Pulmonary CSC

When assessing an arterial blood gas, what does the nurse know to be true about the PaO2: A. It is the primary factor in determining the amount of O2 that binds to hemoglobin. B. It represents about 97% of the oxygen carried by the blood. C. The normal value is not affected the FIO2. D. It does not include the amount of oxygen dissolved in plasma.

A. 3% of oxygen is dissolved in plasma and is represented by the PaO2. 97% of oxygen is combined with hemoglobin. The amount of oxygen dissolved in plasma is not sufficient to meet the oxygen demands of the tissues; however, it is the primary factor in determining the amount of O2 that binds to hemoglobin. PaO2 is affected by alveolar oxygen content which is affected by FIO2.

What compensatory system removes extra interstitial fluid in an effort to prevent pulmonary edema: A. Lymphatic system. B. Sympathetic nervous system. C. Renin-angiotensin-aldosterone system. D. Bronchial blood flow.

A. The lymphatic system can adjust to remove up to ten times the normal amount of fluid during pathological conditions. When the level of fluid exceeds this amount and cannot be removed by lymph drainage, then pulmonary edema occurs. Fluid accumulates first in the interstitium, then in the alveoli because the capillary endothelium is more permeable to water and solute than the alveolar endothelium. Fluid in the interstitium is removed by the lymphatic system. For this reason, the nurse cannot assume that absence of crackles implies normal fluid status. The patient may have normal lung sounds because the lymphatic system is keeping up with the removal of extra fluid and thus preventing pulmonary edema.

Which of the following conditions will alter pulmonary perfusion: A. Right sided heart failure and pneumonia. B. Pulmonary embolus and acute right sided heart failure. C. Pulmonary edema and pulmonary embolus. D. Pulmonary edema and pneumonia.

B. A pulmonary perfusion abnormality is caused by abnormal blood flow. Pulmonary perfusion is the entire output of the right ventricle. An overall reduction in right ventricular cardiac output, which occurs with right sided heart failure, will result in decreased pulmonary perfusion .Obstruction to blood flow caused by a pulmonary embolus decreases pulmonary perfusion. Pulmonary edema and pneumonia alter the alveoli and can cause a barrier to the diffusion of oxygen as well as potential problems with lung compliance and therefore ventilation abnormalities. Pulmonary edema and pneumonia do not directly cause an alteration in blood flow through the pulmonary vessels.

Your patient is being admitted with acute respiratory distress after having progressive flu-like symptoms for the past 3 days. His respiratory rate is 34, he is using accessory muscles of respiration, he is diaphoretic, skin is cool. His BP is 92/54, HR is 112 in sinus tachycardia, his temperature is 39 degrees C. His ABGs are: pH 7.22, PaCO2 58 mmHg, HCO3 27 mEq/L, PaO2 50 mmHg. What would be the best initial therapy: A. Antibiotics to treat his infection. B. Intubation and mechanical ventilation. C. O2 at 6 L/min via nonrebreathing mask to treat his hypoxemia. D. Dopamine to treat his hypotension.

B. This patient is working hard to breathe but is still inadequately ventilating and oxygenating. His ABGs indicate severe respiratory acidosis and hypoxemia. Intubation and mechanical ventilation will improve ventilation and oxygenation as well as reduce the work of breathing. If untreated, this situation is likely to deteriorate into full arrest. Increased work of breathing is an important indicator of impending cardiac or respiratory arrest. Antibiotics will also be necessary if his respiratory failure is due to pneumonia or sepsis, but intubation and mechanical ventilation is the immediate priority.

Which of the following statements is true concerning the physiological impact of a pulmonary embolus: A. Decreased alveolar dead space, increased V/Q ratio. B. Decreased alveolar dead space, decreased V/Q ratio. C. Increased alveolar dead space, increased V/Q ratio. D. Increased alveolar dead space, decreased V/Q ratio.

C. A pulmonary embolus results in a decrease in pulmonary perfusion while ventilation continues. This causes an increased V/Q ratio because ventilation (V) remains constant and perfusion (Q) falls. Alveolar dead space refers to ventilated alveoli that receive no perfusion. Therefore, a pulmonary embolus increases alveolar dead space.

Acute respiratory distress syndrome (ARDS) always involves acute lung injury from a primary pulmonary source such as pneumonia: True False

False ARDS begins with acute lung injury (ALI) either from a primary pulmonary etiology or from a more systemic insult such as sepsis, trauma, or major surgery.

Which of the following is most important to assess for when screening for obstructive sleep apnea (OSA): A. Number of hours slept per night. B. The use of two to pillows at night. C. Insominia. D. Excessive day time sleepiness.

D. A diagnosis of OSA is made when a person has > 5 apneas or hypoapneas per hour of sleep accompanied by excessive daytime sleepiness. Screening for OSA should occur in all cardiovascular patients. High risk features associated with the diagnosis of OSA include: loud snoring, witnessed apneas, excessive daytime sleepiness, morning headaches, hypertension, BMI > 35 kg/m2, neck circumference > 40 cm, and age > 50 years.

What is true regarding acute respiratory distress syndrome (ARDS): A. There is non-cardiac pulmonary edema. B. There is refractory hypoxemia. C. There is impaired removal of CO2. D. All of the above.

D.ARDS is a syndrome of acute respiratory failure characterized by non-cardiac pulmonary edema and manifested by refractory hypoxemia and impaired removal of CO2. ARDS begins with acute lung injury (ALI) either from a primary pulmonary etiology or from a more systemic insult. ARDS is also often accompanied by failure of multiple organs. ARDS does not include very mild or early acute lung injury, but rather involves more severe and diffused lung injury. ARDS is classified based on the degree of hypoxemia: • Mild (PaO2/FIO2 Ratio > 200 mm Hg and ≤ 300 mm Hg) • Moderate (PaO2/FIO2 Ratio > 100 mm Hg ≤ 200 mm Hg) • Severe (PaO2/FIO2 ≤ 100 mm Hg)

Which of the following conditions will result in ventilation to perfusion mismatching: A. Pulmonary tumors. B. Pulmonary embolus. C. Pulmonary edema. D. Bronchitis. E. All of the above.

E. Any condition that causes uneven ventilation or uneven perfusion will result in ventilation and perfusion mismatching. Causes of non-Uniform ventilation due to uneven resistance to airflow: • Bronchoconstriction (asthma) • Collapsed airways (emphysema) • Inflammation (bronchitis). Causes of non-uniform ventilation due to uneven compliance throughout the lung: • Fibrosis • Pulmonary edema • Pneumonia • Atelectasis • Pneumothorax • Tumors • Emphysema • Decreased surfactant. Causes of non-uniform perfusion: • Emboli • Compression of pulmonary capillaries by high alveolar pressures • Tumors • Pneumothorax • Collapse of alveoli • Pulmonary vascular hypotension.

You are caring for a patient with massive atelectasis. What is true regarding this patient's ventilation to perfusion (V/Q) ratio: A. The patient has decreased V/Q ratio. B. The patient's weight is needed to determine the V/Q ratio. C. The patient has a normal V/Q ratio. D. The patient has an increased V/Q ratio.

A. A decreased V/Q ratio is called an intrapulmonary shunt. This occurs when ventilation is less than perfusion. • Results in mixed venous blood perfusing totally collapsed or unventilated alveoli. • No gas exchange occurs and poorly oxygenated blood returns to the left side of the heart (thus the reason for the term intrapulmonary shunt). With a V/Q ratio < 0.8 (decreased V/Q ratio): • Alveolar PO2 falls. • Alveolar PCO2 rises. Massive atelectasis as seen in ARDS will result in a decreased V/Q ratio and intrapulmonary shunting.

Which of the following interventions would NOT result in a decrease in airway resistance: A. Use of a longer endotracheal tube. B. Suctioning. C. Bronchodilators. D. Use of an endotracheal tube with a wider diameter.

A. A wider diameter endotracheal tube, a shorter endotracheal tube, suctioning, and bronchodilators will all decrease airway resistance. A longer endotracheal tube will increase airway resistance.

Arterial blood gas analysis can be used for all of the following EXCEPT: A. Evaluation of tissue oxygenation. B. Evaluation of acid-base status. C. Evaluation of ventilation. D. Evaluation of hypoxemia.

A. ABG analysis provides a pH which indicates acid-base status, a PaO2 which indicates the amount of O2 in arterial blood (presence or absence of hypoxemia), and a PaCO2 which indicates ventilatory status. Tissue oxygenation cannot be accurately evaluated by an arterial blood bas. Global indicators used currently include mixed venous O2 saturation (SvO2), lactic acid levels, base deficit, and arterial-venous pCO2 gradient. Research is currently evaluating the use of new technology to directly assess tissue oxygenation. This technology includes near-infrared spectroscopy that can continuously and non invasively monitor tissue oxygen saturation (StO2).

All of the following will decrease diffusion of oxygen EXCEPT: A. High FIO2. B. Increased thickness of the alveolar capillary membrane. C. Pulmonary resection. D. Low inspired fraction of oxygen.

A. An increase in FIO2 will increase the diffusion of oxygen by increasing the alveolar / arterial gradient. Increased thickness of the alveolar capillary membrane (fluid, fibrotic tissue, etc.) will impede the diffusion of oxygen. Low inspired fraction of oxygen (smoke inhalation, altitude sickness) will decrease the diffusion of oxygen by decreasing the alveolar/arterial gradient. Decreased surface area (resection, tumor, etc.) will also result in a decrease in the diffusion of oxygen

All of the following will interfere with the diffusion of oxygen across the alveolar capillary membrane EXCEPT: A. Narcotic overdose in conscious sedation. B. Fibrotic tissue in pulmonary fibrosis. C. Exudate in pneumonia. D. Fluid in pulmonary edema.

A. Anything that increases the alveolar capillary membrane will interfere with the diffusion of oxygen. Exudate, fluid, and fibrotic tissue will all expand the alveolar capillary membrane and create a barrier to diffusion of oxygen. A narcotic overdose will impact ventilation and can cause respiratory failure but does not interfere with diffusion.

In patients with obstructive airway disease, expiratory airway resistance is most commonly assessed by the following: A. Forced expiratory volume in the first second (FEV1). B. Body plethysmography. C. Volume of air exhaled in one minute. D. Maximum hold time with incentive spirometer.

A. Assessment of expiratory airway resistance is commonly done by assessing forced expiratory volume in the first second (FEV1). Eighty percent of forced vital capacity (FVC) should occur within the first second of forced expiratory effort. A patient with airway obstruction exhales far less than 80% of the FVC within 1 second. Maximum hold time with incentive spirometer is a function of inspiratory effort, not expiratory effort. Body plethysmography is not necessary because expiratory airway resistance can be measured with spirometry. The volume of air exhaled in one minute is minute ventilation. Minute ventilation can be impacted by factors other than expiratory airway resistancE

The following conditions are associated with decreased compliance of the lungs except: A. Bronchitis. B. Interstitial lung disease. C. Atelectasis. D. Pulmonary fibrosis.

A. Atelectasis decreases lung compliance and increases elastic recoil. Restrictive diseases restrict lung expansion due to decreased lung compliance. In pulmonary fibrosis and interstitial lung disease (restrictive diseases), elastin fibers are replaced with scar tissue; causing a decrease in compliance. Obstructive diseases interfere with airflow and increase resistance: • Asthma. • Emphysema. • Bronchitis. • Foreign body obstruction. • Obstructive sleep apnea.

