Tag Archives: echocardiography


Does RV enlargement on echo predict PE?

A nice paper from Annals of Emergency Medicine showing the test characteristcs of some of the common signs we look for on basic 2D echo that suggest the presence of (sub)massive pulmonary embolism:

Right Ventricular Dilatation on Bedside Echocardiography Performed by Emergency Physicians Aids in the Diagnosis of Pulmonary Embolism
Ann Emerg Med. 2014 Jan;63(1):16-24


STUDY OBJECTIVE: The objective of this study was to determine the diagnostic performance of right ventricular dilatation identified by emergency physicians on bedside echocardiography in patients with a suspected or confirmed pulmonary embolism. The secondary objective included an exploratory analysis of the predictive value of a subgroup of findings associated with advanced right ventricular dysfunction (right ventricular hypokinesis, paradoxical septal motion, McConnell’s sign).

METHODS: This was a prospective observational study using a convenience sample of patients with suspected (moderate to high pretest probability) or confirmed pulmonary embolism. Participants had bedside echocardiography evaluating for right ventricular dilatation (defined as right ventricular to left ventricular ratio greater than 1:1) and right ventricular dysfunction (right ventricular hypokinesis, paradoxical septal motion, or McConnell’s sign). The patient’s medical records were reviewed for the final reading on all imaging, disposition, hospital length of stay, 30-day inhospital mortality, and discharge diagnosis.

RESULTS: Thirty of 146 patients had a pulmonary embolism. Right ventricular dilatation on echocardiography had a sensitivity of 50% (95% confidence interval [CI] 32% to 68%), a specificity of 98% (95% CI 95% to 100%), a positive predictive value of 88% (95% CI 66% to 100%), and a negative predictive value of 88% (95% CI 83% to 94%). Positive and negative likelihood ratios were determined to be 29 (95% CI 6.1% to 64%) and 0.51 (95% CI 0.4% to 0.7%), respectively. Ten of 11 patients with right ventricular hypokinesis had a pulmonary embolism. All 6 patients with McConnell’s sign and all 8 patients with paradoxical septal motion had a diagnosis of pulmonary embolism. There was a 96% observed agreement between coinvestigators and principal investigator interpretation of images obtained and recorded.

CONCLUSION: Right ventricular dilatation and right ventricular dysfunction identified on emergency physician performed echocardiography were found to be highly specific for pulmonary embolism but had poor sensitivity. Bedside echocardiography is a useful tool that can be incorporated into the algorithm of patients with a moderate to high pretest probability of pulmonary embolism.

Predicting volume responsiveness

IVCiconOne 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.

Fluid responsiveness assessment – options in the Emergency Department

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.

Echo for cardiac arrest outcome prediction

A meta-analysis of studies evaluation transthoracic echo as a means of predicting return of spontaneous circulation in cardiac arrest (ROSC) provides some likelihood ratios to what we already know: absence of sonographic cardiac activity means a very low chance of ROSC.

The authors report a pooled negative LR of 0.18 (95% CI = 0.10 to 0.31), and a positive likelihood ratio of 4.26 (95% CI = 2.63 to 6.92).

They conclude that focused transthoracic echo is a fairly effective (although not definitive) test for predicting death if no cardiac activity is noted during resuscitation, and recommend interpreting the echo in the light of the test characteristics and the clinical pre-test probability, as one should do for all imaging investigations:


“An elderly patient with an unwitnessed cardiac arrest already has very poor odds for survival. Confirmation of asystole on echo lowers those pretest odds by a factor of 5.6 and therefore might lead to termination of resuscitation. However, in the case of a 50-year-old rescued from drowning, detection of cardiac contractility on echo would increase his already fair odds of survival by a factor of 4.3, prompting continued aggressive resuscitation.”

Only five relatively small studies contributed to the findings. A more definitive answer to this question should be provided in the future by the multi-centre REASON 1 trial.

Objectives:  The objective was to determine if focused transthoracic echocardiography (echo) can be used during resuscitation to predict the outcome of cardiac arrest.

