Category Archives: Acute Med

Acute care of the medically sick adult

Acute Med, All Updates, ICU, Kids, PHARM, Resus, Trauma

Capillary refill time

A review of capillary refill time (CRT) reveals some interesting details about this test:

  • CRT is affected by age – the upper limit of normal for neonates is 3 seconds.
  • It increases with age – one study recommended the upper limit of normal for adult women should be increased to 2.9 seconds and for the elderly to 4.5 seconds.
  • It is affected by multiple external factors (especially ambient temperature).
  • Although it is claimed to have some predictive value in the assessment of dehydration and serious infection in children, studies vary in where and for how long pressure should be applied, and there is poor interobserver reliability.

The latest (5th Edition) of the Advanced Paediatric Life Support Manual states:
‘Poor capillary refill and differential pulse volumes are neither sensitive nor specific indicators of shock in infants and children, but are useful clinical signs when used in conjunction with the other signs described‘
In my view, it is best used as a monitor of trends (in accordance with skin temperature and other markers of perfusion), rather than by placing emphasis on the exact number of seconds of a single reading. See below for a video of my perfectly happy and healthy son demonstrating a CRT of over six seconds in a cool room during an English Summer’s day.
The authors of the review caution:
Operating rooms are cold, patients are often draped, which limits access, and because most anesthetics are potent vasodilators, the use of CRT to guide practice is not justified. The possibility of a false-positive or false-negative assessment is simply too great.


Capillary refill time (CRT) is widely used by health care workers as part of the rapid, structured cardiopulmonary assessment of critically ill patients. Measurement involves the visual inspection of blood returning to distal capillaries after they have been emptied by pressure. It is hypothesized that CRT is a simple measure of alterations in peripheral perfusion. Evidence for the use of CRT in anesthesia is lacking and further research is required, but understanding may be gained from evidence in other fields. In this report, we examine this evidence and factors affecting CRT measurement. Novel approaches to the assessment of CRT are under investigation. In the future, CRT measurement may be achieved using new technologies such as digital videography or modified oxygen saturation probes; these new methods would remove the limitations associated with clinical CRT measurement and may even be able to provide an automated CRT measurement.

Capillary Refill Time: Is It Still a Useful Clinical Sign?
Anesth Analg. 2011 Jul;113(1):120-3
The Capillary Refill Video

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Why I don't give vasopressors in sepsis

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It’s become popular to use the term ‘vasopressors’ or just ‘pressors’ when noradrenaline/norepinephrine or even (in some places still) dopamine are given. I have resisted this trend and continue to use the term ‘vasoactive’ drugs, on the basis that the effects they produce (and that we may desire) are not limited to a pure alpha adrenergic effect on vascular tone, but they have effects on heart rate and contractility too (as well as preload through venous effects). If you don’t believe me about noradrenaline/norepinephrine, then check out one of my favourite critical care papers of all time: the CAT study.
There are of course real pressors out there – phenylephrine acts on alpha receptors, as does methoxamine. Metaraminol predominantly acts on alpha receptors but does also cause some release of noradrenaline/norepinephrine.
Why is this important? All these drugs will fix hypotension, right? Yes, they should. However should blood pressure be our main treatment goal? What we’re really interested in is organ perfusion, which depends on regional blood flow to vital organs. It’s possible that a drug could fix the measured blood pressure and give a nice ‘macroscopic’ number, while at the same time reducing cardiac output and adversely affecting regional blood flow to organs through local vasoconstrictive effects. My view is that this is more likely with pure ‘pressors’ (like phenylephrine), which is why I avoid them in septic shock and opt for catecholamine infusions (noradrenaline/norepinephrine).
This is important in my practice setting of retrieval medicine, where, prior to interfacility transport, physicians might sometimes be tempted to ‘push pressors’ peripherally rather than insert a central venous catheter and commence a catecholamine infusion. While the former approach might be more expeditious and make the vital signs chart look pretty, one wonders about what effect this is having on tissue oxygen delivery.
A fascinating review of papers on pressor physiology1 suggests these agents have the following effects:

