Figure 11-1 illustrates the location of various pulmonary and cardiac structures seen on a CXR (PA view). The following is a short guide to reading a CXR.1. Check exposure technique for lightness or darkness.
2. Verify left and right by looking at the heart shape and stomach bubble, respectively.
3. Check for rotation. Does the thoracic spine shadow align in the center of the sternum between the clavicles?
4. Make sure the CXR is taken in full inspiration (10 posterior or 6 anterior ribs should be visible).
5. Is the film a portable, AP, or PA film? (The heart size cannot be accurately judged from an AP film.)
6. Check the soft tissues for foreign bodies or SC emphysema.
7. Check all visible bones and joints for osteoporosis, old fxs, metastatic lesions, rib notching, or presence of cervical ribs.
8. Look at the diaphragm for tenting, free air, and position.
9. Check hilar and mediastinal areas for the following: size and shape of the aorta, presence of hilar nodes, prominence of hilar blood vessels, elevation of vessels (left slightly higher), and elevation of the left main stem bronchus indicating left atrial enlargement.
10. Look at the heart for size, shape, calcified valves, and enlarged atria.
11. Check the costophrenic angles for fluid or pleural scarring.
12. Check the pulmonary parenchyma for infiltrates, ↑ interstitial markings, masses, absence of nl margins, air bronchograms, or ↑ vascularity and “silhouette” signs.
13. Look at the lateral film for the following: confirmation and position of questionable masses or infiltrates, size of retrosternal air space, AP chest diameter, vertebral bodies for bony lesions or overlying infiltrates, and posterior costophrenic angle for small effusion.
2. Calcifications on Chest X-Ray
Lung neoplasm (primary or metastatic)
Silicosis
Idiopathic pulmonary fibrosis (IPF)
Tuberculosis
Histoplasmosis
Disseminated varicella infection
Mitral stenosis (end-stage)
Secondary hyperparathyroidism3. Cardiac Enlargement
Cardiac Chamber Enlargement
Chronic volume overload
Mitral or aortic regurgitation
Left-to-right shunt (PDA, VSD, AV fistula)
Cardiomyopathy
Ischemic
Nonischemic
Decompensated pressure overload
AS
HTN
High-output states
Severe anemia
Thyrotoxicosis
Bradycardia
Severe sinus bradycardia
FIGURE 11-1 Normal anatomy on the female chest radiograph in the upright posteroanterior projection (A) and in the lateral projection (B). (From Mettler FA: Primary Care Radiology. Philadelphia, Saunders, 2000.)
Left Atrium
LV failure of any cause
Mitral valve disease
MyxomaRight Ventricle
Chronic LV failure of any cause
Chronic volume overload
Tricuspid or pulmonic regurgitation
Left-to-right shunt (ASD)
Decompensated pressure overload
Pulmonic stenosis
Pulmonary HTN
Primary
Secondary (PE, COPD)
Pulmonary veno-occlusive diseaseRight Atrium
Multichamber Enlargement
Hypertrophic cardiomyopathy
Acromegaly
Severe obesityPericardial Disease
Pericardial effusion w/ or w/o tamponade
Effusive constrictive disease
Pericardial cyst, loculated effusionPseudocardiomegaly
Epicardial fat
Chest wall deformity (pectus excavatum, straight back syndrome)
Low lung volumes
AP CXR4. Cavitary Lesion on Chest X-Ray
Necrotizing Infections
Bacteria: anaerobes, Staphylococcus aureus, enteric gram(−) bacteria, Pseudomonas aeruginosa, Legionella species, Haemophilus influenzae, Streptococcus pyogenes, Streptococcus pneumoniae, Rhodococcus, Actinomyces
Mycobacteria: Mycobacterium tuberculosis, Mycobacterium kansasii, Mycobacterium avium-intracellulare
Bacteria-like: Nocardia species
Fungi: Coccidioides immitis, Histoplasma capsulatum, Blastomyces hominis, Aspergillus species, Mucor species
Parasitic: Entamoeba histolytica, Echinococcus, Paragonimus westermaniCavitary Infarction
Bland infarction (w/ or w/o superimposed infection)
Lung contusionSeptic Embolism
Staphylococcus aureus
Anaerobes
OthersVasculitis
Wegener’s granulomatosis
PeriarteritisNeoplasms
Bronchogenic carcinoma
Metastatic carcinoma
LymphomaMiscellaneous Lesions
Cysts, blebs, bullae, or pneumatocele w/ or w/o fluid collections
Sequestration
Empyema w/air-fluid level
Bronchiectasis5. Mediastinal Masses or Widening on Chest X-Ray
Lymphoma: Hodgkin’s disease and non-Hodgkin’s lymphoma
Sarcoidosis
Vascular: aortic aneurysm, ectasia or tortuosity of aorta or bronchocephalic vessels
Carcinoma: lungs, esophagus
Esophageal diverticula
Hiatal hernia
Achalasia
Prominent pulmonary outflow tract: pulmonary HTN, PE, right-to-left shunts
Trauma: mediastinal hemorrhage
Pneumomediastinum
Lymphadenopathy caused by silicosis and other pneumoconioses
Leukemias
Infections: TB, viral (rare), mycoplasmal (rare), fungal, tularemia
Thymoma
Teratoma
Bronchogenic cyst
Pericardial cyst
Neurofibroma, neurosarcoma, ganglioneuromaB. Use and Interpretation of Pulmonary Function Tests
Basic spirometry: Figure 11-2
PFTs in common lung diseases: Table 11-1
Flow volume curves: Figure 11-3
FIGURE 11-2 Basic spirometry. Long volumes obtained with a bell spirometer. (From Kiss GT: Diagnosis and Management of Pulmonary Disease in Primary Practice. Menlo Park, Calif, Addison-Wesley, 1982.)
TABLE 11-1
Pulmonary Function Test Patterns in Common Lung Diseases
| Disorder | Parameter | Bronchodilator Response | |||||
| FVC | FEV1 | FEV1/FVC | RV | TLC | Diffusion (DLCO) | ||
| Asthma | ↓ | ↓ | ↓ | Nl, ↑ | Nl, ↑ | Nl | + |
| Chronic obstructive bronchitis | ↓ | ↓ | ↓ | Nl, ↑ | Nl, ↑ | Nl | − |
| Chronic obstructive bronchitis w/ bronchospasm | ↓ | ↓ | ↓ | Nl, ↑ | Nl, ↑ | Nl | + |
| Emphysema | ↓ | ↓ | ↓ | Nl, ↑ | Nl, ↑ | Nl, ↓ | − |
| Interstitial fibrosis | ↓ | Nl, ↓ | Nl, ↑ | Nl, ↓ | ↓ | ↓ | − |
| Obesity, kyphosis | ↓ | Nl, ↓ | Nl, ↑ | Nl, ↑ | ↓ | Nl | − |
↑, greater than predicted; ↓, less than predicted.
FIGURE 11-3 Flow-volume curves of restrictive disease and various types of obstructive diseases compared with normal curves.
C. Pulmonary Formulas
Lung volumes: Box 11-1
Alveolar-arterial O2 gradient (A-a gradient): Box 11-2
Evaluation of pt in respiratory failure: Box 11-3Box 11-1 Lung Volumes: Normal Volumes in Upright Subjects
| Volume or Capacity | Approximate Value in Upright Subjects |
| Total lung capacity (TLC) | 6 L |
| Vital capacity (VC) | 4.5 L |
| Residual volume (RV) | 1.5 L |
| Inspiratory capacity (IC) | 3 L |
| Functional residual capacity (FRC) | 3 L |
| Inspiratory reserve volume (IRV) | 2.5 L |
| Expiratory reserve volume (ERV) | 1.5 L |
| Tidal volume (VT) | 0.5 L |
| The VC is calculated as:
The RV is calculated as the difference between the FRC and the ERV:
Alternatively, if the TLC and VC are known, the following formula can be used:
|
|
Box 11-2 Alveolar-Arterial Oxygen Gradient (A-a Gradient)
Normal A-a gradient = 5-15 mm
FIO2, fraction of inspired oxygen (normal = 0.21-1.0)
PaCO2, arterial carbon dioxide tension (normal = 35-45 mm Hg)
PaO2, arterial partial pressure of oxygen (normal = 70-100 mm Hg)
Ddx of A-a gradient:
| Abnormality | 15% O2 | 100% O2 |
| Diffusion defect | Increased gradient | Correction of gradient |
| V/Q mismatch | Increased gradient | Partial or complete correction of gradient |
| Right-to-left shunt (intracardiac or pulmonary) | Increased gradient | Increased gradient (no correction) |
Box 11-3 Formulas for Evaluation of Patients in Respiratory Failure
Age-predicted PaO2 = Expected PaO2 − 0.3(age − 25) [expected Pao2 at sea level is 100 mg/Hg]
As a rough rule of thumb: Expected PaO2 ≈ FIO2 (%) × 5
AaDO2 = (FIO2 × [BP∗− 47]) − (PaO2 + PaCO2), where BP = barometric pressure
Pao2/Fio2 ratio
AaDO2, Alveolar-arterial gradient; VD, dead space.
From Vincent JL, Abraham E, Moore FA, et al (eds): Textbook of Critical Care, 6th ed. Philadelphia, Saunders, 2011.
D. Mechanical Ventilation
Indications (Please see section “M” for Respiratory Failure Classification)
1. Clinical assessment: presence of apnea, tachypnea (>40 bpm), or respiratory failure that cannot be adequately corrected by any other means
2. Clinical instability, failure to protect the airway—usually from declining mental status
3. ABGs: severe hypoxemia despite high-flow O2 or significant CO2 retention (e.g., PO2 <50, PCO2 >50)
4. Physiologic parameters are of limited use because many pts w/respiratory insufficiency are unable to perform PFTs, and their respiratory failure mandates immediate intervention. Some of the commonly accepted physiologic parameters for intubation and respiratory support are as follows:
a. VC <10 mL/kg
b. Inspiratory force ≤25 cm H2O
c. FEV1 <10 mL/kg
d. VT <5 mL/kg BW
e. 
E >10 L/min
E >10 L/minf. Ratio of RR (breaths/min) to VT (L) >105
Note: The clinical assessment is the most important determinant of the need for mechanical ventilation because neither physiologic parameters nor ABGs distinguish between acute and chronic respiratory insufficiency (e.g., a PCO2 >60 mm Hg and an RR >30/min may be the “norm” for a pt w/COPD, whereas the same values in a young, otherwise healthy adult are indications for intubation and mechanical ventilation).
ICU Sedation
Commonly used agents are GABA agonists such as propofol and benzos. These agents can cause respiratory depression and delirium. The α-adrenoreceptor agonist dexmedetomidine is as effective for sedation but significantly better in pts at risk for delirium.
Common Modes of Mechanical Ventilation
Invasive mechanical ventilation is defined as ventilatory support supplied through endotracheal intubation. The use of devices that apply intermittent (−) extrathoracic pressure or furnish intermittent positive pressure through a tight-fitting nasal or face mask w/o an artificial airway in place is known as noninvasive ventilation. The delivery of gas under positive pressure into the airways and the lungs is known as positive-pressure ventilation (Table 11-2).
