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Respiratory Emergencies 

Respiratory Emergencies
Chapter:
Respiratory Emergencies
Author(s):

Vivek K. Moitra

and Tricia E. Brentjens

DOI:
10.1093/med/9780199377275.003.0003
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date: 07 April 2020

Acute Lung Injury and Acute Respiratory Distress Syndrome

Definition

Acute onset of bilateral pulmonary infiltrates on noted chest X-ray with pulmonary edema, poor systemic oxygenation, and absence of left atrial hypertension.

Presentation

Patients with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) are often intubated and mechanically ventilated. Their physical exam is notable for reduced breath sounds and possibly wheezing. Increased peak inspiratory and plateau pressures may be seen with positive pressure ventilation. Arterial blood gases may show hypercarbia in the setting of poor lung compliance.

Pathophysiology

The early phase of ARDS is characterized by pulmonary capillary leak and interstitial and alveolar edema. There is a loss of surfactant activity. During the late phase of ARDS, pulmonary fibrosis and decreased lung compliance can develop.

Immediate Management

  • Increase FIO2 and titrate positive end-expiratory pressure (PEEP) to maintain adequate oxygenation.

  • Consider ventilation with low tidal volumes (4–8 cc/kg predicted body weight).

  • Avoid plateau pressures >30 cm H2O.

  • Permissive hypercapnia may be necessary.

  • Consider alternative ventilatory strategies (e.g., airway pressure release ventilation [APRV]).

Differential Diagnosis

  • Pulmonary edema

  • Multilobar pneumonia

  • Diffuse alveolar hemorrhage

  • Pneumonitis

  • Pulmonary embolus

  • Transfusion related acute lung injury (TRALI)

  • Brochiolitis obliterans-organizing pneumonia (BOOP)

Diagnostic Studies

  • Chest X-ray (shows patchy infiltrates that extend to the periphery)

  • Right heart catheterization (CVP or pulmonary artery catheter)

  • Thoracic ultrasound shows B-lines (suggests an interstitial process)

Subsequent Management

  • Treat the precipitating cause of ALI/ARDS.

  • Employ mechanical ventilation as necessary to manage respiratory failure.

  • Transfer the patient to the intensive care unit (ICU) for further management.

  • Neuromuscular blockade may rarely be required to facilitate ventilation and oxygenation.

  • Consider the prone position and nitric oxide therapy for refractory hypoxemia.

  • Consider extracorporeal membrane support if medical management and mechanical ventilation fail.

Risk Factors

  • Sepsis

  • Pneumonia

  • Pneumonitis

  • Pancreatitis

  • Toxic drug reaction

  • Inhalational injury

  • Massive transfusion

  • Mechanical ventilation

Prevention

Early and aggressive treatment of precipitating causes may prevent progression to lung injury.

Special Considerations

  • Patients who come to the operating room with ARDS can present with increased peak airway pressures and high levels of positive end-expiratory pressure (PEEP).

  • Patients often require specialized transport from an ICU (see Transportation of a Critically Ill Patient).

  • The anesthesiologist must be familiar with the patient’s mode of ventilation in order to ensure safe transport. Arterial blood gas samples guide changes to ventilator strategy in the operating room.

Further Reading

Brodie D, Bacchetta M. Extracoporeal membrane oxygenation for ARDS in adults. N Engl J Med. 2011; 365: 1905–1914.Find this resource:

Jason D, Christie P, Lanken, N. Acute lung injury and the acute respiratory distress syndrome. In: Hall JB, Schmidt G, Wood LDH, eds. Principles of Critical Care. 3rd ed. New York: McGraw-Hill; 2005:515–547.Find this resource:

Slutsky AS, Ranieri VM. Ventilator-induced lung injury. N Engl J Med. 2013; 369: 2126–2136.Find this resource:

Bronchospasm

Definition

Spasmodic contraction of bronchial smooth muscle.

Presentation

Decreased SpO2 or an upsloping of the ETCO2 tracing on the capnograph. An increase in peak inspiratory pressure (PIP) may also be seen if the patient is mechanically ventilated. Visible slowing or lack of chest fall may be observed. Wheezing or decreased breath sounds may be heard. Hypotension is a late sign in severe bronchospasm due to hypoxia or auto-PEEP, which decreases venous return.

