I published a case report in the EMJ highlighting the use of intranasal ketamine in a pre-hospital paediatric burns case.
The lad had nasty scalds but did not need iv fluids and had no other indications for an iv line. The vigorous first aid had rendered him cold and veinless and an intraosseous would have been overkill. Ketamine was perfect for the job and Ambulance Service New South Wales paramedics carry a mucosal atomisation device (MAD) for the administration of i.n. fentanyl. I used the MAD to adminster 0.5 mg/kg ketamine, but there is a dead space in the device (0.1 ml) that probably resulted in actual delivery of 0.25mg/kg. This gave great analgesia and compliance enabling us to painlessly apply polyethylene film to the burns.
I received the following email from TIm Wolfe, the inventor of the MAD nasal (reproduced with permission):
Cliff,
Nice contribution to the literature. There is a lot of interest in IN ketamine in these lower doses to treat pain but not cause sedation. You eluded to the military interest and the hospice interest. I think your insights for EMS are also cutting edge – hopefully this will lead others to design a larger trial.
Thanks
Tim Wolfe, MD
In contrast to numerous other European nations, physicians with critical care skills do not consistently form part of the emergency pre-hospital system in the UK. My colleagues and I described the level of cover provided to patients in England, Wales and Northern Ireland, now available as an open access article online.
The BMJ’s press release is headed: ‘Critical care outside hospital ‘incomplete, unpredictable, and inconsistent’ across UK‘, a statement that has captured the interest of some media outlets, including the first place you would look for health news: bigsoccer.com. Pre-hospital physician-based critical care provision. (A) Daylight hours. (B) Hours of darkness.
Background Every day throughout the UK, ambulance services seek medical assistance in providing critically ill or injured patients with pre-hospital care. Objective To identify the current availability and utilisation of physician-based pre-hospital critical care capability across England, Wales and Northern Ireland. Design A postal and telephone survey was undertaken between April and December 2009 of all 13 regional NHS ambulance services, 17 air ambulance charities, 34 organisations affiliated to the British Association for Immediate Care and 215 type 1 emergency departments in England, Wales and Northern Ireland. The survey focused on the availability and use of physician-based pre-hospital critical care support. Results The response rate was 100%. Although nine NHS ambulance services recorded physician attendance at 6155 incidents, few could quantify doctor availability and utilisation. All but one of the British Association for Immediate Care organisations deployed ‘only when available’ and only 45% of active doctors could provide critical care support. Eleven air ambulance services (65%) operated with a doctor but only 5 (29%) operated 7 days a week. Fifty-nine EDs (27%) had a pre-hospital team but only 5 (2%) had 24 h deployable critical care capability and none were used regularly. Conclusion There is wide geographical and diurnal variability in availability and utilisation of physician-based pre-hospital critical care support. Only London ambulance service has access to NHS-commissioned 24 h physician-based pre-hospital critical care support. Throughout the rest of the UK, extensive use is made of volunteer doctors and charity sector providers of varying availability and capability.
Loss of consciousness can occur when a patient is suspended in a harness – ‘suspension syncope’, probably due to factors that include venous pooling in the lower limbs. An evidence based review of this entity was carried out:
The possibility of a fall into rope protection and subsequent suspension exists in some industrial situations. The action to take for the first aid management of rescued victims has not been clear, with some authors advising against standard first aid practices. To clarify the medical evidence relating to harness suspension the UK Health and Safety Executive commissioned an evidence-based review and guideline. Four key questions were posed relating to the incidence, circumstances, recognition and first aid management of the medical effects of harness suspension. A comprehensive literature search returned 60 potential papers with 29 papers being reviewed. The Scottish Intercollegiate Guideline Network (SIGN) methodology was used to critically review the selected papers and develop a guideline. A stakeholders’ workshop was held to review the evidence and draft recommendations. Nine papers formed the basis of the guideline recommendations. No data on the incidence of harness suspension syncope were found. Presyncopal symptoms or syncope are thought to occur with motionless suspension as a consequence of orthostasis leading to hypotension. There was no evidence of any other pathology, despite this being hypothesised by others. No evidence was found that showed the efficacy or safety of positioning a victim in a semirecumbent position. In any case of harness suspension, the standard UK first aid guidance for recovery of a semiconscious or unconscious person in a horizontal position should be followed. Other recommendations included areas for further research and proposals for standard data collection on falls into rope protection.
