Recall that MAP = (cardiac output) x (systemic vascular resistance)

Consequently, a patient can be normotensive due to increased SVR despite a very low cardiac output and shock. In fact, normotensive shock may have worse outcomes compared to patients with isolated hypotension. 

Take home points: 

• Shock does not equal hypotension
• In critically ill patients with reduced cardiac output, additionally use other markers for end-organ perfusion (mental status, renal function/urine output, LFTs, cap refill, lactate etc.) to assess for possible shock

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Question

This is an actual patient case:

65 y/o pt intubated for hemoptysis and started on nebulized transexamic acid. Overnight, the pt is found to have severe breath stacking/auto-PEEPing and consequently is started on neuromuscular blockade. The pt has no history of asthma or COPD and the ETT is clear without obstruction. 

Ventilator waveforms are as shown. What is the issue?

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PEEP is often titrated up along with FiO2 to increase oxygen saturation. Although the potential negative hemodynamic effect of high PEEP is often recognized, it is important to also note that high PEEP can also paradoxically worsen oxygen saturation.

The primary physiologic explanation for this phenomenon in a patient with pulmonary disease is due to the varying impact of PEEP on the intra- vs. extra-alveolar blood vessels. PEEP preferentially distends more normal/compliant lung which causes compression of intra-alveolar vessel at excessively high levels of PEEP. This causes pulmonary blood to be diverted to areas of lower vascular resistance (e.g. consolidated lung which is less distended due to its worsened compliance) and lower VQ matching. Essentially, blood flow to normal/healthy lung is decreased and is instead increased to diseased lung, worsening hypoxemia. 

Bottom line:

High PEEP can potentially worsen hypoxemia and should be considered as an etiology for worsening oxygen saturation, particularly when the hypoxemia is out of proportion to the patient’s radiographic findings.

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DeMasi et al. published a review on the current evidence surrounding peri-intubation and intubation practices. While the actual approach and context to each patient will be different it is good to be aware of the actual evidence base for medical decision-making. 

Preoxygenation

• NIPPV appears to decrease hypoxemia in all subgroups (including in those not requiring supplemental O2 prior to enrollment)
  • PREOXI trial
• Data for HFNC over NRB is inconclusive

Between Induction and Laryngoscopy

• BVM decreased hypoxemia vs. no-ventilation, without a higher risk of aspiration
  • PreVent trial

During Laryngoscopy and Intubation of the Trachea

• Apneic oxygenation may increase the lowest oxygen saturation, but a much smaller benefit than pre-induction PPV

Medications

• Induction
  • Still uncertainty re: differences in patient-centered outcomes for etomidate vs. ketamine
• NMB
  • No rigorous evidence for rocuronium vs. succinylcholine (if no contraindications)

Interventions to Prevent Hypotension

• Peri-intubation IVF boluses have not been shown to prevent hypotension, need for pressors, or cardiac arrest
• Reasonable to have prophylactic vasopressors running or available, but evidence of potential serious dosing errors for push-dose

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These 2 papers challenge management dogmas in critical care that have persisted despite low-quality/absent evidence.

In particular, one explores the dogma, “bicarbonate improves ventricular contractility in severe metabolic acidosis,” with the following points: 

-intracellular pH (which has a large impact on myocardial contractility) correlates poorly with blood gas pH

-many of the studies regarding bicarbonate in severe metabolic acidosis and hemodynamics are done on animal shock models

-two studies in patients with lactic acidosis showed increase in pH with bicarb administration without beneficial impact on hemodynamics (even in pts with pH < 7.1)

-bicarb administration is associated with hypernatremia, hypokalemia, and decreased ionized calcium levels

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Some points from this narrative review:

• much of the existing literature is based on animal models or small human studies
• successful ventilations per compression pause (“synchronous" ventilation, 30:2, without advanced airway) is unsurprisingly important for neurologically intact survival
• no clear difference in outcomes between “synchronous” vs. “asynchronous” (insufflation without pause in CPR) ventilation
• RR below 6 breaths per min were associated with decreased ROSC, whereas faster RR were not associated with worse outcomes (however, be cautious of breathstacking in pts with asthma/COPD)
• chest rise can be detected with TVs as low as 180 mL which is likely not sufficient for CPR
• the benefit of larger tidal volumes (improved oxygenation, less hypercapnia) may outweigh the perceived costs (gastric insufflation, impact on venous return/CO)

Take home pearls:

• use 2-person BVM to ensure adequate TVs and aim for more than just minimal chest rise
• err on the side of moderately larger TVs rather than smaller and moderately faster RR rather than slower (but be cautious in pts with asthma/COPD)

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Many patients present to the ED with hypercarbic respiratory failure (i.e. COPD exacerbation, obesity hypoventilation syndrome etc.). Typically, our first line of treatment is the use of BiPAP, where we set an inspiratory pressure (IPAP) and an expiratory pressure (EPAP). The difference between these two pressures (as well as patient effort) determines the tidal volumes (and consequently minute ventilation) a patient receives in our attempts to help the patient “blow off CO2.” 

