UMEM Educational Pearls - Critical Care

During the height of the pandemic, a large proportion of patients who were referred to our center for VV-ECMO evaluation were on Airway Pressure Release Ventilation (APRV).  Does this ventilation mode offer any advantage?  This new randomized control trial attempted to offer an answer.

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1.Settings: RCT, single center

2. Patients: 90 adults patients with respiratory failure due to COVID-19

3. Intervention: APRV with maximum allowed high pressure of 30 cm H20, at time of 4 seconds.  Low pressure was always 0 cm H20, and expiratory time (T-low) at 0.4-0.6 seconds. This T-low time can be adjusted upon analysis of flow-time curve at expiration.

4. Comparison: Low tidal volume (LTV)  strategy according to ARDSNet protocol.

5. Outcome: Primary outcome was Ventilator Free Days at 28 days.

6.Study Results:

• Baseline characteristics were similar. At randomization, PF ratio for APRV group = 140 (SD 42) vs. 149 (SD 50) for LTV group.
• Median Ventilator Free Day for APRV group: 3.7 [0-15] days vs. 5.2 [0-19] for LTV group ( P = 0.28)
• APRV group had higher PaO2/FiO2 ratio during first 7 days (mean difference = 26, P<0.001)
• ICU length of stay for APRV group: 9 [7-16] vs. 12 [8-17] days (P = 0.17)
• Severe hypercapnia (Pco2 at ≥ 55 along with a pH < 7.15): APRV group = 19 (42%) vs. LTV = 7 (15%), P = 0.009.
• Death at 28 days: 35 (78%) for APRV group, vs. 27 (60%) for LTV group ( P = 0.07)

7.Discussion:

• Hypercapnea was transient and was mostly due to implementation of the ventilator settings.  The protocol recommended reduction of T-high to allow more ventilation, but most clinicians did not want to shorten the T-High, but instead opted for higher T-low.
• Although the number of barotrauma were similar in both group, all 4 cases of barotrauma in the APRV group occurred within a very short period of time (3 weeks), prompted the safety monitoring board to recommend stopping recruitment for COVID-19 patients.

8.Conclusion:

APRV was not associated with more ventilator free days or other outcomes among patients with COVID-19, when compared to Low Tidal Volume strategies in this small RCT.

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The use of catecholamines following OHCA has been a mainstay option for management for decades. Epinephrine is the most commonly used drug for cardiovascular support, but norepinephrine and dobutamine are also used. There is relatively poor data in their use in the out of hospital cardiac arrest (OHCA). This observational multicenter trial in France enrolled 766 patients with persistent requirement for catecholamine infusion post ROSC for 6 hours despite adequate fluid resuscitation. 285 (37%) received epinephrine and 481 (63%) norepinephrine.

Findings

• Deaths from refractory shock (35% vs. 9%, P<0.001) and Recurrent cardiac arrest (9% vs. 3%, P<0.001) were higher in the epinephrine group
• In both univariate/multivariate analyses, use of epinephrine was significantly associated with:
  • All-cause mortality during the hospital stay (83% vs. 61%, P<0.001) / (OR 2.6, 95%CI 1.4–4.7, P=0.002)
  • Cardiovascular-specific mortality (44% vs. 11%, P<0.001) / (aOR 5.5, 95%CI 3.0–10.3, P<0.001)
  • Frequency of unfavorable neurological outcomes (37% vs. 15%, P<0.001) / (aOR 3.0, 95%CI 1.6–5.7, P=0.001)
• While propensity scoring and match analysis largely confirmed these findings, further regression did not associate epinephrine with all-cause mortality.

Limitations:

• Epinephrine arm: significantly longer time to ROSC, lower blood pH at admission, higher rates of unshockable rhythm, higher levels of arterial lactate at admission, lower LV ejection fraction, and higher levels of myocardial dysfunction.
• Propensity matching always has the potential for confounders.

