Pulmonary CSC

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.

What is the best description of a flow cycled breath: A. Each breath is delivered at a preset tidal volume. B. A flow cycled breath is a pressure support breath. C. Each breath is delivered with a high flow of air that has been recycled from the patient's exhalation. D. Each breath is delivered for a preset time at a preset pressure.

B. A flow cycled breath is a pressure support breath. It allows a constant pressure during inspiration. There is no set time in a flow cycled breath. Once a set amount of the peak flow has been delivered, exhalation begins. Flow cycled breaths are used in pressure support ventilation. Note that pressure support ventilation is not the same as pressure controlled ventilation.

You are caring for a patient who has been intubated for 8 days. The patient had a low cuff leak (< 110 mL) during balloon deflation prior to extubation. You recognize your patient to be specifically at risk for: A. Post extubation acute respiratory distress syndrome (ARDS). B. Laryngotracheal edema. C. Tracheal atrophy. D. Re-intubation and long term ventilator dependence.

B. Laryngotracheal edema may occur post-extubation in patients who have been intubated for several days. This may result in upper airway obstruction. Treatment includes epinephrine and steroids. Patients at high risk may be identified by a low cuff leak (< 110 mL) during balloon deflation prior to extubation.

Which patient is unlikely ready for consideration of discontinuation of mechanical ventilation: A. A patient who is able to initiate an inspiratory effort. B. A patient who is not requiring vasopressors for hypotension. C. A patient who is receiving FIO2 of 0.6. D. A patient in whom the underlying cause of respiratory failure has been effectively reversed.

C. A formal assessment for mechanical ventilation discontinuation according to the following parameters: • Reversal of the underlying cause of respiratory failure. • Adequate oxygenation (PaO2/FIO2 > 150-200; PEEP < 5-8cm H2O; FIO2 < 0.4-0.5; and pH > 7.25). • Hemodynamic stability as defined by no active myocardial ischemia and no clinically significant hypotension • Patient ability to initiate an inspiratory effort.

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.

What is the potential benefit of allowing permissive hypercapnia in a patient on mechanical ventilation for acute respiratory distress syndrome (ARDS): A. Acidosis is the preferred environment for cellular function. B. Lowering the respiratory rate allows the alveoli to rest and recover. C. Permissive hypercapnia may be indicated in order to reduce the plateau (and peak) airway pressure and protect the lung. D. Hypercapnia stimulates the patient to use their own respiratory muscles.

C.Decreasing tidal volume is a strategy to lower plateau pressure. A lower tidal volume may cause an increase in PaCO2. Permissive hypercapnia (acceptance of increased PaCO2) may be indicated in order to reduce the plateau (and peak) airway pressure and protect the lung.

Hemodynamic effects of mechanical ventilation include: A. Increased right ventricular stroke volume. B. Increased left ventricular afterload. C. Increased right ventricular preload. D. Increased right ventricular afterload.

C.Hemodynamic effects of mechanical ventilation include: • Decreased venous return (decreased right ventricular preload). • Pulmonary capillary compression and increased right ventricular afterload. • Decreased right ventricular stroke volume. • Decreased left ventricular afterload. Note: The patient's baseline left ventricular function impacts the hemodynamic effects of mechanical ventilation.

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.

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. Suctioning routinely every two hours. C. Prevention of hyperthermia. D. Adequate pharmacological sedation.

B. 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.

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.

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 value during spirometry testing is used to make the diagnosis of chronic obstructive pulmonary disease: A. FEV1 > 80% of predicted. B. FEV1/FVC ratio < 70%. C. FEV1 < 80% of predicted. D. FEV1/FVC ratio > 70%.

B. The formal diagnosis of COPD is made with spirometry. The forced vital capacity (FVC) (volume of air forcibly exhaled after a maximal inspiration) and the forced expiratory volume in the first second (FEV1) are measured after bronchodilator therapy. The ratio of FEV1 / FVC is obtained. A ratio that is than 70% indicates obstruction to airflow. This confirms the diagnosis of COPD. The percent of predicated FEV1 is used to classify the severity of COPD once the diagnosis is made.

What class of medications are used in acute exacerbations of chronic obstructive pulmonary disease (COPD) to improve lung function and hypoxemia, shorten recovery time and length of stay, and reduce the risk for early repeat exacerbation: A. Intravenous beta2-agonsits. B. Antibiotics. C. Systemic corticosteroids. D. Anti virals.

C.Systemic corticosteroids (oral or intravenous) are used in acute exacerbations to improve lung function and hypoxemia, shorten recovery time and length of stay, and reduce the risk for early repeat exacerbation. A dose of 40mg of prednisone or prednisolone for 5 days is often used although the optimal duration of therapy is not certain. Prednisone is activated by the liver into prednisolone. Oral prednisolone is preferred and should always be used in the presence of liver dysfunction.

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.

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.

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.

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.

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.

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.

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.

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.

You are caring for a patient who is intubated and on mechanical ventilation. The high pressure limit alarm sounds. You assess your patient and determine suctioning is needed. After suctioning the high pressure alarm no longer sounds. You conclude: A. Increased airway resistance was the reason for the high pressure alarm to sound. B. Neither increased airway resistance and decreased lung compliance were the reasons for the high pressure alarm to sound. C. Both increased airway resistance and decreased lung compliance were the reasons for the high pressure alarm to sound. D. Decreased lung compliance was the reason for the high pressure alarm to sound.

A. A high pressure alarm is set based on the peak inspiratory pressure. The peak inspiratory pressure takes into account both airway resistance and lung and chest wall compliance. Secretions in the airway increase airway resistance. Since suctioning resolved the alarm issue, you conclude that the alarm was triggered due to increased airway resistance.

You are caring for a patient who is intubated and on mechanical ventilation for acute respiratory failure. The patient has been hemodynamically stable since admission 6 hours ago. Your patient is now profoundly hypotensive and the high pressure alarm on the ventilator is alarming for the first time. What are you concerned is the cause of the patient's change in condition: A. Pneumothorax. B. Pulmonary embolus. C. Hospital acquired pneumonia. D. Acute respiratory distress syndrome (ARDS).

A. A pneumothorax should always be considered when profound hypotension occurs. A chest tube is required when a patient with a pneumothorax is on positive pressure ventilation. A pneumothorax results in a sudden increase in peak inspiratory pressure. Although the patient is at risk for hospital acquired pneumonia, it has only been 6 hours since admission. Pneumonia would not initially present with profound hypotension. Pneumonia can increase airway resistance from increased secretions but would not result in a sudden increase in peak airway pressure. ARDS is not a syndrome that is diagnosed on the day of admission for acute respiratory failure. A pulmonary embolus (PE)is a perfusion abnormality and although a massive PE can cause profound hypotension, it would not cause an airway resistance issue and set off the inspiratory high pressure alarm.

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).

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

A. 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.

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

When caring for a patient who weighs 68.0 kg in acute ventilatory failure due to exacerbation of COPD and is now requiring intubation and mechanical ventilation, the nurse knows the following is true: A. A tidal volume (VT) of 600 ml would be an appropriate initial tidal volume. B. A tidal volume (VT) of 800 ml to start with reevaluation after getting a blood gas. C. The patient's anatomical dead space was approximately 100 ml prior to intubation. D. The patient's maximum PEEP should be no more than 5 cm H2O.

A. Anatomical dead space is approximately 1 ml per pound of ideal body weight. For this patient the anatomic dead space would be approximately 150ml. Recommended initial ventilator settings for a patient with acute respiratory failure include an initial tidal volume (VT) of 8-10 ml / kg. The lower end of the range is often used to prevent further lung injury from volutrauma, particularly in patients with acute lung injury. In patients with acute lung injury, a lower initial tidal volume of 5-8 ml / kg may be used. An initial setting of 5 cm of PEEP is usually used in acute respiratory failure. A patient's maximum PEEP is individualized based on their cardiac output and their oxygenation status. The optimal PEEP is considered the amount of PEEP, which provides the best oxygenation status without an hemodynamic compromise. Remember, PEEP decreases venous return to the heart (preload) and can therefore decrease cardiac output. PEEP should not be initiated or increased in a patient with hypovolemia.

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 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.

A preset volume is delivered at a set rate assuring a minimum number of breaths and tidal volume per minute. If the patient is spontaneously breathing the ventilator will allow the patient to initiate his own breaths and will take over to deliver the preset tidal volume with each patient-initiated breath: A. Assist/control (AC) mode. B. Airway pressure release ventilation (APRV). C. CPAP. D. Synchronized mandatory ventilation (SIMV).

A. Assist/control mode provides a minimum number of breaths at a preset rate and tidal volume but allows the patient to breathe on his own above the preset ventilator rate. Each patient initiated breath is delivered at the same tidal volume as the machine initiated breaths. In SIMV, the ventilator delivers a minimum number of breaths at a preset tidal volume but allows the patient to breathe on his own at his own rate and tidal volume between mandatory ventilator breaths. The SIMV mode is often used in weaning patients who have been on a ventilator for a period of time. Allowing the patient to determine his own tidal volume for patient initiated breaths helps him to assume more of the work of breathing. Airway pressure release ventilation is a mode of ventilation that focuses on mean airway pressure. This mode of ventilation is often used to help open alveoli in patients with acute respiratory distress syndrome (ARDS). In this mode, four parameters are set: T high and low and P high and low. T stands for time and P stands for pressure. The patient breathes at a set pressure for a certain period of time and then is allowed to drop to the low pressure (usually 0) for a very short period of time. CPAP is a non invasive ventilatory strategy that provides continuous pressure (usually 10 cm H20) throughout the breathing cycle in a patient with spontaneous respiration.

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.

Ventilator provides positive pressure throughout the respiratory cycle for each patient initiated breath; tidal volume and rate are controlled by the patient: A. CPAP. B. Synchronized intermittent mandatory ventilation (SIMV). C. Assist/control (AC) mode. D. Airway pressure release ventilation (APRV).

A. CPAP is a non invasive ventilatory strategy that provides continuous pressure (usually 10 cm H20) throughout the breathing cycle in a patient with spontaneous respiration. Respiratory rate and tidal volume are controlled by the patient. In assist control (AC) ventilation, the patient is allowed to initiate breaths above the preset ventilator rate. However, the ventilator will deliver the preset tidal volume for all patient initiated breaths. The patient is not allowed to determine his own tidal volume. Assist control mode is typically the first line mode in acute respiratory failure because the ventilator determines tidal volume and assumes the work of breathing. Synchronized intermittent mandatory ventilation (SIMV). In SIMV, the ventilator delivers a minimum number of breaths at a preset tidal volume but allows the patient to breathe on his own at his own rate and tidal volume between mandatory ventilator breaths. The SIMV mode is often used in weaning patients who have been on a ventilator for a longer period of time. Allowing the patient to determine his own tidal volume for patient initiated breathes helps him to assume more of the work of breathing. Airway pressure release ventilation is a mode of ventilation that focuses on mean airway pressure. This mode of ventilation is often used to help open alveoli in patients with acute respiratory distress syndrome (ARDS). In this mode, four parameters are set: T high and low and P high and low. T stands for time and P stands for pressure. The patient breathes at a set pressure for a certain period of time and then is allowed to drop to the P low (usually 0) for a very short period of time.

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).

When caring for a patient who is intubated and on mechanical ventilation the nurse knows the following to be true regarding cuff pressures for the endotracheal tube: A. Low pressure high volume cuffs are used. B. Cuff pressures need to exceed the capillary filling pressure in the trachea. C. A leak in the cuff can be repaired by injection of a sealant. D. Cuff inflation prevents aspiration of liquids.

A. Cuff pressures should not exceed capillary filling pressure in the trachea (< 25 cm H2O or <20 mmHg). Higher pressures can result in tissue necrosis. An adequately inflated cuff will prevent the aspiration of large particles but not liquids. A leak in the cuff or pilot balloon valve requires replacement.

What are the two most common complications of extracorporeal membrane oxygenation (ECMO): A. Hemorrhage and infection. B. Anaphylaxis and paralysis. C. Anaphylaxis and infection. D. Hemorrhage and paralysis.

A. ECMO allows for gas exchange outside the body. The membrane oxygenator is a key component of ECMO and the system can be configured in three ways: • Venous - arterial: allows for gas exchange and provides hemodynamic support by bypassing the lungs and heart. This system can also work alongside native circulation allowing for a portion of the blood to flow naturally through the heart and lungs. This configuration is indicated in refractory cardiogenic shock or as salvage strategy during cardiac arrest after 10 minutes of unsuccessful advanced cardiac life support. • Venous - venous: facilitates gas exchange but does not provide for hemodynamic support because the blood is returned to the right side of the heart before it enters pulmonary circulation. The circuit pump is necessary to pump venous blood through the membrane oxygenator. This is used as an alternative strategy in adults with ARDS to rest the lungs and avoid insult of mechanical ventilation. • Arterial - venous: This is a pumpless circuit where blood flows from the femoral artery through a membrane and returns to the femoral vein. All hemodynamic support comes from the patient's own cardiac output. Absence of a pump makes this mode easier for transport. However, cardiac function must be well preserved. Hemorrhage and infection are the two most common complications of ECMO.

