Predicting volume responsiveness

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.

 
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
Abstract

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
Abstract

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
Abstract

Hypothermia as an inotrope

This small study supports the hypothesis that therapeutic hypothermia can have positive inotropic effects in patients with cardiogenic shock of ischaemic or non-ischaemic origin.

Cooling resulted in a temperature-dependent decrease in heart rate and temperature-dependent increases in stroke volume index, cardiac index, mean arterial pressure, and cardiac power output. These changes reversed when the patients were rewarmed.

The authors summarise as follows:

In summary, our studies demonstrate that moderate hypothermia is feasible and safe also for patients in cardiogenic shock.

Improved cardiac performance may contribute to the considerable decrease of mortality for survivors of cardiac arrest, and the use of hypothermia can be recommended for patients with a clear indication for cooling and poor cardiac performance.

Moreover, hypothermia might be considered as a positive inotropic intervention during cardiogenic shock.

Moderate hypothermia for severe cardiogenic shock (COOL Shock Study I & II)
Resuscitation. 2013 Mar;84(3):319-25.
Abstract

Don’t ignore the diastolic

Most of us are pretty good at spotting hypotension and activating help or initiating therapy.

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
Click to read abstract

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

Thrombolytic Therapy in Unstable Patients with PE

Most of us would give strong consideration to giving thrombolytics to patients with massive pulmonary embolism (PE), which is in keeping with many guidelines. Some physicians remain reluctant to do so, often citing the lack of good evidence. It is true that large scale RCTs have not been done in this population. The authors of this recent retrospective study state:

There are no definitive trials that prove the value of thrombolytic therapy in unstable patients with pulmonary embolism. It is extremely remote that a randomized controlled trial will be performed in the future. We therefore analyzed the database of the Nationwide Inpatient Sample to test the hypothesis that thrombolytic therapy reduces case fatality rate in unstable patients with acute pulmonary embolism.

They demonstrate a striking difference in mortality when thrombolysis is given to unstable patients with PE, which is further reduced with the addition of a vena cava filter. ‘Unstable’ was defined as having a listed code for shock or ventilator dependence.

Associated comorbid conditions were more often present in those who did not receive thrombolytic therapy than in those who did. However in their discussion the authors add:

Although unstable patients who received thrombolytic therapy had fewer comorbid conditions than those who did not, this would not explain the difference in case fatality rate because unstable patients with a primary diagnosis of pulmonary embolism and none of the comorbid conditions…also showed a lower case fatality rate with thrombolytic therapy. Therefore, differences in comorbid conditions in this group were eliminated as a possible cause of the lower case fatality rate in unstable patients who received thrombolytic therapy.

They round off their conclusion with:

Despite the marked reduction of case fatality rate with thrombolytic therapy in unstable patients, only 30% of unstable patients received it, and the proportion receiving thrombolytic therapy is diminishing. On the basis of these data, thrombolytic therapy in combination with a vena cava filter in unstable patients with acute pulmonary embolism seems indicated.

Many thanks to Dr Daniel Horner for highlighting this paper.

BACKGROUND: Data are sparse and inconsistent regarding whether thrombolytic therapy reduces case fatality rate in unstable patients with acute pulmonary embolism. We tested the hypothesis that thrombolytic therapy reduces case fatality rate in such patients.

METHODS: In-hospital all-cause case fatality rate according to treatment was determined in unstable patients with pulmonary embolism who were discharged from short-stay hospitals throughout the United States from 1999 to 2008 by using data from the Nationwide Inpatient Sample. Unstable patients were in shock or ventilator dependent.

RESULTS: Among unstable patients with pulmonary embolism, 21,390 of 72,230 (30%) received thrombolytic therapy. In-hospital all-cause case fatality rate in unstable patients with thrombolytic therapy was 3105 of 21,390 (15%) versus 23,820 of 50,840 (47%) without thrombolytic therapy (P< .0001). All-cause case fatality rate in unstable patients with thrombolytic therapy plus a vena cava filter was 505 of 6630 (7.6%) versus 4260 of 12,850 (33%) with a filter alone (P<.0001). Case fatality rate attributable to pulmonary embolism in unstable patients was 820 of 9810 (8.4%) with thrombolytic therapy versus 1080 of 2600 (42%) with no thrombolytic therapy (P<.0001). Case fatality rate attributable to pulmonary embolism in unstable patients with thrombolytic therapy plus vena cava filter was 70 of 2590 (2.7%) versus 160 of 600 (27%) with a filter alone (P<.0001).

