NRNP 6566 FINAL EXAM STUDY GUID, Study notes of Nursing

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Final Exam-Study Guide

Week 6 and 7

1. Interpret arterial blood gases (ABG). Differentiate alkalosis/ acidosis and respiratory / metabolic

2. Identify a ventilation – perfusion mismatch and how to treat it If there is a mismatch between the alveolar ventilation and the alveolar blood flow, this will be seen in the V/Q ratio. If the V/Q ratio reduces due to inadequate ventilation, gas exchange within the affected alveoli will be impaired. As a result, the capillary partial pressure of oxygen (pO2) falls and the partial pressure of carbon dioxide (pCO2) rises. To manage this, hypoxic vasoconstriction causes blood to be diverted to better ventilated parts of the lung. However, in most physiological states the hemoglobin in these well-ventilated alveolar capillaries will already be saturated. This means that red cells will be unable to bind additional oxygen to increase the pO2. As a result, the pO2 level of the blood

remains low, which acts as a stimulus to cause hyperventilation, resulting in either normal or low CO2 levels. A mismatch in ventilation and perfusion can arise due to either reduced ventilation of part of the lung or reduced perfusion. Ventilation/perfusion mismatch — Mechanical ventilation can alter two opposing forms of ventilation/perfusion mismatch (V/Q mismatch), dead space (areas that are overventilated relative to perfusion; V>Q) and shunt (areas that are underventilated relative to perfusion; V<Q). By increasing ventilation (V), the institution of positive pressure ventilation will worsen dead space but improve shunt. Increased dead space — Dead space reflects the surface area within the lung that is not involved in gas exchange. It is the sum of the anatomic plus alveolar dead space. Alveolar dead space (also known as physiologic dead space) consists of alveoli that are not involved in gas exchange due to insufficient perfusion (ie, overventilated relative to perfusion). Positive pressure ventilation tends to increase alveolar dead space by increasing ventilation in alveoli that do not have a corresponding increase in perfusion, thereby worsening V/Q mismatch and hypercapnia. Reduced shunt — An intraparenchymal shunt exists where there is blood flow through pulmonary parenchyma that is not involved in gas exchange because of insufficient alveolar ventilation. Patients with respiratory failure frequently have increased intraparenchymal shunting due to areas of focal atelectasis that continue to be perfused (ie, regions that are underventilated relative to perfusion). Treating atelectasis with positive pressure ventilation can reduce intraparenchymal shunting by improving alveolar ventilation, thereby improving V/Q matching and oxygenation. This is particularly true if PEEP is added. (See "Positive end-expiratory pressure (PEEP)" and"Measures of oxygenation and mechanisms of hypoxemia", section on 'V/Q mismatch'.)

3. Be able to calculate an Aa gradient. Be able to interpret an Aa gradient. The alveolar to arterial (A-a) oxygen gradient is a common measure of oxygenation ("A" denotes alveolar and "a" denotes arterial oxygenation). It is the difference between the amount of the oxygen in the alveoli (ie, the alveolar oxygen tension [PAO 2 ]) and the amount of oxygen dissolved in the plasma (PaO 2 ): A-a oxygen gradient = PAO 2 - PaO 2 PaO 2 is measured by arterial blood gas, while PAO 2 is calculated using the alveolar gas equation: PAO 2 = (FiO 2 x [Patm - PH 2 O]) - (PaC O 2 ÷ R)

where FiO 2 is the fraction of inspired oxygen (0.21 at room air), Patm is the atmospheric pressure (760 mmHg at sea level), PH 2 O is the partial pressure of water (47 mmHg at 37ºC), PaCO 2 is the arterial carbon dioxide tension, and R is the respiratory quotient. The respiratory quotient is approximately 0.8 at steady state, but varies according to the relative utilization of carbohydrate, protein, and fat. The A-a gradient calculated using this alveolar gas equation may deviate from the true gradient by up to 10 mmHg. This reflects the equation's simplification from the more rigorous full calculation and the imprecision of several independent variables (eg, FiO 2 and R). The normal A-a gradient varies with age and can be estimated from the following equation, assuming the patient is breathing room air: A-a gradient = 2.5 + 0.21 x age in years The A-a gradient increases with higher FiO 2. When a patient receives a high FiO 2 , both P AO 2 and PaO 2 increase. However, the PAO 2 increases disproportionately, causing the A-a gradient to increase. In one series, the A-a gradient in men breathing air and 100 percent oxygen varied from 8 to 82 mmHg in patients younger than 40 years of age and from 3 to 120 mmHg in patients older than 40 years of age [ 5 ]. Proper determinations of the A-a gradient require exact measurement of FiO 2 such as when patients are breathing room air or are receiving mechanical ventilation. The FiO 2 of patients receiving supplemental oxygen by nasal cannula or mask can be estimated and the A-a gradient approximated but large variations may exist and the A-a gradient may substantially vary from the predicted, limiting its usefulness. The use of a 100 percent non-rebreathing mask reasonably approximates actual delivery of 100 percent oxygen and can be used to measure shunt. Why use the Aa gradient:  The A-a Gradient can help determine the cause of hypoxia; it pinpoints the location of the hypoxia as intra- or extra- pulmonary. When to use the Aa gradient:  Patients with unexplained hypoxia.  Patients with hypoxia exceeding the degree of their clinical illness.