Pathophysiology

Bronchospasm can occur after a mechanical (intubation) or chemical (anaphylatoxin) stimulus activates mast cells, eosinophils, lymphocytes, epithelial cells, and macrophages to release various mediators, such as histamine, to constrict bronchial smooth muscle. The hyperirritable airway is often edematous and produces mucus, which further increases airway resistance and can lead to mucus plugging.

Differential Diagnosis

  • Mechanical obstruction (e.g., kinked endotracheal tube, mucus plug)

  • Pulmonary edema

  • Tension pneumothorax

  • Aspiration pneumonitis

  • Pulmonary embolus

  • Pulmonary edema

  • Endobronchial intubation

Immediate Management

  • Increase FIO2 to 100%.

  • Increase the inspired concentration of a potent volatile anesthetic if one is being used (bronchodilator properties).

  • Administer β‎-agonist bronchodilators (e.g., nebulized albuterol).

  • Consider epinephrine 10–30 mcg IV in refractory cases, titrated to effect.

Diagnostic Studies

Clinical presentation. No specific diagnostic studies.

Subsequent Management

  • If surgery has not started, consider postponing an elective procedure in the setting of unremitting severe bronchospasm.

  • Consider administration of steroids (e.g., hydrocortisone 100 mg IV).

  • Maintain an adequate depth of anesthesia to prevent further bronchospasm.

  • Avoid unnecessary airway manipulation.

  • Avoid triggering agents, such as histamine-releasing drugs.

  • Consider postoperative mechanical ventilation.

Risk Factors

  • History of asthma, chronic obstructive pulmonary disease (COPD), emphysema

  • Recent upper airway infection

  • Airway manipulation

  • Can occur in healthy patients

Prevention

  • If the clinical situation permits, avoid endotracheal intubation in at-risk patients.

  • Consider use of a regional anesthesia technique if the patient has a history of reactive airway disease.

  • Patients with a history of asthma have bronchial hyper-reactivity, and may benefit from preoperative corticosteroid treatment.

  • Intravenous agents, including propofol, ketamine, and lidocaine, may decrease airway resistance.

Special Considerations

  • Even with adequate preparation and implementation of preventive measures, bronchospasm may still occur in the operating room. Avoid elective surgery within 10–14 days of an upper respiratory infection, as the airways can be hyper-reactive during this time period.

Further Reading

Woods BD, Sladen RN. Perioperative considerations for the patient with asthma and bronchospasm. Br J Anaesthesiol. 2009; 103(S1): i57–i65.Find this resource:

Decreased ETCO2 (Intraoperative)

Definition

End tidal CO2 <30 mm Hg

Presentation

A decrease in ETCO2 in a mechanically ventilated patient may occur with either hypocarbia (hyperventilation) or hypercarbia (inability to eliminate CO2). A sudden decrease in ETCO2 may indicate cardiovascular collapse or an embolic phenomenon.

Etiology

Most commonly caused by hyperventilation in a mechanically ventilated patient. It may also reflect increased dead space with a normal PaCO2. Sudden, catastrophic decrease in cardiac output will decrease the ETCO2 because of decreased perfusion (CO2 is not being carried to lungs).

Immediate Management

  • Assess cause of decreased ETCO2

  • Send arterial blood to determine PaCO2

  • Sudden:

    • Consider cardiovascular collapse.

    • Assess perfusion by other means (blood pressure, presence of a pulse oximeter waveform).

    • Assess volume status.

    • Consider providing cardiovascular support using inotropes or vasopressors.

    • If an embolic event is suspected:

      • Adjust head of bed down.

      • Flush the surgical field with saline if air embolus is suspected.

      • Provide hemodynamic support, e.g., epinephrine 4 mcg/min titrate as necessary.

  • Gradual:

    • Decrease minute ventilation (if patient is being ventilated).