CONCLUSION: In-hospital all-cause case fatality rate and case fatality rate attributable to pulmonary embolism in unstable patients was lower in those who received thrombolytic therapy. Thrombolytic therapy resulted in a lower case fatality rate than using vena cava filters alone, and the combination resulted in an even lower case fatality rate. Thrombolytic therapy in combination with a vena cava filter in unstable patients with acute pulmonary embolism seems indicated.

Thrombolytic Therapy in Unstable Patients with Acute Pulmonary Embolism: Saves Lives but Underused
Am J Med. 2012 May;125(5):465-70

Passive leg raise predicted fluid responsiveness in kids

Passive leg raising (PLR) is a great ‘free reversible fluid challenge’ to see if a shocked or hypotensive patient is likely to respond to volume therapy. A new study assesses its applicability in children.

PLR predicted fluid responders with 85% specificity but a lack of response did not rule out fluid responsiveness. Also, the effect of the PLR on cardiac index measured by echocardiography was the only way of predicting response – there was no relation to the more easily monitored effects of PLR on systolic blood pressure or heart rate.

Want to learn how to measure cardiac output using ultrasound? Mike Mallin from the Emergency Ultrasound Podcast shows you how here

OBJECTIVE: Fluid challenge is often used to predict fluid responsiveness in critically ill patients. Inappropriate fluid expansion can lead to some unwanted side effects; therefore, we need a noninvasive predictive parameter to assess fluid responsiveness. We want to assess the hemodynamic parameter changes after passive leg raising, which can mimic fluid expansion, to predict fluid responsiveness in pediatric intensive care unit patients and to get a cutoff value of cardiac index in predicting fluid responsiveness in pediatric patients.

DESIGN: Nonrandomized experimental study.

SETTING: Tertiary academic pediatric intensive care.

PATIENTS: Children admitted to pediatric intensive care.

INTERVENTION: Hemodynamic parameters were assessed at baseline, after passive leg raising, at second baseline, and after volume expansion (10 mL/kg normal saline infusion over 15 mins).

MEASUREMENTS AND MAIN RESULTS: We measured the heart rate, systolic blood pressure, and stroke volume and cardiac index using Doppler echocardiography. The hemodynamic parameter changes induced by passive leg raising were monitored. Among 40 patients included in the study, 20 patients had a cardiac index increase of ≥10% after volume expansion (responders). Changes in heart rate, systolic blood pressure, and stroke volume after passive leg raising did not significantly relate to the response to volume expansion. There was significant relation between changes in cardiac index to predict fluid responsiveness (p = .012, r = .22, 95% confidence interval 1.529 to 31.37). A cardiac index increase by ≥10% induced by passive leg raising predicted preload-dependent status with sensitivity of 55% and specificity of 85% (area under the curve 0.71 ± 0.084, 95% confidence interval 0.546-0.874).

CONCLUSION: The concomitant measurements in cardiac index changes after the passive leg raising maneuver can be helpful in predicting who might have an increase in cardiac index with subsequent fluid resuscitation.

The role of passive leg raising to predict fluid responsiveness in pediatric intensive care unit patients.
Pediatric Critical Care Medicine. 13(3):e155-e160, May 2012

Non-invasive BP in shock

In the management of the shocked patient, we sometimes get a little fixated on the need for an arterial line. This is in part due to previous studies suggesting non-invasive blood pressure (NIBP) measurements were inaccurate in the critically ill. This appears no longer to be the case with modern oscillometric devices and carefully chosen cuff sizes. This recent study showed mean arterial pressure (MAP) measured non-invasively from the arm closely correlated with invasive measurements. NIBP was effective at identifying hypotension and recording the response to therapy. Although patients with severe occlusive arterial disease were excluded, the study did include a number of shocked patients on vasoactive therapies.

Systolic and diastolic pressures were not accurate. This should not be surprising since, as the authors explain:

“oscillometric devices directly measure the MAP and only extrapolate systolic arterial pressure and diastolic arterial pressure, using proprietary algorithms”

Thia study suggests that NIBP measurement of MAP from the arm is accurate but, if contraindicated, the ankle (or even the thigh in older sedated patients) may be a suitable alternative site permitting a reliable detection of hypotensive and therapy-responding patients.

OBJECTIVE: In the critically ill, blood pressure measurements mostly rely on automated oscillometric devices pending the intra-arterial catheter insertion or after its removal. If the arms are inaccessible, the cuff is placed at the ankle or the thigh, but this common practice has never been assessed. We evaluated the reliability of noninvasive blood pressure readings at these anatomic sites.

DESIGN: Prospective observational study.

SETTING: Medical-surgical intensive care unit.