When caring for a patient with a pulmonary embolus secondary to deep vein thrombosis (DVT), what is true regarding the use of compression stockings: A. Stockings should provide a pressure of 30-40 mm Hg at the ankle. B. Compression stockings play no role in the management of DVT. C. Compression stockings should be worn for 4 weeks after diagnosis of DVT. D. Stockings known as "Ted-hose" are designed to provide the amount pf pressure needed in patients with DVT.

A. Early ambulation should always occur with compression stockings. Compression stockings can limit or prevent the extension of thrombus, and prevent post thrombotic syndrome. Stockings should provide a pressure of 30-40 mm Hg at the ankle. The pressure is greatest at the toes and gradually decreases up the level of the thigh. This amount of pressure increases the velocity of blood in the deep veins five times and reduces the amount of blood in the lower extremity deep veins by 70%. Stockings known as "Ted-hose" provide a maximum pressure of 18 mmHg and not recommended for any role in the treatment or prevention of DVT. Compression stockings are recommended for a minimum of 2 years after a DVT. Patients with post thrombotic syndrome will need to wear compression stockings longer. If compression stockings are not effective in reducing the symptoms of post thrombotic syndrome, then intermittent compression device therapy can be tried.

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 the major reason for hypoxemia in a patient with a pulmonary embolus (PE) is: A. Ventilation and perfusion mismatching. B. Diffusion abnormality. C. Intrapulmonary shunting from massive collapse of alveoli. D. Hypercapnic respiratory failure from airway obstruction.

A. Hypoxemia occurs in PE primarily due to ventilation and perfusion mismatching. Some alveolar capillary units have increased V/Q ratio (alveolar dead space) and some alveolar capillary units have decreased V/Q ratio due to increased perfusion from redistributed blood. A decreased V/Q ratio leads to intrapulmonary shunting. Intrapulmonary shunting results in poorly oxygenated blood returning to the left side of the heart because ventilation is insufficient for the amount of perfusion. Other factors can contribute to hypoxemia in PE. For example, if cardiac output falls then oxygen delivery will fall. This will lead to a decrease in the amount of oxygen returned to the right heart via the venous blood. This lower oxygen content in the pulmonary circulation prior to gas exchange contributes further to the hypoxemia.

What is not true in a tension pneumothorax: A. Air rushes out of the pleural space and cannot get back in. B. Can be caused by a clotted water seal drainage system. C. Chest tube or emergency decompression is required. D. It can cause obstructive shock.

A. In a tension pneumothorax air rushes in and cannot escape pleural space. This creates positive pressure in pleural space. The ipsilateral lung collapses. There is a mediastinal shift towards contralateral lung compression with potential tearing of thoracic aorta. The right heart can be compressed, decreasing RV filling with resultant shock.

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.

You are caring for a patient with chronic obstructive pulmonary disease (COPD) who is being admitted for an elective laparoscopic surgery. When doing the admission history, the patient tells you he doesn't want to get addicted to oxygen so he only wears it when he is feeling very short of breath. He estimates he wears it about 2 hours each day. What is your response: A. I would like to discuss with you the reasons why you need to wear your oxygen at least 15 hours each day for you to get the most benefit of the therapy. B. Oxygen is an addictive substance but you would need to wear it 24 hours a day for at least a year to develop an addiction. C. I wish more patients took the responsibility to only where their oxygen when they really needed it. D. Please make sure you wear it at least 2 hours each day or your insurance company might not pay for it.

A. Oxygen should be worn preferably for 24 hours a day in patients with resting hypoxemia. Patients should have the capability of using oxygen during ambulation, including portable capability for use outside the home. Survival benefit requires administration of at least 15 hours out of each day.

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.

What is true regarding the I:E ratio on a ventilator: A. Too short of E time can lead to the development of auto PEEP. B. Normal I:E ratio is 1:4. C. Increasing expiratory time is used as a strategy to increase mean airway pressure and improve oxygenation. D. Patient with chronic obstructive pulmonary disease (COPD) require a longer inspiratory time.

A. The inspiratory/expiratory ratio is monitored during mechanical ventilation. The normal ratio is 1:2. Patients with COPD require longer expiratory times (1:3, 1:4 or perhaps longer). During inverse I:E ventilation, the inspiratory time is increased to improve mean airway pressure and thus improve oxygenation. When expiration time is too short, patients can develop auto PEEP.

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.

What is the most common cause of an exacerbation of chronic obstructive pulmonary disease (COPD): A. Viral infection. B. Missed dose of a medication. C. Exposure to tobacco smoke. D. Bacterial infection.

A. The most common cause of exacerbation is a viral infection of the upper respiratory tract or the tracheobronchial tree.

When initiating warfarin in a patient receiving unfractionated heparin for a known pulmonary embolus (PE) what does the nurse know to be true: A. A paradoxical hypercoagulable state can occur if the unfractionated heparin is discontinued prematurely (before INR is therapeutic for 24 hours). B. Unfractionated heparin should be stopped after the first dose of warfarin to reduce bleeding risks. C. Unfractionated heparin must be changed to another anticoagulant because it cannot be given simultaneous with heparin. D. Unfractionated heparin should be stopped prior to the first dose of warfarin to avoid medication interactions.

A. The parenteral anticoagulation should not be discontinued until the INR is at least 2.0 for 24 hours or no sooner than 5 days. A paradoxical hypercoagulable state can occur if the initial anticoagulation is discontinued prematurely. The reason for this initial paradoxical state is related to action of warfarin prior a therapeutic INR being established. When warfarin is first started, it inhibits protein C and factor VII more than factors II, IX, and X because protein C and factor VII have shorter half-lives than the other factors. The coagulation factor imbalance in the initial stages of warfarin initiation leads to a paradoxical activation of coagulation. This can result in unintended thrombus formation.

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.

A tidal volume typically used for mechanical ventilation in patients with adult respiratory distress to prevent volutrauma is: A. 5 - 8 ml/kg. B. 3 - 5 ml/kg. C. 12 - 20 ml/kg. D. 10 - 15 ml/kg.

A. Tidal volume is the amount of air delivered with each breath. At higher tidal volumes, lung injury can occur from high volumes delivered with each breath. For patients with acute lung injury or acute respiratory distress syndrome (ARDS) lower tidal volumes of 5-8 ml/kg of ideal body weight are used to prevent additional lung injury. Lower tidal volume ventilation may result in allowing the PaCO2 to be a little high; this is called permissive hypercapnia.

Strategies to reduce complications of ventilator therapy include: A. Low tidal volume ventilation with permissive hypercapnia in patients with acute respiratory distress syndrome (ARDS). B. Suctioning q 1-2 hours to prevent infection. C. Avoidance of sedation to prevent damage to respiratory muscles. D Maintain FIO2 at 100% for at least 3 days to improve oxygenation.

A. Two evidence based lung protective strategies in ARDS include lower tidal volume with permissive hypercapnia (prevention of volutrauma) and maintaining a plateau pressure < 30 mmHg (prevention of barotrauma). To reduce the risk of oxygen toxicity, 100% FIO2 should ideally not be used for longer than 24 hours. Routine suctioning should be avoided as a strategy to reduce the risk of ventilator acquired pneumonia. Sedation is important during ventilator therapy for several reasons including reducing anxiety, improving ventilator synchrony, deceasing release of stress hormones, and decreasing tissue oxygen consumption.

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.

When administering a beta 2- agonist for the treatment of chronic obstructive pulmonary disease the nurse incorporates the following knowledge into practice: A. Body tremors can occur in older patients and limit the dose. B. The effects of short acting agents last for 30 minutes to 1 hour. C. The addition of a high dose as needed short acting agent to patients already taking a long acting agent is recommended. D. Short acting agents can only be used PRN with no more than 3 doses a week. E. Beta 2- agonists block the beta 2 receptors.

A.Beta 2- agonists stimulate the beta 2 receptors and this results in a functional block of bronchoconstriction. The effects of short acting agents last for 4 to 6 hours. Short acting agents can be scheduled or taken as needed. Long acting agents have a duration of 12 to 24 hours depending on the agent. The addition of a high dose as needed short acting agent to patients already taking a long acting agent is not recommended. A common side effect of beta 2-agonists is resting tachycardia. Body tremors can occur in older patients and limit the dose.

Which bronchodilator is the least preferred in the treatment of chronic obstructive pulmonary disease (COPD): A. Slow released theophylline. B. Salmeterol. C. Tiotropium. D. Levalbuterol. E. Ipratropium bromide.

A.Methylxanthines: The exact mechanism of these medications is not known. They may act as non-selective phosphodiesterase inhibitors. Slow released theophylline is the most commonly used drug in this class although it is less effective and less well tolerated than the inhaled long acting bronchodilators. It is not recommended if long acting inhaled bronchodilators are affordable. A major problem with drugs in this class is that the therapeutic effect occurs at a near toxic dose. Serious side effects occur including cardiac arrhythmias and grand mal seizures Beta2-agonsits and anticholinergics are the preferred bronchodilators in the treatment of chronic obstructive pulmonary disease. Salmeterol: Long acting beta2- agonist Levalbuterol: Short acting beta2- agonist Ipratropium bromide: Short acting anticholinergic. Tiotropium: Long acting anticholinergic.

When administering a propofol infusion to a patient receiving mechanical ventilation the nurse recognizes the following nursing implications: A. Propofol has a high lipid content and increases the patient's risk for infection. B. Hypertension is a common side effect and can usually be treated by adding a beta blocker to the patient's medication regime. C. Propofol-related infusion syndrome is a common complication that results in the patient having amnesia. D. Propofol provides light enough sedation that it can be continued into the post extubation period.

A.The tubing and any unused portions of propofol emulsion should be discarded after 12 hours because propofol emulsion contains no preservatives and is capable of supporting growth of microorganisms. Strict aseptic technique should be used when handling propofol. Hypotension is a common complication. Hypotension is most commonly associated with bolus dosing and in hypovolemic patients. Hypotension is a result of venous vasodilatation and mild cardiac depressive effects. Propofol-related infusion syndrome is a potentially life threatening complication characterized by the onset of metabolic acidosis, dysrhythmias, hyperkalemia, rhabdomyolysis (or elevated CPK levels), and cardiac failure. Short term administration of large doses or long term administration (>48 hours) at high doses (>80 mcg/kg/min) may increase the risk of propofol infusion syndrome. Propofol decreases awareness and respiratory drive (apnea can occur during therapeutic sedation). Nurses should only use propofol for sedation in patients receiving mechanical ventilation.

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.

When providing sedation to a critically ill patient who is on mechanical ventilation what is the recommended method for determining the amount of sedation needed for the patient: A. Ask the family their perception of the patient's comfort level. B. Following a sedation protocol using a validated sedation scale such as the Richmond Agitation Sedation Scale (RASS). C. Give sedation as ordered and scheduled on the MAR. D. Ask the patient to use a communication board to rate his level of sedation.

B. A target level of sedation is a patient who is calm but easily arousable. The patient should be able to maintain brief eye contact and follow simple instructions, while not exhibiting any signs of agitation. Additionally, the patient should maintain a normal sleep wake cycle. Sedation protocols are effective tools for achieving optimal patient sedation. Two commonly used sedation scales include the: a) Richmond Agitation Sedation Scale (RASS), and b) Riker Sedation-Agitation Scale (SAS). The RASS scale is one of the most validated tools and is frequently recommended for the ease of use, high inter-rater reliability.

The following is true regarding oral care to reduce the risk of ventilator associated pneumonia: A. Brush teeth and gums only twice a day while avoiding the tongue. Brushing of the tongue may dislodge bacteria. B. Brush teeth, gums, and tongue twice a day while moisturizing oral mucosa and lips every 2 to hours. C. Avoid moistening the lips since moisture breeds bacteria. D. Routine use of oral chlorhexidine gluconate (0.12%) is recommended in all patient populations.

B. According to the American Association of Critical Care Nurses' Practice Alert for Oral Care for Patients at Risk for Ventilator Associated Pneumonia the following are the expected practices: 1) Brush teeth, gums and tongue at least twice a day using a soft pediatric or adult toothbrush, 2) Provide oral moisturizing to oral mucosa and lips every 2 to 4 hours, and 3) Use an oral chlorhexidine gluconate (0.12%) rinse twice a day during the perioperative period for adult patients who undergo cardiac surgery. According to a systematic review by Klompas et al. published in JAMA (2014) there is not evidence to support the routine use of oral chlorhexidine gluconate (0.12%) in other populations at this time.

When providing patient education to a patient newly prescribed an anticholinergic bronchodilator, the nurse should inform the patient that the most commonly experienced side effect is: A. Nausea. B. Dry mouth. C. Tremors. D. Headache.

B. Anticholinergic medications block acetylcholine's effect on the muscarinic receptors. Short acting agents can have effects up to 8 hours. The effects of long acting agents range from > 12 hours to > 24 hours. The main side effect of these medications is dry mouth.

What is the preferred initial mode of ventilation in a patient with acute respiratory failure secondary to pulmonary edema: A. Airway pressure release ventilation. B. Assist control. C. High frequency oscillation. D. Synchronized intermittent mandatory ventilation.

