Comments Off on Sepsis research – let’s get some answers
There’s so much debate on which components of Early Goal Directed Therapy in sepsis really make a difference. The good news is that three randomised controlled trials in the UK, Australasia, and North America, aim to answer the question, and the study design from the outset has been a collaboration that will allow the results to be pooled.
The Australasian study (ARISE) and is nearing completion. If you can recruit patients then please do. Listen to a podcast on this fantastic study with lead investigator Dr Anthony Delaney.
Cardiac arrest patients sometimes have unrecognised oesophageal intubations because clinicians omit capnography, based on the assumption that circulatory arrest leads to an absence of exhaled CO2. This is wrong, and reassuringly the latest ILCOR cardiac arrest guidelines recommend waveform capnography during resuscitation.
Of interest is the fact that even corpses have CO2 in their lungs. While not clinically relevant, this may have value when fresh frozen cadavers are used for airway training, since we might be able to supplement the realism of airway instrumentation with the realism of connecting the capnography adaptor and circuit and seeing confirmation on the monitor.
This preliminary study, completed by my Sydney HEMS colleagues, needs further work, but it’s an interesting area.
Sustained life-like waveform capnography after human cadaveric tracheal intubation
Emerg Med J doi:10.1136/emermed-2013-203105
Introduction Fresh frozen cadavers are effective training models for airway management. We hypothesised that residual carbon dioxide (CO2) in cadaveric lung would be detectable using standard clinical monitoring systems, facilitating detection of tracheal tube placement and further enhancing the fidelity of clinical simulation using a cadaveric model.
Methods The tracheas of two fresh frozen unembalmed cadavers were intubated via direct laryngoscopy. Each tracheal tube was connected to a self-inflating bag and a sidestream CO2 detector. The capnograph display was observed and recorded in high-definition video. The cadavers were hand-ventilated with room air until the capnometer reached zero or the waveform approached baseline.
Results A clear capnographic waveform was produced in both cadavers on the first postintubation expiration, simulating the appearances found in the clinical setting. In cadaver one, a consistent capnographic waveform was produced lasting over 100 s. Maximal end-tidal CO2 was 8.5 kPa (65 mm Hg). In cadaver two, a consistent capnographic waveform was produced lasting over 50 s. Maximal end-tidal CO2 was 5.9 kPa (45 mm Hg).
Conclusions We believe this to be the first work to describe and quantify detectable end-tidal capnography in human cadavers. We have demonstrated that tracheal intubation of fresh frozen cadavers can be confirmed by life-like waveform capnography. This requires further validation in a larger sample size.
One of the current Holy Grails of ED critical care is to find a reliable measure of fluid responsiveness in those patients with impaired organ perfusion, such as those with severe sepsis. This would enable us to identify those patients whose cardiac output would be improved by fluid therapy, and avoid subjecting ‘non-responders’ to the risks associated with fluid overload. Thanks to the uptake of early goal-directed therapy in sepsis, under-resuscitation is now much less common in the ED. However a growing evidence base reveals the dangers of over-resuscitation. We have a responsibility to optimise fluid therapy as best we can with the equipment we have, according to the latest evidence.
Inferior Vena Cava Ultrasound
Some tests of fluid responsiveness rely on the effect of respiration-induced changes in pleural pressure on the circulation. Inferior vena cava (IVC) size and degree of inspiratory collapse correlate with central venous pressure (CVP), but CVP is not a reliable predictor of volume status or responsiveness. Skinny, collapsing IVCs detected on ultrasound suggest volume responsiveness, but the lack of this finding does not exclude fluid responsiveness. IVC size and measurement can be affected by patient position, probe position, and a variety of health states from athleticism to increased abdominal pressure.
Pulse Pressure Variation
Respiratory pulse pressure variation derived from an arterial line trace in mechanically ventilated patients who are adequately sedated and receiving large tidal volumes can predict fluid responsiveness too. Variability in tidal volume, the presence of spontaneous breathing activity in a ventilated patient, and cardiac dysrhythmia can all confound the usefulness of this method.
End expiratory occlusion
Another test in mechanically ventilated patients is the end expiratory occlusion test. A positive pressure inspiratory breath cyclically decreases the left cardiac preload. Occluding the circuit at end-expiration prevents this cyclic impediment in left cardiac preload and acts like a fluid challenge. A 15 second expiratory occlusion is performed and an increase in pulse pressure or (if you can measure it) cardiac index predicts fluid responsiveness with a high degree of accuracy. The patient must be able to tolerate the 15 second interruption to ventilation without initiating a spontaneous breath.
Passive Leg Raise
Passive leg raising (PLR) involves measuring cardiac output (or its surrogate, velocity-time integral, or VTI) before and after tilting the semirecumbent patient supine and raising the legs to 45 degrees. This ‘autotransfuses’ blood from the lower limbs to the core and acts as a reversible fluid challenge. An increase in VTI identifies fluid responders. It would be nice if a PLR-induced increase in blood pressure revealed the answer, but BP does not reliably inform us of changes in cardiac output.