PATIENTS: Patients carrying an arterial line with no severe occlusive arterial disease.

INTERVENTION: Each patient underwent a set of three pairs of noninvasive and intra-arterial measurements at each site (arm, ankle, thigh [if Ramsay sedation scale >4]) and, in case of circulatory failure, a second set of measurements after a cardiovascular intervention (volume expansion, change in catecholamine dosage).

MEASUREMENTS AND MAIN RESULTS: In 150 patients, whatever the cuff site, the agreement between invasive and noninvasive readings was markedly higher for mean arterial pressure than for systolic or diastolic pressure. For mean arterial pressure measurement, arm noninvasive blood pressure was reliable (mean bias of 3.4 ± 5.0 mm Hg, lower/upper limit of agreement of -6.3/13.1 mm Hg) contrary to ankle or thigh noninvasive blood pressure (mean bias of 3.1 ± 7.7 mm Hg and 5.7 ± 6.8 mm Hg and lower/upper limits of agreement of -12.1/18.3 mm Hg and -7.7/19.2 mm Hg, respectively). During acute circulatory failure (n = 83), arm noninvasive blood pressure but also ankle and thigh noninvasive blood pressure allowed a reliable detection of 1) invasive mean arterial pressure 10%) increase in invasive mean arterial pressure after a cardiovascular intervention (area under the receiver operating characteristic curve of 0.99 [0.92-1], 0.90 [0.80-0.97], and 0.96 [0.87-0.99], respectively).

CONCLUSION: In our population, arm noninvasive mean arterial pressure readings were accurate. Either the ankle or the thigh may be reliable alternatives, only to detect hypotensive and therapy-responding patients.

Noninvasive monitoring of blood pressure in the critically ill: Reliability according to the cuff site (arm, thigh, or ankle)
Crit Care Med. 2012 Apr;40(4):1207-13

The REAL Shocked Patient

I promised to put some summary notes on the site for those who attended my talk on ‘The REAL Shocked Patient’ for the Australian College of Ambulance Professionals on Tuesday 21st February 2012, so here they are:

Shocked patients are important – they comprise most of the ‘talk and die’ caseload that preoccupies pub conversations between emergency physicians

It’s easy to mistake these patients as less sick than, say, hypoxic ones, but oxygen delivery to the tissues doesn’t just depend on oxygen!

Here’s a dead wombat – someone in the audience knew a worrying amount about wombat anuses.

The 4 Hs and 4 Ts aren’t a very cognitively practical mnemonic for the causes of PEA arrest (which is an extreme form of hypotension)

I prefer the ’3 plus 3′ rule, which breaks down the causes into three – volume, pump, and obstruction. Obstruction is further broken down into three causes, being tension pneumothorax, cardiac tamponade, and pulmonary embolism:

Let’s look at some cases of shock caused by volume deficit, pump falure, or one of the three causes of obstruction to the circulation:

Case 1: The hypotensive motorcyclist
His low back pain suggested pelvic fracture
Think of ‘blood on the floor and four more’ (chest, abdomen, pelvis/retroperitoneum, long bones) and consider non-bleeding causes such as neurogenic (spinal injury), tension pneumothorax, cardiac tamponade, and finally medical causes/iatrogenic (drug) causes.
Don’t underestimate the importance of pelvis and limb splinting as a haemorrhage control technique in blunt trauma
Ultrasound in flight made thoracic or abdominal bleeding very unlikely, and ruled out tamponade and pneumothorax

Although he was hypotensive, no fluids were given, as he was mentating normally and peripherally well perfused, with a radial pulse. If we gave fluid, we would titrate to the presence of a radial pulse (in blunt trauma) but we don’t want to ‘pop the clot’ by elevating the BP, or make him less able to form effective clots by diluting his blood with crystalloid.

Mortality in trauma sharply rises with systolic BP below 105-110, so recalibrate your definition of hypotension in terms of when you might be concerned, and which patients may benefit from triage to a trauma centre.

Case 2: The child crushed by a wall
Caution regarding lower limb infusions in patients with abdominal / pelvic injuries – the fluid may not get to the heart.

The classification of shock into four classes is crap. Never let the absence of a tachycardia reassure you.

Intraosseous is awesome, and EZ-IO has the best track record by far.

Case 3: The boy stabbed in the upper thigh
In penetrating limb trauma, prehospital options include pressure, elevation, tourniquet, and haemostatic dressings. Foley catheters have been used successfully in transition zones such as the neck or groin.