Summary:

Norepinephrine may be a better choice for persistent post-arrest shock. However, this study is not designed to sufficiently address confounders to recommend abandoning epinephrine altogether, but it does give one pause. 

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Acute liver failure is defined as new and rapidly evolving hepatic dysfunction associated with neurologic dysfunction and coagulopathy (INR >1.5). Most common cause of death in these patients are multiorgan failure and sepsis. Drug-induced liver injuy most common cause in US, with viral hepatitis most common cause worldwide.

Management of complications associated with acute liver failure

• Hepatic encephlopathy: Administer lactulose orally or via enema if risk of aspiration. Goal is to slow progression to severe encephalopathy and minimize development of cerebral edema.
• Coagulopathy: Reverse if significant bleeding or if patient needs to have invasive procedure. FFP and 4-factor PCC not indicated in absence of bleeding. Additionally these patients may be vitamin-K deficient for which vitamin K can be given.
• Consider empiric antibiotics due to increased susceptibility to infection.
• Renal dysfunction: correct hypovolemia with fluid resuscitation. May require RRT, continuous preferred for hemodynamic stability.
• If persistent hypotension despite adequate volume resuscitation and pressors, IV hydrocortisone indicated as adrenal insufficiency is common in these patients.
• Early consultation with liver transplant center. King's College Criteria and MELD score are most commonly used prognostic tools.

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How to set the correct PEEP remains one of the most controversial topics in critical care.  In fact, just on UMEM Pearls there are 55 hits when one searches for PEEP, including this relatively recent pearl on PEEP Titration.  

A recent Systematic Review and Network Meta-Analysis looked at existing trials on this issue.  They found that:

1) Higher PEEP strategies were associated with a mortality benefit compared to lower PEEP strategies

2) Lung Recruitment Maneuvers were associated with worse mortality in a dose (length of time of the maneuver) dependent fashion.

This fits with recent literature and trends in critical care and bolsters the feeling many intensivists are increasingly having that we may be under-utilizing PEEP in the average patient.  

Bottom Line: As an extremely broad generalization, we would probably benefit the average patient by favoring higher PEEP strategies, and avoiding lung recruitment maneuvers.  Do keep in mind that it is probably best to continue lower PEEP strategies in patient populations at high risk of negative effects of PEEP (e.g. COPD/asthma, right heart failure, volume depleted with hemodynamic instability, bronchopleural fistula) until these groups are specifically studied.

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Hyperglycemic Hyperosmolar State (HHS)

• Though less common, HHS has a mortality rate that is 10x greater than DKA.
• The hallmark features of HHS include severe hyperglycemia (> 600 mg/dL), hyperosmolality (> 320 mOsm/kg), minimal to no ketosis, and severe dehydration.
• Though the management of HHS is similar to DKA and includes fluid resuscitation, correction of hyperglycemia, and correction of electrolyte abnormalities, it is important to also monitor serum osmolality.
• Too rapid correction of serum osmolality can cause cerebral edema and worsen patient outcomes.
• Current recommendations are to monitor serum osmolality every 1-2 hours with a correction of no more than 3 mOsm/kg/hr.

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The debate is still going on: Whether we should give balanced fluids or normal saline.  

Settings: PLUS study involving 53 ICUs in Australia and New Zealand. This was a double-blinded Randomized Control trial.

• Patients: A total of 5037 adults who were admitted to any ICU.
• Intervention: Balanced multielectrolyte solutions (BMES). Once patient is outside the ICU, the type of fluid was decided by the treating physicians.
• Comparison: Normal saline
• Outcome: 90-day all cause mortality.

