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The Role of Chest Radiography in the Critical Care Unit
3
77
atelectasis is the volume loss secondary to pulmonary brosis and can be seen in
patients with underlying pulmonary disease or as a complication of ARDS.
On CT, atelectasis can often be identied by signs of volume loss. On contrastenhanced CT, atelectasis results in relatively high attenuation of lung parenchyma,
a useful feature distinguishing it from relatively lower attenuating consolidative
processes such as pneumonia.
3.3.4 Aspiration
Intubation, diminished cough reex, sedation, and enteric tube feeds increase aspiration risk. Aspiration can occur in mechanically ventilated patients despite adequate ination of the endotracheal tube cuff. Clinically, aspiration events may go
unnoticed or may be severe, causing respiratory distress. Aspiration can result in
airway obstruction, chemical pneumonitis, or infectious pneumonia, depending on
the volume and type of aspirate. Small amounts of aspirated saliva may result in no
radiographic abnormality, whereas aspiration of large amounts of food substance
increases the likelihood of aspiration pneumonia.
Patchy, ill-dened ground-glass, consolidative, and nodular opacities are the
most frequently encountered radiographic manifestations of aspiration (Fig.3.12).
Opacities typically appear rapidly and are mostly located in the dependent regions
of the lungs: the posterior segment of the upper lobes and the superior and posterior
basal segments of the lower lobes. Opacities may increase in conspicuity over the
rst 1–2 days in aspiration pneumonitis but should resolve rapidly afterward.
Aspiration pneumonia is likely present when opacities persist or increase over several days.
Fig. 3.13 Right basal lung
inhomogeneous
consolidation in keeping
with pneumonia
(Acinetobacter)
78
Fig. 3.14 Bilateral
airspace consolidations
F. Macori
Patchy, dependent ground-glass and consolidative opacities are also seen on CT
“tree-in-bud” opacities that result from inammation of the distal airways. Although
tree-in-bud opacities are nonspecic, when present in a dependent distribution, they
are highly suggestive of aspiration.
3.3.5 Pneumonia
Pneumonia is another cause of pulmonary opacities in ICU patients. Aspiration and
mechanical ventilation are two important risk factors for pneumonia in the ICU
population. Ventilator-associated pneumonia occurs in 9–24% of patients ventilated
for more than 48h. Most pneumonias are caused by mixed anaerobic or, more frequently in the ventilated patient, aerobic gram-negative bacteria such as
Pseudomonas aeruginosa.
Pneumonia may present as a focal consolidation on the chest radiograph
(Fig.3.13); however, it is often multifocal (Fig.3.14). Pneumonia can be difcult to
differentiate from other causes of pulmonary opacities such as atelectasis, aspiration, and pulmonary edema. Typically, pneumonia changes more slowly than these
other entities. In addition, air bronchograms may be seen and differentiated from
those seen in atelectasis by noting the absence of volume loss and crowding of
bronchi.
When ARDS is present, the diagnostic accuracy of CT and chest radiography is
diminished [3, 4]. The presence of underlying consolidation in ARDS limits the
ability to exclude the presence of pneumonia. The incidence of pneumonia in
patients who have diffuse lung injury at autopsy has been reported to be 58%.
ab
The Role of Chest Radiography in the Critical Care Unit
3
Fig. 3.15 Large rightsided pneumothorax with
collapsed lung. No
mediastinal shift. Case
courtesy Prof. Frank
Gaillard—Radiopaedia
rID: 33269
79
Fig. 3.16 Right basal hydropneumothorax (a) conrmed by the CT (b)
3.3.6 Pneumothorax, Pneumomediastinum, andPleural Fluid
Pleural space abnormalities are common in the ICU and can include pneumothorax
and pleural uid. Pneumomediastinum is less common but important to recognize
as it can indicate underlying tracheobronchial injury or alveolar rupture in a
mechanically ventilated patient.
Pneumothorax can be caused by underlying pulmonary disease, trauma, or iatrogenesis. The classic sign of a thin, dense curvilinear pleural line, bordered by lung
on one side and pleural air on the other, may be absent in supine ICU patients.
80
ab
Fig. 3.17 Extensive pneumomediastinum extending into the neck and outlining the pericardium
(a) conrmed by the CT (b). Right internal jugular central venous catheter and a nasogastric
tube in situ
Detection requires a high degree of suspicion. A small pneumothorax can rapidly
progress to tension in a ventilated patient, making recognition critical.
