Respiratory Failure

Description

Respiratory failure is characterized by a reduction in function of the lungs due to lung disease or a skeletal or neuromuscular disorder. It occurs when gas exchange at the lungs is significantly impaired to cause a drop in blood levels of oxygen(hypoxemia) occurring with or without an increase in carbon dioxide levels(hypercapnia). It's usually defined in terms of the gas tensions in the arterial blood, respiratory rate and evidence of increased work of breathing. Respiratory failure can be acute, chronic or acute on chronic. It's a major cause of mortality and morbidity and mortality rates increase with age and presence of co-morbidities.

Respiratory physiology

The respiratory system can be said to consist of two parts: the lung- gas exchanging organ and the respiratory pump- ventilates the lungs. The respiratory pumps consists of the chest wall- respiratory muscles, the respiratory controllers in the CNS and the pathways that connect the central controllers with the respiratory muscles i.e the spinal and peripheral nerves. The act of respiration engages three processes: transfer of oxygen across the alveolus, transfer of oxygen to the tissues and removal of carbon dioxide from the blood into the alveolus and then the environment. The alveolar capillary unit of the lungs are primarily where respiration takes place with exchange of oxygen and carbon dioxide between alveolar gas and blood. Oxygen reversibly binds with hemoglobin after diffusing into the blood. At steady state, rate of carbon dioxide production equals rate of elimination by the lungs. Optimally ventilated alveoli that are not well perfused have a large ventilation to perfusion(V/Q) ratio and are called high V/Q units. High V/Q units act like dead space. Optimally perfused not adequately ventilated alveoli are called low V/Q units and they act like shunt.

Classification of Respiratory Failure

Respiratory failure is classified mechanically based on pathophysiologic derangement in respiratory failure. This classifies RF into 4 types:

1. Type I(Hypoxemic) Respiratory Failure: this is caused by intrinsic lung disease that interferes with oxygen transfer in the lungs. The resulting hypoxemia is from increased shunt fraction, ventilation/perfusion(V/Q) mismatch or a combination of the two. It's characterized by an arterial oxygen tension(PaO₂) < 60mmHg(on room air) with a normal or low arterial carbon dioxide tension(PaCO₂). It is the most common form of respiratory failure and it can be associated with most acute diseases of the lungs that involve fluid filling or collapse of alveolar units. Hypoxaemia resulting from V/Q mismatch or diffusion abnormality can easily be corrected with supplemental oxygen, This is in contrast to hypoxaemia induced purely by increased shunt, it is refractory to supplemental oxygen. Common causes include: acute respiratory distress syndrome(ARDS), COPD, pneumonia, pulmonary edema, pulmonary fibrosis, asthma, pneumothorax, pulmonary embolism, pulmonary hypertension,
2. Type II(Hypercapnic) Respiratory Failure: is characterized by alveolar hypoventilation and increased carbon dioxide pressure(PaCO₂). It is caused by loss of CNS drive, impaired neuromuscular competence, excessive dead space or increased mechanical load. Arterial carbon dioxide pressure PaCO₂ is > 50mmHg. Commonly caused by myasthenia gravis, head injuries, polyneuropathies, muscular dystrophy, kyphoscoliosis, flail chest, obesity hypoventilation syndrome, advanced chronic bronchitis and emphysema.
3. Type III Respiratory Failure: typically occurs in the perioperative period when factors that reduce functional residual capacity(FRC) combine with causes of increased closing volume to produce atelectasis. Commonly caused by inadequate post-operative analgesia, obesity, ascites and excessive airway secretions.
4. Type IV Respiratory Failure: results from hypoperfusion of respiratory muscles in patients in shock. Patients are usually intubated and ventilated in the process of resuscitation for shock. Commonly caused by cardiogenic shock, septic shock and hypovolemic shock.

Respiratory failure can be further classified as acute- develops over minutes to hours with pH < 7.3 or chronic-develops over several days or longer which allows time for renal compensation and increase bicarbonate concentration. pH is usually slightly decreased. Arterial blood gases are not sufficient to clearly distinguish between acute and chronic respiratory failure. Abrupt changes in mental status suggest an acute RF while clinical markers of chronic hypoxemia such as polycythemia or cor pulmonale.

Mechanism of Injury / Pathological Process

Generally, failure of the lung caused by a variety of lung disease leads failure of gas exchange manifested by hypoxemia whilst failure of the pump results in ventilatory failure manifested as hypercapnia. Lung diseases may result in muscle fatigue and ventilatory failure through an imbalance between demands and supplies. Likewise, patients with diseases that involve the ventilatory pump and present with hypercapnia are typically characterized by inability to cough and possibly atelectasis. This aggravates V/Q mismatch resulting in hypoxaemia.

Type I Respiratory failure

Four pathophysiological mechanisms accounts for hypoxaemia in a variety of diseases and this includes: ventilation/perfusion(V/Q) mismatch, increased shunt, diffusion impairment and alveolar hypoventilation.

