Week 11 Final Exam Latest Updated Complete
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THIS EXAM INCLUDES:
• Latest NRNP 6566 Week 11 Final Exam review
• Comprehensive practice questions
• Verified answers with detailed rationales
• High-yield clinical concepts
• Adult acute care management review
• Differential diagnosis and treatment strategies
• Evidence-based practice highlights
• Exam-focused study guide
• Instant digital download
• Updated for the 2026/2027 academic cycle
, Final Exam-Study Guide x x
Week 6 and 7 x x x
1. Interpret arterial blood gases (ABG). Differentiate alkalosis/ acidosis and
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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 alveolar
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xblood flow, this will be seen in the V/Q ratio. If the V/Q ratio reduces due
x x x x x x x x x x x x x x x
xto inadequate ventilation, gas exchange within the affected alveoli will be
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ximpaired. As a result, the capillary partial pressure of oxygen (pO2) falls
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xand the partial pressure of carbon dioxide (pCO2) rises.
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To manage this, hypoxic vasoconstriction causes blood to be diverted to
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better ventilated parts of the lung. However, in most physiological states
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the hemoglobin in these well-ventilated alveolar capillaries will already
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be saturated. This means that red cells will be unable to bind additional
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oxygen to increase the pO2. As a result, the pO2 level of the blood
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, remains low, which acts as a stimulus to cause hyperventilation, resulting
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in either normal or low CO2 levels.
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A mismatch in ventilation and perfusion can arise due to either reduced
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ventilation of part of the lung or reduced perfusion.
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Ventilation/perfusion mismatch — Mechanical ventilation can alter two x x x x x x x
opposing forms of ventilation/perfusion mismatch (V/Q mismatch), dead
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space (areas that are overventilated relative to perfusion; V>Q) and shunt
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(areas that are underventilated relative to perfusion; V<Q). By increasing
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ventilation (V), the institution of positive pressure ventilation will worsen
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dead space but improve shunt.
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Increased dead space — Dead space reflects the surface area within the
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xlung that is not involved in gas exchange. It is the sum of the anatomic
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xplus alveolar dead space. Alveolar dead space (also known as physiologic
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xdead space) consists of alveoli that are not involved in gas exchange due
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xto insufficient perfusion (ie, overventilated relative to perfusion). Positive
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xpressure ventilation tends to increase alveolar dead space by increasing
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xventilation in alveoli that do not have a corresponding increase in
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xperfusion, thereby worsening V/Q mismatch and hypercapnia. x x x x x x
Reduced shunt — An intraparenchymal shunt exists where there is blood
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flow through pulmonary parenchyma that is not involved in gas exchange
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because of insufficient alveolar ventilation. Patients with respiratory
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failure frequently have increased intraparenchymal shunting due to areas
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of focal atelectasis that continue to be perfused (ie, regions that are
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underventilated relative to perfusion). Treating atelectasis with positive
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pressure ventilation can reduce intraparenchymal shunting by improving
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alveolar ventilation, thereby improving V/Q matching and oxygenation.
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This is particularly true if PEEP is added. (See "Positive end-expiratory
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pressure (PEEP)" and "Measures of oxygenation and mechanisms of
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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 of
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oxygenation ("A" denotes alveolar and "a" denotes arterial oxygenation).
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It is the difference between the amount of the oxygen in the alveoli (ie,
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the alveolar oxygen tension [PAO2]) and the amount of oxygen dissolved
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in the plasma (PaO2):
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A-a oxygen gradient = PAO2 - PaO2 x x x x x
PaO2 is measured by arterial blood gas, while PAO2 is calculated using the
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alveolar gas equation:
x x x
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 is
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the atmospheric pressure (760 mmHg at sea level), PH2O is the partial
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pressure of water (47 mmHg at 37ºC), PaCO2 is the arterial carbon dioxide
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tension, and R is the respiratory quotient. The respiratory quotient is
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approximately 0.8 at steady state, but varies according to the relative
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utilization of carbohydrate, protein, and fat.
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The A-a gradient calculated using this alveolar gas equation may deviate
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from the true gradient by up to 10 mmHg. This reflects the equation's
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simplification from the more rigorous full calculation and the imprecision
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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 the
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following equation, assuming the patient is breathing room air:
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A-a gradient = 2.5 + 0.21 x age in years x x x x x x x x
The A-a gradient increases with higher FiO2. When a patient receives a
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high FiO2, both PAO2 and PaO2 increase. However, the PAO2 increases
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disproportionately, causing the A-a gradient to increase. In one series, the
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A-a gradient in men breathing air and 100 percent oxygen varied from 8
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to 82 mmHg in patients younger than 40 years of age and from 3 to 120
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mmHg in patients older than 40 years of age [5].
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Proper determinations of the A-a gradient require exact measurement of
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FiO2 such as when patients are breathing room air or are receiving
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mechanical ventilation. The FiO2 of patients receiving supplemental
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oxygen by nasal cannula or mask can be estimated and the A-a gradient
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approximated but large variations may exist and the A-a gradient may
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substantially vary from the predicted, limiting its usefulness. The use of a
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100 percent non-rebreathing mask reasonably approximates actual
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delivery of 100 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 hypoxia;
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it pinpoints the location of the hypoxia as intra- or extra-
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pulmonary.
When to use the Aa gradient:
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▪ Patients with unexplained hypoxia. x x x
▪ Patients with hypoxia exceeding the degree of their clinical
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illness.
x