Differential Diagnosis

  • Air leak in sample line

  • Gas analyzer error

  • Low ETCO2 with hypocarbia (PaCO2 <35 mm Hg)

  • Hyperventilation

    • High minute ventilation in a mechanically ventilated patient

    • Pain

    • Anxiety

    • Compensation for metabolic acidosis

  • Low ETCO2 with hypercarbia (PaCO2 >45 mm Hg)

    • Pulmonary thromboembolus

    • Air embolus

    • Fat embolus

    • CO2 embolus (laparoscopic surgery)

    • Amniotic fluid embolus

  • Obstruction

    • Mechanical (kinking of tube)

    • Bronchospasm

    • COPD

  • Low cardiac output state

  • Esophageal intubation

Diagnostic Studies

  • Arterial blood gas (ABG) to determine PaCO2

  • Transthoracic or transesophageal echocardiogram to assess cardiac function. Note: An echocardiogram will also detect bubbles if a venous air embolus is the cause.

  • Spiral computed tomography (CT) if a thromboembolic event is suspected

Subsequent Management

  • Correct the underlying cause.

  • Provide hemodynamic support.

  • Intubate the trachea and initiate mechanical ventilation.

Risk Factors

  • Sitting craniotomy or any surgical procedure in which the operative site is above the heart: air embolus

  • Bone cement implantation: fat embolus (see Bone Cement Implantation Syndrome).

  • Hemorrhagic or cardiogenic shock: low cardiac output state

Further Reading

Eisenkraft J, Leibowitz A. Hypoxia and equipment failure. In: Yao F, ed. Anesthesiology: Problem-Oriented Patient Management. 5th ed. New York: Lippincott Williams & Wilkins; 2003:1116–1136.Find this resource:

Difficult Controlled Ventilation

Definition

Inability to effectively oxygenate and/or ventilate a patient who is mechanically ventilated.

Presentation

High peak airway pressures and hypercarbia are observed with difficult controlled ventilation. Patients are often hypoxemic may be hypotensive because increased intrathoracic pressure can decrease venous return.

Etiology

  • High peak airway pressures can be caused by poor compliance of the lung parenchyma and increased resistance to airflow due to:

    • Mucous plug

    • Bronchospasm

    • Pulmonary edema

    • Auto-PEEP

    • Pneumothorax

  • Elevated plateau pressure (the pressure applied to the small airways and the alveoli during positive pressure) suggests poor lung compliance.

  • Low peak airway pressures and loss of measured tidal volumes may indicate an air leak in the circuit or in the tracheobronchial tree (i.e., a bronchopulmonary fistula).

Immediate Management

  • Increase FiO2 to 100% and titrate PEEP to maintain adequate oxygenation.

  • Auscultate breath sounds.

  • Begin manual ventilation.

  • Suction the endotracheal tube.

  • Administer a bronchodilator if bronchospasm is suspected (albuterol 2–4 puffs into the ETT).

  • Administer a diuretic if pulmonary edema is present (furosemide 20 mg IV).

  • Exclude anesthesia gas machine or ventilator failure.

  • Increase the level of sedation and consider neuromuscular blockade if necessary.

Differential Diagnosis

  • Increased resistance to flow

  • Bronchospasm

  • Obstruction

    • Kinked endotracheal tube

    • Mucus plug

    • Decreased lung compliance

    • Inadequate muscle relaxation

    • Tension pneumothorax

    • Auto-PEEP

    • Acute lung injury/acute respiratory distress syndrome

    • Pulmonary edema

    • Aspiration

    • Opioid-induced chest wall rigidity

    • Pulmonary hemorrhage

    • Intra-abdominal hypertension/abdominal compartment syndrome

    • High insufflation pressures in laparoscopic surgery

Diagnostic Studies

  • Measure peak airway pressures.

  • Measure plateau pressure.

  • Perform chest X-ray.

  • Perform thoracic ultrasonography.

Subsequent Management

  • Decrease tidal volume to limit volutrauma.

  • Increase respiratory rate to ensure adequate minute ventilation.

  • Monitor for evidence of auto-PEEP (sudden hypotension, clinical evidence of “breath stacking”).

  • Consider CT scan of the chest if the underlying cause is unknown.

  • Treat the underlying cause of decreased compliance.

  • If conventional mechanical ventilation is inadequate, consider high frequency oscillatory ventilation (HFOV), airway pressure release ventilation (APRV), or extracorporeal membrane oxygenation (ECMO).

Risk Factors

  • Patients with COPD are at risk for auto-PEEP.

