UMEM Educational Pearls - Critical Care

Bicarbonate for severe lactic acidosis from shock?

• In critically ill patients, one of the most common causes of acidosis is hypoperfusion induced lactic acidosis
• Importantly, the source of lactic acid during hypoperfusion/shock is intracellular, and the intracellular compartment is not readily accessible to extracellular bicarb
• Exogenous bicarbonate will certainly raise extracellular pH but does not readily correct intracellular acidosis
• This increase in pH is transient and typically lasts approximately 30 minutes
• In studies to date, exogenous bicarbonate did raise pH, serum bicarbonate concentrations, and P_aCO₂ but importantly did not improve cardiac output, mean arterial pressure, or sensitization to catecholamines
• Take Home Point: Based on available literature, there is no utility to giving bicarbonate in hypoperfusion induced lactic acidosis when the pH is > 7.0

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 Phentolamine for vasopressor extravasation

I was recently informed of a case from an another institution in which a patient was started on a vasopressor medication via a peripheral IV while attempts at central access where attempted.  The patient unfortunately suffered permanent extremity ischemia due to significant extravasation of the vasopressor medication into the soft tissue.

• Phentolamine is reportedly the antidote for vasopressor extravasation into the skin and soft tissues (the evidence is not robust and limited primarily to case reports and animal data)
• Phentolamine is a non-specific alpha-blocking agent that inhibits vasoconstriction and theoretically improves blood flow through the affected area
• Take 5-15 mg of phentolamine and mix in 10 mL of normal saline - inject this into the affected area as soon as possible
• Give the patient concurrent IVFs in the event of some systemic absorption

PEEP in Nonhypoxemic Respiratory Failure

• Patients with ALI/ARDS typically receive PEEP to improve oxygenation
• Patients without ALI/ARDS, however, receive PEEP less frequently (some recent reports indicate that < 50% of these patients receive PEEP)
• A recent study by Spanish investigators found that the use of PEEP (5 - 8 cm H₂0) in nonhypoxemic patients decreased the incidence of ventilator-associated pneumonia and decreased the number of patients who developed hypoxemia
• Interestingly, no differences were found in hospital mortality, duration of mechanical ventilation, or ICU LOS
• Take Home Point: In nonhyoxemic intubated patients, the addition of 5-8 cm H₂0 of PEEP is a reasonable practice and may be beneficial in preventing VAP (pending further study)

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Pressure Regulated Volume Control (PRVC)

• PRVC is a mode of mechanical ventilation that combines both volume and pressure control modes
• The main advantage to PRVC is that the tidal volume / minute ventilation is guaranteed while controlling airway pressures, thereby reducing the risk of ventilator induced lung injury
• In PRVC, the ventilator delivers a pressure-controlled breath, but tidal volume is the key setting
• The ventilator will automatically adjust inspiratory pressures until the desired TV is achieved
• When using PRVC you need to set: target TV, RR, peak pressure alarm, inspiratory time, FiO2, and PEEP

Post-intubation deterioration?  Remember DOPE

• The pneumonic DOPE can help you remember the most common causes of post-intubation hypoxia or deterioration
• Displacement: check the endotracheal tube for displacement (right mainstem) or dislodgement
• Obstruction: check the ETT for obstruction (mucous plug, kink in ventilator tubing)
• Pneumothorax - get an xray
• Equipment failure(unusual): disconnect patient from the ventilator and bag manually   

The Importance of Plateau Pressure

• Alveolar overdistention is a precursor to the development of acute lung injury (ALI)
• Plateau pressure is a measurement of alveolar overdistention, and is the pressure equilibration between the airways and the alveoli
• Plateau pressure is measured by using an inspiratory hold (for at least 3 seconds) at the end of inspiration
• Based on available data, you want to maintain the plateau pressure < 30 cm H₂O
• Remember that patients should be heavily sedated to obtain this measurement - any patient-ventilator asynchrony may provide inaccurate information

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Mechanical Ventilation in Asthma

