Skip to Main Content

Obstetric Intensive Care Manual, 4e

Chapter 12: Respiratory Emergencies During Pregnancy

Alfredo F. Gei; Victor R. Suarez

INTRODUCTION

Respiratory complications during pregnancy are not unusual and can be life threatening. A careful interview and physical examination, a chest x-ray, and an arterial blood analysis are the most useful interventions in the evaluation of these conditions.

Understanding of the cardiorespiratory changes during pregnancy is essential for the diagnosis and treatment of emergencies in normal pregnant women and in women with underlying cardiopulmonary diseases.

BASIC SCIENCE

Oxygen is the basis of every aerobic reaction in our organism. The procurement and delivery of oxygen is a vital process that the pregnant woman has to perform for herself and her unborn child. Nature has ensured adequate mechanisms of adaptation in order to exchange oxygen with air and deliver it to her unborn child (and adapting body) through complex anatomic (Table 12-1) and physiologic changes (Table 12-2).

TABLE 12-1.Anatomic and Physiologic Respiratory Adaptations to Pregnancy

View Table||Download (.pdf)

TABLE 12-1. Anatomic and Physiologic Respiratory Adaptations to Pregnancy

Upper airways

Mucosal edema and friability
Capillary engorgement

(A smaller-sized endotracheal tube may be required for intubation because of swelling of the arytenoid region of the vocal cords)

Chest wall

Increases in chest wall circumference (6 cm)
Elevation of the diaphragm (5 cm)
Widening of the costal angles (from 70° to 104°)
Increase in diaphragmatic excursion (1.5 cm)

(All these changes occur before significant increases in uterine size, maternal body weight, or intra-abdominal pressure)

Respiratory musculature

Respiratory muscle function is unchanged
Diaphragm and intercostals accessory muscles contribute equally to tidal volume during pregnancy
Maximum inspiratory and expiratory pressures are unchanged

TABLE 12-2.Changes in Respiratory Variables During Pregnancy

View Table||Download (.pdf)

TABLE 12-2. Changes in Respiratory Variables During Pregnancy

Parameter

Definition

Change in pregnancy

Respiratory rate

Number of breaths per minute

• No change

Tidal volume

Volume of air inspired and expired at each breath

• Increase up to 40% since early breath pregnancy; remains essentially constant for the remainder of gestation (100-200 mL)

Minute ventilation (RR × Vt)

Total amount of air (gas) inspired and each minute

Sum of the volume of air (gas) participating in gas exchange plus the one filling the airway’s dead space (ie, not participating in gas exchange)

• Increase up to 40% since early pregnancy and remains essentially constant for the remainder of gestation (100-200 mL)

Vital capacity

Maximum volume of air that can be forcibly inspired after a maximum expiration

• Unchanged

Residual volume

Volume of air remaining in the lungs after a maximum expiration

• Decreases by ~20% due to elevation of the diaphragm

Functional residual capacity (FRC)

Volume of air in lungs at resting expiratory level

• Decreases by ~20% due to elevation of the diaphragm

Inspiratory capacity

Maximum volume of air that can be inspired from resting expiratory level

• Increases 100-300 mL (5%-10%) as a result of the reduction in FRC

RR, respiratory rate.

Respiration involves 2 different but interrelated phenomena: ventilation and oxygenation. The evaluation of these processes lays in the interpretation of arterial blood gases variables: Pco₂ and Po₂ (Figs. 12-1 and 12-2).

FIGURE 12-1.

Blood gas analysis I.

View Full Size||Download Slide (.ppt)

FIGURE 12-2.

Evaluation of hypoxemia.

View Full Size||Download Slide (.ppt)

Respiration requires that O₂ be obtained from an extracorporeal source (atmosphere or ventilator), then transferred across the alveolar-endothelial barrier, transported to the different organs in the periphery, and subsequently utilized in aerobic metabolism.

At term, there is a small decrease (200-400 mL, 4%) in total lung capacity. Vital capacity (VC) does not change significantly. Functional residual capacity (FRC) consistently decreases 300 to 500 mL (17%-20%). Changing from a sitting to a supine position at term causes a further decrease (25%) in FRC. This may increase closure of small airways, especially in obese patients in the supine or lithotomy positions.

