Category: Critical Care
Posted: 10/17/2017 by Mike Winters, MBA, MD
(Updated: 11/1/2024)
Click here to contact Mike Winters, MBA, MD
Improving CPR Performance
Nassar BS, et al. Improving CPR performance. Chest. 2017. {epub ahead of print]
Jentzer JC, et al. Improving survival from cardiac arrest: A review of contemporary practice and challenges. Ann Emerg Med. 2016; 68:678-89.
Category: Critical Care
Keywords: liver failure, dialysis, MARS, Molecular Adsorbent Recirculating System (PubMed Search)
Posted: 10/10/2017 by Kami Windsor, MD
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Molecular Adsorbent Recirculating System (MARS) is an artificial liver support system colloquially known in the medical field as "dialysis for the liver."
Take-Home:
1. Consider MARS in your patient with severe acute liver failure due to potentially reversible/recoverable etiology
2. Know if and where MARS is offered near you
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Molecular Adsorbent Recirculating System (MARS) is an artificial liver support system colloquially known in the medical field as "dialysis for the liver."
Its use demonstrates apparent effective replacement of liver function, with consistently-proven improvements in hemodynamics, hepatic encephalopathy, hepatorenal syndrome, drug clearance, hyperbilirubinemia, and other markers of hepatic homeostasis.
It has been repeatedly demonstrated to work well as a short-term bridge to liver recovery or liver transplant in severe ALF of various causes, especially those that are generally reversible with support and time severe trauma, toxic ingestions, and acute alcoholic hepatitis.
Mortality benefit remains unclear and may be dependent on the subtype of acute liver failure. Most of the current literature is made up of case reports, or case studies with small study populations. In acute on chronic liver failure, the 23-patient randomized, controlled RELIEF trial failed to show survival advantage at 28 days. Gerth et al, however, found a 14-day mortality benefit in ACF patients by retrospective analysis, which may indicate that MARS use as a bridge to transplant is the most appropriate utilization in this patient population.
Category: Critical Care
Posted: 10/4/2017 by Ashley Menne, MD
(Updated: 11/1/2024)
Click here to contact Ashley Menne, MD
Risk of Pneumocystis pneumonia (PCP) increases with degree of immunosuppression. If clinical suspicion exists (CD4 <200 with cough, pulmonary infiltrates, hypoxic respiratory failure), it is reasonable to initiate empiric therapy.
First line treatment is trimethoprim-sulfamethoxazole (TMP-SMX) orally or IV for 21 days. IV pentamidine has equivalent efficacy to IV TMP-SMX but greater toxicity and is generally reserved for patients with severe PCP who cannot tolerate or are unresponsive to TMP-SMX.
Importantly, adjunctive corticosteroids have been shown to significantly improve outcomes (mortality, need for ICU admission, need for mechanical ventilation) in HIV-infected patients with moderate to severe PCP (defined by pO2 <70 mmHg on Room Air).
· Ideally steroids should be started BEFORE (or at the same time as) Pneumocystis-specific treatment to prevent/mitigate the sharp deterioration in lung function that occurs in most patients after initiation of PCP treatment. This is thought to be secondary to the intense inflammatory response to lysis of Pneumocystis organisms, which can cause an ARDS-like picture.
· Recommended dosing schedule: 40mg prednisone twice daily for 5 days, then 40mg once daily for 5 days, followed by 20mg once daily for the remaining 11 days of treatment.
Bottom Line: In patients with moderate to severe PCP (pO2 <70 mmHg on RA), don’t forget to initiate adjunctive corticosteroids early (at the same time you initiate empiric therapy for PCP).
Wang RJ, Miller RF, Huang L. Approach to Fungal Infections in Human Immunodeficiency Virus–Infected Individuals. Clin Chest Med. 2017;38(3):465-477. doi:10.1016/j.ccm.2017.04.008.
Bozzette SA, Sattler FR, Chiu J, et al. A Controlled Trial of Early Adjunctive Treatment with Corticosteroids for Pneumocystis carinii Pneumonia in the Acquired Immunodeficiency Syndrome. N Engl J Med. 1990;323(21):1451-1457. doi:10.1056/NEJM199011223232104.