Methods:  A literature search of diagnostic accuracy studies was conducted using MEDLINE via PubMed, EMBASE, CINAHL, and Cochrane Library databases. A hand search of references was performed and experts in the field were contacted. Studies were included for further appraisal and analysis only if the selection criteria and reference standards were met. The eligible studies were appraised and scored by two independent reviewers using a modified quality assessment tool for diagnostic accuracy studies (QUADAS) to select the papers included in the meta-analysis.

Results:  The initial search returned 2,538 unique papers, 11 of which were determined to be relevant after screening criteria were applied by two independent researchers. One additional study was identified after the initial search, totaling 12 studies to be included in our final analysis. The total number of patients in these studies was 568, all of whom had echo during resuscitation efforts to determine the presence or absence of kinetic cardiac activity and were followed up to determine return of spontaneous circulation (ROSC). Meta-analysis of the data showed that as a predictor of ROSC during cardiac arrest, echo had a pooled sensitivity of 91.6% (95% confidence interval [CI] = 84.6% to 96.1%), and specificity was 80.0% (95% CI = 76.1% to 83.6%). The positive likelihood ratio for ROSC was 4.26 (95% CI = 2.63 to 6.92), and negative likelihood ratio was 0.18 (95% CI = 0.10 to 0.31). Heterogeneity of the results (sensitivity) was nonsignificant (Cochran’s Q: χ(2) = 10.63, p = 0.16, and I(2) = 34.1%).

Conclusions:  Echocardiography performed during cardiac arrest that demonstrates an absence of cardiac activity harbors a significantly lower (but not zero) likelihood that a patient will experience ROSC. In selected patients with a higher likelihood of survival from cardiac arrest at presentation, based on established predictors of survival, echo should not be the sole basis for the decision to cease resuscitative efforts. Echo should continue to be used only as an adjunct to clinical assessment in predicting the outcome of resuscitation for cardiac arrest.

Bedside Focused Echocardiography as Predictor of Survival in Cardiac Arrest Patients: A Systematic Review
Acad Emerg Med. 2012 Oct;19(10):1119-1126

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

Posterior pericardiocentesis

Dr Emanuele Catena and colleagues report a case of an adult male who presented 7 days post cardiac surgery with simultaneous pleural and pericardial effucions causing dyspnoea, tachycardia and hypotension.

Old skool pericardiocentesis

His pericardial effusion was posterior which usually requires surgical drainage, but the adjacent left pleural effusion was associated with pulmonary atelectasis and displacement of the lung, allowing them to insert a needle using sonographic guidance first into the pleural space then the pericardial space.

They inserted through the fourth intercostal space 4 cm medially to the left posterior axillary line (with the patient positioned in the semireclining position). They used agitated saline bubbles to confirm first the pleural then the pericardial location of the needle tip. A 30-cm-long catheter was introduced into the posterior pericardium using the Seldinger technique, and serous-haemorrhagic fluid was drained. The catheter was then retracted allowing drainage of the pleural effusion.

The procedure resulted in haemodynamic and respiratory improvement.

The authors summarise:



This case reports the technique of a “back pericardiocentesis” performed under echographic guidance as a valid alternative to surgery in the peculiar situation characterized by the simultaneous presence of a large left pleural effusion. In the presence of a large left pleural effusion, pulmonary atelectasis and displacement of air-filled pulmonary tissue allows ultrasound transmission from a patient’s back to the heart through a liquid interface and needle insertion “from back” to reach the pericardial space.


 

Pericardiocentesis From Back Under Echographic Guidance An Approach for Posterior Pericardial Effusions
Circulation. 2011 Dec 13;124(24):e835-6

Prehospital echo predicts arrest outcome

In hospital, the detection of cardiac standstill with ultrasound predicts a fatal outcome from cardiac arrest with a high degree of accuracy. A similar finding has been made in the prehospital setting. Interestingly, it was a better predictor than other commonly recognised factors associated with outcome: the presence of asystole, down time, bystander CPR, or end-tidal CO2 levels.