BASIC PHYSIOLOGIC OXYGENATION CONCEPTS

O₂ content. The content of oxygen in arterial blood is the sum of that bound to hemoglobin (Hb) and that dissolved in plasma (normally about 1.5%). The main factor that determines the extent of O₂ binding to hemoglobin (saturation) is the Pao₂ (hemoglobin-oxygen dissociation curve). The shape of the curve indicates that unless the steep part of the curve is reached (a drop of Pao₂ to <60 mm Hg), there will not be a significant deleterious effect on Hb saturation and O₂ arterial content.
O₂ affinity. Several factors can change the affinity of Hb for O₂. Acidosis, fever, and increased 2,3-DPG, shift the curve to the right. In the slightly acidic environment of peripheral tissues, a right shift is important to unload O₂ to the cells. Alkalosis, hypothermia, and decreased 2,3-DPG, shift the curve to the left. In the slightly alkalotic environment of the pulmonary capillary, a left shift is important to load O₂ to the red blood cells. Affinity is also shifted to the left in the fetal hemoglobin.
O₂ delivery (Do₂). Systemic O₂ delivery is the product of arterial O₂ content (mL/L of blood) and cardiac output (mL/min).
O₂ consumption (Vo₂). In a normal adult at rest, it is approximately 250 mL/min. During exercise, it can rise to 3000 mL/min. When delivery cannot meet tissue demands, anaerobic metabolism occurs, leading to lactic acidosis.

RESPIRATORY PHYSIOLOGIC ADAPTATIONS OF PREGNANCY

Pregnancy increases O₂ consumption by 15% to 20% (Table 12-3). Half of this increase is associated with the requirements of the feto-placental unit, and the remaining half is secondary to the increased work by the maternal organs (heart, lungs, and kidneys). Increased cardiac output and minute ventilation explain how O₂ consumption increases despite no change in Pao₂ and a decrease in the arteriovenous O₂ difference (a-Vo₂ difference) as a result of an increase in oxygen delivery.

TABLE 12-3.Changes in Oxygenation Variables During Pregnancy

View Table||Download (.pdf)

TABLE 12-3. Changes in Oxygenation Variables During Pregnancy

Parameter

Modification

Magnitude

Peak

Oxygen consumption (Vo₂)

⇑

+20%

+40%-60%

Term

During labor

Oxygen delivery (Do₂)

⇔ ⇑

700-400 mL/min

Term

Resistance of the pulmonary circulation

⇓

–34%

34 wk

Despite the favorable effects of pregnancy (progesterone is a central stimulant) on ventilation, at least half of pregnant women complain of shortness of breath (dyspnea), fatigue, and decreased exercise tolerance during gestation.

OXYGENATION AND ACID-BASE HOMEOSTASIS

Pregnancy is characterized by a chronically compensated respiratory alkalosis due to the hyperventilation (rather than tachypnea) state of pregnancy. Pregnancy’s increase in minute ventilation (progesterone-induced hyperventilation of pregnancy) results in a decrease in Paco₂ to around 30 mm Hg. Maternal pH reflects the chronic compensated mild respiratory alkalosis. Compensation is secondary to the decline in bicarbonate concentration (secondary to increased renal excretion). The net result of these changes is facilitation of CO₂ exchange from fetus to the mother.

Oxygenation is affected in at least one-fourth of pregnant women while in a supine position (lower Pao₂ and larger A-a gradient). These changes are reversed when the maternal position changes to the upright state (Table 12-4).

TABLE 12-4.Changes in Arterial Blood Gases During Pregnancy

View Table||Download (.pdf)

TABLE 12-4. Changes in Arterial Blood Gases During Pregnancy

ABG variable

Nonpregnant adult

Pregnant

pH

7.35-7.43

7.40-7.47

Pco₂ (mm Hg)

37-40

27-34

(there is a compensatory increase in renal bicarbonate excretion)

Po₂ (mm Hg)

103

106-108 (sea level)
01-104 (third trimester)
Can drop to 90 (in the supine position during the II and III trimester)

P(a-a)o₂ (mm Hg)

14

20
+6 (supine position and III trimester)

Bicarbonate (mEq/L)

22-26

18-22

Base deficit (mEq/L)

1

3

CLINICAL IMPLICATIONS

It is not surprising that pregnant women complain of symptoms suggestive of pulmonary or cardiac disease. In most instances, a careful interrogation and physical examination can establish whether these symptoms are physiologic or a possibility of a specific condition that needs to be addressed and evaluated (Fig. 12-3).
Pregnant patients are prone to
- Hypoxemia (due to decreased FRC, increased alveolar ventilation, and increased O₂ consumption)
- Aspiration (slow gastric emptying, functional displacement of lower esophagus)
- Anesthetic overdose (decreased minimal alveolar concentration of anesthetics, decreased functional residual capacity, and increased alveolar ventilation). Induction and emergence of and from general anesthesia occurs more rapidly in pregnant women.