1. IMV: The pt is allowed to breathe spontaneously, and the ventilator delivers a number of machine breaths at a preset rate and volume.
a. Advantages and indications
i. IMV is indicated in the majority of spontaneously breathing pts because it maintains respiratory muscle tone and results in less depression of cardiac output than with ACV.
ii. It is useful for weaning because as the IMV rate is ↓, the pt gradually assumes the bulk of the breathing work.
b. Disadvantages
i. The ↑ work of breathing results in ↑ O2 consumption (deleterious to pts w/myocardial insufficiency).
ii. IMV is not useful in pts w/depressed respiratory drive or impaired neurologic status.
TABLE 11-2
Modes of Positive-Pressure Ventilation
| Mode | Description | Advantages and Disadvantages |
| Controlled mechanical ventilation (CMV) | Ventilator f, inspiratory time, and VT (and thus  E) preset |
Can be used in patients w/sedation or paralysis; ventilator cannot respond to ventilatory needs |
| Assisted mechanical ventilation (AMV) or assist-control ventilation (ACV) | Ventilator VT and inspiratory time preset, but patient can f (and thus  E) |
Ventilator may respond to ventilatory needs; ventilator may undertrigger or overtrigger, depending on sensitivity |
| Intermittent mandatory ventilation (IMV) | Ventilator delivers preset VT, f, and inspiratory time, but patient also can breathe spontaneously | May ↓ asynchronous breathing and sedation requirements; ventilator cannot respond to ventilatory needs |
| Synchronized intermittent mandatory ventilation (SIMV) | Same as IMV, but ventilator breaths delivered only after patient finishes inspiration | Same as IMV, and patient not overinflated by receiving spontaneous and ventilator breaths at same time |
| High-frequency ventilation (HFV) | Ventilator f is and VT may be smaller than VD | May reduce peak airway pressure; may cause auto-PEEP |
| Pressure support ventilation (PSV) | Patient breathes at own f; VT determined by inspiratory pressure and CRS | ↑ comfort and ↓ work of breathing; ventilator cannot respond to ventilatory needs |
| Pressure control ventilation (PCV) | Ventilator peak pressure, f, and respiratory time preset | Peak inspiratory pressures may be ↓; hypoventilation may occur |
| Inverse ratio ventilation (IRV) | Inspiratory time exceeds expiratory time to facilitate inspiration | May improve gas exchange by ↑ time spent on inspiration; may cause auto-PEEP |
| Airway pressure release ventilation (APRV) | Patient receives CPAP at high and low levels to simulate VT | May improve oxygenation at lower airway pressure; hypoventilation may occur |
| Proportional assist ventilation (PAV) | Patient determines own f, VT, pressures, and flows | May amplify spontaneous breathing; depends entirely on patient’s respiratory drive |
CRS, Respiratory system compliance; f, respiratory rate; VD, dead space.
Modified from Goldman L, Schafer AI (eds): Goldman’s Cecil Medicine, 22nd ed. Philadelphia, Saunders, 2004.
iii. It was previously assumed that the degree of respiratory muscle rest was proportional to the level of machine assistance. However, more recent evidence indicates that respiratory-sensor output does not adjust to breath-to-breath changes in respiratory load, and IMV may therefore contribute to the development of respiratory muscle fatigue or prevent recovery from it.
2. ACV: The pt breathes at his or her own rate, and the ventilator senses the inspiratory effort and delivers a preset VT w/each pt effort; if the pt’s RR ↓ past a preset rate, the ventilator delivers tidal breaths at the preset rate.
a. Advantages and indications: ACV is useful in pts w/neuromuscular weakness or CNS disturbances.
b. Disadvantages
i. Tachypnea may result in significant hypocapnia and respiratory alkalosis.
ii. Improper setting of sensitivity to the (−) pressure necessary to trigger the ventilator may result in “fighting the ventilator” when the sensitivity is set too low.
iii. ↑ Sensitivity may result in hyperventilation; sensitivity is generally set so that an inspiratory effort of 2 to 3 cm will trigger ventilation.
iv. The respiratory muscle tone is not well maintained in pts on ACV, and this may result in difficulty w/weaning.
3. CMV: The pt does not breathe spontaneously; the RR is determined by the physician; the ventilator assumes all respiratory work by delivering a preset volume of gas at a preset rate.
a. Advantages and indications
i. CMV is useful in pts who are unable to make an inspiratory effort (e.g., severe CNS dysfunction) and in pts w/excessive agitation or breathing effort.
ii. Pts w/excessive agitation are often sedated w/morphine or benzos and paralyzed w/pancuronium bromide; adequate sedation is necessary to eliminate awareness of paralysis.
iii. Initial pancuronium dose is 0.08 mg/kg IV in adults.
iv. Later incremental doses starting at 0.01 mg/kg may be used as necessary to maintain paralysis; pancuronium should be administered only by or under the supervision of experienced clinicians; a combination of neostigmine and atropine may be used to reverse the action of the pancuronium.
b. Disadvantages: Paralyzed pts on CMV must be closely monitored because ventilator malfunction or disconnection is rapidly fatal.
4. SIMV: A hybrid of ACV and IMV, the ventilator delivers a number of specified breaths/min (as w/IMV). However, at the appropriate interval (e.g., q6sec if machine rate is 10 breaths/min), the machine waits for an ETT pressure deflection to signal pt effort and then delivers a positive-pressure breath; ventilator breaths are thus synchronized w/pt respiratory efforts, as w/assist features of ACV.
5. Other useful ventilation modes are as follows:
a. Pressure control ventilation (PCV): A ventilatory mode in which inspiratory pressure, RR, and inspiratory time (TI) are determined by the ventilator settings. Because inspiratory pressure is the controlled variable, VT during PCV is influenced by the mechanical properties of the respiratory system (resistance and compliance).
b. Pressure support ventilation (PSV): A ventilatory mode in which the pt’s inspiratory effort is supported by a set level of inspiratory pressure. This pressure is maintained until respiratory flow falls below a threshold value, signaling the onset of expiration. VT during PSV is determined by pt effort and the mechanical properties of the lung. PSV differs from PCV in that the RR and the TI are determined by the pt.
c. Inverse ratio ventilation (IRV): A ventilatory strategy in which the inspiratory-to-expiratory ratio is prolonged to 1:1 or greater. In pts w/ARDS, IRV is used to improve oxygenation by increasing mean airway pressure. This modality is used as a salvage Rx when adequate oxygenation cannot be achieved w/conventional ventilation in ARDS. When used, pressure cycled IRV is preferred because of ↓ barotrauma risk.
d. Noninvasive positive-pressure ventilation (NPPV), Continuos positive airway pressure (CPAP), Bi-level positive airway pressure (BiPAP): In NPPV, ventilatory support is delivered by use of a mechanical ventilator connected to a mouthpiece or mask instead of an ETT. It is very useful in pts w/chronic respiratory failure caused by neuromuscular disease or thoracic deformities and in pts w/idiopathic hypoventilation. It improves the pt’s well-being and may eliminate the need for tracheostomies. It is also used in pts as a short-term bridge to avoid intubation and mechanical ventilation, when possible, in conditions that are rapidly reversible, such as hypercarbic respiratory failure in COPD and, importantly, acute pulmonary edema in heart failure. It is also sometimes used as salvage Rx in pts w/any of the indications for intubation who do not want to be intubated. CPAP is applied with an oxygen source connected to either a tight-fitting nasal or full-face mask or via nasal prones. It delivers high concentration of oxygen and maintains (+) airway pressure in the spontaneously breathing patient. It offers the benefit of maintaining alveolar expansion and decreases work of breathing. BiPAP, like CPAP can be provided by mask, but it requires a ventilator to assist with flow delivery. The patients inspiratory effort triggers the BiPAP machine to deliver decelerating flow in order to reach a preset pressure, defined as inspiratory positive airway pressure. When a pt’s own inspiratory flow falls below a preset amount, ventilatory assistance ceases and maintains airway pressure at a predetermined value (usually 5-10 mmHg).
Selection of Ventilator Settings
1. VT IS 10 to 15 mL/kg of ideal BW. Low volume ventilation = 6-8 ml/kg w/ARDS
2. Rate (number of tidal breaths delivered per minute) is 8 to 16, depending on the desired PaCO2 or pH (↑ rate = ↓ PaCO2).
3. Mode is IMV, ACV, CMV (or PCV or PSV, depending on what is available at one’s institution).
4. O2 concentration (FIO2): The initial FIO2 should be 100% unless it is evident that a lower FIO2 will provide adequate oxygenation. The FIO2 should be calibrated down as quickly as possible to prevent O2 toxicity.
5. Obtain ABGs 15 to 30 minutes after initiation of mechanical ventilation.
6. Immediate CXR is indicated after intubation to evaluate for correct placement of ETT.
7. Sedation orders (e.g., morphine, diazepam) are necessary in most pts.
8. PEEP:
a. The application of PEEP may prevent the closure of edematous small airways; it is indicated when arterial oxygenation is inadequate (saturation <90%) despite an FIO2 >50%; it is useful in pts w/diffuse lung edema and refractory hypoxemia caused by intrapulmonary shunting (e.g., ARDS). It is also useful to ↓ the needed FIO2 to ↓ O2 toxicity. In reality, ≥5 mm PEEP is used on virtually everyone, but it can be ↓ if oxygenation is not a problem but intubation-associated hypotension is.
TABLE 11-3
Effects of Ventilator Setting Changes
| Typical Effects on Blood Gases | ||
| Ventilator Setting Changes | PaCO2 | PaO2 |
| ↑ PIP | ↓ | ↑ |
| ↑ PEEP | ↑ | ↑ |
| ↑ Rate (IMV) | ↓ | Minimal ↑ |
| ↑ I/E ratio | No change | ↑ |
| ↑ FIO2 | No change | ↑ |
| ↑ Flow | Minimal ↓ | Minimal ↑ |
| ↑ Power (in HFOV) | ↓ | No change |
↑  (in HFOV) |
Minimal ↓ | ↑ |
HFOV, High-frequency oscillatory ventilation; I/E, inspiratory/expiratory ratio; 
, mean airway pressure; PIP, peak inspiratory pressure.
From Tschudy MM, Arcara KM: The Harriet Lane Handbook, 19th ed. Philadelphia, Mosby, 2012.
TABLE 11-4
Common Ventilator Machine Settings for Various Disorders
| Condition | Mode | Vt,  E |
PEEP (cm H2O) | Pressure Targets | FIO2 |
| Depressed CNS drive | Mandatory ACV, SIMV | Vt = 10 mL/kg E = 6-8 L/min |
0-5 | Peak usually <35 cm H2O | Minimum for Sao2 >90% |
| Neuromuscular insufficiency | Acute: mandatory ACV, SIMV | Vt = 8-10 mL/kg E = 6-8 L/min |
0-5 | Peak usually <35 cm H2O | As above |
| Mild, recovering: SIMV and PSV, PSV alone | Guarantee VT >350 mL w/PSV breaths | 0-5 | |||
| COPD | Early: ACV, SIMV Late: see text |
Vt = 8 mL/kg E: minimize, usually 8-10 L/minPeak flow ≥60 L/min |
0∗ | Plateau <30 cm H2O; monitor for intrinsic PEEP (auto-PEEP) | As above |
∗ PEEP added to obstructive disease only in special circumstances.