  • Patients with diffuse pulmonary injury (infection, sepsis) may develop ARDS as their disease progresses.

Prevention

  • Maintain adequate sedation.

  • Monitor for signs of auto-PEEP.

Special Considerations

  • Patients who are difficult to ventilate may have increased peak airway pressure, require high levels of PEEP, and often require transport to or from an ICU. These patients may require deep sedation and an ICU ventilator in order for safe transport from the ICU to the Operating Room. The anesthesiologist must be familiar with the patient’s mode of ventilation in order to ensure a safe transport (see Transporting the Critically Ill Patient). Arterial blood gas samples can guide changes in ventilator strategy in the operating room.

Further Reading

Brodie D, Bacchetta M. Extracoporeal membrane oxygenation for ARDS in adults. N Engl J Med. 2011; 365: 1905–1914.Find this resource:

Schmidt G. Ventilator waveforms: clinical interpretation. In: Hall JB, Schmidt G, Wood LDH, eds. Principles of Critical Care. 3rd ed. New York: McGraw-Hill; 2005:427–443.Find this resource:

Hemoptysis

Definition

Cough productive of blood or bloody sputum. Massive hemoptysis is the production of 300–600 cc of blood in a 12- to 24-hour period.

Presentation

Reduced breath sounds, frank blood in the sputum, diffuse pulmonary infiltrates on chest X-ray. In an intubated patient, blood may appear in the endotracheal tube. Hypoxia and increased peak inspiratory pressures may occur during positive pressure ventilation in patients with massive hemoptysis. Coagulopathy can trigger hemoptysis, and anemia may be present. Hemoptysis may be the presenting symptom for pulmonary infection or malignancy.

Pathophysiology

Disruption of the pulmonary vessels lining the trachea, bronchi, or alveoli caused by infection, tumor, vascular disorders, or trauma. Coagulopathy may exacerbate bleeding.

Differential Diagnosis

  • Nasal trauma

  • Pharyngeal trauma

  • Gastrointestinal bleeding

Immediate Management

  • Increase FiO2 and titrate PEEP to maintain oxygenation.

  • Inspect the nose and pharynx to exclude an upper-airway source of bleeding.

  • Consider the possibility of a gastrointestinal source of bleeding.

  • Consider bronchoscopy to identify the bleeding site.

  • Consider inserting a double lumen endotracheal tube or bronchial blocker to isolate the bleeding site (see page [link]).

  • If hemoptysis is life-threatening, consider endobronchial ablation, bronchial artery embolization, external beam irradiation, or surgical resection.

Diagnostic Studies

Chest CT and bronchoscopy may localize the source of pulmonary bleeding.

Subsequent Management

  • Identify and treat the cause of a coagulopathy.

  • Consider a surgical consultation if bronchial embolization is unsuccessful or multiple bleeding vessels are seen with angiography.

  • Consider a course of steroids in patients with vasculitis.

  • Consider plasmapheresis in patients with Goodpasture syndrome.

Risk Factors

  • Infection

  • Tumor

  • Pulmonary vascular abnormalities

  • Cardiac causes (e.g., mitral stenosis)

  • Trauma

  • Coagulopathy

  • Pulmonary–renal syndromes (Goodpasture syndrome)

Prevention

  • Avoid unnecessary instrumentation of the airway.

  • Correct underlying coagulopathy (see Coagulopathy).

Special Considerations

  • Frequent suctioning of the endotracheal tube may cause hemoptysis.

Further Reading

Albert R. Massive hemoptysis. In: Hall JB, Schmidt G, Wood LDH, eds. Principles of Critical Care. 3rd ed. New York: McGraw-Hill; 2005:583–585.Find this resource:

Sakr L, Dutau H. Massive hemoptysis: an update on the role of bronchoscopy in diagnosis and management. Respiration. 2010; 80(1): 38–58.Find this resource:

Hypercarbia (Intraoperative)

Definition

Increased arterial partial pressure of carbon dioxide (PaCO2 > 45 mm Hg).

Presentation

Tachycardia, agitation, hypertension, and eventually obtundation.

