Respiratory Failure

Hypoxemic

Hypoxemic respiratory failure is defined by arterial O2saturation <90% while receiving an increased inspired O2 fraction.

Acute hypoxemic respiratory failure can result from pneumonia, pulmonary edema (cardiogenic or noncardiogenic), and alveolar hemorrhage.

Hypoxemia results from ventilation-perfusion mismatch and intrapulmonary shunting.

Present when arterial O2 saturation (Sao2) <90% occurs despite an increased inspired O2 fraction

Results from ventilation-perfusion mismatch or shunt present in:

acute respiratory distress syndrome, heart failure with pulmonary edema, pneumonia, sepsis, complications of surgery and trauma), which accounts for ~65% of all ventilated cases, and

This type occurs with alveolar flooding and subsequent intrapulmonary shunt physiology.

Alveolar flooding may be a consequence of pulmonary edema, pneumonia, or alveolar hemorrhage.

It occurs in clinical settings such as sepsis, gastric aspiration, pneumonia, near-drowning, multiple blood transfusions, and pancreatitis.

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COPD
Pneumonia
Pulmonary edema
Pulmonary fibrosis
Asthma
Pneumothorax
Pulmonary embolism
Pulmonary arterial hypertension
Pneumoconiosis
Granulomatous lung diseases
Cyanotic congenital heart disease
Bronchiectasis
Acute respiratory distress syndrome (ARDS)
Fat embolism syndrome
Kyphoscoliosis
Obesity

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ARF is defined as a sudden (minutes to hours) inability of the lungs to maintain normal respiratory function, resulting in abnormal arterial oxygen or carbon dioxide levels.

Whether classified as Type 1 (hypoxemic) or Type 2 (hypercarbic), ARF represents a major immediate threat to life.

Patients with Type 1 ARF have hypoxemia as their predominant blood gas abnormality. Typically, these patients are anxious and intensely focused on relieving their dyspnea. When you attempt to obtain their history, they may not be able to cooperate, repeating phrases like “I can't breathe” or “Help me.” You may note use of accessory muscles of respiration and, in severe cases, cyanosis. The patient may exhibit unstable vital signs as well. Your differential should include parenchymal and interstitial disease (pneumonia, aspiration, COPD or CHF exacerbation, ARDS) as well as diseases that can cause an acute right-to-left shunt (pulmonary embolism).

Patients with Type 2 ARF have high pCO2 levels as their predominant blood gas problem. They may be hypoxemic as well. These patients can exhibit a “narcosis,” appearing confused, intoxicated, or unresponsive. On physical examination, you may find a tremor or asterixis, peripheral vasodilation with pink nail beds, and significant bradycardia or sinus pauses. Your differential should include disease states that can induce a shallow or inadequate respiratory effort such as asthma or COPD exacerbation in a patient who has “tired out,” neuromuscular issues such as Guillain-Barré syndrome, oversedation with narcotic medications, strokes or brain stem lesions, and structural issues such as severe kyphoscoliosis. In the hospital setting, a few of these issues can combine to turn a chronic condition into an acute problem. For instance, a patient with morbid obesity and resultant sleep apnea who is then hospitalized for a knee replacement and given narcotics for pain control could develop significant hypercarbia due to an acute worsening of the sleep apnea from the sedating effects of the analgesics.

Mechanical Ventialtion

ABGs are essential for the correct diagnosis and treatment of ARF, and doctors should not hesitate to order them when appropriate.
Do not hesitate to intubate and mechanically ventilate a patient with ARF who is not appropriate for or not responding to noninvasive ventilation. A calm, organized intubation is much safer and results in better clinical outcomes than an emergent intubation done after a patient has become unstable or suffered a cardiopulmonary arrest.
Many patients have undiagnosed chronic hypoxia with few clinical signs or symptoms. When hospitalized, the addition of supplemental oxygen, sedating medications, or the stress of an acute illness can cause hypercarbic ARF, which often manifests clinically as altered mental status or delirium.

Respiratory failure is a condition in which the respiratory system fails in one or both of its gas-exchanging functions; that is, oxygenation of, and carbon dioxide elimination {from, mixed venous (pulmonary arterial) blood.

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Hypoxemic respiratory failure is defined by arterial O2saturation <90% while receiving an increased inspired O2 fraction. Acute hypoxemic respiratory failure can result from pneumonia, pulmonary edema (cardiogenic or noncardiogenic), and alveolar hemorrhage. Hypoxemia results from ventilation-perfusion mismatch and intrapulmonary shunting.

