UMEM Educational Pearls - By Kami Windsor

Despite the knowledge that minimizing interruptions in chest compressions during CPR is key to maintaing coronary perfusion pressure and chance of ROSC,^1-4 difficulties in limiting hands-off time remain. 

Dewolf et al.⁵ recently performed a prospective observational study using body cameras to find that 33% (623/1867) of their CPR interruptions were longer than the recommended 10 seconds:

• 51.6% Rhythm/pulse checks
• 11.1% Installation/use mechanical CPR device
•   6.7% Manual CPR provider switch
•   6.2% ETT placement

Previous studies have shown an increase in hands-off time associated with the use of cardiac POCUS during rhythm checks as well.^6,7

Bottom Line:

• Physicians must be mindful of hands-off time to improve their chance of obtaining ROSC, minimizing each CPR interruption to <10 seconds, and maintaining a hands-on time (also known as chest compression fraction) of >80%. 
• Change your pulse check to a rhythm check utilizing arterial line placement, end-tidal monitoring, or US/doppler at the femoral artery in order to minimize the search for a pulse as a reason for prolonged CPR interruption.
• Consider having someone on the team count the seconds out loud during pauses so the entire team is aware of the interruption time and will recognize when CPR needs to be resumed.

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A recent prospective observational study examined the diagnostic usefulness of head-to-pelvis sudden death computed tomography (SDCT) in 104 patients with ROSC and unclear OHCA etiology.

• Obtained within 6 hours of hospital arrival
• Noncontrast head CT + ECG-gated chest CTA with abbreviated coronary imaging + contrasted CT of the abdomen to just below the pelvis. 

Diagnostic performance: 

• Detected 95% of OHCA etiologies diagnosable by CT
• Detected 98% of time-critical diagnoses requiring emergent intervention (including complications of resuscitation)
• The sole reason for diagnosis of OHCA etiology in 13%

Safety:

• 28% of patients with elevated creatinine at 48h (down from 55% at presentation; study excluded GFR < 30ml/min unless treating provider felt the data was needed for care)
• 1% (1 patient) required RRT 
• No false positives noted, no allergic contrast reactions, 1 contrast IV extravasation

Bottom Line: For OHCA without clear etiology, SDCT explicitly including a thoracic CTA may have diagnostic benefit over standard care alone with the added benefit of identification of resuscitation complications. 

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Supplemental oxygen therapy is frequently required for patients presenting with acute respiratory distress and COPD exacerbation. Over-oxygenation can derail compensatory physiologic responses to hypoxia,¹ resulting in worsening VQ mismatch and, to a lesser degree, decreases in minute ventilation, that cause worsened respiratory failure.

The 2012 DECAF (Dyspnea, Eosinopenia, Consolidation, Acidaemia, and Atrial Fibrillation) score was found to predict risk of in-hospital mortality in patients admitted with acute COPD exacerbation.^2,3 Data from the DECAF study’s derivation and external validation cohorts were examined specifically to look at outcome associated with varying levels of oxygen saturation.

• 1027 patients from 6 UK hospitals receiving supplemental oxygen at admission

• Lowest in-hospital mortality seen in the 88-92% cohort 

• Adj OR for in-hospital mortality in ≥97% vs 88-92% group: 2.97 (95% CI 1.58-5.58, p=0.001)

• Adj OR for in-hospital mortality in 93-96% vs 88-92% group: 1.98 (95% CI 1.09-3.60, p=0.025)

• Surprisingly, mortality risk seen more in normocapnic than hypercapnic patients

• Association between admission SpO2 and mortality persisted after adjusting for baseline risk and disease severity using the DECAF and NEWS 2 score

Bottom Line

In patients presenting to the ED with acute COPD exacerbation requiring oxygen supplementation, a target oxygen saturation of 88-92% is associated with the lowest in-hospital mortality, and higher oxygen saturations should be avoided independent of patients' PCO2 levels.