What is true regarding continuous positive airway pressure (CPAP): A. CPAP maintains positive airway pressure at the end of expiration. B. CPAP add pressure during inspiration to decrease work of breathing. C. CPAP is the noninvasive ventilation mode of choice in hypercapnia respiratory failure. D. CPAP controls tidal volume but not respiratory rate.

A. CPAP maintains positive airway pressure at the end of expiration, rather than allowing pressure to return to zero. There are no machine delivered breaths. The patient controls rate and tidal volume. Continuous positive airway pressure accomplishes what positive end expiratory pressure (PEEP) accomplishes as an adjunct to other modes of mechanical ventilation. CPAP is also used in the treatment of obstructive sleep apnea. CPAP is not the noninvasive ventilation mode of choice in hypercapnic respiratory failure because the patient still controls the rate and tidal volume. Biphasic positive airway pressure (BiPAP) combines CPAP with pressure support during inspiration. BiPAP is indicated as a noninvasive mode of ventilation in patients with evidence of inadequate ventilation (i.e. increased work of breathing or elevated PaCO2 on blood gas).

Pulmonary edema impacts the pulmonary system in which of the following ways: A. Interferes with the diffusion of oxygen across the alveolar/ capillary membrane and interferes with effective ventilation by decreasing compliance. B. Interfere with perfusion by blocking pulmonary blood flow and interferes with ventilation by decreasing compliance. C. None of the above. D. Decreases FIO2 and causing pulmonary vasodilation.

A. Excess fluid in the interstitial space as well as any fluid in the alveoli creates a barrier to the diffusion of oxygen by expanding the alveolar/capillary membrane. In addition, the presence of fluid in the alveoli decreases their compliance and can impair effective ventilation. Pulmonary edema does not directly result in blocking pulmonary blood flow. A block in pulmonary blood flow is caused by a perfusion problem such as pulmonary embolus. Pulmonary edema has no effect on FIO2, since FIO2 is inspired O2 and is controlled externally. Pulmonary edema can result in hypoxia which can cause pulmonary vasoconstriction, not dilation.

When caring for a patient with acute respiratory distress syndrome (ARDS) who continues to require a high FIO2 to maintain adequate oxygenation the nurse is concerned about the following: A. Decreased lung compliance as a complication of persistent high FIO2. B. Increased lung compliance as a complication of persistent high FIO2. C. Decreased airway resistance as a complication of persistent high FIO2. D. Increased airway resistance as a complication of persistent high FIO2.

A. High levels of FIO2 for a prolonged period of time can result in oxygen toxicity. One of the complications of oxygen therapy is absorption atelectasis, and a sign of oxygen toxicity is decreased lung compliance. The nurse would be concerned about this complication because decreased lung compliance is also a complication that occurs from the pathophysiological changes in acute respiratory distress syndrome (ARDS). Decreased lung compliance adversely affects ventilation.

What is true regarding normal spontaneous breathing: A. Inspiration is accomplished by causing alveolar pressure to fall below atmospheric pressure. B. Inspiration occurs when pressure at the nose or mouth is raised above alveolar pressure. C. During normal breathing the diaphragm rises to allow for inspiration. D. Normal negative pressure breathing is caused by the relaxation of the inspiratory respiratory muscles.

A. Inspiration is accomplished by causing alveolar pressure to fall below atmospheric pressure. This is called negative pressure breathing because atmospheric pressure is considered 0 cm H2O. Normal negative pressure breathing is caused by the contraction of the inspiratory respiratory muscles, which drops the diaphragm, increases thoracic volume, and lowers intrathoracic pressure. The lowering of the intrathoracic pressure influences the alveolar pressure. A decrease in intrathoracic pressure creates a pressure gradient, referred to as the transpulmonary or distending pressure. This distending pressure causes the alveoli to expand, thus lowering alveolar pressure to allow for inspiration.

You are caring for a patient who is undergoing a transesophageal echocardiogram and the patient has received a topical benzocaine. The patient develops a diffuse cyanosis although oxygen saturations levels do not drop. What problem do you suspect: A. Methemoglobinemia. B. Carbon monoxide poisoning. C. The presence of hemoglobin S. D. Overdose of fluorocarbons.

A. Methemoglobinemia is caused by increased levels of methemoglobin (with iron in the ferric state). Iron atoms in the ferric state will not bind with oxygen. Methemoglobinemia is commonly caused by nitrite poisoning or can be caused by a toxic reaction to oxidant drugs. A common cause of acquired methemoglobinemia is exposure to topical benzocaine during a procedure such as a transesophageal echocardiogram. Intravenous methylene blue is the treatment of choice for methemoglobinemia.

Which of the following statements is true regarding oxygen delivery, consumption, and reserve: A. Oxygen consumption should be independent of oxygen delivery in a healthy person. B. When oxygen delivery to tissues is increased, the tissues automatically consume more oxygen, keeping the reserve at a constant. C. When oxygen reserve falls below 75% anaerobic metabolism occurs. D. A high SvO2 always indicates excellent oxygenation.

A. Oxygen delivery is normally around 1000 ml of oxygen per minute. Oxygen consumption is normally around 250 ml per minute, leaving a reserve (SvO2) of approximately 75%. Patients are at risk for anaerobic metabolism when the venous reserve falls to below 40%. If tissues cannot extract and utilize oxygen, then SvO2 will be high in spite of inadequate tissue oxygenation. Tissues should extract and consume what they need independent of oxygen delivery. In this state, reserve will fall if delivery drops or consumption increases, and reserve will rise if delivery increases or consumption drops. This is referred to as oxygen consumption being independent of delivery. If delivery falls to a critical level, the tissues will no longer be able t extract what they need. This is referred to as oxygen consumption being dependent on delivery. This represents a critical state.

The following assessment findings indicate adequate diffusion of oxygen: A. Normal PaO2 and oxygen saturation. B. Clear lung sounds. C. Normal PaCO2. D. Normal rate and depth of respiration.

A. PaO2 and oxygen saturation are used to assess for adequate diffusion of oxygen. PaCO2, respiratory rate and tidal volume are all used to assess adequacy of ventilation. Clear lung sounds do not assure adequate diffusion of oxygen. For example lung sounds may remain clear in a patient with low inspired fraction of oxygen.

Pulmonary arterial hypertension (previously called 'primary' pulmonary hypertension) is defined as: A. Mean PA pressure > 25 mm Hg; PAOP < 15 mmHg; increased transpulmonary gradient (PA diastolic to PAOP pressure gradient). B. Mean PA pressure > 25 mmHg and PAOP > 25 mmHg. C. Mean PA pressure greater than mean arterial pressure. D. PA systolic of 15-25 mmHg; PA diastolic of 8 - 10 mmHg.

A. Pulmonary artery hypertension (PAH) is elevated PA pressures in the absence of elevated LV pressures. The normal transpulmonary gradient (PA diastolic pressure minus PAOP) is 1-4 mmHg; in PAH this gradient increases due to pulmonary vasoconstriction while LV pressures remain normal. PA systolic of 15-25 mmHg and PA diastolic of 8 - 10 mmHg are normal PA pressures. A mean PA pressure greater than mean arterial pressure is extremely rare and incompatible with life. It can occur in cases of extreme PAH, but that is not how PAH is diagnosed. A mean PA pressure and PAOP both > 25 would indicate left ventricular failure as the cause of PA hypertension, not 'primary' PA hypertension.

Which of the following lung volumes can be measured with spirometry: A. Inspiratory capacity. B. Functional residual capacity. C. Total lung capacity. D. Residual volume.

A. Residual volume cannot be measured with spirometry. Functional residual capacity is the sum of expiratory reserve volume and residual volume so it cannot be measured with spirometry. Total lung capacity also includes residual volume so it cannot be measured with spirometry. Inspiratory capacity is the sum of tidal volume and inspiratory reserve volume which can both be measured with spirometry. To measure any lung volumes that include residual volume other techniques such as nitrogen-washout, helium-dilution, or body plethysmography must be used.

Pulmonary arterial hypertension is diagnosed by: A. Right heart catheterization. B. Left heart catheterization. C. Subtracting CVP from PAOP. D. Calculating the difference between MAP and mean PAP.

A. Right heart catheterization allows measurement of right heart and pulmonary artery pressures; inflation of the balloon on a PA catheter allows measurement of LV end diastolic pressure (PAOP or wedge pressure). The transpulmonary gradient (PA diastolic pressure minus PAOP) can be calculated from these pressure measurements. Left heart catheterization does not give any information about right heart or pulmonary artery pressures or function.

What is true regarding surfactant: A. Surfactant is responsible for decreasing surface tension in the alveoli in response to decreased volume. B. Surfactant results in increased work of breathing. C. Surfactant is responsible for preventing bronchospasm of large airways. D. Surfactant synthesis is dependent predominantly on type 1 alveolar cells.

A. Surfactant is a lipoprotein (phospholipid) that is secreted by Type II alveolar cells. Surfactant is responsible for decreasing surface tension in the alveoli in response to decreased volume. This decrease in surface tension accomplishes two goals: 1) keeps smaller airways open during expiration; 2) improves the ease of alveolar opening during inspiration. A decrease in surfactant results in an increase in surface tension and increased pressure required to open the alveoli.

When caring for a patient with a traditional 3-compartment chest tube unit, the nurse knows that: A. A system valve that is part of the chest tube controls the amount of suction. The amount of suction is limited by the height of the fluid column in the 3rd chamber. B. Turning up the external source of suction causes loud bubbles and increases the amount of suction applied to the system. The loud bubbles assure an adequate level of suction is being maintained. C. When transporting a patient and portable suction is not available it is important to clamp the chest tube. D. The typical amount of suction applied to a chest tube drainage system is negative 60 cm H2O.

A. The typical amount of suction applied to a chest tube is minus 20 cm H2O. Patients with very friable lung tissue may need less suction. The maximum amount of suction that should be applied is minus 40 cm H2O. Chest tubes that have been connected to suction should never be clamped for transport. If portable suction is not available, patients should be transported on water seal (on gravity drainage) with the tubing from the suction chamber open to air. Clamping a chest tube for transport can result in pneumothorax for pleural chest tubes or tamponade for mediastinal chest tubes. The source suction should be adjusted to produce only gentle bubbling in the suction control chamber. Excessive external suction causes loud bubbling, which can interfere with patient rest, and also increases the evaporation of water from the suction control chamber.

When caring for a patient with a chest tube it is important for the nurse to understand that all of the following are true regarding the water seal chamber EXCEPT: A. Constant bubbling in the water seal chamber represents effective functioning. B. It is important for the drainage unit to remain upright in order to maintain an adequate water seal. C. Lack of fluctuation (tidaling) with respiration may indicate a problem in the chamber. D. The water seal allows air to exit the pleural space but prevents air from entering during inhalation.

A. The water seal chamber may bubble gently with insertion, during expiration and with a cough. However, continuous bubbling represents an air leak. The water seal chamber must contain the recommended amount of water to reach the appropriate level and the drainage unit must remain upright at all times in order to assure an adequate water seal. Tidaling (fluctuation with respiration) is normal. A lack of tidaling can indicate a kink. Lack of tidaling may also represent a fully expanded lung. The water seal allows air to exit from the pleural space on exhalation and prevents air from entering the pleural cavity or mediastinum on inhalation.

