31. Mechanical Ventilation in Chronic Obstructive Pulmonary Disease Flashcards
Causes of exacerbation
1) . Viral infection: Rhinovirus or influenza
2) . Bacterial: Haemophilus influenzae, strep pneumoniae, Moraxella catarrhalis or Pseudomonas spp.
3) . Air pollution or other environmental.
4) . PE, PTX or HF.
Goals of Ventilation
1) . Decrease distress
2) . Decrease dynamic hyperinflation
3) . Improve gas exchange
4) . Buy time till cause of exacerbation clears.
Pathophysiology of Respiratory Mechanics
1) . When stable COPD patients have increased flow resistance about 6cm H2O/L/s more than normal. In AECOPD increases another 6.
2) . Bronchospsm, inflammation and mucus.
3) . Motor power increases as needed. 3X higher than normal at baseline and 5 x when in exacerbation.
4) . Normally Exp/Insp flow resistance is 1. With COPD is 3.8 at low volume and 1.6 at high. Higher resistance at low volume due to loss of scaffolding causing dynamic narrowing.
5) . Air trapping is the inability of expiratory muscles to reduce end exp volume below that which would occur with relaxation alone. No elasticity is available to help inspiration. Entire burden is on inspiratory muscles and expiratory muscles are just wasting energy.
Pathophysiology
Dynamic Hyperinflation
Intrinsic PEEP
1) . Inhalation begins before exhalation complete.
2) . Usually associated with increased end expiratoy elastic recoil. Auto-PEEP.
3) . Can vary acutely with mucus plugging, increased tachypnea etc.
4) . Can improve dynamic airway narrowing at the low lung volume but worsens mechanics. 25% of insp muscle effort used to overcome the PEEP.
5) . Impaired length tension reltionship and muscle perfusion. Can cause alveolar distention.
6) . C.O. decreases due to reduced venous return and increased PVR.
Pathophysiology
Respiratory Muscle Function
1). Muscle function deteriorates due to malnutrition, steroids, Also impaired due to shortening of inspiratory muscles with hyperinflation.
Deterioration of Gas Exchange
1) . VQ mismatch and decreased mixed venous return are common causes of hypoxia. Shunt is rare unless pneumonia or pulmonary edema present.
2) . Hypercapnia universally present in COPD patients requiring ventilation. Most commonly have rapid shallow breathing with reduced TE and VT. Thus increased VD/VT that isn’t compensated by increased minute ventilation.
3) . Increased FiO2 sometimes causes greater hypercapnea due to release of hypoxic vasoconstriction and increased dead space and reduced respiratory drive.
Indications for Ventilator Assistance
1) . NIPPV: Success depends on pH. >7.3 85%. <7.3 35% and < 7.25 50% success. Most failure in first few hours BUT there are some late failures so be cautious. Can be successful even if GCS 10 or below due to hypercapnea.
2) Invasive: NIPPV does not protect airway. Not tolerated if insp pressure >25 or FiO2 60%. Also if HD unstable or agitated poorly tolerated.
Goals
1) . Reduce effort, distress, autoPEEP and improve acidosis and hypoxia.
2) Ventilation can worsen PEEPi. If there is still exp flor at the end of exhalation there is PEEPi.
3) . Hypercapnea reducecd by increased VE and decreased CO2 production. BUT increased minute ventilation may worsen dynamic hyperinflation. Permissive acidemia acceptable if no intracranial HTN or HD instability.
4) . Also avoid alkalemia which can cause seizure, coronary vasospasm. Can lead to bicarb wasting and more difficulty weaning.
Mode of Ventilation
Tobin preferences
1). NIPPV: Use PSV w moderate PEEP.
Intrinsic and External PEEP
1) . Best way to reduce PEEPi is reduce minute ventilation. Maylead to alveolar hypoventilation-hypercapnia.
2) . Some times increasing insp flow leads to prolonged expiratory time and allows PEEP to come down. Some times not.
3) . PEEPe added of 5 or less will reduce effort needed to trigger inhalation.
4) . If PEEPi leading to hypotension can given volume or disconnect from ventilator and allow full expiration. Then resume w lower minute ventilation.
5) . Measure PEEPi by occlusion maneuver. Then can add 50% as much external PEEP to improve V/Q without dropping C.O.
Ventilator Dyssynchrony
1) Ineffective triggeing: Premature inspiraory efforts insufficient to overcome dynamic hyperinflation.
2) Neural inhalation: Double triggering when vent doesn’t give enough breath. Flow dysynchrony w excess flow reaises peak pressure.
3) If vent Ti exceeds patients then patient will try to exhale while vent is still delivering a breath.
4) Auto triggering is when vent begins to deliver breath while patient exhaling. Water in tubing and air leaks can contribute.
Hyperinflation
Vent circuit increases resistance p to 10 cm H2O/L/s (normal is negative).
Excessive tidal volume.
Steroid Myopathy
Causes loss of myosin heavy chains. Can also cause rhabdomyolysis or myonecrosis.
Weaning from NIPPV
When FiO2 less than 0.4
Tachypnea resolved.
Decrease Insp and exp pressure by 2cm per hour till down to 10/3 or 5 then try off.
