Introduction to Mechanical Ventilation

Prepared by EK Buzbee 2/08

Revised 2/12/09

The need for mechanical ventilation

Reading assignment:

·  Chang, Mechanical Ventilation Ch. 1

·  Egan’s Fundamentals, Ch. 41

Basic definitions for mechanical ventilation:

The need for mechanical ventilation

Spontaneous breathing is the act of using the patient’s primary and accessory muscle of inspiration to create a driving pressure to move gas into the lungs. The intrapulmonary pressure will be less than zero and inspiration will be triggered by changes in the patient’s CSF pH or low Pa02 in the periphery.

With normal compliance of 100 ml/cmH20 pressure and normal RAW of .5 to 2.5 cm H20/L/second the WOB is easy because the driving pressure is low. [Egan’s pp. 215] With lowered compliance or increased RAW, the driving pressure needed for adequate alveolar ventilation may rise to the point where the patient needs help. The RAW of the intubated patient rises to about 6 cm H20/L/second [Pilbeam pp. 21]

Most [not all] forms of mechanical ventilation will result in the creation of positive pressure in the airway to create the driving pressure needed to move air along. This driving pressure will result in positive pressure inside the thorax for at least part of the breath in contrast to the negative intrathoracic pressures achieved by spontaneous breathing.

The need for mechanical ventilation is usually due to a person’s problem with the ability of the patient to create the driving pressure required to move gas into the alveoli so that diffusion can occur.

·  The driving pressure might be excessive due to decreased compliance or increased RAW,

·  or the patient may lack the ventilatory muscles to initiate a normal driving pressure.

·  The patient may lack the ventilatory drive so that changes in pH or Pa02 have little or no effect on the brain stem.

In this unit we will discuss these problems with spontaneous ventilation. You may need to review your pathology notes for the specific effects of disease states on spontaneous breathing.

Respiratory Failure [Egan’s pp.950-962 & Chang pp. 1-23]

  1. Define respiratory failure [Egan’s pp. 950]

·  Inability to oxygenate the tissues and/or to remove C02

·  Frequently both hypoxemia and hypercapnia are present, but we can have situations in which the patient’s problem is refractory hypoxemia without hypercapnia

·  Specifically, if the Pa02 is less than 60 torr and/or the PaC02 is more than 50 torr in a healthy person breathing room air, we can have respiratory failure.

·  A person with chronic hypercapnia can have both moderate hypoxemia and hypercapnia, but the pH will be WNL-thus this person is not in respiratory failure-- until the hypercapnia rises making the pH is only partially compensated.

  1. List and differentiate the 3 different types of respiratory failure [Egan’s pp.950-962]

·  Acute hypoxemic respiratory failure- Type I in which there is refractory hypoxemia secondary to a number of causes: shunts, V/Q mismatch, alveolar hypoventilation, diffusion issues and decreased Pi02

·  Acute hypercapnia respiratory failure- type II: in which the patient is having problems removing C02.

·  This patient will have acute [uncompensated respiratory] acidosis. This can be due to a number of causes: decreased alveolar ventilation, increased VD ventilation [VD physiological], decreased ventilatory drive, respiratory fatigue & increased WOB.

·  Fatigue and increased WOB can be due to compliance and/or RAW issues

·  Chronic respiratory failure [hypoxemia and hypercapnia] - Type III, This person will have an acute onset on a chronic problem.

·  They will have a baseline ABG that shows chronic moderate hypoxemia with compensated respiratory acidosis, but acute illness will drop the Pa02 and raise the C02 so that the pH is now partially compensated respiratory acidosis

·  This patient could have increased RAW or compliance problems associated with a chronic problems such as COPD, chronic restrictive defects such as pulmonary fibrosis or neuromuscular or neurological disorder

3.  Define the V/Q mismatch. [Egan’s pp. 950-951]

·  One of the causes of acute hypoxemic respiratory failure.

·  As we remember from A & P there are different zone of alveolar ventilation [V] and pulmonary perfusion [Q] in the normal lung.

·  When there is low V/Q, we have low ventilation with good perfusion

·  When there is high V/Q, we have good ventilation with poor perfusion

·  A pathological V/Q mismatch can be due to decreased alveolar ventilation or decreased pulmonary capillary perfusion.

·  Pathological V/Q mismatches could be due to airways issues, such as secretions or bronchospasm or they could be due to alveolar consolidation or inflammation resulting in decreased alveolar ventilation

4.  Discuss the clinical s/s of a V/Q mismatch: [Egan’s pp. 950-951]

·  Hypoxemia that will respond to increased Fi02

  1. Define and discuss shunts and shunt like effects. [Egan’s pp.951-952]

·  One of the causes of acute hypoxemic respiratory failure

·  A shunt is an extreme form of V/Q mismatch in which the patient has [refractory] hypoxemia so that supplementary 02 will not raise the Pa02.