  • conflicting data on changes in myocardial perfusion
  • increase both left and right heart afterload
  • decrease venous compliance with the potential to increase venous return although the impact of this on cardiac output is controversial
  • controversial effect on cerebral bloodflow
  • decrease bloodflow to the kidneys
  • adverse affects on gastrointestinal tract bloodflow


abstract1
Phenylephrine and methoxamine are direct-acting, predominantly α(1) adrenergic receptor (AR) agonists. To better understand their physiologic effects, we screened 463 articles on the basis of PubMed searches of “methoxamine” and “phenylephrine” (limited to human, randomized studies published in English), as well as citations found therein. Relevant articles, as well as those discovered in the peer-review process, were incorporated into this review. Both methoxamine and phenylephrine increase cardiac afterload via several mechanisms, including increased vascular resistance, decreased vascular compliance, and disadvantageous alterations in the pressure waveforms produced by the pulsatile heart. Although pure α(1) agonists increase arterial blood pressure, neither animal nor human studies have ever shown pure α(1)-agonism to produce a favorable change in myocardial energetics because of the resultant increase in myocardial workload. Furthermore, the cost of increased blood pressure after pure α(1)-agonism is almost invariably decreased cardiac output, likely due to increases in venous resistance. The venous system contains α(1) ARs, and though stimulation of α(1) ARs decreases capacitance and may transiently increase venous return, this gain may be offset by changes in afterload, venous compliance, and venous resistance. Data on the effects of α(1) stimulation in the central nervous system show conflicting changes, while experimental animal data suggest that renal blood flow is reduced by α(1)-agonists, and both animal and human data suggest that gastrointestinal perfusion may be reduced by α(1) tone.

A review of clinical articles2 reveals few evidence-based indications for true pressors. Possible situations where they may be of benefit include intraoperative hypotension, aortic stenosis, during cyanotic episodes in Tetralogy of Fallot, and some obstetric situations. In the setting of sepis, phenylephrine has been compared with noradrenaline in which an initial pilot study found a statistically significant reduction in creatinine clearance and increase in arterial lactate after initiating the phenylephrine infusion. However a subsequent randomised controlled comparison of phenylephrine with noradrenaline/norepinephrine did not show differences in cardiopulmonary performance, global oxygen transport, or regional hemodynamics, although there were only 16 patients in each group3.


abstract2
Phenylephrine is a direct-acting, predominantly α(1) adrenergic receptor agonist used by anesthesiologists and intensivists to treat hypotension. A variety of physiologic studies suggest that α-agonists increase cardiac afterload, reduce venous compliance, and reduce renal bloodflow. The effects on gastrointestinal and cerebral perfusion are controversial. To better understand the effects of phenylephrine in a variety of clinical settings, we screened 463 articles on the basis of PubMed searches of “methoxamine,” a long-acting α agonist, and “phenylephrine” (limited to human, randomized studies published in English), as well as citations found therein. Relevant articles, as well as those discovered in the peer-review process, were incorporated into this review. Phenylephrine has been studied as an antihypotensive drug in patients with severe aortic stenosis, as a treatment for decompensated tetralogy of Fallot and hypoxemia during 1-lung ventilation, as well as for the treatment of septic shock, traumatic brain injury, vasospasm status-postsubarachnoid hemorrhage, and hypotension during cesarean delivery. In specific instances (critical aortic stenosis, tetralogy of Fallot, hypotension during cesarean delivery) in which the regional effects of phenylephrine (e.g., decreased heart rate, favorable alterations in Q(p):Q(s) ratio, improved fetal oxygen supply:demand ratio) outweigh its global effects (e.g., decreased cardiac output), phenylephrine may be a rational pharmacologic choice. In pathophysiologic states in which no regional advantages are gained by using an α(1) agonist, alternative vasopressors should be sought.