4. Identify clinical symptoms or conditions indicating a need to intubate and ventilate a patient Neuromuscular depression or failure A. Drugs Opiods Sedatives NM Blockers B. Trauma Spinal Cord injury Phrenic nerve injury C. Disease Guillain Barre syndrome

Amyotrophic Lateral Sclerosis Myasthenia Gravis Shock D. Exhaustion Status asthmaticus Sustained severe work of breathing E. Sustained apnea of any cause Persistent hypoxia (partial pressure of oxygen in arterial blood PaO less than 60mmHg and/or hypercarbia (partial pressure of carbon dioxide in arterial blood PaCO2 greater that 50mmHg refractory to noninvasive supplemental O2 and/or airway maintenance (suctioning and position) A. Diffusion defects Aspiration Pulmonary edema ARDS COPD Pneumonia B. Ventilation defects COPD Pickwickian syndrome Flail chest Pneumothorax Atelectasis C. Perfusion defects Shock PE Malignant arrhythmias

5. Identify clinical signs and symptoms indicating a patient is ready for weaning and extubation. At what point do you start considering whether your patient is ready to come off the ventilator? There are several conditions that should be satisfied before you can consider separating your patient from the ventilator. First, the underlying process that put them on the ventilator should be better or improving. Second, the patient should be able to maintain adequate oxygenation on minimal support (eg. PaO2 > 80 mm Hg on an FIO2 of 0.5 and PEEP < 8. cm H2O). Finally, the patient should be able to maintain an adequate acid- base balance without requiring high levels of minute ventilation (> liters/minute) in order to do so. If higher levels of minute ventilation are required, the ventilatory demands on the patient may be high and they are at risk for tiring out once off they are taken off the ventilator.

How do you determine if the patient is capable of being separated from the ventilator? In the past, clinicians used to look at several different variables, referred to as “weaning parameters” in an effort to assess readiness for separation from the ventilator. For example, if a patient’s vital capacity was > 10 ml/kg, then the patient was likely to tolerate being off the ventilator. None of the different parameters that were used had perfect predictive ability and this approach has since been supplanted by a different strategy utilizing a trial of spontaneous breathing. If patients meet certain criteria on the respiratory therapist’s morning rounds, they are placed on CPAP, t- piece or a low level of pressure support and are monitored for a period of 30-120 minutes while they breathe on their own. An arterial blood gas is usually drawn at the end of this period. A successful trial is one in which the patient looks comfortable, maintains a good respiratory rate (< 25 breaths/minute), takes in sufficient tidal volumes (> 5 ml/kg) and maintains stable vital signs including heart rate, blood pressure and SaO2. The arterial blood gas should also show relatively stable oxygenation and no evidence of increasing PaCO2. Patients can fail the trial for a variety of different reasons including vital sign instability, worsening oxygenation, hypercarbia or other signs of insufficient ventilatory capacity. Patients who pass their trial of spontaneous breathing are deemed ready to be separated from the ventilator. Suppose your patient demonstrates that she can be separated from the ventilator. Should she be extubated? When a patient passes a spontaneous breathing trial, they are ready to be separated from the ventilator. In other words, they no longer need the ventilatory or oxygen support of the machine at their bedside. It is important to remember, however, that the decision to separate a patient from the ventilator is distinct from the decision to remove the endotracheal tube. Some patients can be separated from the ventilator but still require an endotracheal tube. In order to qualify for extubation, patients should be free of upper airway problems, should be able to protect against aspiration of gastric or oral contents and should be able to cough and clear secretions without a need for frequent suctioning. In this case, the patient has a weak cough and copious secretions, problems that would lead you to predict that she might decompensate if extubated. As a result, the endotracheal tube should remain in place until these issues resolve.

6. Prescribe ventilator settings for newly intubated patient. The respiratory therapist suggests you use the volume-targeted Assist Control (AC) mode of mechanical ventilation. How does this work? How does it differ from Synchronized Intermittent Mandatory Ventilation (SIMV) or Pressure Control (PC)? Which mode is better for your patient?