• Approximately 25,000 asthmatics are intubated each year
• Mismanaged mechanical ventilation in asthma carries significant morbidity and mortality
• One of the primary goals of ventilating the asthmatic is to allow for lung deflation
• The most effective way to allow for lung deflation, and reduce hyperinflation, is to reduce minute ventilation (TV x RR)
• Initial tidal volume settings should be 6 ml/kg of predicted body weight; if plateau pressures are > 30 cm H₂O tidal volume should be decreased to 4 - 5 ml/kg
• Reduced respiratory rates will also allow longer exhalation times; initial recommended rates are 6 - 8 breaths per minute
• If plateau pressures are still high despite lowering tidal volume and respiratory rate, you can then shorten the inspiratory time to allow for longer exhalation

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 Noninvasive Ventilation Pearls

• Multiple studies support the use of noninvasive positive pressure ventilation (NPPV) in acute exacerbations of COPD, acute cardiogenic pulmonary edema, and immunocompromised patients (organ transplant) with hypoxic respiratory failure.
• The timing of NPPV initiation is important.  NPPV should be started as soon as possible, as delays increase the likelihood of intubation
• The best predictor of success is a favorable response to NPPV within the first 1 to 2 hours
  • reduction in respiratory rate
  • improvement in pH
  • improved oxygenation
  • reduction in PaCO2
• Also crucial to NPPV success is a well fitting interface (mask)
• Although patients report greater comfort with nasal masks, they also permit more air leakage through the mouth and have been associated with a higher rate of initial intolerance in the acute setting.
• For acute applications of NPPV in the ED, a full face mask is preferred 

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Hypotension begins at 110 mmHg?

• Many of us use the historical SBP cut-off point of 90 mmHg or less to identify hypotension and shock
• Importantly, there is no data to support this arbitrary value
• Particularly in older patients, hypotension, hypoperfusion, and increased mortality may begin sooner than previously realized
• In this study of over 80,000 patients from the National Trauma Data Bank, a SBP < 110 mmHg was found to be more clinically relevant for identifying hypotension and hypoperfusion
• Take Home Point: strongly consider raising your threshold for identifying hypotension and initiating resuscitation, especially in the older trauma patient.

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Passive Leg Raising (PLR)

• We have discussed that static measures of volume (CVP, PA wedge pressures) are not reliable markers of fluid responsiveness
• PLR has recently gained interest as a simple and transient way to assess fluid responsiveness in the critically ill
• Patients are placed in the horizontal position (not Trendelenburg) and the legs are raised to 45 degrees
• A hemodynamic response should be seen in 30 - 90 seconds
• Patients who have improvement in hemodynamics with PLR are said to be fluid responsive (i.e on the ascending portion of their Starling Curve) and require additional volume resuscitation

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Submitted on behalf of Dr. Winters:

Sepsis, Fluids, and ESRD
-ESRD patients are at increased risk of sepsis and bacteremia secondary to
indwelling devices
-Many of are hesitant to aggresively fluid resuscitate patients with ESRD
-Several studies have concluded that volume resuscitation should proceed the
same as patients without ESRD, even if that means more patients are eventually
intubated.

Reference:
Otero RM, et al. Chest 2006;130:1579-95.
 

Acinetobacter in the Critically Ill

• As all of us know, there has been an alarming increase in the incidence of acinetobacter infections
• At present, infections mostly occur in ICU/critically ill patients
• Important risk factors for colonization and infection include mechanical ventilation, recent surgery, tracheostomy, residents of long-term care facilities, central venous catheterization, and enteral feedings
• The most frequent clinical manifestations are ventilator associated pneumonia and bacteremia
• Susceptible strains can be treated with a broad-spectrum cephalosporin, carbapenem, or B-lactam-B-lactamase used alone or in combination with an aminoglycoside
• For resistant strains, the most active agent in vitro are the polymyxins
• The most common adverse effect of the polymyxins is nephrotoxicity (up to 36%)
• Tigecycline has been used but resistance rates are rapidly increasing

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Fluids in Acute Liver Failure

• Acute liver failure is often complicated by intravascular volume depletion - insensible losses, vomiting, poor oral intake
• Early and adequate fluid resuscitation is mandatory
• AVOID lactated Ringer's solution - exogenous lactate load is poorly tolerated by lack of hepatic function
• AVOID dextrose containing water solutions - will lead to hyponatremia and increase the risk of cerebral edema

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COPD and mechanical ventilation