Study Results:

• Patient characteristics:
  • 2515 patients in BMES group vs. 2522 in Saline group.  Characteristics were similar in both groups.
  • Median fluid amount = 3.9L (BMES group) vs. 3.7L (Saline group).
• Primary outcome:
  • Mortality = 21.8% (BMES group) vs. 22.0 (Saline), (OR 0.99, 95% CI 0.86-1.14)
• Secondary outcomes:
  • Requiring Dialysis: OR 0.98 (95% CI 0.83-1.16)
  • Requiring vasopressor: OR 0.92 (95% CI 0.78-1.09)
  • Maximum creatinine level: similar between groups (155.5 umol/L for BMES vs. 154.5 umol/L for Saline group)

Discussion:

• Treatment with saline increased serum chloride, and lower pH than BMES, but kidney function was not affected.

• An updated meta-analysis including this trial was also published in January 2022. This updated meta-analysis showed that the risk ratio for 90-day mortality for BMES was 0.96 (95% CI 0.91-1.01).  This data suggested that using BMES could reduce risk of death (up to 9%) or increase risk of death (up to 1%).
• Appropriate volume resuscitation is still more important than the type of fluid.

Conclusion:

• BME treatment was not associated with improved mortality.

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A prospective, randomized, open-label, parallel assignment, single-center clinical trial performed by an anesthesiology-based Airway Team under emergent circumstances at UT Southwestern.

801 critically ill patients requiring emergency intubation were randomly assigned 1:1 at the time of intubation using standard RSI  doses of etomidate and ketamine.

Primary endpoint: 7-day survival, was statistically and clinically significantly lower in the etomidate group compared with ketamine 77.3% (90/396) vs 85.1% (59/395); NNH = 13.

Secondary endpoints: 28-day survival rate was not statistically or clinically different for etomidate vs ketamine groups was no longer statistically different: 64.1% (142/396) vs 66.8% (131/395). Duration of mechanical ventilation, ICU LOS, use and duration of vasopressor, daily SOFA for 96 hours, adrenal insufficiency not significant.

Other considerations:

1. Similar to a 2009 study, ketamine group had lower blood pressure after RSI, but was not statistically significant. 2

2. Etomidate inhibits 11-beta hydroxylase in the adrenals. Associated with positive ACTH test and high SOFA scores, but not increased mortality.2

3. Ketamine raises ICP… just kidding.

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Clinical pearls for hypothermic cardiac arrest

• VA-ECMO is rewarming strategy of choice – consider transport/contacting nearest ECMO center whenever possible
  • HOPE score predicts survival probability after ECLS rewarming and may guide ECLS decision making. Predictors include age, sex, mechanism of hypothermia, CPR duration, potassium, and core temperature at admission
• If access to ECMO center is not available, use external and internal rewarming strategies: removing wet clothes, forced-air heating blankets, warmed IV fluids (38-42C), thoracic and/or peritoneal lavage
• High-quality continuous CPR is key. Use mechanical CPR when available
• Lack of consensus with regards to ACLS guidelines. European Resuscitation Council recommends up to 3 attempts at defibrillation and withholding epinephrine while core temp is < 30C. AHA states reasonable to follow standard ACLS algorithms. It has been suggested that administering up to 3 shocks and 3 doses of epinephrine while core temp is <30 C is a reasonable approach, with additional doses guided by clinical response
• Resuscitate until core temp is at least 32C (warm and dead). Once rewarmed, consider termination of resuscitation with persistent asystole or K >12

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Background: Conventional medical wisdom long held that patients with pneumothorax (PTX) who require positive pressure ventilation (PPV) should undergo tube thoracostomy to prevent enlarging or tension pneumothorax, even if otherwise they would be managed expectantly.¹

• Small retrospective and observational studies have demonstrated safety to an observational approach for both occult (only detectable on CT) and larger PTXs even in patients requiring noninvasive or invasive mechanical ventilation, whether traumatic/iatrogenic or spontaneous.^2-6
• The Western Trauma Association recently released a guideline for the management of traumatic PTX, which includes observation with 6-hour follow up CXR for patients with small (<20% aka <2cm from chest wall on CXR or <35 mm on CT scan) hemodynamically stable pneumothoraces, even if mechanical ventilation is required.⁷
  • They note a 10% subsequent failure rate (i.e. chest tube requirement) with no difference between patients who do or do not undergo PPV. 
• The OPTICC trial, found however, that while the rate of respiratory distress development was not different between those randomized to observation vs initial chest tube management, there was an increase from a 25% chest tube requirement in the obs group to a 40% failure rate in patients requiring >4 days of mechanical ventilation.⁸ 