Etiology

Hypercarbia is caused by either hypoventilation or increased CO2 production. Hypoventilation due to decreased respiratory drive or airway obstruction in sedated patients often leads to hypercarbia. Poor lung compliance may reduce minute ventilation and cause hypercarbia. Residual anesthetic effects or inadequate reversal of muscle relaxants can cause postoperative hypercarbia. Splinting due to pain can lead to increased dead space, hypoventilation, and hypercarbia. Hypermetabolic states and fever may contribute to increased CO2 production.

Immediate Management

  • Intubate the trachea and initiate mechanical ventilation for severe respiratory acidosis, if the patient is unable to protect his or her airway, or if respiratory failure is imminent.

  • Consider noninvasive positive pressure ventilation (CPAP, BiPap) if airway protection is not required.

  • Increase minute ventilation to reduce PaCO2.

  • Ask the surgeon to lower insufflation pressure during laparoscopic surgery.

  • In a spontaneously breathing patient, consider judicious reversal of opioids with naloxone (naloxone 0.04-mg IV increments).

Differential Diagnosis

  • Hypoventilation

    • Low minute ventilation

    • Narcotics or oversedation

    • Inadequate reversal of muscle relaxant

    • Splinting

  • Malignant hyperthermia (see Special Considerations).

  • Bronchospasm (COPD or asthma exacerbation)

  • Acute lung injury, acute respiratory distress syndrome

  • Severe pneumonia

  • Aspiration

  • Shivering

  • Sepsis

  • CO2 insufflation during laparoscopy

  • Bicarbonate administration

  • Thyrotoxicosis

Diagnostic Studies

Arterial blood gas (ABG) analysis to quantify degree of hypercarbia and acidosis.

Subsequent Management

  • Treat the underlying cause of hypercarbia.

Risk Factors

  • Laparoscopic surgery (insufflation of peritoneal cavity with CO2)

  • Obesity

  • Obstructive sleep apnea (OSA)

  • Chronic CO2 retainers

  • COPD

  • Asthma

  • Poor lung compliance

  • Narcotic administration

Prevention

  • Judicious use of narcotics and other sedatives

  • Adequate reversal of muscle relaxants

  • Adequate minute ventilation, especially in laparoscopic surgery

Special Considerations

  • Hypercarbia causes respiratory acidosis that cannot be compensated for in the acute period. Hypercarbia may cause severe hypertension, hyperkalemia, arrhythmias, myocardial depression, altered mental status, increased intracranial pressure, and increased pulmonary vascular resistance.

  • Rapidly rising ETCO2 in conjunction with tachycardia and rising temperature may be caused by malignant hyperthermia (MH). Malignant hyperthermia must be diagnosed quickly and treatment initiated immediately (see Malignant Hyperthermia).

Further Reading

Lane J. Postoperative respiratory insufficiency. In: Atlee JL, ed. Complications in Anesthesia. 2nd ed. Philadelphia: Saunders Elsevier; 2007:877–880.Find this resource:

Hypoxemia (Intraoperative)

Definition

Decreased partial pressure of oxygen in the blood (PaO2 <60 mm Hg) often manifested by a decrease in SpO2.

Presentation

Decreased SpO2, cyanosis, and possibly hypertension and agitation. Left untreated, hypoxemia may progress to hypotension, bradycardia, arrhythmias, and neurologic and myocardial ischemia.

Etiology

  • Oversedation and/or narcotic overdose can cause hypoventilation and airway obstruction in patients undergoing surgery with monitored anesthetic care (MAC).

  • Decrease in functional residual capacity (FRC)

  • Position (supine position decreases FRC)

  • Atelectasis and alveolar shunting

  • Blunted hypoxic pulmonary vasoconstriction (may be caused by inhaled anesthetics)

  • Ventilation perfusion mismatching

  • Intrapulmonary shunt caused by mainstem bronchus intubation

  • Anesthesia machine malfunction

Immediate Management

  • Increase FIO2 to 100% and titrate PEEP while assessing patient.

  • Ascultate the lung fields to assess breath sounds.

  • Check ETCO2 to ensure that the ETT is in the trachea and that the lungs are being ventilated.

  • If the patient is not already intubated, consider intubation and mechanical ventilation for severe hypoxia or if respiratory failure is imminent.