These review articles reinforce my own bias against the use of pure pressors in septic shock, although clearly more clinical research is needed. I am inclined to agree with the reviewers’ concluding statement:
…in all clinical settings, phenylephrine reduces cardiac output, and in most clinical settings has been shown to significantly increase LV afterload. Thus, only in instances in which its regional effects are thought to outweigh its global effects should phenylephrine be used for the treatment of hypotension.
1. The physiologic implications of isolated alpha(1) adrenergic stimulation
Anesth Analg. 2011 Aug;113(2):284-96
2. The clinical implications of isolated alpha(1) adrenergic stimulation
Anesth Analg. 2011 Aug;113(2):297-304
3. Phenylephrine versus norepinephrine for initial hemodynamic support of patients with septic shock: a randomized, controlled trial
Crit Care. 2008;12(6):R143
Full Text available here

Acute Med, All Updates, PHARM, Resus

Pre-hospital CPAP for pulmonary oedema

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The physician-staffed mobile intensive care units of SAMU (Service d’Aide Médicale Urgente) in France provided the location for this randomised controlled trial of CPAP for acute cardiogenic pulmonary oedema.


STUDY OBJECTIVE: The purpose of this randomized controlled trial was to determine the immediate and delayed effects of noninvasive ventilation for patients in acute cardiogenic pulmonary edema (ACPE) in addition to aggressive usual care in a medical prehospital setting.

METHODS: Out-of-hospital patients in severe ACPE were eligible for the study. Patients were randomized to receive either usual care, including conventional optimal treatment with furosemide, oxygen, and high-dose boluses of isosorbide dinitrate plus oxygen, or conventional medications plus out-of-hospital continuous positive airway pressure (CPAP). The primary outcome was the treatment success defined as all of respiratory rate less than 25 breaths per minute and oxygen saturation of greater than 90% at the end of 1-hour study. Secondary end points included death during 30 days after inclusion. Lengths of intensive care unit and hospital stays were also recorded.

RESULTS: In total, 124 patients were enrolled into the study. The 2 groups had similar baseline characteristics. For the primary outcome analysis, 22 (35.5%) of 62 patients were considered as experiencing a treatment success in the usual care group vs 19 (31.7%) of 60 in the CPAP group (P = .65). Seven patients died within 30 days in the usual care group vs 6 in the CPAP group (P = .52). There were no statistically significant differences between the treatment groups for length of stay either in hospital or in the intensive care unit.

CONCLUSION: In the prehospital setting, in spite of its potential advantages for patients in ACPE, CPAP may not be preferred to a strict optimal intravenous treatment.

Continuous positive airway pressure for cardiogenic pulmonary edema: a randomized study
Am J Emerg Med. 2011 Sep;29(7):775-81

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Still no cardiac arrest survival benefit from epinephrine?

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A double blind randomised controlled trial showed significantly better rates of return of spontaneous circulation and hospital admission with the use of adrenaline (epinephrine) compared with placebo. This effect was observed with both shockable and non-shockable initial cardiac arrest rhythms. There was no statistically significant difference in the primary outcome of survival to hospital discharge.
Interesting but unfortunate political factors appear to have prevented recruitment to the required numbers of patients for this study so it is underpowered for its primary outcome of survival to hospital discharge, which in the adrenaline group was double that in the placebo group, although this did not reach statistical significance. What was supposed to be a multi-centre study became a single centre one and it was not possible to continue as the study drugs reached their expiry date and no additional funding was available.
So do ROSC and survival to admission matter? The authors make the following point:


While not the primary outcome of our study, ROSC is an increasingly important clinical endpoint as the influence of post resuscitation care interventions (i.e.: therapeutic hypothermia, managing underlying cause, organ perfusion and oxygenation) on survival to hospital discharge are recognised.

Optimum dose and timing of adrenaline remain unknown, along with whether it impacts on long-term outcomes.


BACKGROUND: There is little evidence from clinical trials that the use of adrenaline (epinephrine) in treating cardiac arrest improves survival, despite adrenaline being considered standard of care for many decades. The aim of our study was to determine the effect of adrenaline on patient survival to hospital discharge in out of hospital cardiac arrest.

METHODS: We conducted a double blind randomised placebo-controlled trial of adrenaline in out-of-hospital cardiac arrest. Identical study vials containing either adrenaline 1:1000 or placebo (sodium chloride 0.9%) were prepared. Patients were randomly allocated to receive 1ml aliquots of the trial drug according to current advanced life support guidelines. Outcomes assessed included survival to hospital discharge (primary outcome), pre-hospital return of spontaneous circulation (ROSC) and neurological outcome (Cerebral Performance Category Score – CPC).