From Noble J (ed): Textbook of Primary Care Medicine, 2nd ed. St. Louis, Mosby, 1996.
b. PEEP is generally started at 5 cm H2O and by increments of 2 to 5 cm to maintain the PaO2 at 60 mm Hg or greater.
c. The use of PEEP can result in pulmonary barotrauma and hemodynamic compromise (secondary to ↓ right ventricular filling).
d. Pts receiving PEEP should have their cardiac output frequently monitored; the measurement of mixed venous O2 sat is useful to evaluate the effect of PEEP on cardiac output. The surrogate of cardiac output (BP) is fine in most pts.
9. Adjust the initial ventilator setting according to results of the ABGs and clinical response.
a. Use the lowest FIO2 necessary to maintain a PaO2 >60 mm Hg (90% Hgb saturation in pts w/nl pH).
b. Adjust 
E (VT time rate) to nlize the pH and the PaCO2.
E (VT time rate) to nlize the pH and the PaCO2.i. The VT or the rate will ↓ PaCO2 and ↑ pH.
ii. Do not lower the PaCO2 below the “norm” for that pt (e.g., some pts w/COPD should be allowed to maintain their usual mildly ↑ PaCO2 to avoid alkalosis and to provide stimulus for breathing).
10. Effects of ventilator setting changes are described in Table 11-3. Common ventilator machine settings for various disorders are described in Table 11-4 and Box 11-4.
1. Ventilatory mode
Unintubated patients:
NIV for patients with COPD and acute hypercapnic respiratory failure if alert, cooperative, and hemodynamically stable
NIV not routinely recommended for acute hypoxemic respiratory failureIntubated patients:
Assist/control with volume-limited ventilation as initial mode
Consider specific indications for PCV or HFOV (see text) in acute lung injury
SIMV: consider if some respiratory effort, dyssynchrony
PSV: consider if patient’s effort good, ventilatory needs moderate to low, and patient more comfortable during PSV trial2. Oxygenation
If infiltrates on chest radiograph, then
FIO2: begin with 0.8-1.0, reduce according to Spo2
PEEP: begin with 5 cm H2O, increase according to Pao2 or Spo2, FIO2 requirements, and hemodynamic effects; consider PEEP/FIO2 “ladder”; goal of Spo2 >90%, FIO2 ≤0.6
No infiltrates on chest radiograph (COPD, asthma, PTE), FIO2: start at 0.4 and adjust according to Spo2 (consider starting higher if PE is strongly suspected)3. Ventilation
VT: begin with 8 mL/kg PBW; decrease to 6 mL/kg PBW over a few hours if acute lung injury present
Rate: begin with 10-20 breaths/min (10-15 if not acidotic; 15-20 if acidotic); adjust for pH; goal pH >7.3 with maximal rate of 35; may accept lower goal if 
E high4. Secondary modifications
Triggering: in spontaneous modes, adjustment of sensitivity levels to minimize effort
Inspiratory flow rate of 40-80 L/min; higher if tachypneic with respiratory distress or if auto-PEEP present, lower if high pressure in ventilator circuit leads to a high-pressure alarm
Assessment of auto-PEEP, especially in patients with increased airways obstruction (e.g., asthma, COPD)
I/E ratio: 1:2, either set or as function of flow rate; higher (1:3 or more) if auto-PEEP present
Flow pattern: decelerating ramp reduces peak pressure5. Monitoring
Clinical: blood pressure, ECG, observation of ventilatory pattern including assessment of dyssynchrony, effort or work by the patient; assessment of airflow throughout expiratory cycle
Ventilator: VT, 
E, airway pressures (including auto-PEEP), total compliance
ABGs, pulse oximetryHFOV, high-frequency oscillatory ventilation; I/E ratio, inspiratory-to-expiratory ratio; NIV, noninvasive ventilation; PBW, predicted body weight; PTE, pulmonary thromboembolism.
∗ Decisions within this algorithm will be influenced by the specific conditions of the individual patient.
Modified from Goldman L, Schafer AI (eds): Goldman’s Cecil Medicine, 24th ed. Philadelphia, Saunders, 2012.
Major Complications
1. Pulmonary barotrauma (e.g., pneumomediastinum, pneumothorax, SC emphysema, pneumoperitoneum) is generally secondary to high levels of PEEP, excessive VT, high peak airway pressures, and coexistence of significant lung disease.
2. Pulmonary thromboemboli can be prevented by vigorous leg care, antiembolic stockings, and use of prophylactic LMWH.
3. GI bleeding: Prophylaxis w/IV ranitidine 50 mg q8h, PPIs, or sucralfate suspension, 1 g q6h through NG tube, is indicated in most pts on mechanical ventilators.
4. Arrhythmias: Avoid the use of arrhythmogenic drugs and prevent rapid acid-base shifts.
5. Accumulation of large amount of secretions: Frequent respiratory toilet is necessary in all pts on mechanical ventilators. Consider mouth care with chlorhexidine.
6. Others include nosocomial infections, laryngotracheal injury, malnutrition, hypophosphatemia, O2 toxicity, and psychosis. Risk factors for pneumonia are severe illness, old age (>60 years), prior administration of abx, and supine head position. Respiratory ICU pts who are managed in the semirecumbent (30- to 45-degree head-up) position have a lower incidence of nosocomial pneumonia. Use of sucralfate rather than H2 antagonists is also associated w/lower incidence of nosocomial pneumonia. Extubation as rapidly as possible is important to help prevent ventilator-associated pneumonia.
Withdrawal of Mechanical Ventilatory Support
Common Criteria for Ventilator Weaning
1. Improved clinical status (the pt is alert and hemodynamically stable); the process that required mechanical ventilation is reversed.
2. Adequate oxygenation (PaO2 >60 mm Hg w/inspired O2 concentration of 40%)
3. pH 7.33 to 7.48 w/acceptable PaCO2
4. RR ≤25 breaths/min
5. VC ≥10 mL/kg
6. Resting 
E <10 L/min, w/ability to double the resting 
E
E <10 L/min, w/ability to double the resting E7. Peak pressure more (−) than −25 cm H2O
8. VT >5 mL/kg
9. The ratio of respiratory frequency to VT during 1 minute of spontaneous breathing, also known as the rapid shallow breathing index (f/Vt), is a good predictor of a pt’s readiness for weaning; a value of <100 breaths/min/L indicates that weaning probably will be successful, especially if it is confirmed by serial measurements.
Note: The preceding criteria are only guidelines; significant variation may be present (e.g., an RR of 30 breaths/min may be acceptable in a pt w/COPD). Failure to meet these criteria does not mean that the pt will not be weaned successfully. Figure 11-4 is an algorithm for discontinuing ventilation and for extubation.
FIGURE 11-4 Algorithm for assessing whether a patient is ready to be liberated from mechanical ventilation and extubated. P/F, PaO2/FIO2 ratio; WOB, work of breathing. (From Goldman L, Schafer AI [eds]: Goldman’s Cecil Medicine, 24th ed. Philadelphia, Saunders, 2012.)
Methods of Weaning
1. Weaning by IMV
a. Gradually ↓ the IMV as tolerated (e.g., two breaths q3-4h), monitoring ABGs PRN. Monitoring of clinical signs (RR, pt’s comfort, and VT) is usually sufficient to avoid repeated ABGs.
b. Do not change more than one parameter at a time.
c. When the pt is tolerating an IMV of 4 to 6, a trial w/T tube can be attempted. The T tube is attached to the ETT and delivers humidified O2 (FIO2 40%).
d. If the pt tolerates the T tube well, extubation may be attempted.
i. Have adequate equipment and personnel available if reintubation is necessary (start early in the day).
ii. Suction airway and oropharynx.
iii. Deflate cuff and extubate.
iv. Administer O2 by face mask (FIO2 40%-100%).
v. Auscultate the lungs for adequate air movement.
vi. Closely monitor VS.
vii. Obtain ABGs approximately 15 to 30 minutes after extubation.
e. Reintubate if extubation is poorly tolerated.
2. Stable pts w/o pulmonary disease and w/good probability of quick extubation (e.g., after uncomplicated cardiac surgery) may be given a direct trial of T tube (bypassing gradual ↓ of IMV).
3. PSV
a. Titrate pressure to achieve a frequency of ≤25 breaths/min; allow a CPAP of ≤cm H2O.
b. Set pressure support initially at 18.0 ± 6.1 cm H2O, and attempt to reduce this level of support by 2 to 4 cm H2O at least bid.
c. Extubate pts who tolerate a pressure support setting of 5 cm H2O for 2 hr w/no apparent ill effects.
4. Intermittent trials of spontaneous breathing
a. Disconnect the stable pt from the ventilator and allow the pt to breathe spontaneously through either a T-tube circuit or a continuous-flow circuit designed to provide a CPAP of ≤5 cm H2O.
b. Attempt the trial at least bid and gradually ↑ the duration of the trial.
c. Provide ACV for ≥1 hour between the trials.
d. Extubate pts who are able to breathe on their own for ≥2 hr w/o signs of distress.
5. Once-daily trial of spontaneous breathing
a. Disconnect the stable pt from the ventilator and allow him or her to breathe spontaneously through a T-tube circuit for ≤2 hr each day.
b. Extubate pts who tolerate a 2-hour trial w/o signs of distress.
c. Reinstitute ACV for 24 hr if signs of intolerance develop.
Failure to Wean from Mechanical Ventilator
Failure usually results from premature attempts at weaning (e.g., pt is hemodynamically unstable). Other common, reversible causes of failure to wean are as follows:
1. Hypophosphatemia, hypomagnesemia, hypokalemia
2. Drug toxicity (e.g., excessive CNS depression from analgesics, sedatives). Continuous infusions of sedative drugs may prolong the duration of mechanical ventilation. Daily interruption of sedative infusions until the pt is awake ↓ the duration of mechanical ventilation.