• In some studies, the failure rate of non-invasive positive pressure ventilation (CPAP, BiPAP) in acute exacerbations of COPD has been as high as 50%
• When setting the ventilator in patients with COPD, keep in mind that the majority have chronic ventilatory failure with a chronic compensatory respiratory acidosis
• Pearl: Look at the serum bicarbonate level obtained from a recent period of stability
• A recent serum bicarbonate level can provide an indirect indication of the patient's baseline P_aCO₂ if you have no prior ABGs
• Rather than target a P_aCO₂ of 40 mm Hg, manipulate the ventilator to target the patient's baseline serum bicarbonate or a pH of 7.35 - 7.38.

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Acute Lung Injury (ALI) / Acute Respiratory Distress Syndrome (ARDS)

• ALI and ARDS are defined as:
  • bilateral pulmonary infiltrates on CXR
  • pulmonary capillary wedge pressure < 18 mm Hg (no heart failure)
  • P_aO₂ / F_iO₂ < 300 = ALI
  • P_aO₂ / F_iO₂ < 200 = ARDS  
• The current management for patients with ALI or ARDS is low tidal volume ventilation and a conservative fluid management strategy
• Two recent trials (EXPRESS and LOVS) evaluated different applications of PEEP in patients with ALI/ARDS
• Both studies evaluated lower levels of PEEP (5-10) vs. higher levels of PEEP titrated to plateau pressure
• Bottom line: different PEEP strategies did not influence survival, although higher levels did result in improved oxygenation.

Propofol Infusion Syndrome

• Many of us are now using propofol for sedation in our critically ill patients
• Although a great drug, it is important to be aware of "propofol infusion syndrome" (PIS)
• Risk factors for PIS include young age, severe CNS or pulmonary illness, and exogenous catecholamine administration
• Clinical features include: unexplained metabolic acidosis, rhabdomyolysis, hyperlipidemia, hepatomegaly, and cardiovascular instability
• Pearl: It is reported that the development of coved ST elevations in V1-V3 (similar to Brugada syndrome) may be the first sign of cardiac instability with PIS

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Intra-aortic balloon pump counterpulsation

• It is possible that at some point in your career you may need to place an intra-aortic balloon pump (IABP) to temporarily stabilize a patient wth cardiogenic shock
• Optimal performance of the IABP is dependent upon proper positioning in the thoracic aorta
• Traditional teaching has been to insert the IABP via the femoral artery and advance to the level of the aortic knob (via CXR)
• A recent study suggests that using the aortic knob to position the IABP may result in occlusion of the left subclavian artery in a substantial portion of patients (16% in the study)
• Placing the IABP 2 cm above the carina may be a more reliable landmark that using the aortic knob

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Bedside Glucometry in the Critically Ill

• Hyperglycemia is common in critically ill patients
• Depending on the underlying condition (e.g. DKA), you may be instituting an insulin drip and following frequent fingersticks in the ED
• A recent study indicates that bedside glucose values may not accurately reflect serum values in approximately 15% of critically ill patients
• This is more likely to occur in patients with poor peripheral perfusion
• Take Home Point: Interpret bedside glucose readings with caution especially in hypotensive critically ill patients

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Vasopressin for Sepsis

• The VASST trial was recently published in NEJM comparing vasopressin vs. norepinephrine for septic shock
• Unfortunately, there are some issues with the study which I will clarify/expand upon in the next Critical Care Literature Update
• There was a trend towards improved mortality in the vasopressin group receiving low doses of norepinephrine (5 - 14 mcg/min)
• Take Home Point: If you are thinking about adding vasopressin to norepinephrine in patients wtih refractory septic shock, do it early.  In other words, add vasopressin when you find yourself titrating norepinephrine doses to 6, 7, 8 mcg/min

ACTH Stimulation Test

• With the recent publication of the CORTICUS study (along with others), it is becoming clear that the ACTH stimulation test is not reliable in identifying patients with adrenal insufficiency
• In fact, the test is no longer recommended in the evaluation of patients with severe sepsis/septic shock
• Furthermore, if you decide to give steroids to the patient with severe sepsis/septic shock, there is no need to use dexamethasone for fear of "disrupting the ACTH stim test" (hydrocortisone is the preferred agent)