In the supine patient, pleural air initially accumulates in the anteromedial recess,
which is the least dependent location in the hemithorax. Abnormal lucency at the
lung base or projecting over the upper abdomen suggests pneumothorax. A lucent
deep sulcus may be visualized in the medial or lateral hemithorax. In addition,
mediastinum may be unusually well outlined. The lateral decubitus position is the
most sensitive for detecting pleural air but is often impractical. When pneumothorax
is suspected, an upright radiograph should be obtained for conrmation (Fig.3.15).
Tension pneumothorax occurs when intrathoracic pressure is greater than atmospheric pressure. Radiographically, tension pneumothorax is most reliably diagnosed by inversion or attening of the hemidiaphragm. Mediastinal shift may also
be seen but is less reliable and frequently less pronounced in patients with acute
respiratory distress syndrome (ARDS) due to reduced lung compliance.
Skin folds can mimic pneumothoraces, so important distinguishing features
should be recognized. A skin fold is seen as a soft tissue-air interface, with radioopacity on one side and normal lung on the other. In pneumothorax, a pleural line is
often bordered by air on both sides: normal lung and pleural air. The diagnosis may
be more complex when the lung is abnormally opaque, creating the illusion of a soft
tissue-air interface. The opacity is a skin fold if pulmonary vessels extend peripheral
to the interface. If no pulmonary vessels are seen peripherally, then a pneumothorax
is present (Fig.3.16).
Pneumomediastinum is extraluminal air within the mediastinum (Fig.3.17). It
can be seen in tracheobronchial injury, tracheostomy tube placement, mechanically
ventilated patients, asthmatics, and esophageal rupture (although this is a rare
cause). Pulmonary interstitial emphysema in the mechanically ventilated patient is
F. Macori
T
3
he Role of Chest Radiography in the Critical Care Unit
81
a sign of alveolar rupture. Air may dissect the cephalad to the subcutaneous tissues
of the neck and the caudad to the retroperitoneum.
Pleural uid is common in ICU patients and is most frequently transudative. The
supine radiograph is relatively insensitive in detecting pleural uid and often underestimates the amount of pleural uid. On the upright lateral radiograph, blunting of
the costophrenic angle usually occurs when 200mL of uid is present but may be
absent with as much as 500mL.Layering pleural uid is more difcult to detect on
the supine radiograph. The costophrenic angle is often not blunted, and the supine
radiograph may only demonstrate hazy “veil-like” opacication due to layering
pleural uid. The apex is the most dependent location in the supine patient, and
pleural effusion may manifest as an apical cap.
Consolidation, atelectasis, and pleural uid cause opacities on the chest radiograph and frequently coexist, particularly at the thoracic base. CT is useful in differentiating pleural uid from pulmonary parenchymal disease and better
characterizing loculated pleural uid collections. Empyema is suggested when
pleural uid is bordered by enhancing, thick pleura. Hemothorax is suggested by
relatively high-attenuation pleural uid, commonly 35–70 Hounseld units.
References
1. https://www.acr.org/- /media/ACR/Files/Practice- Parameters/Port- Chest- Rad.pdf.
2. Henry TS, Mellnick VM.Multisystem imaging of the critically ill patient. Radiol Clin North
Am. 2020;58(1):xiii. https://doi.org/10.1016/j.rcl.2019.10.001.
Henschk
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Imaging. 1997;21(2):90–103. https://doi.org/10.1016/0899- 7071(95)00097- 6.
Hill JR, Horner PE, Primack SL.
org/10.1016/j.ccm.2007.11.005.
Godo
y MC, Leitman BS, de Groot PM, Vlahos I, Naidich DP.Chest radiography in the ICU:
part 1, evaluation of airway, enteric, and pleural tubes. Am J Roentgenol. 2012;198(3):563–71.
https://doi.org/10.2214/ajr.10.7226.
Godo
y MC, Leitman BS, de Groot PM, Vlahos I, Naidich DP.Chest radiography in the ICU: part
2, evaluation of cardiovascular lines and other devices. Am J Roentgenol. 2012;198(3):572–81.
https://doi.org/10.2214/ajr.11.8124.
Glueck
er T, Capasso P, Schnyder P, Gudinchet F, Schaller MD, Revelly JP, etal. Clinical and
radiologic features of pulmonary edema. Radiographics. 1999;19(6):1507–31.
ICU imaging. Clin Chest Med. 2008;29(1):59–76. https://doi.