Introduction. The prognostic value of emergency echocardiography (EE) in the management of cardiac arrest patients has previously been studied in an in-hospital setting. These studies mainly included patients who underwent cardiopulmonary resuscitation (CPR) by emergency medicine technicians at the scene and who arrived at the emergency department (ED) still in a state of cardiac arrest. In most European countries, cardiac arrest patients are normally treated by physician-staffed emergency medical services (EMS) teams on scene. Transportation to the ED while undergoing CPR is uncommon. Objective. To evaluate the ability of EE to predict outcome in cardiac arrest patients when it is performed by ultrasound-inexperienced emergency physicians on scene.


Methods. We performed a prospective, observational study of nonconsecutive, nontrauma, adult cardiac arrest patients who were treated by physician-staffed urban EMS teams on scene. Participating emergency physicians (EPs) received a two-hour course in EE during CPR. After initial procedures were accomplished, EE was performed during a rhythm and pulse check. A single subxiphoid, four-chamber view was required for study enrollment. We defined sonographic evidence of cardiac kinetic activity as any detected motion of the myocardium, ranging from visible ventricular fibrillation to coordinated ventricular contractions. The CPR had to be continued for at least 15 minutes after the initial echocardiography. No clinical decisions were made based on the results of EE.


Results. Forty-two patients were enrolled in the study. The heart could be visualized successfully in all patients. Five (11.9%) patients survived to hospital admission. Of the 32 patients who had cardiac standstill on initial EE, only one (3.1%) survived to hospital admission, whereas four out of 10 (40%) patients with cardiac movement on initial EE survived to hospital admission (p = 0.008). Neither asystole on initial electrocardiogram nor peak capnography value, age, bystander CPR, or downtime was a significant predictor of survival. Only cardiac movement was associated with survival, and cardiac standstill at any time during CPR resulted in a positive predictive value of 97.1% for death at the scene.


Conclusion. Our results support the idea of focused echocardiography as an additional criterion in the evaluation of outcome in CPR patients and demonstrate its feasibility in the prehospital setting.


Cardiac Movement Identified on Prehospital Echocardiography Predicts Outcome
Prehosp Emerg Care. 2012 Jan 11. [Epub ahead of print]

Thrombolysis in submassive PE – still equipoise?

The AHA has produced a comprehensive guideline on venous thromboembolic disease. Here are some excerpts pertaining to resuscitation room decision making, particularly: ‘should I thrombolyse this patient?’

Definition for massive PE: Acute PE with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left ventricular [LV] dysfunction), pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock).

Definition for submassive PE: Acute PE without systemic hypotension (systolic blood pressure ≥90 mm Hg) but with either RV dysfunction or myocardial necrosis.
RV dysfunction means the presence of at least 1 of the following:

  • RV dilation (apical 4-chamber RV diameter divided by LV diameter >0.9) or RV systolic dysfunction on echocardiography
  • RV dilation (4-chamber RV diameter divided by LV diameter >0.9) on CT
  • Elevation of BNP (>90 pg/mL)
  • Elevation of N-terminal pro-BNP (>500 pg/mL); or
  • Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)

Myocardial necrosis is defined as either of the following:

  • Elevation of troponin I (>0.4 ng/mL) or
    Elevation of troponin T (>0.1 ng/mL)

Odds ratio for short-term mortality for RV dysfunction on echocardiography = 2.53 (95% CI 1.17 to 5.50).

Troponin elevations had an odds ratio for mortality of 5.90 (95% CI 2.68 to 12.95).

Definition for low risk PE: those with normal RV function and no elevations in biomarkers with short-term mortality rates approaching ≈ 1%

Recommendations for Initial Anticoagulation for Acute PE
  • Therapeutic anticoagulation with subcutaneous LMWH, intravenous or subcutaneous UFH with monitoring, unmonitored weight-based subcutaneous UFH, or subcutaneous fondaparinux should be given to patients with objectively confirmed PE and no contraindications to anticoagulation (Class I; Level of Evidence A).
  • Therapeutic anticoagulation during the diagnostic workup should be given to patients with intermediate or high clinical probability of PE and no contraindications to anticoagulation (Class I; Level of Evidence C).