FIGURE 12-3.

Respiratory distress.

View Full Size||Download Slide (.ppt)

RESPIRATORY EMERGENCIES DURING PREGNANCY

The anatomic and physiologic changes of the cardiac (see Chap. 8) and respiratory systems explain why respiratory symptoms are common during pregnancy. The most frequent respiratory complaint is shortness of breath (dyspnea). Other symptoms include cough and hemoptysis. Unfortunately both benign and life-threatening conditions present with similar complaints. A careful evaluation of these symptoms will allow the practitioner to discern between pregnancy-related complaints and a more severe condition. Even when deemed benign, cardiorespiratory symptoms should be noted and evaluated prospectively in subsequent visits of the patient. Some of the conditions that can be suggested by history or physical examination are included in Fig. 12-3. Specific algorithms addressing the evaluation of dyspnea, cough, and hemoptysis (Figs. 12-4,12-5, 12-6) are suggested.

FIGURE 12-4.

Evaluation of dyspnea.

View Full Size||Download Slide (.ppt)

FIGURE 12-5.

Evaluation of cough.

View Full Size||Download Slide (.ppt)

FIGURE 12-6.

Evaluation of hemoptysis.

View Full Size||Download Slide (.ppt)

The most frequent indications for mechanical ventilation among obstetric patients admitted to an ICU are acute respiratory failure (39%) and hemodynamic failure (38%), followed by impaired consciousness (17%) and postoperative ventilation (6%).

Leading causes of acute respiratory distress syndrome (ARDS) during pregnancy are infection, preeclampsia or eclampsia, and aspiration.

The two most helpful clinical adjuncts in the evaluation of respiratory conditions during pregnancy are:

Arterial blood gas interpretation. The changes induced by the pregnant state are summarized in Table 12-4. Figures 12-1 and 12-2 illustrate the evaluation of ventilation and oxygenation through the laboratory analysis of an arterial blood sample.
Chest x-ray interpretation. Table 12-5 summarizes the changes described for pregnancy. Aside from heart enlargement secondary to hypervolemia and cardiac remodeling and some cephalad flow redistribution, all other criteria used to interpret chest radiograms remain the same as in the nonpregnant state. Figure 12-7 provides a guideline for evaluation of chest x-rays and the most common pathologic processes encountered by the site of affliction. As was the case with the arterial blood gases, more than one process may coexist and affect the patient.

FIGURE 12-7.

Evaluation of chest x-ray.

View Full Size||Download Slide (.ppt)

TABLE 12-5.Changes in Chest X-Ray During Pregnancy

View Table||Download (.pdf)

TABLE 12-5. Changes in Chest X-Ray During Pregnancy

Apparent cardiomegaly (enlarged transverse diameter)
Enlarged left atrium (lateral views)
Increased vascular markings
Straightening of left heart border
Postpartum pleural effusion (right-sided)

Multiple intercurrent diseases in the pregnant woman and several conditions specific to pregnancy may compromise the processes of oxygenation or ventilation. While the specific treatment of these conditions may differ, the recognition of the need for supportive respiratory therapy and the prompt institution of adequate ventilation and oxygenation support may be the difference between life and death.

RESPIRATORY FAILURE AND RESPIRATORY SUPPORT

Clinical guidelines for the recognition of respiratory failure (Table 12-6), means to provide noninvasive oxygen (Table 12-7), indications for mechanical ventilation (Table 12-8), indications for endotracheal intubation (Table 12-9), and guidelines for the initiation (Table 12-10) and discontinuation of mechanical ventilation (Table 12-11) are provided. In these situations, the processes of evaluation and treatment are frequently simultaneous (Figs. 12-4 and 12-8).

