How-To: Preoxygenation via SIMV Noninvasive Ventilation

Inspired by a morning report discussion from our very own Lara Vanyo on preoxygenation strategies, I thought it would helpful for a brief run-down on the button-pushing needed to perform preoxygenation by way of noninvasive ventilation. The video below is specific to the vents we have at Sinai–Weingart and Elmer have already shown us how to do the same at Elmhurst on EMCrit.

How-to Video for SIMV Noninvasive Ventilation for Preoxygenation


Picture of SIMV Home Screen on Puritan Bennett 840

Explanation of the Puritan Bennett 840 SIMV Buttons and Settings:

Introduction: The pressure control settings and pressure support settings are the two parts of the NIV settings. The pressure control part runs in the background delivering breaths when the patient is not triggering. The pressure support settings are used when the patient triggers a spontaneous breath.

Rate: Especially important in the hypercapnic patient to control the CO2. The above setting is at 18 breaths per minute, but can be whatever you want.

Pressure Control Settings: This section is for the controlled breaths. PI is the inspiratory pressure that is above PEEP. TI is the inspiratory time that determines how fast a breath is delivered for a pressure control breath. The above setting is IPAP 13 cm H20 and PEEP 3 cm H20 (the Pis above PEEP). The time for controlled breath is 0.9 seconds.

Pressure Support Settings: This section is for the spontaneous breaths (hence support) taken by the patient above the background controlled rate of pressure control. Psupp is the support given to the patient in addition to the spontaneous breath. TI SPONT is the inspiratory time for a supported breath (in contrast to TI of the aforementioned pressure control breath). It is reasonable to set this somewhere between 2.0 and 3.0 seconds depending on patient comfort.

Flow Trigger: VSENS is the flow trigger threshold required prior to breath delivery.

Why pressure control versus volume control for noninvasive ventilation for preoxygenation? After discussing with our respiratory therapist, Judah, volume control is less ideal in noninvasive compared to invasive ventilation as the potential for mask leak in noninvasive introduces potential to inadequately ventilate the patient.

Thanks to Judah, our respiratory therapist, as well as to Dr. Courtney Cassella for the assistance.

That Vitamin C in Sepsis Newsflash

A number of really bright people are still unsure of what to make about the vitamin C, steroids and thiamine newsflash that’s taken Twitter by storm yesterday. At Sinai here we’re the curious types, so we chatted with our pharmacist who similarly didn’t know what to make of the headlines given the lack of a randomized controlled trial. What follows is some of the ground work that’s been done on animal studies and on the molecular level for vitamin C–just to catch us all up to speed while the news / evidence develops. The EMCrit and PulmCrit posts are certainly deeper dives into the purported vitamin C deficiency abnormalities of sepsis–though, normal is often a philosophical debate. Who knows what the bottom line is at this point given the limited evidence, but the following should be informative background knowledge.

 

Most of this is from the Wilson 2009 paper that predates the recent Marik sepsis media storm:

 

Endothelial health

  • Vitamin C modulates endothelial signaling.
  • Improves microvascular function, capillary blood flow and microvascular permeability barrier.
  • In vitro, vitamin C attenuates the lipopolysaccharide (LPS)-mediated increased endothelial permeability (Dimmler 1995).

 

Capillary blood flow

  • Improves the maldistribution of blood flow
    • The maldistribution initially seen in sepsis is characterized by decreased density of the perfused capillaries with a corresponding increase in the proportion of non-perfused capillaries
    • There is decreased availability of nitric oxide (NO) in endothelial cells / platelets. NO appears to keep microvessels patent.
      • There is decreased NO available inside septic endothelial cells and platelets. This may be secondary to reactive oxygen species.
      • Bolus injection of vitamin C immediately after septic insult improves the capillary blood flow in cecal ligation and puncture rat skeletal muscle.

 

 

Vit C and endogenous vasoactive compounds

  • Vit C may increase vasomotor responsiveness by increasing endogenous synthesis of norepinephrine and vasopressin.
  • Glucocorticoids and vit C may act synergistically inducing SVCT to increase vit C uptake intracellularly and restore glucocorticoid receptor function.

