracheal intubation in both normotensive and hypertensive patients (12).

Upadhye SM et al (1996) compared the haemodynamic responses to endotracheal intubation and Laryngeal Mask Airway insertion in 50 adult patients of ASA Grade I undergoing various elective surgical procedures. With similar anaesthesia technique, they observed haemodynamic response of the patients in the form of increases in heart rate, systolic, diastolic and mean blood pressure at similar intervals during intubation and LMA insertion. The increase in heart rate, systolic blood pressure and mean blood pressure was significantly (p<0.01) more in the ETT groups compared to the LMA group. Hence, they concluded that use of LMA might offer some advantage in patients where avoidance of pressor response is of particular concern (13).

Jain MK et al (2010) – Their aim was to see if there was any problem regarding controlled ventilation of patients during Laparoscopic cholecystectomy using PLMA. For this, 10 patients between 21-42 years of age belonging to ASA I-II undergoing elective Laparoscopic Cholecystectomy were selected. Pulse rate, systolic/diastolic/mean blood pressure, ETCO₂, SPO₂, ABG (Na+, K+, Ca++, Cl-1, Glucose, pH, PO₂, PCO₂, HCOзˉ, BEB, An Gap, O₂ content, a/A, PO₂/FiO₂)and peak airway pressure were monitored preoperatively (as base line), just after insufflations of CO₂, 30 min. after insufflations of CO₂, after drain out of CO₂ and after removal of PLMA.

It was seen that all studied variables and ABG mean increased from preoperative point of time to 30 min after insufflations and then slightly decreases from 30 min after insufflations point and remained high during the period of pneumoperitoneum, which came to baseline after gas removal (removal of PLMA point) for almost all the variables except in case of peak airway pressure. They concluded that PLMA can be used as airway maintaining device in case of laparoscopic cholecystectomies (14).

Russo SG et al (2009) examined to see if LMA-ProSeal is an adequate tool for elective postoperative care in the intensive care unit (ICU) and potentially associated with less hemodynamic alteration during extubation in the ICU environment compared to an endotracheal tube. For the study, forty-eight patients were enrolled. The study was planned as a prospective randomized, controlled trial and patients were allocated to either control (ICU-T) or study group (ICU-P). In the ICU-P group, the endotracheal tube was replaced by a PLMA at the end of surgery.

They found that cardiovascular parameters increased significantly less in the ICU-P group: systolic blood pressure increased by 18.10 ± 5.57 mmHg versus 34.65 ± 5.63 mmHg (P < 0.05), mean arterial blood pressure increased by 11.23 ± 3.25 mmHg versus 22.65 ± 3.36 mmHg (P < 0.05), and heart rate increased by 9.3 ± 2.9 versus 12.9 ± 2.2 min (P < 0.05). Ventilation via the PLMA during transfer from the operation room to the ICU as well as during ICU stay was successful and without any adverse events.

They concluded that removal of the PLMA after recovery from anaesthesia was associated with less cardiovascular change compared to the endotracheal tube. Ventilation was possible without reported adverse events during the entire trial. Elective endotracheal tube replacement by the PLMA may be a useful procedure in selected patients (15).

References:

x

1.	Burstein C, Lo Pinto F, Newman W. Electrocardiographic studies during endotracheal intubation. I. Effects during usual routine techniques. Anesthesiology. 1950 Mar; 11(2): p. 224-37.
2.	King B, Harris Jr L, Greifenstein F, Elder Jr J, Dripps R. Reflex circulatory responses to direct laryngoscopy and tracheal intubation performed during general anesthesia. Anesthesiology. 1951 Sept; 12(5): p. 556-66.
3.	Prys-Roberts C, Greene L, Meloche R, Foëx P. Studies of anaesthesia in relation to hypertension. II. Haemodynamic consequences of induction and endotracheal intubation. Br J Anaesth. 1971 Jun; 43(6): p. 531-47.
4.	Kautto U. Attenuation of the circulatory response to laryngoscopy and intubation by fentanyl. Acta Anaesthesiol Scand. 1982 Jun; 26(3): p. 217-21.
5.	Derbyshire D, Chmielewski A, Fell D, Vater M, Achola K, Smith G. Plasma catecholamine responses to tracheal intubation. Br J Anaesth. 1983 Sep; 55(9): p. 855-60.
6.	Shribman A, Smith G, al e. Cardiovascular and catecholamine responses to laryngoscopy with and without tracheal intubation. Br. J. Anaesth. 1987; 59(3): p. 295-299.
7.	Braude N, Clements E, Hodges U, Andrews B. The pressor response and laryngeal mask insertion. A comparison with tracheal intubation. Anaesthesia. 1989 Jul; 44(7): p. 551-4.
8.	Hickey S, Cameron A, Asbury A. Cardiovascular response to insertion of Brain's laryngeal mask. Anaesthesia. 1990 Aug; 45(8): p. 629-33.
9.	Hassan H, El-Sharkawy T, Renck H, al e. Hemodynamic and catecholamine responses to laryngoscopy with vs. without endotracheal intubation. Acta Anaesthesiologica Scandinavica. 1991 July; 35(5): p. 442–447.
10.	Wilson I, Fell D, Robinson S, Smith G. Cardiovascular responses to insertion of the laryngeal mask. Anaesthesia. 1992 Apr; 47(4): p. 300-2.
11.	Brimacombe J. The advantages of the LMA over the tracheal tube or facemask: a meta-analysis. Canadian Journal of Anaesthesia. 1995 November; 42(11): p. 1017-1023.
12.	Fujii Y, Tanaka H, Toyooka H. Circulatory responses to laryngeal mask airway insertion or tracheal intubation in normotensive and hypertensive patients. Can J Anaesth. 1995 Jan; 42(1): p. 32-6.
13.	Upadhye S, Behl S, Kulkarni A, Shah S. Comparison of hemodynamic responses to laryngeal mask airway insertion and endotracheal intubation. Journal of Anaesthesiology Clinical Pharmacology. 1996 Oct; 12(4): p. 279-81.
14.	Jain M, Venugopal M, Tripathi C. Use of proseal LMA (PLMA) for laparoscopic cholecystectomies: An ABG analysis. J Anaesth Clin Pharmacol. 2010; 26(1): p. 87-90.
15.	Russo S, Goetze B, Troche S, Barwing J, Quintel M, Timmermann A. LMA-ProSeal for elective postoperative care on the intensive care unit: a prospective, randomized trial. Anesthesiology. 2009 Jul; 111(1): p. 116-21.

From Andreas Vesalius To Endotracheal Anesthesia

The safe anaesthetic management requires diligent efforts in maintaining an intact functional airway. Endotracheal intubation has been one of the best ways of achieving this goal. Intubation of the trachea for the purpose of resuscitation is three centuries older than anaesthesia itself.  Andreas Vesalius in 1543 reported the first tracheal intubation in an animal (1). In his landmark book published in 1543, De humani corporis fabrica, he described an experiment in which he passed a reed into the trachea of a dying animal whose thorax had been opened and maintained ventilation by blowing into the reed intermittently (2,3). Vesalius wrote that the technique could be life saving.

Human endotracheal intubation was first done by Curry in 1792 (4). At that time, no laryngoscope was invented and intubation was done by tactile method. Frederich Trendelenburg in 1868 manufactured the first cuffed tracheostomy tube (“Trendelenburg’s tampon”) and in 1871 performed the first endotracheal anaesthetic in humans via tracheostomy (1). In 1880, William Macewen, Scottish orthopaedic surgeon started placing metal tubes inside the trachea orally in conscious patients by digital palpation and saw the advantage of this “orotracheal intubation” over tracheostomy. In his paper entitled "clinical observations on the introduction of tracheal tubes by the mouth instead of performing tracheotomy or laryngotomy', he describes in addition two cases of endotracheal intubation lasting at least 36 h. He can, therefore, be said also to have performed the first long-time intubation (5). In 1887, an American paediatrician, Joseph O'Dwyer, described a method of oral tracheal intubation and published a detailed account of 50 patients with croup treated by intubation, 12 (24%) of whom survived (6).

Ivan Magill and Stanley Rowbotham together, they laid the foundations of tracheal anaesthesia (7). In 1922 at the Queen Hospital for Facial and Jaw Injuries in the UK, Ivan Magill and Stanley Rowbotham were working on development of techniques to administer anaesthesia to patients with facial injuries. At the time, the best available method for general anaesthesia in facial surgery was by endotracheal insufflation through the mouth or nose. This involved the use of a gum elastic catheter placed into the pharynx, through which air was driven by a motorised pump with the addition of vaporised ether from Shipway Apparatus heated in hot water (8).

During an extensive surgery on a deformed jaw of a soldier, a catheter had been passed through the nose. However, the deformity and contracture of the lower jaw prevented adequate expiration and the patient's breathing became laboured. Magill passed a second tube through the patient's nose which entered the trachea alongside the catheter which was followed by immediate relief in respiration. These findings later contributed to use of endotracheal intubation during anaesthesia (9).