FIGURE 12-8.

Evaluation of respiratory distress during pregnancy.

View Full Size||Download Slide (.ppt)

TABLE 12-6.Criteria for the Diagnosis of Respiratory Failure

View Table||Download (.pdf)

TABLE 12-6. Criteria for the Diagnosis of Respiratory Failure

Mnemonic: MOVE
1. Mechanical
  1. Vital capacity <15 mL/kg
  2. Maximal inspiratory force (MIF) < –25 cm H₂O
  3. Respiratory rate >35/min
2. Oxygenation
  1. Pao₂ <70 mm Hg with Fio₂ of 0.4
  2. P(a-a)o₂: >350 mm Hg with Fio₂ of 1.0
3. Ventilation
  1. Paco₂ >55 mm Hg (if acute condition)
  2. Dead space/tidal volume (Vd/Vt) >0.6
4. End-inspiratory lung inflation inadequate for adequate gas exchange

TABLE 12-7.Means to Provide Noninvasive Oxygen Therapy

View Table||Download (.pdf)

TABLE 12-7. Means to Provide Noninvasive Oxygen Therapy

Nasal cannulas
- Can provide 24%-40% oxygen with flow rates up to 6 L/min.
- Oxygen at flow rates of 4 L/min or less need not be humidified.
Simple oxygen masks
- Can provide 35%-50%, depending on fit, at flow rates from 5 to 10 L/min.
- Flow rates need to be maintained at 5 L/min or higher to avoid rebreathing exhaled CO₂ that can be retained in the mask.
Partial rebreathing mask (simple mask with a reservoir bag)
- Oxygen flow should be supplied to maintain the reservoir bag at least one-third to one-half full in inspiration.
- At flow rates of 6-10 L/min, the system can provide 40%-70% oxygen.
Nonrebreathing mask (similar to the partial rebreathing mask except it has a series of one-way valves; one valve is between the mask and the bag to prevent exhaled air from returning to the bag)
- The delivered Fio₂ of this system is 60%-80%.
- There should be a minimum flow of 10 L/min.

TABLE 12-8.Indications for Mechanical Ventilation (Invasive or Noninvasive)

View Table||Download (.pdf)

TABLE 12-8. Indications for Mechanical Ventilation (Invasive or Noninvasive)

Severe respiratory or combined respiratory and metabolic acidosis
Sustained respiratory rate of 40/min
Abnormal breathing pattern suggestive of increased respiratory workload and/or respiratory muscle fatigue
Depressed mental status
Severe hypoxemia

TABLE 12-9.Indications for Endotracheal Intubation

View Table||Download (.pdf)

TABLE 12-9. Indications for Endotracheal Intubation

Mnemonic: GARDD

Gastropulmonary reflux and aspiration
Airway obstruction (present or suspected)
Respiratory arrest (actual or impending)
Depressed mental status
Difficulty managing secretions

TABLE 12-10.Guidelines for the Initiation of Mechanical Ventilation

View Table||Download (.pdf)