Differential Diagnosis

  • Esophageal intubation

  • Mechanical disconnect from ventilator or O2 source

  • Right mainstem intubation

  • Airway obstruction

  • Hypoventilation

  • Atelectasis

  • Presence of a mucus plug

  • Bronchospasm

  • Pneumothorax

  • Pulmonary embolus

  • Pulmonary edema

  • Acute lung injury

  • Aspiration

  • Low cardiac output state

Diagnostic Studies

  • Arterial blood gas analysis (ABG) to quantify PaO2

  • Chest X-ray

  • Consider bronchoscopy (assess ETT placement, find a possible obstruction).

  • Thoracic ultrasonography

Subsequent Management

  • Increase FiO2 to maintain oxygenation.

  • Titrate PEEP to improve oxygenation.

  • Treat the underlying cause of hypoxemia.

  • Prepare for endotracheal intubation and mechanical ventilation.

  • Consider nitric oxide therapy for refractory hypoxemia.

  • Consider extracorporeal membrane oxygenation for refractory hypoxemia.

Risk Factors

  • Underlying pulmonary disease

  • Obstructive sleep apnea

  • Aspiration risk

  • Use of narcotics

  • Advanced age

  • Obesity

  • Shivering

Prevention

  • Confirm ETT position with capnography and auscultation.

  • Use narcotics and sedatives carefully in patients who are breathing spontaneously.

  • Ensure that the patient is adequately ventilated.

Special Considerations

  • Intraoperative hypoxemia is one of the most common problems that an anesthesiologist encounters, and should be considered life threatening. Prompt diagnosis and treatment are essential to preventing further complications, such as hypotension, arrhythmias, and end-organ damage.

Further Reading

Lane J. Postoperative respiratory insufficiency. In: Atlee JL, ed. Complications in Anesthesia. 2nd ed. Philadelphia: Saunders Elsevier; 2007:877–880.Find this resource:

Pneumothorax

Definition

Presence of gas, usually air, in the pleural cavity that leads to collapse of the lung. This condition may be life threatening if the gas cannot escape (i.e., tension pneumothorax).

Presentation

A small pneumothorax is often asymptomatic. As the pneumothorax becomes larger, hypoxia, tachypnea, tachycardia, and chest pain may occur. It may be possible to hear hyper-resonance on the affected side with percussion. Decreased or absent breath sounds may also be heard on the affected side. Increased peak airway pressures and plateau pressures occur in mechanically ventilated patients. A tension pneumothorax is often associated with hypotension.

Pathophysiology

A tension pneumothorax occurs when a one-way valve mechanism occurs after injury to the pleural space. With each inspiration, gas is trapped in the pleural space causing collapse of the lung. If intrapleural pressure increases significantly, mediastinal shift causes kinking of major veins at the thoracic inlet of the neck and inferior vena cava, resulting in decreased venous return and hypotension.

Immediate Management

  • Increase FIO2 to 100%.

  • Decompress the pleural space by inserting a large bore needle in the mid-clavicular line in the second intercostal space (Figure 3.1).

  • Insert a chest tube.


Figure 3.1 Decompression of tension pneumothorax.

Figure 3.1 Decompression of tension pneumothorax.

Differential Diagnosis

  • Hemothorax

  • Mucus plug

  • Endobronchial intubation

  • Severe bronchospasm

Diagnostic Studies

  • Auscultation (absent breath sounds on the affected side)

  • Percussion (hyper-resonance).

  • Chest X-ray (lung collapse and mediastinal shift)

  • Thoracic ultrasonography (presence of lung point; absence of lung sliding)

Subsequent Management

  • Bronchoscopy if bronchial tree injury is suspected

  • Surveillance chest X-ray to evaluate progression of pneumothorax

  • Chest tube management

Risk Factors

  • Central line insertion

  • Laparoscopic surgery

  • Excessive tidal volume or peak airway pressure

  • Obstructed chest tube (e.g., kink or clot)

  • Pulmonary blebs

Prevention

  • Avoid excessive tidal volume or peak airway pressure.

  • Chest X-ray or imaging after central line placement to prevent progression of a small pneumothorax to a tension pneumothorax.

Special Considerations

  • Tension pneumothorax should be considered in patients who develop a pulseless electrical activity (PEA) cardiac arrest.