B. Assist control (AC) mode of ventilation is the preferred mode of ventilation in patients with acute respiratory failure associated with increased work of breathing. In AC mode of ventilation the ventilator will allow a patient to initiate a breath, but once initiated the ventilator will take over each breath and do the work of breathing. This includes any breaths above the set rate. In synchronized intermittent mandatory ventilation (SIMV) the patient is responsible for his/her own work of breathing for all breaths above the set rate. Since the patient's respiratory system just failed, it is not preferred to make the patient responsible for any part of the work of breathing. Airway pressure release ventilation (APRV) and high frequency oscillation are considered open lung strategies and are used to recruit alveoli in conditions such as acute respiratory distress syndrome (ARDS) where there are massive amounts of collapsed alveoli.

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.

Complications of neuromuscular blockade include all the following except: A. Prolonged recovery. B. Hypertonicity. C. Myopathy. D. Acute quadriplegic myopathy syndrome.

B. Complications of neuromuscular blockade: • Prolonged recovery from the agents • Myopathy, especially when used with corticosteroids and when used longer than 1 to 2 days. • Acute quadriplegic myopathy syndrome (triad of symptoms): 1) Acute paresis, 2) Myonecrosis (increased CPK enzymes), and 3) Abnormal EMG.

For patients on mechanical ventilation receiving sedation, outcomes of a daily awakening trial include all of the following except: A. Decrease in duration of mechanical ventilation. B. Increase in the number of unplanned extubations. C. Decrease in ICU length of stay. D. Opportunity for neurological evaluation. E. Opportunity to re-titrate sedation.

B. Daily interruption of sedative infusions allows: (a) patients to spend some time awake and interacting, (b) time for a thorough neurological assessment, and (c) opportunity to re-titrate sedatives and analgesics. This daily interruption has been shown to decrease duration of mechanical ventilation and ICU stay while not increasing the number of unplanned extubations. During a daily interruption of sedation the patient should be allowed to wake up or be free of sedation until the patient shows signs of agitation or becoming uncomfortable. A daily interruption may not be appropriate in certain patients (e.g. patient in acute shock or a patient with an open chest). If sedation needs to be resumed after a daily awakening, it should be resumed at ½ the dose prior to awakening and then titrated based on the patient's sedation scale.

Which of the following is not true concerning a spontaneous breathing trial (SBT): A. SBTs administered at least once daily shorten the time to ventilator discontinuation compared to other strategies. B. SBTs should be performed every 72 hours in patients who meet criteria. C. SBTs can be performed with CPAP, low levels of pressure support, or a T piece. D. A SBT should last a minimum of 30 minutes and no longer than 120 minutes.

B. Discontinuation assessments should be done during spontaneous breathing. Tolerance during a SBT is evaluated by work of breathing, adequacy of gas exchange, hemodynamic stability, and subjective comfort. Patients tolerating a SBT lasting 30 to120 minutes should receive prompt consideration for permanent ventilator discontinuation. Key points regarding SBTs include: • There should be close monitoring during the initial few minutes of an SBT to determine if the trial should proceed • A SBT should last a minimum of 30 minutes and no longer than 120 minutes. • SBTs can be performed with CPAP, low levels of pressure support, or a T piece. • Patients who fail a SBT should have an evaluation for any reversible causes. Follow up SBTs should be performed every 24 hours if the patient meets criteria for a SBT. • SBTs administered at least once daily shorten the time to ventilator discontinuation compared to other strategies that do not include daily SBTs. There is no evidence to support more frequent SBTs. • Patients who fail an SBT should return to a stable, non-fatiguing, comfortable form of ventilator support.

Which of the following is not an appropriate nursing intervention in caring for a patient with a chest tube drainage system: A. Reporting continuous bubbling in the waterseal chamber. B. Clamping the chest tube after disconnecting suction in a patient leaving the unit for a diagnostic test. C. Reporting new diminished or any absence of lung sounds. D. Performing gentle milking when drainage is present.

B. Do not clamp chest tube for transport (can cause tension pneumothorax with pleural chest tubes or tamponade with mediastinal chest tubes). Use portable suction if available or transport on gravity drainage with tubing from suction chamber open to air. Leaving the tubing open to air allows a vent for the escape of air. If there is an order for suction and no portable suction is available then obtain an order to transport with gravity drainage. Maintaining patency is a key nursing intervention. Avoid dependent loops in the drainage tubing. Chest tube should be gently milked if there is drainage, but there should be no routine stripping. Aggressive stripping of a mediastinal chest tube can result in a negative 300 cmH2O pressure in the mediastinum and can aggravate bleeding. Reportable conditions in patients with chest tubes include: • Signs and symptoms of increased air leak (increased crepitus, bubbling in the water seal chamber) • Drainage of more than 100 ml in a hour • Tachypnea, hypoxemia, diminished or absent lung sounds • Signs and symptoms of tension pneumothorax or cardiac tamponade (hypotension, jugular venous distention, muffled heart sounds, deviation of the trachea).

You are caring for a patient who has just undergone placement of a central line in the left subclavian to facilitate administration of antibiotics. You patient is complaining of dyspnea. What are you most concerned about as the cause for the dyspnea: A. Atelectasis. B. Pneumothorax. C. Hospital acquired pneumonia. D. Blood stream infection from central line.

B. Dyspnea after a subclavian needle stick should raise suspicion for a pneumothorax. Causes of pneumothorax include: • Blunt trauma (lung laceration by rib fracture) • Positive pressure ventilation • Tracheostomy • Transthoracic needle aspiration procedures • Subclavian needle sticks • Thoracentesis • Pleural or lung biopsies • Post-operative complication of lung resection/pneumonectomy (contralateral pneumothorax). • Cardiopulmonary resuscitation • Spontaneous pneumothorax may occur in younger adults, typically under the age of 40 years. Smoking increases the risk for spontaneous pneumothorax.

What is considered a drawback to the use of high frequency oscillation ventilation in a patient with acute respiratory distress syndrome (ARDS): A. The requirement to be in the prone position. B. The increased amount of sedation required. C. The risk for volutrauma due to high tidal volumes with volume cycled breaths. D. Increased air trapping due to active removal of gas.

B. Features of high frequency oscillation ventilation include: • Oscillates gas (not jet ventilation) and maintains a constant mean airway pressure. • Recruits alveoli and also prevents derecruitment. • Time for recruitment and improvement in oxygenation status generally takes longer than 12 hours. • Gas is both delivered and removed; 1/3 time delivery in and 2/3 time delivery out. • The removal of gas is active rather than passive and thus there is less air trapping. • Tidal volume is intended to be small between 1-3 ml/kg. The small tidal volume is ideal in preventing volutrauma. • Initial setting is usually at 5 to 6 HZ (60 oscillations/HZ). • Oscillation frequencies translate into 180 to 600 breaths / minute. • Adequate humidification is important due to the high flow of gas. • Visible chest movement (wiggle) occurs in response to oscillation. • There is a slight decrease in cardiac output due to decrease in venous return. Patients need an adequate amount of circulating volume when being converted to this mode of ventilation. Most patients are able to hemodynamically tolerate this mode of ventilation. • Heavy sedation is generally required for patients to tolerate this mode. The amount of required sedation is a drawback to this mode of ventilation.

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 is not true regarding the pathophysiology of acute respiratory distress syndrome (ARDS): A. There is uncontrolled activation of coagulation pathways. B. Pulmonary capillary membranes become impermeable to water. C. There is an increase in pulmonary vascular resistance. D. There is impaired production and dysfunction of surfactant. E. There is alveolar collapse and massive atelectasis.

B. In ARDS pulmonary capillary membranes have increased permeability to water and thus non-cardiac pulmonary edema. The key pathophysiological processes involved in ALI and ARDS are: • Stimulation of inflammatory and immune systems including inappropriate leukocyte activity. • Uncontrolled activation of coagulation pathways. • Pulmonary capillary membranes (microvascular endothelium and alveolar type I epithelial cells) are damaged, resulting in an increase in capillary permeability. • Protein containing fluid, inflammatory cells, and inflammatory cytokines leak into the interstitium and alveolar spaces, causing pulmonary edema and rapidly progressive hypoxemia. • Impaired production and dysfunction of surfactant. • Alveolar collapse and massive atelectasis resulting in a decreased V/Q ratio and intrapulmonary shunting as described in Chapter 3. Fluid-filled and collapsed alveoli also decrease the compliance of lung tissue and require high-peak inspiratory pressures to ventilate the lungs. • Pulmonary capillaries constrict to redirect blood away from poorly ventilated alveoli. This increases pulmonary vascular resistance. • There is potential development of pulmonary fibrosis in the chronic phase. • Endothelium and epithelium expand. • Interstitial space expands due to edema. • Protein exudate inside the alveoli produces a hyaline membrane. This destroys the normal structure of the alveoli.

You are caring for a patient receiving high frequency oscillation ventilation for the treatment of acute respiratory distress syndrome (ARDS). What is important to know about the assessment of the patient: A. Absence of a chest wiggle is a sign that all alveoli have been recruited. B. Asymmetry of the body wiggle may be a clinical clue for pneumothorax. C. The patient should be very alert in order to take deep breaths and improve the benefits of the mode of ventilation. D. Inspiratory and expiratory breath sounds are much more pronounced and abnormal sounds are easier to pick up.

B. In high frequency oscillation ventilation there is the absence of true breath sounds as heard during normal inspiration and expiration. This means it is more difficult to detect the presence of a pneumothorax by bedside auscultation. Because higher mean airway pressures are used, patients are at risk for pneumothorax. Asymmetry of the body wiggle may be a clinical clue for pneumothorax. Absence of a chest wiggle indicates an obstruction of air flow. Heavy sedation is generally required for patients to tolerate this mode.

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.

Complications of long term inhaled corticosteroid therapy in patients with chronic obstructive pulmonary disease include: A. Peripheral arterial disease. B. Increased risk for pneumonia. C. Monocular blindness. D. Nephropathy.

B. Inhaled corticosteroids in the treatment of COPD remain controversial and they are used as part of chronic treatment in stable patients only in specific situations. Regular treatment can reduce symptoms and improve quality of life in patients with a FEV1 < 60%. Long term therapy, however, does not modify the long term course of the disease nor does it reduce mortality. Long term treatment with inhaled corticosteroids increases the risk for pneumonia. Inhaled corticosteroids can be used in combination with long acting beta 2-agonists. Long term use of oral steroid therapy in COPD patients can result in steroid myopathy resulting in muscle weakness, decreased functional status, and potential respiratory failure.

What is true regarding the use of bronchodilator therapy in the treatment of chronic obstructive pulmonary disease: A. Short acting agents are preferred over long acting agents. B. Anticholinergics and beta 2-agonists are the primary bronchodilators used in the treatment of COPD. C. The preferred method for delivery is oral. D. Bronchodilators are given to reduce mortality from COPD.

B. Inhaled therapy is the preferred mode of delivery and long acting agents are preferred over short acting agents. Anticholinergics and beta 2-agonists are the primary bronchodilators used in the treatment of COPD. To date there is no definitive evidence that existing medications are able to alter the long term decline in lung function.

When caring for a patient receiving propofol for sedation while on a mechanical ventilation what does the nurse know to be true regarding dosing: A. Propofol is never to be titrated. B. There should be a minimum of 5 minutes between dose adjustment to allow for the peak action of the drug to take effect. C. Propofol is recommended to be given in bolus doses for breakthrough agitation. D. The infusion should be initiated at a rate of 50 mcg/kg/min.

B. Mechanically ventilated patients should have infusion initiated slowly at a rate of 5 mcg/kg/min. The infusion rate should be increased by increments of 5 to 10 mcg/kg/min. There should be a minimum of 5 minutes between dose adjustment to allow for the peak action of the drug to take effect. Most adult patients require a maintenance dose of 5 to 50 mcg/kg/min, although sometimes a higher dose may be required. Nurses should never administer a bolus of propofol.

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.

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 with a history of heart failure who has hypoxemia not resolved with oxygen therapy. D. A patient who has failed weaning from mechanical ventilation after being intubated 4 days ago.

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.

What is not true regarding analgesia and sedation in a patient receiving mechanical ventilation: A. Sedative medications alone are not effective in treating pain and untreated pain increases the risk for delirium. B. Opiates should be used sparingly on an as needed only basis. C. The most valid and reliable indicator of pain is the patient's self-reporting of their perception of pain. D. Pain and sedation should be assessed together.

B. Pain is commonly experienced in the mechanically ventilated patient. Analgesia should always be a priority because pain may manifest as anxiety and agitation and also interfere with adequate sleep. Untreated pain in the mechanically ventilated patient increases the risk for delirium in a patient population already at high risk. Sedative medications alone will not be effective at treating pain. Additionally, pain evokes a stress response that results in several adverse physiological effects including increased myocardial oxygen consumption and promotion of a more hypercoagulable state. Relief of pain is important for physiological homeostasis as well as for patient comfort. Pain and sedation level should be assessed together in the mechanically ventilated patient. The most valid and reliable indicator of pain is the patient's self-reporting of their perception of pain. The numeric rating scale (1-10) is the recommended tool to use in the assessment of pain in the mechanically ventilated patient who is alert and able to participate in the assessment process. If self-report is not an option then subjective observation of pain behaviors (facial expression, movement, etc.) and measurement of physiological parameters (blood pressure, heart rate, and respiratory rate) should be used as part of the pain assessment , although these indices are not always reliable. There are two validated tools for assessing pain in the critically ill patient who cannot verbalize. These tools are the (a) Behavioral Pain Scale and (b) Critical Care Observation Tool. They have been validated in the non-traumatic brain injured patient. Opiates are the most common medications used for analgesia in mechanically ventilated patients. Scheduled opioid doses or a continuous infusion is preferred over as needed dosing in order to assure consistent analgesia. The respiratory depressive effects of opiates are helpful in the mechanically ventilated patient to treat dyspnea, coughing, and ventilator dyssynchrony. Opiates typically do not have hemodynamic effects in patients who are not hypovolemic. Acetaminophen or non-steroidal anti-inflammatory agents (unless contraindicated) are helpful as adjunctive therapy to opioids. Preventing pain is more effective than treating pain and thus providers need to anticipate and treat for any aspects of therapy that cause pain.