Which of the following is not a recommended suctioning practice: A. Each pass of the catheter should last for a maximum of 25 seconds. B. In adult patients 100% FIO2 should be delivered for 30 to 60 seconds prior to suctioning. Hyperoxygenation should also be repeated for 60 seconds post suctioning. C. In deep suctioning the catheter tip should be withdrawn 1 cm after resistance is met before negative pressure is applied. D. The majority of studies indicate that the installation of normal saline is not beneficial and may potentially be harmful. E. Suctioning is done on an as needed basis only to remove secretions.

A. There are two types of suctioning techniques: a) open (involves disconnecting patient from the ventilator, and b) closed (involves a sterile, in-line suction catheter). Strict sterile technique must be used during the open suction technique. There are also two levels of suctioning: a) deep (advancing suction catheter until resistance is met), and b) shallow (inserting the suction catheter to a predetermined depth). Negative pressure is only applied during withdrawal of the suction catheter. In deep suctioning the catheter tip should be withdrawn 1 cm after resistance is met before negative pressure is applied. Shallow suctioning is preferred to prevent tracheal trauma. Each pass of the suction catheter is considered a suctioning event. Each suctioning event should last for a maximum of 15 seconds. The instillation of normal saline prior to suctioning is not recommended. The level of negative pressure is determined by the catheter size and the amount of suction pressure. Smaller suction catheters should be used whenever possible. Suction pressure levels should be set as low as possible while still allowing for adequate clearing of secretions. In adult patients 100% FIO2 should be delivered for 30 to 60 seconds prior to suctioning. Hyperoxygenation should also be repeated for 60 seconds post suctioning. Oxygen saturation levels via pulse oximetry should be monitored during and after suctioning. . Closed suction systems allow for continued ventilation and oxygenation during the suctioning process. Suctioning is done on an as needed basis to remove secretions.

If one of the phrenic nerves gets damaged s a complication of a surgical procedure what is the expected consequence: A. Half of the diaphragm will be paralyzed. B. The patient will have unilateral facial droop. C. The entire diaphragm will be paralyzed resulting in ventilator dependence. D. The patient will have bilateal facial droop.

A. Two phrenic nerves that originate from cervical segments 3-5 innervate the diaphragm. If one phrenic nerve is damaged, half of the diaphragm will be paralyzed.

The two major factors that impact the work of breathing include: A. Airway resistance and compliance of the lungs and chest wall. B. Compliance of the lungs and oxygen saturation level. C. Patient's age and oxygen saturation level. D. Airway resistance and PaO2.

A. Work of breathing is impacted by compliance (elastic work of breathing), and airway resistance (resistive work of breathing). Work of breathing directly impacts the effectiveness of ventilation. Oxygen saturation and PaO2 do not have an immediate or direct effect on the work of breathing. Ventilatory failure can occur at any age if there is increased airway resistance or decreased lung compliance.

The definition of tidal volume (Vt) is: A. Volume of air entering or leaving the nose or mouth per breath. B. Volume of air inhaled into the lungs during maximal forced inspiration, beginning at the end of normal tidal inspiration. C. Volume of air entering or leaving the nose or mouth per minute. D. Volume of air in lungs at end of normal tidal expiration.

A. • Tidal Volume (VT): Volume of air entering or leaving the nose or mouth per breath. • Inspiratory Reserve Volume (IRV): Volume of air inhaled into the lungs during maximal forced inspiration, beginning at the end of normal tidal inspiration. • Expiratory Reserve Volume (ERV): Volume of air expelled during maximal forced expiration, beginning at the end of normal tidal expiration. • Residual Volume (RV): Volume of air left in lungs after maximal forced expiration. In healthy persons this prevents the lungs from collapsing. • Functional Residual Capacity (FRC): Volume of air in lungs at end of normal tidal expiration. This volume includes both expiratory reserve volume and residual volume. • Inspiratory Capacity (IC): Volume of air inhaled into the lungs during a maximal inspiratory effort that begins at the end of normal tidal expiration. This volume includes both normal tidal volume and inspiratory reserve volume. • Vital Capacity (VC): Volume of air expelled from the lungs during maximal forced expiration after maximal forced inspiration. This lung volume excludes the residual volume. • Total Lung Capacity (TLC): The volume of air in the lungs after maximal inspiratory effort. This lung volume includes the residual volume.

Which of the following statements is true regarding alveolar ventilation: A. Alveolar ventilation and tidal volume are equal. B. Alveolar ventilation is minute ventilation minus dead space. C. Alveolar ventilation is not affected by dead space. D. Alveolar ventilation is greater than minute ventilation.

B. Alveolar ventilation is minute ventilation minus dead space. Therefore alveolar ventilation is less than minute ventilation. Some tidal volume occupies dead space, therefore, alveolar ventilation is less than tidal volume. Normal tidal volume is approximately 500 ml per breath and normal alveolar ventilation is approximately 350 ml per breath. As dead space increases, alveolar ventilation decreases.

Outcomes for a patient with status asthmaticus include: A. Increased peak flow rates and decreased FEV1. B. . Normal PaCO2, increased peak flow rates, and increased FEV1. C. Decreased peak flow rates and decreased wheezing. D. Increase PaCO2 and decreased forced expiratory volume (FEV1).

B. Asthma is an obstructive disorder that results in increased airway resistance. The resistive work of breathing is greatest during forced expiration. Increased airway resistance will result in decreased peak flow rates as well as decreased forced expiratory flow volume. Initially in status asthmaticus a patient will hyperventilate. When the PaCO2 rises in status asthmaticus this is a late sign indicating intubation and mechanical ventilation will most likely be needed. Therefore, the goals for treatment include a normal PaCO2 and increased peak flow rates and increased forced expiratory volume. Decreased wheezing would also be a goal of treatment.

A patient presents in acute respiratory distress with a SpO2 of 82% on room air. The patient is placed on a 100% non-rebreather mask. Fifteen minutes after application of 100% FIO2, the patients SpO2 is 84%. The nurse recognizes and anticipates the following: A. The patient is not responding to oxygen therapy and assessment and treatment for pulmonary edema may be needed. B. The patient is not responding to oxygen therapy and may have an unrecognized ventilation problem. C. The patient most likely has a simple diffusion abnormality and needs at least 2 hours of 100% FIO2 therapy to see any potential benefit. D. A SpO2 of 84% is adequate in the patient with respiratory distress for the first 24 hours until the underlying cause can be reversed.

B. If a patient is hypoxemic simply due to a barrier to the diffusion of oxygen, then increasing the FIO2 should increase the PaO2 and oxygen saturation within a short time period because the increased FIO2 results directly in an increased partial pressure of oxygen within the alveoli. For example, if a patient has either pneumonia or pulmonary edema that is affecting the alveolar capillary membrane then there will be a barrier to the diffusion of oxygen across the membrane. If this is a simple diffusion problem the patient will respond favorably to an increase in FIO2. The reason is that an increase in FIO2 results in an increase in the alveolar partial pressure of oxygen and this increases the driving pressure of oxygen by increasing the pressure gradient. When a patient who is hypoxemic does not respond to oxygen therapy, the nurse must consider ventilatory failure as a possible etiology. An elevated PaCO2 on blood gas confirms ventilatory failure. Oxygen therapy will not correct a ventilation problem. Ventilation is determined by rate and tidal volume. Ventilatory failure has to be corrected by increasing either rate or tidal volume through either reversing the underlying cause or offering some type of ventilatory support. Hypoxemia is very dangerous because this adversely affects delivery of oxygen to the tissues. Hypoxemia must be correctly immediately to avoid adverse consequences.

Which of the following statements is not true regarding increased work of breathing: A. Signs of increased work of breathing include: 1) tachypnea, 2) accessory muscle use, 3) tachycardia, and 4) diaphoresis. B. Increased work of breathing is not a concern when oxygen saturation is > or = to 90%. C. BiPAP is an option to support increased work of breathing in patients who are hemodynamically stable and who can maintain an airway. D. Increased work of breathing places the patient at risk for adverse events including a cardiac arrest. E. Increased work of breathing steals significant cardiac output away from other organs.

B. Increased work of breathing steals significant cardiac output away from other organs and therefore places the patient at increased risk for adverse events including cardiac arrest. Increased work of breathing should always be aggressively treated, even if initial oxygen saturation is adequate. Signs of increased work of breathing include: 1) tachypnea, 2) accessory muscle use, 3) tachycardia, and 4) diaphoresis. BiPAP is the initial treatment to support increased work of breathing in a patient who does not have contraindications to noninvasive mechanical ventilation.

When assessing a patient's morning basic metabolic panel, what value correlates closely with the HCO3 (bicarb) on a blood gas: A. Chloride. B. CO2. C. Sodium. D. Potassium.

B. Most the conjugated acid of bicarbonate is in the form of dissolved carbon dioxide (serum CO2) and thus the serum CO2 tracks with the HCO3 level seen on a blood gas panel. However, a serum CO2 alone does not tell the entire picture of acid base balance because you do not know the pH. For example, if CO2 on the basic metabolic panel is elevated, you do not know if you have a primary metabolic alkalosis or if there is compensation for a respiratory acidosis.

Which of the following patients is NOT a candidate for noninvasive positive pressure ventilation: A. A patient with COPD who is experiencing an excessive work of breathing. B. A patient with a high PaCO2 with a decreasing level of consciousness. C. A patient who has failed weaning from mechanical ventilation after being intubated 4 days ago. D. A patient with a history of heart failure who has hypoxemia not resolved with oxygen therapy.

B. Noninvasive positive pressure ventilation should be considered as a first line ventilatory strategy in many patients. It should also be considered as an alternative to failed weaning from traditional mechanical ventilation. Contraindications to noninvasive positive pressure ventilation include decreased level of consciousness due to concern regarding the patient's ability to protect his airway.

What is true regarding auscultation of lung sounds: A. Rhonchi are high pitched adventitious sounds. B. Normal lung sounds are called vesicular lung sounds and has a longer inspiratory phase compared to expiratory phase. C. Wheezes are more prominent during inspiration. D. Bronchial breath sounds are only heard in infants.

B. Normal lung sounds are called vesicular breath sounds. A vesicular breath sound is a low pitched rustling sound with a higher intensity and longer inspiratory phase compared to the expiratory phase. Vesicular breath sounds can be decreased in their intensity due to pulmonary pathophysiology such as pleural effusions, pneumothorax, and emphysema. A bronchial breath sound is tubular in quality and is more pronounced in expiration. Bronchial breath sounds are heard when sound transmission is improved through a consolidated lung. Wheezes are also more prominent during expiration and are the result of oscillation of airways when there is a limitation to airflow. Rhonchi are low pitched vibratory sounds that are created from the interaction between free liquid or mucous and moving air within the lumen of an airway.

Which of following is not considered a component of the gas exchange airways: A. Alveolar ducts. B. Right and left bronchi. C. Respiratory bronchioles. D. Alveolar sacs.