 

 

References

Wilson JX. Mechanism of action of vitamin C in sepsis: ascorbate modulates redox signaling in endothelium. Biofactors. 2009;35(1):5-13.

Wilson JX. Evaluation of vitamin C for adjuvant sepsis therapy. Antioxid Redox Signal 2013;19:2129.

Giving tPA to a patient on aspirin? What about aspirin and Plavix?

Does it matter if my patient getting tPA is on prestroke antiplatelets?

 

The neurology and ED teams have decided to give tissue plasminogen activator (tPA). As an outpatient, the patient is on aspirin and clopidogrel dual antiplatelet therapy. Does it matter that they’re on aspirin and Plavix? Does prestroke antiplatelet therapy in acute ischemic stroke interact with tPA? Contraindications for the use of tPA in acute ischemic stroke have cited coagulopathies as risk factors for bad outcomes in thrombolysis. Specifically, an elevated INR > 1.7 has been listed as a contraindication for the use of tPA in acute ischemic stroke. But, what about antiplatelets? Prestroke antiplatelets have been the subject of a recent meta-analysis by Luo et al to evaluate outcomes of modified Rankin Score (mRS), symptomatic intracranial hemorrhage (sICH) and mortality in the setting of thrombolysis.

 

As the comorbidities between cardiac disease and cerebrovascular disease often overlap, ischemic stroke patients getting tPA may commonly be taking aspirin monotherapy or aspirin-clopidogrel combination therapy. As expected, Luo et al found the risk of sICH was higher in those patients on aspirin-clopidogrel dual therapy (OR 1.88, 95%CI 1.18-3.00). Despite this increased risk in bleeding, prestroke aspirin-clopidogrel dual therapy did not translate into higher mortality nor higher risk for unfavorable mRS. Prestroke aspirin monotherapy did not show any increased risks for mortality nor sICH; however, the odds ratio surprisingly trended towards benefit in terms of favorable mRS (OR 1.11, 95%CI 1.00-1.24).

 

The take-home point of the meta-analysis appears to be that prestroke aspirin-clopidogrel dual therapy puts patients at increased risk for sICH; however, this does not appear to translate into appreciable changes in functional outcome or mortality. Prestroke aspirin monotherapy does not confer this increased risk of sICH or mortality and may even trend towards beneficial functional mRS outcomes.

 

Thanks to Dr. Cappi Lay for the academic discussion on the above topic.

 

References

Luo S, Zhuang M, Zeng W, Tao J. Intravenous Thrombolysis for Acute Ischemic Stroke in Patients Receiving Antiplatelet Therapy: A Systematic Review and Meta-analysis of 19 Studies. J Am Heart Assoc. 2016;5(5)

That Prolonged QT Warning?! Magnesium for Cardiac Arrhythmias

You get a pop-up warning in the electronic medical record about potentially adverse interaction with a prolonged QT interval. What’s the risk, right? Afraid of a little torsades de pointes? Can’t we just give some prophylactic magnesium and call it a day? Let’s see if there’s any literature out there…

First off, let’s review magnesium. A prominent role of magnesium in the body is functioning as a de facto calcium antagonist which will inhibit the torsades de pointes mechanism.1 Furthermore, it’s part of the treatment for digoxin-induced arrhythmias in addition to the antibody fragments. Though not classically an antiarrhythmic, magnesium may convert some arrhythmias and prior work shows low magnesium may be proarrhythmogenic.2

Hypermagnesium is relatively uncommon, especially in the critically ill. However, if it does occur, toxicity manifests as neuromuscular symptoms or EKG changes, starting with widening of the QRS.1 Severe magnesium toxicity may lead to cardiac arrest but can be treated with calcium gluconate or dialysis in addition to standard resuscitative interventions.