Patients requiring long term mechanical ventilation will require a tracheostomy. All of the following are benefits of a tracheostomy in long term mechanical ventilation except: A. Enhanced mobility. B. Decreased security of the airway. C. Opportunity for oral nutrition. D. Decreased airway resistance.

B. Potential benefits to tracheostomy placement for ventilator dependent patients include: • Increased security of airway • Increased effective airway suctioning • Decreased airway resistance • Improved patient comfort • Enhanced patient mobility • Opportunity for articulated speech • Opportunity for oral nutrition. Patients who will benefit from early tracheotomy include: • Those requiring high levels of sedation to tolerate endotracheal tubes • Those with tachypnea in whom a lower airway resistance might have benefit • Those who need the psychological or physical benefits of increased activities allowed by the tracheostomy.

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.

What is correct nursing knowledge regarding the chest tube drainage systems and suction: A. Wet suction units regulate the amount of suction by the suction from the wall unit and not by the height of a column of water in the suction chamber. B. Wet suction units regulate the amount of suction by the height of a column of water in the suction chamber not by the suction from the wall unit. C. Usually -80 cm H2O should be applied to a chest tube drainage system. D. Robust bubbling is needed in order to have an adequate amount of suction.

B. The 3rd compartment of a chest drainage system is connected to the first two sections and provides suction. There are two types of suction units: wet and dry. Wet suction units regulate the amount of suction by the height of a column of water in the suction chamber not by the suction from the wall unit. When a water column is used, only gentle bubbling should occur in the suction chamber. The source of suction should be adjusted to prevent loud bubbling of the water. Excessive external suction results in evacuation of water from the control chamber. The system valve controls the amount of suction and should normally be adjusted to achieve -20 cm H2O of suction. Lower levels of suction may be indicated for patients with friable lung tissue. The goal is to have an adequate amount of suction to keep open the pleural space, but not an excessive amount that will cause damage to the lung tissue. No more than -40 cm H2O should be applied to a chest tube drainage system. Many disposable chest tubes today have a dry suction regulator. This means there is no water in the suction chamber. A mechanical regulator within the unit is used to set the amount of suction applied to the system. The wall vacuum regulator is set at minus 80 cmH2O but the regulator on the unit is set to limit the suction to typically minus 20 cmH2O.

A 70 kg patient is on a ventilator in assist/control mode. The minimum ventilator rate is set at 12 breaths/minute but the patient is breathing at a rate of 18 breaths/minute. The tidal volume is 560 ml/min, the rate is 16, the FIO2 is .80, and (positive end expiratory pressure) PEEP is 5 cmH2O. His ABGs are: pH 7.42, PaCO2 38 mmHg, HCO3 24 mEq/L, PaO2 50 mmHg. His blood pressure is 112/62 mmHg and his heart rate is 82. What would be the best ventilator change to make: A. Increase the tidal volume to 700 ml/min. B. Increase PEEP to 7.5 cm/H2O. C. Increase the FIO2 to 100%. D. Increase the ventilator rate to 20/minute.

B. The ABG shows adequate ventilation, so no change in rate or tidal volume is needed. However, oxygenation is inadequate. Increasing the FIO2 and adding PEEP would both improve oxygenation, but to prevent oxygen toxicity it would be better to add some PEEP before further increasing the FIO2. The patient is not hypotensive so increasing PEEP in this patient is a good option. Increasing the rate or tidal volume would cause the patient to blow off more CO2 and could lead to respiratory alkalosis. Rate and tidal volume affect ventilation but not oxygenation.

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.

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 137.5 and is consistent with acute lung injury or the possible development of acute respiratory distress syndrome (ARDS). C. The ratio is 0.007 and this is diagnostic of ARDS regardless of the length of the time she has been intubated. D. The ratio is 0.72 and this represents an appropriate PaO2 for her FIO2.

B. 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.

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.

What is the most important intervention to reduce mortality in a patient with a non massive pulmonary embolus (PE): A Prophylaxis for deep vein thrombosis. B. Full parenteral anticoagulation. C. Fibrinolytic therapy. D. Surgical pulmonary embolectomy.

B. The mortality in patients with undiagnosed pulmonary embolism is 30%. Treatment with anticoagulation in non-massive PE reduces mortality to less than 5%. Full parenteral anticoagulation with unfractionated heparin, LMWH, or fondaparinux is the priority treatment in any patient with suspected or confirmed PE. Fibrinolytic therapy is indicated in patients with a low risk for bleeding who present with hemodynamic compromise as evidenced by systolic BP < 90 mmHg. Fibrinolytic therapy is not routinely recommended in patients with PE who do not meet these criteria. Catheter based pulmonary embolectomy or surgical pulmonary embolectomy are options when fibrinolytic therapy is contraindicated or when fibrinolytic therapy has failed.

When a pulmonary embolus (PE) occurs there is a humoral response in addition to a mechanical obstruction. What is involved in this humoral response that contributes to the increase in pulmonary vascular resistance (PVR): A. The renin-angiotensin-aldosterone system and sympathetic nervous system are activated. B. Thromboxane-A and serotonin are released. C. Macrophages are deployed to perform phagocytosis of the clot. D. Histamine is released.

B. The obstruction to blood flow is not the only reason for an increase in PVR. When clot is formed there is a humoral response and substances such as thromboxane-A and serotonin are released. These substances are responsible for the vasoconstriction of other vessels within the pulmonary vasculature and this vasoconstriction plays an important role in the hemodynamic compromise of PE.

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.

Which of the following is not among the three most common bacteria associated with chronic obstructive pulmonary disease (COPD) exacerbation are: A. Moraxella catarrhalis. B. Methicillin-resistant Staphylococcus aureus (MRSA). C. Hemophilus influenza. D. Streptococcus pneumoniae.

B. The three most common bacteria associated with COPD exacerbation are Hemophilus influenza, Streptococcus pneumoniae, and Moraxella catarrhalis. Pseudomonas aeruginosa is an important culprit in more advanced COPD. The most common cause of COPD exacerbation however is a viral infection of the upper respiratory tract or the tracheobronchial tree.

The majority of pulmonary emboli(PE) come from thrombus located in the: A. Right ventricle. B. Deep veins of the ileofemoral system. C. Deep veins of the popliteal and tibial arteries. D. Subclavian veins. E. BackNext

B. The vast majority of PE originate from thrombus within the deep veins of lower extremities (ileofemoral system). Thrombi can also originate in the right side of the heart, pelvic veins, and axillary or subclavian veins. Another source of thrombus is around indwelling catheters.

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)

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.

When is the recommended position in the treatment for known or suspected air embolus: A. Trendelenburg, right side lying. B. Trendelenburg, left lateral decubitus position. C. Reverse trendelenburg, left lateral decubitus position. D. Reverse trendelenburg, left lateral decubitus position.

B. Treatment for air embolus at the level of the heart includes: • Trendelenburg position: This helps keep any air in the left ventricle from leaving and entering the coronary arteries or cerebral arteries. • Left lateral decubitus position: This helps keep any air in the right ventricle from leaving it and occluding the pulmonary artery. Additionally, this helps prevent the passage through any patent foramen ovale into the left ventricle. Air trapped in the right ventricle by both the left lateral and trendelenburg position may allow blood to flow under it. • 100% FIO2: This is indicated for both venous and arterial air emboli. Oxygen helps reduce the size of the air bubble and it also helps counteract any ischemia caused by the embolus. • Hyperbaric oxygen therapy is recommended for patients with cardiopulmonary or neurological symptoms. This will help in the removal of nitrogen from the air embolus in addition to improving oxygenation. This treatment is recommended as soon as possible but has been shown to have benefit for up to 30 hours. • The air bubble should be aspirated if possible.

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.

You are caring for a patient receiving mechanical ventilation. What practice does not reduce the risk of ventilator associated pneumonia: A. Oral care including brushing of teeth, gums, and tongue twice a day. B. Routinely changing the patient's ventilator circuit. C. Use of a special endotracheal tube with a lumen above the cuff to allow drainage of secretions in the subglottic area by continuous suctioning. D. Maintaining HOB elevation between 30 and 45 degrees.

B. Ventilator associated pneumonia (VAP) increases a patient's risk of death and therefore prevention is a nursing priority. There is no evidence to support that rates of ventilator associated pneumonia increase with prolonged use of a ventilator circuit and thus ventilator circuits should not be routinely changed. Elevating the HOB 30 degrees or higher significantly reduces gastric reflux and the risk for VAP. Pooling of secretions above the endotracheal tube cuff increases the risk of pulmonary aspiration. Studies on the use of special ET tubes, which remove secretions pooled above the cuff with continuous suction, decrease VAP by 45 to 50 % (American Association of Critical Care Nurses Practice Alert, 2008). Oral care, including brushing of teeth, gums, and tongues twice a day with a soft toothbrush, is an important nursing intervention to reduce the risk of VAP.

Which of the following is true concerning the use of oxygen in patients with chronic obstructive pulmonary disease (COPD): A. Survival benefit requires administration of at least 2 hours out of each day. B. The reversal of hypoxemia is a more important factor than the concern of CO2 retention when using long term oxygen therapy. C. Long term oxygen therapy does not improve survival in patients who have severe resting hypoxemia. D. Once oxygen is started on a patient with stable COPD who is on optimal medical therapy it is used for only the shortest time possible, preferably for less than 3 months.

B. • Long term oxygen therapy can improve survival in patients who have severe resting hypoxemia. The reversal of hypoxemia is a more important factor than the concern of CO2 retention when using long term oxygen therapy. • In patients with stable disease, who are on optimal medical therapy, PaO2 and SaO2 values are confirmed twice over a 3 week period before initiating therapy. Once long term therapy is initiated in a patient on optimal medical therapy, it is considered a long term commitment. •Oxygen therapy is thought to have a reparative effect by reducing pulmonary vasoconstriction and improving ventilation and perfusion matching. Withdrawal of oxygen in these patients results in a decrease in PaO2 and is considered contraindicated. • Some patients not on optimal medical therapy or who have experienced an exacerbation meet criteria for oxygen. Patients may improve with optimal medical therapy or resolution of exacerbation triggers, and no longer meet criteria. In these patients there should be follow up at 1 to 3 months to determine if the patient still meets criteria for long term oxygen therapy. • Oxygen should be worn preferably for 24 hours a day in patients with resting hypoxemia. Patients should have the capability of using oxygen during ambulation, including portable capability for use outside the home. Survival benefit requires administration of at least 15 hours out of each day. • Oxygen is adjusted for rest, exercise, and sleep. Oxygen is used to achieve a rest SpO2 of > 90%. The sleep level of oxygen is prescribed by one of two ways (ab) increasing the flow by1 L during sleep, or (b) using a sleep study to determine the optimal level of oxygen. Exercise oxygen levels should be titrated to maintain a SpO2 > 90%.

There are two modes of ventilation that are referred to as open lung strategies because they are used to open the massive number of collapsed alveoli found in acute respiratory distress syndrome. These two modes are: A. Assist control pressure controlled ventilation and airway pressure release ventilation. B. Adaptive support ventilation and high frequency oscillation. C. Airway pressure release ventilation (APRV) and high frequency oscillation. D. Adaptive support ventilation and assist control pressure controlled ventilation.

C. APRV is a mode of ventilation aimed at opening alveoli and is called an open lung strategy. Open lung strategy means there is a focus on recruiting or opening collapsed alveoli. Open lung ventilation strategies are often considered in patients with ALI or ARDS. This mode combines mechanical ventilation with spontaneous breathing. A high level of CPAP is used during spontaneous breathing with a release level. The release level allows CO2 to be cleared. High frequency oscillation is another mode aimed at recruiting (opening) alveoli, and is also referred to as an open lung strategy. This mode of ventilation oscillates gas (not jet ventilation) and maintains a constant mean airway pressure. All open lung strategies increase mean airway pressure as a means of recruiting alveoli.

Pulmonary embolus can result in what type of shock: A. Cardiogenic. B. Septic. C. Obstructive. D. Hypovolemic. E. Neurogenic.

C. Although the right ventricle fails in a pulmonary embolus (PE) resulting in shock, PE is considered a form of obstructive shock. In PE causing shock there is a physical obstruction to blood flow. Supporting the right ventricle is not sufficient, the obstruction must be removed.

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

C. 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).

What is true concerning the use of benzodiazepines for sedation in the patient receiving mechanical ventilation: A. A continuous infusion is preferred over intermittent dosing. B. Lorazepam has a quicker onset of action compared to midazolam. C. Their use is associated with increased risk of delirium. D. When possible benzodiazepines are the sedative of choice in patients receiving mechanical ventilation.