·  A normal shunt is 2-3% and is due to the anatomical shunting of right-sided blood into the left side of the heart due to bronchial circulation and coronary blood return. A physiological shunt of less than 10% is considered normal

·  A Pathological shunt is higher and may not actually be an interface between the right and left side of the heart. If enough alveoli are collapsed or filled with fluid, the capillaries going to these nonfunctional areas will be desaturated [right-sided blood.]

  1. 10-20% is mild
  2. 20-30% is significant shunt
  3. Over 30% shunt is critical shunt [Chang pp. 15]

·  In these circumstances, merely giving supplementary 02 will not treat the hypoxemia because the alveoli are nonfunctional. A means of opening the alveoli is needed. We will discuss these techniques later.

6.  Discuss decreased Pi02 as a cause of acute hypoxemic respiratory failure

·  A rare cause of respiratory failure is the phenomenon of decreased Pi02 from situations such as high altitude barometric pressures, replacement of 02 by other gases [such as during a fire.]

·  Obviously, if 02 is given soon enough, before the patient losses consciousness and the ability to protect his airway, the patient may not require ventilation.

7.  Discuss the effect of diffusion problems in acute hypoxemic respiratory failure [Egan’s pp. 952]

·  Based on Fick’s law of diffusion through a membrane, the rate of diffusion is inversely proportional to the thickness of the membrane. As the alveolar-capillary membrane is thickening from edema or scarring diffusion of 02 is affected adversely.

·  As alveolar are destroyed by emphysema, the total surface area for gas exchange is decreased so that hypoxic respiratory failure can result

  1. Using 02 indices to identify V/Q mismatches and shunts. [Egan’s pp.953-954]

·  Compare the ratio of Pa02 current and Fi02 current to the Fi02 required to correct the Pa02. Is it possible to correct the Fi02?

·  Use the a/A ratio to determine if there is refractory hypoxemia

·  Is the Fi02 more than 50% with a Pa02 of less than 50 torr; if so there is refractory hypoxemia

  1. Differentiate between alveolar hypoventilation and diffusion problems. [Egan’s pp.953-954]

·  Both are causes of acute hypoxemic respiratory failure

  1. Using 02 indices to differentiate between type I and type II respiratory failure [see mini-clinic Egan’s pp. 954]

·  Look at ABG:

·  is there hypercapnia?

·  Is there respiratory acidosis?

·  If so, then part [or all] of the patient’s problem can be solved by reversing the hypercapnia

·  Calculate the P[A-a]D02:

  1. if the patient is hypoxemic but the P[A-a]D02 is not elevated, the hypoxemia may only be due to the rise in alveolar C02 replacing the alveolar 02. Once we blow off the C02 with increased VE the PA02 thus the Pa02 will rise.

11.  Discuss the effects of decreased ventilatory drive on respiratory failure. [Egan’s pp.955]

·  Another cause of hypercapnia respiratory failure is decreased ventilatory drive due to abnormal brain stem action from neurological injury, or by CNS depressants.

·  A person with chronic hypercapnia whose chronic hypoxia has been over-corrected by supplementary 02 is also suffering CNS depression

“The clinical manifestations of acute hypercapnia are primarily neurological. Acute elevations of PaCO2 greater than 60 mm Hg cause confusion and headache. PaCO2 more than 70 mm Hg produces……CO2 narcosis manifesting as drowsiness, depressed consciousness, or coma. “

http://www.emedicine.com/PED/topic16.htm

12.  Situations that contribute to respiratory failure. [Chang pp.1-23]

·  Conditions that result in increased WOB due to need for excessive driving pressures

  1. increased RAW
  2. decreased lung compliance
  3. Persons at risk for muscle fatigue would be persons with long-term increased WOB, or persons who are malnourished
  4. Persons with severe muscle fatigue need to rest on mechanical ventilation for 24 – 48 hours

2.  V/Q mismatch:

  1. Can be corrected by increasing Fi02

3.  Shunts: because the hypoxemia is unresponsive to Fi02, we may need to mechanically ventilate to increase alveolar ventilation or increase baseline pressure. This may or may not include intubation.

  1. Acute lung injury or ARDS
  2. Shock or other severe decreased C

4.  Situation that result in ineffective ventilator muscle action

i.  Dis-coordination / paralysis from neuromuscular or myopathic disorders

·  VC of less than 20 ml/kg IBW requires some ventilator support. VC of less than 25 ml/kg IBW is associated with decreased ability to cough effectively.