Present when arterial O2 saturation (Sao2) <90% occurs despite an increased inspired O2 fraction

Results from ventilation-perfusion mismatch or shunt present in:

acute respiratory distress syndrome, heart failure with pulmonary edema, pneumonia, sepsis, complications of surgery and trauma), which accounts for ~65% of all ventilated cases, and

This type occurs with alveolar flooding and subsequent intrapulmonary shunt physiology.

Alveolar flooding may be a consequence of pulmonary edema, pneumonia, or alveolar hemorrhage.

It occurs in clinical settings such as sepsis, gastric aspiration, pneumonia, near-drowning, multiple blood transfusions, and pancreatitis.

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ARF is defined as a sudden (minutes to hours) inability of the lungs to maintain normal respiratory function, resulting in abnormal arterial oxygen or carbon dioxide levels.

Whether classified as Type 1 (hypoxemic) or Type 2 (hypercarbic), ARF represents a major immediate threat to homeostasis and is a medical emergency.

Mechanical Ventialtion

ABGs are essential for the correct diagnosis and treatment of ARF, and doctors should not hesitate to order them when appropriate.

Do not hesitate to intubate and mechanically ventilate a patient with ARF who is not appropriate for or not responding to noninvasive ventilation. A calm, organized intubation is much safer and results in better clinical outcomes than an emergent intubation done after a patient has become unstable or suffered a cardiopulmonary arrest.

Many patients have undiagnosed chronic hypoxia with few clinical signs or symptoms. When hospitalized, the addition of supplemental oxygen, sedating medications, or the stress of an acute illness can cause hypercarbic ARF, which often manifests clinically as altered mental status or delirium.

Etiology

Causes
Pathogenesis
Management
Determining the Cause
Study Questions

Hypoxemic
Tab 2
Tab 3

Content 2

Content 3

Augmentation of the patient's ability to exchange gases must proceed quickly and diagnosing the initiating problem are done in parallel.

Supportive Measures
Treatment of the underlying cause.
Tab 3

Supportive measures

Supportive measures which depend on depending on airways management to maintain adequate ventilation and correction of the blood gases abnormalities

Correction of Hypoxemia

The goal is to maintain adequate tissue oxygenation, generally achieved with an arterial oxygen tension (PaO2) of 60 mm Hg or arterial oxygen saturation (SaO2), about 90%.
Un-controlled oxygen supplementation can result in oxygen toxicity and CO2 (carbon dioxide) narcosis. Inspired oxygen concentration should be adjusted at the lowest level, which is sufficient for tissue oxygenation.
Oxygen can be delivered by several routes depending on the clinical situations in which we may use a nasal cannula, simple face mask nonrebreathing mask, or high flow nasal cannula.
Extracorporeal membrane oxygenation may be needed in refractory cases

2. Correction of hypercapnia and respiratory acidosis

This may be achieved by treating the underlying cause or providing ventilatory support.

3. Ventilatory support for the patient with respiratory failure

The goals of ventilatory support in respiratory failure are:

Correct hypoxemia
Correct acute respiratory acidosis
Resting of ventilatory muscles[2]

Non-invasive respiratory support: is ventilatory support without tracheal intubation/ via upper airway. Considered in patients with mild to moderate respiratory failure. Patients should be conscious, have an intact airway and airway protective reflexes. Noninvasive positive pressure ventilation(NIPPV) has been shown to reduce complications, duration of ICU stay and mortality(). It has been suggested that NIPPV is more effective in preventing endotracheal intubation in acute respiratory failure due to COPD than other causes. The etiology of respiratory failure is an important predictor of NIPPV failure.[5]

Invasive respiratory support: indicated in persistent hypoxemia despite receiving maximum oxygen therapy, hypercapnia with impairment of conscious level. Intubation is associated with complications such as aspiration of gastric content, trauma to the teeth, barotraumas, trauma to the trachea etc

Permissive hypercapnia[6] - A ventilatory strategy that allows arterial carbon dioxide(PaCO2) to rise by accepting a lower alveolar minute ventilation to avoid the risk of ventilator-associated lung injury in patients with ALI and minimize intrinsic positive end-expiratory pressure (auto PEEP) in patients with COPD thereby protecting the lungs from barotrauma. Permissive hypercapnia could increase survival in immunocompromised children with severe ARDS[7]

Physiotherapy Management

Physio-therapeutic interventions aim to maximize function in pump and ventilatory systems and improve quality of life.