Bottom Line: The cardiopulmonar-ily stable patient with small PTX doesn’t need empiric tube thoracostomy simply because they’re receiving positive pressure ventilation. If you are unlucky enough to still have them in your ED at day 5 in these COVID times, provide closer monitoring as the observation failure rate may increase dramatically around this time.

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   There are several well known medications that we tend to give by default during cardiac arrests.  It seems like for each of them, every few years someone does an RCT to see if they really help anybody, and we're all disappointed by what they find.  Well... prepare to be disappointed again, I'm afraid.

   These Danish authors randomized 391 patients in cardiac arrest to either calcium or saline (given IV or IO).  They gave 2 doses of either calcium chloride or saline, with the first dose being along with the first epi dose.  Primary outcome was ROSC.  They also looked at modified Rankin at 30 and 90 days.

  The trial was stopped early for harm.  Now, we all know the dangers of interpreting studies that were stopped early, but this doesn't look great for calcium.  19% of the calcium group had ROSC compared to 27% of the saline group (p = 0.09).  Percentage of patients alive, and with favorable mRS at 30 days also both favored the saline group (although also not statistically significantly).  By the way, of the patients who had calcium levels sent, 74% in the calcium group, vs 2% in the saline group, were hypercalcemic.  Whether that had anything to do with the outcome, we may never know.

Bottom Line:  Is this saying that calcium hurts patients in cardiac arrest?  Maybe... but I don't think this is high quality enough data to draw that conclusion.  At the very least, however, just giving everyone in arrest calcium is probably not terribly helpful.  If you have a reason to give it (known severe hypocalcemia, recent parathyroid surgery, suspected hyperkalemia, etc) then go for it, otherwise you can probably focus your resus on more important things.

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The BOUGIE Trial

• More than 1 million patients undergo endotracheal intubation each year in the US.
• Up to 20% of intubations fail on the first attempt, thereby increasing the risk of adverse outcome.
• Over the past several years, many have become comfortable using the bougie as a rescue device when the first attempt at intubation fails with an endotracheal tube with stylet.
• In contrast to its use as a rescue device, should the bougie be used during the first attempt rather than an endotracheal tube with a malleable stylet?
• The BOUGIE Trial compared the effect of using the bougie to an endotracheal tube with stylet on first attempt success in critically ill patients.
• The trial enrolled 1106 patients in 7 EDs and 8 ICUs at 11 hospitals.
• The primary outcome of first pass success was not statistically different between those randomized to bougie and those randomized to endotracheal tube with stylet for the first attempt at intubation.. 
• Though the trial did not find a statistical difference in first pass success rates, the bougie remains an important device in our management of the critically ill airway.

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When we initiate the sepsis bundle in the ED for patients with suspected sepsis, what probability that those patients who received broad spectrum antibiotics in the ED would have bacterial infection.

This study (Shappell et al) provides us with a glimpse of those number.

Settings: Retrospective study of adults presenting to 4 EDs in Massachusetts.

Patients: patients with suspected serious bacterial infection in ED, defined as blood cultures and initiation of at least one broad spectrum antibiotics.  Random selection of 75 patients per hospital.

Patients were categorized in 4 groups:

• Definite bacterial infection: clinical syndrome, pathologic diagnosis of infection (positive cultures from blood, urine; pus; radiographic evidence of abscess, consolidations in lungs)
• Likely bacterial infection: not meeting criteria for definite infection, but having a compatible clinical syndrome responsive to antibiotics and no clear etiology or reason for clinical improvement.
• Unlikely bacterial infection: clinical syndrome consistent with infection, but an alternate diagnosis is more likely.
• Definitely no bacterial infection: there was clear non-infectious diagnosis and no evidence of concurrent bacterial process.