A review of extracorporeal life support for out-of-hospital cardiac arrest was undertaken, looking specifically at studies published in the Japanese literature. The abstract is shown below. Based on these findings, inclusion criteria for a multicentre, prospective non-randomised cohort study were established. The ‘SAVE-J: Study of advanced life support for ventricular fibrillation with extracorporeal circulation in Japan’ was launched and has been ongoing since October 2008 to compare the proportion of patients with a favourable neurological outcome by intention-to-treat in an ECPR group with a non-ECPR group. Inclusion criteria for this new study are:
shockable rhythm on the initial ECG
cardiac arrest on arrival at hospital regardless of the presence of recovery of spontaneous circulation before arrival
arrival at hospital within 45 min of the call for an ambulance or cardiac arrest;
cardiac arrest remaining for more than 15 min after arrival at hospital.
I look forward to seeing the results SAVE-J. If you wish to read more, you can check out the SAVE-J study website.
AIM: Although favourable outcomes in patients receiving extracorporeal cardiopulmonary resuscitation (ECPR) for out-of-hospital cardiac arrest have been frequently reported in Japanese journals since the late 1980s, there has been no meta-analysis of ECPR in Japan. This study reviewed and analysed all previous studies in Japan to clarify the survival rate of patients receiving ECPR. MATERIAL AND METHODS: Case reports, case series and abstracts of scientific meetings of ECPR for out-of-hospital cardiac arrest written in Japanese between 1983 and 2008 were collected. The characteristics and outcomes of patients were investigated, and the influence of publication bias of the case-series studies was examined by the funnel-plot method. RESULTS: There were 1282 out-of-hospital cardiac arrest patients, who received ECPR in 105 reports during the period. The survival rate at discharge given for 516 cases was 26.7±1.4%. The funnel plot presented the relationship between the number of cases of each report and the survival rate at discharge as the reverse-funnel type that centred on the average survival rate. In-depth review of 139 cases found that the rates of good recovery, mild disability, severe disability, vegetative state, death at hospital discharge and non-recorded in all cases were 48.2%, 2.9%, 2.2%, 2.9%, 37.4% and 6.4%, respectively. CONCLUSIONS: Based on the results of previous reports with low publication bias in Japan, ECPR appears to provide a higher survival rate with excellent neurological outcome in patients with out-of-hospital cardiac arrest.
Extracorporeal cardiopulmonary resuscitation for out-of-hospital cardiac arrest: a review of the Japanese literature Resuscitation. 2011 Jan;82(1):10-4
Thanks to neuro-icu.com for highlighting this one: The American Heart Association and American Stroke Association have produced guidelines for the diagnosis and management of cerebral venous thrombosis. Here is a summary of their recommendations. The full text of the guidelines is available via the link at the bottom. Routine Blood Work
In patients with suspected CVT, routine blood studies consisting of a complete blood count, chemistry panel, prothrombin time, and activated partial thromboplastin time should be performed (Class I; Level of Evidence C).
Screening for potential prothrombotic conditions that may predispose a person to CVT (eg, use of contraceptives, underlying inflammatory disease, infectious process) is recommended in the initial clinical assessment (specific recommendations for testing for thrombophilia are found in the long-term management section of this document) (Class I; Level of Evidence C).
A normal D-dimer level according to a sensitive immunoassay or rapid enzyme-linked immunosorbent assay (ELISA) may be considered to help identify patients with low probability of CVT (Class IIb; Level of Evidence B). If there is a strong clinical suspicion of CVT, a normal D-dimer level should not preclude further evaluation.
Common Pitfalls in the Diagnosis of CVT
In patients with lobar ICH of otherwise unclear origin or with cerebral infarction that crosses typical arterial boundaries, imaging of the cerebral venous system should be performed (Class I; Level of Evidence C).
In patients with the clinical features of idiopathic intracranial hypertension, imaging of the cerebral venous system is recommended to exclude CVT (Class I; Level of Evidence C).
In patients with headache associated with atypical features, imaging of the cerebral venous system is reasonable to exclude CVT (Class IIa; Level of Evidence C).
Imaging in the Diagnosis of CVT
Although a plain CT or MRI is useful in the initial evaluation of patients with suspected CVT, a negative plain CT or MRI does not rule out CVT. A venographic study (either CTV or MRV) should be performed in suspected CVT if the plain CT or MRI is negative or to define the extent of CVT if the plain CT or MRI suggests CVT (Class I; Level of Evidence C).