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Background: In respiratory failure due to COPD and cardiogenic pulmonary edema, noninvasive positive pressure ventilation decreases need for intubation and improves mortality,¹ while its utility in other scenarios such as ARDS and pneumonia has yet to be proven.^1,2 We know that patients on NIV with delays to needed intubation have a higher mortality,^1,3 but intubation and mechanical ventilation come with risks that it is preferable to avoid if possible.

So how and when can we determine that NIV is not working?

The HACOR (Heart rate, Acidosis, Consciousness, Oxygenation, Respiratory rate) score at 1 hour after NIV initiation has been demonstrated to be highly predictive of NIV failure requiring intubation.^4,5 

Bottom Line:

• Patients on NIV require close reassessment to prevent worsened survival due to intubation delay should invasive mechanical ventilation be indicated.

• A HACOR score >8 after 1 hour of NIV should prompt intubation in most instances, with strong consideration given to a score >5.

*Note: ABGs were obtained for PaO2 assessment in the above studies -- the use of SpO2 was not evaluated -- but we are often not obtaining ABGs in our ED patients with acute respiratory failure. The following chart provides an estimated SpO2 to PaO2 conversion.

WHO 2001

Caveats: 

1. Pulse oximetry may be inaccurate in darker skin tones (overestimated by ~2%)⁶ and in certain disease processes (e.g. CO poisoning, profound shock states, etc.)
2. The oxyhemoglobin dissociation curve shifts right with increasing pCO2/decreasing pH (lower saturation for a given PaO2).

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As the number of COVID-19 cases rises worldwide, prehospital and emergency department healthcare workers remain at high risk of exposure and infection during CPR for patients with cardiac arrest and potential SARS-CoV-2. 

Existing evidence supports similar cardiac arrest outcomes in airways managed with a supraglottic airway (SGA) compared to endotracheal intubation (ETT).¹  It is generally accepted that the best airway seal is provided with endotracheal intubation + viral filter, but how well do SGAs prevent spread of aerosols? 

In CPR simulation studies:

• Cuffed endotracheal tube + viral filter provides effective seal to prevent aerosolization during CPR.²
• SGA + viral filter decreases AP spread compared to facemask and compared to bag-valve mask ventilation during CPR.³
• Notable aerosolization is seen with SGAs, with no difference between AuraGain, I-gel, LMA Proseal, LMA Supreme, Combitube, or LTS-D.²

• Ventilating through an SGA + viral filter is likely better to limit spread of aerosolized particles than bag-valve mask ventilation.
• SGAs allow egress of aerosolized particles, although the amount and area of distribution in clinical practice is unclear, and endotracheal intubation with a cuffed endotracheal tube remains the best way to avoid ongoing aerosolized particle spread with chest compressions. 
• Appropriate PPE remains crucial to limiting healthcare workers' risk of infection and must be prioritized, even/especially in the management of patients in cardiac arrest. 

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While the invasive monitoring of central venous pressure (CVP) in the critically ill septic patient has gone the way of also transfusing them to a hemoglobin of 10 mg/dL, it remains that an elevated CVP is associated with higher mortality^1,2 and renal failure.^2,3

Extrapolating from existing data looking at hepatic vein, portal vein, and renal vein pulsatility as measures of systemic venous hypertension and congestion,^4,5,6 Beaubien-Souligny et al. developed the venous excess ultrasound (VExUS) grading system incorporating assessment of all 3, plus the IVC, using US to stage severity of venous congestion in post-cardiac surgery patients.⁷ They evaluated several variations, determining that the VExUS-C grading system was most predictive of subsequent renal dysfunction.

(Image from www.pocus101.com)
 

High Points

       VExUS Grade 3 (severe) venous congestion:

• Correlated with higher CVP & NTproBNP levels, as well as overall fluid balance
• Had a 96% specificity for development of subsequent AKI

Caveats

• Evaluating all parameters yields the most benefit to avoid false positives
• Can be difficult to obtain all views (>25% of subjects excluded due to poor US image quality)
• Studied in a limited population, notably not primarily RV failure patients

Clinical Uses

• To limit harmful fluid administration in shock
• To help answer the prerenal vs cardiorenal AKI question in CHF
• To indicate when volume removal (diuresis) should be the strategy, even in patients with vasopressor-dependent shock

A great how-to can be found here:

https://www.pocus101.com/vexus-ultrasound-score-fluid-overload-and-venous-congestion-assessment/

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The RECOVERY (Randomized Evaluation of COVid-19 thERapY) investigators recently published a non-peer reviewed article on their findings utilizing dexamethasone to treat patients with COVID-19. 