Case 4: Haematemesis
Should we apply the same principles of permissive hypotension to patients with ‘medical’ bleeding?
The Trendelenburg position doesn’t make a lot of sense – no need to head down the patient, although the act of elevating the legs may ‘autoinfuse’ a bolus of blood to the core circulation, and is recommended by some bodies as a first aid manoeuvre for hypotensive patients in the field prior to iv fluids.

Case 5: The overdose patient with a low blood pressure but otherwise fine.
When don’t I Worry about hypotension? When the patient is:

• With it
• Warm peripherally
• Weeing
• and (in hospital) Without a raised lactate

Case 6: Two cases of pump failure: STEMI and complete heart block
Adrenaline infusions can be simply made with a 1mg 1:10000 minijet diluted in a litre of saline and dripped through a peripheral line titrated to BP / HR / mentation / pulses.
In complete heart block (or other bradycardias) with hypotension, percussion pacing is an option of you don’t have access to transcutaneous or transvenous pacing. If you get capture, it’s as effective in terms of stroke volume as a pacing wire.

Case 7: Obstructive shock – tamponade cases
…with resolution of hypotension after drainage by emergency physicians who identified the tamponade on ultrasound, even though they didn’t suspect it clinically. It can be a surprise!

Case 8: Obstructive shock – tension pneumothorax
Patients are often agitated and won’t lie flat. They may complain of ‘tight’ breathing. Crackles and/or wheezes may be heard. The classic description of deviated trachea, absent breath sounds, and hyperresonance are the exception, not the rule. Be suspicious and always palpate for subcutaneous emphysema.
Don’t assume a needle decompression will work – there is debate about the best site but in some adults a standard needle won’t reach the pleural space. If you need to place more than one needle, go for it. As physicians, we do thoracostomies to ensure we’ve hit the spot.

Case 9: Obstructive shock – pulmonary embolism
A tough one prehospital, as the hypotensive ones need fibrinolysis. Fluid may help the hypotension but too much can overdistend the right ventricle which can then impair left ventricular filling, and worsen the patient’s circulatory state. Once again, ultrasound may be invaluable in highlighting PE as a possible cause for shock.

Case 10: Penetrating trauma to the ‘box’ – chest and upper abdomen.
If these patients arrest due to tamponade, early (< 10 minutes) clamshell thoracotomy can be life saving, which means it may need to be done pre-hospital by a HEMS physician to provide a chance of survival. Be on the look out for these and if in doubt activate a medical team (in New South Wales). Like with tension pneumothorax, these patients may be extremely agitated as a manifestation of their shock.

Case 11: Confused elderly male with pyrexia and smelly urine who appears ostensibly ‘normotensive’
…but how many 82 year olds do you know with a BP of 110/57? His acute confusion may be a manifestation of shock and he needs aggressive evaluation in hospital including a lactate measurement. Don’t be afraid to give this guy fluids in the field – you can make a big difference here.

Here are five of the myths I promised to expose:

So…shocked patients can talk and die. Don’t let that happen. Shocked patients can be normotensive, and hypotensive patients might not be shocked. Have a plan for how you might evaluate the 3+3 causes in your setting and what you can use from your medication and equipment list to manage volume, pump, and obstruction issues. You will save many lives if you become a serious shock detective.

Vasopressin – what it does and doesn’t do

The current Surviving Sepsis campaign guidelines recommend that vasopressin should not be administered as the initial vasopressor in septic shock, and that vasopressin at constant dosage of 0.03 units/min may be added to norepinephrine with anticipation of an effect equivalent to that of norepinephrine alone. European intensivists conducted a systematic review to determine vasopressin’s risks and benefits in vasodilatory shock. There was no demonstrated survival benefit but its use is associated with a significant reduction in norepinephrine requirement.

Interestingly, the authors point out: ‘Low-dose vasopressin may help to restore blood pressure in patients with hypotension refractory to catecholamines, and may favor pulmonary vasodilation and increase glomerular filtration rate and plasma cortisol levels’.

My take home: consider its use if an apparent vasodilatory shock state is refractory to catecholamines, but don’t stress if you don’t have access to it (or it will complicate practical aspects of organising resuscitation and transfer), since there’s still no clear evidence for outcome benefit.

OBJECTIVE:
To examine the benefits and risks of vasopressin or its analog terlipressin for patients with vasodilatory shock.

DATA SOURCE:
We searched the CENTRAL, MEDLINE, EMBASE, and LILACS databases (up to March 2011) as well as reference lists of articles and proceedings of major meetings; we also contacted trial authors. We considered randomized and quasirandomized trials of vasopressin or terlipressin versus placebo or supportive treatment in adult and pediatric patients with vasodilatory shock. The primary outcome for this review was short-term all-cause mortality.