3. Bronchospasm
4. Excessive secretions
5. Significant acid-base disturbances (e.g., metabolic alkalosis depresses respiratory drive)
6. Hypothyroidism
7. Malnutrition
8. Small-bore ETT (tube >8 mm is preferred)
9. Interference w/chest wall (e.g., chest tube, restraints)
Ventilator-Associated Pneumonia
1. Ventilator-associated pneumonia occurs in 9% to 24% of pts intubated >48 hr.
2. The etiology of ventilator-associated pneumonia varies w/the following factors:
a. Onset <5 days after hospital admission or intubation
b. Presence of risk factors (previous recent abx Rx, corticosteroid use, structural lung disease, and immunosuppression)
3. Pts w/pneumonia diagnosed <5 days after hospital admission or intubation and w/no risk factors can be empirically treated w/one of the following abx:
a. Second- or third-generation cephalosporin
b. β-Lactam w/ or w/o β-lactamase inhibitors
c. Quinolones
4. Pts w/risk factors or those diagnosed 5 days or more after hospital admission or intubation can be empirically treated w/two abx from the following classes:
a. Antipseudomonal lactam agents (e.g., imipenem, meropenem, cefepime, ceftazidime, piperacillin-tazobactam)
b. Quinolones with w/reliable antipseudomonal activity
c. Aminoglycoside
5. Consider addition of vancomycin in institutions w/MRSA.
6. Recommended duration of Rx is 7 days, longer if Pseudomonas infection is diagnosed.
E. Acute Respiratory Distress Syndrome (ARDS)
This form of noncardiogenic pulmonary edema results from acute damage to the alveoli. The definition of ARDS includes the following components: a ratio of PaO2 to the FIO2 ≤200, regardless of the level of PEEP; the detection of bilateral pulmonary infiltrates on the frontal CXR; PAWP ≤18 mm Hg or no clinical evidence of diminished LV function.
Etiology
Sepsis (>40%)
Aspiration: near-drowning, aspiration of gastric contents (>30%)
Trauma (>20%)
Multiple transfusions, blood products
Drugs (OD of morphine, methadone, heroin; reaction to nitrofurantoin)
Noxious inhalation (chlorine gas, high O2 concentration)
Post resuscitation
Cardiopulmonary bypass
Pneumonia
TB
Burns
PancreatitisDiagnosis
Labs
ABGs: initially, varying degrees of hypoxemia, generally resistant to supplemental O2; subsequently, respiratory alkalosis, ↓ PCO2, and widened alveolar-arterial gradient. Hypercapnia occurs as the disease progresses.
Hemodynamic monitoring (when indicated): Although no hemodynamic profile is diagnostic of ARDS, the presence of pulmonary edema, CO, and ↓ PAWP is characteristic of ARDS.Imaging
CXR: Bilateral interstitial infiltrates are usually seen within 24 hr; they are often more prominent in the bases and periphery. Near-total “whiteout” of both lung fields can be seen in advanced stages.Treatment
Identification and Rx of the precipitating condition• Blood and urine cultures and trial of abx in presumed sepsis (routine administration of abx in all cases of ARDS is not recommended)
• Stabilization of bone fx in pts w/major trauma
• Bowel rest and crystalloid resuscitation in pancreatitis
Fluid management: Optimal fluid management is pt specific. Swan-Ganz catheterization may be indicated and is useful to guide fluid replacement. A PCWP of approximately 12 mm Hg is ideal.
DVT prophylaxis
Stress ulcer prophylaxis w/sucralfate suspension (by NG tube) or IV PPIs or IV H2 blockers
F. Asthma
Definition
The National Asthma Education and Prevention Program (NAEPP) guidelines define asthma as “a chronic inflammatory disease of the airways in which many cells and cellular elements play a role: in particular mast cells, neutrophils, eosinophils, T lymphocytes, macrophages, and epithelial cells. In susceptible individuals, this inflammation causes recurrent episodes of coughing (particularly at night or early in the morning), wheezing, breathlessness, and chest tightness. The episodes are usually associated w/widespread but variable airflow obstruction that is reversible either spontaneously or as a result of Rx.” Exposure to relevant allergens precedes symptoms. Other triggers include viral VRIs, cold air, stress, and exercise.
FIGURE 11-5 Ventilatory strategy for patients with ARDS. Several caveats should be considered when using the low VT strategy: (1) VT is based on predicted body weight (PBW), not actual body weight; PBW tends to be about 20% lower than actual BW; (2) the protocol mandates decreases in the VT lower than 6 mL/kg of PBW if the plateau pressure (Pplat) is greater than 30 cm H2O and allows for small increases in VT if the patient is severely distressed and/or if there is breath stacking, as long as Pplat remains at 30 cm H2O or lower; (3) because arterial CO2 levels will rise, pH will fall; acidosis is treated with increasingly aggressive strategies dependent on the arterial pH; (4) the protocol has no specific provisions for the patient with a stiff chest wall, which in this context refers to the rib cage and abdomen; in such patients, it seems reasonable to allow Pplat to increase to more than 30 cm H2O, even though it is not mandated by the protocol; in such cases, the limit on Pplat may be modified based on analysis of abdominal pressure, which can be estimated by measuring bladder pressure. (From Goldman L, Schafer AI [eds]: Goldman’s Cecil Medicine, 24th ed. Philadelphia, Saunders, 2012.)
Status asthmaticus can be defined as a severe continuous bronchospasm.
Diagnosis
For symptomatic adults and children aged >5 yr who can perform spirometry, asthma can be dx after H&P documenting an episodic pattern of respiratory sx and from spirometry that indicates partially reversible airflow obstruction (>12% and 200 mL in 1 FEV1 after inhaling a short bronchodilator or receiving a short [2-3 wk] course of PO corticosteroids).
TABLE 11-5
Relative Severity of an Asthmatic Attack as Indicated by Peak Expiratory Flow Rate, FEV1, and Maximal Midexpiratory Flow Rate
| Test | Predicted Value (%) | Severity of Asthma |
| PEFR | >80 | |
| FEV1 | >80 | No spirometric abnormalities |
| MMEFR | >80 | |
| PEFR | >80 | |
| FEV1 | >70 | Mild asthma |
| MMEFR | 55-75 | |
| PEFR | >60 | |
| FEV1 | 45-70 | Moderate asthma |
| MMEFR | 30-50 | |
| PEFR | <50 | |
| FEV1 | <50 | Severe asthma |
| MMEFR | 10-30 |
From Goldman L, Schafer AI (eds): Goldman’s Cecil Medicine, 24th ed. Philadelphia, Saunders, 2012. In Ferri F: Ferri’s Clinical Advisor: 5 Books in 1. 2013 edition. Philadelphia, Mosby, 2012.
The degree of reversibility measured by spirometry correlates w/airway obstruction. Table 11-5 describes the relative severity of an asthmatic attack as indicated by PEFR, FEV1, and MMEFR.
Physical exam findings vary w/the stage and severity of asthma and may reveal only inspiratory and expiratory phases of respiration. Exam during status asthmaticus may reveal• Tachycardia and tachypnea
• Use of accessory respiratory muscles
• Pulsus paradoxus (inspiratory decline in systolic BP >10 mm Hg)
PFT’s show obstructive pattern
Normal spirometry and high suspicion for asthma → bronchial challenge testing.
Wheezing: Absence of wheezing (silent chest) or ↓ wheezing can indicate worsening obstruction.
ΔMS is generally secondary to hypoxia and hypercapnia and constitutes an indication for urgent intubation.
Paradoxical abd and diaphragmatic movement on inspiration (detected by palpation over the upper part of the abd in a semirecumbent position) is an important sign of impending respiratory crisis and indicates diaphragmatic fatigue.
The following abnlities in VS are indicative of severe asthma exacerbation:• Pulsus paradoxus >18 mm Hg
• RR >30 breaths/min
• Tachycardia w/HR >120 bpm
Labs
ABGs can be used in staging the severity of an asthmatic attack:• Mild: ↓ PaO2 and PaCO2, ↑ pH
• Moderate: ↓ PaO2, nl PaCO2, nl pH
• Severe: marked ↓ PaO2, PaCO2, and ↓ pH
Peak flow <40% or 40%-69% of patients personal best warrants increased frequency of scheduled and PRN SABA Rx as well as systemic steroids (quick taper preferred)Imaging
CXR is usually nl but may show evidence of thoracic hyperinflation (e.g., flattening of the diaphragm, volume over the retrosternal air space).
ECG: Tachycardia and nonspecific ST-T wave changes are common during an asthmatic attack; may also show cor pulmonale, RBBB, RAD, and counterclockwise rotation.Treatment
Table 11-6 describes the classification of asthma severity and therapeutic considerations. A stepwise approach for managing asthma in youths >12 yr and adults is described in Figure 11-7.
The differentiation of asthma from COPD can be challenging. An hx of atopy and intermittent, reactive sx points toward a dx of asthma, whereas smoking and advanced age are more indicative of COPD. Spirometry is useful to distinguish asthma from COPD. Table 11-7 summarizes differentiating features of asthma and COPD.TABLE 11-6
Classifying Asthma Severity and Initiating Treatment in Youths ≥12 Yr and Adults∗
| Components of Severity | Classification of Asthma Severity (≥12 yr) | ||||
| Intermittent | Persistent | ||||
| Mild | Moderate | Severe | |||
| Impairment Normal FEV1/FVC: 8-19 yr, 85%; 20-39 yr, 80%; 40-59 yr, 75%; 60-80 yr, 70% |
Symptoms | ≤2 days/wk | >2 days/wk but not daily | Daily | Throughout the day |
| Night time awakenings | ≤2×/mo | 3-4×/mo | >1×/wk but not nightly | Often 7×/wk | |
| Short-acting β2-agonist use for symptom control (not prevention of EIB) | ≤2 days/wk | >2 days/wk but not daily, and not more than 1× on any day | Daily | Several times per day | |
| Interference with normal activity | None | Minor limitation | Some limitation | Extremely limited | |
| Lung function | Normal FEV1 between exacerbations | ||||
| FEV1 >80% predicted | FEV1 >80% predicted | FEV1 >60% but <80% predicted | FEV1 <60% predicted | ||
| FEV1/FVC normal | FEV1/FVC normal | FEV1/FVC reduced 5% | FEV1/FVC reduced >5% | ||
| Risk | Exacerbations requiring oral systemic corticosteroids | 0-1/yr | ≥2/yr → | ||
| ← Consider severity and interval since last exacerbation. Frequency and severity may fluctuate → over time for patients in any severity category. Relative annual risk of exacerbations may be related to FEV1. |
|||||
| Recommended Step for Initiating Therapy | Step 1 | Step 2 | Step 3 | Step 4 or 5 | |
| Also, consider short course of oral systemic corticosteroids. | |||||
| In 2-6 wk, evaluate level of asthma control that is achieved and adjust therapy accordingly. | |||||
The stepwise approach is meant to assist, not replace, the clinical decision making required to meet individual patient needs.
Level of severity is determined by assessment of both impairment and risk. Assess impairment domain by patient’s/caregiver’s recall of previous 2-4 wk and spirometry. Assign severity to the most severe category in which any feature occurs.
At present, data are inadequate to correlate frequencies of exacerbation with different levels of asthma severity. In general, more frequent and intense exacerbations (e.g., requiring urgent, unscheduled care, hospitalization, or ICU admission) indicate greater underlying disease severity. For treatment purposes, patients who had ≥2 exacerbations requiring oral systemic corticosteroids in the past year may be considered the same as patients who have persistent asthma, even in the absence of impairment levels consistent with persistent asthma.
To access the complete Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma, go to www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
EIB, Exercise-induced bronchospasm
∗ Assessing severity and initiating treatment for patients who are not currently taking long-term control medications.