RESULTS: A total of 4103 cardiac arrests were screened during the study period of which 601 underwent randomisation. Documentation was available for a total of 534 patients: 262 in the placebo group and 272 in the adrenaline group. Groups were well matched for baseline characteristics including age, gender and receiving bystander CPR. ROSC occurred in 22 (8.4%) of patients receiving placebo and 64 (23.5%) who received adrenaline (OR=3.4; 95% CI 2.0-5.6). Survival to hospital discharge occurred in 5 (1.9%) and 11 (4.0%) patients receiving placebo or adrenaline respectively (OR=2.2; 95% CI 0.7-6.3). All but two patients (both in the adrenaline group) had a CPC score of 1-2.

CONCLUSION: Patients receiving adrenaline during cardiac arrest had no statistically significant improvement in the primary outcome of survival to hospital discharge although there was a significantly improved likelihood of achieving ROSC.

Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
Resuscitation. 2011 Sep;82(9):1138-43

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Pre-hospital ECMO

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Two cases are reported of the pre-hospital institution of venoarterial extracorporeal membrane oxygenation (ECMO) for patients in cardiac arrest. One was from France and the other from Germany – both countries with mature physician-staffed pre-hospital systems. The two cases were a 9 yr old drowning victim1 and a 48 year old marathon runner2. They each received BLS then ACLS then ECMO, and both went from asystole to sinus rhythm after the institution of ECMO. Sadly both failed to neurologically recover and died in hospital.
If irreversible anoxic encephalopathy could be detected in the field, patients could be better selected for this intervention. An editorialist3 states:


Until we have a hand held device which can measure neuronal integrity on a cellular level in the field we must use our best judgement, and in many cases give the patient the benefit of the doubt by cannulating them, cooling for 24 h and then making a neurological assessment and withdrawing ECLS if necessary.

Other issues to consider are:

  • Can society afford this level of intervention?
  • Could this intervention, when associated with brain death, result in sufficiently recovered organs for transplantation?
  • How can the infrastructure be created to enable rapid institution of pre-hospital ECMO?

I suspect as the equipment becomes even more portable and self-maintaining, pre-hospital / retrieval physicians already expert in critical care interventions such as seldinger-guided vascular access will be the ones instituting this therapy. In the meantime, we await evidence of outcome benefit and some objective means of case selection.
1. Out-of-hospital extracorporeal life support for cardiac arrest—A case report
Resuscitation. 2011 Sep;82(9):1243-5
2. Out-of-hospital extra-corporeal life support implantation during refractory cardiac arrest in a half-marathon runner
Resuscitation. 2011 Sep;82(9):1239-42
3. Community extracorporeal life support for cardiac arrest – When should it be used?
Resuscitation. 2011 Sep;82(9):1117

Acute Med, All Updates, PHARM, Resus

Mouth-to-nose breathing

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Interesting – mouth to nose breathing was more effective than mouth-to-mouth in simulated resuscitations using anaesthetised, apnoeic patients:


BACKGROUND: The authors hypothesized that mouth ventilation by a resuscitator via the nasal route ensures a more patent airway and more effective ventilation than does ventilation via the oral route and therefore would be the optimal manner to ventilate adult patients in emergencies, such as during cardiopulmonary resuscitation. They tested the hypothesis by comparing the effectiveness of mouth-to-nose breathing (MNB) and mouth-to-mouth breathing (MMB) in anesthetized, apneic, adult subjects without muscle paralysis.

METHODS: Twenty subjects under general anesthesia randomly received MMB and MNB with their heads placed first in a neutral position and then an extended position. A single operator performed MNB and MMB at the target breathing rate of 10 breaths/min, inspiratory:expiratory ratio 1:2 and peak inspiratory airway pressure 24 cm H₂O. A plethysmograph was used to measure the amplitude change during MMB and MNB. The inspiratory and expiratory tidal volumes during MMB and MNB were calculated retrospectively using the calibration curve.