C. Continuous sedation offers the advantage of a more consistent level of sedation but also carries the risk of a deeper than needed level of sedation. Continuous sedation infusions result in longer mechanical ventilation times and longer ICU length of stay, as well as increased risk for delirium. For this reason bolus dosing of benzodiazepines over continuous infusion of benzodiazepines is preferred. However, when possible non benzodiazepines are preferred for sedation due to possible decreased risk of delirium. The onset of action for midazolam is 30 seconds to 5 minutes. Lorazepam has a slower onset of action.

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. Increased lung compliance as a complication of persistent high FIO2. B. Increased airway resistance as a complication of persistent high FIO2. C. Decreased lung compliance as a complication of persistent high FIO2. D. Decreased airway resistance as a complication of persistent high FIO2.

C. 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 co-morbid condition frequently seen in patients with chronic obstructive pulmonary disease (COPD) directly contributes to the patient's decreased activity tolerance: A. Gastroesophageal reflux disease. B. Metabolic syndrome. C. Skeletal muscle dysfunction. D. Lung cancer.

C. Muscle dysfunction occurs frequently in COPD due to loss of muscle cells and the dysfunction of remaining cells. Several factors of COPD contribute to muscle dysfunction including tissue hypoxia, poor nutrition, inactivity, and the inflammatory process. Muscle dysfunction directly contributes to activity intolerance. Other co-morbid conditions seen frequently in patients with COPD include: • Cardiovascular disease. • Metabolic syndrome • Osteoporosis • Depression • Lung cancer.

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.

You have performed a daily awakening trial on a patient who had been appropriately sedated on a propofol drip at 30 mcg/kg/min. The patient awakened and followed simple commands. Thirty minutes after awakening the patient becomes restless and is no longer able to focus on verbal instruction. What is the appropriate action: A. Resume the propofol drip at 30 mcg/kg/min and titrate up to 50 mcg/kg/min to achieve adequate sedation within 5 minutes. B. Call for new sedation orders because the daily awakening trial nullifies the sedation protocol. C. Resume the propofol drip at 15 mcg/kg/min and titrate up if needed at 5 minute intervals. D. Resume the propofol drip at 30 mcg/kg/min.

C. If sedation needs to be resumed after a daily awakening, it should be resumed at ½ the dose prior to awakening and then titrated based on the patient's sedation scale. There should be a minimum of 5 minutes between dose adjustment to allow for the peak action of the drug to take effect.

Which mode of mechanical ventilation is described here: The patient has spontaneous respiratory effort but it is not sufficient for adequate ventilation. He is intubated and mechanically ventilated. The patient receives a preset number of ventilator breaths/minute at a preset tidal volume; these breaths are timed so they are synchronous with the patient's own breathing pattern. The patient is also allowed to initiate and complete additional breaths on his own; however, for these breaths the patient (not the ventilator) will determine the tidal volume: A. Airway pressure release ventilation (APRV). B. Synchronized intermittent mandatory ventilation (SIMV). C. Assist/control (AC). D. CPAP.

C. In SIMV, the ventilator delivers a minimum number of breaths at a preset tidal volume but allows the patient to breathe on his own at his own rate and tidal volume between mandatory ventilator breaths. The SIMV mode is often used in weaning patients who have been on a ventilator for a longer period of time. Allowing the patient to determine his own tidal volume for patient initiated breaths helps him to assume more of the work of breathing. In assist control (AC) ventilation, the patient is also allowed to initiate breaths above the preset rate. However, the ventilator will deliver the preset tidal volume for all patient initiated breaths. The patient will not be allowed to determine his own tidal volume. Assist control mode is typically the first line mode in acute respiratory failure because the ventilator determines tidal volume and assumes the work of breathing. Airway pressure release ventilation is a mode of ventilation that focuses on mean airway pressure. This mode of ventilation is often used to help open alveoli in patients with acute respiratory distress syndrome (ARDS). In this mode, four parameters are set: T high and low and P high and low. T stands for time and P stands for pressure. The patient breathes at a set pressure for a certain period of time and then is allowed to drop to the P low (usually 0) for a very short period of time. CPAP is a non invasive ventilatory strategy that provides continuous pressure (usually 10 cm H20) throughout the breathing cycle in a patient with spontaneous respiration.

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.

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, dyspnea, headache, chest pain, and palpitations. His oxygen saturation remains consistent with his pre-procedural level. What treatment do you anticipate: A. Sublingual nitroglycerin. B. Emergency surgery for tracheostomy. C. Intravenous (IV) methylene blue as the first-line antidotal agent. D. BiPAP with 100% FIO2.

C. 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.

Treatment of pulmonary arterial hypertension (PAH) is aimed at treating the underlying cause and using drugs that reduce pulmonary vascular resistance, including: A. Metoprolol (Lopressor), atenolol (Tenormin), diltiazem (Cardizem). B. Nitroglycerine, dobutamine (Dobutrex), eptifibatide (Integrilin). C. Epoprostenol (Flolan), sildenafil (Viagra, Revatio), iloprost (Ventavis). D. Lisinopril (Zestril), nitroglycerine, verapamil (Calan).

C. Most drugs used to treat PAH cause pulmonary vasodilation and decrease cell proliferation in pulmonary vascular tissue. Such drugs include: prostanoids (e.g. epoprostenol [Flolan], treprostinil [Remodulin], iloprost [Ventavis]); endothelin receptor antagonists (bosentan [Tracleer]; and phosphodiesterase inhibitors (sildenafil [Revatio, also known as Viagra]). Beta blockers can cause pulmonary bronchoconstriction and are not indicated in PAH. Calcium channel blockers can be effective in some patients with PAH because they can cause pulmonary vasodilation, however they have no antiproliferative effects and work only in a small number of patients. Aldosterone blockers are indicated for treating heart failure but have no effect on pulmonary vascular resistance. ACE inhibitors dilate arteries and veins and are used as afterload and preload reducers to treat heart failure and systemic hypertension.

Which of the following is NOT used as a determinant of O2 delivery to the tissues: A. Hemoglobin. B. Cardiac output. C. Blood pressure. D. Arterial oxygen content.

C. O2 delivery is determined by cardiac output, oxygenation of arterial blood, and an adequate hemoglobin to carry O2 to the tissues. Blood pressure is determined by cardiac output and systemic vascular resistance. BP is simply a reflection of pressure in the vascular system, not a determinant of O2 delivery. BP is dependent on an adequate cardiac output and adequate SVR.

Based on the attached waveform what is not true regarding the peak inspiratory pressure: (Plateau is lower that PIP) A. This pressure accounts for both airway resistance (tubing and patient airways) and lung and chest wall compliance. B. It is the pressure needed to get air through airways and distend the lung. C. It is the same as peak flow that is set on the ventilator. D. It is the pressure used to determine ventilator alarm limits.

C. Peak inspiratory pressure is the pressure needed to get air through airways and distend the lung. This pressure accounts for both airway resistance (tubing and patient airways) and lung and chest wall compliance. It is the pressure used to determine high and low alarm limits. The high pressure limit is maximum pressure the ventilator can generate to deliver the preset tidal volume, this is usually 10-20 cm H2O above the peak inspiratory pressure. Peak inspiratory pressure is different from peak flow that is set on the ventilator.

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 are using a chest tube drainage system that requires fluid in the water seal chamber. What is an important nursing consideration: A. Report any tidaling of this chamber immediately. B. Assure that there is continuous bubbling in the water seal chamber. C. Assure that the amount of sterile fluid in the water seal and suction chambers is at the manufacturer recommended level. D. Invert the water seal system at least once every 4 hours.

C. The 2nd compartment is connected to the 1st and creates a water seal. A small amount of sterile water (per manufacturer directions) is injected into the water seal chamber before the drainage system is connected to the patient. The main purpose of the water seal is to allow air to exit from the pleural space on exhalation and prevent air from entering the pleural cavity or mediastinum on inhalation. Air that is allowed to pass through the water seal will bubble out the bottom of the chamber. The water seal chamber is calibrated and should be seen as the window into the pleural space. During gravity drainage the level of water reflects the intrapleural pressure. Some newer systems eliminate the water seal chamber and use a check-valve to serve its purpose. Assure that the amount of sterile fluid in the water seal and suction chambers is at the manufacturer recommended levels when wet systems are used. To maintain an adequate water seal in a wet system it is important to monitor the level of water in the water seal chamber and to keep the chest drainage unit upright at all times. Assess for air leak by checking water seal chamber for bubbles during inspiration. The water seal chamber may bubble gently with insertion, during expiration and with a cough. Continuous bubbling represents an air leak. Some water seal compartments have an air leak meter.

Critically ill patients on mechanical ventilation and those receiving enteral feedings are at high risk for aspiration. What practices are recommended to reduce the risk of aspiration: A. Use liberal sedation to prevent coughing and the risk of aspiration. B. Assess placement of feeding tubes every 12 hours. C. Avoid bolus tube feedings in patients at high risk for aspiration. D. Maintain head of bed elevation at 90 degrees at all time

C. The American Association of Critical Care Nurses has published a Practice Alert for the prevention of aspiration. According to this document, strategies to reduce the risk of aspiration in patients on mechanical ventilation and / or patients receiving enteral tube feedings include the following: 1) Maintain head-of-bed elevation at an angle of 30 to 45 degrees, unless contraindicated, 2) Use sedatives as sparingly as feasible, 3) For tube-fed patients, assess placement of the feeding tube at 4-hour intervals, 4) For patients receiving gastric tube feedings, assess for gastrointestinal intolerance to the feedings at 4-hour intervals, 5) For tube-fed patients, avoid bolus feedings in those at high risk for aspiration, 6) Consult with provider about obtaining a swallowing assessment before oral feedings are started for recently extubated patients who have experienced prolonged intubation, and 7) Maintain endotracheal cuff pressures at an appropriate level, and ensure that secretions are cleared from above the cuff before it is deflated.

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.

What is true regarding chronic bronchitis: A. All patients with chronic bronchitis have chronic obstructive pulmonary disease. B. Chronic bronchitis results in permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of the alveolar wall. C. Chronic bronchitis is defined as a chronic cough and sputum production on a daily basis for a minimum of three months a year, and not less than two consecutive years. D. Chronic bronchitis results in atrophy of the mucous glands.

C. The above statement is the diagnostic criteria for chronic bronchitis when there is no other explanation for the cough. An older definition for chronic obstructive pulmonary disease (COPD) included all patients with emphysema and chronic bronchitis. This is no longer a current definition for COPD. Emphysemic changes are part of the pathophysiology for COPD. Chronic bronchitis is an independent disease entity. Chronic bronchitis can precede or follow the development of airflow limitation that is the hallmark of COPD. In chronic bronchitis mucous glands hypertrophy not atrophy. Enlargement of airspaces and destruction of the alveolar wall is central to emphysema.

What is true regarding symptoms of pulmonary embolus (PE): A. Pleuritic chest pain, shortness of breath, and hypoxemia are present in most patients. B. Pleuritic chest pain is associated with a massive PE. C. Patients with PE may present with atypical symptoms making the diagnosis very difficult. D. All patients with a PE have at least one respiratory symptom.

C. The classic presentation of pleuritic chest pain, shortness of breath, and hypoxemia is not present in the majority of patients with PE. Patients can present with a range of signs and symptoms from catastrophic hemodynamic collapse to nagging nonspecific symptoms. Many patients may present with a progressing shortness of breath or pleuritic chest pain, however, many patients may have no respiratory related complaints. Patients with PE may present with atypical symptoms making the diagnosis very difficult. Examples of atypical presentations include: flank pain, abdominal pain, delirium, and seizures. PE should be considered as a potential diagnosis in any patient with respiratory symptoms in whom there is not another clear etiology. A smaller, more peripheral PE, may be responsible for the symptom of pleuritic chest pain. Pleuritic chest pain of PE is often misdiagnosed as muscular skeletal pain in younger patients. Additionally, there is a higher risk of missing PE in elderly patients because the symptoms are perceived as being chronic.

Your patient with a history of osteoarthritis and TIA is admitted for anterior wall MI. On hospital day 3 he develops acute onset dyspnea with a productive cough of pink sputum. The patient is tachycardic and has inspiratory crackles as well as inspiratory and expiratory wheezes throughout the lung fields. Cardiac auscultation reveals an audible S3. The most likely explanation is: A. Hospital acquired pneumonia. B. Acute respiratory distress syndrome (ARDS). C. Pulmonary edema. D. Pulmonary embolus.

C. The most likely explanation is pulmonary edema given the recent anterior wall MI and current audible S3. Anterior wall MI patients are at risk for residual left ventricular dysfunction and the development of heart failure. A S3 is an extra heart sound heard early in diastole when the atria are attempting to empty into an already full ventricle. ARDS does not present with a sudden onset. Pneumonia can cause tachycardia, adventitious breath sounds, and a productive cough. Sputum, however, is typically not pink (blood tinged) and patients with pneumonia typically show clinical signs of dehydration as opposed to fluid overload. Pulmonary emboli will not typically produce a pink or blood tinged sputum unless a pulmonary infarction has occurred as a complication of a pulmonary embolus. Pulmonary infarction is not a common complication. In a medium-sized pulmonary embolus, an accentuated S2 can often be auscultated. Pneumonia and pulmonary emboli also frequently present with pleuritic chest pain.

