A 58-year-old man is admitted to the intensive care unit with increasing dyspnea after developing influenza symptoms 3 days previously. On physical examination, his temperature is 39.1 °C (102.3 °F), pulse rate is 110/min, and bloodpressure is 135/83 mm Hg. He weighs 73 kg (161 lb). He is using accessory muscles of respiration, and he has finecrackles throughout all lung fields. Cardiac examination is unremarkable, and no edema is noted. Chest radiographyshows diffuse infiltrates throughout both lungs with patchy areas of consolidation. The patient has a history of moderate obstructive lung disease secondary to smoking. Several months before hospitalization his forced expiratory volume in 1sec (FEV1) was 53% of predicted, and he had normal oxygen saturation and no hypercapnia.Shortly after hospitalization, he is intubated because of increasing hypoxemia and hypercapnia. Subsequent arterial blood gases with the patient breathing 100% oxygen and 10 cm H2O of positive end-expiratory pressure are PO2, 68mm Hg; PCO2, 65 mm Hg; pH, 7.23; and bicarbonate, 26 meq/L. Tidal volume is 450 mL, respiration rate is 25/min,inspiratory flow rate is 100 L/min, and inspiratory/expiratory ratio is 1:5. Peak airway and plateau ventilatory pressures are 48 cm H2O and 32 cm H2O.
Which of the following is the best option?
( A ) Increase the tidal volume
( B ) Increase the respiration rate
( C ) Increase the positive end-expiratory pressure
( D ) Decrease the positive end-expiratory pressure
( E ) Administer sodium bicarbonate, intravenously
The key to this question is to recognize that this patient remains acidotic and hypercarbic despite intubation. In order to "blow off" more carbon dioxide and normalize blood pH, you must increase minute ventilation (MV). If you remember that MV=TV X RR, you can quickly recognize that the two ways to decrease carbon dioxide is to increase the RR or increase theTV.
k guys this is the explanation, if u guys can understand it plz do elaborate... coz iam sorta :O...
Ans. E
In patients with acute respiratory distress syndrome, mortality was significantly improved by ventilating patients with tidalvolumes of 6 mL/kg of ideal body weight and keeping plateau ventilatory pressure at =30 cm H2O.
If changes in respirator settings required to prevent hypercapnia have associated untoward effects, it is reasonable to allow arterial PCO2 to rise and, if necessary, prevent acidemia by administration of buffer ïƒ as in this case!! ( don™t increase tidal volume here ïƒ low Vt is good for this ïƒ remember Permissive Hypercapnia)
Increasing PEEP is not good here. Raising PEEP is undesirable because this will narrow the pressure difference between the plateau ventilatory pressure and the PEEP, decreasing the pressure available to deliver the tidal volume. This will reduce the tidal volume and exacerbate hypercapnia. PEEP should remain unchanged because the patient has acceptable oxygenation with the present setting. The level of PEEP cannot be reduced since reduction likely will lead to unacceptable hypoxemia. The patient is barely at an acceptable level without any reduction.
Increasing the respiration rate likely will increase auto-positive end-expiratory pressure (PEEP) in this patient with chronic obstructive pulmonary disease ( they have proloned expiration!) by œbreath stacking, that is, delivering the next breath before the previous breath is completely expired.This will also raise the plateau ventilatory pressure above a desirable range.
EEE never never the bicorb is normal it's BBBB just need to wash some
CO2
pH GOAL: 7.30-7.45
Acidosis Management: (pH < 7.30)
If pH 7.15-7.30: Increase RR until pH > 7.30 or PaCO2 < 25 (Maximum set RR = 35).
.
If pH < 7.15: Increase RR to 35.
If pH remains < 7.15, VT may be increased in 1 ml/kg steps until pH > 7.15 (Pplat target of 30 may be exceeded).
May give NaHCO3
Alkalosis Management: (pH > 7.45) Decrease vent rate if possible.
source
http://www.ardsnet.org/system/files/Vent...l+Card.pdf
No carb at this point