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Examen

NRNP 6566 WEEK 11 FINAL EXAM LATEST UPDATED COMPLETE SOLUTIONS GRADED A+ 2025 / 2026 NEWEST EDITION INSTANT DOWNLOAD

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NRNP 6566 WEEK 11 FINAL EXAM LATEST UPDATE GRADED A+ 2025 NRNP 6566 WEEK 11 FINAL EXAM LATEST UPDATE WITH COMPLETE SOLUTIONS GRADED A+ NRNP 6566 WEEK 11 FINAL EXAM LATEST UPDATE WITH COMPLETE SOLUTIONS GRADED A+ NRNP 6566 WEEK 11 FINAL EXAM LATEST UPDATE GRADED A+ 2025 NRNP 6566 WEEK 11 FINAL EXAM LATEST UPDATE WITH COMPLETE SOLUTIONS GRADED A+ NRNP 6566 WEEK 11 FINAL EXAM LATEST UPDATE WITH COMPLETE SOLUTIONS GRADED A+

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Institución
NRNP 6566 / NRNP6566
Grado
NRNP 6566 / NRNP6566

Información del documento

Subido en
19 de junio de 2025
Número de páginas
64
Escrito en
2024/2025
Tipo
Examen
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Preguntas y respuestas

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NRNP 6566 f




FINAL EXAM f




STUDYGUIDE f




Week 6 and 7f f f




1. Interpret arterial blood gases (ABG). Differentiate alkalosis/ acidosis
f f f f f f f


and respiratory / metabolic
f f f f

,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
f f f f f f f f f f


alveolar blood flow, this will be seen in the V/Q ratio. If the V/Q ratio
f f f f f f f f f f f f f f f


reduces due to inadequate ventilation, gas exchange within the
f f f f f f f f f


affected alveoli will be impaired. As a result, the capillary partial
f f f f f f f f f f f


pressure of oxygen (pO2) falls and the partial pressure of carbon
f f f f f f f f f f f


dioxide (pCO2) rises.
f f f




To manage this, hypoxic vasoconstriction causes blood to be
f f f f f f f f


diverted to better ventilated parts of the lung. However, in most
f f f f f f f f f f f


physiological states the hemoglobin in these well-ventilated alveolar
f f f f f f f f


capillaries will already be saturated. This means that red cells will be
f f f f f f f f f f f f


unable to bind additional oxygen to increase the pO2. As a result, the
f f f f f f f f f f f f f


pO2 level of the blood
f f f f f

, remains low, which acts as a stimulus to cause hyperventilation,
f f f f f f f f f


resulting in either normal or low CO2 levels.
f f f f f f f f




A mismatch in ventilation and perfusion can arise due to either
f f f f f f f f f f


reduced ventilation of part of the lung or reduced perfusion.
f f f f f f f f f f




Ventilation/perfusion mismatch — Mechanical ventilation can alter f f f f f f


two opposing forms of ventilation/perfusion mismatch (V/Q
f f f f f f f


mismatch), dead space (areas that are overventilated relative to
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perfusion; V>Q) and shunt (areas that are underventilated relative to
f f f f f f f f f f


perfusion; V<Q). By increasing ventilation (V), the institution of
f f f f f f f f f


positive pressure ventilation will worsen dead space but improve
f f f f f f f f f


shunt.
f




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
f f f f f f f f f f f


involved in gas exchange due to insufficient perfusion (ie,
f f f f f f f f f


overventilated relative to perfusion). Positive pressure ventilation
f f f f f f f


tends to increase alveolar dead space by increasing ventilation in
f f f f f f f f f f


alveoli that do not have a corresponding increase in perfusion,
f f f f f f f f f f


thereby worsening V/Q mismatch and hypercapnia.
f f f f f f




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
f f f f f f f f f f f


exchange because of insufficient alveolar ventilation. Patients with
f f f f f f f f


respiratory failure frequently have increased intraparenchymal
f f f f f f


shunting due to areas of focal atelectasis that continue to be perfused
f f f f f f f f f f f f