Further Reading

Ali J. Torso trauma. In: Hall JB, Schmidt G, Wood LDH, eds. Principles of Critical Care. 3rd ed. New York: McGraw-Hill; 2005:1421–1441.Find this resource:

Pulmonary Edema

Definition

The abnormal accumulation of extravascular fluid in the lung parenchyma.

Presentation

The first signs of pulmonary edema in an anesthetized patient are often hypoxemia and decreased SpO2. Rales or wheezing are heard over the lung fields. Frothy sputum may be noted in the endotracheal tube. In an awake patient, respiratory distress, tachycardia, and agitation. Jugular venous distention may be seen on physical examination.

Pathophysiology

  • High pulmonary and venous hydrostatic pressure (cardiogenic) or increased capillary permeability (noncardiogenic).

  • Cardiogenic pulmonary edema is caused by impaired venous drainage from the pulmonary vasculature to the left atrium. This often occurs when the left atrial pressure is high in the setting of left ventricular dysfunction and/or valvular abnormalities.

  • Negative pressure or postobstruction pulmonary edema occurs when negative intrapleural pressure increases the pulmonary hydrostatic pressure gradient, causing fluid to move from the pulmonary vasculature to the interstitium.

Immediate Management

  • Increase FIO2 to 100% and titrate PEEP to maintain oxygenation.

  • Initiate diuresis (start with furosemide 20 mg IV).

  • Intubate the trachea and begin positive pressure ventilation if the patient is hypoxic or respiratory failure is imminent.

  • If cardiogenic pulmonary edema is suspected, consider afterload reduction with nitroglycerine (infusion starting at 0.5 mcg/kg/min) and support blood pressure with vasopressors (see Congestive Heart Failure).

  • Treat the underlying cause.

Differential Diagnosis

  • Aspiration pneumonitis

  • Acute lung injury/ARDS

  • Neurogenic pulmonary edema

  • Aspiration pneumonitis

  • Fat embolism

  • TACO (transfusion-associated circulatory overload)

  • TRALI (transfusion-related acute lung injury)

Diagnostic Studies

  • Chext X-ray (bilateral pulmonary infiltrates and edema around pulmonary arteries)

  • Pulmonary artery catheter or echocardiogram can differentiate between cardiogenic and noncardiogenic pulmonary edema.

  • Thoracic ultrasonography (presence of B lines)

Subsequent Management

  • Ventilatory support, including PEEP

  • Serial arterial blood gas measurements

  • Central venous pressure monitoring may aid in medical management, for example, diuresis.

Risk Factors

  • Cardiogenic

    • Systolic dysfunction

    • Diastolic dysfunction

    • Volume overload

    • Myocardial infarction

    • Valvular abnormalities

  • Respiratory

    • Negative pressure

    • Laryngospasm

    • Upper airway obstruction

    • Upper airway tumor or foreign body

    • Tonsillar hypertrophy

Prevention

  • Avoid fluid overload in a patient with compromised myocardial function.

  • Ensure adequate perfusion pressure and avoid tachycardia in patients with coronary artery disease.

  • Identify patients at risk for airway obstruction.

Special Considerations

  • Negative pressure pulmonary edema often resolves within 24 hours. Cardiogenic pulmonary edema may occur 2–3 days postoperatively when fluids are mobilized.

Further Reading

Ali J. Special considerations in the surgical patient. In: Hall JB, Schmidt G, Wood LDH, eds. Principles of Critical Care. 3rd ed. New York: McGraw-Hill; 2005:1321–1330.Find this resource:

Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, et al. Focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines developed in collaboration with the International Society for Heart and Lung Transplantation. J Am Coll Cardiol. 2009; 53(15): e1–e90.Find this resource:

Pulmonary Thromboembolism

Definition

Obstruction of a pulmonary artery or one of its branches, most commonly by a venous thrombus that becomes dislodged and eventually travels to the lungs. Pulmonary embolus may also be caused by fat, air, carbon dioxide, or amniotic fluid emboli.

Presentation

The signs and symptoms may be subtle. Small emboli may go undetected; unexplained fever, tachycardia, and rales may be the only presenting symptoms. Some patients may present with a triad of dyspnea, hemoptysis, and chest pain. Patients with large emboli may present with sudden hypoxia, hypercarbia, tachypnea, decreased ETCO2, and circulatory collapse.