TABLE 12-10. Guidelines for the Initiation of Mechanical Ventilation

Primary goals of ventilatory support are
- Adequate oxygenation/ventilation
- Reduced work of breathing
- Synchrony between patient and ventilator
- Avoidance of high-end inspiration alveolar pressures
Five subsets of patients can be identified
- Normal lung mechanics and gas exchange (example: drug overdose)
  - Settings: ACV/PSV; Fio₂ of 0.5-1.0; TV: 8-15 mL/kg; RR: 8-12/min; inspiratory flow rate of 40-60 L/min; add sighs 6/h at 1.5 times Vt or PEEP of 5-7.5 cm H₂O to prevent atelectasis
- Severe airflow obstruction (example: drug overdose)
  - Settings: ACV/SIMV; Fio₂ of 0.5-1.0; TV: 5-7 mL/kg; RR: 12-15/min; inspiratory flow rate of 40-60 L/min; add PEEP if patient is triggering. Goals are to minimize alveolar overdistention (plat <30 cm H₂O) and to minimize alveolar dynamic hyperinflation auto-PEEP <10 cm H₂O or end-expiratory lung volumes <20 mL/kg
- Acute or chronic respiratory failure (example: status asthmaticus)
  - Settings: SIMV/ACV; Fio₂ of 0.4-0.6; TV: 5-7 mL/kg; RR: 24-28/min; inspiratory flow rate of 40-60 L/min
- Acute hypoxemic respiratory failure (example: ARDS)
  - Settings: ACV/PCV; Fio₂ of 1.0; TV: 5-7 mL/kg; RR: 24-28/min; minimal PEEP to keep Sao₂ of 90%. If volume is held constant, PEEP increases peak inspiratory airway pressure, a potentially undesirable effect in ARDS; PEEP levels >15 cm H₂O are rarely necessary
- Restrictive lung or chest wall disease (example: sarcoidosis)
  - Settings: Fio₂ of 0.5-1.0; TV: 5-7 mL/kg; RR: 18-24/min
Other recommendations
- Avoid high inspiratory peak pressures (>30 cm H₂O)
- Target pH and not Pco₂ to make changes to respiratory rate and minute ventilation
- Use PEEP in diffuse lung injury to support oxygenation and reduce the Fio₂
- Set trigger sensitivity to allow a minimal patient effort to initiate the inspiration
- In patients at risk, avoid choosing ventilator settings that limit expiratory time and cause or worsen auto-PEEP
- When poor oxygenation, inadequate ventilation, or excessively high-peak inspiratory pressures are thought to be related to patient intolerance of ventilator settings and are not corrected by ventilator adjustment, consider sedation, analgesia, and/or neuromuscular blockade

TABLE 12-11.Criteria for Determining Readiness for Extubation

View Table||Download (.pdf)

TABLE 12-11. Criteria for Determining Readiness for Extubation

Pao₂ >80 torr on Fio₂ of 0.6
Paco₂ <45 torr
Respiratory rate: <35 breaths/min
Tidal volume: >5 mL/kg
Vital capacity: >10 mL/kg
Minute ventilation: <10 L/min
Negative inspiratory force (NIF): < –20 cm H₂O
Shallow breathing index (respiratory frequency/tidal volume): <80

SPECIFIC CONDITIONS

In addition, an algorithm for the evaluation and treatment of acute asthma is provided (Fig. 12-9) and a table with risk factors for asthma mortality included (Table 12-12). Separate tables are provided covering the general principles of management of pulmonary edema (Table 12-13), the selection of antibiotic therapy for the treatment of community-acquired pneumonia (Table 12-14), the severity of community-acquired pneumonia (Table 12-15), the diagnosis of ARDS (Table 12-16), and principles of management of ARDS (Table 12-17).

FIGURE 12-9.

Evaluation of asthma.

View Full Size||Download Slide (.ppt)

TABLE 12-12.Risk Factors of Death From Asthma

View Table||Download (.pdf)

TABLE 12-12. Risk Factors of Death From Asthma

History of sudden severe exacerbations
Prior intubations
Prior admission to an ICU due to asthma
>2 hospitalizations per year
>3 ER visits for asthma
Hospitalization or ER visit within last 30 d
Use of >2 canisters of β₂ per month
Current use of steroids or recent withdrawal from them
Comorbidity (cardiovascular or COPD)
Serious psychiatric illness
Illicit drug use
Poor perception of air flow or severity
Low socioeconomic status
Sensitivity to mold

TABLE 12-13.Principles of Management of Pulmonary Edema

View Table||Download (.pdf)

TABLE 12-13. Principles of Management of Pulmonary Edema

Diagnosis
- Progressive (not sudden) shortness of breath
- Desaturation
- Tachypnea
- Occasionally hypertension
- Bilateral crackles
- S3/Gallop (not always)
Predisposing factors
- Fluid overload
- Preeclampsia
- Tocolytic treatment
- Uncontrolled hypertension
Management
- Semi-Fowler position: Elevate head and chest to improve ventilation.
- Oxygen: Administer at 10 L/min via nonrebreather face mask or with CPAP (intubation may be required).
- Continuous pulse oxymetry and cardiac monitoring.
- Establish IV access; limit intravenous fluid infusion (30-50 mL/h)
- Identify and control predisposing factor(s).
Pharmacologic therapy
- Morphine sulfate: 3-5 mg IV may be given; (avoid in the presence of altered consciousness, increased intracranial pressure, or severe COPD)
- Furosemide: 20-40 mg IV; repeat as necessary (do not use more than 120 mg/h and give slowly to prevent ototoxicity)
- Nitroglycerin: 2 in of paste to chest or 1 pill (1/150) until IV access is secured or no other therapy available
- Hydralazine: 5-10 mg IV may be considered if severe hypertension is mediating the pulmonary edema
Monitor
- Input and output
- Blood pressure and fetal heart rate monitoring if appropriate according to GA

