Given a critically ill patient, the resident must be able to determine the presence or absence of respiratory failure, provide for its emergency support, and have a plan of action to subsequently investigate and manage the problem. These actions must be based on a sound knowledge of respiratory physiology, pathology, pathophysiology, and pharmacology.
- Recognize the clinical signs and symptoms of acute respiratory failure; Describe the clinical presentation of acute respiratory failure. Describe a brief directed physical exam and assessment of a patient presenting with acute respiratory distress
- Define and classify acute respiratory failure.
- Describe the various etiologies of acute respiratory failure.
- Describe the pathophysiology of hypoxemic respiratory failure, list the 6 causes of hypoxemia, and write the alveolar-arterial gas equation;
- Describe the appropriate management of hypoxemic respiratory failure;
- Describe the pathophysiology of hypercapnic respiratory failure, and list the physiologic causes of hypercapnia;
- Discuss the role of oxygen therapy in the treatment of hypercapnic respiratory failure;
- List the differential diagnosis for an exacerbation of COPD;
- Describe the appropriate management of hypercapnic respiratory failure.
Acute Respiratory Failure:
The loss of the ability to ventilate adequately or to provide sufficient oxygen to the blood and systemic organs. The pulmonary system is no longer able to meet the metabolic demands of the body with respect to oxygenation of the blood and/or CO2 elimination.
- Type 1 (Hypoxemic ) - PO2 < 50 mmHg on room air. Usually seen in patients with acute pulmonary edema or acute lung injury. These disorders interfere with the lung's ability to oxygenate blood as it flows through the pulmonary vasculature.
- Type 2 (Hypercapnic/ Ventilatory ) - PCO2 > 50 mmHg (if not a chronic CO2 retainer). This is usually seen in patients with an increased work of breathing due to airflow obstruction or decreased respiratory system compliance, with decreased respiratory muscle power due to neuromuscular disease, or with central respiratory failure and decreased respiratory drive.
- Type 3 (Peri-operative). This is generally a subset of type 1 failure but is sometimes considered separately because it is so common.
- Type 4 (Shock) - secondary to cardiovascular instability.
ARF can result from a variety of etiologies. It can result from primary pulmonary pathologies or can be initiated by extra-pulmonary pathology. Causes are often multifactorial. Acute respiratory failure can be caused by abnormalities in:
- CNS ( drugs, metabolic encephalopathy, CNS infections, increased ICP, OSA, Central alveolar hypoventilation)
- spinal cord (trauma, transverse myelitis)
- neuromuscular system ( polio, tetanus, M.S., M.Gravis, Guillain-Barre, critical care or steroid myopathy)
- chest wall ( Kyphoscoliosis, obesity)
- upper airways ( obstruction from tissue enlargement, infection, mass; vocal cord paralysis, tracheomalacia)
- lower airways ( bronchospasm, CHF, infection)
- lung parenchyma ( infection, interstitial lung disease)
- cardiovascular system
Hypoxemic Respiratory Failure (Type 1):
Physiologic Causes of Hypoxemia
- Low FiO2 (high altitude)
- V/Q mismatch (low V/Q)
- Shunt (Qs/Qt)
- Diffusion abnormality
- Venous admixture ( low mixed venous oxygen)
Low FiO2 is the primary cause of ARF only at altitude. However, it should be kept in mind that any patient who suddenly desaturates while on oxygen may have had their oxygen source disconnected or interrupted. Hypoventilation can be ruled in or out with the use of the alveolar-air gas equation. A normal A-a gradient indicates that hypoventilation is the cause.
PAO2 = FIO2 (PBarometric - 47) - 1.25PaCO2)
Occasionally a patient with a sub-clinical intra-pulmonary shunt may become hypoxemic due to venous admixture. In this situation inadequate oxygen delivery to the periphery results in increased peripheral oxygen extraction and thus the return of blood with a very low mixed venous oxygen saturation. The relatively small shunt in the lungs is normally not clinically obvious, but is great enough so that if extremely desaturated blood returns to the lungs it will not be adequately re-oxygenated. Thus patient hemodynamics and the possibility of a low-flow state should be kept in mind as a possible cause of hypoxemia.