Rx: Dexamethasone 6mg daily* x 10 days (PO or IV) *or steroid equivalent

• 2104 in the dexamethasone group vs 4321 in the “usual care” group
• Did not exclude children or pregnant/breastfeeding mothers
• Follow-up at 28 days, hospital discharge, or death

Primary outcome:         All-cause mortality at 28-days

Secondary outcomes: 

• Major arrhythmia
• Time to discharge from hospital
• Duration of mechanical ventilation
• Need for renal replacement therapy
• In patients not ventilated at enrollment, need for intubation/ECMO & death

Results:

• Decrease in overall mortality at 28-days with 3% absolute risk reduction.
  • NNT of 25 in patients requiring O2, HFNC, or NIV
  • NNT of 8 in patients requiring invasive mechanical ventilation
• More mortality benefit seen the higher the respiratory support required, with no benefit and apparent trend towards increased mortality in the group not requiring any respiratory support at all. 
• When stratified by symptoms < or > 7 days, mortality benefit only seen in the >7 days group (which was more of the ventilated patients).
• Less progression to intubation, shorter hospital duration, greater likelihood of hospital discharge.

Limitations:

• Not yet peer-reviewed, haven't seen all the data, additional analyses could be helpful in determining if treatment effect is real
• Unblinded study
• 7% of control group received dexamethasone

Bottom Line: Strongly consider admininstering dexamethasone to your patients with known COVID-19 who require respiratory support, and look for the peer-reviewed publication from the RECOVERY Trial investigators.

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Background:

· Empiric broad spectrum antibiotic therapy is a mainstay of the management of critically ill patients with septic shock.

· Vancomycin is widely used for the coverage of potential MRSA infection

• PROS: cheap, widely available, relatively widespread tissue penetration when given IV, and is generally well-tolerated

• CONS: has a complicated dosing regimen requiring specifically-timed serum concentration sampling and subsequent dose changes, frequently subtherapeutic, carries a risk of AKI especially when used concomitantly with piperacillin/tazobactam,¹ as it commonly is during empiric therapy for septic shock.         

· Continuous infusion of vancomycin has been repeatedly demonstrated to reach target serum concentrations faster, maintain consistent serum vancomycin levels better, with fewer serum concentration sampling required, and less overall vancomycin required to do so, in both adult and pediatric populations.^2-5

Current Article: 

Flannery AH, Bissell BD, Bastin MT, et al. Continuous Versus Intermittent Infusion of Vancomycin and the Risk of Acute Kidney Injury in Critically Ill Adults: a Systematic Review and Meta-Analysis. Crit Care Med. 2020;48(6):912-8.

· Systematic review and meta-analysis of 11 studies for a total of 2123 patients

· Comparing continuous versus intermittent vancomycin infusion.

· Primary outcome of AKI, secondary outcome of mortality

· Found a reduction in the incidence of AKI in the continuous infusion cohort:

• OR 0.47 (95% CI 0.34-0.65) even when taking into account trough levels /area under the curve concentrations and the severity of AKI examined by the individual studies.

· No association between infusion strategy and mortality

Considerations:

· Initial loading dose used in most of the studies (15 mk/kg) probably underdosed, current recommendation for 25mg/kg initial loading dose⁷ (which is not even always effective by itself)⁸ (Reardon)

· Continuous infusion may be difficult with limited IV access

· AKI associated with increased hospital stay, costs, mortality (although didn’t pan out in study) – worth preventing if possible.

Take Home:

· Give a 25-30mk/kg loading dose of vancomycin in critically ill patients with suspicion of MRSA to achieve target serum concentrations sooner.

