I have always had a problem with the ATLS classification of hypovolaemic shock, and omit it from teaching as any clinical applicability and reproducibility seem to be entirely lost on me. I was therefore reassured to read that real physiological data from the extensive national trauma registry in the UK (TARN) of 107,649 adult blunt trauma patients do not strongly support this classification. A key observation we regularly make in trauma patients is the frequent presence of normo- or bradycardia in hypovolaemic patients, which is well documented in the literature.
An excellent discussion section in this paper states: ‘it is clear that the ATLS classification of shock that associates increasing blood loss with an increasing heart rate, is too simplistic. In addition, blunt injury, which forms the majority of trauma in the UK, is usually a combination of haemorrhage and tissue injury and the classification fails to consider the effect of tissue injury‘
Testing the validity of the ATLS classification of hypovolaemic shock
Resuscitation. 2010 Sep;81(9):1142-7
Category Archives: Resus
Life-saving medicine
Burr holes by emergency physicians
Emergency physicians at Hennepin County Medical Centre (HCMC) are trained in skull trephination (drilling a burr hole) for patients with coma, anisocoria and epidural (extradural) haematoma (EDH) who have not responded to osmotic agents and hyperventilation. This may be particularly applicable in centres remote from neurosurgical centres where delays caused by interfacility transfer are associated with increased morbidity and mortality.
Dr Smith and colleagues from HCMC describe a series of five talk-and-deteriorate patients with EDH who underwent skull trephination. 3 had complete recovery without disability, and 2 others had mild to moderate disability but with good to excellent cognitive function. None had complications from the procedure other than external bleeding from the already lacerated middle meningeal artery. In 4 of 5 cases, the times were recorded. Mean time from ED presentation to trephination was 55 min, and mean time from ED to craniotomy was 173 min. The mean time saved was 118 min, or approximately 2 h.
All trephinations were done by emergency physicians, who had received training in skull trephination as part of the HCMC Emergency Medicine Residency or as part of the Comprehensive Advanced Life Support (CALS) course. Training was very brief and involved discussion of the treatment of EDH, review of a CT scan of EDH, and hands-on practice on the skull of a dead sheep, using the Galt trephinator.
An excellent point made by the authors reminds us that patients with EDH who talk-and-deteriorate (those with the traditionally described “lucid interval”) have minimal primary brain injury and frequently have no brain parenchymal injury. Thus, if the EDH is rapidly decompressed, the outcome is significantly better than for deterioration due to other aetiologies. The authors recommend in EDH that the procedure should be done within 60–90 min of onset of anisocoria. A review of other studies on the procedure would suggest that case selection is critical in defining the appropriateness of the procedure: talk-and-deteriorate, coma, anisocoria, and a delay to neurosurgical decompression.
Emergency Department Skull Trephination for Epidural Hematoma in Patients Who Are Awake But Deteriorate Rapidly
J Emerg Med. 2010 Sep;39(3):377-83
capnometry versus pulse oximetry during procedural sedation
During emergency department procedural sedation, some clinicians (myself included) advocate non-invasive capnography for the early detection of apnoea. Others argue against routine administration of oxygen so that if desaturation occurs it provides an earlier more correctable warning of respiratory depression than if it occurs on supplemental oxygen. A Canadian study using prospective data from research on propofol with either ketamine or fentanyl compared changes in capnography with desaturation in sedated patients breathing only room air. Desaturation detectable by pulse oximeter occurred before overt changes in capnometry were identified.
It’s hard to ascertain the relevance of this finding. The authors wisely state ‘these findings should not be extrapolated to patients administered supplemental oxygen where it is possible capnometry may be helpful’. Since I use capnography in the hope that it will assist in the earlier detection of ketamine-associated laryngospasm in children, I’m not going to discard it in favour of waiting for the saturation to fall. Perhaps we just need to be clear that capnography may be more useful at detecting apnoea than hypoventilation.
A comparative evaluation of capnometry versus pulse oximetry during procedural sedation and analgesia on room air
CJEM. 2010 Sep;12(5):397-404
Echo in life support feasible
Emergency physicians in Cambridge and Ipswich in the UK prospectively documented their echo use in cardiac arrest. Images were easily acquired, were quickly obtained, and influenced management. In keeping with previous studies, absence of ventricular wall motion predicted lack of return of spontaneous circulation, with a negative predictive value of 97%.
An evaluation of echo in life support (ELS): is it feasible? What does it add?