An early follow-up CTV or MRV is recommended in CVT patients with persistent or evolving symptoms despite medical treatment or with symptoms suggestive of propagation of thrombus (Class I; Level of Evidence C).
In patients with previous CVT who present with recurrent symptoms suggestive of CVT, repeat CTV or MRV is recommended (Class I; Level of Evidence C).
Gradient echo T2 susceptibility-weighted images combined with magnetic resonance can be useful to improve the accuracy of CVT diagnosis (Class IIa; Level of Evidence B).
Catheter cerebral angiography can be useful in patients with inconclusive CTV or MRV in whom a clinical suspicion for CVT remains high (Class IIa; Level of Evidence C).
A follow-up CTV or MRV at 3 to 6 months after diagnosis is reasonable to assess for recanalization of the occluded cortical vein/sinuses in stable patients (Class IIa; Level of Evidence C).
Management and Treatment
Patients with CVT and a suspected bacterial infection should receive appropriate antibiotics and surgical drainage of purulent collections of infectious sources associated with CVT when appropriate (Class I; Level of Evidence C).
In patients with CVT and increased intracranial pressure, monitoring for progressive visual loss is recommended, and when this is observed, increased intracranial pressure should be treated urgently (Class I; Level of Evidence C).
In patients with CVT and a single seizure with parenchymal lesions, early initiation of antiepileptic drugs for a defined duration is recommended to prevent further seizures (Class I; Level of Evidence B).
In patients with CVT and a single seizure without parenchymal lesions, early initiation of antiepileptic drugs for a defined duration is probably recommended to prevent further seizures (Class IIa; Level of Evidence C).
In the absence of seizures, the routine use of antiepileptic drugs in patients with CVT is not recommended (Class III; Level of Evidence C).
For patients with CVT, initial anticoagulation with adjusted-dose UFH or weight-based LMWH in full anticoagulant doses is reasonable, followed by vitamin K antagonists, regardless of the presence of ICH (Class IIa; Level of Evidence B).
Admission to a stroke unit is reasonable for treatment and for prevention of clinical complications of patients with CVT (Class IIa; Level of Evidence C).
In patients with CVT and increased intracranial pressure, it is reasonable to initiate treatment with acetazolamide. Other therapies (lumbar puncture, optic nerve decompression, or shunts) can be effective if there is progressive visual loss. (Class IIa; Level of Evidence C).
Endovascular intervention may be considered if deterioration occurs despite intensive anticoagulation treatment (Class IIb; Level of Evidence C). In patients with neurological deterioration due to severe mass effect or intracranial hemorrhage causing intractable intracranial hypertension, decompressive hemicraniectomy may be considered (Class IIb; Level of Evidence C).
For patients with CVT, steroid medications are not recommended, even in the presence of parenchymal brain lesions on CT/MRI, unless needed for another underlying disease (Class III; Level of Evidence B).
Long-Term Management and Recurrence of CVT
Testing for prothrombotic conditions, including protein C, protein S, antithrombin deficiency, antiphospholipid syndrome, prothrombin G20210A mutation, and factor V Leiden, can be beneficial for the management of patients with CVT. Testing for protein C, protein S, and antithrombin deficiency is generally indicated 2 to 4 weeks after completion of anticoagulation. There is a very limited value of testing in the acute setting or in patients taking warfarin. (Class IIa; Level of Evidence B).
In patients with provoked CVT (associated with a transient risk factor), vitamin K antagonists may be continued for 3 to 6 months, with a target INR of 2.0 to 3.0 (Table 3) (Class IIb; Level of Evidence C).
In patients with unprovoked CVT, vitamin K antagonists may be continued for 6 to 12 months, with a target INR of 2.0 to 3.0 (Class IIb; Level of Evidence C).
For patients with recurrent CVT, VTE after CVT, or first CVT with severe thrombophilia (ie, homozygous prothrombin G20210A; homozygous factor V Leiden; deficiencies of protein C, protein S, or antithrombin; combined thrombophilia defects; or antiphospholipid syndrome), indefinite anticoagulation may be considered, with a target INR of 2.0 to 3.0 (Class IIb; Level of Evidence C).
Consultation with a physician with expertise in thrombosis may be considered to assist in the pro- thrombotic testing and care of patients with CVT (Class IIb; Level of Evidence C).