Part II
Pulmonary Critical Care
Chapter 4
The Basics ofMechanical Ventilation
TylerPeck andRichardM.Schwartzstein
4.1 Introduction
One of the most frequently used lifesaving interventions for critically ill patients is
mechanical ventilation—the use of a machine that pumps gas, using positive pressure, into the lungs to ensure adequate exchange of oxygen and carbon dioxide to
sustain life. Scenarios necessitating the use of mechanical ventilation include severe
life-threatening respiratory failure due to respiratory system disease (e.g., pulmonary pathologies like pneumonia and acute asthma exacerbation, or neuromuscular
diseases like Guillain-Barré syndrome and myasthenic crisis), protection of the airway from aspiration and adequate ventilation in patients with impaired consciousness, and maintenance of respiratory function during and after sedation–anesthesia
used for surgery. The safe and effective use of mechanical ventilation requires collaboration of the entire intensive care unit (ICU) team, including critical care
pharmacists.
While initial forms of mechanical ventilation included negative-pressure ventila-
tion with devices such as the iron lung used widely during the polio epidemic of the
1950s, positive-pressure ventilation is the primary method of mechanical ventilation today. Positive-pressure ventilation can be delivered noninvasively via mask,
nasal prongs, or helmet into the patient’s upper airway (commonly referred to as
noninvasive positive-pressure ventilation [NIPPV]) or invasively via laryngeal mask
airway, endotracheal tube, or tracheostomy into the patient’s lower airway. While
NIPPV is an important critical care modality, this chapter focuses on invasive
mechanical ventilation. Modern ventilators are complex computers that allow users
to set a wide array of variables related to ventilation and provide advanced monitoring of patient physiology and patient-ventilator interactions.
T. Peck · R. M. Schwartzstein (*)
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
e-mail: rschwart@bidmc.harvard.edu
Switzerland AG 2025
Y. Alzaidi, M. A. Gebily (eds.), The Pharmacist’s Expanded Role in Critical
Care Medicine, https://doi.org/10.1007/978-3-031-77335-8_4
85© The Author(s), under exclusive license to Springer Nature
86
During the use of mechanical ventilation, pharmacists ensure appropriate sup-
port by recommending effective pharmacotherapy, particularly sedation and analgesia, reviewing medication regimens for efcacy and safety, and identifying potential
medication adverse effects and interactions. This chapter serves to provide an overview of mechanical ventilation relevant to the critical care pharmacist, encompassing indications for its use, basic terminology and physiology, role of pharmacotherapy,
common ventilator modes and settings, pathways forward after initiation of mechanical ventilation, and examples of common disease states in which mechanical ventilation is used.
T. Peck and R. M. Schwartzstein
4.2 Physiology ofRespiration andMechanical Ventilation
The physiology of respiration in mechanically ventilated patients is decidedly different from that of spontaneously breathing patients. Spontaneous breathing relies
on the coordinated contraction and relaxation of respiratory muscles, primarily the
diaphragm. During inhalation, the diaphragm contracts and lowers, expanding the
chest cavity and lowering intrathoracic pressure. This pressure change creates a gradient, drawing air into the lungs. Conversely, exhalation is a passive process driven
by the natural recoil of the lungs and chest wall. Gas exchange occurs by diffusion
across the alveolar-capillary membrane in the lungs, where oxygen crosses from
alveoli into the bloodstream, while carbon dioxide moves in the opposite direction.
Mechanical ventilation disrupts this natural physiology. In mechanically venti-
lated patients, an external device (ventilator) takes over the work of breathing. The
ventilator delivers pressurized gas directly into the airways, bypassing the upper
airway and relying on an endotracheal tube or tracheostomy for gas delivery into the
lower airways. Positive pressure is maintained throughout the respiratory cycle
(although may return to zero during expiration in some patients) and is the hallmark
of mechanical ventilation. This positive pressure inates the lungs, replacing the role
of the diaphragm during inhalation. While gas exchange continues to occur passively across the alveolar-capillary membrane, the entire respiratory process becomes
dependent on the ventilator settings and proper functioning of the ventilator circuit.
This shift from spontaneous to mechanical ventilation necessitates close moni-
toring and careful adjustments to ensure adequate gas exchange and prevent
complications.
4.3 Indications forMechanical Ventilation
The initiation of mechanical ventilation is warranted for critically ill patients who
are unable to maintain adequate ventilation and gas exchange on their own. This
inability to maintain respiratory function can be due to various reasons, each of
which is an indication for the use of mechanical ventilation.
4 The Basics ofMechanical Ventilation
87
• Acute hypoxemic respiratory failure—Hypoxemia is a state of abnormally low
blood oxygen levels which, in severe cases, can threaten life because of
inadequate oxygen supply to tissues to allow cellular respiration and function.
