Ch. 19 Reading Flashcards
clinical condition in which the pulmonary system fails to maintain adequate gas exchange.
ALF results from a deficiency in the performance of the pulmonary system
The causes of ALF may be classified as extrapulmonary or intrapulmonary, depending on the origin of the patient’s primary disorder. Extrapulmonary causes include disorders that affect the brain, the spinal cord, the neuromuscular system, the thorax, the pleura, and the upper airways. Intrapulmonary causes include disorders that affect the lower airways and alveoli, the pulmonary circulation, and the alveolar-capillary membrane.
Assessment and dx
Medical management
Nursing managment
Acute lung failure
The clinical manifestations commonly seen in patients with ALF are usually related to the development of hypoxemia, hypercapnia, and acidosis. ALF is generally accepted as being present when the PaO2 is less than 60 mm Hg. If the patient is also experiencing hypercapnia, the PaCO2 will be greater than 45 mm Hg. In patients with chronically elevated PaCO2 levels, these criteria must be broadened to include a pH less than 7.35.
Tests include bronchoscopy for airway surveillance or specimen retrieval, chest radiography, thoracic ultrasound, thoracic computed tomography (CT), and selected lung function studies.
Assessment and dx - Acute lung failure
aimed at treating the underlying cause, promoting adequate gas exchange, correcting acidosis, initiating nutrition support, and preventing complications.
Oxygenation
Ventilation
Pharmacology
Acidosis
Nutrition support
Complications
Medical management - Acute lung failure
include supplemental oxygen administration, with either a low-flow system or a high-flow system, and the use of positive pressure ventilation.
The goal is to keep the tissues’ needs satisfied but not produce hypoxemia or hyperoxemia.
Supplemental oxygen administration is effective in treating hypoxemia related to alveolar hypoventilation and V/Q mis-matching.
Oxygenation
include the use of nonin-vasive and invasive mechanical ventilation. Depending on the underlying cause and the severity of the ALF, the patient may be treated initially with noninvasive ventilation.
The selection of ventilatory mode and settings depends on the patient’s underlying condition, severity of respiratory failure, and body size. Initially, the patient is started on volume ventilation in the assist/control mode. In a patient with chronic hypercapnia, the settings are adjusted to keep the ABG values within the parameters expected to be maintained by the patient after extubation.
Ventilation
Medications to facilitate dilation of the airways may also be beneficial in the treatment of ALF. Bronchodilators, such as beta-2 agonists and anticholinergic agents, aid in smooth muscle relaxation and are of particular benefit to patients with airflow limitations. Methylxanthines, such as aminophylline, are no longer recommended because of their negative side effects. Steroids also are often administered to decrease airway inflammation and enhance the effects of the beta-2 agonists.
Neuromuscular paralysis may be necessary to facilitate optimal ventilation.
Pharmacology
Hypoxemia causes impaired tissue perfusion, which leads to the production of lactic acid and the development of metabolic acidosis.
Impaired ventilation leads to the accumulation of carbon dioxide and the development of respiratory acidosis.
Sodium bicarbonate may be used if metabolic acidosis is severe (pH less than 7.2), refractory to therapy, and causing dysrhythmias or hemodynamic instability.
Acidosis
Failure to provide the patient with adequate nutrition support leads to the development of malnutrition. Both malnutrition and over-feeding can interfere with the performance of the pulmonary system, further perpetuating ALF. Malnutrition decreases the patient’s ventilatory drive and muscle strength, whereas over-feeding increases carbon dioxide production, which increases the patient’s ventilatory demand, resulting in respiratory muscle fatigue.
The enteral route is the preferred method nutrition support is initiated before the third day of mechanical ventilation for well-nourished patients and within 24 hours for malnourished patients.
Nutrition support
experience many complications including ischemic-anoxic encephalopathy, cardiac dysrhythmias, venous thromboembolism (VTE), and stress ulcers.
Ischemic-anoxic encephalopathy: hypoxemia, hypercapnia, and acidosis.
Dysrhythmias: hypoxemia, acidosis, electrolyte imbalances, and the administration of beta-2 agonists; Maintaining oxygenation, normalizing electrolytes, and monitoring medication levels facilitate the prevention and treatment of encephalopathy and dysrhythmias.
VTE: venous stasis resulting from immobility and can be prevented through the use of intermittent pneumatic compression devices and low-dose unfractionated heparin or low molecular-weight heparin (LMWH); be prevented through the use of histamine receptor antagonists and proton pump inhibitors.
at risk for the complications associated with the artificial airway, mechanical ventilation, enteral and parenteral nutrition, and vascular access devices.
Complications
Nursing actions are driven by the specific cause of the respiratory failure, although there are some common interventions that are appropriate for all patients with ALF.
Optimize oxygenation and ventilation
Educate the patient and family
Nursing managment - Acute lung failure
positioning, preventing desaturation, and promoting secretion clearance (providing adequate systemic hydration, humidifying supplemental oxygen, coughing, and suctioning)
Optimize oxygenation and ventilation
Early in the patient’s hospital stay, the patient and family are taught about ALF, its causes, and its treatment. Closer to discharge, patient and family education focuses on the interventions necessary for preventing the reoccurrence of the precipitating disorder
Importance of participating in a pulmonary rehabilitation program is stressed.
Educate the patient and family
is a systemic process that is considered to be the pulmonary manifestation of multiple-organ dysfunction syndrome. It is characterized by noncardiac pulmonary edema and disruption of the alveolar-capillary membrane as a result of injury to either the pulmonary vasculature or the airways.