RESULTS: All data are presented as medians (interquartile ranges). The rates of effective ventilation (expired volume > estimated anatomic dead space) during MNB and MMB were 91.1% (42.4-100%) and 43.1% (42.5-100%) (P < 0.001), and expired tidal volume with MMB 130.5 ml (44.0-372.8 ml) was significantly lower than with MNB 324.5 ml (140.8-509.0 ml), regardless of the head position (P < 0.001).
CONCLUSIONS: Direct mouth ventilation delivered exclusively via the nose is significantly more effective than that delivered via the mouth in anesthetized, apneic adult subjects without muscle paralysis. Additional studies are needed to establish whether using this breathing technique during emergency situations will improve patient outcomes.

Effectiveness of breathing through nasal and oral routes in unconscious apneic adult human subjects: a prospective randomized crossover trial
Anesthesiology. 2011 Jul;115(1):129-35

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Nitric oxide for right ventricular cardiogenic shock

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A case report describes a patient with right ventricular cardiogenic shock due to a dissected right coronary artery1. There was deterioration despite fluid, inotropic and intraaortic balloon pump therapy, followed by improvement with the introduction of inhaled nitric oxide (iNO) at 12 to 15 ppm (a selective pulmonary vasodilator), to the point where vasoactive medication was withdrawn. The cessation of iNO was associated with deterioration which resolved with its reintroduction. It was more gradually withdrawn and the patient made a good recovery.
The rationale for the use of iNO in patients with acute RV heart failure due to MI is afterload reduction without systemic hypotension.
It has been shown to improve haemodynamics in RV MI patients with cardiogenic shock in a previous case series2 (abstract below) in which its effects on pulmonary vasodilation are thought be beneficial. In RV MI with shock increased pulmonary vascular tone is postulated to result from the following mechanisms:

  • A low cardiac output results in a decreased mixed venous blood oxygen content, which enhances pulmonary artery vasoconstriction.
  • The intravenous infusion of alpha-adrenergic vasoconstrictors can contribute to pulmonary vasoconstriction.
  • Mechanical ventilation with positive end-expiratory pressure can increase the pulmonary vascular resistance through compression of the pulmonary vasculature.
  • Interstitial pulmonary edema, which may occur in some patients with coexisting LV dysfunction, can also cause pulmonary constriction

OBJECTIVES: We sought to determine whether or not inhaled nitric oxide (NO) could improve hemodynamic function in patients with right ventricular myocardial infarction (RVMI) and cardiogenic shock (CS).

BACKGROUND: Inhaled NO is a selective pulmonary vasodilator that can decrease right ventricular afterload.

METHODS: Thirteen patients (7 males and 6 females, age 65 +/- 3 years) presenting with electrocardiographic, echocardiographic, and hemodynamic evidence of acute inferior myocardial infarction associated with RVMI and CS were studied. After administration of supplemental oxygen (inspired oxygen fraction [F(i)O(2)] = 1.0), hemodynamic measurements were recorded before, during inhalation of NO (80 ppm at F(i)O(2) = 0.90) for 10 min, and 10 min after NO inhalation was discontinued (F(i)O(2) = 1.0).

RESULTS: Breathing NO decreased the mean right atrial pressure by 12 +/- 3%, mean pulmonary arterial pressure by 13 +/- 2%, and pulmonary vascular resistance by 36 +/- 8% (all p < 0.05). Nitric oxide inhalation increased the cardiac index by 24 +/- 11% and the stroke volume index by 23 +/- 12% (p < 0.05). The NO administration did not change systemic arterial or pulmonary capillary wedge pressures. Contrast echocardiography identified three patients with a patent foramen ovale and right-to-left shunt flow while breathing at F(i)O(2) = 1.0. Breathing NO decreased shunt flow by 56 +/- 5% (p < 0.05) and was associated with markedly improved systemic oxygen saturation.

CONCLUSIONS: Nitric oxide inhalation results in acute hemodynamic improvement when administered to patients with RVMI and CS.