Management of Late Complications (Other Than Recurrent VTE)
In patients with a history of CVT who complain of new, persisting, or severe headache, evaluation for CVT recurrence and intracranial hypertension should be considered (Class I; Level of Evidence C)
CVT in pregnancy
For women with CVT during pregnancy, LMWH in full anticoagulant doses should be continued throughout pregnancy, and LMWH or vitamin K antagonist with a target INR of 2.0 to 3.0 should be continued for at least 6 weeks postpartum (for a total minimum duration of therapy of 6 months) (Class I; Level of Evidence C).
It is reasonable to advise women with a history of CVT that future pregnancy is not contraindicated. Further investigations regarding the underlying cause and a formal consultation with a hematologist and/or maternal fetal medicine specialist are reasonable. (Class IIa; Level of Evidence B).
It is reasonable to treat acute CVT during pregnancy with full-dose LMWH rather than UFH (Class IIa; Level of Evidence C).
For women with a history of CVT, prophylaxis with LMWH during future pregnancies and the postpartum period is probably recommended (Class IIa; Level of Evidence C).
Children
Supportive measures for children with CVT should include appropriate hydration, control of epileptic seizures, and treatment of elevated intracranial pressure (Class I; Level of Evidence C).
Given the potential for visual loss owing to severe or long-standing increased intracranial pressure in children with CVT, periodic assessments of the visual fields and visual acuity should be performed, and appropriate measures to control elevated intracranial pressure and its complications should be instituted (Class I; Level of Evidence C).
In all pediatric patients, if initial anticoagulation treatment is withheld, repeat neuroimaging including venous imaging in the first week after diagnosis is recommended to monitor for propagation of the initial thrombus or new infarcts or hemorrhage (Class I; Level of Evidence C).
In children with acute CVT diagnosed beyond the first 28 days of life, it is reasonable to treat with full-dose LMWH even in the presence of intracra- nial hemorrhage (Class IIa; Level of Evidence C).
In children with acute CVT diagnosed beyond the first 28 days of life, it is reasonable to continue LMWH or oral vitamin K antagonists for 3 to 6 months (Class IIa; Level of Evidence C).
In all pediatric patients with acute CVT, if initial anticoagulation is started, it is reasonable to perform a head CT or MRI scan in the initial week after treatment to monitor for additional hemor- rhage (Class IIa; Level of Evidence C).
Children with CVT may benefit from thrombophilia testing to identify underlying coagulation defects, some of which could affect the risk of subsequent rethromboses and influence therapeutic decisions (Class IIb; Level of Evidence B).
Children with CVT may benefit from investigation for underlying infections with blood cultures and sinus radiographs (Class IIb; Level of Evidence B).
In neonates with acute CVT, treatment with LMWH or UFH may be considered (Class IIb; Level of Evidence B).
Given the frequency of epileptic seizures in children with an acute CVT, continuous electroencephalography monitoring may be considered for individuals who are unconscious or mechanically ventilated (Class IIb; Level of Evidence C).
In neonates with acute CVT, continuation of LMWH for 6 weeks to 3 months may be considered (Class IIb; Level of Evidence C).
The usefulness and safety of endovascular intervention are uncertain in pediatric patients, and its use may only be considered in carefully selected patients with progressive neurological deterioration despite intensive and therapeutic levels of anticoagulant treatment (Class IIb; Level of Evidence C).
Diagnosis and Management of Cerebral Venous Thrombosis: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association Stroke. 2011 Feb 3. [Epub ahead of print] Full Text
A retrospective study of out-of-hospital cardiac arrest patients attended by a French pre-hospital system was performed to assess the predictive factors for positive coronary angiography.