Hypomagnesium is more common and is seen in 65% of intensive care patients.3 More pertinent to the undifferentiated ED patient, we consider administering magnesium when attempting to avert ventricular arrhythmias. For torsades de pointes, 2g of magnesium sulfate is the drug of choice. Though solid clinical data is lacking, small studies have demonstrated suppression of monomorphic ventricular tachycardia.4 A meta-analysis by Shiga et al in 2004 showed how it has potential (at least in the cardiac surgery population) to be used prophylactically to avert supraventricular and ventricular arrhythmias.5 So, in short, it’s unclear how low our threshold for giving prophylactic magnesium should be when there’s risk of prolonged QT. Strong evidence is lacking; however, the cardiac surgery population appears to get some benefit.

References
1. Herroeder S, Schönherr ME, De hert SG, Hollmann MW. Magnesium–essentials for anesthesiologists. Anesthesiology. 2011;114(4):971-93.
2. Moran JL, Gallagher J, Peake SL, Cunningham DN, Salagaras M, Leppard P: Parenteral magnesium sulfate versus amiodarone in the therapy of atrial tachyarrhythmias: A prospective, randomized study. Crit Care Med 1995; 23:1816–24
3. Rubeiz GJ, Thill-Baharozian M, Hardie D, Carlson RW: Association of hypomagnesemia and mortality in acutely ill medical patients. Crit Care Med 1993; 21:203–9Rubeiz, GJ Thill-Baharozian, M Hardie, D Carlson, RW
4. Ceremuzynski L, Gebalska J, Wolk R, Makowska E: Hypomagnesemia in heart failure with ventricular arrhythmias. Beneficial effects of magnesium supplementation. J Intern Med 2000; 247:78–86
5. Shiga T, Wajima Z, Inoue T, Ogawa R. Magnesium prophylaxis for arrhythmias after cardiac surgery: a meta-analysis of randomized controlled trials. Am J Med. 2004;117(5):325-33.

The 52 in 52 Review: Comparison of Dopamine and Norepinephrine in the Treatment of Shock

The 52 in 52 Review: Comparison of Dopamine and Norepinephrine in the Treatment of Shock

 

Article Citation: De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362(9):779-89.

 

What We Already Know About the Topic: The recent 2016 Surviving Sepsis Campaign Guidelines continue a strong recommendation for norepinephrine as the first-line vasoactive agent in the treatment of septic shock. Furthermore, the use of dopamine is a weak recommendation in selected patients at low risk for tachyarrhythmias and bradycardia.1 Using low-dose dopamine for purported renal protection has a strong negative recommendation.

 

Why This Study Is Important: This study laid the groundwork for the recommendations for norepinephrine as the first line pressor in septic shock. It would later become the largest of the included studies in a meta-analysis by the same lead author, De Backer et al, in 2012 which found mortality and arrhythmia risks with dopamine.2

 

Brief Overview of the Study: The multicenter, randomized trial assigned 1,679 patients to either dopamine or norepinephrine and evaluated the primary outcome of rate of death at 28-days. Secondary endpoints included number of days without need for organ support and occurrence of adverse events.

 

Limitations: Open label norepinephrine was used after the maximum doses of norepinephrine or dopamine were used.

 

Take Home Points: In the treatment of shock, the use of either dopamine or norepinephrine showed similar 28-day mortality. However, the use of dopamine was associated with greater incidence of arrhythmias.

 

References:

 

  1. Rhodes A, Evans LE, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017;
  2. DeBacker D, Aldecoa C, Njimi H, et al. Dopamine versus norepinephrine in the treatment of septic shock: a meta-analysis. Crit Care Med. 2012;40(3):725-30.

 

The 52 in 52 Review: Lactate Clearance vs Central Venous Oxygen Saturation as Goals of Early Sepsis Therapy

Article Citation: Jones AE, Shapiro NI, Trzeciak S, et al. Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial. JAMA. 2010;303(8):739-46.

 

What We Already Know About the Topic: Lactate physiology can assist in triaging the severity of illness for septic patients. While the underlying pathophysiology can be either type A (oxygen-dependent tissue dysoxia) or type B (upregulated sympathomimetic response), the elevation of lactate correlates with illness severity. Central venous oxygen saturation or mixed venous oxygen saturation (ScvO2 or SvO2) is not necessarily required for adequate sepsis resuscitation as seen in the triad of large scale studies (i.e. ProMISe, ARISE, ProCESS) following Rivers’ landmark early goal directed therapy work.