1. Use of inhaled nitric oxide in the treatment of right ventricular myocardial infarction
Am J Emerg Med. 2011 May;29(4):473.e3-5
2. Hemodynamic effects of inhaled nitric oxide in right ventricular myocardial infarction and cardiogenic shock
J Am Coll Cardiol. 2004 Aug 18;44(4):793-8

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Early CT may rule out subarachnoid haemorrhage

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A multicentre Canadian study challenges the practice of routine lumbar puncture after negative CT in patients with suspected subarachnoid haemorrhage. CT scanning within six hours was highly sensitive, although a few cases of initially misinterpreted CTs “illustrate the importance of having a qualified radiologist with a high level of skill interpreting the head scans in a timely manner“.

Nearly 2% of patients were lost to all follow-up; the authors point out that even if a quarter of these patients could have experienced a subarachnoid haemorrhage, the corresponding negative likelihood ratio for a computed tomography performed within six hours rises to only 0.024 (0.007 to 0.07). They assert:

Such a likelihood ratio could be incorporated into the informed discussion surrounding the risks and benefits of lumbar puncture after negative results on computed tomography for this diagnosis

They point out that when CT imaging is obtained more than six hours after headache onset, clinicians should continue to be cautious because of the decreasing sensitivity for subarachnoid haemorrhage beyond this time.


Objective To measure the sensitivity of modern third generation computed tomography in emergency patients being evaluated for possible subarachnoid haemorrhage, especially when carried out within six hours of headache onset.

Design Prospective cohort study. Setting 11 tertiary care emergency departments across Canada, 2000-9.

Participants Neurologically intact adults with a new acute headache peaking in intensity within one hour of onset in whom a computed tomography was ordered by the treating physician to rule out subarachnoid haemorrhage.

Main outcome measures Subarachnoid haemorrhage was defined by any of subarachnoid blood on computed tomography, xanthochromia in cerebrospinal fluid, or any red blood cells in final tube of cerebrospinal fluid collected with positive results on cerebral angiography.

Results Of the 3132 patients enrolled (mean age 45.1, 2571 (82.1%) with worst headache ever), 240 had subarachnoid haemorrhage (7.7%). The sensitivity of computed tomography overall for subarachnoid
haemorrhage was 92.9% (95% confidence interval 89.0% to 95.5%), the specificity was 100% (99.9% to 100%), the negative predictive value was 99.4% (99.1% to 99.6%), and the positive predictive value was 100% (98.3% to 100%). For the 953 patients scanned within six hours of headache onset, all 121 patients with subarachnoid haemorrhage were identified by computed tomography, yielding a sensitivity of 100% (97.0% to 100.0%), specificity of 100% (99.5% to 100%), negative predictive value of 100% (99.5% to 100%), and positive predictive value of 100% (96.9% to 100%).

Conclusion Modern third generation computed tomography is extremely sensitive in identifying subarachnoid haemorrhage when it is carried out within six hours of headache onset and interpreted by a qualified radiologist

Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study
BMJ. 2011 Jul 18;343:d4277

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What do I do with a high sensitivity troponin?

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Newer high-sensitivity troponin tests can be positive in patients who would have negative tests with the ‘traditional’ assay, which can result in confusion about what to do with the patient, particularly those patients without an obvious cardiac presentation. A recent study1 shows that the majority of patients that fall into this group had non-cardiac discharge diagnoses.


Background: High sensitivity troponin T (hsTnT) detects lower levels of troponin T with greater precision than the 4th generation (cTnT) assay. However, the clinical implications of this are uncertain.

Objectives: Primary: Describe the proportion of patients who test ‘positive’ with hsTnT but negative with cTnT. Secondary: Determine proportion in each group with an adverse event (representation, AMI or died) within 90 days of the index test.

Method: 161 patients samples were tested with cTnT and hsTNT assays. McNemar’s test was used to compare paired samples. Electronic medical records were reviewed, with discharge diagnosis and 90 day outcomes determined blind to hsTnT results. Patients were then classified as ‘TnT negative’ (hsTnT was <0.014 mcg/mL), 'new positive' (hsTnT was ≥0.014 mcg/mL and cTnT <0.03 mcg/mL) and 'TnT positive' (cTNT was ≥0.03 mcg/mL)
Results: Positive results more than doubled with the hsTnT assay (50% vs 22%, P < 0.001). 81 patients were ‘TnT negative’, 44 were ‘new positive’ and 36 ‘cTnT positive’. The discharge diagnosis for ‘new positives’ was AMI in 4 (9%), other cardiac in 13 (30%) and non-cardiac in 27 (61%). At 90 days adverse events occurred in 30%, 54% and 50% of the groups respectively. There were no late cases of AMI or cardiovascular death in ‘new positive’ patients.