 

Patients treated with a fibrinolytic agent have faster restoration of lung perfusion. At 24 hours, patients treated with heparin have no substantial improvement in pulmonary blood flow, whereas patients treated with adjunctive fibrinolysis manifest a 30% to 35% reduction in total perfusion defect. However, by 7 days, blood flow improves similarly (≈65% to 70% reduction in total defect).

Thirteen placebo-controlled randomized trials of fibrinolysis for acute PE have been published, but only a subset evaluated massive PE specifically.
When Wan et al restricted their analysis to those trials with massive PE, they identified a significant reduction in recurrent PE or death from 19.0% with heparin alone to 9.4% with fibrinolysis (odds ratio 0.45, 95% CI 0.22 to 0.90).

Data from registries indicate that the short-term mortality rate directly attributable to submassive PE treated with heparin anticoagulation is probably < 3.0%. The implication is that even if adjunctive fibrinolytic therapy has extremely high efficacy, for example, a 30% relative reduction in mortality, the effect size on mortality due to submassive PE is probably < 1%. Thus, secondary adverse outcomes such as persistent RV dysfunction, chronic thromboembolic pulmonary hypertension, and impaired quality of life represent appropriate surrogate goals of treatment.

Data suggest that compared with heparin alone, heparin plus fibrinolysis yields a significant favorable change in right ventricular systolic pressure and pulmonary arterial pressure incident between the time of diagnosis and follow-up. Patients with low-risk PE have an unfavorable risk-benefit ratio with fibrinolysis. Patients with PE that causes hypotension probably do benefit from fibrinolysis. Management of submassive PE crosses the zone of equipoise, requiring the clinician to use clinical judgment.

An algorithm is proposed:

Two criteria can be used to assist in determining whether a patient is more likely to benefit from fibrinolysis: (1) Evidence of present or developing circulatory or respiratory insufficiency; or (2) evidence of moderate to severe RV injury.

Evidence of circulatory failure includes any episode of hypotension or a persistent shock index (heart rate in beats per minute divided by systolic blood pressure in millimeters of mercury) >1

The definition of respiratory insufficiency may include hypoxemia, defined as a pulse oximetry reading < 95% when the patient is breathing room air and clinical judgment that the patient appears to be in respiratory distress. Alternatively, respiratory distress can be quantified by the numeric Borg score, which assesses the severity of dyspnea from 0 to 10 (0=no dyspnea and 10=sensation of choking to death).

Evidence of moderate to severe RV injury may be derived from Doppler echocardiography that demonstrates any degree of RV hypokinesis, McConnell’s sign (a distinct regional pattern of RV dysfunction with akinesis of the mid free wall but normal motion at the apex), interventricular septal shift or bowing, or an estimated RVSP > 40 mm Hg.

Biomarker evidence of moderate to severe RV injury includes major elevation of troponin measurement or brain natriuretic peptides.

Two trials are currently ongoing that aim to assess effect of thrombolysis on patients with submassive PE: PEITHO and TOPCOAT