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.

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. Dopamine to treat his hypotension. C. Intubation and mechanical ventilation. D. O2 at 6 L/min via nonrebreathing mask to treat his hypoxemia.

C. 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.

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.

Complications of positive end expiratory pressure (PEEP) as an adjunct to mechanical ventilation include all of the following EXCEPT: A. Pulmonary hypoperfusion. B. Hypotension. C. Volutrauma. D. Barotrauma.

C. Volutrauma occurs when tidal volume is too high, not when pressure is too high. Hypotension can occur with PEEP when cardiac output is decreased as a result of decreased venous return to the heart. An increase in intrathoracic pressure due to PEEP decreases cardiac preload. Therefore PEEP should not be initiated in hypovolemic states. Barotrauma can result from increased pressure at the end of expiration. Regional pulmonary hypoperfusion can occur from compression of pulmonary capillaries surrounding overdistended alveoli.

Which of the following post-op CABG patients is NOT ready to be weaned from mechanical ventilation despite adequate ABGs: A. Patient on SIMV rate of 6 and FIO2 40%. B. Patient with cardiac index of 2.4 L/min/m2, HR 100, chest tube drainage 30 ml/hr. C. Patient requiring 10 cm H2O PEEP and FIO2 of 50% to maintain adequate PO2. D. Patient receiving dexmedetomidine.

C. Weaning criteria generally include the following: patient is awake with stimulation; not receiving neuromuscular blockade, long-acting or high dose narcotics, or Propofol (dexmedetomidine is OK because it provides anxiolysis and sedation without depressing respirations); hemodynamically stable with CI > 2.2 L/min/m2, HR < 120, systolic BP stable at 100-140 mmHg with or without medication; chest tube drainage < 50 ml/hr; ABGs on mechanical ventilation: PaO2 > 75 mmHg on < 50% FIO2, pCO2 < 50 mmHg, PEEP < 7.5 cm H2O.

In caring for a patient with chest tubes the nurse knows the following to be true concerning drainage: A. Aggressive stripping is necessary to keep the drainage tube patent. B. Dumping of blood into the chest tube with a position change is usually related to a new bleed. C. A patient with decreased breath sounds and increased inspiratory pressures on the ventilator but with no drainage in the chest tube might have a collection of undrained blood in the pleural space. D. Chest tubes can safely be removed as long as the amount of drainage is < 500 ml per 8 hours.

C.A change in patient condition, such as decreased breath sounds and increased inspiratory pressures on the ventilator alarm, may indicate blood in the pleural space that has not been effectively drained by the chest tube. Aggressive stripping of the chest tube can cause a negative pressure of over 300 cm of H2O and this can cause further bleeding and is painful for the patient. When a dumping of blood occurs with a position change this can represent either new or old blood. The color of the blood as well as other changes in the patient condition can be used to help assess the acuity of the bleeding. Chest tubes are typically not removed until the amount of drainage is less than 50 to 100 ml for a 24-hour period of time. After CABG surgery chest tubes are typically removed when drainage is less than 100 ml for eight hours.

What is true regarding airway pressure release ventilation (APRV): A. The mean airway pressure is lowered allowing for re-expansion of collapsed alveoli. B. It is an ideal mode of ventilation for patients with chronic obstructive pulmonary disease. C. The release time is short enough time to prevent alveolar collapse and yet a long enough time to allow for adequate exhalation of CO2. D. This mode of ventilation is not tolerated well in patients who are spontaneously breathiNG

C.APRV works well with spontaneous breathing because the patient's spontaneous breathing is not interrupted by a ventilator preset respiratory rate. This results in improved ventilator synchrony allowing for greater patient comfort and less sedation. Two pressure levels are used: 1) P High. The high pressure is typically set at 20-30 cm H2O, and 2) P Low. The low pressure is typically set between 0 and 5 cmH2O. P low is also known as the release pressure. One inspiratory time is used: T High. This is the amount of time the patient will breathe at the high pressure, typically 4 to 6 seconds. One expiratory time is used: T Low. This is the amount of time allowed for the release or the amount of time at the low pressure. It is typically a very short time, such as 0.2 to 0.8 seconds. The goal is a short enough time to prevent alveolar collapse and yet a long enough time to allow for adequate exhalation of CO2. The mean airway pressure is increased in this mode of ventilation because the patient is breathing at P High for approximately 80-95% of the respiratory cycle. Spontaneous breathing and thus the use of the patient's own inspiratory muscles helps to improve ventilation to nondependent lung regions. This improves ventilation and perfusion matching. This mode of ventilation is not suited for patients with COPD who require longer expiratory times. The short release time in this mode of ventilation will not allow for adequate removal of CO2 in these patients. Careful monitoring of minute ventilation is required when using this mode. There is a potential to under ventilate due to the short release time.

What is true regarding a massive pulmonary embolus (PE): A. A massive PE is defined as a PE that results in an extended length of stay. B. Mortality from a massive PE has been reduced to less than 5% with current treatment strategies. C. It is the type of PE that occurs in the majority of patients. D. A massive PE is defined by a presenting systolic BP of < 90 mmHg.

D. A massive PE is defined as a presenting systolic BP of < 90 mmHg. Blood pressure is low due to right ventricular failure. Mortality rates associated with massive PE range from 30% to 60% and most deaths occur within the first 1 to 2 hours. Massive PE is present in less than 5% of patients presenting with PE.

When providing sedation to a critically ill patient in the medical intensive care unit who is on mechanical ventilation for sepsis secondary to pneumonia, the nurse know the following is an appropriate level of sedation: A. The appropriate level of sedation is when sedation is only given in response to agitation. B. A deep enough level of sedation that results in eye opening only to painful stimuli. C. A light enough level of sedation that the patient can use his call light to request prn pain medication. D. The appropriate level of sedation is when the patient is able to maintain brief eye contact and follow simple instructions, while not exhibiting any signs of agitation.

D. A target level of sedation is a patient who is calm but easily arousable. The patient should be able to maintain brief eye contact and follow simple instructions, while not exhibiting any signs of agitation. Additionally, the patient should maintain a normal sleep wake cycle. Sedation protocols are effective tools for achieving optimal patient sedation. Two commonly used sedation scales include the: a) Richmond Agitation Sedation Scale (RASS), and b) Riker Sedation-Agitation Scale (SAS). The RASS scale is one of the most validated tools and is frequently recommended for the ease of use, high inter-rater reliability.

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.

What are potential consequences of increased pulmonary vascular resistance (PVR) and increased pulmonary artery (PA) pressures that occur when a patient has a pulmonary embolus (PE): A. Tricuspid valve regurgitation. B. Right ventricular dilatation and pressure overload. C. Bulging of the interventricular septum into the left ventricle. D. All of the above.

D. An increase in PVR and / or PA pressure increases the workload of the right ventricle. The end result of increased right ventricular work is right ventricular dilatation, hypokinesis, and ultimate right ventricular failure. Tricuspid valve regurgitation also develops due to annular dilatation. Right heart failure secondary to a pulmonary etiology is called cor pulmonale. Right ventricular dilatation and pressure overload results in a leftward shift of the septum. The interventricular septum can bulge toward the left ventricle and impair filling of the left ventricle during diastole. Increased right ventricular pressure can also lead to myocardial ischemia due to compression of branches of the right coronary artery.

Mechanical ventilation can be used to accomplish which of the following: A. Achieve adequate ventilation. B. Decrease the work of breathing. C. Achieve adequate oxygenation. D. All of the above.

D. Mechanical ventilation can improve ventilation by delivering a guaranteed ventilatory rate and tidal volume. It can also improve oxygenation by increasing the driving pressure of oxygen across the alveolar/capillary membrane through higher FIO2 and the use of PEEP. The use of positive pressure ventilation helps decrease the work of breathing because the ventilator can assume the 'work of breathing' for the patient. Assist control mode with adequate sedation is the best mode for decreasing the work of breathing.

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.

What best describes the pathophysiology that leads to airflow limitation in chronic obstructive pulmonary disease (COPD): A. Obstruction of large airways due to hyperplasia. B. Destruction of the alveoli and other lung structures (termed emphysema) only. C. Small airway disease from inflammation (termed obstructive bronchiolitis) only. D. Mixture of small airway disease from inflammation (termed obstructive bronchiolitis) and destruction of the alveoli and other lung structures (termed emphysema).

D. Chronic airflow limitation results from a mixture of small airway disease (termed obstructive bronchiolitis) and destruction of the alveoli and other lung structures (termed emphysema). Chronic inflammation causes narrowing of the small airways, and inflammation also contributes to the destruction of the lung parenchyma. During the destructive process, there is a loss of alveolar attachments to the small airways and there is also a loss of the elastic recoil of lung tissue. The result of these structural changes is the inability of the airways to remain open during expiration. The airflow limitation in COPD is caused by both the inflammatory changes in the small airways and by the destruction of the lung structures. These processes increase with disease severity and persist even after smoking cessation.

Which of the following statements is not true regarding chronic obstructive pulmonary disease (COPD): A. It is progressive. B. It is characterized by a persistent airflow limitation. C. There is an enhanced chronic inflammatory response. D. It is not preventable.

D. Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation that is usually progressive in nature. A noxious stimulus (often cigarette smoke) triggers an enhanced chronic inflammatory response. The severity of the disease is affected by exacerbations and co-morbid conditions. COPD is the third leading cause of death in the United States. COPD is a condition that is both preventable and treatable.

Decreased expiratory airflow is central to chronic obstructive pulmonary disease (COPD). As a result of this pathophysiology what can occur to lung volumes: A. Total lung capacity can decrease. B. Residual volume can decrease. C. Inspiratory capacity can increase. D. Functional residual capacity can increase.

D. Decreased expiratory airflow is central to COPD pathophysiology and, as a result, residual volume, functional residual capacity, and total lung capacity can increase. Functional residual capacity and total lung volume contain residual volume which can increase in COPD due to expiratory airflow limitations. Inspiratory capacity is reduced in COPD, especially during exercise.

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.

Your patient has a cardiac index of 1.9, a Hgb of 9.8 and an SaO2 of 88%. What interventions would improve your patient's delivery of oxygen: A. Increase the SaO2 to 95%. B. Increase the cardiac index to 2.4. C. Increase the hemoglobin to 12.0. D. All of the above.

D. Delivery of oxygen is determined by cardiac output, hemoglobin, and oxygen saturation. All 3 of the interventions above will increase the delivery of oxygen to the tissues. However, of the three determinants of oxygen delivery, cardiac output is the most important.

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.

Your patient is being mechanically ventilated in assist control mode of ventilation. The ventilator is using time cycled breaths. What is true regarding this type of ventilator breath: A. Each breath is delivered for a preset time at a preset pressure. B. Tidal volume is not guaranteed. C. This type of breath is used in pressure control ventilation. D. All of the above.

D. Each breath is delivered at a constant pressure (i.e. 20 cm H2O) for a preset time (i.e. 2 seconds). Time cycled breathing is used in pressure control ventilation. With type if breath tidal volume is not guaranteed and may be inadequate if lungs have decreased compliance. With decreased compliance of the lungs, more pressure is required to deliver the same tidal volume. If pressure is preset, it may not be high enough to deliver adequate tidal volume. The advantage of this type of breath is that it prevents barotrauma.

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.

When caring for a patient with evidence of a pneumothorax on the chest x-ray, what do you know to be true: A. A chest tube is required if the patient is symptomatic. B. Lung collapse results in decreased surface area for gas exchange. C. Normal negative intrapleural pressure has been disrupted. D. All of the above.

D. In a pneumothorax there is a disruption of normal negative intrapleural pressure resulting in lung collapse and decreased surface area for gas exchange. Acute respiratory failure can result. A chest tube is required for pneumothorax > approximately 15%, or if the patient is symptomatic.

What is true regarding inverse ratio ventilation: A. The purpose is to increase mean airway pressure to improve oxygenation and / or recruit alveoli. B. Adequate sedation is of particular importance. C. The patient is at increased risk for auto peep. D. All of the above.

D. In inverse ratio ventilation the inspiration to expiration ratio is adjusted to allow for more time than normal during inspiration. The normal inspiration to expiration time ratio is 1:2. Allowing for more time during inspiration increases the mean airway pressure and can optimize oxygenation. This strategy is sometimes used to help recruit or open collapsed alveoli. The inspiratory time can be increased on a ventilator by increasing VT and decreasing peak flow rate (gas takes longer to enter alveoli). Inverse ratio ventilation can be achieve with both volume cycled and time cycled breaths. The most common delivery is with time cycled breaths (pressure controlled ventilation). When inspiratory time increases, expiratory time decreases, and there is the risk for auto PEEP. Adequate sedation is required for this mode of ventilation since it does not mimic normal physiology.

To compensate for an increase in pulmonary vascular resistance (PVR) from a pulmonary embolus (PE) what occurs: A. Pulmonary capillaries vasoconstrict to even pressures throughout the pulmonary vasculature. B. Systemic pressures increase to provide more blood flow to the right side of the heart. C. Pulmonary artery pressure decreases and pulmonary capillaries constrict. D. Pulmonary artery pressure rises and pulmonary capillaries are recruited.

