Category Archives: ICU

Stuff relevant to patients on ICU

Upper GI bleeding guideline update

The UK’s National Institute for Health and Clinical Excellence has issued updated guidance on the management of acute upper gastrointestinal bleeding.
The initial resuscitation section recommends haemostatic blood product resuscitation for unstable patients in line with massive transfusion practice in trauma.
A risk assessment is recommended using the Blatchford score pre-endoscopy at first assessment, and the full Rockall score after endoscopy.
Consider early discharge for patients with a pre-endoscopy Blatchford score of 0.
In non-varicesal haemorrhage, acid-suppression drugs (proton pump inhibitors or H2-receptor antagonists) before endoscopy are not recommended.
Terlipressin should be given to patients with suspected variceal bleeding at presentation and continued until definitive haemostasis has been achieved, or after 5 days, unless there is another indication for its use.
Prophylactic antibiotic therapy should be offered at presentation to patients with suspected or confirmed variceal bleeding.

Click image to go to interactive pathway on NICE website

National Institute for Health and Clinical Excellence: CG141 Acute upper GI bleeding: NICE guideline
http://guidance.nice.org.uk/CG141/NICEGuidance/pdf/English

Confidential stuff – in hospital cardiac arrests

A new report describes room for improvement in the care of cardiac arrest patients in hospital1.
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
[EXPAND Click to read abstract]


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.

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3. In-hospital cardiac arrest: is it time for an in-hospital ‘chain of prevention’?
Resuscitation. 2010 Sep;81(9):1209-11
[EXPAND Click to read abstract]


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.

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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

Hypotonic Versus Isotonic Fluids After Surgery for Children

Kids in hospital with injury, infection or other illness, and those undergoing the physiological stress of surgery, produce (appropriately) elevated antidiuretic hormone levels which contribute to the risk of hyponatraemia by impairing free water excretion in the kidney.
Deaths have occurred on general paediatric and surgery wards when fluid regimens containing low concentrations of sodium (classically 0.18% or 0.225% NaCl) have resulted in hyponatraemia in children without adequate electrolyte monitoring, leading some bodies to recommend at least 0.45% NaCl solutions for maintenance fluid therapy in children.
However two recent studies1,2 on postoperative children show an increased risk of hyponatraemia even with 0.45% saline, when compared with 0.9% saline or Hartmann’s solution (Hartmann’s is similar – almost identical – to Ringer’s lactate).
I like the fact that paediatricians used Hartmann’s in one of these studies1. I have worked with several paediatricians who never use Hartmann’s, either from lack of experience or because of concern about its lactate content (not appreciating the lactate is metabolised by the liver to bicarbonate).
This is ironic, since Alexis Hartmann (1898–1964) was a paediatrician.
Want more fluid therapy irony? The ‘balanced salt solution’ used by Brits and Australasians is Hartmann’s solution – named after an American. The one used by Americans is Lactated Ringer’s solution – named after the British physician Sydney Ringer (1834-1910).
Medical history enthusiasts can read more about Hartmann and Ringer here.
1. A randomised controlled trial of Hartmann’s solution versus half normal saline in postoperative paediatric spinal instrumentation and craniotomy patients.
Arch Dis Child. 2012 Jun;97(6):491-6
[EXPAND Click to read abstract]

OBJECTIVE: To compare the difference in plasma sodium at 16-18 h following major surgery in children who were prescribed either Hartmann’s and 5% dextrose or 0.45% saline and 5% dextrose.
DESIGN: A prospective, randomised, open label study.
SETTING: The paediatric intensive care unit (650 admissions per annum) in a tertiary children’s hospital in Brisbane, Australia.
PATIENTS: The study group comprised 82 children undergoing spinal instrumentation, craniotomy for brain tumour resection, or cranial vault remodelling.
INTERVENTIONS: Patients received either Hartmann’s and 5% dextrose at full maintenance rate or 0.45% saline and 5% dextrose at two-thirds maintenance rate.
MAIN OUTCOMES MEASURES: Primary outcome measure: plasma sodium at 16-18 h postoperatively; secondary outcome measure: number of fluid boluses administered.
RESULTS: Mean postoperative plasma sodium levels of children receiving 0.45% saline and 5% dextrose were 1.4 mmol/l (95% CI 0.4 to 2.5) lower than those receiving Hartmann’s and 5% dextrose (p=0.008). In the 0.45% saline group, seven patients (18%) became hyponatraemic (Na <135 mmol/l) at 16-18 h postoperatively; in the Hartmann’s group no patient became hyponatraemic (p=0.01). No child in either fluid group became hypernatraemic.
CONCLUSIONS: The postoperative fall in plasma sodium was smaller in children who received Hartmann’s and 5% dextrose compared to those who received 0.45% saline and 5% dextrose. It is suggested that Hartmann’s and 5% dextrose should be administered at full maintenance rate postoperatively to children who have undergone major surgery in preference to hypotonic fluids.