From National Asthma Education and Prevention Program: Expert Panel Report 3: Guidelines for Diagnosis and Management of Asthma. NIH publication 08-4051. Bethesda, Md, National Institutes of Health, 2007.
G. Chronic Obstructive Pulmonary Disease (COPD)
Definition
COPD is an inflammatory respiratory disease caused by exposure to tobacco smoke. It is characterized by the presence of airflow limitation that is not fully reversible. Traditionally, COPD was described as encompassing emphysema, characterized by loss of lung elasticity and destruction of lung parenchyma w/enlargement of air spaces, and chronic bronchitis, characterized by obstruction of small airways and productive cough >3 mo in duration for >2 successive years. These terms are no longer included in the formal definition of COPD, although they are still used clinically.
FIGURE 11-7 Stepwise approach for managing asthma in youth ≥12 yr old and in adults. EIB, Exercise-induced bronchospasm; ICS, inhaled corticosteroid; LABA, inhaled long-acting β2-agonist; LTRA, leukotriene receptor antagonist; SABA, inhaled short-acting β2-agonist. (From National Asthma Education and Prevention Program: Expert Panel Report 3: Guidelines for Diagnosis and Management of Asthma. NIH publication 08-4051. Bethesda, Md, National Institutes of Health, 2007.)
TABLE 11-7
Differentiating Features of COPD and Asthma
| COPD | Asthma | |
| Smoker or ex-smoker | Most | Possibly |
| Symptoms <35 yr of age | Rare | Common |
| Atopic features (rhinitis, eczema) | Uncommon | Common |
| Cellular infiltrate | Macrophages, neutrophils, CD8+ T cells | Eosinophils, CD4+ T cells |
| Cough and sputum | Daily/common | Intermittent |
| Breathlessness | Persistent and progressive | Variable |
| Night time symptoms | Uncommon | Common |
| Significant diurnal or day-to-day variability of symptoms | Uncommon | Common |
| Bronchodilator response (FEV1 and PEFR) | <15% | >20% |
| Corticosteroid response | Poor | Good |
From Ballinger A: Kumar & Clark’s Essentials of Clinical Medicine, 5th ed. Edinburgh, Saunders, 2012.
TABLE 11-8
Classification of COPD Severity (GOLD Criteria)
| Stage | Function | Symptoms |
| Stage I: mild | FEV1/FVC <70% FEV1 ≥80% predicted |
Chronic cough, none/mild breathlessness |
| Stage II: moderate | FEV1/FVC <70% 50% ≤ FEV1 <80% predicted |
Breathlessness on exertion |
| Stage III: severe | FEV1/FVC <70% 30% ≤ FEV1 <50% predicted |
Breathless on minimal exertion; possible weight loss and depression |
| Stage IV: very severe | FEV1/FVC <70% FEV1 <30% predicted or FEV1 <50% predicted plus respiratory failure |
Breathless at rest |
Modified from Global Strategy for the Diagnosis, Management and Prevention of COPD. Available at: www.goldcopd.com
Etiology
Tobacco exposure
Occupational exposure to pulmonary toxins (e.g., dust, noxious gases, vapors, fumes, cadmium, coal, silica). The industries w/the highest exposure risk are plastics, leather, rubber, and textiles.
Atmospheric pollution
AAT deficiency (<1% of pts w/COPD)Diagnosis
H&P
Peripheral cyanosis, productive cough, tachypnea, tachycardia
Dyspnea, pursed-lip breathing w/use of accessory muscles for respiration, ↓ breath sounds, wheezing
Acute exacerbation of COPD is mainly a clinical dx and generally is manifested w/worsening dyspnea, sputum purulence, and volume.Classification
Imaging
CXR: hyperinflation w/flattened diaphragm, tenting of the diaphragm at the rib, and retrosternal chest space, ↑ AP diameter
↓ Vascular markings and bullae in pts w/“emphysema”
Thickened bronchial markings and enlarged right side of the heart in pts w/“chronic bronchitis”Treatment
H. Pulmonary Vascular Disease
1. Pulmonary Embolism (PE)
Definition
Lodging of a thrombus or other embolic material from a distant site in the pulmonary circulation
Etiology
Risk factors for PE:• Hematologic disease (e.g., factor V Leiden mutation, antithrombin III deficiency, protein C deficiency, protein S deficiency, lupus anticoagulant, PV, dysfibrinogenemia, PNH, acquired protein C resistance w/o factor V Leiden, G20210A prothrombin mutation)
• Prolonged immobilization, ↓ mobility
• Postoperative state, major surgery
• Trauma to lower extremities, immobilizer or cast
• Estrogen-containing birth control pills, hormone replacement Rx
• Prior h/o DVT or PE
TABLE 11-9
Guideline Recommendations for Hospital Management of COPD Exacerbations
| Global Initiative for Chronic Obstructive Lung Disease∗ | American Thoracic Society/European Respiratory Society† | National Institute for Clinical Excellence‡ | |
| Date of statement | 2010 | 2004 | 2010 |
| Diagnostic testing | Chest radiograph, oximetry, ABGs, and ECG. Other testing as warranted by clinical indication. | Chest radiograph, oxygen saturation, ABGs, ECG, sputum Gram stain, and culture | Chest radiograph, ABG, ECG, complete blood count, sputum smear and culture, blood cultures if febrile |
| Bronchodilator therapy | Inhaled short-acting ß2-agonist is recommended. Consider ipratropium if inadequate clinical response. Consider theophylline or aminophylline as second-line intravenous therapy. | Inhaled short-acting ß2-agonist and/or ipratropium with spacer or nebulizer, as needed | Administer inhaled drugs by nebulizer or handheld inhaler. Specific agents and dosing regimens are not specified. Consider theophylline if response to inhaled bronchodilators is inadequate. |
| Antibiotics | Recommended if (1) increases in dyspnea, sputum volume, and sputum purulence all are present; (2) increase in sputum purulence along with increase in either dyspnea or sputum volume; or (3) need for assisted ventilation. See original document for complex treatment algorithm. | Base choice on local bacterial resistance patterns. Consider amoxicillin/clavulanate or respiratory fluoroquinolones. If Pseudomonas species and/or other Enterobacteriaceae are suspected, consider combination therapy. | Administer only if history of purulent sputum. Initiate with an aminopenicillin, a macrolide, or a tetracycline, taking into account local bacterial resistance patterns. Adjust therapy according to sputum and blood cultures. |
| Systemic corticosteroids | Daily prednisolone 30-40 mg (or its equivalent) orally for 7-10 days | Daily prednisone 30-40 mg orally for 10-14 days; equivalent dose intravenously if unable to tolerate oral intake Consider inhaled corticosteroids. | Daily prednisolone 30 mg (or its equivalent) orally for 7-14 days |
| Supplemental oxygen | Maintain oxygen saturation >90%. Monitor ABGs for hypercapnia and acidosis. | Maintain oxygen saturation >90%. Monitor ABGs for hypercapnia and acidosis. | Maintain oxygen saturation within the individualized target range. Monitor ABGs. |
| Assisted ventilation | Indications for NPPV include severe dyspnea, acidosis (pH ≤7.35) and/or hypercapnia (PCO2 >45 mm Hg), and RR >25 breaths/min. Contraindications to NPPV include respiratory arrest, hemodynamic instability, impaired mental status, copious bronchial secretions, and extreme obesity. Intubate if contraindication to NPPV or failure of NPPV (worsening ABGs or clinical status). Consider likelihood of recovery and patient’s wishes and expectations before intubation. | Consider with pH <7.35 and PCO2 >45-60 mm Hg and RR >24 breaths/min. Institute NPPV in a controlled environment, unless there are contraindications (e.g., respiratory arrest, hemodynamic instability, impaired mental status, copious bronchial secretions, and extreme obesity). Intubate if contraindication to NPPV or failure of NPPV (worsening ABGs or clinical status). | NPPV treatment of choice for persistent hypercapnic respiratory failure. Consider functional status, body mass index, home oxygen, comorbidities, prior ICU admissions, age, and FEV1 when assessing suitability for intubation and ventilation. |
∗ Data from http://www.goldcopd.com.
† Data from MacNee W: Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper. Eur Respir J 23:932-946, 2004.
‡ Data from http://www.nice.org.uk.
From Goldman L, Schafer AI (eds): Goldman’s Cecil Medicine, 24th ed. Philadelphia, Saunders, 2012.
TABLE 11-10
Wells Clinical Prediction Rule for Likelihood of Pulmonary Embolism
| Variable | Points |
| Predisposing Factors | |
| Previous VTE | 1.5 |
| Recent surgery or immobilization | 1.5 |
| Cancer | 1 |
| Symptoms | |
| Hemoptysis | 1 |
| Signs | |
| HR >100 bpm | 1.5 |
| Clinical signs of DVT | 3 |
| Clinical Judgment | |
| Alternative diagnosis less likely than PE | 3 |
| Clinical Probability | Total Points |
| Low | <2 |
| Moderate | 2-6 |
| High | >6 |
Modified from Wells PS, Ginsberg JS, Anderson DR, et al: Use of a clinical model for safe management of patients with suspected pulmonary embolism. Ann Intern Med 129:997-1005, 1998.
• CHF
• Pregnancy and early puerperium
• Visceral cancer (lung, pancreas, alimentary and GU tracts)
• Spinal cord injury
• Prolonged air travel
• Central venous catheterization
• Advanced age
• Obesity, smoking
• COPD, DM, acute medical illness
Diagnosis
H&P
Most common physical finding: tachypnea
Chest pain: may be nonpleuritic or pleuritic (infarction)
Syncope (massive PE)
Hemoptysis, cough
Evidence of DVT: may be present (e.g., swelling and tenderness of extremities)
Cardiac exam: tachycardia, pulmonic component of S2, murmur of tricuspid insufficiency, RV heave, right-sided S3
Pulmonary exam: rales, localized wheezing, friction rubLabs
ABGs: ↓ PaO2 and PaCO2, ↑ pH
A-a O2 gradient (measure of the difference in O2 concentration between alveoli and arterial blood): An nl A-a gradient makes the dx of PE unlikely.
Plasma D-dimer by ELISA: An nl plasma D-dimer level is useful to r/o PE in pts w/nondiagnostic lung scan and a low pretest probability of PE. However, it cannot “rule in” PE because it is ↑ w/many other disorders (e.g., metastatic cancer, trauma, sepsis, postoperative state).Imaging
CXR: ↑ diaphragm, pleural effusion, dilation of pulmonary artery, infiltrate or consolidation, abrupt vessel cutoff, or atelectasis. A wedge-shaped consolidation in the middle and lower lobes suggests a pulmonary infarction and is known as Hampton’s hump.
Spiral CT: excellent modality for dx PE (Fig. 11-8). It can also detect other pulmonary disease that can mimic PE.
Lung scan (in pt w/nl CXR):• An nl lung scan does r/o PE.
• A V/Q mismatch suggests PE, and a lung scan interpretation of high probability is confirmatory.