Timing: Within 1 week of known clinical insult or new or worsening respiratory symptoms
Chest imaging: Bilateral opacities not fully explained by effusions, lobar/lung collapse, or nodules
Origin of edema: Respiratory failure not fully explained by heart failure or fluid overload; objective assessment needed to exclude hydrostatic edema if no risk factor present
Oxygenation: Mild (200 mm Hg less than PaO2/fraction of inspired oxygen [FIO2] less than or equal to 300 mm Hg with positive end-expiratory airway pressure [PEEP] or continuous positive airway pressure [CPAP] greater than or equal to 5 cm H2O); moderate (100 mm Hg less than PaO2/FIO2 less than or equal to 200 mm Hg with PEEP greater than or equal to 5 cm H2O); or severe (PaO2/FIO2 less than or equal to 100 mm Hg with PEEP greater than or equal to 5 cm H2O).
Exudative phase
Fibroproliferative phase
Assessment and dx
Medical management
Nursing management
Acute Respiratory Distress Syndrome
Within the first 72 hours after the initial insult, the exudative phase or acute phase ensues. Once released, the mediators cause injury to the pulmonary capillaries, resulting in increased capillary membrane permeability leading to the leakage of fluid filled with protein, blood cells, fibrin, and activated cellular and humoral mediators into the pulmonary interstitium. Hypoxemia occurs as a result of intrapulmonary shunting and V/Q mismatching secondary to compression, collapse, and flooding of the alveoli and small airways.
Exudative phase - Acute Respiratory Distress Syndrome
begins as disordered healing and starts in the lungs. Cellular granulation and collagen deposition occur within the alveolar-capillary membrane. The alveoli become enlarged and irregularly shaped (fibrotic), and the pulmonary capillaries become scarred and obliterated. This leads to further stiffening of the lungs, increasing pulmonary hypertension, and continued hypoxemia.
Fibroproliferative phase - Acute Respiratory Distress Syndrome
During the exudative phase, the patient presents with tachypnea, restlessness, apprehension, and moderate increase in accessory muscle use. During the fibroproliferative phase, the patient’s signs and symptoms progress to agitation, dyspnea, fatigue, excessive accessory muscle use, and fine crackles as respiratory failure develops.
Initially the chest radiograph may be normal, because changes in the lungs do not become evident for up to 24 hours. As the pulmonary edema becomes apparent, diffuse, patchy interstitial and alveolar infiltrates appear. This progresses to multifocal consolidation of the lungs, which appears as a “whiteout” on the chest radiograph.
Assessment and dx - Acute Respiratory Distress Syndrome
treating the underlying cause, promoting gas exchange, supporting tissue oxygenation, and preventing complications. Given the severity of hypoxemia, the patient is intubated and mechanically ventilated to facilitate adequate gas exchange.
Ventilation
Oxygen therapy
Tissue perfusion
Medical management - Acute Respiratory Distress Syndrome
Low tidal volume
Permissive hypercapnia
Pressure control ventilation
Inverse ratio ventilation
High-frequency oscillatory ventilation
Ventilation
Low tidal volume ventilation uses smaller
tidal volumes (6 mL/kg) to ventilate the patient in an attempt to
limit the effects of barotrauma and volutrauma.
Goal: provide the maximum tidal volume possible, while maintaining
end-inspiratory plateau pressure less than 30 cm H2O.
allow
for adequate carbon dioxide elimination, the respiratory rate is
increased to 20 to 30 breaths/min.42,43
Low tidal volume
Allow for adequate carbon dioxide elimination, the respiratory rate is increased to 20 to 30 breaths/min.
As a general rule, the patient’s PaCO2 should not rise faster than 10 mm Hg per hour and overall should not exceed 80 to 100 mm Hg. Because of the negative cardiopulmonary effects of severe acidosis, the arterial pH is generally maintained at 7.20 or greater.
is contraindicated in patients with increased intracranial pressure, pulmonary hypertension, seizures, and heart failure.
Permissive hypercapnia
In pressure control ventilation mode, each breath is delivered or augmented with a preset amount of inspiratory pressure as opposed to tidal volume, which is used in volume ventilation. Thus the actual tidal volume the patient receives varies from breath to breath. Pressure control ventilation is used to limit and control the amount of pressure in the lungs and decrease the incidence of volutrauma. The goal is to keep the patient’s plateau pressure (end-inspiratory static pressure) lower than 30 cm H2O.
Known problem with this mode of ventilation is that as the patient’s lungs get stiffer, it becomes harder and harder to maintain an adequate tidal volume, and severe hypercapnia can occur.
Pressure control ventilation
prolongs the inspiratory time and shortens the expiratory time, thus reversing the normal inspiratory-to-expiratory ratio. The goal of IRV is to maintain a more constant mean airway pressure throughout the ventilatory cycle, which helps keep alveoli open and participating in gas exchange. It also increases FRC and decreases the work of breathing. In addition, as the breath is delivered over a longer period of time, the peak inspiratory pressure in the lungs is decreased. A major disadvantage to IRV is the development of auto-PEEP. As the expiratory phase of ventilation is shortened, air can become trapped in the lower airways, creating unintentional PEEP (or auto-PEEP), which can cause hemodynamic compromise and worsening gas exchange. Patients on IRV usually require heavy sedation with neuromuscular blockade to prevent them from fighting the ventilator.
Inverse ratio ventilation