Outcome: Prevalence of each category.

Study Results: 300 patients who received broad spectrum antibiotics.

1. Prevalence of bacterial infection:
   1. 81 (27%) had definite bacterial infection
   2. 104 (34.7%) had likely bacterial infection
   3. 55 (18.3%) had unlikely bacterial infection
   4. 49 (16.3%) with definitely no bacterial infection
2. For 96 patients with suspicion of sepsis vs. the rest of the cohort (P = 0.36)
   1. Definite 42.7%
   2. Likely 29.2%
   3. Unlikely 16.7%
   4. Definitely no 11.5%

       3. For patients who were admitted to the ICU (P = 0.26)

  a.   Definite 16.5%

                b.   Likely 8.6%

  c.   Unlikely 16.4%

                d.   Definitely no 20.4%

4. Source of infection

5.  Definite/Likely bacterial infection
   1. GU = 69 (35%)
   2. Respiratory = 48 (24.4%)
   3. Skin or soft tissue = 45 (22.8%)
   4. Bacteremia or endovascular = 42 (21.3%)
   5. Abdominal = 24 (12.2%) 
6. Unlikely/definitely not bacterial infection

1. Viral = 27%
2. Volume overload/cardiac disease = 10%
3. Hypovolemia = 8%

Discussion:

1. Slightly more than half of the patient we covered with broad spectrum antibiotics would have definitely or likely bacterial infection.
2. This study agreed with previous studies (2), which suggested that for patients treated prophylactically for sepsis, 13% had a “none” likelihood, 30% of only "possible" likelihood for bacterial infection.
3. The study highlighted that it was not easy for Emergency clinicians to recognize bacterial infection when we operate on a limited source of information and a limited timeline (think about the bundle of sepsis).
4. However, overtreatment is also bad, so we just need to be cognizant.

Conclusion:

Approximately 30% of patients who had blood cultures drawn and received broad spectrum antibiotics in ED have low likelihood of bacterial infection.

Reference:

1. Shappell CN, Klompas M, Ochoa A, Rhee C; CDC Prevention Epicenters Program. Likelihood of Bacterial Infection in Patients Treated With Broad-Spectrum IV Antibiotics in the Emergency Department. Crit Care Med. 2021 Nov 1;49(11):e1144-e1150. doi: 10.1097/CCM.0000000000005090. PMID: 33967206; PMCID: PMC8516665.

2. Klein Klouwenberg PM, Cremer OL, van Vught LA, Ong DS, Frencken JF, Schultz MJ, Bonten MJ, van der Poll T. Likelihood of infection in patients with presumed sepsis at the time of intensive care unit admission: a cohort study. Crit Care. 2015 Sep 7;19(1):319. doi: 10.1186/s13054-015-1035-1. PMID: 26346055; PMCID: PMC4562354.

Clinical Pearls for Variceal Hemorrhage

-lower mortality with “restrictive” (Hgb 7-9 g/dL) rather than liberal strategy

• although you should c/w your blood resuscitation according to hemodynamics

-antibiotic “prophylaxis” reduces mortality

• use ceftriaxone rather than quinolone 2/2 increasing resistance

-no need to correct INR with FFP

• FFP transfusions may actually be associated with worse outcomes (e.g. inc’d mortality)

-vasoactives (i.e. octreotide, somatostatin, terlipressin) alone may actually control bleeding

-for your ICU boarders...if persistent or severe rebleeding (despite endoscopic therapy), rescue TIPS is therapy of choice (call IR)

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Myocarditis is a potentially fatal inflammatory disorder of the heart. Viral infection is the most common cause but can also result from toxic, autoimmune, or other infectious etiologies. Complications include life-threatening dysrhythmias, heart failure, and fulminant myocarditis. Typically affects young patients (20-50 years old).