The causes of hypoxemia are impaired diffusion capacity (difculty in oxygen
moving from the alveolar compartment into the bloodstream; of note, because of
the rapid equilibrium of oxygen between the alveolus and the blood, this mechanism only causes hypoxemia if there is an increase in the ow of blood through
the pulmonary capillaries—i.e., a high cardiac output state as in exercise),
hypoventilation (inadequate refreshment of gas in the alveoli as oxygen is
removed by red blood cells, such that there is low oxygen availability for absorption into the pulmonary capillaries), ventilation-perfusion mismatch (poor
matching of blood ow to the areas of the lung with the best supply of oxygen),
shunt (blood ow through an abnormal pathway that bypasses the blood-alveolar
interface), and low inhaled partial pressure of oxygen (uncommon at sea level).
When blood oxygen levels are low due to diseases like pneumonia or acute respiratory distress syndrome (ARDS), mechanical ventilation provides the maximum possible delivery of oxygen to the alveoli, allowing for improved blood
oxygen levels.
• Acute hypercarbic respiratory failure—Hypercarbia, or elevated carbon dioxide
level in the blood, represents the inability of the respiratory system to remove
enough of this waste product of cellular respiration to maintain a safe tissue
environment. A common cause of this type of respiratory failure is an acute exacerbation of chronic obstructive pulmonary disease (COPD), in which obstructive
airway disease causes severe impairment of alveolar ventilation and an accumulation of alveolar carbon dioxide ensues. Acute elevation of CO2 levels in the
blood is associated with respiratory acidosis and can cause worsening encephalopathy and eventually coma.
• Altered consciousness—Adequate respiration requires a patent airway through
which alveolar gas can be exchanged with ambient air in the environment. States
of altered consciousness can lead to airway obstruction due to aspiration of oropharyngeal contents (saliva, ingested food/liquid, etc.) and collapse of airway
soft tissues (tongue occlusion of the airway). Any cause of severe encephalopathy can contribute to this process, including both primary neurologic pathology
(e.g., stroke and seizure) and secondary causes (e.g., intoxication, sedating medications, and uremia).
Inability to maintain adequate ventilation
•
without primary pulmonary disease—
Some patients are unable to ventilate adequately due to impaired activation of
respiratory muscles without an underlying lung disease. This includes patients
with neuromuscular weakness: for example, patients with spinal cord or phrenic
nerve injury can be left unable to contract the diaphragm and thus have impaired
ability to generate air movement. Alternatively, decreased respiratory muscle
function can be caused by impaired respiratory drive due to a more central neurologic problem—this is the case with opioid overdose in which activation of
opioid receptors in the brainstem causes inhibition of neurons that typically stimulate breathing.
88
e (PEEP)
Time
Pressure
T. Peck and R. M. Schwartzstein
4.4 Terminology Used inMechanical Ventilation
Healthcare providers share a common language to describe the many parameters
relevant to the use of mechanical ventilation. Familiarity with a few basic terms
used to describe the settings and measurements in mechanical ventilation will allow
pharmacists to understand this aspect of critical care management and communicate
effectively with ICU team members.
Fraction of inspired oxygen (FiO
in the gas delivered to the patient from the ventilator. Ambient air (also called room
air) in the environment typically contains 21% oxygen (FiO2 = 0.21); ventilators can
deliver up to 100% oxygen (or FiO2 = 1.0) as selected by the clinician.
Airway pressure is the measured pressure in the patient’s airway and can be mea-
sured at various stages of the respiratory cycle. A few examples of airway pressure
are as follows:
• Positive end-expiratory pressure (PEEP) is the constant positive pressure applied
to the airways at the end of exhalation before the next breath is initiated.
Clinicians set the PEEP delivered by the ventilator. PEEP helps keep alveoli
open (or “recruited”) during expiration, which improves gas exchange and prevents lung injury from repeated closure–reopening of alveoli. High PEEP can
cause overdistension of the lung tissue, which can impair gas exchange and
cause decreased cardiac output (and hypotension) due to increased intrathoracic
pressure and decreased venous return of blood to the heart.
• Peak pressure (P
) is the highest pressure reached in the airway during inspira-
peak
tion and is generated by the movement of air through the respiratory system
(Fig.4.1).
) refers to the fraction or percentage of oxygen
2
Peak pressure (P
Fig. 4.1 Peak pressure and positive end-expiratory pressure (PEEP). During inspiration on
positive- pressure ventilation, the airway pressure rises from the PEEP to the highest pressure of the
respiratory cycle, known as the P
peak
peak
)
Positive end-expiratory pressur