In Assist Control (AC) ventilation, the clinician determines the tidal volume and the respiratory rate for the patient. The machine guarantees that the patient will receive the set number of breaths at the desired tidal volume each minute. Patients can also initiate their own breaths (i.e. take breaths above the rate set on the ventilator by the clinician); patient-initiated breaths are delivered at the full tidal volume that has been set on the machine. In SIMV, the clinician also sets the rate and tidal volume and the machine guarantees the patient will receive the set number of breaths at the desired tidal volume each minute. Patients can also initiate their own breaths, but on the extra breaths in SIMV, the patient only gets as much tidal volume as they are capable of taking in on their own; the ventilator does not guarantee a set tidal volume for these breaths. Weak patients may draw small tidal volumes on these extra breaths while strong patients may take in larger tidal volumes. Pressure control ventilation is quite different than either volume targeted AC or SIMV. In this mode, the clinician sets the peak inflation pressure and respiratory rate but does not specify the tidal volume. Instead, the tidal volume received by the patient varies based on the compliance of the respiratory system and the level of airway resistance. If a patient, for example, has a very compliant respiratory system (emphysema), they will receive a large tidal volume for a set pressure whereas a patient with low respiratory system compliance (ARDS) will only receive a small tidal volume. At present, there is no evidence that a particular mode of mechanical ventilation is associated with a mortality benefit compared to the other modes. Evidence exists for improvements in short-term physiologic variables with one mode compared to another (which is largely a function of how the comparison is set up), but there are no solid data to support a preference for one mode over another. This is a subject of intense debate and the choice of mode tends to be very physician-, respiratory therapist-, and institution- dependent. In the University of Washington system, the pulmonary and critical care physicians tend to ventilate most of our patients using volume- targeted Assist Control mode and to use pressure control ventilation only in situations in which the patient has a very poor response to standard measures. Suppose you put the patient on a volume-targeted Assist Control mode of mechanical ventilation. How do you choose the tidal volume? The tidal volume is chosen based on the patient’s weight. It is critical, however, to make sure you use the correct weight in the calculations. The size of the lungs is largely a function of a person’s height. Therefore, rather than using the patient’s actual weight to determine the tidal volume, you should, instead, use the patient’s ideal body weight, the value of which is derived from the patient’s height. To calculate the ideal body weight in kilograms, you can use the following formulas: Men: [(height in inches – 60) X 2.2] + 50

Women: [(height in inches – 60) X 2.2] + 45 Failure to use the correct weight can lead to disastrous consequences for the patient. If you were to put a 150 kg person on a tidal volume of 10 ml/kg of their actual body weight, you would end up delivering tidal volumes of 1.5L and, as a result, would significantly increase the risk of barotrauma and ventilator-induced lung injury. Once you know the ideal body weight, you can choose the tidal volume for the patient. The majority of patients are placed on a tidal volume corresponding to 8- 10 ml/kg of their ideal body weight. In order to decrease the risk of air-trapping and barotrauma, patients intubated for COPD or asthma exacerbations are often placed on 6-8 ml/kg of their ideal body weight. Patients who develop ARDS are placed on 4-6 ml/kg of their ideal body weight but are not typically started at these low levels. Instead, they are started on 8-10 ml/kg and the tidal volume is gradually decreased over a period of time. Finally, many ventilator-dependent patients with spinal cord injuries are maintained on higher tidal volumes ranging from 12 ml/kg to as high as 20 ml/kg of their ideal body weight. Proponents of this practice argue that it improves patient comfort and prevents mucous plugging and atelectasis which predispose to pulmonary complications in this patient population. The data supporting this practice is actually quite limited and there is considerable debate as to the safety and efficacy of such high tidal volumes in these patients. The patient in this case is 6-foot tall (72 inches). Using the formula above, his ideal body weight is about 76kg. Therefore, you would place him on a tidal volume between 600 and 750 ml, which corresponds to between 8 and 10 ml/kg. What respiratory rate should you choose for the patient? Contrary to the popular, but erroneous, practice of choosing the ubiquitous respiratory rate of “12” because “that is what I’ve always seen other people do,” the respiratory rate should be selected based on an assessment of the patient’s minute ventilation requirements. For example, a patient with a normal bicarbonate of 24 who was intubated for a procedure may only need 6-8 liters/minute of ventilation whereas a patient in severe sepsis with a bicarbonate of 10 may require upwards of 20- liters/minute of ventilation to maintain an adequate acid-base status. Once you derive an estimate of the minute ventilation (VE ) needs of the patient, you can use your previously determined tidal volume and simple division to calculate an appropriate respiratory rate (RR = VE/tidal volume) This practice is particularly important in the period immediately following intubation. Most patients receive paralytic agents for intubation and, as a result, have no ability to mount respiratory efforts for 15 to 60 minutes following the procedure. They are dependent on you to choose the correct rate and give them an adequate amount of minute ventilation. Failure to do so will lead to increasing respiratory acidosis and worsening pH. As the paralytic agent wears off and sedative needs decrease, the patients will often set the respiratory rate on their own to match their minute ventilation needs.