All these tests have limitations. Pulse pressure variation fails in patients with low respiratory system compliance, such as is found in ARDS(1). End-expiratory occlusion and PLR work in low respiratory system compliance, but the former still requires mechanical ventilation, and the latter requires a means of estimating cardiac output or a surrogate – oesophageal Doppler, the velocity-time integral measured by transthoracic echocardiography, and femoral artery flow (measured by arterial Doppler) have all been used. Non-invasive cardiac output monitors that are not operator dependent exist, such as the NICOM(TM) bioreactance device. Bioreactance cardiac output measurement is based on an analysis of relative phase shifts of an oscillating current that occurs when this current traverses the thoracic cavity. Its advantages are that it is noninvasive, it does not require endotracheal intubation or an arterial line, and it provides a good estimate of stroke volume in patients with atrial fibrillation.
A recent study evaluating the combination of PLR with NICOM(TM) bioreactance monitoring revealed that another tool could indicate volume responsiveness: an increase in carotid blood flow after PLR, as measured by carotid Doppler flow imaging(2). A threshold increase in carotid Doppler flow imaging of 20% for predicting volume responsiveness had a sensitivity and specificity of 94% and 86%, respectively. This was studied in a heterogenous group of hemodynamically unstable patients, suggesting applicability to the kind of patients who present to the ED, although numbers were small so more validation is required.
End-tidal carbon dioxide
End-tidal carbon dioxide (ETCO2) levels depend on cardiac output. Increasing cardiac output with a fluid challenge or PLR increases ETCO2,as long as ventilatory and metabolic conditions remain stable. In a recent small study, a PLR-induced increase in ETCO2 ≥ 5 % predicted a fluid-induced increase in cardiac index ≥ 15 % with sensitivity of 71 % (95 % confidence interval: 48-89 %) and specificity of 100 (82-100) %(3). The maximal effects of PLR on CI and ETCO2 were observed within 1 min.
So what can I use?
In summary, differentiating fluid responders from non-responders in the ED remains a challenge. The method used depends on available equipment and expertise, and whether the patient is spontaneously breathing or mechanically ventilated. The NICOM(TM) shows great promise but until your department can afford one, ultrasound is the way to go; small collapsing IVCs suggest fluid responders. Learning to measure a VTI on transthoracic echo or carotid Doppler flow will help you assess the response to a PLR in spontaneously ventilating patients. If they’re mechanically ventilated, then looking for an ETCO2 rise after PLR could be a simpler alternative.
Inferior Vena Cava Ultrasound
Helpful if skinny / large degree of respirophasic collapse – suggests fluid responsive – ventilated or spontaneous breathing
Passive Leg Raise
Good in ventilated or spontaneous breathing patients; need to measure cardiac output or a surrogate, such as VTI (echo), NICOM(TM), carotid Doppler flow, or ETCO2 (if ventilation and metabolic status constant)
Pulse Pressure Variation
Requires full mechanical ventilation; no good if low respiratory compliance / disturbed heart-lung interaction
End expiratory occlusion
Requires mechanical ventilation and patient tolerance of 15 seconds of apnoea. Acts like a passive leg raise so need a measure of cardiac output or surrogate
I look forward to more studies on these modalities, and to trying some of them in the resus room at every available opportunity.
1. Passive leg-raising and end-expiratory occlusion tests perform better than pulse pressure variation in patients with low respiratory system compliance
Crit Care Med. 2012 Jan;40(1):152-7
OBJECTIVES: We tested whether the poor ability of pulse pressure variation to predict fluid responsiveness in cases of acute respiratory distress syndrome was related to low lung compliance. We also tested whether the changes in cardiac index induced by passive leg-raising and by an end-expiratory occlusion test were better than pulse pressure variation at predicting fluid responsiveness in acute respiratory distress syndrome patients.
DESIGN: Prospective study.
SETTING: Medical intensive care unit.
PATIENTS: We included 54 patients with circulatory shock (63 ± 13 yrs; Simplified Acute Physiology Score II, 63 ± 24). Twenty-seven patients had acute respiratory distress syndrome (compliance of the respiratory system, 22 ± 3 mL/cm H2O). In nonacute respiratory distress syndrome patients, the compliance of the respiratory system was 45 ± 9 mL/cm H2O.