In mechanically ventilated patients, early physiotherapy has been shown to improve quality of life and to prevent ICU-associated complications like de-conditioning, ventilator dependency and respiratory conditions.
Main indications for physiotherapy are excessive pulmonary secretions and atelectasis.
Timely physical therapy interventions may improve gas exchange and reverse pathological progression thereby avoiding ventilation.

Interventions include:

Positioning: the use of specific body position aimed at improving ventilation/perfusion(V/Q) matching, promoting mucociliary clearance, improving aeration via increased lung volumes and reducing the work of breathing.[8] These include:
- Prone: helps to improve V/Q matching, redistribute edema and increase functional residual capacity(FRC) in patients with acute respiratory distress syndrome. It has been shown to result in oxygenation for 52-92% of patients with severe acute respiratory failure.[9][10]
- Side-lying: with affected lungs uppermost to improve aeration through increased lung volumes in patients with unilateral lung disease.
- Semi-recumbent: 450 head-up position serves to prevent the risk of gastroesophageal reflux and aspiration.
- Upright: helps to improve lung volumes and decrease work of breathing in patients that are being weaned from mechanical ventilator.

Postural drainage and Percussion: uses gravitational effects to facilitate mucociliary clearance
Suction: used for clearing secretions when the patient cannot do so independently (Guglielminotti et al recommended a saw-tooth pattern seen on ventilator’s flow-volume loop and/or respiratory sounds over the trachea as good indicators for tracheal suction in a ventilated patient).[11]
Manual Hyperinflation: aims to re-inflate atelectatic areas of the lung as such improving pulmonary compliance[12] and facilitate the clearance of pulmonary secretions when used with other techniques.
Active cycle of breathing technique[13] and manual techniques such as shaking and vibration to facilitate mucus clearance
Limb exercises: passive, active-assisted, active exercises may optimize oxygen transport and reduce the effects of immobility.[8]
Inspiratory muscle training: aims to improve inspiratory muscle strength and it facilitates weaning from mechanical ventilation. It has be shown to improve whole body exercise performance, particularly in less fit subjects.[14] The study by Hoffman L et showed positive outcomes with inspiratory muscle training in patients with advanced lung disease.[15]
Early mobilisation: improves function, mobility and quality of life[16][17][18]

2) Hypercarbic respiratory failure is characterized by alveolar hypoventilation and respiratory acidosis. Hypercarbic respiratory failure results from decreased minute ventilation and/or increased physiologic dead space. Conditions associated with hypercarbic respiratory failure include neuromuscular diseases (e.g., myasthenia gravis), disease processes causing diminished respiratory drive (e.g., drug overdose, brainstem injury), and respiratory diseases associated with respiratory muscle fatigue (e.g., exacerbations of asthma and chronic obstructive pulmonary disease [COPD]). In acute hypercarbic respiratory failure, PaCO2 is typically >50 mmHg. With acute-on-chronic respiratory failure, as is often seen with COPD exacerbations, considerably higher PaCO2 values may be observed. The degree of respiratory acidosis, the pt’s mental status, and the pt’s degree of respiratory distress are better indicators of the need for mechanical ventilation than a specific PaCO2level in acute-on-chronic respiratory failure.

Hypercarbic respiratory failure is characterized by alveolar hypoventilation and respiratory acidosis.

Hypercarbic respiratory failure results from decreased minute ventilation and/or increased physiologic dead space. Conditions associated with hypercarbic respiratory failure include neuromuscular diseases (e.g., myasthenia gravis), disease processes causing diminished respiratory drive (e.g., drug overdose, brainstem injury), and respiratory diseases associated with respiratory muscle fatigue (e.g., exacerbations of asthma and chronic obstructive pulmonary disease [COPD]). In acute hypercarbic respiratory failure, PaCO2 is typically >50 mmHg. With acute-on-chronic respiratory failure, as is often seen with COPD exacerbations, considerably higher PaCO2 values may be observed. The degree of respiratory acidosis, the pt’s mental status, and the pt’s degree of respiratory distress are better indicators of the need for mechanical ventilation than a specific PaCO2 level in acute-on-chronic respiratory failure.

This type of respiratory failure is a consequence of alveolar hypoventilation and results from the inability to eliminate carbon dioxide effectively.

Mechanisms are categorized by

impaired central nervous system (CNS) drive to breathe
- drug overdose
- brainstem injury
- sleep-disordered breathing
- severe hypothyroidism.
impaired strength with failure of neuromuscular function in the respiratory system,
and increased load(s) on the respiratory system. Reduced strength can be due to impaired neuromuscular transmission (e.g., myasthenia gravis, Guillain-Barré syndrome, amyotrophic lateral sclerosis) or respiratory muscle weakness (e.g., myopathy, electrolyte derangements, fatigue).

