September 29, 2016

  This blog post is the second part of a series of 3, on a recent lecture I was asked to give  on Critical Care Updates: Resuscitation Sequence Intubation. This talk was mostly derived from a podcast by Scott Weingart (Twitter: @EMCrit) where he talked about the physiologic killers during preintubation and perintubation. In this podcast, Scott mentions the HOp killers: Hypotension, Hypoxemia, and Metabolic Acidosis (pH) as the physiologic causes of pre-intubation/peri-intubation morbidity and mortality. Taking care of these critically ill patients that require intubation can be a high stress situation, with little room for error.  In part two of this series we will discuss some useful strategies at the bedside to help us reduce pre-intubation/peri-intubation hypoxemia.

September 26, 2016

  This blog post is the first part of a series of 3, on a recent lecture I was asked to give  on Critical Care Updates: Resuscitation Sequence Intubation. This talk was mostly derived from a podcast by Scott Weingart (Twitter: @EMCrit) where he talked about the physiologic killers during preintubation and perintubation. In this podcast, Scott mentions the HOp killers: Hypotension, Hypoxemia, and Metabolic Acidosis (pH) as the physiologic causes of pre-intubation/peri-intubation morbidity and mortality. Taking care of these critically ill patients that require intubation can be a high stress situation, with little room for error.  In part one of this series we will discuss some useful strategies at the bedside to help us reduce pre-intubation/peri-intubation hypotension.

September 22, 2016

The focus of this talk is on how to cognitively offload our minds as we are running a resuscitation. ACLS provides us with a framework in treating adult victims of Cardiac Arrest (CA) or other cardiopulmonary emergencies. This helps get providers who don't commonly deal with CA, to improve things, such as the quality of CPR, minimizing interruptions during CPR for pulse checks, and the timing/dosing of epinephrine. Emergency Medicine (EM) and the prehospital world are different than many environments in medicine. We get minimal information at the time of patient arrival while at the same time the disease process that is taking place has not quite defined itself.  We are constantly expected to acutely manage and resuscitate anyone who comes in our doors 24-7-365, many times without crucial information. Our job therefore should be to ensure coronary and cerebral perfusion are at their highest quality, but also simultaneously putting the pieces of the puzzle together to figure out why our patient is in CA. It can be very difficult to do both and many times we sacrifice one for the other. It is therefore important to cognitively offload ourselves during the resuscitation of our patients in CA and focus our attention on why they are in CA. As a disclosure for this lecture I did state that some of the recommendations made have evidence to support them and others are more theoretical and certainly up for discussion.

August 4, 2016

Background: Hemorrhagic stroke accounts for only 11-22% of all strokes but up to 50% of all stroke mortality. Additionally, there is significant disability associated with the disease in survivors. Much of our attention in the Emergency Department (ED) is guided towards preventing expansion of bleeding and secondary injury after the initial insult. Physiologically, controlling blood pressure has always appeared to be a reasonable goal as it may decrease hematoma expansion and thus mortality. However, there is little high-quality evidence to guide clinicians in determining what the goal blood pressure should be and whether there’s truly a patient centered benefit to aggressive blood pressure management. The recently published INTERACT-2 trial demonstrated no benefit for death or disability for aggressive blood pressure control when started within 6 hours of symptom onset (though the authors touted benefits seen only after ordinal analysis) but some critics have argued that treatment should be started earlier.

June 23, 2016

Background: The best way to resuscitate critically ill patients with fluids has been a hotly debated topic in the FOAMed and Critical Care worlds. Fluids are important to optimize stroke volume and distal tissue perfusion, however, the administration of excessive fluids for shock can increase a patient’s morbidity and mortality by causing volume overload, which may lead to tissue edema and subsequently inadequate blood flow to tissues [1]. Accurately predicting when, whom, and how much fluid to administer remains a very challenging clinical question as only half of critically ill patients increase their cardiac output in response to the administration of fluids (i.e. the patient is preload or fluid responsive) [1]. Clinical signs and pressure/volumetric static variables are unreliable predictors of fluid responsiveness [1]. Ventilator-induced dynamic variables such as stroke volume variation and pulse pressure variation, however, have been shown to be more accurate in predicating fluid responsiveness. These tests can only be applied when several criteria are present (e.g., sinus heart rate, mechanical ventilation with a tidal volume of 8-10cc/kg of ideal body weight). Passive leg raise (PLR) is another method to assess preload responsiveness. PLR produces a temporary and reversible increase in ventricular preload through an increase in venous return from the lower extremities, which mimics fluid administration without actually having to give exogenous fluids. This sounds great in theory, but PLR requires a hemodynamic assessment to be made during the maneuver to determine if the patient is preload responsive or not. There are multiple techniques for assessing changes in stroke volume but the diagnostic performance of each method still remains unknown. The two most commonly described methods are changes in pulse pressure variation and variables of flow.