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)

Dialysis Disequilibrium Syndrome (DDS)

• Although typically seen in ESRD patients who are being initiated on hemodialysis, DDS can be seen in the critically ill
• Critically ill patients at risk for DDS include recent CVA, head trauma, subdural hematoma, hyponatremia,, hypertensive emergency, and hepatic encephalopathy
• Mild cases are characterized by restlessness, nausea, vomiting, headache, disorientation, and tremors
• More severe symptoms include seizures and coma
• The exact pathogenesis is debated but centers around acute cerebral edema
• Treatment of DDS primarily centers around manipulation of hemodialysis
• For the EP: patients with DDS presenting with seizures can be treated by rapidly increasing plasma osmolality with either hypertonic saline or mannitol (12.5 gms)  

Guidewire length for central venous catheterization

• 18 cm should be considered the upper limit of guidewire insertion during internal jugular or subclavian central venous catheterization (16cm for right IJ)
• There is the Peres Nomogram for determining guidewire length, which is based on patient height
• However, height is less reliable in predicting safe guidewire length

Potassium Phosphate ("K-phos")

Over the weekend, I had a patient with Dr. Scott that had a phosphate of 0.8 mmol/L.  Phosphate < 1.0 mmol/L is an indication for IV repletion.  IV repletion involves giving potassium phosphate.  An important clinical question, therefore, is how much potassium does the patient actually get?

• 1 mmol of IV phosphate delivers 1.46 mEq of potassium
• Recommended infusion rate is 5 mmol/hr
• Rapid infusion may lead to severe hypocalcemia, hypotension, acute renal failure, hypomagnesemia, and hypernatremia

Coagulopathy and Trauma

• When resuscitating a trauma patient recall that the "lethal triad" consists of acidosis, hypothermia, and coagulopathy
• Coagulopathy is induced by the combination of direct loss of clotting factors, consumption in clot formation, dilutional due to crystalloid administration, acidosis, and hypothermia
• When giving PRBCs in trauma resuscitation, don't forget to give FFP
• The ratio to remember is 1U of FFP for every 2U PRBCs

Aspiration Pneumonitis

• Aspiration pneumonitis is an acute lung injury resulting from the aspiration of gastric contents
• It is an inflammatory condition rather than infectious
• Despite the inflammation, corticosteroids have been shown to have no effect on mortality
• Aspiration pneumonitis is self limited
• Antibiotics are generally held for 24 to 48 hours
• When to consider empiric broad spectrum antibiotics in the ED:  Gastric contents are sterile in most patients.  Patients who may have colonization/contamination of gastric contents are more likely to progress from pneumonitis to pneumonia.  Consider empiric antibiotics for aspiration pneumonitis in the patient with SBO, gastroparesis, those receiving enteral feeds through a G- or J-tube, and those on chronic PPI's/antacids.

D-Dimer in the Critically Ill

• Diagnosis of VTE in the critically ill can be challenging and these patients are at high risk for the disease
• Only 3.6% - 16% of critically ill patients have a negative d-dimer, regardless of the presence or absence of VTE
• Even in patients with low pretest probability, d-dimer in the critically ill is of limited utility

Crowther MA, et al. Neither baseline tests of molecular hypercoagulability nor D-dimer levels predict deep venous thrombosis in critically ill medical-surgical patients. Intensive Care Med 2005;31(1):48-55.