5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory
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RR = respiratory rate, Pplat = plateau pressure (airway pressure), VT = tidal volume, PEEP = positive end expiratory pressure.
*To review the complete recommendations of ARDSnet mechanical ventilation protocol, criteria for mechanical ventilation, oxygenation goals, plateau pressure goals, pH goals, and mechanical ventilation weaning protocol, go to: http://www.ardsnet.org
Finally, the patient's PaCO2 is often allowed to increase (permissive hypercapnia) as a trade-off to protect the lungs
from high airway pressures. In most cases, an increased ventilatory rate adequately offsets the decreased tidal volume used in the management of ARDS. The PaCO2, however, should not be permitted to increase to the point of severe acidosis
(e.g., a pH below 7.2).2
To summarize, the therapeutic goal of mechanical ventilation of the ARDS patient is to maintain (1) a low tidal volume, between 6 to 8 mL/kg; (2) a high respiratory rate, but not greater than 35 breaths/min; (3) an alveolar plateau pressure between 25 and 30 cm H2O; (4) an oxygenation level between PaO2 55 and 80 mm Hg or an SpO2 between 88% and 95%,
and (5) the pH between 7.30 and 7.45.
26 mEq/L, PaO
26, PaO
24 mEq/L, PaO
24, PaOwith bilateral diffuse infiltrates and atelectasis, worse on the right side. Purulent sputum. PA pressure (mean) 27 mm Hg.
A
•Severe ARDS (symptoms associated with ARDS: bilateral infiltrates on CXR, PaO2/FIO2 ratio is 38 on ventilator settings that include PEEP >20 cm H2O).
•Persistent coma (physical examination)
•Aspiration pneumonitis—progressing to ARDS with bilateral infiltrates and atelectasis (CXR, bronchial breath sounds)
•Increasing airway secretions with infection (fever, coarse crackles, and purulent sputum)
•Acute ventilatory failure on present ventilator settings (but acceptable hypercapnia in this case)
•Severe hypoxemia (ABGs, extremely low PaO2/FIO2 ratio: 38)
P Call physician to discuss worsening PaO2 and to confirm an acceptable hypercapnia level and
PEEP upper limit. Airway Clearance Therapy Protocol (suction PRN). Adjust Mechanical Ventilation Protocol (titrate tidal volume and rate to raise PaCO2 to permissive hypercapnia
range). Repeat Gram stain and culture sputum. Closely monitor and reevaluate.
After 3 hours it was apparent that current management would not be successful; the physician decided to alert the extracorporeal membrane oxygenation (ECMO) team and place the patient on extracorporeal membrane oxygenation. This was done, and the patient was maintained on ECMO for 13 hours, when she developed ventricular tachycardia followed by ventricular fibrillation. Attempts to reestablish normal cardiac function were not successful, and the patient was pronounced dead 45 minutes later.
Discussion
This was possibly a preventable death. Gastric lavage should never be performed on an unconscious patient unless the airway is first protected with a cuffed endotracheal tube. This is one of the very few categoric imperatives in pulmonary medicine. The following three causative factors known to produce ARDS may have been operative in this patient: (1) drug overdose, (2) aspiration of gastric contents, and (3) breathing an excessive FIO2 for a long period. As time progressed, the
patient's lungs became stiffer and physiologically nonfunctional as a result of the anatomic alterations associated with ARDS. The PaO2/FIO2 ratio helped detect this and raises the point that an initial (or very early) ABG at a known FIO2
should be established in patients who are acutely ill.
As documented in the first assessment, her crackles, refractory hypoxemia, and radiograph findings all reflected the pathophysiologic changes seen in patients with atelectasis (see Fig. 10.7) and/or increased alveolar-capillary membrane thickening (see Fig. 10.9). Aggressive lung expansion therapy (see Protocol 10.3), in the form of PEEP, was used with mechanical ventilation from the start. Unfortunately, severe ARDS was confirmed 15 hours later—that is, when the respiratory symptoms associated with ARDS were present in less than 1 week, bilateral infiltrates were seen on the chest radiograph, and the PaO2/FIO2 ratio was only 38 on ventilator settings that include PEEP greater than 20 cm H2O (see Box
28.3, The Berlin Definition of Acute Respiratory Distress Syndrome). The respiratory therapist's immediate reduction in the tidal volume of the patient to 300 mL, increase in respiratory rate to 20 breaths/min, and permissive hypercapnia were all clearly indicated and appropriate.
Unfortunately, these therapeutic techniques and use of ECMO to manage the condition were not enough in the final analysis.
Self-Assessment Questions
1.In response to injury, the lungs of a patient with ARDS undergo which of the following changes?