MEASUREMENTS AND MAIN RESULTS: We measured the response of cardiac index (transpulmonary thermodilution) to fluid administration (500 mL saline). Before fluid administration, we recorded pulse pressure variation and the changes in pulse contour analysis-derived cardiac index induced by passive leg-raising and end-expiratory occlusion. Fluid increased cardiac index ≥ 15% (44% ± 39%) in 30 “responders.” Pulse pressure variation was significantly correlated with compliance of the respiratory system (r = .58), but not with tidal volume. The higher the compliance of the respiratory system, the better the prediction of fluid responsiveness by pulse pressure variation. A compliance of the respiratory system of 30 mL/cm H2O was the best cut-off for discriminating patients regarding the ability of pulse pressure variation to predict fluid responsiveness. If compliance of the respiratory system was >30 mL/cm H2O, then the area under the receiver-operating characteristics curve for predicting fluid responsiveness was not different for pulse pressure variation and the passive leg-raising and end-expiratory occlusion tests (0.98 ± 0.03, 0.91 ± 0.06, and 0.97 ± 0.03, respectively). By contrast, if compliance of the respiratory system was ≤ 30 mL/cm H2O, then the area under the receiver-operating characteristics curve was significantly lower for pulse pressure variation than for the passive leg-raising and end-expiratory occlusion tests (0.69 ± 0.10, 0.94 ± 0.05, and 0.93 ± 0.05, respectively).
CONCLUSIONS: The ability of pulse pressure variation to predict fluid responsiveness was inversely related to compliance of the respiratory system. If compliance of the respiratory system was ≤ 30 mL/cm H2O, then pulse pressure variation became less accurate for predicting fluid responsiveness. However, the passive leg-raising and end-expiratory occlusion tests remained valuable in such cases.
2. The use of bioreactance and carotid doppler to determine volume responsiveness and blood flow redistribution following passive leg raising in hemodynamically unstable patients
Chest. 2013 Feb 1;143(2):364-70
BACKGROUND: The clinical assessment of intravascular volume status and volume responsiveness is one of the most difficult tasks in critical care medicine. Furthermore, accumulating evidence suggests that both inadequate and overzealous fluid resuscitation are associated with poor outcomes. The objective of this study was to determine the predictive value of passive leg raising (PLR)- induced changes in stroke volume index (SVI) as assessed by bioreactance in predicting volume responsiveness in a heterogenous group of patients in the ICU. A secondary end point was to evaluate the change in carotid Doppler fl ow following the PLR maneuver.
METHODS: During an 8-month period, we collected clinical, hemodynamic, and carotid Doppler data on hemodynamically unstable patients in the ICU who underwent a PLR maneuver as part of our resuscitation protocol. A patient whose SVI increased by . 10% following a fluid challenge was considered a fluid responder.
RESULTS: A complete data set was available for 34 patients. Twenty-two patients (65%) had severe sepsis/septic shock, whereas 21 (62%) required vasopressor support and 19 (56%) required mechanical ventilation. Eighteen patients (53%) were volume responders. The PLR maneuver had a sensitivity of 94% and a specificity of 100% for predicting volume responsiveness (one false negative result). In the 19 patients undergoing mechanical ventilation, the stroke volume variation was 18.0% 5.1% in the responders and 14.8% 3.4% in the nonresponders ( P 5 .15). Carotid blood fl ow increased by 79% 32% after the PLR in the responders compared with 0.1% 14% in the nonresponders ( P , .0001). There was a strong correlation between the percent change in SVI by PLR and the concomitant percent change in carotid blood fl ow ( r 5 0.59, P 5 .0003). Using a threshold increase in carotid Doppler fl ow imaging of 20% for predicting volume responsiveness, there were two false positive results and one false negative result, giving a sensitivity and specificity of 94% and 86%, respectively. We noted a significant increase in the diameter of the common carotid artery in the fluid responders.
CONCLUSIONS: Monitoring the hemodynamic response to a PLR maneuver using bioreactance provides an accurate method of assessing volume responsiveness in critically ill patients. In addition, the study suggests that changes in carotid blood fl ow following a PLR maneuver may be a useful adjunctive method for determining fluid responsiveness in hemodynamically unstable patients.
3. End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test
Intensive Care Med. 2013 Jan;39(1):93-100
PURPOSE: In stable ventilatory and metabolic conditions, changes in end-tidal carbon dioxide (EtCO(2)) might reflect changes in cardiac index (CI). We tested whether EtCO(2) detects changes in CI induced by volume expansion and whether changes in EtCO(2) during passive leg raising (PLR) predict fluid responsiveness. We compared EtCO(2) and arterial pulse pressure for this purpose.
METHODS: We included 65 patients [Simplified Acute Physiology Score (SAPS) II = 57 ± 19, 37 males, under mechanical ventilation without spontaneous breathing, 15 % with chronic obstructive pulmonary disease, baseline CI = 2.9 ± 1.1 L/min/m(2)] in whom a fluid challenge was decided due to circulatory failure and who were monitored by an expiratory-CO(2) sensor and a PiCCO2 device. In all patients, we measured arterial pressure, EtCO(2), and CI before and after a fluid challenge. In 40 patients, PLR was performed before fluid administration. The PLR-induced changes in arterial pressure, EtCO(2), and CI were recorded.