B. Right and left bronchi are part of the conducting airway system. Gas exchange airways include: • Respiratory bronchioles are the transition between conducting airways and gas exchange airways. Alveoli begin to appear at the level of the respiratory bronchioles. Each portion of the lung supplied by a terminal respiratory bronchiole is called the acinus. • Alveolar ducts. • Alveolar sacs contain alveoli that are structurally interdependent - this helps prevent the collapse of individual alveoli. • Alveoli: Alveoli are made up of two types of alveolar cells: Type I and II.

Treatment strategies in an elderly patient with pneumonia should include all the following EXCEPT: A. Timely antibiotics. B. Sedatives to promote sleep. C. Mucolytics / expectorants / bronchodilators. D. Hydration.

B. Sedatives should be avoided because the patient needs to be as awake as possible to participate in deep breathing and incentive spirometry. Pneumonia causes stimulation of goblet cells to increase mucous production. Excessive mucous results in increased airway resistance and can be managed with mucolytics / expectorants / bronchodilators. Pneumonia results in clinical signs of dehydration due to tachypnea, so patients will require hydration. Timely antibiotics are essential to treatment in bacterial pneumonia. Deep breathing and incentive spirometry help prevent atelectasis and improve lung compliance.

A patient presents to the ED in acute respiratory distress. Pulse oximetry on room air is 82%. A blood gas is drawn and the PaCO2 is 42 mmHg. The most appropriate initial treatment is: A. Spiral CT to rule out pulmonary embolus (PE). B. Administration of 100% oxygen via non rebreather mask. C. Apply oxygen at 4L and send to radiology for chest X-ray. D. Immediate intubation for acute ventilatory failure.

B. The PaCO2 is normal so the patient is not in acute ventilatory failure and therefore immediate intubation is not indicated. Although a PE is a possible etiology, a CT is a diagnostic test and not a treatment. The patient's oxygen saturation level warrants treatment. Oxygen at 4 L nasal cannula will most likely not deliver a high enough FIO2 to correct this apparent diffusion problem. Also, the patient most likely warrants a portable chest x-ray due to respiratory distress. The best answer is to apply a non rebreather mask for administration of 100% FIO2.

Your patient is on 60% FIO2 and has a PaO2 of 70 mmHg. His PaCO2 is 48 mmHg. After assessing the PaO2 / FIO2 ratio you know: A. Your patient's oxyhemoglobin curve has shifted to the right and his SaO2 will be lower than expected. B. Your patient has a clinically significant intrapulmonary shunt such as that caused by acute respiratory distress syndrome (ARDS). C. Your patient's oxyhemoglobin curve has shifted to the left and his SaO2 will be higher than expected. D. Your patient's expected PaO2 is only 90 mmHg so he has only a minor intrapulmonary shunt.

B. The PaO2 / FIO2 ratio is calculated by dividing the PaO2 of 70 by the FIO2 of .6 (70/.6). When calculating the PaO2/FIO2 ratio the decimal is always used for the FIO2. In this question the PaO2 /FIO2 ratio is 117. A PaO2/FIO2 ratio of < 200 is one of the criteria required for a diagnosis of ARDs. The expected PaO2 for a given FIO2 can be calculated by taking the FIO2 (not a decimal) multiplying x 6 and then subtracting the PaCO2. For this patient the expected PaO2 would be (60 x 6) - 48 or 312 mm Hg. You do not have enough information in this question to know about the relationship between oxygen and hemoglobin (oxyhemoglobin curve). The things that alter the relationship between oxygen and hemoglobin include acid base balance, temperature, and levels of 2,3 DPG.

Which of these parameters is the best indicator of tissue oxygenation: A. SaO2. B. SvO2. C. DO2. D. PaCO2.

B. The best indicator of tissue oxygenation is SvO2 because it represents venous reserve. Venous reserve is the difference between oxygen delivery and oxygen consumption. When tissues are unable to use oxygen (such as in sepsis), SvO2 increases because less O2 is used, resulting in more O2 in venous blood. PaCO2 is the best indicator for the effectiveness of alveolar ventilation. SaO2 indicates the percentage of hemoglobin that is saturated with oxygen but does not indicate tissue utilization of O2. DO2 represents the delivery of oxygen to the tissues. Although DO2 is very important for tissue oxygenation, it only tells you what is delivered to the tissues and does not take into account what is utilized by the tissues.

What is true regarding the role of kidneys in regulating acid base balance: A. When compensating for alkalosis the urine will become more acidic. B. There is an inverse relationship between renal K+ secretion and renal H+ secretion. Therefore, alterations in acid base balance cause an alteration in K+ balance. C. In an acidosis the kidneys will decreases HCO3- reabsorption and decreases hydrogen ion secretion. D. They can fully compensate for a respiratory or metabolic disorder (not involving the kidneys) within hours.

B. The kidneys can compensate for respiratory disorders and for metabolic disorders not involving the kidneys. They responds within 48 hours, but complete compensation may take several days. The kidneys regulate excretion or retention of HCO3- and the excretion of H+ and non-volatile acids. • If pH is down (acidosis): Kidney retains HCO3- and excretes fixed acids. • If pH is up (alkalosis): Kidney decreases HCO3- reabsorption and decreases hydrogen ion secretion. There is an inverse relationship between renal K+ secretion and renal H+ secretion. Therefore, alterations in acid base balance cause an alteration in K+ balance. Normally the kidneys secrete about 70 mEq of H+ and reabsorb about 70 mEq of HCO3- daily. This process can increase greatly during acidosis, acidifying the urine to a pH as low as 4.0 to 5.0.

Your patient's blood gas report is: pH 7.35 PaCO2 49 mmHg PaO2 60 mmHg HCO3 29 mEq/L Oxygen saturation 90% This represents: A. Metabolic alkalosis with severe hypoxemia. B. Compensated respiratory acidosis with mild hypoxemia. C. Respiratory alkalosis with attempted metabolic compensation. D. Compensated metabolic acidosis with adequate oxygenation.

B. The pH of 7.35 is on the acidotic side of perfect normal (7.40) but is within the normal range of 7.35 - 7.45, indicating a compensated acidosis. (In uncompensated acidosis the pH would be outside the normal range: < 7.35) The PaCO2 is the respiratory parameter and the value of 49 mmHg is also on the acidotic side of normal PaCO2 (35-45 mmHg). Since the respiratory parameter matches the acidotic pH, the primary problem is respiratory acidosis. The HCO3 is the metabolic parameter and the value of 29 mmHg is on the alkalotic side (normal 22-27 mmHg) because it is compensating for the respiratory acidosis. To be a compensated metabolic acidosis the HCO3 would be low (on the acid side of normal) and the PaCO2 would also be low (on the alkalotic side of normal) in order to compensate for the metabolic acidosis. To be an alkalosis the pH would need to be greater than 7.45.

What is true regarding the diffusion of gases across the alveolar capillary membrane: A. Diffusion of oxygen occurs predominantly in the bronchi. B. Diffusion of oxygen occurs because the alveolar partial pressure of oxygen is higher than partial pressure of oxygen in mixed venous blood. C. The lower the pressure gradient, the more the diffusion of a gas. D. Oxygen is the only gas to diffuse across the alveolar capillary membrane.

B. The primary purpose of the pulmonary system is gas exchange (diffusion). Gas exchange occurs at the alveolar capillary unit. Diffusion does not occur in the conducting airways. Diffusion is the net movement of molecules from an area where a gas exerts a higher partial pressure to an area where the gas exerts a lower partial pressure. The diffusion of each gas across the alveolar capillary membrane occurs according to its individual partial pressure. Both oxygen and CO2 diffuse across the alveolar capillary membrane. However, CO2 is more diffusible than oxygen, and barriers to diffusion impact the diffusion of oxygen more than the diffusion of CO2. Therefore, in discussing diffusion, the focus is on the diffusion of oxygen across the alveolar capillary membrane.

You are caring for a patient with a diagnosis of acute respiratory distress syndrome (ARDS). The patient is on FIO2 of 0.8 with a PaO2 of 80 mmHg. What do you know about the severity of the patient's ARDS: A. This is moderate ARDS. B. This is severe ARDS. C. This does not meet criteria for ARDS. D. This is mild ARDS.

B. This patient has a PaO2/FIO2 ratio to 100. ARDS is classified based on the degree of hypoxemia: • Mild (PaO2/FIO2 Ratio > 200 mm Hg and ≤ 300 mm Hg) • Moderate (PaO2/FIO2 Ratio > 100 mm Hg ≤ 200 mm Hg) • Severe (PaO2/FIO2 ≤ 100 mm Hg)

What is true regarding alveolar cells: A. Type 1 alveolar cells are resistant to injury. B. Type 1 alveolar cells are responsible for keeping fluid out of alveoli. C. The primary role of type 2 alveolar cells is to engage in phagocytosis. D. Type 2 alveolar cells are the most abundant of the alveolar cells.

B. Type I alveolar cells are flat, squamous epithelial cells and comprise approximately 90% of the alveolar surface area. These cells are designed for gas exchange and are sensitive to injury. They help prevent fluid entry into the alveoli. Type II alveolar cells secrete key components for pulmonary surfactant synthesis and are also capable for generating into Type I cells in response to injury. In addition to Types I and II alveolar cells, there are alveolar macrophages that engage in the phagocytosis of foreign materials.

A patient is admitted with chronic obstructive pulmonary disease with a history of chronic hypoxemia and chronic anemia. The nurse recognizes the impact of the patient's history on the relationship between oxygen and hemoglobin in the following way: A. The patient has an decreased production of 2,3 DPG and a shift in the oxyhemoglobin curve to the right. B. The patient has an increased production of 2,3 DPG and a shift in the oxyhemoglobin curve to the left. C. The patient has an increased production of 2,3 DPG and a shift in the oxyhemoglobin curve to the right. D. The patient has an decreased production of 2,3 DPG and a shift in the oxyhemoglobin curve to the left.

C. 2,3 DPG (Diphosphoglycerate) is a substance in the erythrocyte which affects the affinity of hemoglobin for oxygen. It binds to hemoglobin and decreases the affinity of hemoglobin for oxygen. 2,3 DPG is produced by erythrocytes during their normal glycolysis. Levels of 2,3 DPG are increased in certain conditions including: chronic hypoxemia, anemia, and hyperthyroidism. Levels of 2,3 DPG are decreased in certain conditions such as: following massive transfusion of banked blood, hypophosphatemia, and hypothyroidism. A rise in 2,3 DPG levels will cause a shift in the oxyhemoglobin curve to the right and a decrease in 2,3 DPG levels will cause a shift in the oxyhemoglobin curve to the left. When the oxyhemoglobin curve shifts from normal there is a change in the relationship between oxygen and hemoglobin. A shift to the right refers to a decrease in affinity between oxygen and hemoglobin where the patient will have a lower than expected SpO2 for a given PaO2. A shift to the left refers to an increased affinity between oxygen and hemoglobin. Although this may seem like a benign issue at the lung level, it becomes a devastating issue at the tissue level because hemoglobin does not want to release oxygen for use at the tissue level.

A patient is admitted three weeks post coronary artery bypass surgery with bilateral pleural effusions. The nurse recognizes the following regarding the patient's pleural effusions: A. Fluid in the pleural space will increase airway resistance. B. Fluid in the pleural space will decrease airway resistance. C. Fluid in the pleural space will decrease lung compliance. D. Fluid in the pleural space will increase lung compliance.