Emerg Med J. 2010 Oct 4. [Epub ahead of print]
McConnell's sign revisited
In acute pulmonary embolism, a well-recognised pattern of right ventricular wall motion reported by McConnell is characterised by normal RV apex (RVa) contractility with akinesia of the RV free wall. A study using an echo techique called longitudinal velocity vector imaging (VVI) was conducted to describe RVa mechanics in relation to the rest of the RV in patients with a proven acute PE (aPE) and to compare these results to healthy volunteers and to patients with known chronic pulmonary hypertension (cPH). There were no significant differences in segmental strain patterns between the aPE and cPH groups. The authors suggest that McConnell’s sign is probably a visual illusion; preserved RVa contractility might be due to tethering of the RVa to a hyperdynamic left ventricle in the presence of an acutely dilated RV and this is the most likely explanation of the regional pattern of RV dysfunction seen in aPE patients.
Video describing McConnell’s sign from YouTube:
Right Ventricular Apical Contractility in Acute Pulmonary Embolism: The McConnell Sign Revisited
Echocardiography. 2010 Jul;27(6):614-20
Two smaller lines may be quicker
Using Poiseuille’s law and standardized gauge sizes, an 18-gauge (g) intravenous catheter (IV) should be 2.5 times faster than a 20-g IV, but this is not borne out by observation, in vitro testing, and manufacturer’s data. A nice simple study on normal volunteers compared simultaneous flow rates between a single 18G iv in one arm with two 20G ivs in the other arm. The two smaller ones provided significantly faster flow than the single larger one, although flow rates were slower than manufacturer’s estimates. This is in keeping with this other study on cannula flow rates.
Are 2 smaller intravenous catheters as good as 1 larger intravenous catheter?
Am J Emerg Med. 2010 Jul;28(6):724-7
Can we tell if AF is new?
One of the dilemmas in selecting appropriate therapy for atrial fibrillation in the emergency situation is determining whether the AF is of acute onset or not. AF causes release of natriuretic peptide from the heart, so measuring these peptides may give a clue to the recency of onset if the kinetics are known. This of course can only apply to those patients without heart failure, who have another cause for elevated natriuretic peptide levels.
A study of N-terminal pro-BNP levels in patients with acute onset AF, and without clinical or radiological evidence of heart failure, showed the pattern of rise and fall. The key finding in this study is the rapid rise of plasma NT-proBNP levels to peak followed by a rapid decline, probably due to depletion of the granules in atrial myocytes in which pro-BNP is stored.
The authors describe the following implication of the study:
According to our observations, a rising trend is markedly indicative of the fact that AF onset did not happen more than 24–48 h before presentation. As a consequence, obtaining two to three plasma NT-proBNP levels within 24 h of presentation in patients with AF without heart failure who cannot satisfactorily pinpoint the time of onset may assist in determining whether the onset of the arrhythmia was recent. Such information is pertinent to decisions concerning anticoagulation and cardioversion.
Short-term fluctuations of plasma NT-proBNP levels in patients with new-onset atrial fibrillation: a way to assess time of onset?
Heart. 2010 Jul;96(13):1033-6
Pre-hospital cooling post arrest
An Australian randomised controlled trial assessed the effect of pre-hospital cooling (using 2 litres ice cold Hartmann’s) of post-cardiac arrest patients on functional status at hospital discharge. The intervention group were marginally cooler on arrival but did not have improved outcomes.
The authors conclude: In adults who have been resuscitated from out-of-hospital cardiac arrest with an initial cardiac rhythm of ventricular fibrillation, paramedic cooling with a rapid infusion of large-volume, ice-cold intravenous fluid decreased core temperature at hospital arrival but was not shown to improve outcome at hospital discharge compared with cooling commenced in the hospital.
Induction of Therapeutic Hypothermia by Paramedics After Resuscitation From Out-of-Hospital Ventricular Fibrillation Cardiac Arrest
Circulation. 2010 Aug 17;122(7):737-42 Free Full Text
One issue from this study was that relatively short urban pre-hospital transport times meant some patients did not get the full two litres, and some had already received room temperature fluids during the cardiac arrest resuscitation. The authors suggest further study should involved initiating cooling during the arrest. In fact a European study has done just that, using a device call a RhinoChill (a portable transnasal cooling device) to lower temperature during arrest in a randomised controlled trial. This trial showed pre-hospital intra-arrest transnasal cooling is safe and feasible and is associated with a significant improvement in the time intervals required to cool patients.