TABLE 12-14.Empirical Selection of Antibiotics for Patients With Community-Acquired Pneumonia

View Table||Download (.pdf)

TABLE 12-14. Empirical Selection of Antibiotics for Patients With Community-Acquired Pneumonia

Specific therapy is desirable within 8 h of onset of empirical therapy to narrow the spectrum and direct the treatment.

Hospitalized patients
1. General medical ward
  - A respiratory fluoroquinolone (moxifloxacin, gemifloxacin, or levofloxacin)
    or
  - A β-lactam combined plus a macrolide or a respiratory fluoroquinolone
2. Intensive care unit
  - A β-lactam (cefotaxime, ceftriaxone, or ampicillin-sulbactam)
    
    plus either azithromycin or a fluoroquinolone
    
    (for PCN-allergic patients, a respiratory fluoroquinolone, and aztreonam are recommended)
3. Special considerations
  - Cover for Pseudomonas if structural lung disease (bronchiectasis), use of steroids or prior antibiotic therapy (particularly fluoroquinolones).
    - Antipseudomonal β-lactam agents (piperacillin-tazobactam, cefepime, imipenem, or meropenem) plus a fluoroquinolone (ciprofloxacin or levofloxacin), or
    - β-Lactam agents (piperacillin-tazobactam, cefepime, imipenem, or meropenem) plus an aminoglycoside and azithromycin, or
    - β-Lactam agents (piperacillin-tazobactam, cefepime, imipenem, or meropenem) plus an aminoglycoside and fluoroquinolone
    (for PCN-allergic patients, substitute aztreonam for the β-lactam)
  - If MRSA (increased risk if injection drug abuse, end-stage renal disease, prior influenza, or prior antibiotic therapy (particularly fluoroquinolones): Add vancomycin or linezolid.
  - If aspiration is suspected (history seizures including eclampsia, risk if injection drug abuse, end-stage renal disease, prior influenza or prior antibiotic therapy (particularly fluoroquinolones)): β-Lactam agents/β-lactamase inhibitor (piperacillin-tazobactam, ticarcillin-clavulanate, ampicillin-sulbactam, or amoxicillin-clavulanate)
  - If influenza: Oseltamivir or zanamivir.
  - If pandemic influenza: Consider in addition to oseltamivir antibacterial agents targeting S. pneumoniae and S. aureus

NOTE

Once the etiology of CAP has been identified by microbiologic methods, antimicrobial therapy should be directed at that pathogen.

Reproduced with permission from IDSA/ATS Guidelines for CAP in Adults. CID. 2007;44(suppl 2):27-72.

TABLE 12-15.Severity of Community-Acquired Pneumonia

View Table||Download (.pdf)

TABLE 12-15. Severity of Community-Acquired Pneumonia

Mnemonic: SMART-COP

S: Systolic blood pressure (low)
M: Multilobal chest radiographic involvement
A: Albumin (low)
R: Respiratory rate (high)
T: Tachycardia
C: Confusion
O: Oxygenation (poor)
P: Arterial pH (low)
All factors are given 1 point with exception of systolic blood pressure, poor oxygenation, and low pH (scored 2 points each).
A score of 3 or greater identifies patients at high risk of requiring intensive respiratory or vasopressor support.

Reproduced with permission from Charles PG, Wolfe R, Whitby M, et al. SMART-COP: a tool for predicting the need for intensive respiratory or vasopressor support in community-acquired pneumonia. Clin Infect Dis. 2008;47:375-384.