Figure 11-9 is a diagnostic algorithm incorporating the Wells criteria, D-dimer testing, and V/Q scan.
FIGURE 11-8 Integrated strategy for diagnosis of pulmonary embolism (PE) using clinical probability assessment, measurement of D-dimer, and computer tomography angiography (CTA) as primary imaging test. Patients with low clinical probability (i.e., PE unlikely, negative D-dimer) need no further testing, but if D-dimer is positive, they should proceed to CTA, and if this is nondiagnostic, to ultrasonography of legs. Then either treat or repeat ultrasound in 1 week. Patients with high clinical probability (i.e., PE likely) need not have D-dimer measure but should proceed directly to CTA. If CTA is not diagnostic, options are to perform ultrasonography of legs or proceed to pulmonary angiogram. If ultrasound of legs is negative, options are to repeat in 1 week or proceed to pulmonary angiography. (From Vincent JL, Abraham E, Moore FA, et al [eds]: Textbook of Critical Care, 6th ed. Philadelphia, Saunders, 2011.)
FIGURE 11-9 Integrated strategy for diagnosis of suspected PE using clinical probability assessment, measurement of D-dimer, and V/Q scan as primary imaging test. Patients with low clinical probability (i.e., PE unlikely, negative D-dimer) need no further investigation. If D-dimer is positive, V/Q scan performed; if not diagnostic, proceed to ultrasound. Then either treat or repeat ultrasound in 1 week. Patients with high probability (i.e., PE likely) need not have D-dimer measured but should proceed directly to V/Q scan. If V/Q scan not diagnostic, options are to perform CTA, pulmonary angiography, or ultrasonography of legs. If ultrasonography is negative, either repeat in 1 week or perform pulmonary angiogram. (From Vincent JL, Abraham E, Moore FA, et al [eds]: Textbook of Critical Care, 6th ed. Philadelphia, Saunders, 2011.)
Angiography: Pulmonary angiography is the gold standard; however, it is invasive, expensive, and not readily available in some clinical settings. False(+) pulmonary angiograms may result from mediastinal disorders such as radiation fibrosis and tumors.
CTA is an accurate, noninvasive tool in the dx of PE at the main, lobar, and segmental pulmonary artery levels. A major advantage of CTA over standard pulmonary angiography is its ability to dx intrathoracic disease other than PE that may account for the pt’s clinical picture. It is also less invasive, less costly, and more widely available. Its major shortcoming is its poor sensitivity for subsegmental emboli. It is contraindicated in patients with GFR<30/renal failure.
Gadolinium-enhanced MRA of the pulmonary arteries has a moderate sensitivity and high specificity for the dx of PE; MRA is best reserved for selected pts when CT scan and lung scan are inconclusive and the risk of pulmonary angiography is high.
ECG: abnl in 85% of pts w/acute PE. Frequent abnlities are sinus tachycardia; S1,Q3,T3 pattern (10% of pts); S1,S2,S3 pattern; T wave inversion in V1 to V6; acute RBBB; new-onset AF; ST-segment depression in lead II; RV strain.Treatment
See the section on venous thromboembolism in Chapter 7 for Rx of PE.
Acute pulmonary artery embolectomy may be indicated in a pt w/massive PE and refractory hypotension.2. Pulmonary Hypertension
Definition
Mean PAP >25 mm Hg at rest or >30 mm Hg w/exercise. Sustained ↑ in PAP secondary to pulmonary venous pressure, hypoxic pulmonary vasoconstriction, or flow is referred to as secondary pulmonary HTN.
Etiology and Classification
Diagnosis
H&P
Exertional dyspnea: most common presenting sx (60%)
Fatigue and weakness
Syncope, classically exertion related or after a warm shower w/peripheral vasodilation
Chest pain
Hoarse voice from compression of recurrent laryngeal nerve by an enlarged pulmonary artery (Ortner’s syndrome)
Loud P2 component of the second heart sound and paradoxical splitting of second heart sound
Right-sided S4
JVD
Abd distention/ascites
Prominent parasternal (RV) impulse
Holosystolic TR murmur heard best along the left fourth parasternal line that ↑ in intensity w/inspiration
Peripheral edemaLabs
CBC: nl or may show secondary polycythemia
ANA (r/o connective tissue disease), HIV, LFTs, antiphospholipid Abs
ABGs: ↓ PO2 and SaO2
PFTs: r/o obstructive or restrictive lung disease
Overnight sleep study: r/o sleep apnea/hypopneaImaging
ECG: RA enlargement (tall P wave >2.5 mV in leads II, III, aVF) and RV enlargement (RAD >100 and R wave > S wave in lead V1)
CXR: enlargement of the main and hilar pulmonary arteries w/rapid tapering of the distal vessels, described as peripheral oligemia. RV enlargement may be evident on lateral films.
Spiral CT or V/Q scan: r/o PE
Doppler echo: assesses ventricular function, excludes significant valvular disease, and visualizes abnl shunting of blood between heart chambers if present. It also provides an estimate of the pulmonary artery systolic pressure.TABLE 11-11
Updated Clinical Classification of Pulmonary Hypertension
Group 1
Pulmonary Arterial Hypertension (PAH)
Idiopathic PAH
Heritable
BMPR2
ALK1, endoglin (with or without hereditary hemorrhagic telangiectasia)
Unknown
Drug- and toxin-induced
Associated with
Connective tissue diseases
HIV infection
Portal hypertension
Congenital heart diseases
Schistosomiasis
Chronic hemolytic anemia
Persistent Pulmonary Hypertension of the Newborn
Pulmonary Veno-occlusive Disease with Left-to-Right Shunts and/or Pulmonary Capillary Hemangiomatosis
Group 2
Pulmonary Hypertension Secondary to Left-Sided Heart Disease
Systolic dysfunction
Diastolic dysfunction
Valvular disease
Group 3
Pulmonary Hypertension Secondary to Lung Diseases and/or Hypoxia
COPD
Interstitial lung disease
Other Pulmonary Diseases with Mixed Restrictive and Obstructive Pattern
Sleep-disordered breathing
Alveolar hypoventilation disorders
Chronic exposure to high altitude
Developmental abnormalities
Group 4
Chronic Thromboembolic Pulmonary Hypertension (50% have no hx of DVT/PE)
Group 5
Pulmonary Hypertension with Unclear Multifactorial Mechanisms
Hematologic disorders: myeloproliferative disorders, splenectomy
Systemic disorders: sarcoidosis, pulmonary Langerhans cell histiocytosis: lymphangioleiomyomatosis, neurofibromatosis, vasculitis
Metabolic disorders: glycogen storage disease, Gaucher’s disease, thyroid disorders
Others: tumoral obstruction, fibrosing mediastinitis, chronic renal failure on dialysis
ALK1, Activin receptor-like kinase type 1; BMPR2, bone morphogenetic protein receptor type 2.
Modified From Simonneau G et al: Updated clinical classification of pulmonary hypertension. J Am Coll Cardiol 54:S43-S54, 2009.
Treatment
Acute Rx
Diuretics (e.g., furosemide 40-80 mg qd)
Digoxin in pts w/AF
Short-acting vasodilators: IV adenosine, epoprostenol, or inhaled nitric oxideChronic Rx
CCB (diltiazem, amlodipine, or nifedipine)
Prostanoids (epoprostenol, treprostinil, and iloprost) act as potent vasodilators of pulmonary arteries and inhibitors of Plt aggregation.
Endothelin receptor antagonists: bosentan, ambrisentan, and sitaxsentan
Phosphodiesterase inhibitors: sildenafil and tadalafil
Warfarin Rx w/goal INR 1.5 to 2.0 is recommended for all pts w/PPH and although not proven may be indicated in secondary pulmonary HTN.
Lung transplantation and heart-lung transplantation are other options in pts w/end-stage class IV disease. Atrial septostomy may be performed as a bridge to transplantation.TABLE 11-12
Overview of Idiopathic Interstitial Pneumonias
| Diagnosis | Clinical Findings | HRCT Features | Differential Diagnosis |
| UIP/IPF | 40-70 yr, M>F; >6-mo dyspnea, cough, crackles, clubbing; poor response to steroids | Peripheral, basal, subpleural reticulation and honeycombing, ± ground-glass opacity | Collagen vascular disease, asbestosis, CHP, scleroderma, drugs (bleomycin, methotrexate) |
| NSIP | 40-50 yr, M = F; dyspnea, cough, fatigue, crackles; may respond to steroids | Bilateral, patchy, subpleural ground-glass opacity, ± reticulation | Collagen vascular disease, CHP, DIP |
| RB-ILD | 30-50 yr, M > F; dyspnea, cough | Ground-glass, centrilobular nodules, ± centrilobular emphysema | Hypersensitivity pneumonitis |
| AIP/diffuse alveolar damage | Any age, M = F; acute-onset dyspnea, diffuse crackles and consolidation | Ground-glass consolidation, traction bronchiectasis, and architectural distortion | ARDS, infection, edema, hemorrhage |
| COP | Mean 55 yr, M = F; <3-mo hx of cough, dyspnea, fever; may respond to steroids | Subpleural and peribronchial consolidation, ± nodules in lower zones; atoll sign (ring-shaped opacity) | Collagen vascular disease, infection, vasculitis, sarcoidosis, lymphoma, alveolar carcinoma |
| DIP | 30-54 yr, M > F; insidious onset weeks to months of dyspnea, cough | Ground-glass opacity, lower zone, peripheral | Hypersensitivity pneumonitis, NSIP |
| LIP | Any age, F > M | Ground-glass opacity, ± poorly defined centrilobular nodules, thin-walled cysts, and air trapping | DIP, NSIP, hypersensitivity pneumonitis |
AIP, Acute interstitial pneumonia; CHP, chronic hypersensitivity pneumonitis; COP, cryptogenic organizing pneumonia; DIP, desquamative interstitial pneumonitis; IPF, idiopathic pulmonary fibrosis; LIP, lymphoid interstitial pneumonia; NSIP, nonspecific interstitial pneumonia; RB-ILD, respiratory bronchiolitis–associated interstitial lung disease; UIP, usual interstitial pneumonia.
From Ferri F: Ferri’s Clinical Advisor: 5 Books in 1. 2013 edition. Philadelphia, Mosby, 2012.
I. Diffuse Parenchymal Lung Disease
1. Interstitial Lung Disease (ILD)
ILD includes a large group of nonmalignant disorders characterized by diffuse damage to the lung parenchyma by inflammation and fibrosis or granulomatous reaction in interstitial or vascular areas. Table 11-12 provides an overview of idiopathic interstitial pneumonias.
Diagnosis
H&P
Dyspnea
Tachypnea
Bibasilar end-inspiratory dry crackles
Pulmonary HTN
Cyanosis, clubbingLabs
ABGs: nl or may show respiratory alkalosis
ANA, ANCA, ACE level, RF, LDH
Bronchoscopy and BAL may help identify type of ILD. However, their role in defining the stage of disease and the response to Rx is controversial.