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2. Hypotonic versus isotonic maintenance fluids after surgery for children: a randomized controlled trial
Pediatrics. 2011 Nov;128(5):857-66.
[EXPAND Click to read abstract]

OBJECTIVE: The objective of this randomized controlled trial was to evaluate the risk of hyponatremia following administration of a isotonic (0.9% saline) compared to a hypotonic (0.45% saline) parenteral maintenance solution (PMS) for 48 hours to postoperative pediatric patients.
METHODS: Surgical patients 6 months to 16 years of age with an expected postoperative stay of >24 hours were eligible. Patients with an uncorrected baseline plasma sodium level abnormality, hemodynamic instability, chronic diuretic use, previous enrollment, and those for whom either hypotonic PMS or isotonic PMS was considered contraindicated or necessary, were excluded. A fully blinded randomized controlled trial was performed. The primary outcome was acute hyponatremia. Secondary outcomes included severe hyponatremia, hypernatremia, adverse events attributable to acute plasma sodium level changes, and antidiuretic hormone levels.
RESULTS: A total of 258 patients were enrolled and assigned randomly to receive hypotonic PMS (N = 130) or isotonic PMS (N = 128). Baseline characteristics were similar for the 2 groups. Hypotonic PMS significantly increased the risk of hyponatremia, compared with isotonic PMS (40.8% vs 22.7%; relative risk: 1.82 [95% confidence interval: 1.21-2.74]; P = .004). Admission to the pediatric critical care unit was not an independent risk factor for the development of hyponatremia. Isotonic PMS did not increase the risk of hypernatremia (relative risk: 1.30 [95% confidence interval: 0.30-5.59]; P = .722). Antidiuretic hormone levels and adverse events were not significantly different between the groups.
CONCLUSION: Hypotonic Versus Isotonic Maintenance Fluids After Surgery for Children: A Randomized Controlled Trial.

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Not a pin cushion

This is the daughter of my friend. Avery is only seven months old and has survived a critical illness and is thankfully now fully recovered. Her Dad has nothing but praise for the medical and nursing staff who cared for her. But one thing could have been better. Avery endured multiple attempts at vascular access without ultrasound guidance.

If you were her parent, and you were an emergency physician with galaxy-class expertise in emergency ultrasound, how would you react? Complaints? Incident forms? Outrage?
How about education? For free. Accompanied by lavish praise for the experts who treated Avery and made her better.
Avery’s Dad is ultrasound podcaster and gentleman Dr Matt Dawson. He is offering FREE ultrasound training to anyone who wants to improve their vascular access skills.
Are there nurses, physicians, or technicians in your ED or ICU that could improve their care with this training? Please consider sending them for this training. To register for the course, and to read Avery’s full story, go to notapincushion.com.
And if you’re already comfortable with ultrasound-guided vascular access, then visit the site anyway, as there is some education here for all of us: how to turn a gut-wrenchingly distressing experience into something positive that will benefit countless others. I am thoroughly inspired.
Best wishes to an amazing family.
Cliff

End-Tidal CO2 as a Predictor of Cardiac Arrest Survival



In one of largest studies to date of prehospital capnography in cardiac arrest, an initial EtCO2 >10 mmHg (1.3 kPa) was associated with an almost five-fold higher rate of return of spontaneous circulation (ROSC). In addition, a decrease in the EtCO2 during resuscitative events of >25% was associated with a significant increase in mortality, independent of other variables known to affect outcome.

The authors conclude: “EtCO2 values should be included as important variables in protocols to terminate or continue resuscitation in the prehospital setting“.


OBJECTIVE: The objective of this study was to evaluate initial end-tidal CO2 (EtCO2) as a predictor of survival in out-of-hospital cardiac arrest.

METHODS: This was a retrospective study of all adult, non-traumatic, out-of-hospital, cardiac arrests during 2006 and 2007 in Los Angeles, California. The primary outcome variable was attaining return of spontaneous circulation (ROSC) in the field. All demographic information was reviewed and logistic regression analysis was performed to determine which variables of the cardiac arrest were significantly associated with ROSC.