· Continuous vancomycin is a viable option and could be considered in ED boarders, especially if there is concern for impending renal injury.

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There is currently a high, and appropriate, concern regarding the aerosolization of viral particles during various methods of respiratory support. While studies are limited, here is some of the currently available data (mostly-simulated) on the approximate maximum distances of particle spread:

Nasal Cannula 5LPM:¹ 1 ft 4.5 in

Non-Rebreather Mask, 6-12LPM: 4 in, minimal change with increasing flows¹

High Flow Nasal Cannula

• Simulation:² 30 LPM = 5.6 in / 60 LPM = 8.1 in
• Actual volunteers:³
  • Use of HFNC decreased aerosol dispersion during “violent exhalation” through nares
  • No difference in aerosol dispersion w/normal breathing using HFNC until 60lpm
  • Max spread = 14.4 ft without HFNC (violent exhalation) and 6.2 ft with HFNC (violent exhalation); aerosols airborne for max of 43 seconds

CPAP (20 cmH2O) provided by oronasal mask with good fit (leak from exhaust port):² 11.5 in

Bilevel positive airway pressure w/ oronasal mask (IPAP 10-18/EPAP 4): max dispersal:⁴ 1 ft 7.7 in

Bilevel positive airway pressure with full facemask⁵ (IPAP 18 / EPAP 5): 2 ft 8 in

Bilevel positive airway pressure with helmet:⁴

• IPAP 20 / EPAP 10 = 9 in
• Using helmet w/ air cushion = negligible dispersal

Utility of Surgical Mask:⁶

• No therapy:                 31% of exhaled particles travel, some >3.3 ft
• No therapy + mask:    5% of exhaled particles leak, some >3.3 ft
• 6LPM O2 + mask:       6.9% of exhaled particles leak, some >3.3 ft
• High Velocity Nasal Insufflation (40LPM) + mask: 15.9% of exhaled particles leak, some >3.3 ft

Bottom Line: 

In vivo data from actual patients is lacking, however there is potentially lower risk of aerosol spread with HFNC than regular nasal cannula, perhaps due to higher likelihood of a tighter nare/nasal cannula interface. Nonrebreather mask performs well indirectly with the shortest dispersal distance. Noninvasive positive pressure ventilation with an oronasal mask and good seal has a relatively short dispersal distance, and a surgical mask over respiratory support interventions actively decreases amount, if not distance, of particle spread. Use of appropriate PPE and negative pressure rooms, if available, remains key.

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With ED-boarding of critically-ill patients becoming more common, it is likely that ED physicians may find themselves caring for a patient who develops ACS – that is, abdominal compartment syndrome. While intraabdominal hypertension (IAH) is common and is defined as intraabdominal pressure > 12 mmHg, ACS is defined as a sustained intraabdominal pressure > 20mmHg with associated organ injury.

WHY you need to know it:

ACS → Increased mortality & recognition is key to appropriate management

WHO is at risk:

• Decreased abdominal wall compliance (obese, post-surgical)
• Increased intrabadominal contents (hemoperitoneum, ascites, tumor)
• Increased intraluminal contents (gastroparesis, ileus)
• Capillary leak / aggressive fluid resuscitation (sepsis, burns)

HOW it kills:

• Decreased blood flow to organs due to extraluminal pressure (mesenteric, renal, hepatic ischemia)
• Decreased diaphragmatic mobility, hypoventilation/oxygenation
• Decreased venous return, decreased cardiac output

→ Lactic acidosis, respiratory acidosis, multisystem organ failure, cardiovascular collapse & death

WHEN to consider it:

• Most patients who develop ACS are already intubated or altered – but consider in responsive patients c/o severe abdominal pain, marked distension, and SOB with tachypnea
• Intubated patients – recurrent, ongoing high pressure alarms with relatively low lung volumes, tachypnea
• Abdomen distended and minimally ballotable
• New / worsening oliguria / anuria
• Labs demonstrate increased creatinine, LFTs, lactate elevated “out of proportion” to patient presentation prior to decompensation 
• Imaging may reveal underlying etiology or sequelae of ACS but cannot rule it out