·  inspiratory max pressure measures weakness of inspiratory chest wall muscles and diaphragm. a need for mechanical ventilation is seen with a [PI max] less -30 cmH20

o  expiratory max pressure measures weakness of the abdominal muscles. a need for mechanical ventilation is seen with a [PE max] less than + 40 cmH20

o  be aware that facial weakness can result in false values for these two figures if the patient cannot seal properly—needless to say, that alone tells us we have problems

ii.  Chest trauma such as flail chest

  1. Electrolyte imbalance such as hyperkalemia that affects muscle action: Go here for a cases study of a patient who suffered prolonged paralysis from hyperkalemia

http://www.aana.com/uploadedFiles/Resources/Publications/AANA_Journal_-_Public/2005/December_2005/p437-441.pdf

iv.  High doses of steroids particularly with persons in sepsis, who have been sedated & paralyzed & ventilated for a period of time resulting in myopathy

v.  Persons at risk for muscle fatigue would be persons with long-term increased WOB, or persons who are malnourished.

5.  Situations that result in increased VD ventilation

i.  anatomical VD

  1. conducting airways. Comprises about 30% of the VD of the body.
  2. is equal to 1 ml / pound of IBW
  3. Is always present, but can be reduced by tracheostomy which bypasses upper airways
  4. VD/VT ratio will change, as the patient’s VT varies but the VD will stay the same

If the patient’s IBW is / His VD anatomical is / If his VT is / his VD/VT ratio is
100 pounds / 100 ml / 500 / 100/500 = .20 20% of his VT is VD
88 pounds / 600
135 pounds / 800
180 pounds / 900

ii. alveolar VD

1.  when an alveoli gets ventilation but no perfusion, it is considered alveolar VD

  1. as CO drops or there are problems with pulmonary blood flow the alveolar VD will rise above baseline

iii.  physiological VD

  1. is the sum of the anatomical VD + the alveolar VD
  2. VD /VT in normal circumstances, will be more or less equal to the anatomical VD/VT
  3. rises in the physiological VD are usually due to rises in the alveolar VD
  4. the normal VD /VT is about .3 or 30%. It is not uncommon for mechanically ventilated persons to have VD /VT of .6 and higher.
  5. VT - VD = alveolar ventilation
  6. Alveolar ventilation results in gas exchange
  7. if physiological VD is excessive, we can increase the VT to get the alveolar ventilation back to an effective level
  8. Failure to get the VD /VT below .6 will prevent successful weaning of a patient from mechanical ventilation.

His VD anatomical is / If his VT is / his VD/VT ratio is: / Is this excessive?
50 ml / 500 / 50/500 = .10
125 ml / 600
88 ml / 800
120 ml / 900

13.  Clinical signs and symptoms of respiratory failure in the adult patient. [Egan’s pp. 921-923]

·  inadequate alveolar ventilation: decreased peripheral air movement, crackles, significant atelectasis or consolidation on X-ray

·  inadequate lung expansion: poor chest movement; weak cough decreased peripheral air movement, crackles, significant atelectasis or consolidation on X-ray

·  poor muscle strength: inability to cough or protect airway decreased peripheral air movement, crackles, significant atelectasis or consolidation on X-ray

·  increased WOB: tachypnic, retractions, flaring, muscle tremor, altered LOC

·  hypoxemic respiratory failure: s/s of hypoxemia, tachycardia, tachypnea, cyanosis, confusion

14.  Parameters associated with a need for mechanical ventilation [Egan’s pp. 950-962]

·  s/s of inadequate alveolar ventilation: hypercapnia above 55 torr pH below 7.20

·  s/s of inadequate lung expansion: VT less than 5 ml/kg IBW, VC less than 10 ml/kg IBW requires full ventilator support, and RR over 35 bpm

·  s/s poor muscle strength : MIP less than -20 cmH20, VC less than 10 ml/kg and MVV less than 2x VE

·  s/s of increased WOB: VE more than 10 LPM & VD/VT more than .6

·  s/s hypoxemic respiratory failure: P(A-a)D02 on 100% more than 350 mmHg & Pa02/Fi02 less than 200.

15.  Arterial blood gases associated with respiratory failure. [Egan’s pp. 950-952, 953, 955-956]

·  Acute respiratory acidosis with moderate/severe hypoxemia

·  Partially compensated respiratory acidosis with moderate / severe hypoxemia. Chronic patient is no longer compensating effectively.

·  Panic values on ABG: hypercapnia above 55 torr pH below 7.20

·  Serial ABG in which the trend is to see PaC02 rise each time

  1. The effects of decreased compliance or increased RAW on the driving pressure required to ventilate the patient. [Chang’s pp. 3-10]

·  Bedside measurement of the RAW

RAW = P1 - P2

Flow rate in liters/second

See page 8 Figure 1-2 and 1-3 of Chang.