However, the two most common causes of hypoxemic respiratory failure in the ICU are V/Q mismatch and shunt. These can be distinguished from each other by their response to oxygen. V/Q mismatch responds very readily to oxygen whereas shunt is very oxygen insensitive. A classic cause of V/Q mismatch is a COPD exacerbation. In shunt, alveolar capillary perfusion is much greater than alveolar oxygenation due to collapse and derecruitment of alveoli. This means that venous blood does not come in contact with oxygen as it is "shunted" by the collapsed or fluid -filled alveoli. Therapy for shunt is directed at re-opening or recruiting collapsed alveoli, preventing derecruitment, diminishing lung water, and improving pulmonary hypoxic vasoconstriction. Some causes of shunt include ;
- Cardiogenic pulmonary edema
- Noncardiogenic pulmonary edema (ARDS)
- Lung hemorrhage
Therapies for acute hypoxemic respiratory failure include;
- Prone Position
- Permissive hypercapnia
- Inverse Ratio Ventilation or Pressure Control Ventilation
- Nitric oxide
- ECMO / ECCOR / Partial Liquid Ventilation
Type 2 ( Ventilatory /Hypercapnic Respiratory Failure):
Physiologic causes of Hypercapnia:
- Increased CO2 production (fever, sepsis, burns, overfeeding)
- Decreased alveolar ventilation
- decreased RR
- decreased tidal volume (Vt)
- increased dead space (Vd)
The cause of hypercapnia is often independent of hypoxemia. Hypercapnia results from either increased CO2 production secondary to increased metabolism (sepsis, fever, burns, overfeeding), or decreased CO2 excretion. CO2excretion is inversely proportional to alveolar ventilation (VA). VA is decreased if total minute ventilation is decreased - secondary to either a decreased respiratory rate (f) or a decrease in tidal volume (Vt); or if the deadspace fraction of the tidal volume is increased (Vd/ Vt).
PACO2 = k x VCO2 / VA, therefore....
PACO2 = k x VCO2 / VE(1 - Vd/ Vt) = k x VCO2 / (Vt x f) (1- Vd/ Vt)
since VA = (Vt - Vd)f
where VCO2 is carbon dioxide production, VA is alveolar ventilation, VE is total minute ventilation, and Vd/Vt is the fraction of dead space over tidal volume.
Causes of decreased alveolar ventilation:
- Decreased CNS drive ( CNS lesion, overdose, anesthesia). The patient is unable to sense the increased PaCO2. The patient "won't breathe".
- Neuromuscular disease ( Myasthenia Gravis, ALS, Guillian-Barre , Botulism, spinal cord disease, myopathies, etc.). The patient is unable to neurologically signal the muscles of respiration or has significant intrinsic respiratory muscle weakness. The patient "can't breathe".
- Increased Work Of Breathing leading to respiratory muscle fatigue and inadequate ventilation.
- Asthma/ COPD
- Pulmonary fibrosis
- Increased Physiologic Dead Space (Vd). When blood flow to some alveoli is significantly diminished, CO2 is not transferred from the pulmonary circulation to the alveoli and CO2 rich blood is returned to the left atrium. Causes of increased dead space ventilation include pulmonary embolus, hypovolemia, poor cardiac output, and alveolar over distension. Dead space can be quantified using the Bohr equation and a Douglas bag, or with the use of a "metabolic cart".
Evaluation of Hypercapnia:
The physiologic reasons for hypercapnia can be determined at the bedside.
- Minute Ventilation, RR, Vt,
- Assessment of patient's work of breathing - accessory respiratory muscle use, indrawing, retractions, abdominal paradox.
- NIF (negative inspiratory force). This is a measure of the patient's respiratory system muscle strength. It is obtained by having the patient fully exhale. Occluding the patient's airway or endotracheal tube for 20 seconds, then measuring the maximal pressure the patient can generate upon inspiration. NIF's less than -20 to -25 cm H2O suggest that the patient does not have adequate respiratory muscle strength to support ventilation on his own.
- P0.1 max. This measurement of the degree of pressure drop during the first 100 milliseconds of a patient initiated breath is an estimate of the patient's respiratory drive. A low P0.1 max suggests that the patient has a low drive and a central hypoventilation syndrome.