C. Fluid in the pleural space is one physiological condition that will decrease the compliance of the lungs. Other factors that affect compliance of the lungs include: atelectasis, decreased surfactant production, and any restrictive disorder such as pulmonary fibrosis or interstitial lung disease. Obstructive disorders such as asthma, chronic bronchitis, emphysema, and obstructive sleep apnea affect the airways and therefore increase resistance. Secretions and foreign bodies in the airways will also increase resistance.

The following conditions will alter the affinity between oxygen and hemoglobin resulting a shift in the oxyhemoglobin curve to the left: A. Hyperthermia. B. Chronic anemia. C. Hypothermia. D. Metabolic acidosis.

C. Hypothermia results in an increased affinity between oxygen and hemoglobin and shifts the oxyhemoglobin curve to the left. Acidosis results in an decreased affinity between oxygen and hemoglobin and shifts the oxyhemoglobin curve to the right. Anemia results in an increase in 2-3 DPG, decreasing the affinity between oxygen and hemoglobin. This shifts the oxyhemoglobin curve to the right. Hyperthermia decreases the affinity between oxygen and hemoglobin and shifts the oxyhemoglobin to the right. This illustration shows an easy way to remember which factors shift the curve to the right: rise in 2-3-DPG, H+ concentration (acidosis), temperature (hyperthermia). Opposite factors shift the curve to the left.

When caring for the patient with COPD who is a CO2 retainer, it is important to remember that: A. The patient should never be given more that 2L of oxygen via nasal cannula. B. Delivering oxygen decreases the CO2 which is the patient's drive to breathe. C. Oxygen saturations greater than 90 - 92% should be avoided. D. It is safe to place the patient on 100% non-rebreather as long as you check the oxygen saturation every 4 hours.

C. In healthy people, CO2 levels control ventilation. A patient who is a chronic CO2 retainer develops a hypoxic drive to breathe based on an oxygen saturation somewhere between 90 - 92%. A patient who is a chronic CO2 retainer who is significantly hypoxemic can have as much oxygen as needed to achieve a SaO2 of 90-92%. Patients who are chronic CO2 retainers, who require high levels of oxygen therapy for significant hypoxemia, need to be assessed frequently to assure saturation levels do not rise to a level that knocks out the patient's hypoxic drive to breathe.

What is true regarding the cause of obstructive sleep apnea (OSA): A. The most cause in adults is related to a genetic varation in airway size that does not produce symptoms until adulthood. B. It occurs as a result of episodes of lower airway obstruction. C. The primary problem in obstructive sleep apnea is an anatomically small pharyngeal airway. D. The pharyngeal airway during does not fully open during sleep.

C. Obstructive sleep apnea (OSA) occurs as a result of episodes of upper airway obstruction from collapse of the pharyngeal airway during sleep. The primary problem in obstructive sleep apnea is an anatomically small pharyngeal airway. In adults this is most commonly due to obesity.

Which of the following therapies will not increase the diffusion of oxygen across the alveolar capillary membrane: A. Addition of continuous positive airway pressure (CPAP). B. Increased FIO2. C. Increased tidal volume. D. Increased positive end expiratory pressure (PEEP).

C. Oxygen therapy (increased FIO2), and positive end expiratory pressure (PEEP) or continuous positive airway pressure (CPAP), are used to promote the diffusion of oxygen across the membrane. An increase in FIO2 will increase the alveolar oxygen content and thus the gradient across the alveolar capillary membrane. Adding positive pressure will increase the driving pressure across the membrane. Tidal volume and respiratory rate are used to manipulate ventilation.

Which of the following is the best assessment parameter in evaluating the effectiveness of a patient's ventilation: A. PaO2. B. SaO2. C. PaCO2. D. SVO2.

C. PaCO2 is the best assessment parameter in evaluating the effectiveness of a patient's ventilation. Hypoventilation is the only physiological explanation for a rise in the patient's PaCO2. SVO2 is the best global indicator of the balance between oxygen supply and demand but it is not the most specific and direct assessment of the patient's ventilation. PaO2 and SaO2 are parameters used to assess the patient's oxygenation status. Although both will eventually fall when a patient fails to adequately ventilate they are not the most specific and direct assessment of the patient's ventilation.

12 hours after surgery for a compound femur fracture the patient complains of chest pain and severe SOB. RR is 32. The patient has petechiae on the chest and in the axillary area. ABGs on 4L NC: pH 7.5, PaCO2 27 mmHg, PaO2 66 mmHg. The most likely explanation is: A. Early onset acute respiratory distress syndrome (ARDS). B. Hospital acquired pneumonia. C. Fat embolus. D. Tension pneumothorax.

C. Respiratory alkalosis is a common finding in pulmonary embolus. Orthopedic surgery or fractures involving long bones are risk factors for the complication of fat embolus. Transient petechiae is a specific assessment finding in fat embolus. The most likely explanation for these symptoms point to fat embolus because of the patient's recent surgery for a compound femur fracture.

When a patient is placed on supplemental oxygen the nurse knows the following to be true: A. The driving pressure of oxygen across the alveolar capillary membrane is decreased. B. Supplemental oxygenation is beneficial in patients who are not hypoxemic. C. The FIO2 is increased and the partial pressure of oxygen within the alveoli is increased. D. The FIO2 is increased and the partial pressure of oxygen within the alveoli is decreased.

C. Room air breathing is at an FIO2 (fraction of inspired oxygen) of .21. Adding supplemental oxygen increases the FIO2. Breathing an FIO2 of .21 results in an alveolar partial pressure of oxygen of approximately 104 mm Hg. As the FIO2 increases the partial pressure of oxygen in the alveoli increases, and this increases the driving pressure of oxygen across the alveolar capillary membrane. Remember, gases will diffuse across the alveolar capillary membrane based on a concentration gradient. Higher FIO2 is used to increase the partial pressure of alveolar oxygen and thus increase the gradient. This is why oxygen therapy can be used to counteract barriers to the diffusion of oxygen across the alveolar capillary membrane. Oxygenating patients who are not hypoxemic can be dangerous and result in hyper oxygenation with associated poor outcomes.

When screening for obstructive sleep apnea (OSA), the following patient complaint is the most specific to OSA: A. Paroxysmal nocturnal dyspnea. B. Insomnia. C. Excessive day time sleepiness. D. Shortness of breath with exertion.

C. Screening for OSA should occur in all cardiovascular patients. High risk features associated with the diagnosis of OSA include: loud snoring, witnessed apneas, excessive daytime sleepiness, morning headaches, hypertension, BMI > 35 kg/m2, neck circumference > 40 cm, and age > 50 years. Insomnia is defined as inability to fall asleep or to stay asleep as long as desired. The inability to fall asleep is not specifically associated with OSA. Paroxysmal nocturnal dyspnea is more associated with left sided volume overload from heart failure than with OSA. Shortness of breath with exertion is a symptom that can be associated with many cardiac and pulmonary disorders.

You have a patient admitted with pneumonia who is now on a ventilator with acute respiratory distress syndrome (ARDS). The ventilator settings are TV 600 ml, rate 14, and 12 cm of PEEP. The FIO2 is at 50% and the PaO2 on the last blood gas was 94 mmHg. PaCO2 was 42 mmHg. Based on the PaO2 / FIO2 ratio what do you conclude: A. The patient needs more tidal volume to improve oxygenation. B. The patient is most likely ready for extubation. C. The patient is still demonstrating active ARDS. D. PEEP should be discontinued.

C. The PaO2 / FIO2 ratio is calculated by dividing the PaO2 of 94 by the FIO2 of .5 (94/.5). When calculating the PaO2/FIO2 ratio the decimal is always used for the FIO2. In this question the PaO2 /FIO2 ratio is 188. A PaO2/FIO2 ratio of < 200 is one of the criteria required for a diagnosis of ARDs. This patient is still demonstrating active ARDS and is not ready for extubation. The 12 cm of PEEP delivered by the ventilator is helping support oxygenation by increasing the driving pressure of oxygen across the alveolar capillary membrane. Tidal volume impacts ventilation but does not affect oxygenation, therefore changing the tidal volume will not help.

A patient with this blood gas, most likely has which of the following diagnoses: PH 7.37 PCO2 44 mmHg PaO2 140 mmHg HCO3 25 mEq/L FIO2 100% A. Pulmonary embolus. B. Left lower lobe pneumonia. C. Acute respiratory distress syndrome (ARDS). D. Acute exacerbation of chronic obstructive pulmonary disease (COPD) with ventilatory failure.

C. This blood gas is most consistent with a patient who has ARDS because the PaO2 / FIO2 ratio is only 140. A PaO2 / FIO2 ratio of < 200 is one of the diagnostic criteria for ARDS because it indicates a significant intrapulmonary shunt. A patient with pneumonia isolated to the left lower lobe would most likely not have such a severe intrapulmonary shunt. Although a pulmonary embolus can cause hypoxemia and intrapulmonary shunting, a pulmonary embolus usually presents with hypocapnia producing a respiratory alkalosis. This blood gas does not indicate ventilatory failure because the PaCO2 is normal.

In caring for a patient with an elevated PaCO2 the nurse knows the following methods can be used to treat alveolar hypoventilation: A. Increasing FIO2 and increasing respiratory rate. B. Increasing FIO2 and increasing PEEP. C. Increasing respiratory rate and increasing tidal volume. D. Increasing tidal volume and increasing PEEP.

C. Ventilation is respiratory rate X tidal volume. To correct inadequate ventilation one must improve respiratory rate, tidal volume or both. Strategies might include reversing sedation, using an ambu bag, non-invasive positive pressure ventilation, or intubating and mechanically ventilating a patient. Increasing FIO2 and PEEP are strategies that can be used to improve the diffusion of oxygen across the alveolar capillary membrane. Increasing FIO2 and PEEP are not effective strategies to improve alveolar hypoventilation.

Pulmonary arterial hypertension eventually leads to signs of: A. Decreased cerebral perfusion. B. Left ventricular failure. D. Coronary insufficiency. C. Right ventricular failure.

C.Right heart failure can occur due to chronically elevated PA pressures that increase the work load of the right ventricle. Signs of right heart failure include elevated neck veins, peripheral edema, hepatomegaly, ascites, reduced exercise capacity, and sometimes tricuspid regurgitation. Decreased cerebral perfusion and signs of coronary insufficiency could eventually develop if right ventricular failure is severe enough to significantly limit LV filling, therefore decreasing the ability of the LV to perfuse the rest of the body. Left ventricular failure is usually caused by decreased LV function secondary to MI, aortic or mitral valve disease, chronic systemic hypertension, or cardiomyopathy. PA hypertension affects right ventricular function, not left ventricular function.

One of the goals in treating acute respiratory distress syndrome (ARDS) is to reduce oxygen consumption. This can be achieved by all of the following EXCEPT: A. Alternating nursing interventions with periods of rest. B. Prevention of hyperthermia. C. Suctioning routinely every two hours. D. Adequate pharmacological sedation.

C.Routine suctioning every two hours is not recommended. Suctioning a patient can elicit a cough as well as the gag reflex. Any activity that causes patient discomfort can cause an increase in oxygen consumption. Suctioning must be performed when clinically indicated in acute respiratory distress syndrome (ARDS) to prevent secretions from increasing airway resistance. However, suctioning is not a strategy used to decrease oxygen consumption. All of the other three interventions will decrease oxygen consumption.