If you are having trouble with continued hypercarbia despite the use of BiPAP, another NIPPV mode that can be trialed is Average Volume-Assured Pressure Support (AVAPS). With BiPAP the patient receives the same fixed IPAP no matter what, even if their tidal volumes are lower than what is needed. With AVAPS, the ventilator will self-titrate the IPAP and increase (or decrease) the IPAP to reach the tidal volumes that you set, increasing the odds the patient will achieve the minute ventilation you are trying to achieve.

(AVAPS is essentially a non-invasive version of PRVC)

Initial settings (ask your RTs for help!):

• The target tidal volume is set to 8 ml/kg of ideal weight 
• The maximal IPAP value is generally fixed at 20-25 cm H2O
• The minimal IPAP value equals to EPAP + 4 cm H2O
• The value of the minimal inspiratory pressure is no less than 8 cmH2O and commonly higher
• The respiratory rate is set at 2-3 BPM below the resting respiratory rate

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Background:

           -Muscle rigidity has been described as a side-effect of fentanyl, specifically activation of expiratory muscles 

           -Excessive expiratory muscle use acts as “anti-PEEP,” causing lung derecruitment and hypoxemia

           -End-expiratory lung volume (EELV) has been used as a surrogate for lung recruitment

Study:

          -Small, two center, observational study (46 patients with ARDS)

          -50% of  patients had a significant increase in EELV after administration of neuromuscular blockade (NMB)

          -Statistically significant correlation between a higher dosage of fentanyl and a greater increase in EELV after NMB

Takeaways:

          -NMB can improve lung recruitment for a subset of patients with ARDS, particularly in patients with significant expiratory muscle use (this can be seen on your physical exam of your intubated ED boarding patient)

          -Although this was not the main point of this study, consider fentanyl-associated “anti-PEEP,” particularly in patients receiving fentanyl whose hypoxemia and/or ventilator mechanics are disproportionate to their imaging

                    -This can be assessed with NMB (but ensure the patient will have adequate minute ventilation first)

                    -Naloxone has also been shown to reverse fentanyl-associated rigidity, but obviously would induce patient discomfort/withdrawal

*Of note, because this was an observational trial, it is possible that the patients with increased work of breathing were simply given more fentanyl. Regardless, these findings are consistent with previously documented physiologic side effects of fentanyl.

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IVC POCUS is often misapplied in attempts to assess volume status and/or volume “responsiveness.” Here are some important concepts to understand when using IVC POCUS to guide management:

1. IVC measurement is not a reliable predictor of fluid responsiveness
2. Venodilation and obstructive pathology can decrease and increase (respectively) IVC size without any change in actual blood volume or “volume status”
3. IVC size/variation is affected by multiple factors including spontaneous breathing vs. mechanical ventilation (AND actual ventilator settings), and degree of respiratory effort (in both spontaneous and mechanically ventilated patients) so there are no true “cut off” points that determine volume responsiveness
4. Attempting to maximize cardiac output/oxygen delivery (macrocirculation) through IVF can actually cause venous congestion and worsen microcirculation and organ function
5. Some patients with a plethoric IVC (tamponade or tension pneumothorax) may actually benefit from IVF in the acute setting
6. Examine the entire IVC (cephalad and distal portion) and in the short and long axis (the IVC is actually elliptoid, rather than a true cylinder)
7. Interpret IVC size in relation to RA/RV function (pts with chronically elevated RA pressures may have a chronically dilated IVC)

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Background:
There has been interest in vitamin C as an adjunctive therapy in patients with systemic inflammation and vasoplegia to reduce inflammation. While it was suggested that vitamin C may have some benefit (along with hydrocortisone and thiamine) in septic shock, the LOVIT trial showed possible harm from high-dose vitamin C administration in septic ICU patients. The  VALENCIA trial sought to evaluate whether vitamin C could reduce the duration of vasopressor therapy in patients with moderate vasoplegic shock.

