Category Archives: ICU

Stuff relevant to patients on ICU

Flying Docs and Airways

Flying Doctor Minh Le Cong describes the profile and success rates of emergency endotracheal intubation conducted by the Queensland Royal Flying Doctor Service aeromedical retrieval team, comprising a doctor and flight nurse. It would be interesting to know how many more patients have been added to the registry since this was submitted. An important contribution to the literature in retrieval medicine.


Objective To describe the profile and success rates of emergency endotracheal intubation conducted by the Queensland Royal Flying Doctor Service aeromedical retrieval team comprising a doctor and flight nurse.

Method Each intubator completed a study questionnaire at the time of each intubation for indications, complications, overall success, drugs utilised and deployment of rescue airway devices/adjuncts.

Results 76 patients were intubated; 72 intubations were successful. None required surgical airway and three were managed with laryngeal mask airways; the remaining failure was managed with simple airway positioning for transport. There were two cardiac arrests during intubation. Thiopentone and suxamethonium were the predominant drugs used to facilitate intubation.

Conclusion Despite a low rate of endotracheal intubation, the high success rate was similar to other aeromedical organisations’ published airway data. This study demonstrates the utility of the laryngeal mask airway device in the retrieval and transport setting, in particular for managing a failed intubation.

Flying doctor emergency airway registry: a 3-year, prospective, observational study of endotracheal intubation by the Queensland Section of the Royal Flying Doctor Service of Australia
Emerg Med J. 2010 Sep 15. [Epub ahead of print]
Those interested in learning more about this registry, including how often capnography was used, more information about the asystolic arrests, and whether they tried a blind digital intubation, can check this link to a presentation about the registry.

End tidal CO2 in cardiac arrest

Measuring end-tidal CO2 in cardiac arrest patients is helpful for

  1. confirming tracheal tube placement
  2. assessing the effectiveness of chest compressions
  3. predicting likelihood of return of spontaneous circulation (ROSC), in that a persistently low ETCO2 tends to predict death, whereas a high or rising ETCO2 is associated with a higher chance of ROSC.

It may be however that its predictive ability depends on the type of cardiac arrest, and how far into the resuscitation you’ve got when you measure the ETCO2. Consider this new study from Slovenian pre-hospital emergency physicians:
Methods: The study included two cohorts of patients: cardiac arrest due to asphyxia with initial rhythm asystole or pulseless electrical activity (PEA), and cardiac arrest due to arrhythmia with initial rhythm VF or pulseless VT. The causes of asphyxia were: asthma, severe acute respiratory failure, tumor of the airway, suicide by hanging, acute intoxication, pneumonia and a foreign body in the airway.PetCO2 was measured for both groups immediately after intubation and repeatedly every minute, both for patients with or without return of spontaneous circulation (ROSC). We compared the dynamic pattern of PetCO2 between groups. Resuscitation procedures were performed by an emergency medical team (emergency medical physician and two emergency medical technicians or registered nurses) in accordance with 2005 ERC Guideline
Results: Between June 2006 and June 2009 resuscitation was attempted in 325 patients and in this study we included 51 patients with asphyxial cardiac arrest and 63 patients with VF/VT cardiac arrest. The initial values of PetCO2 were significantly higher in the group with asphyxial cardiac arrest (6.74 ± 4.22 kilopascals (kPa) versus 4.51 ± 2.47 kPa; P = 0.004). In the group with asphyxial cardiac arrest, the initial values of PetCO2 did not show a significant difference when we compared patients with and without ROSC (6.96 ± 3.63 kPa versus 5.77 ± 4.64 kPa; P = 0.313). We confirmed significantly higher initial PetCO2 values for those with ROSC in the group with primary cardiac arrest (4.62 ± 2.46 kPa versus 3.29 ± 1.76 kPa; P = 0.041).

A significant difference in PetCO2 values for those with and without ROSC was achieved after five minutes of CPR in both groups (asphyxial arrest: 6.09 ± 2.63 kPa versus 4.47 ± 3.35 kPa; P = 0.006; primary arrest: 5.63 ± 2.01 kPa versus 4.26 ± 1.86; P = 0.015)
In mmHg, the PetCO2 values for those with and without ROSC after five minutes of CPR was: asphyxial arrest: 42.3 ± 20 mmHg versus 34 ± 25.5 mmHg; P = 0.006; primary arrest: 42.8 ± 15.3 mmHg versus 32.3 ± 14.1 mmHg; P = 0.015
Graphically, this difference in ROSC vs non-ROSC PetCO2 for both groups appeared to be even greater at ten minutes, with higher statistically significance (p<0.001), although the values of PetCO2 are not given in the paper.
In all patients with ROSC the initial PetCO2 was again higher than 1.33 kPa (10.1 mmHg).
Conclusions: The dynamic pattern of PetCO2 values during out-of-hospital CPR showed higher values of PetCO2 in the first two minutes of CPR in asphyxia, and a prognostic value of initial PetCO2 only in primary VF/VT cardiac arrest. A prognostic value of PetCO2 for ROSC was achieved after the fifth minute of CPR in both groups and remained present until final values. This difference seems to be a useful criterion in pre-hospital diagnostic procedures and attendance of cardiac arrest.
The authors summarise with the following key messages:

  • Initial values of PetCO2 are higher in asphyxial cardiac arrest than in primary cardiac arrest.
  • Initial values of PetCO2 in asphyxial cardiac arrest do not have a prognostic value for resuscitation outcome.
  • The prognostic value of PetCO2 for ROSC was achieved after the fifth minute of CPR in both groups and remained present until the final values.
  • The values of PetCO2 seem to be useful in differentiating the causes of cardiac arrest in a pre-hospital setting.

I think that last one’s a bit of a stretch. For me, this paper confirms that the longer you are into a cardiac arrest resuscitation, the worse news a low PetCO2 is. The lack of predictive value of initial PetCO2, particularly in the asphyxia group, is interesting but not surprising.
The dynamic pattern of end-tidal carbon dioxide during cardiopulmonary resuscitation: difference between asphyxial cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest
Critical Care 2011, 15:R13

Propofol and the heart

I don’t normally blog about animal studies, but on reading a review of recent(-ish) shock research I was interested in the following piece that describes the effect of diffrent induction agents on rat heart muscle:
Sedation is frequently necessary in patients with septic shock, and therefore Zausig and colleagues investigated the effects of dose-dependent effects of various induction agents (propofol, midazolam, s(+)-ketamine, methohexitone, etomidate) in a Langendorff heart preparation from rats rendered septic by CLP. Propofol exerted the most pronounced depressant effects on both the maximal systolic contraction and the minimal diastolic relaxation, and cardiac work. Furthermore, propofol only adversely deleteriously affected the myocardial oxygen supply- demand ratio. In contrast, s(+)-ketamine was associated with the best maintenance of cardiac function. Within the limits of the study – that is, the use of an ex vivo isolated organ model – the authors concluded that s(+)-ketamine may be an alternative to the comparably inert etomidate, the use of which is, however, limited due to its endocrine side effects.

Of course we should be cautious about extrapolating animal lab work to clinical practice, but this supports my position of vehement opposition to the injudicious use of propofol for RSI in critically ill patients!
Year in review 2009: Critical Care – shock
Critical Care 2010, 14:239 Full text

Prone ventilation in ARDS

Prone ventilation can improve refractory hypoxaemia in ARDS but its effects on mortality have not been impressive in some studies which may be underpowered or include patients with less severe hypoxaemia. An updated meta-analysis showed significantly reduced ICU mortality in the four recent studies that enrolled only patients with ARDS, as opposed to ARDS/ALI (odds ratio = 0.71; 95% confidence interval = 0.5 to 0.99; P = 0.048; number needed to treat = 11). There may also be benefit from a greater duration of prone positioning.

An updated study-level meta-analysis of randomised controlled trials on proning in ARDS and acute lung injury
Critical Care 2011, 15:R6 Full text

Extracorporeal CPR

Extracorporeal cardiopulmonary resuscitation (E-CPR) using extracorporeal membrane oxygenation (ECMO) support during inhospital cardiac arrest has been attempted to improve the outcome of cardiopulmonary resuscitation (CPR). A retrospective, single-center, observational study from Korea analysed a total of 406 adult patients with witnessed inhospital cardiac arrest receiving cardiopulmonary resuscitation for >10 mins.
How their system works: An ECMO cart was transported to the CPR site within 5–10 mins during the day and within 10–20 mins during the night shift. The decision to use E-CPR was dependent on the CPR team leader. Application of ECMO was usually considered under conditions of prolonged arrest (when there was no ROSC after 10–20 mins of CPR), recurrent arrest (when ROSC could not be maintained), or when the patient could not be expected to recover as a result of underlying severe left ventricular dysfunction or coronary artery disease despite a short CPR duration (end-stage heart failure requiring transplantation, left main coronary artery occlusion, etc)
The primary end point was a survival discharge with minimal neurologic impairment.

No. ECMO. I said ECMO.

