The desire to produce my own Podcast has been burning away for a while now. I can’t offer clinical pearls in the beautiful ways that EMCrit or EMRAP do, but I do want to share the news about the great resuscitation practitioners that have inspired me and continue to do so.
You have to start somewhere – I’m hoping to improve at this and would welcome any constructive feedback. Click the link below to download. If you play it in iTunes the chapter headings should be available as should links to the websites referred to in the podcast.
Enjoy!
Resus.ME! May 2011
Category Archives: All Updates
STEMI criteria vary with age and sex
On reading through the 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science – Part 10: Acute Coronary Syndromes, I found a reminder that the ECG criteria for diagnosing ST-elevation myocardial infarction (STEMI) vary according to age and sex. From the original article in the Journal of the American College of Cardiology:
The threshold values of ST-segment elevation of 0.2 mV (2 mm) in some leads and 0.1 mV (1 mm) in others results from recognition that some elevation of the junction of the QRS complex and the ST segment (the J point) in most chest leads is normal. Recent studies have revealed that the threshold values are dependent on gender, age, and ECG lead ([8], [9], [10], [11] and [12]). In healthy individuals, the amplitude of the ST junction is generally highest in leads V2 and V3 and is greater in men than in women.
Recommendations
- For men 40 years of age and older, the threshold value for abnormal J-point elevation should be 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads.
- For men less than 40 years of age, the threshold values for abnormal J-point elevation in leads V2 and V3 should be 0.25 mV (2.5 mm).
- For women, the threshold value for abnormal J-point elevation should be 0.15 mV (1.5 mm) in leads V2 and V3 and greater than 0.1 mV (1 mm) in all other leads.
- For men and women, the threshold for abnormal J-point elevation in V3R and V4R should be 0.05 mV (0.5 mm), except for males less than 30 years of age, for whom 0.1 mV (1 mm) is more appropriate.
- For men and women, the threshold value for abnormal J- point elevation in V7 through V9 should be 0.05 mV (0.5 mm).
- For men and women of all ages, the threshold value for abnormal J-point depression should be −0.05 mV (−0.5 mm) in leads V2 and V3 and −0.1 mV (−1 mm) in all other leads.
What does establishment of abnormal J-point mean for STEMI diagnosis? The AHA/ECC guidelines state the following:
ST-segment elevation… is characterized by ST-segment elevation in 2 or more contiguous leads and is classified as ST-segment elevation MI (STEMI). Threshold values for ST-segment elevation consistent with STEMI are:
- J-point elevation 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men ≥40 years old);
- J-point elevation 0.25 mV (2.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men <40 years old);
- J-point elevation 0.15 mV (1.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (women).
So, in summary:
Older men – 2mm in V2/V3 and 1mm everywhere else
Younger men – 2.5 mm in V2/V3 and 1mm everywhere else
Women – 1.5 mm in V2/V3 and 1mm everywhere else
Shouldn’t be too difficult to remember.
Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation. 2010 Nov 2;122(18 Suppl 3):S787-817
AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology.
J Am Coll Cardiol. 2009 Mar 17;53(11):1003-11
'Sensitive' troponin assays do not rule out at ED presentation
An assessment of new ‘sensitive’ troponin assays at presentation of chest pain patients in a real-world ED setting showed that a single troponin I assay at ED presentation has insufficient sensitivity for clinical use to rule out MI. Author Anne-Maree Kelly discusses the current requirement for a minimum interval after an episode of chest pain to ensure adequate sensitivity: Currently in Australia the recommended minimum interval is 8 h after symptom onset. New evidence suggests that a shorter interval might be appropriate with the sensitive assays. Keller et al. reported 100% sensitivity at 3 h after ED presentation. Macrae et al. suggested that an assay 6 h from pain onset or serial assays 3 h apart with one at least 6 h from pain onset has high diagnostic accuracy. Although further research in an ED chest pain cohort is needed, the weight of evidence suggests a reduction in the minimum interval from pain onset to 6 h might be appropriate.
Aim: Troponin assays have high diagnostic value for myocardial infarction (MI), but sensitivity has been weak early after chest pain onset. New, so-called ‘sensitive’ troponin assays have recently been introduced. Two studies report high sensitivity for assays taken at ED presentation, but studied selected populations. Our aim was to evaluate the diagnostic performance for MI of a sensitive troponin assay measured at ED presentation in an unselected chest pain population without ECG evidence of ischaemia.