 

Why This Study is Important: In the following seven years since this landmark study, the use of lactate clearance has replaced the routine use of ScvO2 to guide resuscitation in sepsis and septic shock. The recent 2016 Surviving Sepsis Guidelines (Rhodes et al 2016) recommend targeting lactate clearance in contrast to the prior 2012 recommendations of targeting ScvO2 or SvO2 of 70% or 65%, respectively.

 

Brief Overview of the Study: As a multicenter randomized controlled noninferiority trial, Jones et al assigned 300 severely septic or septic shock patients to either a group targeting ScvO2 of at least 70% or a lactate clearance of 10%. Both groups were resuscitated to normalized central venous pressure (CVP) and mean arterial pressure (MAP). The primary outcome evaluated was absolute in-hospital mortality rate with a noninferiority threshold of Δ -10%. The authors concluded that the intent-to-treat mortality difference of 6% did not meet the predefined -10% threshold.

 

Limitations: The lack of blinding in the study makes the finding susceptible to treatment bias. Furthermore, knowledge that the study was ongoing makes the findings susceptible to the Hawthorne effect. Despite the multicenter nature of the trial, the 3 institutions of the study were emergency departments which used quantitative resuscitation; therefore, the findings may not be generalizable to other types of centers.

 

Take Home Points: Using lactate clearance as marker for resuscitation of sepsis and septic shock patients is non-inferior to ScvO2 goals. This study’s conclusions have been reflected in the 2016 Surviving Sepsis Guidelines which offer a weak, low quality evidence recommendation for guiding resuscitation with normalizing lactate. There is no longer a goal for ScvO2 or SvO2.

 

References:

 

Rhodes A, Evans LE, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017;

 

Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580-637.

Don’t Forget The Right Ventricle

The Right Ventricle

The right ventricle (RV) has been getting more coverage lately from the Wilcox et al review article in Annals to the continued coverage in many critical care circles where anesthesia and emergency medicine overlap.(1)  Furthermore, the increased presence of VADs and physiology-centric thinking in the resuscitation units of the ED require facility with manipulation of the RV.

Danger with Positive Pressure

The RV’s lower pressures, structural design, and interdependence with the left ventricle (LV) create unfavorable hemodynamic interactions for the RV and positive pressure ventilation.(2) Most easily appreciated when separating preload and afterload, the conceptual challenge with positive pressure is seen in the following diagram from derangedphysiology.com. Intrathoracic pressure from either non-invasive or mechanical ventilation decreases RA preload and increases RV afterload. Proceed with caution when intubating pulmonary hypertension or RV failure patients.

Structure

Anatomically, the RV is crescent-shaped in longitudinal cross-section and triangular in axial cross-section. The deep longitudinal fibers of the RV pull it from apex to base of the heart. Additionally, there is small contribution from inward motion of the RV free wall as well as left ventricular traction on the RV.

Ventricular Interdependence

Compared to the LV, the RV’s thin wall and lower resistance circuit means it contracts throughout systole; it has no isovolumic relaxation phase. Any acute rise in right sided pressures (e.g. PE, tamponade, RV infarct) push the septum to the left, impairing LV diastolic filling and contractility.

References

  1. Wilcox SR, Kabrhel C, Channick RN. Pulmonary Hypertension and Right Ventricular Failure in Emergency Medicine. Ann Emerg Med. 2015;66(6):619-28.
  2. Deranged Physiology: Effects of Positive Pressure Ventilation on Cardiovascular Physiology. Deranged Physiology. http://www.derangedphysiology.com/main/core-topics-intensive-care/mechanical-ventilation-0/Chapter%202.1.7/effects-positive-pressure-ventilation-cardiovascular-physiology. Accessed March 14, 2017.
  3. Ibrahim BS. Right Ventricular Failure. European Society of Cardiology. https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-14/Right-ventricular-failure. Published December 12, 2016. Accessed March 14, 2017.