RESULTS: There were 3,121 cardiac arrests included in the study, of which 1,689 (54.4%) were witnessed, and 516 (16.9%) were primary ventricular fibrillation (VF). The mean initial EtCO2 was 18.7 (95%CI = 18.2-19.3) for all patients. Return of spontaneous circulation was achieved in 695 patients (22.4%) for which the mean initial EtCO2 was 27.6 (95%CI = 26.3-29.0). For patients who failed to achieve ROSC, the mean EtCO2 was 16.0 (95%CI = 15.5-16.5). The following variables were significantly associated with achieving ROSC: witnessed arrest (OR = 1.51; 95%CI = 1.07-2.12); initial EtCO2 >10 (OR = 4.79; 95%CI = 3.10-4.42); and EtCO2 dropping <25% during the resuscitation (OR = 2.82; 95%CI = 2.01-3.97).The combination of male gender, lack of bystander cardiopulmonary resuscitation, unwitnessed collapse, non-vfib arrest, initial EtCO2 ≤10 and EtCO2 falling > 25% was 97% predictive of failure to achieve ROSC.

CONCLUSIONS: An initial EtCO2 >10 and the absence of a falling EtCO2 >25% from baseline were significantly associated with achieving ROSC in out-of-hospital cardiac arrest. These additional variables should be incorporated in termination of resuscitation algorithms in the prehospital setting.

End-Tidal CO2 as a Predictor of Survival in Out-of-Hospital Cardiac Arres
Prehosp Disaster Med. 2011 Jun;26(3):148-50

Nitrate bolus in acute heart failure

Despite intravenous nitrate boluses being used in original studies demonstrating benefit in acute heart failure1,2, I regularly meet reluctance from both physicians and nurses in the emergency department to give them.
Their resistance seems to be based on a concern for inducing hypotension, and they prefer to ‘titrate up’ an infusion.
iv nitrate options include nitroglycerin (GTN), and isosorbide dinitrate (ISDN). Studies have used ISDN 4mg every 4 mins, ISDN 3mg every 5 mins, and GTN 2mg every 3 mins3.
There are a number of reasons to avoid starting with a low rate infusion in a sick heart failure patient.
Matthew Reed highlighted cannula size as an important factor4:


If a GTN infusion is commenced at a rate of 1 ml/h, a critically unwell patient with a large cannula—for example, a grey cannula (16G) — will have to wait over 6 min for the drug to enter the body. This compares with 1.5 min for a pink cannula (20G) at the same infusion rate. If a large-diameter cannula is chosen for these patients, then a fast initial infusion rate should also be chosen to ensure that the GTN begins to act quickly.

Alistair Steel subsequently pointed out further reasons to avoid slow infusions5:


(1) mechanical slack within an infusion device may mean an infusion set at 1 ml/h will take many minutes for the driver to contact and advance the syringe plunger. For this reason, infusions should be purged before patient connection.

(2) the pharmacokinetics of the drug should be considered. At low infusion rates it will take significant time for a steady state to be achieved (a drug such as GTN, with a half-life of 2 min, would require 10 min to achieve steady state). For clinical effects to be seen quickly, a bolus should be given before commencing infusions.

(3) the use of 1 ml/h infusions (8 µg/min using a 0.5% solution) may be excessively cautious – the British National Formulary recommends a therapeutic dose range from 10 to 200 µg/min. Furthermore, there is emerging evidence that, when used for decompensated heart failure, higher doses of GTN are associated with more favourable outcomes.

(4) at low infusion rates any obstruction in the intravenous system will take a proportionally longer time to become apparent, as it will take longer for the pressure to build up and trigger the syringe pump’s high pressure alarm.
.

Now a recent study confirms such a regimen can be used safely in the elderly. ISDN 3mg bolus treatment was not associated with higher rates of hypotension in the elderly population treated for heart failure in the emergency department. Despite a small study and a retrospective design, this lends support to the practice of iv bolus nitrate therapy for acute heart failure, even in the elderly.
1. Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema
Lancet. 1998 Feb 7;351(9100):389-93
2. High-doses intravenous isosorbide dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema
J Am Coll Cardiol. 2000 Sep;36(3):832-7 Free Full Text
3. Managing acute pulmonary oedema with high or standard dose nitrate
Emerg Med J. 2009 May;26(5):357-8
4. Administering a glyceryl trinitrate infusion: big is not always best
Emerg Med J 2007;24:423-424
5. Administering a glyceryl trinitrate infusion: faster is better than slower
Emerg Med J. 2008 Jan;25(1):60
6. Isosorbide dinitrate bolus for heart failure in elderly emergency patients: a retrospective study
Eur J Emerg Med. 2011 Oct;18(5):272-5

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