TABLE 12-16.Consensus Criteria for the Diagnosis of ARDS

View Table||Download (.pdf)

TABLE 12-16. Consensus Criteria for the Diagnosis of ARDS

Acute onset
History compatible with specific risk factors
- Trauma
- Severe shock
- Sepsis (septic abortion included)
- Aspiration
- Venous fluid, fat, or amniotic fluid embolism
- Pneumonia
- Pancreatitis
- Blood transfusion
- Seizures (including eclampsia)
- Overdose
- Abruptio placentae
- Dead fetus syndrome or retained products of conception
- Diabetic ketoacidosis
Clinical exclusion of cardiogenic pulmonary edema (or PCWP <18 mm Hg)
Respiratory distress
Diffuse bilateral patchy opacities in chest x-ray
Pao₂/Fio₂ of <200^a

^aAcute lung injury: Less severe form of ARDS with a Pao₂/Fio₂ between 201 and 300.

TABLE 12-17.Principles of Treatment of ARDS

View Table||Download (.pdf)

TABLE 12-17. Principles of Treatment of ARDS

Therapeutic goals
- Adequate oxygenation
- Avoidance of barotraumas/volutrauma with treatment
- Avoidance of cardiovascular compromise
Management
- Semi-Fowler position: Elevate head and chest to improve ventilation.
- Oxygen: Administer at 10 L/min via nonrebreather face mask or with CPAP (intubation may be required).
- Continuous pulse oxymetry and cardiac monitoring.
- Establish IV access. Consider placement of arterial line and a central line.
- Identify and control predisposing factor(s).
Pharmacologic therapy: Not specific available. In severe cases consult pulmonary services for consideration of nitric oxide, pulmonary vasodilatation, corticosteroids, exogenous surfactant administration, prone ventilation, or extracellular membrane oxygenation (ECMO)
Monitor
- Input and output
- Blood pressure and fetal heart rate monitoring if appropriate according to GA

Abbreviations Used

View Table||Download (.pdf)

Abbreviations Used

BP

Blood pressure

Hb

Hemoglobin

ICU

Intensive care unit

O₂

Pao₂

Arterial oxygen’s partial pressure

Paco₂

Arterial carbon dioxide’s partial pressure

P(A-a)o₂

Alveolar-arterial oxygen difference

PEEP

Positive end-expiratory pressure

PCN

Penicillin

SOB

Shortness of breath

Vd

Dead space

Vt

Tidal volume

Wga

Weeks of gestational age

ECF

Extracellular fluid

AG

Anion gap

SUGGESTED READING

Al-Ansari MA, Hameed AA, Al-Jawder SE et al.. Use of noninvasive positive-pressure ventilation during pregnancy: case series. Ann Thorac Med. 2007;2:23–25. [PubMed: 19724671]

American Association for Respiratory Care (AARC) Clinical Practice Guideline. Oxygen therapy for adults in the acute care facility—2002 revision and update. Respir Care. 2002;47:717–720.

American Association for Respiratory Care (AARC) Clinical Practice Guideline. Removal of the endotracheal tube—2007 revision and update. Respir Care. 2007;52:81–93.

American College of Emergency Physicians (ACEP). Clinical policy for the initial approach to adults presenting with the chief complaint of chest pain, with no history of trauma. Ann Emerg Med. 1995;25:274. [PubMed: 7832368]

American College of Emergency Physicians (ACEP). Critical issues in the evaluation and management of adult patients presenting to the emergency department with suspected pulmonary embolism. Ann Emerg Med. 2011;57:628–652. [PubMed: 21621092]

American Society of Anesthesiologists. Practice guidelines for management of the difficult airway. Anesthesiology. 2013;118:1–20. [PubMed: 23208520]

American Thoracic Society. The diagnostic approach to acute venous thromboembolism. Am J Respir Care Med. 1999; 160:1043.

Bandi VD, Munnur U, Matthay MA. Acute lung injury and acute respiratory distress syndrome in pregnancy. Crit Care Clin. 2004;20:577–607. [PubMed: 15388190]

Bourjeily G, Paidas M, Khalil H et al.. Pulmonary embolism in pregnancy. Lancet. 2010;375(9713):500–512. [PubMed: 19889451]

Brito V, Niederman MS. Pneumonia complicating pregnancy. Clin Chest Med. 2011;32(1):121–132. [PubMed: 21277454]

Catanzarite V, Willms D, Wong D et al.. Acute respiratory distress syndrome in pregnancy and the puerperium: causes, courses, and outcomes. Obstet Gynecol. 2001;97:760–764. [PubMed: 11339930]

Charles PG, Wolfe R, Whitby M et al.. SMART-COP: a tool for predicting the need for intensive respiratory or vasopressor support in community-acquired pneumonia. Clin Infect Dis. 2008;47:375–384. [PubMed: 18558884]

Cole DE, Taylor TL, McCullough DM et al.. Acute respiratory distress syndrome in pregnancy. Crit Care Med. 2005; 33:269S–278S.