- central hypoventilation vs. Neuromuscular weakness
- "won’t breathe vs. can’t breathe"
- central = low P0.1 with normal NIF
- Neuromuscular weakness = normal P0.1 with low NIF
- Metabolic cart
- calculates VCO2, and Vd/ Vt
ICU Alveolar Hypoventilation:
- Central / Brainstem depression (drugs, obesity)
- Neuropathic (MG, Guillian-Barre, MS, Botulism, Phrenic nerve injury, ICU polyneuropathy)
- Myopathic (Mg, PO4, ICU myopathy)
Abnormalities in Lung Mechanics:
There are many possible etiologies for acute respiratory failure and the diagnosis is often unclear or uncertain during the critical first few minutes after presentation. Since it is often necessary to initiate treatment before a clear diagnosis can be established, taking a pathophysiologic approach towards the patient can be useful. To that end, the "respiratory equation of motion" can provide a useful conceptual framework in determining why the patient is unable to sustain adequate minute ventilation.
Work Of Breathing (WOB) = Resistance + Elastance + Threshold load + Inertia
Pmuscle + Papplied = E(Vt) + R(V)+ threshold load + Inertia
Pmuscle is the pressure supplied by the Inspiratory respiratory muscles; Papplied is the inspiratory pressure provided by mechanical means (i.e., a ventilator); E is the elastance of the system; R is the respiratory system resistance; Threshold load is the amount of PEEPi or intrinsic PEEP the patient must overcome before inspiratory flow can begin; Vt and V are the tidal volume and the flow rate respectively; Inertia is a property of all mass and has minimal contributions and thus can be ignored clinically.
More simply put, acute respiratory failure results when there is an imbalance between the respiratory muscle power available (supply) versus the muscle power needed (demand). This usually occurs when the respiratory loads are increased to the point where the respiratory muscles begin to fatigue and fail. As examples, acute bronchospasm due to asthma or COPD places an increased resistive load on the respiratory system, acute pulmonary edema decreases lung compliance and thus places an increased elastance load on the system, and in COPD intrinsic PEEP increases the threshold load. The object of medical therapy is to decrease or reverse these acute respiratory loads thereby decreasing demand on fatiguing respiratory muscles. If this is not successful, then ventilation needs to be aided by mechanical means. Recruitment of accessory muscles of respiration and abdominal paradox are clinical signs that the respiratory muscles do not have enough power on their own to meet demand. Any patient with these signs will need to have the loads reduced or eventually, ventilation aided by mechanical means.
Type 3 (Peri-operative) Respiratory Failure:
Type 3 respiratory failure can be considered as a subtype of type 1 failure. However, acute respiratory failure is common in the post-operative period with atelectasis being the most frequent cause. Thus measures to reverse atelectasis are paramount.In general residual anesthesia effects, post-operative pain, and abnormal abdominal mechanics contribute to decreasing FRC and progressive collapse of dependant lung units.
Causes of post-operative atelectasis include:
- decreased FRC
- Supine/ obese/ ascites
- upper abdominal incision
- airway secretions
Therapy is directed at reversing the atelectasis.
- Turn patient q1-2h
- Chest physiotherapy
- Incentive spirometry
- Treat incisional pain (may include epidural anesthesia or patient controlled analgesia)
- Ventilate at 45 degrees upright
- Drain ascites
- Re-expansion of lobar collapse
- Avoid overhydration
Type 4 (Shock);
Hypoperfusion can lead to respiratory failure.Ventilator therapy is often instituted in order to minimize the steal of the limited cardiac output by the overworking respiratory muscles until the etiology of the hypoperfusion state is identified and corrected.
Clinical Signs and Symptoms of Acute Respiratory Failure
Clinical manifestations of respiratory distress reflect signs and symptoms of hypoxemia, hypercapnia, or the increased work of breathing necessary. These include
- Altered mental status (agitation, somnolence)
- Peripheral or central cyanosis or decreased oxygen saturation on pulse oximetry
- Manifestations of a "stress response" including tachycardia, hypertension, and diaphoresis
- Evidence of increased respiratory work of breathing including accessory muscle use, nasal flaring, intercostal indrawing, suprasternal or supraclavicular retractions, tachypnea
- Evidence of diaphragmatic fatigue (abdominal paradox)
- Abnormal arterial blood gas results
ARF : CXR Findings
- Clear CXR with hypoxemia and normocapnia.- Pulmonary embolus, R to L shunt, Shock
- Diffusely white (opacified) CXR with hypoxemia and normocapnia - ARDS, NCPE, CHF, pulmonary fibrosis
- Localized infiltrate - pneumonia, atelectasis, infarct
- Clear CXR with hypercapnia - COPD, asthma, overdose, neuromuscular weakness
Acute Respiratory Failure with COPD: Differential Dx.:
- LV failure (pulmonary edema)
- Pulmonary embolus
- Drugs ( beta blockers )
Management of Acute Respiratory Failure
The management of acute respiratory failure can be divided into an urgent resuscitation phase followed by a phase of ongoing care. The goal of the urgent resuscitation phase is to stabilize the patient as much as possible and to prevent any further life-threatening deterioration. Once these goals are accomplished the focus should then shift towards diagnosis of the underlying process, and then the institution of therapy targeted at reversing the primary etiology of the ARF.