The overall load on the respiratory system can be subclassified into resistive loads (e.g., bronchospasm), loads due to reduced lung compliance (e.g., alveolar edema, atelectasis, intrinsic positive end-expiratory pressure [auto-PEEP]—see below), loads due to reduced chest wall compliance (e.g., pneumothorax, pleural effusion, abdominal distention), and loads due to increased minute ventilation requirements (e.g., pulmonary embolus with increased dead-space fraction, sepsis).

The mainstays of therapy for type II respiratory failure are directed at reversing the underlying cause(s) of ventilatory failure. Noninvasive positive-pressure ventilation with a tight-fitting facial or nasal mask, with avoidance of endotracheal intubation, often stabilizes these patients. This approach has been shown to be beneficial in treating patients with exacerbations of chronic obstructive pulmonary disease; it has been tested less extensively in other kinds of respiratory failure but may be attempted nonetheless in the absence of contraindications (hemodynamic instability, inability to protect the airway, respiratory arrest).

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Treatment for both Type 1 and Type 2 ARF is aimed at stabilizing and reversing the derangements in the patient's ability to properly exchange gases in the lung. Diagnosing and treating the underlying issue is important, but acute strategies to augment oxygenation and support the ventilatory release of CO2 must also be utilized to relieve the patient's symptoms and prevent organ failure.

In patients with Type 1 ARF, providing supplemental oxygen is key. This can be done most easily through a nasal cannula, the use of which allows patients to continue to eat, drink, and speak easily. Unfortunately, since much of the oxygen supplied is lost to the air around the patient, oxygen by nasal cannula is only useful for patients who require low flow rates (2–5 L) to support their oxygen levels. Patients who require higher flow rates of oxygen require venturi masks, which can deliver FiO2s of up to 50% or non-rebreather masks, which have a 1-way valve that prevents exhaled gases from diluting the delivered oxygen, resulting in 80% to 90% O2 concentrations. All of these methods of increased oxygen delivery should be used cautiously in patients with chronic lung disease, in whom an increased pO2 can result in the loss of their hypoxic drive and subsequent retention of pCO2. Although these patients may initially present as Type 1 ARF, they may need treatment strategies more in line with Type 2 ARF patients, as described below. Patients exhibiting severe levels of hypoxia, unstable vital signs, mental status changes that make them unable to protect their airway, or stridor should proceed immediately to intubation and mechanical ventilation.

Patients with Type 2 ARF require ventilatory support so that they can “blow off” their excess CO2. They may also need supplemental oxygen. As above, patients who are hemodynamically unstable or unable to protect their airway should be intubated and ventilated. In more stable patients, a course of noninvasive ventilation can be very helpful. Two types of noninvasive ventilation are commonly used—continuous positive airway pressure (CPAP) masks and bilevel positive airway pressure (BiPAP) masks.

CPAP masks are tight-fitting apparati that support the patient's ventilatory effort by adding a few centimeters of pressure to the air they breathe. This decreases the workload of breathing and gives patients some rest so that they can improve their ventilatory effort. Supplemental levels of oxygen can be given through the mask if needed. BiPAP masks provide heavier pressure with inhalation and a lower level of pressure with exhalation. This decreases the workload of breathing and improves gas exchange by preventing alveolar collapse on exhalation.

It is important to remember that noninvasive methods of supporting ventilation are only for temporary use while the underlying cause of ARF is diagnosed and treated. Patients who are on CPAP or BiPAP therapy for ARF should be reassessed with an ABG 1 hour after beginning treatment. If significant improvement in their pCO2 and pO2 levels is not seen after this period of time, patients should be intubated and mechanically ventilated.

An initial workup including a cardiac and pulmonary examination, chest x-ray, ABG, and EKG should point you in the right direction by helping to classify the ARF and generate a differential diagnosis as to the cause.

Content 3

EKG should point you in the right direction by helping to classify the ARF and generate a differential diagnosis as to the cause.Content 6

A 72-year-old man with no known pulmonary history admitted to the hospital with E. coli sepsis due to cholecystitis. He receives antibiotics, fluids, and narcotic analgesia. On hospital day 3, he gets out of bed to go to the bathroom and becomes “winded.” When you arrive to see him, he is sitting on the edge of his bed with his elbows on his knees, breathing at 30 breaths/min. He states he cannot catch his breath. His pulse ox registers an SaO2 of 87%.

What is your differential diagnosis for the patient's acute respiratory failure (ARF)?

Hypoxemic

Physiotherapy Management

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Diseases and Disorders