WHAT to do:

1. Confirm diagnosis with bladder pressure (via urinary catheter) *see cited paper for how-to in the ED*
2. Emergent surgical consultation (emergent laparotomy → improved hemodynamics, organ function, & survival. 
3. Optimize abdominal perfusion pressure (MAP - intraabdominal pressure; recommended > 60mmHg) as much as possible:

• Adequate analgeisia and sedation, if needed, to avoid agitation
• Avoid intubation if able, to avoid the positive pressure. In intubated patients, aim for low PEEPs and plateau pressures and consider short-term paralytic
• Lower the head of bed (supine to 30mmHg) to minimize abdominal "crunch"
• Aim for intravascular euvolemia. If volume overload is a contributing factor then IVF for hypotension will worsen the ACS -- start vasopressor instaed
• Evacuate intraluminal contents if able (NGT/rectal tube for decompression, consider erythromycin/reglan, or neostigmine for colonic pseudoobstruction)
• Evacuate intraabdominal extraluminal contents if able (therapeutic paracentesis for ascites(
• Burn patients with restrictive abdominal eschar should get escharotomy

Bottom Line: Abdominal compartment syndrome is an affliction of the critically ill, is assosciated with worsened mortality, and requires aggressive measures to lower the intraabdominal pressure while obtaining emergent surgical consultation for potential emergent laparotomy. 

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The arrival of a critically ill pregnant patient to the ED can be anxiety-provoking for emergency physicians as two lives and outcomes must be considered.

Some basic tenets of care, regardless of underlying issue, include:

• Obtain IV access above the diaphragm to avoid delay/prevention of administered products reaching central circulation due to compression of the IVC by the gravid uterus. 

• Provide supplemental oxygen as needed to maintain a saturation of >95% which corresponds to a PaO2 >70 mmHg. A PaO2 <60 mmHg is associated with fetal hypoxemia which will quickly lead to fetal acidosis and bradycardia. 

• Goal maternal PaCO2 is 28-32 mmHg; this respiratory alkalosis maintains a CO2 gradient to help shift offload fetal CO2 into the maternal circulation for clearance. 

• Hypotensive pregnant patients with a large uterus (20+ weeks) should be turned to the left lateral decubitus position or tilted leftward by at least 15 degrees to offload aortocaval compression and minimize secondary decrease in venous return) by the gravid uterus. 

• In cases of maternal cardiac arrest, the patient should be kept supine for chest compressions with the gravid uterus manually displaced to the left.

• Keeping the mother alive is the best way to keep the fetus alive. Standard sedatives, vasopressors, and inotropes are okay if they are needed. Exception for ketamine, which has mixed effects in existing studies and while low doses are probably safe if needed, use as a firstline agent is not recommended. Notify the NICU team of medications given to mother if there is a precipitous delivery.

• Fetal tococardiometry monitoring if available, or regular POCUS assessment of FHR, in all viable pregnancies.

Finally, once critical illness is identified the OB and NICU teams should be consulted immediately. Fetal distress in a viable pregnancy may be an indication for delivery, and initiation of the transfer process should occur if the supportive specialties are not in-house.

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When managing cardiac arrest, it is important to differentiate PEA, the presence of organized electrical activity without a pulse, from "pseudo-PEA,"where there is no pulse but there IS cardiac activity visualized on ultrasound. 

Why: 

• Pseudo-PEA is essentially a profound, low-flow shock state that often has reversible causes, such as hypovolemia, massive PE, tension pneumothorax, etcetera.
• Compared to PEA, with appropriate care patients with pseudo-PEA have a higher rate of ROSC as well as overall survival.

How: 

• POCUS during rhythm check in cardiac arrest. Be careful not to prolong the pause in compressions; acquire the US, if needed, for review once hands are back on the chest. 