RESULTS: Considering the whole population, the fluid-induced changes in EtCO(2) and CI were correlated (r (2) = 0.45, p = 0.0001). Considering the 40 patients in whom PLR was performed, volume expansion increased CI ≥ 15 % in 21 “volume responders.” A PLR-induced increase in EtCO(2) ≥ 5 % predicted a fluid-induced increase in CI ≥ 15 % with sensitivity of 71 % (95 % confidence interval: 48-89 %) and specificity of 100 (82-100) %. The prediction ability of the PLR-induced changes in CI was not different. The area under the receiver-operating characteristic (ROC) curve for the PLR-induced changes in pulse pressure was not significantly different from 0.5.
CONCLUSION: The changes in EtCO(2) induced by a PLR test predicted fluid responsiveness with reliability, while the changes in arterial pulse pressure did not.
Comments Off on Identifying the febrile kid who’s too tachypnoeic
Body temperature raises heart rate and respiratory rate in kids, potentially affecting our interpretation of these clinical signs.
Dutch investigators developed centile charts of respiratory rates for specific body temperatures (derivation study), so that abnormally high rates could be identified as a means of predicting lower respiratory infection (validation set).
Respiratory rate increased overall by 2.2 breaths/min per 1°C rise (standard error 0.2) after accounting for age and temperature in the model, which is similar to a previous UK study that suggested a rise in respiratory rate of around 0.5-2 breaths per minute and an increase in heart rate of about 10 beats per minute for every 1 degree celcius above normal.
Cut-off values at the 97th centile were more useful in detecting the presence of LRTI than existing (Advanced Paediatric Life Support) respiratory rate thresholds.
The respiratory rate charts are available here.
Derivation and validation of age and temperature specific reference values and centile charts to predict lower respiratory tract infection in children with fever: prospective observational study
BMJ. 2012 Jul 3;345:e4224
Comments Off on Targeted ICP reduction in TBI
A South American randomised controlled trial has demonstrated no improvement in mortality when traumatic brain injured patients had therapy targeted at keeping intracranial pressure below or equal to 20 mmHg as measured by an intraparenchymal monitor. The control group’s management was guided by neurologic examination and serial CT imaging(1).
Editorialist Dr Ropper summarises what we should do with this information well(2):
“[The authors]…do not advocate abandoning the treatment of elevated intracranial pressure any more than the authors of studies on wedge pressure reject the administration of fluid boluses in the treatment of shock”
Intracranial-pressure monitoring is considered the standard of care for severe traumatic brain injury and is used frequently, but the efficacy of treatment based on monitoring in improving the outcome has not been rigorously assessed.
We conducted a multicenter, controlled trial in which 324 patients 13 years of age or older who had severe traumatic brain injury and were being treated in intensive care units (ICUs) in Bolivia or Ecuador were randomly assigned to one of two specific protocols: guidelines-based management in which a protocol for monitoring intraparenchymal intracranial pressure was used (pressure-monitoring group) or a protocol in which treatment was based on imaging and clinical examination (imaging–clinical examination group). The primary outcome was a composite of survival time, impaired consciousness, and functional status at 3 months and 6 months and neuropsychological status at 6 months; neuropsychological status was assessed by an examiner who was unaware of protocol assignment. This composite measure was based on performance across 21 measures of functional and cognitive status and calculated as a percentile (with 0 indicating the worst performance, and 100 the best performance).
There was no significant between-group difference in the primary outcome, a composite measure based on percentile performance across 21 measures of functional and cognitive status (score, 56 in the pressure-monitoring group vs. 53 in the imaging–clinical examination group; P=0.49). Six-month mortality was 39% in the pressure-monitoring group and 41% in the imaging–clinical examination group (P=0.60). The median length of stay in the ICU was similar in the two groups (12 days in the pressure-monitoring group and 9 days in the imaging–clinical examination group; P=0.25), although the number of days of brain-specific treatments (e.g., administration of hyperosmolar fluids and the use of hyperventilation) in the ICU was higher in the imaging–clinical examination group than in the pressure-monitoring group (4.8 vs. 3.4, P=0.002). The distribution of serious adverse events was similar in the two groups.
For patients with severe traumatic brain injury, care focused on maintaining monitored intracranial pressure at 20 mm Hg or less was not shown to be superior to care based on imaging and clinical examination
1. A Trial of Intracranial-Pressure Monitoring in Traumatic Brain Injury
N Eng J Med 367;26:2471-2381 Full Text
2. Brain in a Box
N Eng J Med DOI: 10.1056/NEJMe1212289 Full Text
Comments Off on Aeromedical retrieval: invasive vs noninvasive blood pressure
The chaps from the Emergency Medical Retrieval Service in the UK compared invasive (IABP) and non-invasive blood pressure (NIBP) measurements on the ground and in the air. They concluded that NIBP was unreliable, although it was no worse in the aeromedical environment than in the hospital. Not surprisingly there was a better correlation between the mean IABP and NIBP than systolic or diastolic pressures (oscillometric NIBP devices measure the mean BP and derive systolic and diastolic using an algorithm specific to the device).