Study:
-double-blinded RCT at two tertiary centers, 71 patients (36 to placebo, 35 to vitamin C)
-adult patients with vasoplegic shock of any cause
-vasopressor requirement >10 μg/min of norepi after hypovolemia was excluded
-notable exclusion criteria: end-stage renal failure and expected survival <12 hrs

Results:
-65 pts with septic shock, 6 pts with non-infectious cause
-no significant difference in the duration of vasopressors between the treatment group (median, 44 h [95% CI, 37-54 hrs]) and the control group (55 hrs [95% CI, 33-66 hrs])
-also no statistically significant difference in the vasopressor dose at 12 hourly time points, ICU or 28-day mortality and ICU or hospital length of stay

Take-home points:
Small study that ultimately may be under-powered but did not show that vitamin C reduces vasopressor duration in moderate vasoplegic shock

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Hypoxemic respiratory failure is a common presentation of critically ill patients. If the degree of hypoxemia is severe and disproportionate to the patient's radiographic findings and not responding to increasing FiO2, a right-to-left shunt should be considered. To evaluate for an anatomic shunt, an intravenous agitated saline contrast (ASC) echocardiographic evaluation can be conducted by an ED provider at the bedside.

Technique:

1. Use two operators, nursing can perform the ASC with the physician obtaining the echo views
2. Set-up:
   • 20 gauge (or larger) PIV in the AC fossa or more proximal is sufficient (does not have to be a CVC)
   • Flush PIV aggressively prior to attempt to make sure it won't blow
   • Obtain 3-way stopcock and 2 10 cc syringes
   • One port is connected to the PIV, and a second port to an empty 10cc syringe with the plunger fully depressed 
   • Third port connected to a syringe filled with 9ccs of saline and 1cc of air (eject 1cc of saline from the syringe of normal saline (NS) and replace it with air)
3. Echo technique:
   • Any view where the RA, LA, and IAS can be seen will suffice
   • Apical 4-chamber view is favored, with a focus on the bilateral atria (can also do sub-xiphoid)
4. Procedure:
   • With the equipment connected to the PIV, bubbles are created by turning the stopcock valve to “off” toward the patient and alternately depressing the plungers on the 2 syringes to send the air/NS mixture back-and-forth between them (should be done forcefully)
   • Push ASC completely into one of the syringes and quickly turn the stopcock “off” toward the other, and inject the ASC into patient while maintaining echo view and actively recording

Interpretation:

1. Quality control check:
   •  A vigorous injection should result in dense opacification of the RA
     • If the chamber is not densely opacified, likely technique issue and the exam should not be interpreted
2. The LA should be examined for a period of at least 10 full beats
3. Timing when microbubbles are seen in the LA:
   • Immediately (within 3-6 beats is a typically used cutoff):  likely to be intracardiac (most likely PFO)
     • Under ideal circumstances, bubbles can be seen to transit across the septum in real time
   • After the 3-6 beat cutoff: more likely to be due to a transpulmonary shunt, either an AVM or hepatopulmonary syndrome, depending on the clinical circumstances
     • Further workup might include a CT angiogram of the chest or workup for cirrhosis
4. Rough qualitative interpretation
   • no bubbles
   • a small number (roughly <10)
   • a large number (roughly >10)
   • enough to completely opacify the LA
   • (Significant continuous hypoxemia requires significant continuous right-to-left shunting, and thus the ongoing passage of many ASC bubbles)

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Background: 

There have been a few studies that suggested that there may be some neuroprotective effect with a higher MAP goal in post-arrest patients. However, these studies were small and/or observational. 

Intervention:

-The BOX trial was a double-blind, dual-center (Denmark), randomized trial 

-Study population: >18 yo, OHCA of presumed cardiac cause

-Pts randomized to higher (77 mmHg) vs. lower (63 mmHg) MAP goal

-double-blinded by attaching a module that reported a BP that was 10% higher or lower than the pt’s actual BP

-Notable exclusion criteria:

-unwitnessed asystole or suspected intracranial bleeding/stroke

Results/Primary outcome:

-No sig difference in composite of death + Cerebral Performance Category of 3 or 4  (3= severe disability, 4= coma) within 90 days