What:

• In addition to searching for & addressing reversible causes of the pseudo-PEA, manage the profound shock state with pressors and/or inotropic support.
• In EDs where TEE is utilized during cardiac arrest resuscitations, strongly consider synchronization of external compressions with intrinsic cardiac activity to potentially improve ventricular filling and therefore coronary perfusion pressure.

Bottom Line: Pseudo-PEA is different from PEA. Utilize POCUS during your cardiac arrests to identify it and to help diagnose reversible causes, and treat it as a profound shock state with the appropriate supportive measures, i.e. pressors or inotropy. 

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The U.S. is currently experiencing an epidemic of a severe lung disease termed Vaping-Associated Pulmonary Illness (VAPI), with over 500 cases and 7 deaths across 38 states and 1 U.S. territory since July 2019.

The clinical presentation of VAPI varies -- 

• Respiratory (SOB, cough, chest pain), constitutional (fever, tachycardia, headache, dizziness), and potentially GI symptoms (vomiting, diarrhea) after the use of vaping devices. GI symptoms may precede respiratory issues.
• Can take days or worsen over weeks and can present or end up with severe respiratory failure

Diagnostics --

• Labs nonspecific: Leukocytosis, elevated ESR, no specific infectious etiology
• Chest CT generally with bilateral infiltrates
• Bronchoscopy with BAL demonstrates PMNs and may have lipid-laden macrophages on Oil red O or Sudan staining

Treatment is supportive +/- steroids -- 

• Current recommendations to treat similarly to ARDS in intubated patients
• Potential benefit to steroids if not contraindicated

Bottom Line: Include vaping-associated pulmonary illness in your differential for patients presenting with acute lung disease.

• Ask patients about use of e-cigarette/vaping devices.
• Notify the CDC or your state health department of any suspected cases.
• Counsel your patients to avoid the use of these devices, at the very least until the specific causative agent is found.

Show Additional Information

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Managing the intubated patient with exacerbation of severe obstructive lung disease, especially asthma, can be very challenging as it carries higher risks of barotrauma due to higher pulmonary pressures and circulatory collapse due to auto-PEEP and decreased venous return. When measures such as medical therapy and noninvasive positive-pressure ventilation fail to prevent intubation, here are some tips to help:

1. Utilize a volume control ventilation mode to ensure a set tidal volume delivery / minute ventilation, as pressure-targeted modes will be more difficult due to the high pulmonary pressures in acute obstructive lung disease.

2. Set a low RR in order to allow for full exhalation, avoiding air-trapping / breath-stacking and circulatory collapse due to decreased venous return. This may require deep sedation and potentially paralysis.

• Permissive hypercapnea to >7.2 is generally well-tolerated except for pregnant patients, patients with high ICP, or patients with severe pulmonary hypertension

3. Increase your inspiratory flow by shortening your inspiratory time (thereby increasing your time for exhalation.

4. Monitor for auto-PEEP:

• Check your flow curve -- the waveform should return to zero before the start of the next inhalation, otherwise the next breath has been given before the patient has fully exhaled.
• Perform an expiratory hold at the end of exhalation. PEEP greater than set PEEP = auto-PEEP.

5. Peak inspiratory pressures will be high -- what is more important is the plateau pressure, measured by performing an inspiratory hold at the end of inspiration. Provided your plateau pressure remains <30, you don't need to worry as much about the peak pressure alarms.

6. If your patient acutely decompensates in terms of hemodynamics and oxygenation -- first attempt to decompress their likely auto-PEEPed lungs by popping them off the ventilator and manually press on their chest to assist with exhalation of stacked breaths allowing venous return to the heart.

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Background:  Previous systematic reviews^1,2,3 have indicated that the absence of cardiac activity on point-of-care ultrasound (POCUS) during cardiac arrest confers a low likelihood of return of spontaneous circulation (ROSC), but included heterogenous populations (both traumatic and atraumatic cardiac arrest, shockable and nonshockable rhythms).

The SHoC investigators⁴ are the first to publish their review of nontraumatic cardiac arrests with nonshockable rhythms, evaluating POCUS as predictor of ROSC, survival to admission (SHA), and survival to discharge (SHD) in cardiac arrests occurring out-of-hospital or in the ED.