In their summary, they recommend:
- IABP monitoring should be used in any unwell patient in whom accurate blood pressure measurement is desirable.
- The aeromedical transport environment does not lead to less precise NIBP results than the non-transport environment.
- Where NIBP measurement is the only option, the mean blood pressure should be used in preference to systolic measurements
Blood pressure measurement is an essential physiological measurement for all critically ill patients. Previous work has shown that non-invasive blood pressure is not an accurate reflection of invasive blood pressure measurement. In a transport environment, the effects of motion and vibration may make non-invasive blood pressure less accurate.
Consecutive critically ill patients transported by a dedicated aeromedical retrieval and critical care transfer service with simultaneous invasive and non-invasive blood pressure measurements were analysed. Two sets of measurements were recorded, first in a hospital environment before departure (pre-flight) and a second during aeromedical transport (in-flight).
A total of 56 complete sets of data were analysed. Bland-Altman plots showed limits of agreement (precision) for pre-flight systolic blood pressure were -37.3 mmHg to 30.0 mmHg, and for pre-flight mean arterial pressure -20.5 mmHg to 25.0 mmHg. The limits of agreement for in-flight systolic blood pressure were -40.6 mmHg to 33.1 mmHg, while those for in-flight mean blood pressure in-flight were -23.6 mmHg to 24.6 mmHg. The bias for the four conditions ranged from 0.5 to -3.8 mmHg. There were no significant differences in values between pre-flight and in-flight blood pressure measurements for all categories of blood pressure measurement.
Thus, our data show that non-invasive blood pressure is not a precise reflection of invasive intra-arterial blood pressure. Mean blood pressure measured non-invasively may be a better marker of invasive blood pressure than systolic blood pressure. Our data show no evidence of non-invasive blood pressures being less accurate in an aeromedical transport environment.
Comparison of non-invasive and invasive blood pressure in aeromedical care
Anaesthesia. 2012 Dec;67(12):1343-7
I previously noted an article demonstrating that a ‘lowish’ – as opposed to a low – systolic blood pressure is a reason to be vigilant in blunt trauma patients, as a significant increase in mortality has been demonstrated with a systolic blood pressure (SBP) < 110 mmHg.
The same researchers have found similar results in patients with penetrating trauma.
Compared with the reference group with SBP 110-129mmHg, mortality was doubled at SBP 90-109mmHg, was four-fold higher at 70-89mmHg and 10-fold higher at <70mmHg. SBP values ≥150mmHg were associated with decreased mortality.
Systolic blood pressure below 110 mmHg is associated with increased mortality in penetrating major trauma patients: Multicentre cohort study
Resuscitation. 2012 Apr;83(4):476-81
INTRODUCTION: Non-invasive systolic blood pressure (SBP) measurement is a commonly used triaging tool for trauma patients. A SBP of <90mmHg has represented the threshold for hypotension for many years, but recent studies have suggested redefining hypotension at lower levels. We therefore examined the association between SBP and mortality in penetrating trauma patients.
METHODS: We conducted a prospective cohort study in adult (≥16 years) penetrating trauma patients. Patients were admitted to hospitals belonging to the Trauma Audit and Research Network (TARN) between 2000 and 2009. The main outcome measure was the association between SBP and mortality at 30 days. Multivariate logistic regression models adjusted for the influence of age, gender, Injury Severity Score (ISS) and Glasgow Coma Score (GCS) on mortality were used. RESULTS: 3444 patients with a median age of 30 years (IQR 22.5-41.4), SBP of 126mmHg (IQR 107-142), ISS of 9 (IQR 9-14) and GCS of 15 (IQR 15-15), were analysed. Multivariable logistic regression analysis adjusted for age, gender, severity of injury and level of consciousness showed a cut-off for SBP at <110mmHg, after which increased mortality was observed. Compared with the reference group with SBP 110-129mmHg, mortality was doubled at SBP 90-109mmHg, was four-fold higher at 70-89mmHg and 10-fold higher at <70mmHg. SBP values ≥150mmHg were associated with decreased mortality.
CONCLUSION: We recommend that penetrating trauma patients with a SBP<110mmHg are triaged to resuscitation areas within dedicated, appropriately specialised, high-level care trauma centres.
But ‘hypotension’ in many practitioners’ minds refers to a low systolic blood pressure. Who pays serious attention to the diastolic blood pressure? A low diastolic in a sick patient to me is a warning sign that their mean arterial pressure (MAP) is – or will be – low. After all, we spend about twice as long in diastole as in systole, so the diastolic pressure contributes more to the MAP than does the systolic.