Which of these patients has acute ventilatory failure and would benefit from mechanical ventilation: A. pH = 7.50, PaCO2 = 30, HCO3 = 24, PaO2 = 75. B. pH = 7.32, PaCO2 = 48, HCO3 = 20, PaO2 = 80. C. pH = 7.35, PaCO2 = 56, HCO3 = 30, PaO2 =65. D. pH = 7.20, PaCO2 = 58, HCO3 = 24, PaO2 = 52.

D. Acute ventilatory failure presents as hypercapnia (high PaCO2) and acidosis (low pH). The PaCO2 is the ventilatory parameter; hypoventilation causes the PaCO2 to rise because the alveoli are not able to remove CO2. This hypercapnia must be accompanied by acidosis to be an indication for mechanical ventilation. Hypercapnia that is due to chronic lung disease (like COPD) is not accompanied by acidosis because of an increased HCO3 due to renal compensation (this example: pH = 7.35, PaCO2 = 56, HCO3 = 30, PaO2 =65). In this example: pH = 7.32, PaCO2 = 48, HCO3 = 20, PaO2 = 80, the pH is slightly on the acidotic side and the PaCO2 is a little elevated but this mild hypoventilation might respond to deep breathing and incentive spirometry. Good pulmonary toilet, pain control to allow for deep inspiration, or other interventions to reverse the cause of hypoventilation could fix this situation. In this example: pH = 7.50, PaCO2 = 30, HCO3 = 24, PaO2 = 75, the pH is alkalotic and the PaCO2 is a little low, indicating respiratory alkalosis due to hyperventilation. Common causes of hyperventilation include hypoxemia (as indicated by the PaO2 of 75) and compensation for metabolic acidosis. The patient breathes deeper and faster in an effort to oxygenate better or in an effort to produce respiratory alkalosis as a compensation for metabolic acidosis.

A patient with a history of COPD presents with the following blood gases: pH 7.26 PaCO2 68 mmHg PaO2 56 mmHg HCO3 30 mEq/L These represent which of the following: A. Acute metabolic acidosis. B. COPD with compensated respiratory acidosis. C. Acute respiratory alkalosis. D. Acute ventilatory failure with hypoxemia.

D. Although some patients with COPD can be chronic CO2 retainers, these patients should compensate and have a normal pH. When a CO2 retainer becomes acidotic, this indicates acute ventilatory failure. An elevated PaCO2 is an indication of ventilatory failure. This is not an acute respiratory alkalosis because the pH is low and it is not a metabolic acidosis because the HCO3 is high.

When caring for a critically ill patient, the nurse understands the following regarding the physiological implications of pulmonary vascular resistance (PVR) and pulmonary arterial pressure (PAP): A. Similar to the left ventricle, the right ventricle is capable of pumping against very high pulmonary pressures for an extended period of time without failing. B. A patient on positive pressure mechanical ventilation with PEEP will receive the benefit of lowered pulmonary vascular resistance. C. The advantage of an inhaled pulmonary vasodilator is that it will only reach capillaries serving ventilated alveoli. D. Hypercapnia and alveolar hypoxia will result in an decreased PVR.

D. An inhaled pulmonary vasodilator has the advantage of reaching only the pulmonary capillaries that are surrounding the well-ventilated alveoli. The right ventricle will fail much sooner than the left ventricle in response to working against higher pressures. The right ventricle is a thin walled ventricle used to pumping against resistance 1/10 that of systemic vascular resistance. Positive pressure ventilation and PEEP result in compression of alveolar and extra alveolar vessels and this results in an increase in pulmonary vascular resistance. Hypercapnia and alveolar hypoxia result in an increase in PVR. Pulmonary vessels vasoconstrict in response to hypoxia to divert blood away from poorly ventilated alveoli.

Which of the following pathological conditions does not directly impact the diffusion of oxygen: A. Smoke inhalation. B. Pulmonary resection. C. Pulmonary edema. D. Asthma.

D. Asthma is an obstructive disorder that impacts airways resistance and ventilation. The following factors adversely impact how well oxygen is able to diffuse from the alveoli through the alveolar capillary membrane and into the blood. Increased thickness of alveolar capillary membrane: • Interstitial or alveolar edema. • Interstitial or alveolar fibrosis. Decrease in available alveolar / capillary surface area: • Pulmonary resection. • Emphysema. • Tumors. • Any ventilation to perfusion mismatching. Decreased driving pressure of oxygen (decreased partial pressure of oxygen in the alveoli): • Low inspired fraction of O2 (smoke inhalation). • Low barometric pressure (high altitudes).

What is true regarding carbon monoxide: A. It has a low affinity for hemoglobin. B. It's presence promotes the release of oxygen from hemoglobin at the tissue level. C. It has a definitive odor that provides a warning of its presence. D. Low levels can result in dangerously high levels of carboxyhemoglobin.

D. Carbon monoxide has a high affinity for hemoglobin and limits the ability of oxygen to bind with hemoglobin. It also shifts the oxyhemoglobin curve (discussed below) to the left and prevents the unloading of oxygen at the tissues. Carbon monoxide is very dangerous because low levels of carbon monoxide can result in dangerously high levels of carboxyhemoglobin. Carbon monoxide is colorless, odorless, and tasteless. Tobacco smoking and / or living in urban areas can cause small amounts of carboxyhemoglobin to be present in the blood.

The following nursing interventions can be used to increase compliance of the lungs or chest wall: A. Proper patient positioning. B. Incentive spirometry. C. Deep breathing exercises. D. All of the above.

D. Deep breathing exercises and incentive spirometry can help improve compliance of the lungs; proper patient positioning (such as in a full upright position) can help improve compliance of the chest wall.

You are caring for a patient who is intubated and on mechanical ventilation after being admitted for sepsis. The ventilator settings include: Tidal volume of 600 ml, rate of 14, FIO2 of 0.8, and positive end expiratory pressure (PEEP) of 12 cm H2O. The last blood gas results are: pH 7.36, PaCO2 47 mmHg, PaO2 110 mmHg, and HCO3 20. What is true regarding the patient's PaO2 / FIO2 ratio: A. The ratio is 1.375 and is consistent the adequate diffusion of oxygen. B. The ratio is 0.007 and this is diagnostic of ARDS regardless of the length of the time she has been intubated. C. The ratio is 0.72 and this represents an appropriate PaO2 for her FIO2. D. The ratio is 137.5 and is consistent with acute lung injury or the possible development of acute respiratory distress syndrome (ARDS).

D. The PaO2/FIO2 ratio is determined by dividing the PaO2 by the FIO2 (decimal). • Normal PAO2/FIO2 Ratio > 350. • Acute lung injury (ALI) < 300. • Acute respiratory distress syndrome (ARDS) < 200. The PaO2/FIO2 ratio is only one criteria for the diagnosis of ARDS.

In caring for a patient with acute lung injury, the nurse knows the following to be true regarding hypoxic pulmonary vasoconstriction: A. This response is limited due to a smaller amount of vascular smooth muscle in the pulmonary system compared to the peripheral arterial system. B. Pulmonary artery vasoconstriction places strain on the right heart. C. Some pulmonary arteries vasoconstrict to divert blood away from poorly ventilated alveoli. D. All of the above.

D. During hypoxic pulmonary vasoconstriction, blood is diverted away from poorly ventilated alveoli. There is also a vasoconstrictive response in response to more global hypoxia. The vasoconstrictive response increases pulmonary artery pressure and recruits (opens up) pulmonary capillaries to improve ventilation and perfusion matching. This compensatory response has limitations because of the small amount of vascular smooth muscle in the pulmonary arteries, compared to the amount of vascular smooth muscle in the systemic arteriole system. Hypoxic vasoconstriction greatly increases the workload of the right ventricle. Additionally, the increased pulmonary artery pressure may lead to pulmonary edema.

A patient presents to the emergency department in status asthmaticus. The nurse recognizes that the following is a late sign and anticipates that intubation will most likely be necessary: A. pH > 7.45. B. Tachypnea. C. Expiratory wheezing. D. Elevated PaCO2.

D. Expiratory wheezing, tachypnea, and respiratory alkalosis are all signs that occur early in status asthmaticus. When a patient's PaCO2 rises this is a late sign of ineffective ventilation and the patient will most likely need to be intubated until the cause of the exacerbation can be eliminated or treated.

All of the following are considered conducting airways EXCEPT for: A. Bronchi. B. Trachea. C. Pharynx. D. Alveolar ducts.

D. No gas exchange occurs in the conducting airways. The nose, pharynx, larynx, trachea, and bronchi are all considered conducting airways. The gas exchange airways begin in the respiratory bronchioles and also include the alveolar ducts, and the alveoli.

All of the following can cause an obstruction to airflow and increase airway resistance EXCEPT: A. Sleep apnea. B. Bronchitis. C. Asthma. D. Atelectasis.

D. Obstructive disease process such as emphysema, chronic bronchitis and asthma all increase airway resistance as a component of the disease process. Sleep apnea and foreign objects can also cause an obstruction to airflow. Atelectasis results in decreased lung compliance rather than increased airway resistance.

The most common condition predisposing your patient to acute respiratory distress syndrome (ARDS) is: A. Acute bronchitis. B. Intubation for an orthopedic surgical procedure. C. Chronic obstructive pulmonary disease (COPD). D. Pneumonia.

D. Pneumonia is the most common cause of acute lung injury (ALI) and acute respiratory distress syndrome (ARDs). ARDS develops within 24 to 72 hours of the initial predisposing insult (i.e. pneumonia) causing ALI.

A (polysomnography) sleep study is ordered in a patient identified as having high risk features for obstructive sleep apnea. What is true regarding a sleep study findings and the diagnosis of obstructive sleep apnea: A. A diagnosis of OSA is made when a person has > 5 apneas or hypoapneas per hour of sleep accompanied by excessive daytime sleepiness. B. Apnea is defined as a > 10 second pause in respiration in spite of ongoing ventilator effort. C. Hypoapnea is a decrease in respiration associated with a drop in oxygen saturation or arousal from sleep. D. All of the above.

D. Polysomnography performed in a sleep lab is typically used to make the diagnosis of OSA or other forms of sleep disordered breathing. As implied in the name, polysomnography, monitors multiple physiological variables. Home based sleep studies are appropriate in selected patients and use less comprehensive physiological monitoring. Apnea is defined as a > 10 second pause in respiration in spite of ongoing ventilator effort. Hypoapnea is a decrease in respiration associated with a drop in oxygen saturation or arousal from sleep. A diagnosis of OSA is made when a person has > 5 apneas or hypoapneas per hour of sleep accompanied by excessive daytime sleepiness

What factors can interfere with accuracy of SpO2 monitoring: A. SpO2 below 70%. B. Abnormal hemoglobin, such as carboxyhemoglobin or methemoglobin. C. Hemoglobin < 5 g/dL or hematocrit <15%. D. All of the above.

D. Several factors can interfere with the accuracy of pulse oximetry. • Hemoglobin < 5 g/dL or hematocrit <15%. • Abnormal hemoglobin, such as carboxyhemoglobin or methemoglobin. These forms of hemoglobin are not distinguishable from oxyhemoglobin. • SpO2 below 70%. • State of low blood flow, such as with hypotension or vasoconstriction. • IV dyes, fingernail polish, and some skin pigmentations.