Recommendations for Fibrinolysis for Acute PE
  • Fibrinolysis is reasonable for patients with massive acute PE and acceptable risk of bleeding complications (Class IIa; Level of Evidence B).
  • Fibrinolysis may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory insufficiency, severe RV dysfunction, or major myocardial necrosis) and low risk of bleeding complications (Class IIb; Level of Evidence C).
  • Fibrinolysis is not recommended for patients with low-risk PE (Class III; Level of Evidence B) or submassive acute PE with minor RV dysfunction, minor myocardial necrosis, and no clinical worsening (Class III; Level of Evidence B).
  • Fibrinolysis is not recommended for undifferentiated cardiac arrest (Class III; Level of Evidence B).
Recommendations for Catheter Embolectomy and Fragmentation
  • Depending on local expertise, either catheter embolectomy and fragmentation or surgical embolectomy is reasonable for patients with massive PE and contraindications to fibrinolysis (Class IIa; Level of Evidence C).
  • Catheter embolectomy and fragmentation or surgical embolectomy is reasonable for patients with massive PE who remain unstable after receiving fibrinolysis (Class IIa; Level of Evidence C).
  • For patients with massive PE who cannot receive fibrinolysis or who remain unstable after fibrinolysis, it is reasonable to consider transfer to an institution experienced in either catheter embolectomy or surgical embolectomy if these procedures are not available locally and safe transfer can be achieved (Class IIa; Level of Evidence C).
  • Either catheter embolectomy or surgical embolectomy may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory failure, severe RV dysfunction, or major myocardial necrosis) (Class IIb; Level of Evidence C).
  • Catheter embolectomy and surgical thrombectomy are not recommended for patients with low-risk PE or submassive acute PE with minor RV dysfunction, minor myocardial necrosis, and no clinical worsening (Class III; Level of Evidence C).

 

Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension
Circulation. 2011 Apr 26;123(16):1788-1830 (Free Full Text)

An easily missed cause of shock

A potentially reversible cause of haemodynamic shock in critically ill patients is left ventricular outflow tract obstruction (LVOTO). We are familiar with this phenomenon in conditions such as hypertrophic cardiomyopathy (HCM), but LVOTO can occur in the absence of HCM and result in hypotension that may be refractory to catecholamines. In fact, vasoactive drugs are often the precipitant.

A case is reported of an intubated elderly man with pneumonia and COPD who upon starting dopamine and furosemide for hypotension and anuria developed severe haemodynamic deterioration1. Echo revealed a hyperkinetic left ventricle with mild concentric hypertrophy, septal wall thickness of 12 mm (normal range up to 10mm), and a reduced end-diastolic diameter. Systolic anterior motion (SAM) of the anterior mitral leaflet causing a significant left ventricular outflow tract obstruction (LVOTO), with a peak gradient of 100 mmHg, was detected. The patient improved with discontinuation of vasoactive drugs and fluid loading. A follow up cardiac MR showed a structurally normal LV.

The authors describe the factors that combine to produce this syndrome:

  • Anatomical substrate – Left ventricular hypertrophy due to hypertension, mitral valve repair, previous aortic valve replacement, abnormalities of the mitral subvalvular apparatus, sigmoid septum and a steep aortic root angle.
  •  
  • Precipitating factors – Drug therapies such as catecholamine infusion or diuretics, which respectively enhance the contractility of the basal segments and reduce the left ventricular cavity, emotional stress (like described in the apical ballooning syndrome), hypovolaemia, dehydration, sepsis, and myocardial infarction; hypovolaemia and mechanical ventilation further exacerbate underfilling of the LV and dynamic LVOTO.

In a review article on the topic, Dr Chockalingam and colleagues describe structural and functional factors in this finely crafted explanation2:

The asymmetrically hypertrophied septum, progressive narrowing of the LVOT during systole, and direction of the bloodstream cause drag forces and a Venturi effect on the anterior mitral leaflet, which results in SAM of the anterior mitral leaflet. This movement results in the anterior mitral leaflet contacting the septum for a period of systole, effectively obstructing the path of ventricular outflow. Failure of the anterior mitral leaflet to coapt with the posterior leaflet in systole results in MR. The degree and duration of mitral SAM determine the severity of the dynamic LVOTO gradients and MR.

Although classically described with hypertrophic cardiomyopathy, SAM and LVOTO can independently result from various clinical settings such as LV hypertrophy (hypertension or sigmoid septum), reduced LV chamber size (dehydration, bleeding, or diuresis), mitral valve abnormalities (redundant, long anterior leaflet), and hypercontractility (stress, anxiety, or inotropic agents). Dynamic LVOTO may occur with acute coronary syndrome and often presents with shock and a new systolic murmur3. The presence of a new murmur in a shocked ACS patient should therefore prompt consideration of the following diagnoses:

  • Acute mitral valve dysfunction
  • Ventricular septal defect
  • Free wall rupture
  • Dynamic LVOTO

Treatment is aimed at alleviating the causes and should be individualised. Options include coronary revascularisation, volume therapy, beta blockade, removing afterload reduction (vasodilators and balloon pumps can exacerbate LVOTO), and alpha agonists such as phenylephrine.