A recent study showed that a low diastolic BP was one of several factors predictive of cardiac arrest on hospital wards: the most accurate predictors were maximum respiratory rate, heart rate, pulse pressure index, and minimum diastolic BP. These factors were more predictive than some of the variables included in the commonly used Early Warning Scores that trigger an emergency review.
The ‘pulse pressure index’ examined in the study is the pulse pressure divided by the systolic blood pressure (ie. [SBP-DBP]/SBP) which of course will be higher with lower diastolic blood pressures.
Importantly, the authors point out:
“In addition, our findings suggest that for many patients there is ample time prior to cardiac arrest to provide potentially life-saving interventions.”
…suggesting that there is still room for improvement in the identification and management of patients at risk for cardiac arrest, as the NCEPOD report ‘Cardiac Arrest Procedures: Time to Intervene?’ also showed.
They also recommend:
“…although systolic BP is commonly used in rapid response team activation criteria, incorporation of pulse pressure, pulse pressure index, or diastolic BP in place of systolic BP into the predictive model may be superior.”
Perhaps this may remind all of us to keep an eye on the diastolic as well as systolic BP when patients first present to us, and to include the importance of recognising diastolic hypotension in the teaching we provide our medical, paramedical and nursing students.
Predicting Cardiac Arrest on the Wards: A Nested Case-Control Study
Chest. 2012 May;141(5):1170-6 Free Full Text here
Background: Current rapid response team activation criteria were not statistically derived using ward vital signs, and the best vital sign predictors of cardiac arrest (CA) have not been determined. In addition, it is unknown when vital signs begin to accurately detect this event prior to CA.
Methods: We conducted a nested case-control study of 88 patients experiencing CA on the wards of a university hospital between November 2008 and January 2011, matched 1:4 to 352 control subjects residing on the same ward at the same time as the case CA. Vital signs and Modified Early Warning Scores (MEWS) were compared on admission and during the 48 h preceding CA.
Results: Case patients were older (64 ± 16 years vs 58 ± 18 years; P = .002) and more likely to have had a prior ICU admission than control subjects (41% vs 24%; P = .001), but had similar admission MEWS (2.2 ± 1.3 vs 2.0 ± 1.3; P = .28). In the 48 h preceding CA, maximum MEWS was the best predictor (area under the receiver operating characteristic curve [AUC] 0.77; 95% CI, 0.71-0.82), followed by maximum respiratory rate (AUC 0.72; 95% CI, 0.65-0.78), maximum heart rate (AUC 0.68; 95% CI, 0.61-0.74), maximum pulse pressure index (AUC 0.61; 95% CI, 0.54-0.68), and minimum diastolic BP (AUC 0.60; 95% CI, 0.53-0.67). By 48 h prior to CA, the MEWS was higher in cases (P = .005), with increasing disparity leading up to the event.
Conclusions: The MEWS was significantly different between patients experiencing CA and control patients by 48 h prior to the event, but includes poor predictors of CA such as temperature and omits significant predictors such as diastolic BP and pulse pressure index.
The National Confidential Enquiry into Patient Outcome and Death (NCEPOD) aimed to describe variability and identify remediable factors in the process of care of adult patients who receive resuscitation in hospital, including factors which may affect the decision to initiate the resuscitation attempt, the outcome and the quality of care following the resuscitation attempt, and antecedents in the preceding 48 hours that may have offered opportunities for intervention to prevent cardiac arrest.
Data were captured over a 14 day study period in late 2010 from UK hospitals, and were reviewed by an expert panel.
The summary is available here. I have picked out some findings of interest:
- An adequate history was not recorded in 70/489 cases (14%) and clinical examination was incomplete at first contact in 117/479 cases (24%).
- Appreciation of the severity of the situation was lacking in 74/416 (18%).
- Timely escalation to more senior doctors was lacking in 61/347 (18%).
- Decisions about CPR status were documented in the admission notes in 44/435 cases (10%). This is despite the high incidence of chronic disease and almost one in four cases being expected to be rapidly fatal on admission.
- Where time to first consultant review could be identified it was more than 12 hours in 95/198 cases (48%).
- Appreciation of urgency, supervision of junior doctors and the seeking of advice from senior doctors were rated ‘poor’ by Advisors.
- Physiological instability was noted in 322/444 (73%) of patients who subsequently had a cardiac arrest.
- Advisors considered that warning signs for cardiac arrest were present in 344/462 (75%) of cases. These warning signs were recognised poorly, acted on infrequently, and escalated to more senior doctors infrequently.
- There was no evidence of escalation to more senior staff in patients who had multiple reviews.
- Advisors considered that the cardiac arrest was predictable in 289/454 (64%) and potentially avoidable in 156/413 (38%) of cases.