Methods: This is a sub-study of a prospective cohort study of adult patients with potentially cardiac chest pain who underwent evaluation for acute coronary syndrome. Patients with clear ECG evidence of acute ischaemia or an alternative diagnosis were excluded. Data collected included demographic, clinical, ECG, biomarker and outcome data. A ‘positive’ troponin was defined as >99th percentile of the assay used. MI diagnosis was as judged by the treating cardiologist. The outcomes of interest were sensitivity, specificity and likelihood ratios (LR) for positive troponin assay taken at ED presentation. Data were analysed by clinical performance analysis.
Results: Totally 952 were studied. Median age was 61 years; 56.4% were male and median TIMI score was 2. There were 129 MI (13.6, 95% CI 11.5-15.9). Sensitivity of TnI at ED presentation was 76.7% (95% CI 68.5-83.7%), specificity 93.6% (95% CI 91.7-95.1%), with LR positive 11.92 and LR negative 0.25.
Conclusion: Sensitive TnI assay at ED presentation has insufficient diagnostic accuracy for detection of MI. Serial biomarker assays in patients with negative initial TnI are required.
Performance of a sensitive troponin assay in the early diagnosis of acute myocardial infarction in the emergency department.
Emerg Med Australas. 2011 Apr;23(2):181-5
Intravenous lipid emulsion as antidote
Emergency physician intensivist Grant Cave and colleagues review the literature on intravenous lipid emulsion (ILE) therapy for human poisoning in this month’s Emergency Medicine Australasia
Intravenous lipid emulsion (ILE) has been demonstrated to be effective in amelioration of cardiovascular and central nervous system sequelae of local-anaesthetic and non-local-anaesthetic drug toxicity in animal models. Sequestration of lipophilic toxins to an expanded plasma lipid phase is credited as the predominant beneficial mechanism of action of ILE. Systematic review of published human experience is however lacking. We determined to report a comprehensive literature search of all human reports of ILE application in drug poisoning. Forty-two cases of ILE use (19 local-anaesthetic, 23 non-local-anaesthetic) were identified, with anecdotal reports of successful resuscitation from cardiovascular collapse and central nervous system depression associated with ILE administration in lipophilic toxin overdose. Although significant heterogeneity was observed in both agents of intoxication, and reported outcomes; case report data suggest a possible benefit of ILE in potentially life-threatening cardio-toxicity from bupivacaine, mepivacaine, ropivacaine, haloperidol, tricyclic antidepressants, lipophilic beta blockers and calcium channel blockers. Further controlled study and systematic evaluation of human cases is required to define the clinical role of ILE in acute poisonings.
Review article: Intravenous lipid emulsion as antidote: A summary of published human experience.
Emerg Med Australas. 2011 Apr;23(2):123-41
An editorial by Guy Weinberg, the researcher who first demonstrated the effect of ILE on bupivacaine toxicity, has some interesting observations and recommendations:
- Each of the first six case reports of lipid resuscitation from local anaesthetic systemic toxicity (LAST) were noted to have one or more of either underlying ischaemia, conduction defect or low cardiac output. For patients in these susceptible groups, reduce the dose of local anaesthetics used in nerve blocks
- There is laboratory evidence that epinephrine (adrenaline) can impair lipid resuscitation. Weinberg believes that epinephrine should be used only in small doses, if at all, in treating LAST
- In bupivacaine toxicity, use it early rather than later, as outcomes are likely to be better when intervention occurs before tissue perfusion has been compromised and too much pressor therapy has been used
Weinberg informs us that more examples of lipid resuscitation can be found at the educational website: http://www.lipidrescue.org/ and the registry site: http://www.lipidregistry.org/.
Intravenous lipid emulsion: Why wait to save a life?
Emerg Med Australas. 2011 Apr;23(2):113-5
In his editorial Weinberg refers to the review article by Jamaty et al, whose suggested regimen included 20% ILE 1.5mL/kg bolus then 0.25–0.5 mL/kg/min for 30–60 min.
OBJECTIVE: To assess the evidence regarding the efficacy and safety of intravenous fat emulsion (IFE) in the management of poisoned patients.
METHODS: We performed a systematic review of the literature with no time or language restriction. The electronic databases were searched from their inception until June 1, 2009 (Medline, EMBASE, ISI web of science, Biological abstract, LILACS, ChemIndex, Toxnet, and Proquest). We also examined the references of identified articles and the gray literature. The target interventions eligible for inclusion were administration of any IFE before, during, or after poisoning in human or animals. All types of studies were reviewed. Eligibility for inclusion and study quality scores, based on criteria by Jadad and the STROBE statement, were evaluated by independent investigators. The primary outcome was mortality. Secondary outcomes included neurologic, hemodynamic, and electrocardiographic variables, as well as adverse effects.