When assessing the PaO2 on an arterial blood gas, what does the nurse know to be true: A. The normal value of 80 to 100 mmHg is true for patients on .21 FIO2. B. An increase in alveolar oxygen content should result in an increase in PaO2. C. An increase in FIO2 should result in an increase in PaO2. D. All of the above.

D. The PaO2 on blood gas cannot accurately be assessed without the considering the FIO2. This is because an increase in FIO2 will result in an increased partial pressure of oxygen in the alveoli. The more oxygen content in the alveoli the more oxygen that should be diffused across the alveolar capillary membrane and thus resulting in a higher PaO2. The majority of the oxygen in the alveoli should diffuse across the alveolar capillary membrane and end up in the arterial blood.

In assessing acid base balance, what is true regarding the anion gap: A. The anion gap is the sum of potassium, sodium, and calcium divided by the blood pH. B. If blood pH is low the anion gap will always be greater than normal. C. The anion gap is used to determine the cause of metabolic alkalosis. D. The most common etiology of normal anion gap acidosis is diarrhea.

D. The anion gap is used to help determine the cause of the patient's metabolic acidosis. The anion gap is determined by summing the plasma chloride and bicarbonate levels, then subtracting from the sum of the patient's sodium and potassium level. • Anion gap = [Na+ + K+] - [Cl- + HCO3-]. Note: The serum CO2 can be used as a surrogate for HCO3-. • Alternative formula for anion gap: Because K+ is a small number it will not significantly affect the calculated anion gap. For this reason many people in daily clinical practice use the following formula: Na+ - [Cl- + HCO3-]. • A normal anion gap is 12 + or - 4 mEq/L. An increased anion gap typically indicates an increased concentration of anions other than Cl- and HCO3-. Causes of increased concentrations of these other anions include lactic acidosis, ketoacidosis, ingestion of anions such as salicylate, or renal retention of anions such as sulfate, phosphate, and urate. • The most common etiology of normal anion gap acidosis is diarrhea. Renal tubular acidosis is the second most common etiology. Both diarrhea and renal tubular acidosis result in a loss of bicarbonate ions. To compensate for a lowered bicarbonate concentration there is an increase in plasma chloride. For this reason normal ion gap acidosis is often referred to as hyperchloremic acidosis.

Which of the following statements is true regarding pulmonary perfusion: A. Pulmonary perfusion occurs prior to ventilation. B. Pulmonary capillaries are slightly larger than the average erythrocyte. C. There are less pulmonary capillaries than there are pulmonary alveoli. D. The dependent areas of the lungs receive the best perfusion.

D. The most dependent areas of the lung receive the best perfusion. Dependent areas of the lung represent Zone 3 of perfusion. Zone 3 is always perfused. Ventilation and perfusion occur simultaneously. Ventilation and perfusion are prerequisites for diffusion of oxygen across the alveolar capillary membrane. There are many more capillaries than alveoli. This allows each alveolus to be engulfed in pulmonary capillaries. Pulmonary capillaries are actually slightly smaller than the average red blood cell, requiring the red blood cell to change shape each time it passes through the pulmonary capillaries.

Which of the following statements is NOT true regarding PaCO2: A. PaCO2 is the best indicator of the effectiveness of alveolar ventilation. B. Alveolar hypoventilation will result in an increase in PaCO2. C. The brain adjusts alveolar ventilation to maintain PaCO2 close to 40 mmHg. D. There are multiple physiological explanations for an elevated PaCO2.

D. The only physiological explanation for an elevated PaCO2 is alveolar hypoventilation. Chemoreceptors near the medulla sense pH and adjust ventilation accordingly to keep the PaCO2 close to 40 mmHg. The PaCO2 is the best indicator of effective alveolar ventilation. Alveolar hypoventilation will result in an increase in PaCO2 and alveolar hyperventilation will result in a decrease in PaCO2.

A shift of the oxyhemoglobin curve to the left means: A. Hemoglobin releases oxygen more easily. B. Tissues have improved oxygenation due to increased SaO2. C. The SaO2 for a PaO2 of 60 mmHg is expected to be < 90%. D. Hemoglobin binds with oxygen more tightly.

D. The oxyhemoglobin curve shows the relationship between PaO2 (partial pressure of O2 in plasma) and SaO2 (percentage of O2 combined with hemoglobin). On a normal curve when the PaO2 is 60 mmHg, SaO2 is 90%. This normal curve occurs at 37 degrees C, pH 7.4, and PCO2 of 40 mmHg. A shift to the left causes hemoglobin to have a higher affinity for O2 so they bind more tightly together. It is easier for hemoglobin to pick up O2 in the lungs but more difficult for O2 to dissociate from hemoglobin at the tissue level. Therefore, tissues are less well oxygenated with a shift to the left. With a shift to the left, the SaO2 for a PaO2 of 60 mmHg is expected to be > 90%. This illustration shows the oxyhemoglobin dissociation curve and factors that shift it to the left and to the right.

A patient with a history of COPD is admitted to the critical care unit following the onset of SOB, fever, and flu-like symptoms at home. He is in acute respiratory distress on admission with the following VS: BP 160/80 mmHg, HR 120 in atrial fibrillation, RR 26 breaths/minute. His ABGs on room air are: pH = 7.28 pCO2 = 64 mmHg HCO3 = 32 mEq/L PaO2 = 54 mmHg His ABGs indicate which of the following: A. Respiratory acidosis with adequate oxygenation. B. Respiratory alkalosis with hypoxemia. C. Metabolic acidosis with hypoxemia. D. Respiratory acidosis with hypoxemia.

D. The pH of 7.28 is acidotic. CO2 is an acid, and the pCO2 (respiratory parameter) of 64 mmHg is also acidotic; therefore this is a respiratory acidosis. A normal PaO2 on room air is 80-100 mmHg. This PaO2 is 54 mmHg, indicating hypoxemia. HCO3 (bicarbonate) is the metabolic parameter, and bicarbonate is a base. Normal HCO3 is 22-26 mEq/L, so this HCO3 of 32 indicates that the kidneys are retaining HCO3 to compensate for the respiratory acidosis. In metabolic acidosis, the HCO3 would be low. Normal pH is 7.35 - 7.45. In alkalosis, the pH would be higher than 7.45. In acidosis, the pH is lower than 7.35.

A patient in acute respiratory distress presents with the following blood gases on 4 L nasal cannula. What do you anticipate being the initial treatment strategy as a result of the blood gases: pH 7.40 PaCO2 40 mmHg PaO2 60 mmHg O2 Saturation 90% A. Decreasing oxygen to avoid oxygen toxicity. B. Short acting beta agonist. C. Intubation. D. Increase in oxygen therapy.

D. The patient's blood gas represents a normal PaCO2 and therefore normal alveolar ventilation. Intubation may be an initial treatment strategy in a patient with acute ventilatory failure as indicated by an elevated PaCO2. The patient's blood gas represents mild hypoxemia most likely due to a barrier to diffusion of oxygen. Increasing oxygen therapy will increase the alveolar oxygen content and help increase the diffusion of oxygen across the alveolar capillary membrane. Oxygen diffuses based on a pressure gradient. When alveolar FIO2 is increased the gradient is increased. Oxygen toxicity is a potential complication of oxygen therapy. To avoid the risk it is ideal to use 40% or less FIO2 for long term oxygen therapy. However, oxygen therapy should never be withheld in a patient who is hypoxemic due to the concern of oxygen toxicity. A short acting beta agonist can be used as a bronchodilator in a patient with increased airway resistance. Increased resistance will impact ventilation. There is no evidence of ventilation problems on this blood gas.

You are caring for an obese male patient with no previously diagnosed medical problems who is admitted for hypertensive urgency directly from the office of his primary care physician during a routine visit. His blood pressure is now controlled after treatment with an IV antihypertensive agent and the start of two oral agents. All other assessment findings have been normal during the day and afternoon shifts. During the night you observe that he has intermittent episodes of hypoxemia based on his SpO2 readings. Based on your patient's risk factors and your observation, you recognize this patient most likely has the following condition: A. Resistant hypertension. B. Drug toxicity. C. Early sepsis. D. Obstructive sleep apnea.

D. The primary problem in obstructive sleep apnea is an anatomically small pharyngeal airway. In adults this is most commonly due to obesity. OSA increases the risk for hypertension, CAD, atrial and ventricular arrhythmias, and stroke. Screening for OSA should occur in all cardiovascular patients. High risk features associated with the diagnosis of OSA include: loud snoring, witnessed apnea, excessive daytime sleepiness, morning headaches, hypertension, BMI > 35 kg/m2, neck circumference > 40 cm, and age > 50 years. Overnight pulse oximetry can be used as a screening tool in patients who are hospitalized. Nurses can identify patients at risk and notify providers. This can lead to appropriate diagnosis, treatment, and reduction of risk. The patient's hypertension is not considered resistant because the blood pressure is controlled on two oral agents. There are no specific assessment findings related to sepsis or drug toxicity.

When using incentive spirometry the nurse knows that this therapy most directly supports ventilation through which mechanism: A. Activating the respiratory center in the brain to stimulate ventilation. B. Clearing secretions and therefore improving airway resistance. C. Increasing pulmonary perfusion to already well ventilated alveoli. D. Preventing atelectasis and therefore supporting lung compliance.

D. There are two factors that directly impact the work of breathing and thus ventilation. These two factors are compliance (of the lung and chest wall) and airway resistance. Incentive spirometry most directly works to support ventilation by preventing atelectasis and maintaining normal lung compliance. Atelectasis will decrease lung compliance. A cough in the presence of secretions will clear the airway and improve airway resistance. The pons and medulla comprise the respiratory centers in the brain and control respiration through the autonomic nervous system. Perfusion involves blood flow from the right ventricle through the pulmonary arteriole system. Incentive spirometry does not directly impact pulmonary perfusion.

During the admission assessment your patient (admitted for atrial fibrillation) tells you he no longer wears his CPAP (continuous positive airway pressure) mask because he has not been having any problems sleeping at night. Your most appropriate response in providing information to your patient is: A. I think this is something you need to discuss with the doctor who ordered your CPAP. We will need to focus on the atrial fibrillation this admission since that is why you came to the hospital. You can ask your primary care physician at your next visit to discontinue your CPAP since you no longer need it. B. I am glad that you are sleeping well and no longer need the CPAP. Please make sure you use it again if you start to have a hard time falling asleep at night. C. I will update your electronic medical record to state that you refuse treatment for your sleep apnea. D. I would like us to talk more about the benefits of your CPAP mask. Your sleep apnea has many health risks. The purpose of the CPAP mask is to reduce those risks. Although you feel you are sleeping well, your untreated sleep apnea may be placing you at risk for several health disorders. I am concerned that your sleep apnea may also be contributing to your atrial fibrillation.

