Published flow rates for cannulae are derived from a test in which fluid runs through a perfectly straight cannula into an open receptacle. Laminar flow is expected in such a model in which the Hagen-Poisseuille formula tells us that flow is proportional to the fourth power of the radius. In this study manufacturers’ published flow rates were compared with an artifical vein model. Hartmann’s flowed faster than Gelofusine. For all cannulas flow was less than the manufacturers’ published rates. Although the radius was the biggest determinant of flow rate, the fourth power could not be used, suggesting a mixture of laminar and turbulent flow. The addition of pressurised infusions increased the flow rate with increasing pressure. Although the vein model used has limitations, and many other factors may influence flow rate in the clinical setting, the authors’ conclusions are helpful:
While the effect of radius is less than commonly believed, it is still important. However, clinicians should be aware of the limitations of increasing radius and use other strategies to increase flow when needed. These could include use of pressure, choice of fluid to be infused, and using multiple cannulae in parallel.
Fluid flow through intravenous cannulae in a clinical model
Anesth Analg. 2009 Apr;108(4):1198-202
Category Archives: ICU
Stuff relevant to patients on ICU
ETCO2 all over the place in trauma
In 180 intubated trauma patients in the ED, there was little correlation between arterial carbon dioxide tension (PaCO2) and end-tidal carbon dioxide levels (ETCO2) (R2 = 0.277). In fact, in those patients ventilated to the ‘normal range’ of 35-40 mmHg (4.6-5.2 kPa), PaCO2 was over 50 mmHg 30% of the time. Slightly reassuring that in isolated brain injury the correlation was better (r2 = 0.52)
The Utility of Early End-Tidal Capnography in Monitoring Ventilation Status After Severe Injury
J Trauma. 2009 Jan;66(1):26-31
Blood product ratios and survival bias
Haemostatic resuscitation of trauma patients, using high ratios of fresh frozen plasma (FFP) to packed red cells (PRBC), is growing in popularity as a result of military experience. Few data support the practice in civilian trauma. It is possible that some of the demonstrated mortality benefit is a result of survival bias: it takes time to obtain FFP, by which time severely injured patients may be dead. Therefore, those that receive large ratios of FFP:PRBC must have survived long enough to receive it. In other words FFP doesn’t lead to survival, but survival leads to FFP. Some evidence in favour of this explanation is provided on a study of 134 patients in the Journal of Trauma. Reanalysing data to correct for survival bias made an apparently significant survival benefit from high FFP:PRBC ratios go away. An interesting paper, although unlikely to dissuade us from paying attention to coagulopathy in trauma. I suspect the debate on optimal blood product resuscitation will be around for a while.
The Relationship of Blood Product Ratio to Mortality: Survival Benefit or Survival Bias?
J Trauma. 2009 Feb;66(2):358-62
Sodium lactate for raised ICP
Lactate may be an important metabolic substrate for injured brain and sodium lactate may have beneficial effects on cerebral oedema and cerebral blood flow. Sodium lactate was compared with 20% mannitol in severely brain injured patients with cranial hypertension in a randomised controlled trial. Sodium lactate was more likely to lower ICP, and to have a sustained effect on ICP. A nonsignificant improvement in one year outcome was seen with sodium lactate, although the study was not powered for this endpoint. These promising findings should prompt a larger multicentre study.
Sodium lactate versus mannitol in the treatment of intracranial hypertensive episodes in severe traumatic brain-injured patients
Intensive Care Med. 2009 Mar;35(3):471-9
Is defib danger overstated
No rescuer or bystander has ever been seriously harmed by receiving an inadvertent shock while in direct or indirect contact with a patient during defibrillation. New evidence suggests that it might even be electrically safe for the rescuer to continue chest compressions during defibrillation if self-adhesive defibrillation electrodes are used and examination gloves are worn. This paper reviews the existing evidence, but warns more definite data are needed to make absolutely sure that there is no risk before defibrillation safety recommendations are changed.
Is external defibrillation an electric threat for bystanders?
Resuscitation. 2009 Apr;80(4):395-401
Transfusion and ARDS
Blood transfusion in trauma is a risk factor for acute respiratory distress syndrome (ARDS). An analysis of 14070 patients in a trauma database showed that 521 (4.6%) developed ARDS. Logisitc regression analysis demonstrated that, independent of injury type, injury severity, or pneumonia, (1) early PRBCs transfusion of more than 5 units during the first 24 h of hospital admission predicted ARDS and (2) each unit of PRBCs transfused early after admission increased the risk of ARDS by 6%.