Montaner JS, Lawson LM, Levitt N, Belzberg A, Schechter MT, Ruedy J. Corticosteroids prevent early deterioration in patients with moderately severe Pneumocystis carinii pneumonia and the acquired immunodeficiency syndrome (AIDS). Ann Intern Med. 1990;113(1):14-20. http://www.ncbi.nlm.nih.gov/pubmed/2190515.
Category: Critical Care
Posted: 9/19/2017 by Mike Winters, MBA, MD
(Updated: 11/1/2024)
Click here to contact Mike Winters, MBA, MD
Post-Arrest Tidal Volume Setting
Beitler JR, et al. Favorable neurocognitive outcome with low tidal volume ventilation after cardiac arrest. Am J Respir Crit Care Med. 2017; 195:1196-1206.
Category: Critical Care
Keywords: respiratory failure, pulmonary edema, airway obstruction (PubMed Search)
Posted: 9/12/2017 by Kami Windsor, MD
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Negative-pressure pulmonary edema (NPPE) is a well-documented entity that occurs after a patient makes strong inspiratory effort against a blocked airway. The negative pressure causes hydrostatic edema that can be life-threatening if not recognized, but if treated quickly and appropriately, usually resolves after 24-48 hours. These patients may have any type of airway obstruction, whether due to edema secondary to infection or allergy, laryngospasm, or traumatic disruption of the airway, such as in attempted hangings.
Management:
1. Alleviate or bypass the airway obstruction.
· Usually via intubation; may require a surgical airway
· If obstruction in an intubated patient is due to biting on tube or dyssynchrony, add bite-block (if not already in place), sedation, and even paralysis if needed.
2. Provide positive pressure ventilation and oxygen supplementation.
3. Use low tidal volume ventilation.
4. In severe hypoxemia without shock, add a diuretic agent and consider additional measures such as proning and even ECMO if the hypoxemia is refractory to standard therapy.
Negative-pressure pulmonary edema (NPPE), also called post-obstructive pulmonary edema, can occur after any event in which a patient exerts strong inspiratory effort against an obstructed airway. This obstruction can be essentially due to any cause; in adults it is most well-documented secondary to post-extubation laryngospasm, in children the etiology is usually infectious, such as in epiglottitis. It has also been documented secondary to laryngeal edema, tumor, trauma, biting on an endotracheal tube, vent dyssynchrony, as well as disruptions to breathing mechanics during generalized seizures, among other causes.
It is noted that many of the documented cases involve patients who are relatively young and otherwise healthy, and thus capable of creating a strong negative intrathoracic pressure. The pathophysiology is thought to be related to hydrostatic mechanisms rather than a “leaky-capillary” permeability edema, and it usually resolves quickly if managed appropriately, within 24-48 hours. Diffuse alveolar hemorrhage, related to capillary rupture from the negative pressure, has been documented to occur in severe cases but is rare.
Consider the diagnosis in patients with an appropriate clinical picture or witnessed event leading to abrupt respiratory distress and/or failure. The diagnosis is even more strongly supported if they had absence of respiratory symptoms, or a clear chest x-ray prior to the event, with a chest x-ray demonstrating pulmonary edema afterwards.
Appropriate management of these patients includes:
1. Alleviation or bypass of the upper airway obstruction, which usually requires intubation.
· Depending on the etiology of obstruction (e.g. epiglottitis), endo/nasotracheal intubation may be difficult and a surgical airway may be necessary. Be prepared for this possibility.
· Ventilated patients who develop NPPE may require sedation to prevent biting on the ETT or to promote vent synchrony
2. Provide with positive-pressure ventilation to counteract the negative airway pressures, and oxygen supplementation to decrease pulmonary vascular resistance.
3. Lung-protective ventilation with low tidal volumes is generally accepted as the preferred ventilation strategy in these patients, extrapolated from data regarding its use in acute lung injury.
4. In cases of moderate to severe hypoxemia without the presence of shock, add a diuretic agent.
5. For refractory hypoxemia, consider early utilization of additional therapies, including neuromuscular blockade, proning, and ECMO.
Bhattacharya M, Kallet RJ, Ware LB, Matthay MA. Negative-pressure pulmonary edema. Chest. 2016;150(4):927-33.
Contou D, Voiriot G, Djibre et al. Clinical features of patients with diffuse alveolar hemorrhage due to negative-pressure pulmonary edema. Lung. 2017;195(4):477-487.