OBJECTIVES: Coronary angiography is often performed in survivors of out-of-hospital cardiac arrest, but little is known about the factors predictive of a positive coronary angiography. Our aim was to determine these factors. METHODS: In this 7-year retrospective study (January 2000-December 2006) conducted by a French out-of-hospital emergency medical unit, data were collected according to Utstein style guidelines on all out-of-hospital cardiac arrest patients with suspected coronary disease who recovered spontaneous cardiac activity and underwent early coronary angiography. Coronary angiography was considered positive if a lesion resulting in more than a 50% reduction in luminal diameter was observed or if there was a thrombus at an occlusion site. RESULTS: Among the 4621 patients from whom data were collected, 445 were successfully resuscitated and admitted to hospital. Of these, 133 were taken directly to the coronary angiography unit, 95 (71%) had at least one significant lesion, 71 (53%) underwent a percutaneous coronary intervention, and 30 survived [23%, 95% confidence interval (CI): 16-30]. According to multivariate analysis, the factors predictive of a positive coronary angiography were a history of diabetes [odds ratio (OR): 7.1, 95% CI: 1.4-36], ST segment depression on the out-of-hospital ECG (OR: 5.4, 95% CI: 1.1-27.8), a history of coronary disease (OR: 5.3, 95% CI: 1.4-20.1), cardiac arrest in a public place (OR: 3.7, 95% CI: 1.3-10.7), and ventricular fibrillation or ventricular tachycardia as initial rhythm (OR: 3.1, 95% CI: 1.1-8.6). CONCLUSION: Among the factors identified, diabetes and a history of coronary artery were strong predictors for a positive coronary angiography, whereas ST segment elevation was not as predictive as expected.
A potentially reversible cause of haemodynamic shock in critically ill patients is left ventricular outflow tract obstruction (LVOTO). We are familiar with this phenomenon in conditions such as hypertrophic cardiomyopathy (HCM), but LVOTO can occur in the absence of HCM and result in hypotension that may be refractory to catecholamines. In fact, vasoactive drugs are often the precipitant.
A case is reported of an intubated elderly man with pneumonia and COPD who upon starting dopamine and furosemide for hypotension and anuria developed severe haemodynamic deterioration1. Echo revealed a hyperkinetic left ventricle with mild concentric hypertrophy, septal wall thickness of 12 mm (normal range up to 10mm), and a reduced end-diastolic diameter. Systolic anterior motion (SAM) of the anterior mitral leaflet causing a significant left ventricular outflow tract obstruction (LVOTO), with a peak gradient of 100 mmHg, was detected. The patient improved with discontinuation of vasoactive drugs and fluid loading. A follow up cardiac MR showed a structurally normal LV.
The authors describe the factors that combine to produce this syndrome:
Anatomical substrate – Left ventricular hypertrophy due to hypertension, mitral valve repair, previous aortic valve replacement, abnormalities of the mitral subvalvular apparatus, sigmoid septum and a steep aortic root angle.
Precipitating factors – Drug therapies such as catecholamine infusion or diuretics, which respectively enhance the contractility of the basal segments and reduce the left ventricular cavity, emotional stress (like described in the apical ballooning syndrome), hypovolaemia, dehydration, sepsis, and myocardial infarction; hypovolaemia and mechanical ventilation further exacerbate underfilling of the LV and dynamic LVOTO.
In a review article on the topic, Dr Chockalingam and colleagues describe structural and functional factors in this finely crafted explanation2:
The asymmetrically hypertrophied septum, progressive narrowing of the LVOT during systole, and direction of the bloodstream cause drag forces and a Venturi effect on the anterior mitral leaflet, which results in SAM of the anterior mitral leaflet. This movement results in the anterior mitral leaflet contacting the septum for a period of systole, effectively obstructing the path of ventricular outflow. Failure of the anterior mitral leaflet to coapt with the posterior leaflet in systole results in MR. The degree and duration of mitral SAM determine the severity of the dynamic LVOTO gradients and MR.
Although classically described with hypertrophic cardiomyopathy, SAM and LVOTO can independently result from various clinical settings such as LV hypertrophy (hypertension or sigmoid septum), reduced LV chamber size (dehydration, bleeding, or diuresis), mitral valve abnormalities (redundant, long anterior leaflet), and hypercontractility (stress, anxiety, or inotropic agents). Dynamic LVOTO may occur with acute coronary syndrome and often presents with shock and a new systolic murmur3. The presence of a new murmur in a shocked ACS patient should therefore prompt consideration of the following diagnoses:
Acute mitral valve dysfunction
Ventricular septal defect
Free wall rupture
Dynamic LVOTO
Treatment is aimed at alleviating the causes and should be individualised. Options include coronary revascularisation, volume therapy, beta blockade, removing afterload reduction (vasodilators and balloon pumps can exacerbate LVOTO), and alpha agonists such as phenylephrine.
In summary, dynamic LVOTO:
is a potentially reversible cause of haemodynamic shock in critically ill patients
should be considered in critically ill patients whose shock fails to improve or worsen with inotropic medication
should be considered in patients with ACS, shock, and a new systolic murmur
can result from combinations of LV hypertrophy, reduced LV chamber size (dehydration, bleeding, or diuresis), mitral valve abnormalities, and hypercontractility (stress, anxiety, or inotropic agents)
is yet another reason why the haemodynamic monitor of choice in shocked patients should be echocardiography!