RESULTS: Of the 938 publications identified by the search strategies, 74 met the inclusion criteria. We identified 23 animal trials, 50 human, and 1 animal case reports. Overall, the quality of evidence was weak and significant heterogeneity prevented data pooling. Available data suggest some benefits of IFE in bupivacaine, verapamil, chlorpromazine, and some tricyclic antidepressants and beta-blockers toxicity. No trial assessed the safety of IFE in the treatment of acute poisoning.
CONCLUSION: The evidence for the efficacy of IFE in reducing mortality and improving hemodynamic, electrocardiographic, and neurological parameters in the poisoned patients is solely based on animal studies and human case reports. The safety of IFE has not been established.
Lipid emulsions in the treatment of acute poisoning: a systematic review of human and animal studies.
Clin Toxicol (Phila). 2010 Jan;48(1):1-27
The Guidelines from the Association of Anaesthetists of Great Britain and Ireland, also endorsed by the Australian and New Zealand College of Anaesthetists, outline the dose and indications for ILE in LAST. The full guideline can be accessed by clicking the image below:
Triple marker panel for AMI
A large Asian/Australasian study examined a 2hr triple-marker test in patients presenting with chest pain.
BACKGROUND: Patients with chest pain contribute substantially to emergency department attendances, lengthy hospital stay, and inpatient admissions. A reliable, reproducible, and fast process to identify patients presenting with chest pain who have a low short-term risk of a major adverse cardiac event is needed to facilitate early discharge. We aimed to prospectively validate the safety of a predefined 2-h accelerated diagnostic protocol (ADP) to assess patients presenting to the emergency department with chest pain symptoms suggestive of acute coronary syndrome.
METHODS: This observational study was undertaken in 14 emergency departments in nine countries in the Asia-Pacific region, in patients aged 18 years and older with at least 5 min of chest pain. The ADP included use of a structured pre-test probability scoring method (Thrombolysis in Myocardial Infarction [TIMI] score), electrocardiograph, and point-of-care biomarker panel of troponin, creatine kinase MB, and myoglobin. The primary endpoint was major adverse cardiac events within 30 days after initial presentation (including initial hospital attendance). This trial is registered with the Australia-New Zealand Clinical Trials Registry, number ACTRN12609000283279.
FINDINGS: 3582 consecutive patients were recruited and completed 30-day follow-up. 421 (11.8%) patients had a major adverse cardiac event. The ADP classified 352 (9.8%) patients as low risk and potentially suitable for early discharge. A major adverse cardiac event occurred in three (0.9%) of these patients, giving the ADP a sensitivity of 99.3% (95% CI 97.9-99.8), a negative predictive value of 99.1% (97.3-99.8), and a specificity of 11.0% (10.0-12.2).
INTERPRETATION: This novel ADP identifies patients at very low risk of a short-term major adverse cardiac event who might be suitable for early discharge. Such an approach could be used to decrease the overall observation periods and admissions for chest pain. The components needed for the implementation of this strategy are widely available. The ADP has the potential to affect health-service delivery worldwide.
A 2-h diagnostic protocol to assess patients with chest pain symptoms in the Asia-Pacific region (ASPECT): a prospective observational validation study.
Lancet. 2011 Mar 26;377(9771):1077-84
Full text link available at time of writing
In an accompanying editorial, nicely entitled ‘Acute MI: triple-markers resurrected or Bayesian dice?’ Dr Rick Body notes that the point-of-care triple-marker test has a relatively low sensitivity, at just 82.9%, when used alone, and the sensitivity only increased to 99.3% in the current study because it was used in an already-selected low-risk population. He writes: “Most people will probably consider this net risk to be statistically acceptable. However, if properly informed, low-risk patients might feel differently about the relative merits of waiting for definitive six-hour laboratory-based troponin testing or going home after two hours on the basis of results from a test that correctly identifies serious coronary disease, when present, in just over eight of 10 occasions.”
Dr Body has a new blog at The Bodsblog where we’re likely to be informed other data relevant to emergency cardiology as they emerge.
Point-of-care panel assessment using a similar triple-marker test at presentation and 90 minutes was also examined in the RATPAC study, in which it increased successful discharge home and reduced median length of stay, but did not alter overall hospital bed use.
Colorimetric CO2 detectors and newborns
Colorimetric CO2 detectors may fail to indicate successful tracheal tube placement in adults in certain circumstances, such as low cardiac output states, and waveform capnography is considered the gold standard. We now have data that demonstrate their inadequacy for neonatal intubation. Ideally, waveform devices should be used by all professionals who intubate patients – from paramedics to neonatologists.