 

In summary, dynamic LVOTO:
  • is a potentially reversible cause of haemodynamic shock in critically ill patients
  • should be considered in critically ill patients whose shock fails to improve or worsen with inotropic medication
  • should be considered in patients with ACS, shock, and a new systolic murmur
  • can result from combinations of LV hypertrophy, reduced LV chamber size (dehydration, bleeding, or diuresis), mitral valve abnormalities, and hypercontractility (stress, anxiety, or inotropic agents)
  • is yet another reason why the haemodynamic monitor of choice in shocked patients should be echocardiography!

Echo showing systolic anterior motion of the mitral valve

1. Pathophysiology of Dynamic Left Ventricular Outflow Tract Obstruction in a Critically Ill Patient Echocardiography. 2010 Nov;27(10):E122-4

2. Dynamic Left Ventricular Outflow Tract Obstruction in Acute Myocardial Infarction With Shock Circulation. 2007 Jul 31;116(5):e110-3 Free Full Text 3. Dynamic left ventricular outflow tract obstruction in acute coronary syndromes: an important cause of new systolic murmur and cardiogenic shock Mayo Clin Proc. 1999 Sep;74(9):901-6

Pre-hospital Echo

Pre-hospital physicians in Germany performed basic echo on patients with symptoms either of profound hypotension and/or severe dyspnoea/tachypnoea where judged by the physician to be in a ‘peri-resuscitation’ state, and on patients undergoing CPR. Features noted were; cardiac motion (present or absent), ventricular function (normal, moderately impaired, severely impaired, absent), right ventricular dilatation or pericardial collection.

A few interesting findings to note:

  • In almost all patients an interpretable view was achieved; in the CPR patients, the subcostal view was best
  • In PEA patients, there was a difference in survival to admission (to discharge isn’t documented) between those with and without sonographically evident cardiac wall motion (21/38 = 55% vs 1/13 = 8%)
  • In ‘suspected asystole’, some patients had sonographically evident cardiac wall motion, and 9/37 (24%) of these survived to hospital admission vs 4/37 (11%) with no wall motion. On this point, the authors note: ‘The ECG performance and interpretation were by experienced practitioners, and this therefore raises questions regarding the accuracy of an ECG diagnosis of asystole in the pre-hospital setting‘.

Purpose of the study: Focused ultrasound is increasingly used in the emergency setting, with an ALS- compliant focused echocardiography algorithm proposed as an adjunct in peri-resuscitation care (FEEL). The purpose of this study was to evaluate the feasibility of FEEL in pre-hospital resuscitation, the incidence of potentially treatable conditions detected, and the influence on patient management.

Patients, materials and methods: A prospective observational study in a pre-hospital emergency setting in patients actively undergoing cardio-pulmonary resuscitation or in a shock state. The FEEL protocol was applied by trained emergency doctors, following which a standardised report sheet was completed, including echo findings and any echo-directed change in management. These reports were then analysed independently.

Results: A total of 230 patients were included, with 204 undergoing a FEEL examination during ongoing cardiac arrest (100) and in a shock state (104). Images of diagnostic quality were obtained in 96%. In 35% of those with an ECG diagnosis of asystole, and 58% of those with PEA, coordinated cardiac motion was detected, and associated with increased survival. Echocardiographic findings altered management in 78% of cases.

Conclusions: Application of ALS-compliant echocardiography in pre-hospital care is feasible, and alters diagnosis and management in a significant number of patients. Further research into its effect on patient outcomes is warranted.

Focused echocardiographic evaluation in life support and peri-resuscitation of
emergency patients: A prospective trial

Resuscitation. 2010 Nov;81(11):1527-33