Category: Critical Care
Keywords: Mechanical ventilation, sedation (PubMed Search)
Posted: 8/30/2017 by Kami Windsor, MD
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Background: Sedation and analgesia are key components for mechanically ventilated patients. While significant data exists regarding how to manage sedation and analgesia in the ICU setting, very little data exists on management in the ED.
Data: A prospective, single-center, observational study of mechanically-ventilated adult patients used linear regression to identify ED sedation practices and outcomes, with a focus on sedation characteristics using the Richmond Agitation-Sedation Scale (RASS).
Findings:
Bottom line: Avoid early deep sedation in your intubated patients as this may be directly associated with increased mortality. Instead, a goal RASS of 0 to -2 should be appropriate for most non-paralyzed, mechanically-ventilated ED patients, extrapoloating from ICU guidelines.
Stephens, R.J., et al., Analgosedation Practices and the Impact of Sedation Depth on Clinical Outcomes Among Patients Requiring Mechanical Ventilation in the ED: A Cohort Study. Chest, 2017 [Epub ahead of print].
Barr J, Fraser GL, Puntillo K, Ely EW, Gélinas C, Dasta JF, Davidson JE, Devlin JW, Kress JP, Joffe AM, et al.; American College of Critical Care Medicine. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Crit Care Med 2013;41:263–306.
Category: Critical Care
Posted: 8/22/2017 by Mike Winters, MBA, MD
Click here to contact Mike Winters, MBA, MD
Hyponatremic Encephalopathy
Archinger SG, Ayus JC. Treatment of hyponatremic encephalopathy in the critically ill. Crit Care Med. 2017; epub ahead of print.
Category: Critical Care
Keywords: autoimmune, rheumatology, thrombosis, hematology (PubMed Search)
Posted: 8/15/2017 by Kami Windsor, MD
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Catastrophic Antiphospholipid Syndrome (CAPS):
A life-threatening “thrombotic storm” of multi-organ micro & macro thrombosis in patients with antiphospholipid syndrome (known or unknown).
Triggered circulating antibodies (usually by infection, but can be prompted by malignancy, pregnancy, and lupus itself) cause endothelial disruption and inflammation leading to prothrombotic state, commonly with SIRS response.
Mortality is high at an estimated 40%.
Confirm diagnosis with antiphospholipid antibody titers.
Treat ASAP with unfractionated heparin, corticosteroids, and Hematology consultation for plasma exchange and/or IVIG.
Kazzaz NM, McCune WJ, Knight JS. Treatment of catastrophic antiphospholipid syndrome. Curr Opin Rheumatol. 2016;28(3):218-27.
Cervera R, Rodriguez-Pinto I, Colafrancesco S, et al. 14th International Congress on Antiphospholipid Antibodies Task Force. Report on catastrophic antiphospholipid syndrome. Autoimmun Rev 2014; 13:699–707.
Category: Critical Care
Keywords: RV dysfunction, APRV, echo, ultrasound (PubMed Search)
Posted: 8/1/2017 by Daniel Haase, MD
Click here to contact Daniel Haase, MD
--RV systolic function is negatively affected by high RV afterload
--High mean airway pressures on the ventilator (particularly in modes such as APRV [airway pressure release ventilation]) can induce RV dysfunction
*****CLICK BELOW FOR A GREAT CASE!!!*****
A 25yoF with ARDS is on APRV (36/0 and 5/0.5). She is on norepi to maintain a MAP >65. A bedside echo reveals a dilated, dysfunctional RV.
--Open "A4C end diastole"
Measurement of TAPSE confirms the RV dysfunction, but also reveals the cause.
--Open "TAPSE"
Every 5th beat, the TAPSE significantly improves to "normal" range. The four beats inbetween are abnormal. The 5th normal beat coincides with the APRV relase, when airway pressures are zero! Thus, this change in RV function is from the ventilator alone. The TAPSE decreases by almost 40%!
--Open "TAPSE measured"
Be careful with high mean airway pressures in patients with known or suspected RV dysfunction. This is why we try to avoid intubation in HD significant pulmonary embolism!