Crapo RO. Normal cardiopulmonary physiology during pregnancy. Clin Obstet Gynecol. 1999;39:3.

Deblieux PM, Summer WR. Acute respiratory failure in pregnancy. Clin Obstet Gynecol. 1996;39:143. [PubMed: 8635295]

Dennis AT, Solnordal CB. Acute pulmonary oedema in pregnant women. Anaesthesia. 2012;67:646–659. [PubMed: 22420683]

Gei AF, Vadhera RB, Hankins GDV. Embolism during pregnancy: thrombus, air, and amniotic fluid. Anesthesiology Clin N Am. 2003;21:165.

Goodnight WH, Soper DE. Pneumonia in pregnancy. Crit Care Med. 2005;33:S390–S397. [PubMed: 16215363]

Goodrum LA. Pneumonia in pregnancy. Semin Perinatol. 1997;21:276. [PubMed: 9298716]

Graves CR. Pneumonia in pregnancy. Clin Obstet Gynecol. 2010;53(2):329–336. [PubMed: 20436308]

Ie S, Rubio ER, Alper B et al.. Respiratory complications of pregnancy. Obstet Gynecol Surv. 2001;57:39–46.

Keenan SP, Sinuff T, Burns KEA et al.. (Canadian Critical Care Trials Group/Canadian Critical Care Society Noninvasive Ventilation Guidelines Group). Clinical practice guidelines for the use of noninvasive positive-pressure ventilation and noninvasive continuous positive airway pressure in the acute care setting. CMAJ. 2011;183(3):E195–E214. [PubMed: 21324867]

King TE. Restrictive lung disease in pregnancy. Clin Chest Med. 1992;13:607. [PubMed: 1478021]

Lee RW. Pulmonary embolism. Chest Surg Clin N Am. 2002;12:417. [PubMed: 12122832]

Mandell LA, Wunderink RG, Anzueto A et al.. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. CID. 2007; 44:S27–S72.

Miller MA, Chalhoub M, Bourjeily G. Peripartum pulmonary embolism. Clin Chest Med. 2011;32(1):147–164. [PubMed: 21277456]

National Asthma Education and Prevention Program. Quick reference from the Working Group report on managing asthma during pregnancy: recommendations for pharmacologic treatment. update 2004. NIH publication no. 05-5236. March 2005.

O’Day M. Cardiorespiratory physiological adaptation of pregnancy. Semin Perinatol. 1997;21:268. [PubMed: 9298715]

Rowe TF. Acute gastric aspiration: prevention and treatment. Semin Perinatol. 1997;21:313. [PubMed: 9298720]

Saade GR. Human immunodeficiency virus (HIV)-related pulmonary complications in pregnancy. Semin Perinatol. 1997;21:336. [PubMed: 9298723]

Schatz M, Dombrowski MP. Asthma in pregnancy. N Engl J Med. 2009;360(18):1862–1869. [PubMed: 19403904]

Spiropoulos K, Prodromaki E, Tsapanos V. Effect of body position on PaO₂ and PaCO₂ during pregnancy. Gynecol Obstet Invest. 2004;58:22–25. [PubMed: 15028865]

Van Hook JW. Acute respiratory distress syndrome in pregnancy. Semin Perinatol. 1997;21:320. [PubMed: 9298721]

Vasquez DN, Estenssoro E, Canales HS et al.. Clinical characteristics and outcomes of obstetric patients requiring ICU admission. Chest. 2007;131:718–724. [PubMed: 17356085]

Williams JW Jr, Cox CE, Hargett CW et al.. Noninvasive positive-pressure ventilation (NPPV) for acute respiratory failure. Comparative Effectiveness Review 68. AHRQ publication no. 12-EHC089-EF. Rockville, MD: Agency for Healthcare Research and Quality; 2012.

Zimmerman JL. Fundamental Critical Care Support. 4th ed. Mount Prospect, IL: Society of Critical Care Medicine; 2007.

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.