Blind nasal intubation was first developed and described by Magill in 1928, with a demonstration given to the Society of Anaesthetics (Liverpool) in 1932 (9). Great achievement was recorded in the field on endotracheal anaesthesia during the First World War and post war period. The contribution of Ivan Magill and Stanley Rowbotham was the hallmark of endotracheal anaesthesia since 1934.

References:

1. Ezri T, Evron S, Hadad H, Roth Y. Tracheostomy and endotracheal intubation: a short history. Harefuah. 2005 Dec; 144(12): p. 891-3.
2. Baker AB. Artificial respiration, the history of an idea. Med Hist. 1971 Oct; 15(4): p. 336–351.
3. Garrison DH., Hast MH. The Fabric of the Human Body,An Annotated Translation of the 1543 and 1555 Editions of “De Humani Corporis Fabrica”: Northwestern University; 2003.
4. Paul AK. Essentials of Anaesthesiology. 7th ed.: Jaypee Brothers; 2006.
5. Brandt L, Pokar H, Schütte H. 100 years of intubation anesthesia. William Macewen, a pioneer of endotracheal intubation. Anaesthesist. 1983 May; 32(5): p. 200-4.
6. Opinel A, Gachelin G. French 19th century contributions to the development of treatments for diphtheria. J R Soc Med. 2011 Apr; 104(4): p. 173–178.
7. Condon H, Gilchrist E. Stanley Rowbotham. Twentieth century pioneer anaesthetist. Anaesthesia. 1986 Jan; 41(1): p. 46-52.
8. Magill I. Blind nasal intubation. Anaesthesia. 1975 Jul; 30(4): p. 476-9.
9. McLachlan G. Sir Ivan Magill KCVO, DSc, MB, BCh, BAO, FRCS, FFARCS (Hon), FFARCSI (Hon), DA, (1888-1986). Ulster Med J. 2008 Sep; 77(3): p. 146–152.

oxygen delivery

Awake Intubation (procedure in brief) 

Succinylcholine vs Rocuronium

	Succinylcholine	Rocuronium
Chemical structure	Structurally two acetyl choline molecules joined together	Aminosteroid
Classification	Depolarising neuromuscular blocker	Non-depolarising neuromuscular blocker
Fasciculation	Yes ( causes post-op myalgia)	No
Metabolism	·         Rapidly metabolised by pseudocholinesterase ·         Duration of action prolonged in Pseudocholinesterase deficiency	·         Eliminated primarily by liver and slightly by kidney ·         Elimination half life longer as compared to Sch.
Dosage	·         Used for intubation only now-a-days ·         1-1.5 mg/kg iv ·         4-5 mg/kg im (onset delayed)	·         Used for both intubation as well as during maintenance ·         Intubation: 0.6-1.2mg /kg iv ·         Intubation: 1mg/kg im (infants) and 2mg/kg im (children) àonset delayed (3-6min) ·         Maintenance: 0.15 mg/kg every 20 mins ·         Continuous infusion: 5-12µg/kg/min
Onset of action after iv induction dose (onset to maximum twitch depression)	30-60secs	60-90 secs
Duration of action	3-5 mins (phase 1 block)	·         Duration of action (duration to return to ≥ 25% of control twitch height): 20-35 min ·         Clinical duration (duration to return to Train-of-four >0.9): 55-80 min
Reversal with Sugammadex	Not possible	Possible Dose: ·         4 mg/kg iv when recovery has reached 1-2 post-tetanic counts ·         2 mg/kg iv if recovery has occurred upto reappearance of T2 ·         Immediate reversal: 16 mg/kg iv (recovery of T4/T1 ratio to 0.9 by 1.5 min)
Systemic effects	·         Causes bradycardia (especially when a second dose is given after 3-8mins) ·         Hyperkalemia (increases K+ by 0.5 mEq/L) ·         Transient increase in intracranial, intraocular and intragastric pressure	·         Mostly cardiostable ·         Mild vagolytic
Malignant hyperthermia risk	Yes	No
Use in burn patients	Avoid beyond 2 days till 2 yrs after burn (risk of hyperkalemia)	Can be used safely
Apnoea time (time available until critical desaturation occurs in the absence of ventilation after administration of the drug)	Less (because of fasciculation which uses up oxygen)	More
Paediatric usage	Usually avoided especially in case of unknown/undiagnosed myopathy	Can be used safely
Shelf life	Stable at room temperature for upto 14 days	Stable at room temperature for upto 12 weeks

Awake Intubation (procedure in brief)