85 patients underwent E-CPR and 321 underwent C- CPR. ECMO implantation was successful in 94.1% (80 of 85) in the E-CPR group, except for three cannulation failures and two ECMO flow failures. There was a signficantly greater proportion of patients with primary cardiac disease in the E-CPR group. Propensity score matching was used to balance the baseline characteristics and cardiopulmonary resuscitation variables that could potentially affect prognosis. In the matched population (n = 120), the survival discharge rate with minimal neurologic impairment in the extracorporeal cardiopulmonary resuscitation group was significantly higher than that in the conventional cardiopulmonary resuscitation group (odds ratio of mortality or significant neurologic deficit, 0.17; 95% confidence interval, 0.04-0.68; p = .012). In addition, there was a significant difference in the 6-month survival rates with minimal neurologic impairment (hazard ratio, 0.48; 95% confidence interval, 0.29-0.77; p = .003; p <.001 by stratified log-rank test). In the subgroup based on cardiac origin, extracorporeal cardiopulmonary resuscitation also showed benefits for survival discharge (odds ratio, 0.19; 95% confidence interval, 0.04-0.82; p = .026) and 6-month survival with minimal neurologic impairment (hazard ratio, 0.56; 95% confidence interval, 0.33-0.97; p = .038; p = .013 by stratified log-rank test).
The authors conclude that extracorporeal cardiopulmonary resuscitation showed a survival benefit over conventional cardiopulmonary resuscitation in patients who received cardiopulmonary resuscitation for >10 mins after witnessed inhospital arrest, especially in cases of cardiac origin. These results contrast with these recently published French findings in patients receiving ECMO after out-of-hospital cardiac arrest.
Extracorporeal cardiopulmonary resuscitation in patients with inhospital cardiac arrest: A comparison with conventional cardiopulmonary resuscitation
Crit Care Med. 2011 Jan;39(1):1-7

Paediatric airway gems

Dr Rich Levitan has made an enormous contribution to the science and practice of emergency airway management, as his bibliography demonstrates. In a new article in Emergency Physicians Monthly entitled ‘Demystifying Pediatric Laryngoscopy’, Rich covers some great tips for optimising laryngoscopic view in kids.
Check this excerpt out for an example:
During laryngoscopy in infants the epiglottis and uvula are often touching; the epiglottis may be located within an inch of the mouth. Often the epiglottis lies against the posterior pharynx, and it is critical to have a Yankauer to dab the posterior pharynx as the laryngoscope is advanced. Hyperextension of the head pushes the base of tongue and epiglottis backwards against the posterior pharyngeal wall, and makes epiglottis identification more difficult
Gems like this come thick and fast when you hear or read what Rich has to say. Seven years ago I was left reeling after finishing his ‘Airway Cam Guide to Intubation and Practical Emergency Airway Management‘ which profoundly influenced the way I practice and teach emergency airway skills, including on the Critical Care for Emergency Physicians course.

I’ve finally gotten round to booking a place on one of his courses in March in Baltimore. I’ll let you know how it goes. In the mean time, I’d like to point you toward his training videos as a great educational resource, like this one that demonstrates for novice laryngoscopists the difference between the appearances of trachea and oesophagus, the former having recognisable, defined posterior cartilagenous structures:

Demystifying Pediatric Laryngoscopy
Emergency Physicians Monthly January 19, 2011

Sux vs Roc in ED RSI

Suxamethonium and rocuronium were compared in a database of prospectively recorded cases of RSI in the emergency department.
A total of 327 RSI were included in the final analyses. All patients received etomidate as the induction sedative and were successfully intubated. Of these, 113 and 214 intubations were performed using succinylcholine and rocuronium, respectively.

  • The rate of first-attempt intubation success was similar between the succinylcholine and rocuronium groups (72.6% vs. 72.9%, p = 0.95).
  • Median doses used for succinylcholine and rocuronium were 1.65 mg/kg (interquartile range [IQR] = 1.26–1.95 mg/kg) and 1.19 mg/kg (IQR = 1–1.45 mg/kg), respectively.
  • The median dose of etomidate was 0.25 mg/kg in both groups.

In this study succinylcholine and rocuronium were equivalent with regard to first-attempt intubation success in the ED. This finding is consistent with previous investigations that used doses between 0.9 and 1.2 mg/kg and found similar intubating conditions to succinylcholine at these higher doses; subgroup analyses of studies using a lower rocuronium dose of 0.6 to 0.7 mg/kg had a relative risk favoring succinylcholine for excellent intubating conditions.
The low (in my view) rate of first-attempt intubation success in both groups was (72.6% vs. 72.9%), does make one wonder whether the intubating clinicians optimised their strategy for first-pass success.
Comparison of Succinylcholine and Rocuronium for First-attempt Intubation Success in the Emergency Department
Acad Emerg Med. 2011;18:11-14

Hole in the head? Don't waste the window!