• Diagnosis can be challenging. Presentation can range from nonspecific symptoms and normal hemodynamics to cardiogenic shock.
• Dyspnea was found to be the most common presenting symptom in one study
• Other symptoms include fever, malaise, chest pain, palpitations, fatigue, nausea, vomiting
• Consider the diagnosis in young patient with suspected sepsis but worsens with IV fluids with signs of volume overload
• Initial assessment should include ECG, CBC, CMP, inflammatory markers, cardiac biomarkers, CXR. Obtaining an echo is important. Perform POCUS to assess for global hypokinesis, reduced EF, wall motion abnormalities, pericardial effusion, B-lines.

ED management pearls

• Initiate vasopressors and inotropic support if hemodynamically unstable: norepinephrine + inotropic agent (e.g. milrinone, dobutamine) is recommended. In a few studies, epinephrine was associated with increased mortality when used in cardiogenic shock.
• Diurese if evidence of volume overload
• NIPPV or intubation if respiratory failure
• Avoid NSAIDs which may worsen mortality
• Consider mechanical circulatory support (e.g. ECMO, IABP, VAD) in refractory hypotension despite appropriate medical therapy

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Fever has long been understood to be associated with worse outcomes in patients post-cardiac arrest. Whether ascribing to the goal of 33-34°C, 36°C, or simply <38°C, close monitoring and management of core temperatures are a tenet of post-cardiac arrest care.

A recently published study compared the effectiveness of several methods in maintaining temperatures <38°C…

• Both ICHA and OHCA, shockable and unshockable, nontraumatic arrests
• Single center retrospective cohort study looking at 1/2012 – 9/2015
• Treatment and temperatures over first 48 hours

Results:

Maintenance of temp <38°C:

• Antipyretics only group: 57.7% 
• Invasive cooling by intravascular catheter +/- antipyretics:  82.1%

Mean change in temp from baseline:

• Antipyretics only: +1.1°C
• Intravascular alone: -3.4°C
• Antipyretics + Intravascular cooling: -5.2°C

Limitations:

• Varied range of antipyretic dosing per body weight
• No mention of noninvasive cooling methods (cooling pads, ice packs, etc.)
• Patients w/ intravascular cooling likely getting more aggressive care in general
• Not powered for clinical outcomes assessment

Bottom Line:

• Antipyretics alone greatly ineffective at preventing fever 
• Even with invasive cooling -- not meeting goal 18% of the time
• With longer ED boarding times nationwide, we must pay active attention to body temperature management and not assume that that we can set it and forget it, even with techniques as invasive as intravascular cooling.

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The debate around post-arrest management recently has revolved around whether therapeutic hypothermia should go cold, or LESS cold.  But what if we went MORE cold?  While recent TTM trials have compared temps such as 33 to 36 and 33 to 37.5 or less, a recent trial called CAPITAL CHILL looked at 34C vs 31C.  There is a solid physiologic basis for cooling post-arrest patients, so do they do better if we lower their temp even further?  Maybe we're not going cold enough with 33?

Bottom Line: No, 31C is not better than 34C for post-arrest patients.  This study compared death and poor neurologic outcome at 180 days with 31 and 34C targets for post-arrest patients, and found no difference (in fact the 31C group did slightly, but not significantly, worse on the primary outcome, and worse on a few secondary outcomes).  

While debate remains for 33 vs 36 vs afebrile, the literature does not currently support consideration of temps below 33.  

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Initial Mechanical Ventilation Settings for the Intubated Asthmatic

• Approximately 2% of adult patients who present with an acute asthma exacerbation will require intubation and mechanical ventilation.
• It is critical to provide the intubated asthmatic with sufficient time for exhalation.
• Initial recommended settings for mechanical ventilation include:
  • Tidal volume: 6-8 ml/kg ideal body weight
  • Respiratory rate: 6-10 breaths per minute
  • PEEP: 0-5 cm H2O
  • Inspiratory flow rate: 80-120 L/min
• Permissive hypercapnea is tolerated to a pH of approximately 7.15

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Background: A cornerstone of therapy for cardiogenic shock is inotropic support with medications including dobutamine, epinephrine and milrinone.  Few studies have examined these head-to-head and between dobutamine and milrinone (including only one RCT of 36 patients)

The investigators conducted a RCT of milrinone versus dobutamine for cardiogenic shock in a single quaternary care center cardiac ICU.