1708011802_TAPSE_measured.jpg (166 Kb)
Category: Critical Care
Posted: 7/25/2017 by Mike Winters, MBA, MD
(Updated: 11/1/2024)
Click here to contact Mike Winters, MBA, MD
Improving Resuscitation Performance
Lauria M, et al. Psychological skills to improve emergency care providers' performance under stress. Ann Emerg Med. 2017; epub ahead of print.
Category: Critical Care
Keywords: Resuscitation, CPR, family, policy (PubMed Search)
Posted: 7/17/2017 by Kami Windsor, MD
Click here to contact Kami Windsor, MD
When surveyed, half of general medicine patients interviewed stated that they would prefer to have a loved one present if they were to develop cardiac arrest and require CPR. So far, studies have demonstrated that…
Allowing family presence during CPR is associated with the following benefits to family members:
And is NOT associated with a difference in:
Several studies have demonstrated benefits to patient family members who are offered the opportunity to witness ongoing CPR when their loved one develops cardiac arrest. These benefits--decreased rates of PTSD-related symptoms, anxiety, depression (including need for medication, professional treatment, and suicide attempts), and complicated grief--have been shown to persist at 1 year post-resuscitation event.
Themes that arise when discussing the resuscitations with family members afterward include:
1. The feeling of active involvement in the resuscitation process
2. Communication with the resuscitation team
3. Perception of the reality of death
4. Experience of and reaction to witnessing (or not witnessing) the resuscitation
Twelve percent of family members who chose to NOT be present during CPR expressed regret at their choice, versus three percent of relatives who chose to be present.
Negative outcomes cited by family members who witnessed CPR involved feeling like they were not being communicated with, or that their loved one was being over-zealously resuscitated.
Category: Critical Care
Keywords: CPR, ventilation, respiratory rate, PaCO2 (PubMed Search)
Posted: 6/27/2017 by Mike Winters, MBA, MD
Click here to contact Mike Winters, MBA, MD
Ventilation During Cardiopulmonary Resuscitation
Chang MP, Idris AH. The past, present, and future of ventilation during cardiopulmonary resuscitation. Curr Opin Crit Care 2017; 23:188-192.
Category: Critical Care
Keywords: ACLS, cardiac arrest, resuscitation, epinephrine (PubMed Search)
Posted: 6/13/2017 by Kami Windsor, MD
Click here to contact Kami Windsor, MD
In patients with persistent VT/VF cardiac arrest, giving epinephrine before the 2nd defibrillation attempt (which should follow initial shock and 2 minutes of CPR) is associated with decreased ROSC, decreased hospital survival, and decreased functional outcome.
Take Home Point:
"Electricity before Epi" in patients with persistent VT/VF arrest, at least for the initial epinephrine dose.
Background Info:
While the ACLS algorithm does recommend initial defibrillation followed by 2 minutes of CPR and repeated shock if the shockable rhythm persists, the 2015 AHA Guidelines update admits that there is insufficient evidence to comment on “optimal timing” of epinephrine administration in these patients.
A 2016 study of 2794 patients across 310 hospitals looked at patients with cardiac arrest with initial shockable rhythm and found that compared to patients who received epinephrine after the second defibrillation attempt, patients who received epinephrine in the first 2 minutes before the 2nd shock had:
The benefit of 2nd-shock-first was maintained when groups were matched using a propensity score accounting for baseline characteristics of the patients, events, and hospitals.
References:
Part 7: Adult Advanced Cardiovascular Life Support: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Link MS, Berkow LC, Kudenchuk PJ, et al. Circulation. 2015;132(18 Suppl 2):S444-64.
Early administration of epinephrine (adrenaline) in patients with cardiac arrest with initial shockable rhythm in hospital: propensity score matched analysis. Andersen LW, Kurth T, Chase M, et al. BMJ. 2016;353:i1577.
Category: Critical Care
Keywords: POCUS, Massive PE (PubMed Search)
Posted: 6/6/2017 by Rory Spiegel, MD
(Updated: 11/1/2024)
Click here to contact Rory Spiegel, MD
The poor sensitivity of bedside echocardiography to identify all-comers with pulmonary embolism is well documented. Most series cite a sensitivity and specificity of 31% to 72% and 87% to 98%, respectively (1,2). But as Nazerian et al demonstrate in their recent publication in Internal and Emergency Medicine, the diagnostic performance of bedside echocardiography is far more reliable in the subset of patients presenting in shock (3).