Zampieri and colleagues from Brazil report the use of brain ultrasound in two ICU patients who had had hemicraniectomies.
One of the patients had a subarachnoid haemorrhage with hydrocephalus and an infarct due to vasospasm requiring hemicraniectomy, who subsequently deteriorated with decreasing ventricular catheter drainage, raising suspicion of acute hydrocephalus. Brain ultrasonography confirmed moderate hydrocephalus which was seen to improve after catheter desobstruction.

a Ultrasonography showing moderate hydrocephalus with the catheter tip inside lateral ventricle (white arrow). b Image after catheter cleaning showing the decompressed lateral ventricle

The authors note: ‘standard ultrasonography can be performed through a hemicraniectomy field and may be helpful in a small group of patients. Since decompressive hemicraniectomy is increasingly being used in critical care medicine, bedside evaluation of the brain using the hemicraniectomy as an insonation window could be useful as a noninvasive triage tool and reduce the need for patient transport to the imaging center.’
Use of ultrasonography in hemicraniectomized patients: a report of two cases
Intensive Care Med. 2010 Dec;36(12):2161-2
Not got a hole in the skull? Could try a bony ultrasound window – compare the clear scans above with this scan of an extradural haematoma

Hypothermia and hypokalaemia

We all like to treat selected post cardiac arrest patients with hypothermia now, but isn’t hypothermia associated with a drop in potassium, which of course can precipitate pesky ventricular dysrhythmias in patients who would really rather not arrest again. Maybe the hypothermia itself is protective against the dysrhythmias?
A study from the Mayo Clinic updates our knowledge of this area:

METHODS: We retrospectively analyzed potassium variability with Therapeutic Hypothermia (TH) and performed correlative analysis of QT intervals and the incidence of ventricular arrhythmia.
RESULTS: We enrolled 94 sequential patients with OHCA, and serum potassium was followed intensively. The average initial potassium value was 3.9±0.7 mmol/l and decreased to a nadir of 3.2±0.7 mmol/l at 10 h after initiation of cooling (p<0.001). Eleven patients developed sustained polymorphic ventricular tachycardia (PVT) with eight of these occurring during the cooling phase. The corrected QT interval prolonged in relation to the development of hypothermia (p<0.001). Hypokalemia was significantly associated with the development of PVT (p=0.002), with this arrhythmia being most likely to develop in patients with serum potassium values of less than 2.5 mmol/l (p=0.002). Rebound hyperkalemia did not reach concerning levels (maximum 4.26±0.8 mmol/l at 40 h) and was not associated with the occurrence of ventricular arrhythmia. Furthermore, repletion of serum potassium did not correlate with the development of ventricular arrhythmia.
CONCLUSIONS: Therapeutic hypothermia is associated with a significant decline in serum potassium during cooling. Hypothermic core temperatures do not appear to protect against ventricular arrhythmia in the context of severe hypokalemia and cautious supplementation to maintain potassium at 3.0 mmol/l appears to be both safe and effective.
Hypokalemia during the cooling phase of therapeutic hypothermia and its impact on arrhythmogenesis
Resuscitation. 2010 Dec;81(12):1632-6

Bleeding Tracheostomy

Adapted from the UK Intensive Care Society’s ‘Standards for the care of adult patients with a temporary tracheostomy

Bleeding from an established tracheostomy (ie. ‘late bleeding’, as to opposed to peri-operative bleeding that is more common and often benign) may occur because of erosion of blood vessels in and around the stoma site. This is more likely if there has been infection of the stoma site. Such bleeding may settle with conservative management. More worryingly, however, is the prospect of such bleeding being the result of erosion of a major artery in the root of the neck where there has been pressure from the tracheostomy tube itself or the cuff tube. Most commonly, this erosion occurs into the right brachiocephalic artery (also known as the innominate artery), resulting in a tracheo-innominate artery fistula. This situation may be heralded in the preceding hours by a small, apparently insignificant, sentinel bleed. Bleeding from such a fistula will be massive. THIS IS A LIFE-THREATENING EMERGENCY and so decisions need to be rapidly made.

  1. Call for help– senior medical and nursing staff, other health professionals with tracheostomy care skills (e.g. respiratory therapist, physiotherapist).
  2. Clear airway – blood clots may need to be suctioned.
  3. Replace blood products as required
  4. Bleeding may be temporarily reduced or stopped by applying finger pressure to the root of the neck in the sternal notch, or by inflating the tracheostomy tube cuff (if present) with a 50ml syringe of air. This inflation should be done slowly and steadily to inflate the balloon to a maximum volume without bursting it. Depending on the type and size of the tracheostomy tube this may be anywhere between 10 and 35 ml.
  5. Urgent referral for surgical exploration must now be made, if not already done so. In addition to an ENT or maxillofacial surgeon, it may be necessary to get help from a vascular surgeon. Sometimes, the damage can only be repaired utilising cardio-pulmonary bypass, and so a cardiothoracic surgeon may also be needed to help.
  6. Consider palliation – it is well recognised that fatalities occur in this situation, and that this may be the mode of death for some patients with head and neck cancers