2022 / 2023 NRNP 6566 Final Exam Study Guide | Week 6 – 11 Fully Covered

2022 / 2023 NRNP 6566 Final Exam Study Guide Week 6 – 11 Fully Covered   Week 6 and 7 1. Interpret arterial blood gases (ABG). Differentiate alkalosis/ acidosis and respiratory / metabolic 2. Identify a ventilation – perfusion mismatch and how to treat it If there is a mismatch between the alveolar ventilation and the alveolar blood flow, this will be seen in the V/Q ratio. If the V/Q ratio reduces due to inadequate ventilation, gas exchange within the affected alveoli will be impaired. As a result, the capillary partial pressure of oxygen (pO2) falls and the partial pressure of carbon dioxide (pCO2) rises. To manage this, hypoxic vasoconstriction causes blood to be diverted to better ventilated parts of the lung. However, in most physiological states the hemoglobin in these well-ventilated alveolar capillaries will already be saturated. This means that red cells will be unable to bind additional oxygen to increase the pO2. As a result, the pO2 level of the blood remains low, which acts as a stimulus to cause hyperventilation, resulting in either normal or low CO2 levels. A mismatch in ventilation and perfusion can arise due to either reduced ventilation of part of the lung or reduced perfusion. Ventilation/perfusion mismatch — Mechanical ventilation can alter two opposing forms of ventilation/perfusion mismatch (V/Q mismatch), dead space (areas that are overventilated relative to perfusion; VQ) and shunt (areas that are underventilated relative to perfusion; VQ). By increasing ventilation (V), the institution of positive pressure ventilation will worsen dead space but improve shunt. Increased dead space — Dead space reflects the surface area within the lung that is not involved in gas exchange. It is the sum of the anatomic plus alveolar dead space. Alveolar dead space (also known as physiologic dead space) consists of alveoli that are not involved in gas exchange due to insufficient perfusion (ie, overventilated relative to perfusion). Positive pressure ventilation tends to increase alveolar dead space by increasing ventilation in alveoli that do not have a corresponding increase in perfusion, thereby worsening V/Q mismatch and hypercapnia. Reduced shunt — An intraparenchymal shunt exists where there is blood flow through pulmonary parenchyma that is not involved in gas exchange because of insufficient alveolar ventilation. Patients with respiratory failure frequently have increased intraparenchymal shunting due to areas of focal atelectasis that continue to be perfused (ie, regions that are underventilated relative to perfusion). Treating atelectasis with positive pressure ventilation can reduce intraparenchymal shunting by improving alveolar ventilation, thereby improving V/Q matching and oxygenation. This is particularly true if PEEP is added. (See "Positive end-expiratory pressure (PEEP)" and "Measures of oxygenation and mechanisms of hypoxemia", section on 'V/Q mismatch'.) 3. Be able to calculate an Aa gradient. Be able to interpret an Aa gradient. The alveolar to arterial (A-a) oxygen gradient is a common measure of oxygenation ("A" denotes alveolar and "a" denotes arterial oxygenation). It is the difference between the amount of the oxygen in the alveoli (ie, the alveolar oxygen tension [PAO2]) and the amount of oxygen dissolved in the plasma (PaO2): A-a oxygen gradient = PAO2 - PaO2 PaO2 is measured by arterial blood gas, while PAO2 is calculated using the alveolar gas equation: PAO2 = (FiO2 x [Patm - PH2O]) - (PaCO2 ÷ R) where FiO2 is the fraction of inspired oxygen (0.21 at room air), Patm is the atmospheric pressure (760 mmHg at sea level), PH2O is the partial pressure of water (47 mmHg at 37ºC), PaCO2 is the arterial carbon dioxide tension, and R is the respiratory quotient. The respiratory quotient is approximately 0.8 at steady state, but varies according to the relative utilization of carbohydrate, protein, and fat. The A-a gradient calculated using this alveolar gas equation may deviate from the true gradient by up to 10 mmHg. This reflects the equation's simplification from the more rigorous full calculation and the imprecision of several independent variables (eg, FiO2 and R). The normal A-a gradient varies with age and can be estimated from the following equation, assuming the patient is breathing room air: A-a gradient = 2.5 + 0.21 x age in years The A-a gradient increases with higher FiO2. When a patient receives a high FiO2, both PAO2 and PaO2 increase. However, the PAO2 increases disproportionately, causing the A-a gradient to increase. In one series, the A-a gradient in men breathing air and 100 percent oxygen varied from 8 to 82 mmHg in patients younger than 40 years of age and from 3 to 120 mmHg in patients older than 40 years of age [5]. Proper determinations of the A-a gradient require exact measurement of FiO2 such as when patients are breathing room air or are receiving mechanical ventilation. The FiO2 of patients receiving supplemental oxygen by nasal cannula or mask can be estimated and the A-a gradient approximated but large variations may exist and the A-a gradient may substantially vary from the predicted, limiting its usefulness. The use of a 100 percent non-rebreathing mask reasonably approximates actual delivery of 100 percent oxygen and can be used to measure shunt. Why use the Aa gradient: ▪ The A-a Gradient can help determine the cause of hypoxia; it pinpoints the location of the hypoxia as intra- or extra- pulmonary. When to use the Aa gradient: ▪ Patients with unexplained hypoxia. ▪ Patients with hypoxia exceeding the degree of their clinical illness. 4. Identify clinical symptoms or conditions indicating a need to intubate and ventilate a patient Neuromuscular depression or failure A. Drugs Opiods Sedatives NM Blockers B. Trauma