Pathophysiology

Pulmonary thromboembolism occurs when a venous thrombus is dislodged and travels to the lungs. This occurs most commonly in the setting of venous stasis or injury, and most thrombi originate in the lower extremity deep vein system. Pulmonary embolism can also be caused by air, fat, carbon dioxide, or amniotic fluid emboli. Gas exchange becomes impaired as dead space increases. A widened alveolar to arterial gradient is often seen. Right ventricular afterload increases.

Differential Diagnosis

  • Thromboembolism

  • Air embolism

  • Fat embolism

  • Amniotic fluid embolism

  • Acute myocardial infarction

  • Severe bronchospasm

  • Anaphylaxis

  • Pneumothorax

Immediate Management

  • Increase FIO2 to 100% to maintain oxygenation.

  • Consider intubation and mechanical ventilation if hypoxia is severe.

  • Support the circulation with fluid, vasopressors, and inotropes.

  • Consider right ventricular afterload reduction with nitric oxide.

  • Begin systemic anticoagulation if not contraindicated and a thromboembolism is diagnosed (heparin 80 U/kg IV bolus, then 18 U/kg per h IV, titrated to therapeutic INR)

  • NOTE: Consider thrombolytic therapy or embolectomy if the patient is hemodynamically unstable.

Diagnostic Studies

  • Helical chest computed tomography angiography

  • D-dimer is of limited value, as levels are often elevated in the perioperative setting.

  • Ventilation-perfusion scan

  • Noninvasive venous Doppler studies to assess for deep venous thrombosis

  • Echocardiography to evaluate for right ventricular dilation or strain

Subsequent Management

  • Identify the source of the embolism.

  • Continue anticoagulation if indicated.

  • Consider inserting an inferior vena cava filter if anticoagulation is contraindicated.

Risk Factors

  • Thromboembolism

    • Malignancy

    • Surgery and trauma

    • Immobility

    • Pregnancy

    • Hypercoagulable states

    • Obesity

    • Indwelling central lines

  • Other embolic events

    • Sitting craniotomy (air embolus)

    • Laparoscopic surgery (CO2 embolus)

    • Hip replacement (fat embolus)

Prevention

  • Intermittent compression stockings

  • Subcutaneous (SC) heparin (e.g., 5000 U SC) in high-risk patients

  • Early mobilization after surgery

Special Considerations

  • The decision to administer anticoagulants or thrombolytics may be complicated in postoperative patients, and must take into consideration the risk of postoperative bleeding.

  • Brain natriuretic peptide levels predict right ventricular dysfunction and mortality.

  • Pulmonary embolus should be considered in patients with PEA.

Further Reading

Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension. Circulation. 2011; 123: 1788–1818.Find this resource:

Respiratory Precautions

Bioterrorism, severe acute respiratory syndrome (SARS), multi-drug resistant tuberculosis, and H1N1 influenza have brought new concerns to the health care provider, and especially the anesthesiologist. Anesthesiologists must provide rapid and appropriate care when managing an airway, while at the same time making sure to protect themselves from communicable diseases.

The Centers for Disease Control and Prevention (CDC) recommends use of N95 respirator masks while caring for patients with suspected H1N1. The N95 mask is tighter-fitting than a traditional face mask (Figure 3.2). An N95 respirator covers the nose and mouth and is designed to have a tight fit. If worn correctly, it should filter out at least 95% of particles as small as 0.3 µm.


Figure 3.2 Standard fluid shield mask (top) and N95 respirator (bottom).

Figure 3.2 Standard fluid shield mask (top) and N95 respirator (bottom).

The use of eye protection in the form of fluid shields or goggles is also recommended to protect against contact with sputum, gastric contents, or other bodily fluids while securing a patient’s airway. Additionally, wearing a gown may further protect the anesthesiologist as well as other patients.

If a bioterrorism strike is suspected, gown, gloves, N95 respirators, and fluid shields should be worn. Immediately contact local authorities and the CDC for likely pathogens and take further proper precautions, including potentially a splash protective suit and a self-contained breathing apparatus.