1.Atelectasis
2.Decreased alveolar-capillary membrane permeability
3.Interstitial and intraalveolar edema
4.Hemorrhagic alveolar consolidation
a.1 and 3 only
b.2 and 4 only
c.1, 2, and 4 only
d.1, 3, and 4 only
2.Which of the following is/are recommended ventilation strategies for most patients with ARDS? 1. High tidal volumes
2. Low respiratory rates
3.High respiratory rates
4.Low tidal volumes
a.1 only
b.3 and 4 only
c.1 and 3 only
d.2 and 4 only
3.Common chest assessment findings in ARDS include the following: 1. Diminished breath sounds
2.Dull percussion note
3.Bronchial breath sounds
4.Crackles
a.1 only
b.3 only
PA R T X I
Neuro-Respiratory Disorders
OUTLINE
Chapter 29 Guillain-Barré Syndrome Chapter 30 Myasthenia Gravis
Chapter 31 Cardiopulmonary Assessment and Care of Patients with Neuromuscular Disease
Plasma Exchange
Plasmapheresis
Stryker Frame
Anatomic Alterations of the Lungs Associated With Guillain-Barré Syndrome1
Guillain-Barré syndrome (GBS) is an autoimmune disease that causes an acute peripheral nervous system disorder (called polyneuropathy) that results in a flaccid paralysis of the skeletal muscles and loss of muscle reflexes. Box 29.1 lists other names in the literature for GBS. In severe cases, paralysis of the diaphragm and ventilatory failure can develop. Clinically, this is a medical emergency. In these cases, mechanical ventilation is required. If the patient is not properly managed (e.g., via the Airway Clearance Therapy Protocol, Protocol 10.2, Ventilator Initiation and Management Protocol, Protocol 11.1, and Ventilator Weaning Protocol, Protocol 11.2), mucus accumulation with airway obstruction, alveolar consolidation, and atelectasis may develop.
Box 29.1
Other Names Found in the Literature for Guillain-Barré Syndrome
•Landry-Guillain-Barré-Strohl syndrome
•Acute idiopathic polyneuritis
•Postinfectious polyneuritis
•Landry paralysis
•Acute postinfectious polyneuropathy
•Acute polyradiculitis
•Polyradiculoneuropathy
The major pathologic or structural changes of the lungs associated with poorly managed GBS are as follows:
•Mucus accumulation
•Airway obstruction
•Alveolar consolidation
•Atelectasis
Etiology and Epidemiology
GBS occurs worldwide with an overall incidence of 1 to 2 per 100,000 people. The incidence of GBS is slightly more frequent in males than in females. The incidence is greater in people over 50 years of age. GBS is 50% to 60% more common in whites than blacks. There is no obvious seasonal clustering of cases. As shown in Table 29.1, there are several different subtypes of GBS.
TABLE 29.1
Subtypes of Guillain-Barré Syndrome*
Acute inflammatory |
AIDP is the most common form of GBS in North America and Europe, representing about |
demyelinating |
75% to 80% of cases. AIDP falls into the classic category that affects motor, sensory, and |
polyneuropathy |
autonomic nerves in a symmetric fashion. |
(AIDP) |
|
Acute motor axonal |
AMAN is similar to AIDP, but without sensory symptoms, affects the motor axons of the |
neuropathy (AMAN) |
nerves. |
Acute motor and |
AMSAN is a severe variant of GBS that is more prevalent in Asia, Central America, and South |
sensory axonal |
America. AMSAN causes severe, rapid destruction to nerves throughout the body. |
neuropathy (AMSAN) |
|
Miller Fisher syndrome |
MFS is characterized by double vision, loss of balance, and loss of deep tendon reflexes |
(MFS) |
|
*All share the characteristic of being “rapid onset.” |
|
From GBS/CIDP Foundation: Everything you need to know. Retrieved from https://www.gbs-cidp.org/gbs/all-about-gbs/.
Although the precise cause of GBS is not fully understood, it is known that all forms of GBS are autoimmune diseases that develop from an immune response to foreign antigens (e.g., an infectious agent) that attack the nerve tissues. For example, acute inflammatory demyelinating polyradiculopathy (AIDP) is thought to be caused by an immunologic attack that results in peripheral nerve demyelination and inflammation. Lymphocytes and macrophages appear to attack and strip off the myelin sheath of the peripheral nerves and leave swelling and fragmentation of the neural axon. It is believed that the myelin sheath covering the peripheral nerves (or the myelin-producing Schwann cell) is the actual target of the immune attack. Microscopically, the nerves show demyelination, inflammation, lymphocytes, macrophages, and edema. As the anatomic alterations of the peripheral nerves intensify, the ability of the neurons to transmit impulses to the muscles decreases, and eventually paralysis ensues (Fig. 29.1).