Intra-arrest transnasal evaporative cooling: a randomized, prehospital, multicenter study (PRINCE: Pre-ROSC IntraNasal Cooling Effectiveness)
Circulation. 2010 Aug 17;122(7):729-36
Inferior MI – check V1 too
Lead V1 directly faces the right ventricle and during an inferior AMI may exhibit ST elevation with concomitant right ventricular infarction. Lead V1 also faces the endocardial surface of the posterolateral left ventricle, and ST depression may reflect concomitant posterolateral infarction (as the “mirror image” of ST elevation involving posterolateral epicardial leads). In this situation, V3 also shows ST depression. In lead V1, however, ST elevation from right ventricular AMI may potentially cancel out the ST depression from posterolateral AMI to give an isoelectric ST level. Diagnosis of right ventricular infarction during an inferior AMI may therefore be aided by evaluating both V1 and V3 ST levels. Both right ventricular infarction and postero-lateral infarction worsen the prognosis of an inferior AMI.
In 7967 patients with acute inferior myocardial infarction in the Hirulog and Early Reperfusion or Occlusion-2 (HERO-2) trial, V1 ST levels were analyzed with adjustment for lead V3 ST level for predicting 30-day mortality.
V1 ST elevation at baseline, analyzed as a continuous variable, was associated with higher mortality. Unadjusted, each 0.5-mm-step increase in ST level above the isoelectric level was associated with ~25% increase in 30-day mortality; this was true whether V3 ST depression was present or not. The odds ratio for mortality was 1.21 (95% confidence interval, 1.07 to 1.37) after adjustment for inferolateral ST elevation and clinical factors and 1.24 (95% confidence interval, 1.09 to 1.40) if also adjusted for V3 ST level. In contrast, lead V1 ST depression was not associated with mortality after adjustment for V3 ST level. V1 ST elevation ≥1 mm, analyzed dichotomously in all patients, was associated with higher mortality. The odds ratio was 1.28 (95% confidence interval, 1.01 to 1.61) unadjusted, 1.51 (95% confidence interval, 1.19 to 1.92) adjusted for V3 ST level, and 1.35 (95% confidence interval, 1.04 to 1.76) adjusted for ECG and clinical factors. Persistence of V1 ST elevation ≥1 mm 60 minutes after fibrinolysis was associated with higher mortality (10.8% versus 5.5%, P<0.001).
The authors conclude that V1 ST elevation identifies patients with acute inferior myocardial infarction who are at higher risk, although because no myocardial imaging was performed, could only speculate that the mechanistic link between V1 elevation and increased mortality is due to the occurrence of right ventricular infarction.
This is important to know about in terms of prognostication, but is it useful in the diagnosis of right ventricular AMI? The authors acknowledge that the ECG diagnosis of right ventricular infarction is classically made by recording lead V4R. In an autopsy study of 43 patients, ST elevation in lead V4R had higher sensitivity and specificity than ST elevation in lead V1 in diagnosing right ventricular infarction. Similarly, ST elevation in leads V7 through V9 adds significantly to precordial ST depression in aiding the diagnosis of posterolateral AMI. The authors contend that recording leads V4R and V7 through V9 is an additional step in the performance of a standard 12-lead ECG and, although recommended, may not be routinely performed.
I will continue to do a V4R in all inferior AMIs, and a V7-8 at least in patients with ST depression in V1-3.
Prognostic Value of Lead V1 ST Elevation During Acute Inferior Myocardial Infarction
Circulation. 2010 Aug 3;122(5):463-9
Unilateral pulmonary oedema worse
A few years ago in the Emergency Department I managed a sick hypotensive, hypoxic 20-something year old with a unilateral lung white-out and air bronchograms as pneumonia/septic shock. He died subsequently of refractory pulmonary oedema on the ICU, where the diagnosis of acute pulmonary oedema due to severe aortic stenosis was delayed. Post mortem findings showed pulmonary oedema but no pneumonia. A kind radiologist told me the chest x-ray would certainly have fitted with pneumonia. After this case I learned to echo sick hypotensive patients in the ED.
Circulation reports 869 cardiogenic pulmonary oedema patients, of which 2.1% had unilateral pulmonary oedema (UPE). In patients with UPE, blood pressure was significantly lower (P<=0.01), whereas noninvasive or invasive ventilation and catecholamines were used more frequently (P=0.0004 and P<0.0001, respectively). The prevalence of severe mitral regurgitation in patients with bilateral pulmonary edema and UPE was 6% and 100%, respectively (P<0.0001). In patients with UPE, use of antibiotic therapy and delay in treatment were significantly higher (P<0.0001 and P=0.003, respectively). In-hospital mortality was 9%: 39% for UPE versus 8% for bilateral pulmonary edema (odds ratio, 6.9; 95% confidence interval, 2.6 to 18; P<0.001). In multivariate analysis, unilateral location of pulmonary edema was independently related to death.
Prevalence, Characteristics, and Outcomes of Patients Presenting With Cardiogenic Unilateral Pulmonary Edema
Circulation. 2010 Sep 14;122(11):1109-15