72
year old male presents to the ER with lethargy, fatigue, exertions dyspnea,
fever of 102 and hypotension. He is mildly hypoxic per ed reports. He’s placed
on 3L, diagnosed with pna based on a chest film demonstrating bilateral multi
focal opacities with superimposed edema, started on abx and given a 30ml/kg
fluid challenge. He is noted to have a creatinine of 5.2 which is new, a
potassium of 5.9 and a bicarbonate of 15. First lactate is 6. After fluids
lactate is 3 and His map is around 75 and he is admitted to SDU. Around 2 am you
are called by the night nurse that his saturation’s have worsened greatly and
he is more tachypneic. He is now on bipap, presumably started by the floor
intern. Nurse said he has crackles. No fever. He is awake and answers questions
but does appear labored pausing to speak partial sentences. His stat chest xry
looks wet but with persistent infiltrated that appear worsened. You pull up old
records and note his eF last month was 55%. There is also a mention of history
of adrenal insufficiency but he is not on glucocorticoids. He has no peripheral
edema. Current bipap settings are 18/10 @100%.
Abg 7.21/38/51/14 with sat of 82%.
3)after appropriately intubation him, what is your mode of ventilation and your initial settings?
4)if you intubate him and his saturation’s still do not improve, what is your next step?
We don't have a set of vitals including ht and weight but the patient appears to be increasing work of breathing and is elderly at 72 years of age. I would begin by placing the patient on AC mode to relieve the work of breathing and start with a rate of 16 with a PEEP of 5. Tidal volume would be 6 Ml/KG and Fio2 of 70 %. If saturation remains poor, PEEP could be increased to recruit more alveoli and Fio2 increased to provide greater O2 supply. ( Owens, The Ventilator Book)
ReplyDeleteVent Settings: AC TV 6ccs/kg based on ideal body weight. RR 20.FiO2 100%. PEEP 5. Repeat ABG in 60 minutes and change settings based on ABG, the RR is higher for now to help compensate for the Acidosis which is Metabolic presumed due to a PCO2 of 38.
ReplyDeleteFor his Hypoxia: Find the source- Listen to lungs, make sure the ETT is placed correctly, Stat CXR, Stat ABG, I would check for auto-peep, Review CXR to see if he would benefit from lasix but acutely I would disconnect the VENT and see if provided breaths through an ambubag helps oxygenate him. I would also attempt to increase his PEEP, I am already at 100% FiO2, , if he isn’t making urine and he is fluid overload and his K remains elevated- may need emergent dialysis, Or does he have a PE? Will need to evaluate pt and see what his WELLS score is. I would check a PaO2/FiO2 ratio however this seems like he is fluid overloaded in acute renal failure which is likely the source of his hypoxia. But he could be in acute adrenal crisis from this ?hx of adrenal insuff. I would give him dexamethasone and order labs to confirm adrenal insuff.
In addition to stated above by Patel and Baker:
ReplyDeleteIn addition to protective lung ventilation, the following treatments may also be helpful:
◾conservative fluid management
◾While many patients with ARDS have concurrent hypotension or shock and require fluid resuscitation, too much added fluid to increased capillary permeability leads to pulmonary edema that exacerbates lung injury. You might hear attendings and respiratory therapists say, “Dry lungs are happy lungs.”
◾The FACTT trial showed that a conservative fluid strategy decreased duration of mechanical ventilation, compared with a liberal strategy.
◾neuromuscular blockade
◾Synchrony between the patient’s respiration and the ventilator improves oxygen by ensuring the right tidal volume (rather than the patient trying to exhale when the ventilator is delivering a breath) and prevents injury (e.g., panel E in the figure above depicting high transpulmonary pressure generated by the patient trying to inhale on top of the ventilator delivering a breath). Synchrony can be enhanced with the use of neuromuscular blocking agents (NMBA).
◾The ACURASYS trial showed that the use of the NMBA cisatracurium within 48 hours of mechanical ventilation in patients with a P/F ratio <150 reduced 90-day mortality, compared with placebo (31.6% vs. 40.7%) and increased the number of ventilator-free days.
◾Much of the benefit of cisatracurium in the ACURASYS trial is thought to be from minimizing ventilator-induced lung injury from dyssynchrony, once again illustrating the key principle of avoiding harm when treating ARDS. Other benefits include the possible anti-inflammatory effects of NMBA and decreased oxygen requirement by muscle paralysis (see figure below). One negative aspect of NMBA use is heavy sedation, which is associated with definite adverse effects.