STUDY SELECTION:
We identified 10 randomized trials (1,134 patients). Six studies were considered for the main analysis on mortality in adults.

DATA EXTRACTION AND SYNTHESIS:
The crude short-term mortality was 206 of 512 (40.2%) in vasopressin/terlipressin-treated patients and 198 of 461 (42.9%) in controls [six trials, risk ratio (RR) = 0.91; 95% confidence interval (CI) 0.79-1.05; P = 0.21; I (2) = 0%]. There were 49 of 463 (10.6%) patients with serious adverse events in the vasopressin/terlipressin arm and 51 of 431 (11.8%) in the control arm (four trials, RR = 0.90; 95% CI 0.49-1.67; P = 0.75; I (2) = 26%). Metaregression analysis showed negative correlation between vasopressin dose and norepinephrine dose (P = 0.03).

CONCLUSIONS:
Overall, use of vasopressin or terlipressin did not produce any survival benefit in the short term in patients with vasodilatory shock. Physicians may value the sparing effects of vasopressin/terlipressin on norepinephrine requirement given its apparent safe profile.

Vasopressin for treatment of vasodilatory shock: an ESICM systematic review and meta-analysis
Intensive Care Med. 2012 Jan;38(1):9-19

Circulatory support in cardiogenic shock

An editorial¹ reviewing options for circulatory support in patients with cardiogenic shock argues that traditional inotrope therapy may be replaced by newer alternatives that have a less detrimental effect on myocardial oxygen demand.

Newer inotropic agents include levosimendan, istaroxime, and omecamtiv mecarbil. Mechanical therapies include intra-aortic balloon pumps (IABP), ventricular assist devices (VAD), and extracorporeal membrane oxygenation (ECMO).

Intra-aortic balloon pump in the resus room

Levosimendan is an inodilator, with the following characteristics:

• stabilises the myocardial calcium-troponin C complex
• activates adenosine triphosphate (ATP)-sensitive potassium channels in vascular smooth muscle and cardiac mitochondria,
• acts as a traditional phosphodiesterase inhibitor at higher doses
• improved cardiac output and a reduction in filling pressures compared with dobutamine
• may also improve diastolic function by increasing relaxation rate
• modulates the neuroendocrine response to heart failure by reducing brain natriuretic peptide levels
• has anti-apoptotic and anti-inflammatory effects
• renal function may also improve
• is associated with a similar risk of ventricular arrhythmias to dobutamine
• increases risk of new onset atrial fibrillation
• has conflicting literature surrounding mortality
• has shown a lack of consistent outcome benefits in studies
• may be useful in postmyocardial infarction cardiac dysfunction and septic shock through increasing coronary flow and attenuating inflammatory activation, respectively².

Istaroxime, a novel inotrope with positive lusitropic (cardiac relaxant) effects³:

• is an inhibitor of the sodium-potassium-ATPase (resulting, like digoxin, in elevated intracellular calcium) with additional stimulatory effects on the sarcoplasmic reticulum calcium pump (SERCA)
• provides a dose-dependant increase in cardiac output without significant change in heart rate or arrhythmia
• in one study reducesd pulmonary capillary wedge pressure, increased systolic blood pressure, and reduced heart rate and left ventricular end-diastolic volume
• requires further clinical evaluation.

Omecamtiv mecarbil is a cardiac myosin activator. This new drug:

• improves myocardial contraction by increasing the hydrolysis of ATP by myosin ATPase
• this produces the power stroke between actin and myosin and subsequent shortening of sarcomere length
• in phase-2a studies in patients with systolic heart failure it demonstrated improved stroke volume without an increase in heart rate, although cardiac ischaemia emerged at high plasma concentrations^4,5.

1. Do inotropes really have a future?
Anaesthesia. 2011 Nov;66(11):972-6.

2. Inotropes in cardiac patients: update 2011
Curr Opin Crit Care. 2010 Oct;16(5):432-41
Abstract

3. Combining SERCA2a activation and Na-K ATPase inhibition: a promising new approach to managing acute heart failure syndromes with low cardiac output.
Discov Med. 2011 Aug;12(63):141-51 Free Full Text
Abstract

4. Dose-dependent augmentation of cardiac systolic function with the selective cardiac myosin activator, omecamtiv mecarbil: a first-in-man study
Lancet. 2011 Aug 20;378(9792):667-75
Abstract

5. The effects of the cardiac myosin activator, omecamtiv mecarbil, on cardiac function in systolic heart failure: a double-blind, placebo-controlled, crossover, dose-ranging phase 2 trial
Lancet. 2011 Aug 20;378(9792):676-83
Abstract

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