- Airway control
- Ventilator management
- Stabilization of the circulation
- Bronchodilators/ Steroids
- Differential diagnosis and investigations
- Therapeutic plan tailored to diagnosis
Almost all patients with ARF require supplemental oxygen. All should be placed on a pulse oximeter and oxygen saturation should generally be maintained above 90%. Oxygen diffuses from the alveolus across the alveolar membrane into capillary blood. The rate of diffusion is driven by the oxygen partial-pressure gradient. Therefore increasing the PAO2 with supplementary oxygen should improve the transfer of oxygen into the pulmonary capillary blood.
There are several different devices that can be used to deliver oxygen. They differ in terms of whether the are open or closed systems, whether they deliver low or high oxygen concentrations, and whether they are low or high flow systems. Their effectiveness depends upon whether they can deliver enough oxygen at a sufficient flow rate to meet the patients demands. Non-intubated patients spontaneously breathing through an open system will "entrain" some room air from their environment with each breath. Thus the ultimate oxygen concentration delivered to them will depend upon how much was delivered by the oxygen device and how much was entrained room air. The lower the flow delivered by the oxygen device, and the higher the patient's own inspiratory flow is, the more room that will be entrained resulting in a lower oxygen concentration. For example, a tachypneic patient will likely have a high respiratory drive and high inspiratory flows. He will require a high flow system in order to prevent significant entrainment of room air and thus dilution of the delivered oxygen.
- Nasal cannula; Low-flow, low oxygen concentration, open device. 100 % oxygen is delivered through cannulae at 0.5 to 6 L/min. Higher flow rates do not increase the FIO2 significantly and lead to drying of the mucosa and patient discomfort. The resulting FIO2 depends upon the patient's minute ventilation and how much room air is entrained. Thus it cannot be precisely controlled. The maximal oxygen concentration at the trachea is not likely to exceed 40 to 50 %. Nasal prongs are generally used for relatively stable patients who do not require high FIO2 or precise control of their FIO2.
- Venturi masks. These are variable oxygen concentration, low to moderate flow, open devices. These air entrainment masks deliver 100% oxygen through a jet-mixing device that causes a controlled entrainment of air and thus allows for deliver of precise oxygen concentrations from 24 to 50 %. These masks are useful in patients with COPD in whom a precise titration of oxygen concentration may be desirable in order to minimize an increase in PCO2.
- Reservoir Face Masks. These are high flow, high oxygen, open devices designed to minimize entrainment of air in patients with high inspiratory flow demands. These masks incorporate a reservoir bag that is filled with 100% oxygen. If the patient makes an inspiratory effort generating a flow higher than the wall circuit can deliver, the reservoir of oxygen will be emptied to minimize entrainment of room air.. The use of "tusks" on the facemask is a similar principle. The bag should be at least partially distended throughout the respiratory cycle.
- Resuscitation Bag-Mask-Valve Unit. High oxygen, high flow device. The oxygen flow should be kept high (15 L/min) when this device is used. When the mask is held firmly over the face with a good facemask seal, entrainment of room air is minimized.
- Non-Invasive Positive Pressure Ventilation (NPPV). NPPV provides ventilatory assistance, positive pressure, and a controlled oxygen concentration using a tight-fitting facemask as the interface between the patient and the ventilator instead of an endotracheal tube. It can be used in order to avoid or prevent intubation in carefully selected patients.
- Introduction to Mechanical Ventilation
Patrick Melanson, MD, FRCPC