D. This statement demonstrates an understanding of two important points: 1) The patient may not have a clear understanding of the adverse implications of untreated sleep apnea, and 2) The patient's untreated sleep apnea may be a contributing factor to his atrial fibrillation. Many patients think of obstructive sleep apnea (OSA) only as a nuisance disorder that results in snoring and poor sleep. Instructing patients on the physiological implications of OSA and the associated adverse consequences can assist in gaining buy-in to treatment. It is important to note that the patient demonstrates a misunderstanding regarding his diagnosis and treatment rather than a refusal of the treatment. Additionally, the nurse needs to take responsibility for patient education and counseling regarding the patient's health issues at every opportunity.

Which of the following treatments will not improve the ventilatory status of your patient: A. Using BiPAP in a patient with increased work of breathing. B. Reversing sedation in an over sedated patient. C. Increasing the respiratory rate on the ventilator in a patient who is hpercapnic. D. Increasing the FIO2 in a patient who is hypoxemic.

D. Treatment for inadequate ventilation includes improving rate or tidal volume by: • Reversing sedation or other reversible causes if applicable. • Supporting the patient with noninvasive positive pressure ventilation. • Ventilation with ambu bag. • Intubation and mechanical ventilation with adjustments as necessary in rate or tidal volume. Increasing FIO2 does not improve ventilation.

What is true regarding the pleura: A. Intrapleural pressure is less than the pressure inside the lungs. B. Abnormal fluid accumulation (beyond 15 to 25 ml) in the pleural space is called pleural effusion. C. There are both visceral and parietal pleura. D. All of the above.

D. • Parietal pleura lines the chest wall and contains many nerve fibers. • Visceral pleura lies over the lung parenchyma and does not contain nerve fibers. • The intrapleural space is the fluid-filled space between the visceral and parietal pleural. There small amount of serous fluid in the intrapleural space allows the pleurae to slide over each other during inspiration and expiration. • Abnormal fluid accumulation (beyond 15 to 25 ml) in the pleural space is called pleural effusion. • Intrapleural pressure is less than the pressure in the lungs, and this negative pressure keeps the lungs inflated (loss in negative pressure results in pneumothorax). • Normal negative intrathoracic pressure refers to the pressure of -3 to -5 cm H2O (below atmospheric pressure) in the intrapleural space.

The progress note written on your patient today indicates she has a large A-a gradient. You know this means: A. There is dysfunction at the site of the lung. B. A significant amount of alveolar oxygen content is not diffusing into the arterial blood. C. Although the patient is receiving increased FIO2, it is not resulting in an increase PaO2. D. All of the above.

D. • The A-a gradient is the alveolar (A) to arterial (a) oxygen pressure difference. The difference between alveolar (A) and arterial (a) oxygen should be small. This is because the majority of the oxygen within the alveoli should diffuse across the alveolar capillary membrane and enter the blood. • Normal A-a Gradient = 5-15 mmHg (normal PAO2 = 100 mmHg and normal PaO2 = 80 to 100 mmHg). The A-a gradient provides an index of gas transfer (diffusion). A large A-a gradient (a significant amount of alveolar oxygen not diffusing into the blood) generally indicates that the lung is the site of dysfunction. Causes of a large A-a gradient include: • Simple diffusion impairment, such as in pulmonary edema where interstitial fluid creates a barrier to diffusion. • Diffusion impairment caused by significant ventilation and perfusion mismatching, i.e. intrapulmonary shunt.

Which clinical parameter differentiates cardiac pulmonary edema from non-cardiac pulmonary edema: A. Right atrial pressure. B. Pulmonary artery systolic pressure. C. Chest x-ray findings. D. Pulmonary artery occlusive pressure (PAOP) or pulmonary capillary wedge pressure (PCWP).

D.Pulmonary edema is the presence of extravascular accumulation of fluid in the lungs. Pulmonary edema can be classified as cardiogenic or non-cardiogenic. Cardiogenic pulmonary edema is accompanied by an elevated pulmonary artery occlusive pressure (PAOP). Non cardiogenic pulmonary edema is diagnosed when pulmonary edema exists in the presence of a normal PAOP. Non cardiogenic pulmonary edema is seen with acute lung injury and acute respiratory distress syndrome.

A shift of the oxyhemoglobin dissociation curve to the left can be caused by all of the following EXCEPT: A. Decreased 2,3-DPG. B. Alkalemia. C. Low PCO2. D. Hypothermia. E. Hypokalemia.

E. Hypokalemia does not directly affect the oxyhemoglobin dissociation curve. The following will shift the oxyhemoglobin curve to the left: hypothermia, alkalosis, a decrease in 2-3 DPG. This illustration shows the oxyhemoglobin dissociation curve and factors that shift it to the left and to the right.

You are caring for a patient who has high risk features of obstructive sleep apnea (OSA). The patient does not want to have a sleep study because he states he sleeps fine. When counseling him about the potential impact of OSA on his heatlh, if indeed he does have it, you might include the following information: A. Sleep apnea can cause insulin resistance. B. Sleep apnea can cause high levels of blood pressure during the night. C. Sleep apnea can alter your fluid balance. D. Sleep apnea can cause Intermittent drops in your oxygen saturation and can cause you to retain CO2. E. All of the above.

E. OSA has multiple physiological implications that account for these adverse outcomes. Examples of the major physiological consequences of OSA include: • Intermittent hypoxemia and CO2 retention with oxygen saturation dropping to as low as 60% or less. • Decreased quality sleep time due to post apnea arousals. • Blood pressure elevations (as high as 240/130 mmHg) due to chemoreceptor induced sympathetic nervous system stimulation (from CO2 retention) resulting in vasoconstriction. • Altered fluid balance due to compensatory renin-angiotensin-aldosterone system involvement. • Increased pro-inflammatory and pro-thrombotic mediators released secondary to hypoxemia. • Insulin resistance due to increased circulating catecholamines. • Endothelial dysfunction due to multiple potential factors including increased pro-inflammatory mediators, sympathetic nervous system stimulation, and increased oxidative stress. • Increased afterload and impaired diastolic function due to intrathoracic pressure changes.

Which of the following is true regarding obstructive sleep apnea: A. It is caused by collapse of the pharyngeal airway. B. It is treated with continuous positive airway pressure (CPAP). C. It is a > 10 second pause in respiration associated with ongoing ventilatory effort. D. It results in physiological consequences including endothelial and ventricular dysfunction. E. All of the above.

E. Obstructive sleep apnea (OSA) occurs as a result of episodes of upper airway obstruction from collapse of the pharyngeal airway during sleep. Apnea is defined as a > 10 second pause in respiration in spite of ongoing ventilatory effort. OSA is treated with continuous positive airway pressure (CPAP). The major barrier is the patient's ability to tolerate the therapy. OSA has multiple physiological implications that account for these adverse outcomes. Examples of the major physiological consequences of OSA include: • Intermittent hypoxemia and CO2 retention with oxygen saturation dropping to as low as 60% or less. • Decreased quality sleep time due to post apnea arousals. • Blood pressure elevations (as high as 240/130 mmHg) due to chemoreceptor induced sympathetic nervous system stimulation (from CO2 retention) resulting in vasoconstriction. • Altered fluid balance due to compensatory renin-angiotensin-aldosterone system involvement. • Increased pro-inflammatory and pro-thrombotic mediators released secondary to hypoxemia. • Insulin resistance due to increased circulating catecholamines. • Endothelial dysfunction due to multiple potential factors including increased pro-inflammatory mediators, sympathetic nervous system stimulation, and increased oxidative stress. • Increased afterload and impaired diastolic function due to intrathoracic pressure changes.

What do you know is true regarding pulmonary vascular resistance: A. An increase in cardiac output during exercise will decrease pulmonary vascular resistance. B. Positive pressure ventilation and positive end expiratory pressure (PEEP) increase pulmonary vascular resistance. C. Pulmonary vascular resistance is evenly distributed between the pulmonary arteries, the pulmonary capillaries, and the pulmonary veins. D. An increase in pulmonary vascular resistance increases the workload of the right ventricle. E. All the above.

E. Pulmonary vessels are thin walled and have less vascular smooth muscle than vessels in the systemic circulation. Normal pulmonary vascular resistance (PVR) is about 1/10 of systemic vascular resistance. Pulmonary vascular resistance is evenly distributed between the pulmonary arteries, the pulmonary capillaries, and the pulmonary veins. This is different compared to systemic circulation whereby approximately 70% of the resistance comes from the arterioles. An increase in PVR increases the workload of the right ventricle in the same way that an increase in SVR increases the workload of the left ventricle. During positive pressure mechanical ventilation, both the alveolar and extra-alveolar vessels are compressed during lung inflation. With the addition of positive end expiratory pressure (PEEP), these vessels remain compressed during expiration as well. PVR is thus increased. An increase in cardiac output from the right ventricle (as during exercise) causes a slight increase in pulmonary artery pressure (PAP) which results in a decrease in PVR. Other causes of increased PVR: • Epinephrine and norepinephrine. • Histamine / influx of inflammatory mediators. • Thromboxane / platelet activation and aggregation. • Alveolar hypoxia (local vasoconstriction). • Hypercapnia / acidosis. • Hypothermia. • Pulmonary endothelial dysfunction.

When assessing acid base balance, what is true regarding base deficit or base excess: A. The result is the number of mEq of acid or base needed to titrate one liter of blood to a pH of 7.4 at a normal temperature and a normal PaCO2. B. < -2 (base deficit) represents metabolic acidosis or metabolic compensation for respiratory alkalosis. C. Normal value is + 2 to -2 mEq/L. E. All of the above.

E. The base excess or base deficit is the number of mEq of acid or base needed to titrate one liter of blood to a pH of 7.4 at a temperature of 37 degrees Celsius and with a constant PCO2 of 40 mmHg. Normal: + 2 to -2 mEq/L. • > +2 = metabolic alkalosis or metabolic compensation for respiratory acidosis. • < -2 (base deficit) = metabolic acidosis or metabolic compensation for respiratory alkalosis. Base deficit can be used to estimate how much sodium bicarbonate (in mEq) to give a patient. This is determined by multiplying the base deficit by the patient's estimated extracellular fluid space. Extracellular fluid space is estimated at 0.3 times the lean body mass in kilograms.

You are caring for a patient and when doing his admission history the wife tells you she has frequently noticed he stops breathing at night. The patient's physician has previously recommended a sleep study but the patient thinks his sleep problem is an annoyance that he is willing to live with. When counseling your patient you explain that obstructive sleep apnea (OSA) is associated with an increased risk of: A. Hypertension. B. Stroke. C. Cardiac arrhythmias. D. CAD. E. All of the above.

E. The effect of OSA is altered cardiopulmonary function which places patients at increased risk for cardiovascular disorders and death. OSA increases the risk for hypertension, CAD, and atrial and ventricular arrhythmias, and stroke. The associated risk is pronounced in men than in women. Additionally there is evidence that OSA increases mortality risk in those patients with cardiovascular disease.

What is true regarding the role of the respiratory system in acid base balance: A. In metabolic acidosis there is an increase in the rate and depth of respiration to blow off CO2. B. It responds within minutes. C. It regulates the excretion or retention of carbonic acid (the only acid excreted as a gas by the lungs). D. It compensates only for metabolic disorders. E. All of the above.

E. The respiratory system compensates only for metabolic disorders and does so quickly within minutes. In metabolic acidosis there is an increase in the rate and depth of respiration to blow off CO2. The respiratory system regulates the excretion or retention of carbonic acid (the only acid excreted as a gas by the lungs).