-133 patients (34%) in the high-target group vs 127 patients (32%) in the low-target group (hazard ratio, 1.08;95%CI, 0.84 to 1.37; P=0.56)

Caveats/Takeaways:

-Mean difference in BP was 10.7 mmHg (95[CI], 10.0 to 11.4) which is still relatively clinically significant, but was lower than their goal difference of 14 mmHg

-They used IVF to target a CVP of 10 mmHg prior to initiation of norepi and used dopamine "if necessary"

-Consider generalizability given study population was patients with presumed cardiac cause of arrest

-Keeping a lower MAP goal of >65 mmHg is reasonable in post-arrest patients

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DOSE VF (DOuble SEquential External Defibrillation for Refractory VF) Trial 

Background - High quality data regarding the use of double sequential external defibrillation (DSED) and vector-change (VC) defibrillation in refractory vfib is limited

Study

-Three-group, cluster-randomized, controlled trial in six Canadian paramedic services

-Study population: 

-OHCA with refractory vfib (initial presenting rhythm of vfib or pulseless VT that was still present after three consecutive rhythm analyses and standard defibrillations separated by 2 minute intervals of CPR) of presumed cardiac etiology (405 patients)

-Some notable exclusion criteria: 

-suspected drug overdose, hypothermia, traumatic cardiac arrest

-Protocol:

-First 3 defib attempts in the standard (anterior-lateral) position

-If remained in vfib after three consecutive shocks randomized to one of:

1. Standard defib for all subsequent attempts (136 pts)

2. VC defib (all subsequent attempts in anterior-posterior position) (144 pts)

3. DSED (applied second set of pads in AP position) with near simultaneously (<1 sec) defib shocks (125 pts)

Results

-Primary outcome: survival to hospital discharge

-38 patients (30.4%) in the DSED group vs. 18 (13.3%) in the standard group (RR 2.21; 95% CI, 1.33 to 3.67) (Fragility index of 9)

-31 patients (21.7%)  in the VC group (RR [vs. standard], 1.71; 95% CI, 1.01 to 2.88) (Fragility index of 1)

-Notable secondary outcome: survival with a good neurologic outcome

-34 patients (27.4%) who received DSED vs. 15 patients (11.2%)  with standard defibrillation (RR, 2.21; 95% CI, 1.26 to 3.88)

Takeaways/Caveats:

-68% of arrests witnessed, 58% received bystander CPR, median response time of 7.4-7.8 min

-Did not reach planned sample size 2/2 COVID pandemic

-No reporting of post-arrest care (e.g. TTM, PCI)

-Overall rates of survival and good neuro outcome on the higher side even with standard of care

-More/larger studies needed, but can consider DSED for refractory vfib, particularly if you are in a setting without more advanced circulatory support/resources

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Point-of-care ultrasound compression of the carotid artery for pulse determination in cardiopulmonary resuscitation

Background:

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Tachyarrhythmias in the setting of high-dose vasopressors due to septic shock are not uncommon. Aside from amiodarone, some providers may not know of alternative therapeutic options in the setting of septic shock. In addition, some may view the use of a beta-blocker as counter-intuitive or counter-productive in the setting of norepinephrine usage.

However, there have been multiple smaller studies evaluating using esmolol (and other short-acting beta-blockers) in the setting of tachycardia, septic shock and pressors. Outcomes regarding the theoretical benefits of beta-blockade in sepsis (i.e. decreased mortality/morbidity 2/2 decreased sympathetic innervation, inflammation, myocardial demand etc.) have been varied. However, esmolol has been demonstrated multiple times to be effective at reducing heart rate without significant adverse outcomes (i.e. no sig diff in mortality, refractory shock, or time on vasopressors).  

Caveats/pitfalls

-most of the studies discuss “adequate resuscitation” prior to initiation of esmolol

-not studied in patients that also had significant cardiac dysfunction 

-be aware that esmolol gtts can be a lot of volume and pts can become volume overloaded if boarding in the ED for an extended period of time

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-If the patient is able to maintain mentation/airway/SpO2/hemodynamics and cough up blood, intubation is not immediately necessary

• an ETT will actually reduce the diameter of the airway and can impede clearance and precipitate respiratory failure

-If you do intubate, intubate with the largest ETT possibly to faciliate bronchoscopic interventions and clearance of blood

• Men: 8.5 or above; Women: 8.0 or above

-The CT scan that typically needs to be ordered is a CTA (not CTPA) with IV con

• 90% of life-threatening hemoptysis from the bronchial arteries

-See if you can find prior/recent imaging in the immediate setting (e.g. pre-existing mass/cavitation on R/L/upper/lower lobes) 