Echo showing systolic anterior motion of the mitral valve
A Swiss study examined the on site triage decision making of pre-hospital emergency physicians. Dispatch of the physicians was coordinated by trained nurses or paramedics.
OBJECTIVE: Accurate identification of major trauma patients in the prehospital setting positively affects survival and resource utilization. Triage algorithms using predictive criteria of injury severity have been identified in paramedic-based prehospital systems. Our rescue system is based on prehospital paramedics and emergency physicians. The aim of this study was to evaluate the accuracy of the prehospital triage performed by physicians and to identify the predictive factors leading to errors of triage. METHODS: Retrospective study of trauma patients triaged by physicians. Prehospital triage was analyzed using criteria defining major trauma victims (MTVs, Injury Severity Score >15, admission to ICU, need for immediate surgery and death within 48 h). Adequate triage was defined as MTVs oriented to the trauma centre or non-MTV (NMTV) oriented to regional hospitals. RESULTS: One thousand six hundred and eighti-five patients (blunt trauma 96%) were included (558 MTV and 1127 NMTV). Triage was adequate in 1455 patients (86.4%). Overtriage occurred in 171 cases (10.1%) and undertriage in 59 cases (3.5%). Sensitivity and specificity was 90 and 85%, respectively, whereas positive predictive value and negative predictive value were 75 and 94%, respectively. Using logistic regression analysis, significant (P<0.05) predictors of undertriage were head or thorax injuries (odds ratio >2.5). Predictors of overtriage were paediatric age group, pedestrian or 2 wheel-vehicle road traffic accidents (odds ratio >2.0). CONCLUSION: Physicians using clinical judgement provide effective prehospital triage of trauma patients. Only a few factors predicting errors in triage process were identified in this study.
Accuracy of prehospital triage of trauma patients by emergency physicians: a retrospective study in western Switzerland Eur J Emerg Med. 2011 Apr;18(2):86-93
Oxygen therapy in normoxic acute coronary syndrome patients is controversial, and a previous systematic review cautioned against it in uncomplicated MI. A volunteer study using cardiac imaging demonstrates the effects of supplemental oxygen on coronary blood flow.
OBJECTIVES: Oxygen (O2) is a cornerstone in the treatment of critically ill patients, and the guidelines prescribe 10-15 l of O2/min even to those who are initially normoxic. Studies using indirect or invasive methods suggest, however, that supplemental O2 may have negative cardiovascular effects. The aim of this study was to test the hypothesis, using noninvasive cardiac magnetic resonance imaging, that inhaled supplemental O2 decreases cardiac output (CO) and coronary blood flow in healthy individuals. METHODS: Sixteen healthy individuals inhaled O2 at 1, 8 and 15 l/min through a standard reservoir bag mask. A 1.5 T magnetic resonance imaging scanner was used to measure stroke volume, CO and coronary sinus blood flow. Left ventricular (LV) perfusion was calculated as coronary sinus blood flow/LV mass. RESULTS: The O2 response was dose-dependent. At 15 l of O2/min, blood partial pressure of O2 increased from an average 11.7 to 51.0 kPa with no significant changes in blood partial pressure of CO2 or arterial blood pressure. At the same dose, LV perfusion decreased by 23% (P=0.005) and CO decreased by 10% (P=0.003) owing to a decrease in heart rate (by 9%, P<0.002), with no significant changes in stroke volume or LV dimensions. Owing to the decreased CO and LV perfusion, systemic and coronary O2 delivery fell by 4 and 11% at 8 l of O2/min, despite the increased blood oxygen content. CONCLUSION: Our data indicate that O2 administration decreases CO, LV perfusion and systemic and coronary O2 delivery in healthy individuals. Further research should address the effects of O2 therapy in normoxic patients.
A way of improving glottic visualisation when attempting fibreoptic intubation is for an assistant to perform a jaw thrust manoeuvre. This is nicely demonstrated in a video on the New England Journal website. However my retrieval medicine colleague and anaesthetist Dr Anthony Lewis pointed out the following situation and its solution:
What if they are a ‘difficult airway’ and you the jaw can’t move? Get your Magills forceps, grab the tongue and pull the tongue out. Very nice!