- The Advisors reported problems during the resuscitation attempt in 91/526 cases (17%). Of these, 36/91 were associated with airway management.
- Survival to discharge after in-hospital cardiac arrest was 14.6% (85/581).
- Only 9/165 (5.5%) patients who had an arrest in asystole survived to hospital discharge.
- Survival to discharge after a cardiac arrest at night was much lower than after a cardiac arrest during the day time (13/176; 7.4% v 44/218; 20.1%).
In the opinion of the treating clinicians, earlier treatment of the problem and better monitoring may have improved outcome:
Compare these findings with a smaller scale confidential enquiry into the care of patients who ended up in intensive care units, published exactly 14 years ago by McQuillan et al2:
“The main causes of suboptimal care were failure of organisation, lack of knowledge, failure to appreciate clinical urgency, lack of supervision, and failure to seek advice.”
One of the co-authors of the McQuillan study, Professor Gary Smith , has spent years improving training in and awareness of the importance of recognition of critical illness, and pioneered the “ALERT” Course TM: Acute Life-threatening Emergencies, Recognition, and Treatment. Professor Smith provides commentary on the NCEPOD report and the slides are available here, including a reminder of the ‘Chain of Prevention’3.
It’s a shame these issues remain a problem but it is heartening to see NCEPOD tackle this important topic and provide recommendations that UK hospitals will have to act upon. It is further credit to the vision of Pete McQuillan, Gary Smith and their colleague Bruce Taylor (another co-author of the 1998 confidential inquiry). These guys opened my eyes to the world of critical care and trained me for 18 months on their ICU, which remains a beacon site for critical care expertise and training. Without their inspiration, I may not have ended up in emergency medicine-critical care and I doubt very much that Resus.ME would exist.
1. Cardiac Arrest Procedures: Time to Intervene? (2012)
National Confidential Enquiry into Patient Outcome and Death (NCEPOD)
2. Confidential inquiry into quality of care before admission to intensive care
BMJ 1998 Jun 20;316(7148):1853-8 Free Full Text
OBJECTIVE: To examine the prevalence, nature, causes, and consequences of suboptimal care before admission to intensive care units, and to suggest possible solutions.
DESIGN: Prospective confidential inquiry on the basis of structured interviews and questionnaires.
SETTING: A large district general hospital and a teaching hospital.
SUBJECTS: A cohort of 100 consecutive adult emergency admissions, 50 in each centre.
MAIN OUTCOME MEASURES: Opinions of two external assessors on quality of care especially recognition, investigation, monitoring, and management of abnormalities of airway, breathing, and circulation, and oxygen therapy and monitoring.
RESULTS: Assessors agreed that 20 patients were well managed (group 1) and 54 patients received suboptimal care (group 2). Assessors disagreed on quality of management of 26 patients (group 3). The casemix and severity of illness, defined by the acute physiology and chronic health evaluation (APACHE II) score, were similar between centres and the three groups. In groups 1, 2, and 3 intensive care mortalities were 5 (25%), 26 (48%), and 6 (23%) respectively (P=0.04) (group 1 versus group 2, P=0.07). Hospital mortalities were 7 (35%), 30 (56%), and 8 (31%) (P=0.07) and standardised hospital mortality ratios (95% confidence intervals) were 1.23 (0.49 to 2.54), 1.4 (0.94 to 2.0), and 1.26 (0.54 to 2.48) respectively. Admission to intensive care was considered late in 37 (69%) patients in group 2. Overall, a minimum of 4.5% and a maximum of 41% of admissions were considered potentially avoidable. Suboptimal care contributed to morbidity or mortality in most instances. The main causes of suboptimal care were failure of organisation, lack of knowledge, failure to appreciate clinical urgency, lack of supervision, and failure to seek advice.
CONCLUSIONS: The management of airway, breathing, and circulation, and oxygen therapy and monitoring in severely ill patients before admissionto intensive care units may frequently be suboptimal. Major consequences may include increased morbidity and mortality and requirement forintensive care. Possible solutions include improved teaching, establishment of medical emergency teams, and widespread debate on the structure and process of acute care.
3. In-hospital cardiac arrest: is it time for an in-hospital ‘chain of prevention’?
Resuscitation. 2010 Sep;81(9):1209-11
The ‘chain of survival’ has been a useful tool for improving the understanding of, and the quality of the response to, cardiac arrest for many years. In the 2005 European Resuscitation Council Guidelines the importance of recognising critical illness and preventing cardiac arrest was highlighted by their inclusion as the first link in a new four-ring ‘chain of survival’. However, recognising critical illness and preventing cardiac arrest are complex tasks, each requiring the presence of several essential steps to ensure clinical success. This article proposes the adoption of an additional chain for in-hospital settings–a ‘chain of prevention’–to assist hospitals in structuring their care processes to prevent and detect patient deterioration and cardiac arrest. The five rings of the chain represent ‘staff education’, ‘monitoring’, ‘recognition’, the ‘call for help’ and the ‘response’. It is believed that a ‘chain of prevention’ has the potential to be understood well by hospital clinical staff of all grades, disciplines and specialties, patients, and their families and friends. The chain provides a structure for research to identify the importance of each of the various components of rapid response systems.