◾prone positioning
◾Patients typically lay supine in the intensive care unit (ICU); this position is associated with negative gravitational effects on the posterior lung regions, causing the heart to compress the left lung and more dependent atelectasis from interstitial edema. Placing patients in the prone position allows more lung regions to be functional and improves V/Q mismatch.
◾The PROSEVA trial showed that, compared with supine positioning, prone positioning within 36 hours of mechanical ventilation in patients with a P/F ratio <150 reduced 28-day (16.0% vs. 32.8%) and 90-day mortality.
◾Prone positioning requires an experienced nursing team to move the patient safely and prevent subsequent complications (e.g., pressure ulcers, extubation, intravenous decannulation), thus limiting its widespread adoption.
After exhausting the established therapies described above, the following additional treatments may be attempted for refractory hypoxemia, although strong evidence of benefit is lacking.
◾ airway pressure release ventilation (APRV): APRV is a mode of ventilation that inverts the pressure settings; a continuous high positive airway pressure is applied and intermittently released, allowing ventilation with the goal of sustaining lung recruitment.
◾ extracorporeal membrane oxygenation (ECMO): ECMO is reserved for the sickest patients (resources differ on the exact indications, but generally P/F ratio <60–80). Read more on ECMO in this NEJM review and on the Extracorporeal Life Support Organization website.
◾ inhaled nitric oxide: Inhaled nitric oxide can decrease pulmonary vascular resistance locally in ventilated areas of the lung and shunt more blood to that area, thus improving V/Q mismatch and oxygenation. Small trials (e.g., Rossaint R et al.) have shown benefit, but the effect may be transient.
http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf?utm_medium=referral&utm_source=r360&utm_campaign=criticalcare
ReplyDeleteGood responses. Key points were recognition of ARDS, understanding low TV mechanical ventilation, reducing interstitial non-cardiogenic pulmonary edema, NMB and troubleshooting the ventilator. The appropriate mode of sedation can be either PC or AC so long as the plateue pressures remain under 30, auto peep is controlled and pH is >7.25. Ideal body weight is used to calculate TV if using AC with a target of 6ml/kg. Important note is that minute ventilation is affected by TV and RR. So in a pt like this receiving a TV which could be as low as 300ml depending on their size, the RR will probably need to be 24-28, max of 30, to maintain minute ventilation. If a RR of 30 is not capable of keeping the pCO2 low enough to allow for a pH >7.25, the TV will need to be increased to 8ml/kg. Note I said >7.25, not normal range. This is the concept of permissive hypercapnia and is something everyone should be comfortable with. Sedation is very important for these pt’s. A RR of 30 with a TV of 350 is not a comfortable way to breath for most pt’s so heavy amounts of sedation is often needed and this in fact is the answer to the first question if the sats are dropping. Is the pt synchonus with the vent or combative? Often time’s ventilator dyssynchrony in ARDS pts is encountered and is fixed frequently by adjusting sedation. Important to remember to treat with both a sedative and an opiate. Again, this isn’t comfortable for the pt so try to be mindful of sedation levels. If the pt is appropriately sedated, on appropriate low TV MV, has Pplat<30, pH>7.25, and a saturation >88/pO2>60, you are doing your job well. If these parameters are not being met, additional changes need to be made. NMB is an important concept and goes along with ventilator synchrony and sedation. It is particularly helpful in pts with poor chest wall compliance or in pts on high levels of sedation who are still managing to trigger the vent and breath well over the high set RR. As Jessica mentioned, Nimbex is the preferred choice. (bonus question, why is it preferred? What is its method of metabolism and clearance from the system?). The additional modalities of prone ventilation, APRV and ECMO are additional strategies used to treat refractory ARDS with an inability to ventilate and maintain saturations using conventional LowTV/High peep strategies. Speaking of Peep, familiarize yourself with the Peep ladder and appropriate increase to peep levels and fio2 to manage the hypoxemia. These are not pts we start on 5 of peep which is simply the amount of end expiratory pressure needed to overcome the resistance of the endotracheal tube. We frequently start with Peeps in the 10 range and often run 12-16. Proteinaceous alveolar edema and end expiratory collapse is an important concept to grasp in terms of understanding why the pts need more peep. Last point, ARDS pts share one thing in common with all of our other intubated pts, the endotracheal tube and the ventilator circuit. So always remember, if a pt isn’t ventilating well, remember to check the tube and that it hasn’t been pulled out, advanced into the right mainstem, the cuff hasn’t ruptured, the circuit isn’t disconnected somewhere, pt hasn’t developed a PTX, etc. Common things still happen in sick pts. Good responses by all. ARDS is an important topic and something we encounter frequently. Familiarize yourself with the guidelines.
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