(ie, regions that are underventilated relative to perfusion). Treating
f f f f f f f f f


atelectasis with positive pressure ventilation can reduce
f f f f f f f


intraparenchymal shunting by improving alveolar ventilation, thereby
f f f f f f f


improving V/Q matching and oxygenation.
f f f f f


This is particularly true if PEEP is added. (See "Positive end-
f f f f f f f f f f


expiratory pressure (PEEP)" and "Measures of oxygenation and f f f f f f f


mechanisms of hypoxemia", section on 'V/Q mismatch'.)
f f f f f f f




3. Be able to calculate an Aa gradient. Be able to interpret an Aa gradient.
f f f f f f f f f f f f f




The alveolar to arterial (A-a) oxygen gradient is a common measure
f f f f f f f f f f


of oxygenation ("A" denotes alveolar and "a" denotes arterial
f f f f f f f f f


oxygenation). It is the difference between the amount of the oxygen
f f f f f f f f f f f


in the alveoli (ie, the alveolar oxygen tension [PAO2]) and the amount
f f f f f f f f f f f f


of oxygen dissolved in the plasma (PaO2):
f f f f f f f




A-a oxygen gradient = PAO2 - PaO2
f f f f f f




PaO2 is measured by arterial blood gas, while PAO2 is calculated
f f f f f f f f f f


using the alveolar gas equation:
f f f f f




PAO2 = (FiO2 x [Patm - PH2O]) - (PaCO2 ÷ R)
f f f f f f f f f f

, where FiO2 is the fraction of inspired oxygen (0.21 at room air), Patm
f f f f f f f f f f f f


is the atmospheric pressure (760 mmHg at sea level), PH2O is the
f f f f f f f f f f f f


partial pressure of water (47 mmHg at 37ºC), PaCO2 is the arterial
f f f f f f f f f f f f


carbon dioxide tension, and R is the respiratory quotient. The
f f f f f f f f f f


respiratory quotient is approximately 0.8 at steady state, but varies
f f f f f f f f f f


according to the relative utilization of carbohydrate, protein, and fat.
f f f f f f f f f f




The A-a gradient calculated using this alveolar gas equation may
f f f f f f f f f


deviate from the true gradient by up to 10 mmHg. This reflects the
f f f f f f f f f f f f f


equation's simplification from the more rigorous full calculation and
f f f f f f f f f


the imprecision of several independent variables (eg, FiO2 and R).
f f f f f f f f f f




The normal A-a gradient varies with age and can be estimated from
f f f f f f f f f f f


the following equation, assuming the patient is breathing room air:
f f f f f f f f f f




A-a gradient = 2.5 + 0.21 x age in years
f f f f f f f f f




The A-a gradient increases with higher FiO2. When a patient receives
f f f f f f f f f f


a high FiO2, both PAO2 and PaO2 increase. However, the PAO2
f f f f f f f f f f f


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
f f f f f f f f f f f f


oxygen varied from 8 to 82 mmHg in patients younger than 40 years
f f f f f f f f f f f f f


of age and from 3 to 120 mmHg in patients older than 40 years of age
f f f f f f f f f f f f f f f f


[5].
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Proper determinations of the A-a gradient require exact
f f f f f f f


measurement of FiO2 such as when patients are breathing room air
f f f f f f f f f f f


or are receiving mechanical ventilation. The FiO2 of patients
f f f f f f f f f


receiving supplemental oxygen by nasal cannula or mask can be
f f f f f f f f f f


estimated and the A-a gradient approximated but large variations
f f f f f f f f f


may exist and the A-a gradient may substantially vary from the
f f f f f f f f f f f


predicted, limiting its usefulness. The use of a 100 percent non-
f f f f f f f f f f f


rebreathing mask reasonably approximates actual delivery of 100 f f f f f f f


percent oxygen and can be used to measure shunt.
f f f f f f f f f




Why use the Aa gradient:
f f f f




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.
f f
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