Bx is the most effective method for confirming dx and assessing disease activity.Imaging (Box 11-5)
CXR, HRCT: bibasilar reticular pattern
PFTs: Well-defined patterns in PFTs are usually consistent w/restrictive defect (↓ FRC, RV, and TLC) resulting from ↓ lung compliance caused by alveolar wall thickening from inflammation and fibrosis. Diffusing capacity ↓ from inflammation and thickening of alveolar walls, although nonspecific. FEV1/FVC is usually nl or because lung stiffness keeps small airways open, although some conditions (e.g., sarcoidosis) may ↓ airflow.Box 11-5 Radiographic Features That Suggest Specific Causes of Interstitial Lung Disease
Hilar or Mediastinal Lymphadenopathy
Sarcoidosis
Berylliosis
Silicosis (eggshell calcification)
Lymphocytic interstitial pneumonia
Amyloidosis
Gaucher’s disease
Pleural Disease
Asbestosis (pleural effusion, thickening, plaques, mesothelioma)
Systemic rheumatic disorders
Lymphangioleiomyomatosis (chylous effusion)
Nitrofurantoin
Radiation pneumonitis
Pneumothorax
Histiocytosis X
Lymphangioleiomyomatosis
Neurofibromatosis
Tuberous sclerosis
Preserved Lung Volumes or Hyperinflation
Bronchiolitis obliterans organizing pneumonia
Chronic hypersensitivity pneumonitis
Histiocytosis X
Lymphangioleiomyomatosis
Neurofibromatosis
Sarcoidosis
Tuberous sclerosis
Upper Lobe Distribution
Ankylosing spondylitis
Berylliosis
Histiocytosis X
Silicosis
Chronic hypersensitivity pneumonitis
Necrobiotic nodules of rheumatoid arthritis
From Goldman L, Ausiello D (eds): Cecil Textbook of Medicine, 22nd ed. Philadelphia, Saunders, 2004.
Treatment
Prednisone 0.5 to 1 mg/kg qd × 4 to 12 wk, then re-evaluate; if stable, taper; if not, maintain × another 4 to 12 wk; if still not improved, add cyclophosphamide or azathioprine.
Supplemental O2 PRN in pts w/hypoxemia; avoidance of tobacco and occupational exposuresJ. Granulomatous Lung Disease
1. Sarcoidosis
Chronic systemic granulomatous disease of unknown cause, characterized histologically by the presence of nonspecific, noncaseating granulomas
Diagnosis
H&P
Clinical manifestations often vary w/stage of the disease and degree of organ involvement; pts may be asymptomatic, but CXR may demonstrate findings consistent w/sarcoidosis (see the later section on imaging). Nearly 50% of pts w/sarcoidosis are dx by incidental findings on CXR. Frequent manifestations:• Pulmonary manifestations: dry, nonproductive cough; dyspnea; chest discomfort
• Constitutional sx: fatigue, weight loss, anorexia, malaise
• Visual disturbances: blurred vision, ocular discomfort, conjunctivitis, iritis, uveitis (65% of pts)
• Dermatologic manifestations: erythema nodosum (10% of pts), macules, papules, SC nodules, hyperpigmentation, lupus pernio (indurated violaceous lesions on the nose, lips, ears, cheeks that can erode into underlying cartilage and bone)
• Myocardial disturbances (5% of pts): arrhythmias, cardiomyopathy
• Splenomegaly, hepatomegaly
• Rheumatologic manifestations: arthralgias have been reported in up to 40% of pts
• Neurologic and other manifestations: cranial nerve palsies, diabetes insipidus, meningeal involvement, parotid enlargement, hypothalamic and pituitary lesions, peripheral adenopathy
Labs
Hypergammaglobulinemia, anemia, leukopenia
LFT abnlities
Hypercalcemia (11% of pts), hypercalciuria (40% of pts): secondary to GI absorption, abnl vitamin D metabolism, and calcitriol production by sarcoid granuloma
ACE in 60% of pts; nonspecific and generally not useful as a dx tool and in following the course of the diseaseImaging
CXR and chest CT• Adenopathy of the hilar and paratracheal nodes
• Parenchymal changes may also be present, depending on the stage of the disease: stage 0, nl x-ray; stage I, bilateral hilar adenopathy; stage II, stage I plus pulmonary infiltrate; stage III, pulmonary infiltrate w/o adenopathy; stage IV, advanced fibrosis w/evidence of honeycombing, hilar retraction, bullae, cysts, and emphysema.
PFTs (spirometry and diffusing capacity of the lung for CO): may be nl or may reveal a restrictive pattern or obstructive pattern
18FDG-PET: useful in identifying sites for dx bx in pts w/o apparent lung involvement
18FDG-PET and MRI w/gadolinium: useful in pts w/suspected cardiac and neurologic involvementTreatment
Most pts will not require any Rx.
Corticosteroids should be considered in pts w/severe sx (e.g., dyspnea; chest pain; hypercalcemia; ocular, CNS, or cardiac involvement; and progressive pulmonary disease).
MTX 7.5 to 15 mg once/wk: in pts w/progressive disease refractory to corticosteroids
Hydroxychloroquine: effective for chronic disfiguring skin lesions, hypercalcemia, and neurologic involvement
NSAIDs: useful for musculoskeletal sx and erythema nodosumPrognosis
Most pts w/sarcoidosis have spontaneous remission within 2 yr and do not require Rx. Their course can be followed by periodic clinical evaluation, CXR, and PFTs.
However, 25% to 33% of pts have unrelenting disease leading to clinically significant organ impairment. Adverse prognostic factors are age at onset >40 yr, cardiac involvement, neurosarcoidosis, progressive pulmonary fibrosis, chronic hypercalcemia, chronic uveitis, involvement of nasal mucosa, nephrocalcinosis, and presence of cystic bone lesions and lupus pernio.2. Granulomatosis with Polyangiitis (Wegener’s Granulomatosis)
Multisystem disease generally consisting of the classic triad of:• Necrotizing granulomatous lesions in the upper or lower respiratory tracts
• Generalized focal necrotizing vasculitis involving both arteries and veins
• Focal GN of the kidneys
“Limited forms” of the disease can also occur and may evolve into the classic triad. Granulomatosis with polyangiitis can be classified by the “ELK” classification, which identifies the three major sites of involvement: E, ears, nose, and throat or respiratory tract; L, lungs; K, kidneys.Diagnosis
H&P
Clinical manifestations often vary w/the stage of the disease and degree of organ involvement.
Frequent manifestations:• Upper respiratory tract: chronic sinusitis, chronic otitis media, mastoiditis, nasal crusting, obstruction and epistaxis, nasal septal perforation, nasal lacrimal duct stenosis, saddle nose deformities (resulting from cartilage destruction)
• Lung: hemoptysis, multiple nodules, diffuse alveolar pattern
• Kidney: renal insufficiency, GN
• Skin: necrotizing skin lesions
• Nervous system: mononeuritis multiplex, cranial nerve involvement
• Joints: monarthritis or polyarthritis (nondeforming), usually affecting large joints
• Mouth: chronic ulcerative lesions of the oral mucosa, “mulberry” gingivitis
• Eye: proptosis, uveitis, episcleritis, retinal and optic nerve vasculitis
Labs
(+) test result for cytoplasmic pattern of ANCA (cANCA)
Other labs: anemia, leukocytosis, hematuria, RBC casts, and proteinuria; ↑ serum Cr, ↓ CrCl, ↑ ESR, (+) RF, and ↑ CRP
Bx of one or more affected organs should be attempted; the most reliable source for tissue dx is the lung. Lesions in the nasopharynx (if present) can be easily sampled.Imaging
CXR: bilateral multiple nodules, cavitated mass lesions, pleural effusion (20%)
PFTs: useful in detecting stenosis of the airwaysTreatment
Prednisone 60 to 80 mg/day and cyclophosphamide 2 mg/kg. Once the disease is under control, prednisone is tapered and cyclophosphamide is continued. Other potentially useful agents in pts intolerant of cyclophosphamide are azathioprine, MTX, and mycophenolate mofetil.
TMP-SMX: useful alternative in pts w/lesions limited to the upper or lower respiratory tracts in absence of vasculitis or nephritis. Rx w/TMP-SMX (160 mg/800 mg bid) also ↓ the incidence of relapses in pts w/Wegener’s granulomatosis in remission. It is also useful in preventing Pneumocystis pneumonia, which occurs in 10% of pts receiving induction Rx. When used for prophylaxis, dose of TMP-SMX (160 mg/800 mg) is 1 tablet 3×/wk.K. Pleural Disease
1. Pleural Effusion/Thoracentesis
Indications
1. Presence of any pleural effusion of unknown cause
2. Relief of dyspnea caused by large pleural effusion
Contraindications
1. Clotting abnlities
2. Thrombocytopenia
3. Uncooperative pt or pt w/severe cough or hiccups
Localization of Pleural Effusion
1. Physical examination: dullness to percussion, loss of tactile fremitus
2. CXR: PA view is usually sufficient in identifying the fluid collection; but in case of equivocal effusions, a lateral decubitus CXR can demonstrate layering out of the pleural fluid. Effusions >1 cm on a lateral decubitus film are usually sufficiently large to be removed at the bedside w/o additional imaging.
3. Fluoroscopy, ultrasonography, or CT guidance in performing thoracentesis if the fluid collection has the following qualities:
a. <10 mm thick
b. Not freely movable on the lateral decubitus x-ray view
Procedure
1. Position pt in a sitting position w/arms and head supported on a bedside adjustable table.
2. Identify the area of effusion by gentle percussion.
3. Clean the area w/povidone-iodine solution and maintain strict aseptic technique.
4. Insert the needle in the posterior chest (≈5 to 10 cm lateral to the spine, in the midpoint between the spine and the posterior axillary line) in one to two interspaces below the point of dullness to percussion.
5. Anesthetize the skin and SC tissues w/1% to 2% lidocaine, using a 25-gauge needle.
6. Make sure that the needle is positioned and advanced above the superior margin of the rib (the intercostal nerve and the blood supply are located near the inferior margin). “Walk” the needle over the superior margin of the rib and deeper into the interspace, to anesthetize the intercostal muscle layers.
7. Apply (−) pressure as the needle is advanced. In thin pts, this needle is often sufficiently long to reach the pleural space. If pleural fluid is withdrawn, anesthetize the pleura adequately and note the depth at which it was reached. If it is not reached, use a longer, 20- to 22-gauge syringe w/1% to 2% lidocaine, advance it slowly w/(−) pressure along the same tract as the prior needle, anesthetize the pleura adequately, and advance the needle into the pleural space. If the purpose of the thoracentesis is for dx only, a 30- to 50-mL syringe may then be attached and pleural fluid withdrawn for diagnostic studies. If the purpose of the thoracentesis is fluid removal, proceed further as below. Place a clamp on the needle at skin level to mark the depth, then remove the needle and note the depth of insertion needed for the thoracentesis needle.
8. In the previous puncture site, insert a 17-gauge needle (flat bevel) attached to a 30-mL syringe via a three-way stopcock connected to a drainage tube.