Comments Off on Is diastolic worse than systolic dysfunction in sepsis?
Septic myocardial dysfunction is a well recognised contributor to shock in sepsis but for many of us we assume this to be gross systolic impairment. Interestingly a recent study highlights that patients with severe sepsis and septic shock frequently have diastolic dysfunction1. They found that diastolic dysfunction was the strongest independent predictor of early mortality, even after adjusting for the APACHE-II score and other predictors of mortality.
In this study, 9.1% of severe sepsis/septic shock patients had isolated systolic dysfunction, 14.1% had combined systolic and diastolic dysfunction, and 38% had isolated diastolic dysfunction.
Importantly, the authors point out that although diastolic dysfunction is associated with age, hypertension, diabetes mellitus, and ischaemic heart disease, diastolic dysfunction is a stronger independent predictor of mortality than age and the other co-morbidities. However, a limitation of the study acknowledged by the authors is that it did not include follow-up echocardiography examinations, so we do not know whether sepsis was responsible for a transient diastolic dysfunction or whether the observed diastolic dysfunction was a pre-existing condition.
Both troponin and NT-ProBNP elevations also predicted mortality.
Want to know how to measure diastolic dysfunction? These authors measured mitral annular early-diastolic peak velocity, or the e’-wave (called ‘e prime’). It is a way of seeing how fast myocardial tissue relaxes in diastole, and if its peak velocity is slow (in this case < 8cm/s) there is diastolic dysfunction. We measure speed using Doppler, and in this case we’re looking at the speed of heart tissue (as opposed to the blood cells within the heart chambers) so we do ‘Tissue Doppler Imaging’, or TDI. You need an echo machine with pulsed-wave Doppler, and you need to be able to get an apical view. This is explained really nicely here2 but if you don’t have the time or the echopassion to read a whole article on TDI watch this one minute video (BY emergency physicians FOR emergency physicians!) on diastology, where TDI measurement of e’ is shown from 45 seconds into the video.
For reference, there is some more detail on diastolic function measurements at the Echobasics site.
If you think you can cope with any more of this level of awesomeness and want these geniuses to talk to you from your smartphone in the ED then get the free One Minute Ultrasound app for Android or Apple devices.
AIMS: Systolic dysfunction in septic shock is well recognized and, paradoxically, predicts better outcome. In contrast, diastolic dysfunction is often ignored and its role in determining early mortality from sepsis has not been adequately investigated.
METHODS AND RESULTS: A cohort of 262 intensive care unit patients with severe sepsis or septic shock underwent two echocardiography examinations early in the course of their disease. All clinical, laboratory, and survival data were prospectively collected. Ninety-five (36%) patients died in the hospital. Reduced mitral annular e’-wave was the strongest predictor of mortality, even after adjusting for the APACHE-II score, low urine output, low left ventricular stroke volume index, and lowest oxygen saturation, the other independent predictors of mortality (Cox’s proportional hazards: Wald = 21.5, 16.3, 9.91, 7.0 and 6.6, P< 0.0001, <0.0001, 0.002, 0.008, and 0.010, respectively). Patients with systolic dysfunction only (left ventricular ejection fraction ≤50%), diastolic dysfunction only (e’-wave <8 cm/s), or combined systolic and diastolic dysfunction (9.1, 40.4, and 14.1% of the patients, respectively) had higher mortality than those with no diastolic or systolic dysfunction (hazard ratio = 2.9, 6.0, 6.2, P= 0.035, <0.0001, <0.0001, respectively) and had significantly higher serum levels of high-sensitivity troponin-T and N-terminal pro-B-type natriuretic peptide (NT-proBNP). High-sensitivity troponin-T was only minimally elevated, whereas serum levels of NT-proBNP were markedly elevated [median (inter-quartile range): 0.07 (0.02-0.17) ng/mL and 5762 (1001-15 962) pg/mL, respectively], though both predicted mortality even after adjusting for highest creatinine levels (Wald = 5.8, 21.4 and 2.3, P= 0.015, <0.001 and 0.13).
CONCLUSION: Diastolic dysfunction is common and is a major predictor of mortality in severe sepsis and septic shock.
1. Diastolic dysfunction and mortality in severe sepsis and septic shock
Eur Heart J. 2012 Apr;33(7):895-903
2. A clinician’s guide to tissue Doppler imaging
Circulation. 2006 Mar 14;113(10):e396-8 Free Full Text