• 10 studies, 1485 patients
• Compared to absence of cardiac activity, presence of cardiac activity = higher odds, increased incidence of ROSC, SHA, and SHD
• Pooled sensitivity for ROSC, SHA, SHD relatively low (60%, 75%, 69%, respectively)
  • On subgroup analysis, sensitivity higher in PEA group (77%) than asystole group (25%)

Bottom Line:  In nontraumatic cardiac arrest with non-shockable rhythms, the absence of cardiac activity on POCUS may not, on its own, be as strong an indicator of poor outcome as previously thought.

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When managing transplant patients it is important to keep in mind the anatomic and physiologic changes that occur with the complete extraction of one person's body part to replace another's. 

For cardiac transplant patients with symptomatic bradycardia:

• Remember that due to lack of autonomic/vagal innervation, resting HR should be around 90 bpm.
• HR will not respond to atropine. Use direct sympathomimetics like epinephrine instead.
• If medication is unsuccessful, proceed to transcutaneous or transvenous pacing.

For cardiac transplant patients with tachyarrythmias:

• They are particularly sensitive to adenosine; for SVT start with 1 to 3mg adenosine push (3mg is usually effective) to avoid sustained bradycardia or asystole.
• Digoxin is not effective as an antiarrhythmic.
• Diltiazem can decrease the metabolism of calcineurin inhibitor immunosuppressive agents (such as cyclosporine and tacrolimus), so while it can be used there may need to be dose adjustments to these medications. 

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The PROTRACH study recently compared preoxygenation with standard bag valve mask (BVM) at 15 lpm to preoxygenation + apneic oxygenation with high flow nasal cannula 60 lpm/100% FiO2 in patients undergoing rapid sequence intubation.

• There was no significant difference in the primary outcome of median lowest SpO2 during intubation. 
• There were more intubation complications in the BVM group compared to the HFNC group:
  • Severe complications: SpO2 <80%, severe hypotension (SBP < 80mmHg or vasopressor initiation/increase by 30%), and cardiac arrest (6% HFNC vs 16% BVM, RR 0.38, 95% CI 0.15-0.95, p=0.03). 
  • Moderate complications: aspiration, cardiac arrhythmia, agitation, and esophageal intubation (0% HFNC vs 7% BVM, p= 0.01). 
• There was no difference in ventilator days, ICU length of stay, or mortality.

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Despite ongoing research and efforts to improve our care of patients with ARDS, it remains an entity with high morbidity and mortality. Early recognition of the disease process and appropriate management by emergency physicians can have profound effects on the patient's course, especially in centers where ICU boarding continues to be an issue.

Recognition of ARDS (Berlin criteria)

• Acute in onset
• Bilateral infiltrates on chest imaging not due to cardiac failure/volume overload
• PaO2 : FiO2 < 300 despite PEEP of at least 5cmH2O 
• This is the standard ED patient who gets intubated with multifocal pneumonia and has continued hypoxemia

*An ABG should be obtained in the ED if physicians are unable to wean down FiO2 from high settings, if oxygenation by pulse ox is marginal, or if the patient is in a shock state.

Tenets of ARDS Management:

• Low tidal volume ventilation (6-8ml/kg ideal body weight*)
• Maintain plateau pressures (Pplat) < 30 cmH2O
• Driving pressure (Pplat – PEEP) < 15 cmH2O
• Goal PaO2 > 55-60 
• Permissive hypercapnia to pH >7.2

*IBW Males = 50 + 2.3 x [Height (in) - 60]   /  IBW Females = 45.5 + 2.3 x [Height (in) - 60]

Strategies for Refractory Hypoxemia in the ED:  You can't prone the patient, but what else can you do? 