• having a level of suspicion for location/lateralization is helpful for the performing bronchoscopist to allow them to empirically occlude a location with an endobronchial blocker in a crashing hypoxemic patient if visualization is difficult 2/2 blood

-Get these meds ready before the bronchoscopist gets to the bedside to expedite care: 

• iced/cold saline, thrombin, code-dose epi (which will be diluted)
• there is also some (not great) data for intravenous TXA and improved outcomes

-If the pt's vent suddenly has new high peak pressures or decreased volumes after placement of endobronchial blocker, be concerned that the blocker has migrated

• this can happen even with 1 cm movement of the ETT or blocker, or extension of the patient's neck
• know where the ETT is secured as well as the endobronchial blocker (analagous to locking of a transvenous pacer)
• pts with endobronchial blockers should also be on continuous neuromuscular blockade

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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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Clinical Question:

• Does dexmedetomidine lead to better short-term and long-term outcomes than propofol in mechanically ventilated adults with sepsis?

Methods:

• Multicenter (13 US hospitals), double-blinded, 422 mechanically ventilated patients with sepsis
• Notable exclusion criteria: pregnant, 2nd- or 3rd-degree heart block or persistent bradycardia requiring intervention, indication for bzds, expected to have NMB > 48 hrs, already had received mechanical ventilation >96 hrs
• Pain was treated with opioid pushes or fentanyl gtt
• Primary end point: number of calendar days alive without delirium or coma during the 14-day intervention period
  • Secondary efficacy end points included ventilator-free days at 28 days, death at 90 days, and global cognition at 6 months

Results:

• No sig difference in adjusted number of days alive without delirium or coma over the 14-day intervention period  (dexmedetomidine: 10.7 days vs. propofol: 10.8 days; OR, 0.96; 95% CI, 0.74 to 1.26; P = 0.79
  • No sig differences in the number of ventilator-free days at 28 days, in death at 90 days, or global cognitiion at 6 months
• Other notable findings:
  • Fewer patients in the dexmedetomidine group had ARDS or signs of trial drug withdrawal
  • Fewer patients in the propofol group extubated themselves
  • Open-label propofol received by 13% in the dexmedetomidine group and 8% in the propofol group) and dexmedetomidine (4% in the dexmedetomidine group and 3% in the propofol group)
  • Rescue midazolam was used in about half the patients, most often for procedural sedation or during NMB, 42% received antipsychotics
  • Similar proportions of patients had organ dysfunction, hypotension, or severe lactic acidosis
  • Symptomatic bradycardia requiring discontinuation of the trial drug was similar in the two groups

Take-home points:

• Dexmedetomidine or propofol are reasonable options for septic patients requiring mechanical ventilation without notable differences in delirium or mortality

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Study Question: What is the association of relative hypotension (degree and duration of MPP deficit) in patients with vasopressor-dependent shock with the incidence of new significant AKI and major adverse kidney events (MAKE)? 

• Mean Perfusion Pressure (MPP) = MAP - CVP
• MAKE-14: composite measure of death, new initiation of RRT, or doubling of serum creatinine from the premorbid level at Day 14
• Basal MPP estimated using pre-illness BP readings in the chart, basal CVP estimated using prior echo findings or estimated mean values

Methods:

• Multicenter, prospective observational cohort study with 302 patients
• Notable exclusion criteria:
  • age < 40, trauma as primary reason for ICU admission, active bleeding, unavailability of at least two preillness BP readings, pregnancy, "any condition specifically requiring a higher or a lower blood pressure target in the view of a treating clinician"

Results:

• for every percentage increase in the time-weighted average MPP deficit, the odds of developing new significant AKI and MAKE-14 increased by 5.6% (95% CI, 2.2–9.1; P = 0.001) and 5.9% (95% CI, 2.2–9.8; P = 0.002), respectively.
• Relationships between the risks of developing new significant AKI or MAKE-14 and the percentage of time spent with a MAP < 65 mm Hg were not statistically significant 

Take-aways:

• Critically ill patients in shock who had higher and longer degrees of relative hypotension compared to their baseline BPs had a higher incidence of adverse kidney outcomes
• Sidenote: also consider venous congestion/volume overload when thinking about end-organ damage (e.g. MPP not just MAP)

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