Of the 105 patients included in the final analysis, in 43 (40.9%) PE was determined to be the etiology of their shock. Bedside echo demonstrated notable diagnostic prowess when employed in this subset of patients, sensitivity (91%), specificity (87%), –LR (0.11), +LR (7.03). The sensitivity and –LR were further augmented when the venous US of the LE was included (sensitivity of 95% and –LR of 0.06) in the diagnostic workup.
1. Dresden S, Mitchell P, Rahimi L, et al. Right ventricular dilatation on bedside echocardiography performed by emergency physicians aids in the diagnosis of pulmonary embolism. Ann Emerg Med. 2014;63(1):16-24.
2. Nazerian P, Vanni S, Volpicelli G, et al. Accuracy of point-of-care multiorgan ultrasonography for the diagnosis of pulmonary embolism. Chest. 2014;145(5):950-957.
3. Nazerian P, Volpicelli G, Gigli C, Lamorte A, Grifoni S, Vanni S. Diagnostic accuracy of focused cardiac and venous ultrasound examinations in patients with shock and suspected pulmonary embolism. Intern Emerg Med. 2017;
Category: Critical Care
Posted: 5/23/2017 by Mike Winters, MBA, MD
(Updated: 11/1/2024)
Click here to contact Mike Winters, MBA, MD
Antibiotics in Sepsis
Leisman D, et al. Delayed second-dose antibiotics for patients admitted from the emergency department with sepsis: prevalence, risk factors, and outcomes. Crit Care Med. 2017; 45:956-65.
Category: Critical Care
Posted: 5/16/2017 by Kami Windsor, MD
Click here to contact Kami Windsor, MD
High flow nasal cannula (HFNC) is a valid option in the management of acute hypoxic respiratory failure (AHRF) without hypercapnia, as evidenced by multiple studies including the FLORALI trial. Failure of HFNC, however, may result in delayed intubation and worsened clinical outcomes.
Factors predicting HFNC failure and subsequent intubation include:
Consider whether or not HFNC is appropriate in your patient with AHRF, and if you use it, reevaluate your patient to ensure improvement, or escalate their respiratory support.
For patients with acute hypoxic respiratory failure without hypercapnia, the FLORALI trial demonstrated that high flow nasal cannula (HFNC) therapy increases ventilator-free days, reduces 90-day mortality, and is associated with better comfort and lower dyspnea severity when compared to conventional oxygen therapy and non-invasive ventilation (NIV). Failure of HFNC, however, may result in delayed intubation and worse clinical outcomes in patients with acute hypoxic respiratory failure. So how do we predict in the ED which patients are going to fail?
Sztrymf et al. evaluated patients placed on HFNC for nonhypercapneic acute hypoxic respiratory failure, who later went on to require endotracheal intubation. The cohort who failed HFNC had significantly:
- higher RR at 30 & 45 minutes after initiation of HFNC
- lower SpO2% at 15, 30, and 60 minutes
- higher incidence of paradoxical breathing (thoracoabdominal dyssynchrony) at 15, 30, 60, and 120 minutes
In an observational study of patients with ARDS,* Messika et al. found that factors predicting HFNC failure included:
- a higher Simplified Acute Physiology Score II (SAPS II; 46 v. 29, p=.001)
- additional organ system failure (mostly hemodynamic or neurological)
- trends towards lower PaO2:FiO2 ratios and higher RR
So don’t set it and forget it! Consider a different method of respiratory support if your patient has multi-organ system failure, especially if they are in shock or have altered mental status. If you do use HFNC, reevaluate your patient at 15 minutes and again at 30 minutes to make sure their respiratory rate and SpO2 have improved and that there is no paradoxic breathing (or it is resolving). If not, move on to NIV or invasive mechanical ventilation.
*acute respiratory failure occurring within 1 week of known clinical insult with PaO2:FiO2 <300mmHg and bilateral opacities on chest x-ray not attributable to cardiac failure/volume overload
1. Frat JP, Thille AW, Mercat A, et al. High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. N Engl J Med. 2015;372:2185–96.
2. Sztrymf B, Messika J, Bertrand F, et al. Beneficial effects of humidified high flow nasal oxygen in critical care patients: a prospective pilot study. Intensive Care Med. 2011;37:1780–6.