9. Slowly advance the needle (above the superior margin of the rib) and gently aspirate while advancing.
10. Keep a clamp or a hemostat on the needle at the level previously marked to prevent it from inadvertently advancing forward. Many thoracentesis kits have a catheter that may be advanced over the needle to remove the risk of a sharp needle within the pleural space.
11. Remove the necessary amount of pleural fluid (usually 100 mL for diagnostic studies), but do not remove >1000 mL of fluid at any one time because of risk of pulmonary edema or hypotension (pneumothorax from needle laceration of the visceral pleura is also much more likely to occur if an effusion is completely drained).
12. Gently remove the needle.
13. Obtain measurements of serum LDH, alb, glucose, and total protein levels.
14. Process the pleural fluid; the initial laboratory studies should be aimed only at distinguishing an exudate from a transudate (Fig. 11-10).
a. Tube 1: protein, LDH, alb
b. Tubes 2, 3, 4: Save the fluid until further notice. In selected pts w/suspected empyema, ascertaining a pH level may be useful (generally <7.0).
TABLE 11-13
Evaluation of Pleural and Peritoneal Effusions
| Test | Exudate | Transudate |
| Fluid LDH | >200 IU/dL | <200 IU/dL |
| Fluid protein | >3 g | <3 g |
| Fluid-to-serum LDH ratio | >0.6 IU/dL | <0.6 IU/dL |
| Fluid-to-serum protein ratio | >0.5 IU/dL | <0.5 IU/dL |
| Specific gravity | >1.016 | <1.016 |
| Appearance | Cloudy | Clear, thin |
| Viscous | Nonclotting |
From Weissleder R, Wittenberg J, Harisinghani M, Chen JW (eds): Primer of Diagnostic Imaging, 5th ed. St. Louis, Mosby, 2011.
L. Lung Cancer
The WHO distinguishes 12 types of pulmonary neoplasms. Among them, the major types are squamous cell carcinoma, adenocarcinoma, small cell carcinoma, and large cell carcinoma. However, the crucial difference in the dx of lung cancer is between small cell (SCLC) and non–small cell lung cancer (NSCLC) types because the prognosis and therapeutic approach are different. NSCLC consists of 3 main histologic subtypes (adenocarcinoma, squamous cell, and large cell carcinoma) compromising >80% of all lung cancers. Bronchoalveolar carcinoma, another type of lung cancer, accounts for ≈5% of all lung cancers. Table 11-14 describes selected characteristics of lung carcinomas.
Diagnosis
H&P
Cough, hemoptysis, dyspnea, wheezing
Chest, shoulder, and bone pain
Weight loss, fatigue, fever, anorexia, dysphagia
FIGURE 11-10 Diagnostic thoracentesis algorithm. (From Ferri FF: Ferri’s Best Test: A Practical Guide to Clinical Laboratory Medicine and Diagnostic Imaging, 2nd ed. Philadelphia, Mosby, 2010.)
TABLE 11-14
Selected Characteristics of Lung Carcinomas
| Histologic Cell Type | Percentage of Total (%) | Frequent Location | Initial Metastases | Comments |
| Adenocarcinoma | 35 | Midlung and periphery | Lymphatics | Associated w/peripheral scars |
| Squamous cells (epidermoid) | 20-30 | Central | Local invasion | Frequent cavitation and obstructive phenomena |
| Small cell (oat cell) | 20 | Central | Lymphatics | Cavitation rare Associated w/deletion of short arm of chromosome 3 |
| Large cell | 15-20 | Periphery | CNS, mediastinum | Rapid growth rate w/early metastases |
| Bronchioloalveolar | 5 | Periphery, may be bilateral | Lymphatics, hematogenous, and local invasion | No correlation w/cigarette smoking Cavitation rare |
Paraneoplastic syndromes:• Lambert-Eaton syndrome: myopathy involving proximal muscle groups
• Endocrine manifestations: hypercalcemia, ectopic ACTH, SIADH
• Neurologic: subacute cerebellar degeneration, peripheral neuropathy, cortical degeneration
• Musculoskeletal: polymyositis, clubbing, hypertrophic pulmonary osteoarthropathy
• Hematologic or vascular: migratory thrombophlebitis, marantic thrombosis, anemia, thrombocytosis, or thrombocytopenia
• Cutaneous: acanthosis nigricans, dermatomyositis
Pleural effusion (10% of pts), recurrent pneumonias (secondary to obstruction), localized wheezing
SVC syndrome
Horner’s syndrome: constricted pupil, ptosis, facial anhidrosis caused by spinal cord damage between C8 and T1 secondary to a superior sulcus tumor (bronchogenic carcinoma of the extreme lung apex). A superior sulcus tumor associated w/ipsilateral Horner’s syndrome and shoulder pain is known as a Pancoast tumor.Procedures
Flexible fiberoptic bronchoscopy: Brush and bx specimens are obtained from any visualized endobronchial lesions and other abnormal areas identified through endobronchial ultrasonography guidance.
Transthoracic FNAB w/fluoroscopic or CT scan guidance is used to evaluate peripheral pulmonary nodules.
Mediastinoscopy and anteromedial sternotomy is indicated in suspected tumor involvement of the mediastinum.
Bone marrow aspiration is performed in selected pts w/SCLC w/LDH or cytopenia.
PFTs are performed determine whether the pt can tolerate any loss of lung tissue. The postop predicted pulmonary function = preop function − calculated % of lung function to be lost with surgery. Pneumonectomy is possible if the pt has a preoperative FEV1 >2 L, or if the maximal voluntary ventilation is >50% of predicted capacity. Individuals w/FEV1 >1.5 L are suitable for lobectomy w/o further evaluation unless there is evidence of ILD or undue dyspnea on exertion. In that case, DLCO should be measured. If the DLCO is <80% predicted nl, the pt is not clearly operable; if the postop predicted FEV1 and DLCO are >40%, surgery is possible.
Genetic mutations testing of lung specimen: detection of epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK)Imaging
CXR
CT chest
PET w/18F-fluorodeoxyglucose (18FDG-PET): for preop staging of NSCLC
CT of liver and brain; bone scan in all pts w/SCLC and pts w/NSCLC suspected of involving these organsStaging
The international staging system for NSCLC: Stage I is N0 (no lymph node involvement). Stage II (N1 [spread to ipsilateral bronchopulmonary or hilar lymph nodes]) includes localized tumors for which surgical resection is the preferred Rx. Stage III is subdivided into IIIA (potentially resectable) and IIIB. The surgical management of stage IIIA disease (N2 [involvement of ipsilateral mediastinal nodes]) is controversial. Only 20% of N2 disease is considered minimal disease (involvement of only one node) and technically resectable. Stage IV indicates metastatic disease. The pathologic staging system uses a tumor–nodal involvement–metastasis system.
In pts w/SCLC, the staging system from the Veterans Administration Lung Cancer Study Group contains two stages:• Limited stage disease: confined to the regional lymph nodes and to one hemithorax (excluding pleural surfaces)
• Extensive stage disease: spread beyond the confines of limited-stage disease
Treatment
NSCLC
Surgical resection (lobectomy, pneumonectomy)• Indicated in pts w/limited disease (stage I or II). This represents 15% to 30% of diagnosed cases. Lobectomy can be performed by VATS with less morbidity and shorter hospitalization.
• Preoperative chemoRx: consider in pts w/more advanced disease (stage IIIA) who are being considered for surgery. Gene expression profiles that predict the risk of recurrence in pts w/early-stage (IA) NSCLC have been identified. These pts are at high risk for recurrence and may also benefit from adjuvant chemoRx.
• Postoperative adjuvant chemoRx (chemoRx given after surgical resection of an apparently localized tumor to eradicate occult mets) w/vinorelbine plus cisplatin: consider in pts w/completely resected stage IB or stage II NSCLC and good performance status. Adjuvant chemoRx is generally indicated for pts w/resected tumors that are stages IIA through IIIA.
Rx of unresectable NSCLC• RadioRx can be used alone or in combination w/chemoRx; it is used primarily for Rx of CNS and skeletal mets, SVC, and obstructive atelectasis. Although thoracic radioRx is generally considered standard Rx for stage III disease, it has limited effect on survival. Palliative radioRx should be delayed until sx occur because immediate Rx offers no advantage over delayed Rx and results in more adverse events from the radioRx.
• ChemoRx: Current drugs of choice are paclitaxel + either carboplatin or cisplatin; cisplatin + vinorelbine; gemcitabine + cisplatin; carboplatin or cisplatin + docetaxel. The overall results are disappointing, and none of the standard regimens for NSCLC is clearly superior to the others. The addition of bevacizumab to paclitaxel + carboplatin results in significant survival benefit but carries a risk of Rx-related death. Gefitinib and erlotinib are PO inhibitors of EGFR tyrosine kinase. Both agents are approved only for pts in whom at least one prior chemoRx regimen has failed. The inhibition of ALK in lung tumors with crizotinib, an orally available small-molecule inhibitor of the ALK tyrosine kinase, has resulted in tumor shrinkage and significantly prolonged progression-free survival.
• The addition of chemoRx to radioRx improves survival in pts w/locally advanced, unresectable NSCLC. The absolute benefit is relatively small, however, and should be balanced against the toxicity associated w/the addition of chemoRx.
SCLC
Limited stage disease: standard Rxs include thoracic radioRx and chemoRx (cisplatin and etoposide)
Extensive stage disease: standard Rxs include combination chemoRx (cisplatin or carboplatin + etoposide or combination of irinotecan and cisplatin)
Prophylactic cranial irradiation: for pts in complete remission to ↓ the risk of CNS metastasisM. Respiratory Failure Classification
A. Hypoxemic (“Type I”) Respiratory Failure
↓ in oxyhemoglobin that does not correct with supp. O2
PaO2 (ambient air) ≤ 60 mmHg
PCO2 typically normal or < 40 mmHg
Hypoxemia is the result of persistent perfusion of lung units that are not ventilating as a result of fluid (pus, blood, edema) or alveolar collapse => intrapulmonary shunt physiology results in inability to correct with supp. O2. Hypoxemia can be corrected with administration of PEEP which “results” and opens up collapsed/fliud-filled alveoli.• Examples: ARDS, CHF, Atelectasis, Pneumonia
B. Hypercapnic (“Type II”) Respiratory Failure
Occurs as a result of insufficient alveolar ventilation from ↑CO2
PaO2 ↓
PCO2 ↑ as a result of ↑CO2 production and/or decreased alveolar ventilation (secondary to respiratory muscle weakness/excessive mechanical work of breathing, decreased respiratory drive, and lung diseases with impaired gas exchange such as: COPD)• Examples: COPD/Asthma (obstructive lung disease), Neuromuscular disease (Myasthenia Gravis, GBS when VC < 15-20 cc/kg and NIF < 30). Restrictive Lung Disease (Extrapulmonary – kyphoscoliosis, ascites, and Intrapulmonary – Fibrotic Lung disease)
