FINAL EXAM f
STUDYGUIDE f
Week 6 and 7f f f
1. Interpret arterial blood gases (ABG). Differentiate alkalosis/ acidosis
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and respiratory / metabolic
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,2. Identify a ventilation – perfusion mismatch and how to treat it
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If there is a mismatch between the alveolar ventilation and the
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alveolar blood flow, this will be seen in the V/Q ratio. If the V/Q ratio
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reduces due to inadequate ventilation, gas exchange within the
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affected alveoli will be impaired. As a result, the capillary partial
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pressure of oxygen (pO2) falls and the partial pressure of carbon
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dioxide (pCO2) rises.
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To manage this, hypoxic vasoconstriction causes blood to be
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diverted to better ventilated parts of the lung. However, in most
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physiological states the hemoglobin in these well-ventilated alveolar
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capillaries will already be saturated. This means that red cells will be
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unable to bind additional oxygen to increase the pO2. As a result, the
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pO2 level of the blood
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, remains low, which acts as a stimulus to cause hyperventilation,
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resulting in either normal or low CO2 levels.
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A mismatch in ventilation and perfusion can arise due to either
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reduced ventilation of part of the lung or reduced perfusion.
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Ventilation/perfusion mismatch — Mechanical ventilation can alter f f f f f f
two opposing forms of ventilation/perfusion mismatch (V/Q
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mismatch), dead space (areas that are overventilated relative to
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perfusion; V>Q) and shunt (areas that are underventilated relative to
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perfusion; V<Q). By increasing ventilation (V), the institution of
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positive pressure ventilation will worsen dead space but improve
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shunt.
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Increased dead space — Dead space reflects the surface area f f f f f f f f f
within the lung that is not involved in gas exchange. It is the sum of
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the anatomic plus alveolar dead space. Alveolar dead space (also
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known as physiologic dead space) consists of alveoli that are not
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involved in gas exchange due to insufficient perfusion (ie,
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overventilated relative to perfusion). Positive pressure ventilation
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tends to increase alveolar dead space by increasing ventilation in
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alveoli that do not have a corresponding increase in perfusion,
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thereby worsening V/Q mismatch and hypercapnia.
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Reduced shunt — An intraparenchymal shunt exists where there is f f f f f f f f f
blood flow through pulmonary parenchyma that is not involved in gas
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exchange because of insufficient alveolar ventilation. Patients with
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respiratory failure frequently have increased intraparenchymal
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shunting due to areas of focal atelectasis that continue to be perfused
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(ie, regions that are underventilated relative to perfusion). Treating
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atelectasis with positive pressure ventilation can reduce
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intraparenchymal shunting by improving alveolar ventilation, thereby
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improving V/Q matching and oxygenation.
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This is particularly true if PEEP is added. (See "Positive end-
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expiratory pressure (PEEP)" and "Measures of oxygenation and f f f f f f f
mechanisms of hypoxemia", section on 'V/Q mismatch'.)
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3. Be able to calculate an Aa gradient. Be able to interpret an Aa gradient.
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The alveolar to arterial (A-a) oxygen gradient is a common measure
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of oxygenation ("A" denotes alveolar and "a" denotes arterial
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oxygenation). It is the difference between the amount of the oxygen
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in the alveoli (ie, the alveolar oxygen tension [PAO2]) and the amount
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of oxygen dissolved in the plasma (PaO2):
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A-a oxygen gradient = PAO2 - PaO2
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PaO2 is measured by arterial blood gas, while PAO2 is calculated
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using the alveolar gas equation:
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PAO2 = (FiO2 x [Patm - PH2O]) - (PaCO2 ÷ R)
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, where FiO2 is the fraction of inspired oxygen (0.21 at room air), Patm
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is the atmospheric pressure (760 mmHg at sea level), PH2O is the
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partial pressure of water (47 mmHg at 37ºC), PaCO2 is the arterial
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carbon dioxide tension, and R is the respiratory quotient. The
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respiratory quotient is approximately 0.8 at steady state, but varies
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according to the relative utilization of carbohydrate, protein, and fat.
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The A-a gradient calculated using this alveolar gas equation may
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deviate from the true gradient by up to 10 mmHg. This reflects the
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equation's simplification from the more rigorous full calculation and
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the imprecision of several independent variables (eg, FiO2 and R).
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The normal A-a gradient varies with age and can be estimated from
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the following equation, assuming the patient is breathing room air:
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A-a gradient = 2.5 + 0.21 x age in years
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The A-a gradient increases with higher FiO2. When a patient receives
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a high FiO2, both PAO2 and PaO2 increase. However, the PAO2
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increases disproportionately, causing the A-a gradient to increase. In
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one series, the A-a gradient in men breathing air and 100 percent
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oxygen varied from 8 to 82 mmHg in patients younger than 40 years
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of age and from 3 to 120 mmHg in patients older than 40 years of age
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[5].
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Proper determinations of the A-a gradient require exact
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measurement of FiO2 such as when patients are breathing room air
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or are receiving mechanical ventilation. The FiO2 of patients
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receiving supplemental oxygen by nasal cannula or mask can be
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estimated and the A-a gradient approximated but large variations
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may exist and the A-a gradient may substantially vary from the
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predicted, limiting its usefulness. The use of a 100 percent non-
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rebreathing mask reasonably approximates actual delivery of 100 f f f f f f f
percent oxygen and can be used to measure shunt.
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Why use the Aa gradient:
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The A-a Gradient can help determine the cause of
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hypoxia; it pinpoints the location of the hypoxia as
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intra- or extra- pulmonary.
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When to use the Aa gradient:
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Patients with unexplained hypoxia. f f f
Patients with hypoxia exceeding the degree of their f f f f f f f
clinical illness.
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