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
Scoop minimises cervical movement
A cadaveric study using a 3-dimensional electromagnetic tracking device to asses cervical motion compared the application of a scoop stretcher with two other manual transfer techniques, including log rolling onto an extrication (spine) board. The scoop method restricted cervical spine movement more than log rolling, although this was not statistically significant.
The authors conclude: the effectiveness of the scoop stretcher to limit spinal motion in the destabilized spine is comparable or better than manual techniques currently being used by primary responders.
Are scoop stretchers suitable for use on spine-injured patients?
Am J Emerg Med. 2010 Sep;28(7):751-6
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
Fancy new ACS tests
It’s hard to keep track of all new proposed biomarkers that may be useful in the work up of acute coronary syndrome (ACS) patients. We’re all used to troponin now – so we really want to know how novel tests measure up against the existing standard, in particular for the timeframe in which troponin is less helpful, namely the first six hours.
A systematic review examine the evidence for the following biomarkers in the early assessment (ie, within 6 h of symptom onset) of suspected ACS:
- CK-MB: CK-MB and 2 h ΔCK-MB have potential in diagnosing AMI in the first hours after symptom onset. Whether CK-MB has value in the early diagnostic assessment of ACS in addition to clinical symptoms, ECG or other markers has rarely been studied.
- myoglobin: myoglobin might be of value in early ruling out of AMI and ACS in suspected patients because of the relatively high NPV; its PPV, however, is low. However, it is not yet known whether myoglobin has diagnostic value in addition to symptoms, signs and other diagnostic tests (eg, ECG), because of the lack of multivariable analysis
- heart-type fatty acid binding protein (H-FABP): H-FABP seems to have some potential as an early diagnostic marker of AMI or ACS, but its value in addition to clinical features and other markers has not been studied
- ischemia modified albumin (IMA): IMA could be a potential marker for early ruling out of ACS in chest pain patients because of its relatively high NPV, especially combined with cTn and ECG. However, its PPV is low. Importantly; IMA seems to add relevant diagnostic information to more readily available diagnostic parameters. However, problems with the stability of IMA and its lack of cardiospecificity have been reported
- pregnancy-associated plasma protein A: contradictory results indicate that the diagnostic value of PAPP-A in patients suspected of having ACS has not been evaluated properly
- glycogen phosphorylase isoenzyme BB: GPBB might be a marker for myocardial ischaemia and myocardial necrosis, although the available research is limited and does not assess the added value of the marker.
- myeloid-related protein 8/14: more research is needed to evaluate the (added) diagnostic value of MRP 8/14 in patients suspected of having ACS.
The authors also point out the introduction of high-sensitivity troponin assays may further improve diagnosis of ACS. They refer to a study in patients with suspected AMI presenting at the emergency department, which showed that a sensitive cTnI assay had a higher NPV than a standard cTnT assay and comparable PPV for detecting AMI within 6 h of symptom onset. The PPV was 79.3% and 80.7%, respectively; the NPVs were 95.3% and 88%. The Full Text of this high-sensitivity troponin paper is here
The review makes the following conclusions:
- current guidelines advocate the use of cardiac troponin or CK-MB when cTn is not available, and myoglobin in the first 6 h in addition to cTn
- IMA and H-FABP seem to be promising diagnostic biomarkers in the early diagnostic assessment of patients suspected of having ACS
- There is an urgent need for adequately designed studies of (novel) ACS markers and their combinations against contemporary troponin assays
Novel biochemical markers in suspected acute coronary syndrome: systematic review and critical appraisal
Heart. 2010 Jul;96(13):1001-1
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
Pneumonia scores equivalent
Got a favourite assessment tool for classifying the severity of community acquired pneumonia? Two systematic reviews showed no significant differences in performance between Pneumonia Severity Index (PSI) and various versions of CURB (CURB, CURB-65, and CRB-65).
An accompanying editorial* opines that CRB-65 is the simplest tool and can easily be remembered. It also discusses some of the more subtle strengths and weaknesses of the tools.
Severity assessment tools for predicting mortality in hospitalised patients with community-acquired pneumonia. Systematic review and meta-analysis
Thorax. 2010 Oct;65(10):878-83
Value of severity scales in predicting mortality from community-acquired pneumonia: systematic review and meta-analysis
Thorax. 2010 Oct;65(10):884-90
*Severity scores for CAP. ‘Much workload for the next bias’
Thorax 2010 Oct;65:853-855
Give all sick patients oestrogen?
A thought provoking article in Critical Care Medicine outlines basic science, animal, and human studies that suggest oestrogen may have a protective effect in a wide range of critical illnesses from cardiac arrest to trauma to stroke. It urges clinical trials of sex hormones, some of which are underway. Regarding traumatic brain injury, the authors state: “To date, studied interventions to treat the effects of secondary injury, such as induced hypothermia or sedative-hypnotic coma, have had disappointing results… Clearly, EMS (or emergency department) infusion of a single IV bolus of estrogen, a therapy shown in the laboratory to be a strong, direct, easy-to-deliver antioxidant, antiapoptotic, and anti-inflammatory intervention, has a much better chance of decreasing the severity of injury.”
Bold? Let’s see if studies such as this one show this intervention to be so beneficial.
Rationale for routine and immediate administration of intravenous estrogen for all critically ill and injured patients
Critical Care Medicine. 38(10):S620-S629, October 2010
ABCDE of ICU cognitive outcomes
Applying best evidence using simple easily remembered tools appeals to my small and busy brain. A system of minimising the impact of intensive care on long term brain function is proposed using an ABCDE mnemonic: awakening, spontaneous breathing trials, coordinating these two with target-based sedation, delirium monitoring and scoring, and early mobility therapy / exercise.
A screening, prevention, and restoration model for saving the injured brain in intensive care unit survivors
Critical Care Medicine Oct 2010;38(10):S683-S691