3. Messika J, Ben Ahmed K, Gaudry S, et al. Use of high-flow nasal cannula oxygen therapy in subjects with ARDS: a 1-year observational study. Respir Care. 2015;60(2):162-9.
4. Hernandez G, Roca O, Colinas L. High-flow nasal cannula support therapy: new insights and improving performance. Crit Care. 2017;21(1):62.
Category: Critical Care
Posted: 4/25/2017 by Mike Winters, MBA, MD
(Updated: 11/1/2024)
Click here to contact Mike Winters, MBA, MD
Ventilator Settings for the Post-Arrest Patient
Jentzer JC, et al. Recent developments in the management of patients resuscitated from cardiac arrest. J Crit Care. 2017; 39:97-107.
Category: Critical Care
Keywords: Central venous catheter, ultrasound (PubMed Search)
Posted: 4/18/2017 by Kami Windsor, MD
(Updated: 11/1/2024)
Click here to contact Kami Windsor, MD
Save time by using bedside ultrasound to confirm above-the-diaphragm central venous catheter (CVC) placement rather than waiting for chest x-ray confirmation:
1. Perform rapid push of saline (it doesn’t have to be agitated) through CVC while cardiac probe is placed with right atrium in view. Immediate visualization of bubbles (or “atrial swirl”) essentially confirms correct placement.
2. Perform the usual search for ipsilateral lung-sliding and the waves-on-the-beach to rule out procedural pneumothorax.
It makes sense that it’s going to be faster for you to use that internal jugular/subclavian central venous catheter (CVC) you just placed if you confirm with bedside ultrasound instead of waiting for the radiology tech to get the chest x-ray. But what’s the data?
Using pooled data from of 15 studies with 1553 CVC placements, Ablordeppey et al. found that ultrasound had a sensitivity of 86% and 98% specificity for detecting catheter malposition, with a positive likelihood ratio (LR) of 31.1 and a negative LR of 0.25. There was an almost 100% sensitivity and specificity for pneumothorax detection, and reduced confirmation time by 58 minutes.These findings are generally consistent across the board for the other studies out there.
1. Ablordeppey EA, Drewry AM, Beyer AB, et al. Diagnostic accuracy of central venous catheter confirmation by bedside ultrasound versus chest radiography in critically ill patients: a systematic review and meta-analysis. Crit Care Med. 2017; 45(4): 715-24.
2. Gekle R, Dubensky L, Haddad S, et al. Saline flush test: Can bedside sonography replace conventional radiography for confirmation of above-the-diaphragm central venous catheter placement? J Ultrasound Med. 2015;34(7):1295-9.
3. Weekes AJ, Johnson DA, Keller SM. Central vascular catheter placement evaluation using saline flush and bedside echocardiography. Acad Emerg Med. 2014; 21:65-72.
Category: Critical Care
Keywords: Hyperoxia, Mechanical Ventilation (PubMed Search)
Posted: 4/11/2017 by Rory Spiegel, MD
(Updated: 11/1/2024)
Click here to contact Rory Spiegel, MD
The deleterious effects of hyperoxia are becoming more and more apparent. But obtaining a blood gas to ensure normoxia in a busy Emergency Department can be burdensome. And while the utilization of a non-invasive pulse oximeter seems ideal, the threshold that best limits the rate of hyperoxia is unclear.
Durlinger et al in a prospective observational study demonstrated that an oxygen saturation 95% or less effectively limited the number of patients with hyperoxia (PaO2 of greater than 100 mm Hg). Conversely when an SpO2 of 100% was maintained, 84% of the patients demonstrated a PaO2 of greater than 100 mm Hg.
Durlinger EM, Spoelstra-de man AM, Smit B, et al. Hyperoxia: At what level of SpO2 is a patient safe? A study in mechanically ventilated ICU patients. J Crit Care. 2017;
Category: Critical Care
Posted: 3/28/2017 by Mike Winters, MBA, MD
(Updated: 11/1/2024)
Click here to contact Mike Winters, MBA, MD
DSI, Ketamine, and Apnea
Driver BE, Reardon RF. Apnea after low-dose ketamine sedation during attempted delayed sequence intubation. Ann Emerg Med 2017; 69:34-35.