Conclusion: Many patients with diagnoses other than AMI will have hsTNT above the reference level. Indiscriminate testing with hsTnT might lead to more patients requiring serial troponin testing and/or invasive further tests, which will have process and resource implications for EDs and health services.

An accompanying editorial2 highlights that:

Elevations are seen in pathological conditions, including structural heart disease, renal impairment and pulmonary embolism, but might also be seen in extreme exertion, such as marathon runners. It is now clear that when using a highly sensitive assay, circulating levels of troponin will be detected in many normal people.

The editorial makes the interesting observation that the duration of rise may help elucidate the cause; ischaemic elevation of troponin falls rapidly, since the rise might be due to the release of small amounts of troponin that exist free within the cytoplasm, in contrast to the more persistent elevation seen with myocardial necrosis. The editorialist provides the following caution:


Overall, our practice for ordering troponin will need to be urgently reviewed. Single troponin values will continue to be of little to no use in defining disease states in the ED. Identifying a chronic versus an acute elevation will only be revealed by serial troponin testing. The time interval between testing is currently contentious.

High sensitivity troponins are referred to in the newly published 2011 Addendum to the National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand Guidelines for the Management of Acute Coronary Syndromes (full text link below)3:

RECOMMENDED PROTOCOL FOR TROPONIN TESTING USING HIGH SENSITIVITY ASSAYS IN “RULING-OUT” ACS

  • All patients with a suspected ACS should undergo troponin testing on arrival at ED to ‘rule in’ ACS within the differential diagnosis
  • For a patient with a positive troponin result or a change in troponin levels over time, neither ACS nor other significant pathology (e.g. pulmonary embolus, aortic dissection, and sepsis) can be excluded. These patients are at higher risk of subsequent events. A positive result should be considered within the entire clinical context (history, examination, ECG findings and other investigations). Further investigations directed at all plausible clinical diagnoses should be considered and, if ACS is thought to be the likely cause, these patients may require cardiology assessment.
  • All patients with a negative result should undergo repeat testing 3–4 hours later.
  • The testing interval to ‘rule out’ MI may be reduced to 3 hours, provided that one sample is taken at least 6 hours after symptom onset:
  • Patients with a negative result at 3 hours after presentation and at least 6 hours after the onset of pain should be considered for early assessment by non-invasive anatomic or functional testing, as determined by local availability.
  • For patients presenting more than 6 hours after pain onset, a single high sensitivity troponin assay is sufficient to rule out myocardial infarction in the absence of ongoing chest pain.

High sensitivity troponin assays have an increased sensitivity for the detection of “myonecrosis”, but a reduced specificity for the diagnosis of “MI”. A positive result (≥99th centile for reference population OR where there is a change of ≥50% above an initial baseline level) should be interpreted in the context of the entire clinical presentation and does not necessarily represent an indication for coronary angiography. The management MI secondary to other conditions (e.g. anaemia, thyrotoxicosis, and sepsis) should be primarily directed at those conditions.
The finding of troponin concentrations that remain stable over time suggests that the presence of troponin is due to chronic disease. Acute exacerbations of chronic disease that result in elevated troponin levels can mimic an MI release pattern.

1. Clinical diagnosis and outcomes for Troponin T ‘positive’ patients assessed by a high sensitivity compared with a 4th generation assay
Emerg Med Australas. 2011 Aug;23(4):490-501
2. Troponin: A risk-defining biomarker for emergency department physicians
Emerg Med Australas. 2011 Aug;23(4):391-4
3. 2011 Addendum to the National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand Guidelines for the Management of Acute Coronary Syndromes
Heart, Lung and Circulation 2011 Aug;28(8):487-502 Free Full Text