AIM: Clinical assessment and end-tidal CO(2) (ETCO(2)) detectors are routinely used to verify endotracheal tube (ETT) placement. However, ETCO(2) detectors may mislead clinicians by failing to identify correct placement under a variety of conditions. A flow sensor measures gas flow in and out of an ETT. We reviewed video recordings of neonatal resuscitations to compare a colorimetric CO(2) detector (Pedi-Cap®) with flow sensor recordings for assessing ETT placement.
METHODS: We reviewed recordings of infants <32 weeks gestation born between February 2007 and January 2010. Airway pressures and gas flow were recorded with a respiratory function monitor. Video recording were used (i) to identify infants who were intubated in the delivery room and (ii) to observe colour change of the ETCO(2) detector. Flow sensor recordings were used to confirm whether the tube was in the trachea or not. RESULTS: Of the 210 infants recorded, 44 infants were intubated in the delivery room. Data from 77 intubation attempts were analysed. In 35 intubations of 20 infants both a PediCap® and flow sensor were available for analysis. In 21 (60%) intubations, both methods correctly identified successful ETT placement and in 3 (9%) both indicated the ETT was not in the trachea. In the remaining 11 (31%) intubations the PediCap® failed to change colour despite the flow wave indicating correct ETT placement.
CONCLUSION: Colorimetric CO(2) detectors may mislead clinicians intubating very preterm infants in the delivery room. They may fail to change colour in spite of correct tube placement in up to one third of the cases.
Assessment of flow waves and colorimetric CO2 detector for endotracheal tube placement during neonatal resuscitation
Resuscitation. 2011 Mar;82(3):307-12
LRAs for acute asthma?
As far as I’m concerned the jury is still out here since this small study was terminated early, more patients in the montelukast group received magnesium and / or aminophylline, and it is unclear how the groups compared with regard to other other acute therapies such as beta-agonists and steroids.
BACKGROUND: Although leukotriene receptor antagonists have an established role in the management of patients with chronic asthma, their efficacy in an acute asthma exacerbation is not fully known.
METHODS: 87 adults with acute asthma requiring hospitalisation were randomly assigned to receive either montelukast 10 mg or placebo on admission and every evening thereafter for 4 weeks (when they were reviewed as outpatients). All patients were admitted under the care of a consultant chest physician and received full care for acute asthma according to the British Thoracic Society guidelines. The primary end point was the difference in peak expiratory flow (PEF) between active and placebo treatment the morning following admission.
RESULTS: Primary end point data were analysed for 73 patients. At study entry, patients who received montelukast (n=37) had a mean (±SD) PEF of 227.6 (±56.9) l/min (47.6% predicted) and those who received placebo (n=36) had a PEF of 240.3 (±99.8) l/min (49.6% predicted). The morning after admission, patients who received montelukast achieved a PEF of 389.6 (±109.7) l/min (81.4% predicted) compared with 332.3 (±124.9) l/min (69.8% predicted) for placebo (p=0.046). The mean difference between treatment groups was 57.4 l/min (95% CI of 1.15 to 113.6 l/min or 1.95-21.2% predicted).
CONCLUSION: In acute asthma exacerbations the additional administration of oral montelukast results in a significantly higher PEF the morning after admission than that achievable with current standard treatment.
Oral montelukast in acute asthma exacerbations: a randomised, double-blind, placebo-controlled trial
Thorax. 2011 Jan;66(1):7-11
Vasoactive drugs in cardiogenic shock
I’m always on the look-out for evidence to guide vasoactive drug therapy, an area where much dogma is spouted by many who have not read the literature. Here’s a small (note: pilot) study comparing two strategies for cardiogenic shock. The higher heart rate and lactate with epinephrine (adrenaline) are consistent with the findings of the great CAT study; this is of interest, but not necessarily clinically significant nor practice changing.
OBJECTIVE: There is no study that has compared, in a randomized manner, which vasopressor is most suitable in optimizing both systemic and regional hemodynamics in cardiogenic shock patients. Hence, the present study was designed to compare epinephrine and norepinephrine-dobutamine in dopamine-resistant cardiogenic shock.
DESIGN: Open, randomized interventional human study.
SETTING: Medical intensive care unit in a university hospital.
PATIENTS: Thirty patients with a cardiac index of <2.2 L/min/m and a mean arterial pressure of <60 mm Hg resistant to combined dopamine-dobutamine treatment and signs of shock. Patients were not included in cases of cardiogenic shock secondary to acute ischemic events such as myocardial infarction. Noninclusion criteria also included immediate indication of mechanical assistance.
INTERVENTIONS: Patients were randomized to receive an infusion of either norepinephrine-dobutamine or epinephrine titrated to obtain a mean arterial pressure of between 65 and 70 mm Hg with a stable or increased cardiac index.