What should the FIO2 and PEEP be set at? In the majority of cases patients are initially placed on an FIO2 of 1.0 and a PEEP of 5 cm H2O.If the initial ABG drawn 30 to 60 minutes after intubation reveals an adequate PaO2 (above 65 mm Hg) the FIO2 can be turned down to a lower level. Further adjustments are made in the FIO2 based on the patient’s oxygen saturation and blood gases are not necessary for every change in this parameter. It is not uncommon to hear comments about maintaining patients on too high an inspired oxygen concentration for too long a period, as there is concern about provoking oxygen toxicity in the lungs. This concern is largely based on the results of laboratory studies in animal and normal human volunteers and concrete evidence of its occurrence in critically ill ICU patients is lacking. If a patient requires a high FIO2 in order to maintain adequate oxygenation then they should receive those high levels for as long as necessary. The PEEP is typically not decreased below 5 cm H2O but can be increased as necessary (up to 15 to 20 cm H20) to support oxygenation in patients with severe hypoxemia (discussed further below). It tends to be a more effective tool in diffuse, rather than focal, lung processes such as ARDS.

7. Describe static and plateau pressures on a ventilator Measurement of peak pressures and plateau pressures may be helpful in identifying the location of resistance, especially if graphical representation of airway pressures is available. Peak pressure is a measure of airway resistance and compliance including the tubing and bronchial tree. Plateau pressure is thought to reflect alveolar pressure and pulmonary compliance and can be measured by applying a brief inspiratory pause after ventilation. High peak pressure with normal plateau pressures indicates increased resistance to flow, such as endotracheal tube obstruction or bronchospasm. An increase in both peak and plateau pressures suggest decreased lung compliance, which may be seen in disease states such as pneumonia, ARDS, pulmonary edema, and abdominal distention. What do “static” pressures represent on the ventilator? The static or “plateau” pressure is representative of the compliance of the respiratory system (lung, chest wall and abdomen). In essence, it is telling you how much pressure is necessary to inflate the alveoli with each breath. Any problem which causes a fall in the compliance of the respiratory system will cause static pressures to rise. Examples of such problems include the onset of ARDS or pulmonary edema, large pleural effusions, pneumothorax, abdominal distention, or circumferential chest wall burns. The ventilator does not display this pressure with every breath. Instead, you must use an inspiratory pause maneuver to see this value. Plateau pressure is the static pressure achieved at the end of a full inspiration. To measure plateau pressure, we need to perform an inspiratory hold on the ventilator to permit for the pressure to equalize through the system. Plateau pressure is a measure of alveolar pressure and

lung compliance. Normal plateau pressure is below 30 cm H20, and higher pressure can generate barotrauma What do “peak” pressures represent on the ventilator? The peak pressure is representative of the resistance in the system from the ventilator tubing all the way down to the segmental bronchi. Anything that affects the resistance of these tubes (mucous plugging, bronchospasm, blood clots, and kinked endotracheal tube) will cause the peak pressure to rise. The machine displays the peak pressure with every breath. It is important to know that, while some of the same factors contribute to both peak and static airway pressures, a number of things that affect peak pressure are external to the patient and do not necessarily reflect a change in the compliance of the patient’s lung. Peak pressure is the pressure achieved during inspiration when the air is being pushed into the lungs and is a measure of airway resistance. Elevated peak pressure – do inspiratory hold and check plateau pressure.  If elevated peak pressure and normal plateau pressure = airway resistance and normal compliance. Causes: kinked ETT, mucus plug, bronchospasm  If both peak and plateau are elevated causes: mainstem intubation (unilateral breath sounds), pneumothorax (needs CT placement), atelectasis (percussion and recruitment), pulmonary edema (diuresis, inotropes, high PEEP), and ARDS (low TV and high PEEP).

8. Be able to adjust ventilator settings based on the patient’s condition and ABG results.  An ABG Is written or expressed by pH/pCO2/pO2/HCO 3  Normal ABG o pH 7.35-7. o pCO2 35- o pO2 80-100 mmHg o SaO2 95-100% o HCO3 22-  Vent adjustments can include the FiO2, RR, TV by decreasing or increasing to rectify acid-base imbalance