D. In response to an increase in PVR, the pulmonary artery (PA) pressure can double to compensate. In patients with previous pulmonary hypertension, PA pressures rise to even higher levels. An increased PA pressure results in the recruitment (opening) of more pulmonary capillaries and this lowers resistance. In response to higher pressure, capillaries also distend and this distention further lowers resistance.

You are caring for a patient on a ventilator with elevated plateau pressures secondary to decreased lung or chest wall compliance. What strategies may be effective in improving compliance: A. Thoracentesis for the treatment of a large pleural effusion. B. Diuretics to improve pulmonary edema. C. Nasogastric tube prevent abdominal distention. D. All of the above.

D. Interventions to improve compliance include: • Prevent abdominal distention. • Thoracentesis or chest tube for pleural effusion. • Diuretics for pulmonary edema. • Antibiotics for pneumonia

What is true regarding delirium in patients receiving mechanical ventilation: A. Sedative agents are more likely to exacerbate rather than treat hypoactive delirium. B. The treatment of hypoactive delirium is not fully understood. C. The more hypoactive form of delirium is more common in mechanically ventilated patients. D. All of the above.

D. It does appear that commonly used sedative agents are more likely to exacerbate rather than treat hypoactive delirium. The more hypoactive form of delirium is more common in mechanically ventilated patients. The response of hypoactive delirium to medications used to treat hyperactive delirium is not fully understood.

You are caring for patient presenting with shortness of breath and progressive chest pain who has just been diagnosed with a pulmonary embolus (PE). You vital sign assessment includes BP 82/60 mmHg, HR 117, and RR 22. Your patient has cool extremities. What do you know to be true: A. Intravenous fluids and inotropes if needed will correct your patient's hypotension. B. Your patient will benefit from insertion of an intra aortic balloon pump. C. Your patient's blood pressure will need to be monitored every 2 hours for the first 24 hours to assure it remains above 80 mmHg systolic. D. Your patient is experiencing a massive PE.

D. Patients with massive PE will present in shock. A PE is determined to be massive based on its impact on cardiac function, not by its location on an imaging study. This is important because it is cardiac function rather than anatomic location that is associated with adverse outcomes. However, the presence of central PE in a patient who is stable is a marker for increased risk of clinical decompensation and mortality. An intra aortic balloon pump in used to reduce afterload in left ventricular failure. A PE causes right ventricular failure. Intravenous fluids and inotropes will not be sufficient because a PE causes obstructive shock.

The most common physical exam finding in pulmonary embolus (PE) is: A. Hypoxemia. B. Cough. C. Hemoptysis. D. Tachypnea.

D. Physical exam findings vary greatly between massive and non-massive PE, and PE complicated by pulmonary infarction versus PE not complicated by pulmonary infarction. PE results in hyperventilation, and therefore; the most common physical sign, present in almost everyone with PE, is tachypnea (defined as respiratory rate > 16 per minute). Other physical signs include: • Dyspnea, rales, cough, hemoptysis • Accentuated 2nd heart sound, presence of right sided S3 or S4, new systolic murmur of tricuspid regurgitation • Tachycardia, low grade fever, diaphoresis • Signs of thrombophlebitis, lower extremity peripheral edema • Hypoxemia, cyanosis.

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.

Which of the following statements is accurate concerning SvO2 and SCvO2 monitoring:. A. They can both be obtained without the use of a pulmonary artery catheter. B. Only SvO2 can be used to evaluate the balance between O2 delivery and consumption. C. Normal SCvO2 is about 90% and normal SvO2 is 80%, but they trend together. D. Both are affected by cardiac output, arterial O2 saturation, Hgb, and O2 consumption by tissues.

D. SvO2 measures mixed venous oxygen saturation from the pulmonary artery and includes blood returning to the heart from the whole body. SCvO2 measures venous oxygen saturation of blood from the superior vena cava and only includes blood from the head and upper extremities. SvO2 is obtained from the distal port of a pulmonary artery catheter, but SCvO2 only requires a CVP catheter placed in the superior vena cava. They both reflect the balance between O2 delivery (determined by cardiac output, arterial O2 saturation, and Hgb) and O2 consumption by the tissues. The SCvO2 is normally slightly lower than the SvO2 but can be up to 7% higher than SvO2 in critically ill patients. However, the two values tend to trend together. Normal SCvO2 is about 70%, normal SvO2 is 60-80%

Pharmacological prophylaxis of deep vein thrombosis (DVT) in the acutely ill patient can be achieved by all of the following except: A. Low-molecular-weight heparin (LMWH). B. Low-dose unfractionated heparin BID or TID. C. Fondaparinux. D. Clopidogrel.

D. The American College of Chest Physicians makes the following recommendations: • For acutely ill hospitalized medical patients at increased risk of thrombosis, the following three pharmacological approaches are an option for prophylaxis: (a) low-molecular-weight heparin (LMWH), (b) low-dose unfractionated heparin BID or TID, or (c) fondaparinux. Fondaparinux is not recommended for prophylaxis in the critically ill patient. • For acutely ill hospitalized medical patients at low risk of thrombosis prophylaxis can be achieved by one of the above three pharmacological options or with mechanical prophylaxis. • For acutely ill hospitalized medical patients who are bleeding or who at high risk for bleeding, anticoagulant prophylaxis should not be used.

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 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.

Nursing care considerations when caring for a patient with a tracheostomy include: A. Clean disposable inner cannulas. B. Recognition that dislodgement is highest in tracheostomies that have been in place between 6 months and one year. C. Treat a new tracheostomy as a stage I pressure ulcer. D. Be prepared for complications by having the following readily available: ambu bag and mask, suction equipment, tube obturator, and intubation supplies.

D. The most common method of tracheostomy placement is with a percutaneous dilational technique using bronchoscopic guidance. Care of a tracheostomy includes: • Keep tube secure. Risk for dislodgement is high for first 3 to 5 days after insertion. • Keep the stoma clean and dry and assess for skin breakdown under and around the neck plate. Treat a new tracheostomy as a surgical wound. • Exchange (if disposable) or clean the inner cannula. Be prepared for complications by having the following readily available: ambu bag and mask, suction equipment, tube obturator, and intubation supplies.

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.

The nurse recognizes that when placing a patient on mechanical ventilation the following changes occur: A. Breathing changes from positive pressure to negative pressure and dead space increases. B. Breathing changes from positive pressure to negative pressure and dead space decreases. C. Breathing changes from negative pressure to positive pressure and dead space decreases. D. Breathing changes from negative pressure to positive pressure and dead space increases.

D. The normal process of breathing is negative pressure ventilation. Contraction of inspiratory muscles results in a lower intrathoracic pressure. This creates a distending pressure and the alveoli expand. With expansion the alveolar pressure is lowered and inspiration occurs. The result is negative pressure breathing. When a patient is placed on mechanical ventilation, negative pressure ventilation is replaced by the forced delivery of positive pressure breaths. Dead space is the term used to describe places where there is air, but where this air does not participate in gas exchange. All people have a normal amount of anatomical dead space. Our conducting airways comprise our anatomical dead space because there are no pulmonary capillaries present next to our conducting airways and therefore no gas exchange occurs. When a patient is intubated and mechanically ventilated, the additional tubing (although not anatomical) adds to the amount of dead space.

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.

What blood cell is the primary culprit in chronic obstructive pulmonary disease for releasing enzymes that are responsible for digesting elastin: A. Eosinophil. B. Platelet. C. Reticulocyte. D. Neutrophil.

D. The pathological changes in COPD are multifactorial. The most understood pathophysiological process involves neutrophil granulocytes (also called neutrophils). Neutrophils are the most abundant of the white blood cells (leukocytes). Cigarette smoke results in an influx of neutrophils. In COPD, increased numbers of neutrophils and macrophages release enzymes that are responsible for digesting elastin (elastases). The neutrophil elastase is the primary culprit although others are also involved. Neutrophil elastase is intended to destroy bacteria, but in COPD it is present in excess, and results in the destruction of elastin within the lung tissues. Elastin is a protein found in connective tissue. In COPD the body's antiproteases (substances that prevent the digestion of proteins) cannot counteract the increased number of digestive enzymes released from the neutrophils and macrophages.

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.

As a nurse providing patient education to a patient with chronic obstructive pulmonary disease (COPD)what do you know about the use of inhalers: A. Lack of instruction by a health care provider is often a reason for the improper use of an inhaler. B. Failure to use inhalation devices correctly results in increased emergency department visits and hospital admissions. C. Proper technique for use varies based on the type of inhaler device prescribed. D. All of the above.

D. There are several inhaled delivery options and correct inhaled technique is an important aspect in effective treatment. Failure to use inhalation devices correctly results in increased emergency department visits, hospital admissions, and increased use of corticosteroids and antibiotics. Factors associated with improper use of inhaled devices are (a) advanced age, (b) lower levels of education, and most significantly (c) lack of instruction by a health care provider. The choice of inhaler device is dependent on prescriber preferences and patient ability to use the device. Options and variation include dry powder inhalers, metered dose inhaler, breath activated devices and supplemental spacer devices.

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.

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 does not meet criteria for ARDS. B. This is mild ARDS. C. This is moderate ARDS. D. This is severe ARDS.

D. 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)

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.

Your patient is being mechanically ventilated in assist control mode of ventilation. The ventilator is using volume cycled breaths. What is true regarding this type of ventilator breath: A. This type of breath eliminates the ability of the patient to initiate a breath. B. This type of breath is used in pressure control ventilation. C. The tidal volume per breath will vary based on the compliance of the lungs. D. Each breath delivers a preset tidal volume.

D. Volume cycled breaths can be used in the assist control mode of ventilation or in the synchronized intermittent mandatory ventilation mode. With volume cycled breaths each breath is delivered at a preset tidal volume. Exhalation begins after the set volume has been delivered. Volume cycled breathing is used in volume controlled ventilation. With this volume cycles breathing the volume is controlled but the pressure required to deliver the volume varies based on the compliance of the lungs.

When assessing for train of four for the appropriate response in a patient receiving neuromuscular blockade what is the goal: A. Dose that results in 4 twitches (out of a possible 4) in response to peripheral nerve stimulation. B. Dose that results in 0 twitches (out of a possible 4) in response to peripheral nerve stimulation. C. Dose that results in 2 to 3 twitches (out of a possible 4) in response to peripheral nerve stimulation. D. Dose that results in 1 to 2 twitches (out of a possible 4) in response to peripheral nerve stimulation.

D. When monitoring train of four for appropriate amount of blockade, an adjustment of neuromuscular blockade should occur to achieve 1 to 2 twitches (out of a possible 4) in response to peripheral nerve stimulation. A commonly used muscle nerve combination is the ulnar nerve and adductor pollicus.

Clinical implications directly associated with chronic obstructive pulmonary disease (COPD) include the following except: A. Chronic hypoxemia leading to tissue hypoxia. B. Exertional dyspnea due to hyperinflation. C. Respiratory failure due to ventilation and perfusion mismatching. D. Left sided heart failure.

D. • Hyperinflation reduces inspiratory capacity and causes exertional dyspnea. • Ventilation and perfusion (V/Q) mismatching can result in oxygenation failure and hypercapnia. • Chronic hypoxemia produces tissue hypoxia. • Right-sided heart failure can occur as a complication of COPD. COPD results in increased pulmonary artery pressure and increased in pulmonary vascular resistance increasing the workload of the right heart. Right sided heart failure as a result of a primary pulmonary etiology is referred to as cor pulmonale.

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.

You are caring for a patient with a history of chronic obstructive pulmonary disease (COPD), chronic heart failure with reduced ejection fraction, and chronic anemia. The patient is admitted with sepsis. When planning nursing activities such as bathing, what are important considerations: A. The measurement of central venous oxygen saturation in this patient would not be valid due to his history of chronic heart failure. B. Nursing interventions such as bathing and turning will not have any impact in a patient with these medical conditions. However, in a patient with a head injury, nursing interventions can increase intracranial pressure. C. Patients with sepsis have a decrease in metabolic demand and oxygen needs which is a protective factor in patients with comorbid conditions. Nursing activities have a negligible impact on oxygen needs, and therefore there are no special considerations. D. Oxygen delivery is compromised due to the patient's chronic medical conditions; oxygen consumption is increased due to sepsis; oxygen reserve is at risk; nursing activities that increase oxygen consumption should be limited and spaced out with rest periods between during the acute illness.

D.Oxygen delivery is determined by cardiac output, hemoglobin, and oxygen saturation. The patient's chronic medical conditions have an impact on these three components of oxygen delivery. Fever, shivering, sepsis, and multi organ failure all increase oxygen consumption. When delivery is reduced and consumption is increased, the patient's reserve will fall. Nursing interventions such as suctioning, turning, and bathing all impact oxygen demand. Other things such as weights, venipuncture, portable chest x-rays, and non family persons in the room also increase oxygen consumption.

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.

Which of the following could be responsible for a low SvO2 in a critically ill patient: A. Cardiac disease causing a decrease in cardiac output. B. Trauma causing hemorrhage. C. Pulmonary disease causing hypoxemia. D. All of the above.