MAIN RESULTS: Both regimens increased cardiac index and oxygen-derived parameters in a similar manner. Patients in the norepinephrine-dobutamine group demonstrated heart rates lower (p<.05) than those in the epinephrine group. Epinephrine infusion was associated with new arrhythmias in three patients. When compared to baseline values, after 6 hrs, epinephrine infusion was associated with an increase in lactate level (p<.01), whereas this level decreased in the norepinephrine-dobutamine group. Tonometered PCO2 gap, a surrogate for splanchnic perfusion adequacy, increased in the epinephrine-treated group (p<.01) while decreasing in the norepinephrine group (p<.01). Diuresis increased in both groups but significantly more so in the norepinephrine-dobutamine group, whereas plasma creatinine decreased in both groups.
CONCLUSIONS: When considering global hemodynamic effects, epinephrine is as effective as norepinephrine-dobutamine. Nevertheless, epinephrine is associated with a transient lactic acidosis, higher heart rate and arrhythmia, and inadequate gastric mucosa perfusion. Thus, the combination norepinephrine-dobutamine appears to be a more reliable and safer strategy.
Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study
Crit Care Med. 2011 Mar;39(3):450-5
Thrombolysis for PE after limb surgery
A patient develops shock and dyspnoea on the orthopaedic ward after a total knee replacement and massive pulmonary embolism is confirmed radiologically. Would you give a fibrinolytic or is it contraindicated? Harry Wright and colleagues did, but before giving 50 mg of intravenous rtPA they applied a tourniquet (Cryocuff) to the limb to limit the proportion of the systemic thrombolytic agent that would reach the site of the surgery. The tourniquet was inflated just before the infusion and was left on for one hour. There was some oozing of blood from the postoperative wound, which settled with bandage compression. The authors state that the inflation time of one hour was sufficient for the thrombolytic agent to be largely eliminated from the circulation, since alteplase has a plasma half-life of less than five minutes, although some plasminogen activator activity does persist for up to four hours.
The patient was well at three month follow up. They suggest:
Given the success in this case, we believe that major limb surgery no longer represents a contraindication to thrombolysis.
Thrombolysis for postoperative pulmonary embolism: limiting the risk of haemorrhage
Thorax. 2011 May;66(5):452
Disposable flexible intubating scope
There is now a single use flexible intubating device that compares favourably with conventional fibreoptic devices. It does not have fibreoptic cables, but rather has a small camera at its tip illuminated by an LED. The image is transmitted via a cable in the device to a reusable screen. Dr Cook’s team in Bath, England have an extensive track record of evaluating new airway devices, and they report their assessment of this gadget in a manikin-based study. I think this may extend the airway management options to departments or teams for whom the cost and maintenance of conventional fibreoptic equipment is prohibitive.
We compared the Ambu aScope™ with a conventional fibrescope in two simulated settings. First, 22 volunteers performed paired oral and nasal fibreoptic intubations in three different manikins: the Laerdal Airway Trainer, Bill 1 and the Airsim (a total of 264 intubations). Second, 21 volunteers intubated the Airway Trainer manikin via three supraglottic airways: classic and intubating laryngeal mask airways and i-gel (a total of 66 intubations). Performance of the aScope was good with few failures and infrequent problems. In the first study, choice of fibrescope had an impact on the number of user-reported problems (p=0.004), and user-assessed ratings of ease of endoscopy (p<0.001) and overall usefulness (p<0.001), but not on time to intubate (p=0.19), or ease of railroading (p=0.72). The manikin chosen and route of endoscopy had more consistent effects on performance: best performance was via the nasal route in the Airway Trainer manikin. In the second study, the choice of fibrescope did not significantly affect any performance outcome (p=0.3), but there was a significant difference in the speed of intubation between the devices (p=0.02) with the i-gel the fastest intubation conduit (mean (SD) intubation time i-gel 18.5(6.8)s, intubating laryngeal mask airway = 24.1(11.2)s, classic laryngeal mask airway = 31.4(32.5)s, p=0.02). We conclude that the aScope performs well in simulated fibreoptic intubation and (if adapted for untimed use) would be a useful training tool for both simulated fibreoptic intubation and conduit-assisted intubation. The choice of manikin and conduit are also important in the success of such training. This manikin study does not predict performance in humans and a clinical study is required.
Evaluation of a single-use intubating videoscope (Ambu aScopeTM) in three airway training manikins for oral intubation, nasal intubation and intubation via three supraglottic airway devices
Anaesthesia. 2011 Apr;66(4):293-9