Inclusion: Patients over 18 with cardiogenic shock (largely clinical determination)

Exclusion: Out-of-hospital cardiac arrest, pregnancy, prior initiation of dobutamine or milrinone, or physician discretion.

Methods: 1:1 randomization stratified by affected ventricle (LV vs RV). Primary outcome was a composite of in-hospital death, resuscitated cardiac arrest, cardiac transplant, mechanical circulator support, nonfatal MI, TIA, stroke, or renal replacement therapy. Powered to detect a 20% improvement in this measure in the milrinone group (192 pts).

Results:  192 patients enrolled (96 in each arm). Average age was 70, 36% female, 90% LV dysfunction, 67% ischemic disease, 33% non-ischemic, average LVEF 25%, 68% on vasopressors. ICU admission to randomization was 23+/-92.6h for dobutamine and 17.6+/-50.6h for milrinone arms. 80% were SCAI class C shock.

Primary outcome for milrinone 49% versus dobutamine 54%, HR 0.9(0.69-1.19), p=0.47, death was the primary driver of the composite (37% vs 43%).  Arrythmia requiring intervention was not different between groups (50% vs 46%). No difference in a host of other endpoints including AKI (92% vs 90%), RRT (22% vs 17%), HR, lactate, MAP, UOP, and creatinine.

Discussion: No significant differences observed in outcomes for patients with cardiogenic shock randomized to milrinone versus dobutamine.  The trial addressed an important clinical question for management of cardiogenic shock and relied largely on clinical diagnosis for inclusion and likely reflected a somewhat broad range of patients. The trial was too small given observed treatment effects and few patients with RV failure. Notably, similar rates of adverse events observed in each group.  

Many limitations for practice including a single specialized ICU setting, limited information on events leading to ICU admission including invasive or medical interventions during the index visit and no long term follow-up.  Time to randomization, exclusion of cardiac arrest, and lack of reporting pre-ICU setting (ED, floor, cath lab) also significantly limits utility in an emergency setting.

Bottom Line: 192 patient single-center cardiac ICU-based trial shows no difference in composite or secondary endpoints between milrinone and dobutamine for cardiogenic shock, adds to a body of very limited RCTs comparing inotropes in cardiogenic shock but provides no practice changing evidence.

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Intubation considerations

• Use large ET tube (at least 8.0 if possible): minimizes airway resistance, facilitates aggressive pulmonary toilet and bronchoscopy if needed
• Consider using ketamine as induction agent as it has bronchodilator properties and can maintain blood pressure
• Appropriate choices for initial sedation includes propofol, fentanyl, and ketamine

Vent management strategies

• No overall outcome differences between volume vs pressure control modes. Volume control has been recommended as initial mode due to familiarity and ensures your set tidal volume will be delivered.
• Goal is to minimize autoPEEP, which occurs from incomplete exhalation prior to initiation of next inhaled breath. This can be achieved by adjusting a few vent settings: decreasing RR, decreasing I:E ratio, decreasing inspiratory time, or increasing inspiratory flow rate. Allow for permissive hypercapnia, pH >7.2 has been advocated though precise target is unknown.
• If patient becomes hemodynamically unstable, consider first disconnecting the ventilator from the ET tube and manually decompress the chest to facilitate exhalation.
• Peak inspiratory pressures are expected to be high in the acute severe asthmatic. More important is to keep plateau pressures <30 cm H₂O to prevent lung injury.
• Don't forget to continue asthma-directed therapy. Administer albuterol via in-line nebulization unit of the vent.

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