1. Escalate PEEP in stepwise fashion

• ex: 2cmH20 every 10 minutes
• can use ARDSnet PEEP/FiO2 table as guide

2. Recruitment maneuvers

• "20 of PEEP for 20 seconds" or "30 for 30"
• if patient is "PEEP responsive," leave PEEP on a higher setting than when you started (ex: 10 instead of 5, 16 instead of 10)
• Risk of barotrauma with higher PEEPs and hypotension in underresuscitated or hemodynamically unstable patients due to decreased venous return

3. Appropriate sedation and neuromuscular blockade

• promotes patient synchrony with lung protective settings
• can result in improved oxygenation by itself

4. Inhaled pulmonary vasodilators (inhaled prostaglandins, nitric oxide) if known or suspected right heart failure or pulmonary hypertension

Bottom Line: Emergency physicians are the first line of defense against ARDS. Early recognition of the disease process and appropriate management is important to improve outcomes AND to help ICU physicians triage which patients need to be emergently proned or even who should potentially be referred for ECMO. 

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Neutropenic enterocolitis can occur in immunosuppressed patients, classically those being treated for malignancy (hematologic much more commonly than solid tumor). When involving the cecum specifically, it is known as "typhlitis."

It should be considered in any febrile neutropenic patients with abdominal pain or other symptoms of GI discomfort (diarrhea, vomiting, lower GI bleeding), and can be confirmed with CT imaging.

A recent study found that invasive fungal disease, most often candidemia, occurred in 20% of febrile neutropenic patients with CT-confirmed enteritis, a rate that increased to 30% if the patient was in septic shock.

Take Home: 

1. Have a lower threshold for abdominal CT imaging in your patients with febrile neutropenia and abdominal pain/GI symptoms, especially if they are critically ill.

2. Consider addition of IV antifungal therapy if they are hemodynamically unstable with enterocolitis on CT.

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Historically, there has been very limited data regarding the epidemiology of OHCA in pregnant females. Two recently-published studies tried to shed some light on the issue.

Both Maurin et al.¹ and Lipowicz et al.² looked at all-cause out-of-hospital maternal cardiac arrest (MCA) data in terms of numbers and management, in Paris and Toronto respectively, from 2009/2010 to 2014. Collectively, they found: 

• MCA was relatively rare: 0.8 MCA per 1000 OHCA (Maurin) and 1.71 MCA per 100,000 pregnant females (Lipowicz)
• Low incidence of bystander CPR in witnessed MCA (33% and 0%)
• Adherence to PMCS guidelines was poor 
• Maternal survival was lower than what has been previously quoted for in-hospital CA: 12.5 and 16.7% compared to 40-50%^3,4

A few reminders from the 2015 AHA guidelines for the management of cardiac arrest in pregnancy: 

• Hand location for chest compressions should be in the center of the chest as for nonpregnant patients (previous recommendations had been to shift upward to accommodate for the gravid uterus but there is no data to support this).

• Chest compressions should be performed with the patient supine, using manual lateral uterine displacement for aortocaval decompression. Left lateral tilt position is no longer recommended due to poorer quality of cardiac compressions, the lack of full aortocaval decompression, and further complication of other procedures such as airway management.

• IV or IO access should be obtained above the diaphragm, to ensure no interference to flow to the heart by the gravid uterus.

• Rate and depth of chest compressions, ACLS drugs and doses, and defibrillation all remain the same as in nonpregnant OHCA patients.
  • NB: As opposed to nonpregnant patients periarrest, oxygen saturation in the pregnant female should be maintained at 95% or greater, or PaO2 > 70mmHg, to ensure appropriate oxygen delivery to the fetus. The goal PCO2 is ~28-32 mmHg, to facilitate fetal CO2 removal.⁶  

• If advanced airway is pursued, the most experienced provider should perform intubation due to the higher intrinsic difficulties, more rapid decompensation, and propensity for airway trauma and bleeding in the pregnant female.

• Perimortem c-section should occur within the first 5 minutes of cardiac arrest / arrival to the ED in ongoing arrest. 

Bottom Line: Although maternal cardiac arrest is relatively rare, survival in OHCA is lower than perhaps previously thought. Areas to improve include public education on the importance of bystander CPR in pregnant females, and appropriate physician adherence to PMCS recommendations, with decreased on-scene time by EMS in order to decrease time to PMCS. 

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