Early packed red blood cell transfusion and acute respiratory distress syndrome after trauma.
Anesthesiology. 2009 Feb;110(2):351-60
Delays to neurosurgery
Further evidence from the UK shows that patients with acute traumatic brain injury suffer delays in the neurosurgical evacuation of intracranial haematomas which are increased from an average of 3.7 hours to 5.4 hours if they have to undergo interhospital transfer. Coordinated regional trauma systems please!
A prospective study of the time to evacuate acute subdural and extradural haematomas.
Anaesthesia. 2009 Mar;64(3):277-81
Ventilator-associated tracheobronchitis
Ventilator associated pneumonia (VAP) is a well recognised complication of ICU care, but colonisation and infection further up the respiratory tract may be a risk factor for VAP that is worth identifying and treating. Ventilator-associated tracheobronchitis (VAT) has similar diagnostic criteria to VAP, but without the radiographic infiltrates.
Ventilator-associated tracheobronchitis: the impact of targeted antibiotic therapy on patient outcomes
Chest. 2009 Feb;135(2):521-8
oxygen for myocardial infarction – harmful?
Hyperoxia may reduce coronary artery blood flow, increase systemic vascular resistance, and decrease cardiac output. This paper argues that if the baseline arterial oxygen saturations are >90%, high concentration oxygen does not increase oxygen transport, as the reductions in cardiac output are in excess of the increase in oxygen content. The balance of the limited evidence that exists suggests that the routine use of oxygen in uncomplicated MI (no failure or shock) may increase infarct size and possibly increase the risk of mortality, owing to its haemodynamic effects, including a reduction in coronary blood flow.
Routine use of oxygen in the treatment of myocardial infarction: systematic review
Heart. 2009 Mar;95(3):198-202
End expiratory occlusion
OBJECTIVE: During mechanical ventilation, inspiration cyclically decreases the left cardiac preload. Thus, an end-expiratory occlusion may prevent the cyclic impediment in left cardiac preload and may act like a fluid challenge. We tested whether this could serve as a functional test for fluid responsiveness in patients with circulatory failure.
DESIGN: Prospective study.
SETTING: Medical intensive care unit.
PATIENTS: Thirty-four mechanically ventilated patients with shock in whom volume expansion was planned.
INTERVENTION: A 15-second end-expiratory occlusion followed by a 500 mL saline infusion.
MEASUREMENTS: Arterial pressure and pulse contour-derived cardiac index (PiCCOplus) at baseline, during passive leg raising (PLR), during the 5-last seconds of the end-expiratory occlusion, and after volume expansion.
MAIN RESULTS: Volume expansion increased cardiac index by >15% (2.4 +/- 1.0 to 3.3 +/- 1.2 L/min/m, p < 0.05) in 23 patients ("responders"). Before volume expansion, the end-expiratory occlusion significantly increased arterial pulse pressure by 15% +/- 15% and cardiac index by 12% +/- 11% in responders whereas arterial pulse pressure and cardiac index did not change significantly in nonresponders. Fluid responsiveness was predicted by an increase in pulse pressure >or=5% during the end-expiratory occlusion with a sensitivity and a specificity of 87% and 100%, respectively, and by an increase in cardiac index >or=5% during the end-expiratory occlusion with a sensitivity and a specificity of 91% and 100%, respectively. The response of pulse pressure and cardiac index to the end-expiratory occlusion predicted fluid responsiveness with an accuracy that was similar to the response of cardiac index to PLR and that was significantly better than the response of pulse pressure to PLR (receiver operating characteristic curves area 0.957 [95% confidence interval [CI:] 0.825-0.994], 0.972 [95% CI: 0.849-0.995], 0.937 [95% CI: 0.797-0.990], and 0.675 [95% CI: 0.497-0.829], respectively).
CONCLUSIONS:The hemodynamic response to an end-expiratory occlusion can predict volume responsiveness in mechanically ventilated patients.
Predicting volume responsiveness by using the end-expiratory occlusion in mechanically ventilated intensive care unit patients.
Crit Care Med. 2009 Mar;37(3):951-6