D.SvO2 is the O2 saturation of venous blood after the blood has circulated through the body and O2 has been extracted by the tissues. Normal SvO2 is 60-75%. A decrease in SvO2 can result from decreased O2 delivery to tissues due to decreased cardiac output from cardiac disease, decreased arterial O2 saturation due to pulmonary disease, or decreased HCT or Hgb due to excessive bleeding. A low SvO2 can also be due to an increase in O2 consumption by the tissues due to shivering, fever, agitation, increased work of breathing, or nursing care activities.

Which of the following is the best description of adaptive support ventilation: A. The ventilator will adjust the respiratory rate (mandatory breaths) to assure adequate minute ventilation. B. The goal is to limit the complications associated with high plateau pressures. C. The ventilator makes adjustments on a breath to breath basis. D. The ventilator can change modes from assist control to synchronized intermittent mandatory ventilation to pressure support. E. All of the above.

E. Adaptive support ventilation is a mode of ventilation that makes adjustments on a breath to breath basis. When a patient has no spontaneous breathing the ventilator uses an AC mode with pressure controlled breaths. When the patient is breathing spontaneously, but below target, the ventilator changes to a SIMV mode with pressure controlled breaths. If the patient is breathing spontaneously above target, the ventilator changes to the pressure support mode using flow cycled breathes. This mode of ventilation adapts to patient characteristics by increasing or decreasing support. The goal of adaptive support ventilation is to limit the complications associated with high plateau pressures. Therefore, a plateau pressure limit is set and tidal volume varies breath to breath. The ventilator will adjust the respiratory rate (mandatory breaths) to assure adequate minute ventilation. The pressure limits for both mandatory and spontaneous breaths are also capable of being adjusted to assure adequate minute ventilation. The ventilator also adjusts the inspiration to expiration ratio to prevent auto peep.

What are clinical signs of a severe exacerbation of chronic obstructive pulmonary disease (COPD): A. Altered mental status. B. Evidence of right sided heart failure. C. Paradoxical chest wall movement. D. Use of accessory muscles when breathing. E. All of the above.

E. Clinical Signs of Severe Exacerbation of COPD: ▪ Use of accessory muscles when breathing ▪ Paradoxical chest wall movement ▪ New or worsened central cyanosis ▪ Altered mental status ▪ Evidence of right sided heart failure

Which of the following is not considered an acceptable parameter for weaning a patient from the ventilator after an episode of acute respiratory failure: A. Minute ventilation: < 10 L. B. Rapid shallow breathing index (respiratory rate/tidal volume ): < 100 breaths/min/L. C. Tidal volume: > 5 ml/kg. D. Respiratory rate: < 30 per minute. E. Negative inspiratory force of at least -5 to -10 cm H2O.

E. Criteria for weaning from a ventilator: • Alert • Stable vital signs • Intact gag reflex • Arterial PaO2 > 60 mm Hg on FIO2 < 0.50 and PEEP of 0 to 5 cm of H20 • Ventilation status: - Respiratory rate: < 30 per minute - Tidal volume: > 5 ml/kg - Rapid shallow breathing index (respiratory rate/tidal volume ): < 100 breaths/min/L - Vital capacity: > 10 ml/kg, ideally 15 ml/kg - Minute ventilation: < 10 L - Negative inspiratory force of at least -25 to -30 cm H2O

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.

The following clinical features place your patient at risk for deep vein thrombosis (DVT) and pulmonary embolus(PE): A. Stroke. B. Heart failure. C. Chronic obstructive pulmonary disease (COPD). D. Smoking. E. All of the above.

E. In the Prospective Investigation of Pulmonary Embolism Diagnosis II study, 94% of the patients with PE had at least one of the following: • Immobilization • Travel of 4 hours or more in the past month • Surgery within the last 3 months • Malignancy, especially lung cancer • Current or past history of thrombophlebitis • Trauma to the lower extremities and pelvis during the past 3 months • Smoking • Central venous instrumentation within the past 3 months • Stroke, paresis, or paralysis • Prior pulmonary embolus • Heart failure • Chronic obstructive pulmonary disease

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.

The following ECG signs may be present in a patient presenting with pulmonary embolus (PE): A. S1, Q3, T3. B. Right atrial enlargement. C. Large R waves in V1 and V2. D. Right axis deviation. E. All of the above.

E. Only about 20% of patients with PE will have evidence of PE on the ECG, thus the absence of ECG signs cannot be used to rule out PE. ECG signs of PE are generally nonspecific. Patients may have sinus tachycardia or atrial fibrillation. There may also be small T wave inversions in both the limb and chest leads. An S wave in lead 1, a Q wave in lead III, and an inverted T wave in lead III (S1, Q3, T3) point to a PE in a patient in whom there is already a high level of suspicion. Patients may also have ECG signs of right ventricular hypertrophy as a result of pulmonary HTN associated with PE. Right axis deviation is often the first ECG sign of right ventricular hypertrophy. Other ECG signs include: • Large R waves in V1 and V2 • Deep S waves in leads V5 and V6 • Right atrial enlargement (tall P waves in lead II or dominant first ½ of P wave in V1) • Incomplete right bundle branch block (RBBB) • Delayed intrinsicoid deflection (measured from beginning of QRS complex to peak of R wave) in leads V1 and V2.

What benefits have been shown when pulmonary rehabilitation is a part of the treatment plan in patients with chronic obstructive pulmonary disease (COPD): A. Reduces hospitalizations. B. Reduces anxiety and depression. C. Enhanced effect of long term bronchodilators. D. Increased exercise capacity. E. All of the above.

E. Pulmonary rehabilitation supplements pharmacological therapy by addressing issues that are not directly impacted by medications. The minimum length of time for an effective rehabilitation program is 6 weeks, however, the longer the program the more benefit achieved. Pulmonary rehabilitation is a comprehensive program including: exercise training, nutritional support, education, assessment of functional status and dyspnea severity, and social support. Benefits of pulmonary rehabilitation include the following: • Improves perceived breathlessness and increases exercise capacity, • Enhances effect of long term bronchodilators • Reduces anxiety and depression and improves health-related quality of life • Reduces hospitalization and length of stay, enhances recovery after exacerbation, and improves survival.

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.

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

E. 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.

You are caring for a patient with a chest tube in place for treatment of a pneumothorax. What is true regarding the waterseal chamber: A. Lack of tidaling may indicate a kink. B. The main purpose of the water seal is to allow air to exit from the pleural space on exhalation and prevent air from entering the pleural cavity or mediastinum on inhalation. C. Continuous bubbling represents an air leak. D. The chamber may bubble gently during expiration. E. All of the above.

E. The 2nd compartment is connected to the 1st and creates a water seal. A small amount of sterile water (per manufacturer directions) is injected into the water seal chamber before the drainage system is connected to the patient. The main purpose of the water seal is to allow air to exit from the pleural space on exhalation and prevent air from entering the pleural cavity or mediastinum on inhalation. Air that is allowed to pass through the water seal will bubble out the bottom of the chamber. The water seal chamber is calibrated and should be seen as the window into the pleural space. During gravity drainage the level of water reflects the intrapleural pressure. Some newer systems eliminate the water seal chamber and use a check-valve to serve its purpose. Assure that the amount of sterile fluid in the water seal and suction chambers is at the manufacturer recommended levels when wet systems are used. To maintain an adequate water seal in a wet system it is important to monitor the level of water in the water seal chamber and to keep the chest drainage unit upright at all times. Assess for air leak by checking water seal chamber for bubbles during inspiration. The water seal chamber may bubble gently with insertion, during expiration and with a cough. Continuous bubbling represents an air leak. Some water seal compartments have an air leak meter. Check for system leaks by clamping before each connection (system may need to be replaced). Check for leak where tube enters chest. Check chest x-ray to assure last hole of chest tube is inside chest. Assess the water seal chamber for slight fluctuation. Slight fluctuation (tidaling) in the water seal level (rising during spontaneous inspiration and falling during expiration) is normal. Lack of fluctuation with respiration may indicate kinking or other problems interfering with drainage. A slow gradual rise in the water level is consistent with an increase in intrapleural pressure. This is a desired outcome as normal intrapleural pressure is restored and the lung re-expands.

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.

According to the attached image, what is true concerning the plateau pressure: Plateau is lower that PIP A. This is the pressure needed to keep alveoli distended. B. It is measured by holding inspiration after delivered tidal volume is complete. C. Decreasing tidal volume is a strategy to lower plateau pressure. D. The plateau pressure takes airway resistance out of the equation and is therefore used to reflect lung and chest wall compliance. E. All of the above.

E. The inspiratory plateau pressure is measured by holding inspiration after delivered tidal volume is complete. This measurement takes airway resistance out of the equation. The plateau pressure is reflective of the pressure in the alveoli at the end of inspiration. This is the pressure needed to keep alveoli distended (independent of resistance). The plateau pressure therefore reflects lung and chest wall compliance. Decreasing tidal volume is a strategy to lower plateau pressure. A lower tidal may cause an increase in PaCO2. Permissive hypercapnia (acceptance of increased PaCO2) may be indicated in order to reduce the plateau (and peak) airway pressure and protect the lung.

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).

The following is a potential etiology of hypotension in a patient receiving mechanical ventilation: A. Tension pneumothorax. B. Over sedation. C. Decreased preload. D. Auto PEEP. E. All of the above.

E. There are several reasons why a patient receiving mechanical ventilation may be hypotensive: 1) Sedation is used for intubation and for comfort while on mechanical ventilation. Hypotension may occur as a side effect of sedatives or over sedation. 2) Positive pressure ventilation and positive end expiratory pressure (PEEP) decrease venous return to the heart and will cause hypotension in any patient who does not have adequate circulating volume. 3) The development of auto peep can cause hypotension. Suspect this in patients with chronic obstructive lung disease who need a longer than normal expiratory time. 4) A tension pneumothorax should always be ruled out as a cause of hypotension because it is a form of obstructive shock. A pneumothorax results in a sudden increase in peak inspiratory pressure.

The critical care nurse knows the following is true regarding sedation and neuromuscular blockade in patients receiving mechanical ventilation: A. Neuromuscular blockade should seldom be needed in patients who receive adequate analgesia and sedation. B. Prior to determining if a patient needs neuromuscular blockade, it is imperative to assure the patient has adequate analgesia and sedation. C. Sedation is required before and throughout the administration of neuromuscular blockade. D. Sedation to achieve complete amnesia is required when neuromuscular blockade is utilized. E. All of the above.

E.Neuromuscular blockade is most typically not needed for mechanically ventilated patients. Prior to determining if a patient needs neuromuscular blockade, it is imperative to assure the patient has adequate analgesia and sedation. If neuromuscular blockade is needed, sedation is required before and throughout administration. Sedation to achieve complete amnesia is required when neuromuscular blockade is utilized.

When providing care to a patient who is on mechanical ventilation what principles guide your decision making regarding sedation and analgesia: A. Acetaminophen or non-steroidal anti-inflammatory agents (unless contraindicated) are helpful as adjunctive therapy to opioids. B. There are two validated tools for assessing pain in the critically ill patient who cannot verbalize. These tools are the (a) Behavioral Pain Scale and (b) Critical Care Observation Tool. C. Analgesia should always be a priority because pain may manifest as anxiety and agitation and result in delirium. D. The respiratory depressive effects of opiates are helpful in the mechanically ventilated patient to treat dyspnea, coughing, and ventilator dyssynchrony. E. All of the above.

E.Pain is commonly experienced in the mechanically ventilated patient. Analgesia should always be a priority because pain may manifest as anxiety and agitation and also interfere with adequate sleep. Untreated pain in the mechanically ventilated patient increases the risk for delirium in a patient population already at high risk. Sedative medications alone will not be effective at treating pain. Additionally, pain evokes a stress response that results in several adverse physiological effects including increased myocardial oxygen consumption and promotion of a more hypercoagulable state. Relief of pain is important for physiological homeostasis as well as for patient comfort. Pain and sedation level should be assessed together in the mechanically ventilated patient. The most valid and reliable indicator of pain is the patient's self-reporting of their perception of pain. The numeric rating scale (1-10) is the recommended tool to use in the assessment of pain in the mechanically ventilated patient who is alert and able to participate in the assessment process. If self-report is not an option then subjective observation of pain behaviors (facial expression, movement, etc.) and measurement of physiological parameters (blood pressure, heart rate, and respiratory rate) should be used as part of the pain assessment , although these indices are not always reliable. There are two validated tools for assessing pain in the critically ill patient who cannot verbalize. These tools are the (a) Behavioral Pain Scale and (b) Critical Care Observation Tool. They have been validated in the non-traumatic brain injured patient. Opiates are the most common medications used for analgesia in mechanically ventilated patients. Scheduled opioid doses or a continuous infusion is preferred over as needed dosing in order to assure consistent analgesia. The respiratory depressive effects of opiates are helpful in the mechanically ventilated patient to treat dyspnea, coughing, and ventilator dyssynchrony. Opiates typically do not have hemodynamic effects in patients who are not hypovolemic. Acetaminophen or non-steroidal anti-inflammatory agents (unless contraindicated) are helpful as adjunctive therapy to opioids. Preventing pain is more effective than treating pain and thus providers need to anticipate and treat for any aspects of therapy that cause pain.

Combing bronchodilators with different mechanisms of action and different durations is contraindicated: False True

False Combing bronchodilators with different mechanisms of action and different durations increases the effectiveness of bronchodilation.