• V/Q mismatch(low V/Q), which is the most common mechanism develops when there are lung regions with a greater reduction in ventilation than in perfusion.
• In shunt, there is a bypass of ventilated alveoli by intrapulmonary or intracardiac deoxygenated mixed venous blood resulting in venous admixture.
• Diffusion pathway for oxygen from the alveolar space to the pulmonary capillaries can be increased by diseases which in turn decreases capillary surface area prevents complete equilibrium of alveolar oxygen with pulmonary capillary blood.
• In underlying pulmonary disease, there is broadening of the alveolar/arterial gradient- either due to V/Q mismatch or shunt or diffusion impairment results in severe hypoxemia while for hypoxaemia accompanying hypoventilation(without underlying pulmonary disease) the alveolar/arterial gradient is normal

Type II Respiratory failure

Pump failure leading to hypercapnia are caused by three major factors which includes: inadequate output of the respiratory centers controlling the muscles, mechanical defect in the chest wall , excessive inspiratory load

• inadequate output of the respiratory centers controlling the muscles results in an insufficient respiratory drive for the demand or the respiratory centers my reflexively modify their output to prevent respiratory muscle injury and avoid fatigue. Insufficient activation from the CNS either temporarily- from anesthesia, drug overdose or permanently- diseases of the medulla results in inadequate respiratory efforts and hypoventilation ensues.
• mechanical defects in the chest wall as in flail chest, diseases of the nerves(Gullain-Barre syndrome) and anterior horn cells(poliomyelitis) or diseases of the respiratory muscles(myopathies)
• excessive inspiratory load fatigues the inspiratory muscles- they are unable to generate an adequate pleural pressure even though there is an adequate respiratory drive and an intact chest wall. Factors that increase inspiratory muscle energy demand and/or decrease energy supplies predisposes respiratory muscles to fatigue.

Etiology

Respiratory failure occurs when there is a dysfunction of one or more of the components of the respiratory system. The etiology of respiratory failure can be grouped according to the primary abnormality and the individual components of the respiratory system.

Central nervous system dysfunction

• drug overdose- narcotics/sedatives
• brain-stem lesion
• metabolic disorders- myxedema, chronic metabolic acidosis
• central hypoventilation

Peripheral nervous system dysfunction

• myasthenia gravis
• gullain-barre syndrome
• muscular dystophy

Chest wall dysfunction

• kyphoscoliosis
• obesity

Airway dysfunction

• Upper airway- acute epiglottitis, tumors involving trachea
• Lower airway- COPD, asthma, cystic fibosis

Alveolar dysfunction

• pulmonary edema- cardiogenic & non-cardiogenic
• pneumonia
• pulmonary hemorrhage

Pulmonary circulation dysfunction

• acute pulmonary embolism
• pulmonary hypertension
• arteriovenous malformation

Clinical Presentation

Presentation of respiratory failure is dependent on the underlying cause and associated hypoxemia or hypercapnia. Common presentations include:

• Dyspnoea
• Tachypnoea
• Restlessness
• Confusion
• Anxiety
• Cynaosis- central
• Tachycardia
• Pulmonary hypertension
• Loss of consciouness

Diagnostic Procedures

A combination of medical history, physical findings, laboratory investigations and imaging are used to establish the diagnosis of respiratory failure.

Medical history aims to gather information about history of diseases/conditions that could lead to respiratory failure,

Physical findings signs suggests possible underlying cause of respiratory failure, Includes:

• hypotension usually with signs of poor perfusion suggest severe sepsis or pulmonary embolus
• hypertension usually with signs of poor perfusion suggests cardiogenic pulmonary edema
• wheeze & stridor suggest airway obstruction
• tachycardia and arrhythmias may be the cause of cardiogenic pulmonary edema
• elevated jugular venous pressure suggests right ventricular dysfunction
• respiratory rate < 12b/m in spontaneously breathing patient with hypoxia or hypercarbia and acidemia suggest nervous system dysfunction
• paradoxical respiratory motion suggest muscular dysfunction

Laboratory Investigations

• Arterial blood gases- measures oxygen and carbon dioxide levels in the blood

• Full blood count- may indicate anemia which can contribute to tissue hypoxia; polycythaemia may indicate chronic hypoxaemic respiratory failure; thrombocytopenia may suggest sepsis
• Renal function tests and liver function tests- may indicate the etiology of respiratory failure or identify complications associated with it.
• Pulmonary function test- identifies obstruction, restriction and gas diffusion abnormalities. Normal values for forced expiratory volume in 1 second(FEV₁) and forced vital capacity(FVC) suggest a disturbance in respiratory control. Decrease in FEV₁ to FVC ratio indicates airflow obstruction. A decrease in FEV₁ and FVC and maintenance of FEV₁ to FVC ratio suggest restrictive lung disease.
• Electrocardiography(ECG)- determines if respiratory failure is from a cardiovascular cause, may detect dysarryhtmias from hypoxaemia or acidosis
• Echocardiography- needed when a cardiac cause of acute respiratory failure is suspected. Findings such as left ventricular dilatation, regional/global wall motion abnormalities or severe mitral regurgitation verify the diagnosis of cardiogenic pulmonary edema. Normal heart size and normal systolic and diastolic function in a patient with pulmonary edema suggests acute respiratory distress syndrome
• Chest radiography- reveals the cause of respiratory failure
• Serum creatinine kinase with fractionation and troponin I- excludes recent myocardial infarction in a patient with RF. Elevated levels of creatinine kinase with normal troponin I levelss may indicate myositis- causes respiratory failure occasionally
• Thyroid function tests- hypothyrodism may cause chronic hypercapnic respiratory failure

Complications

Multiple organ-system complications involving the cardiovascular, pulmonary, gastrointestinal systems may occcur subsequent to respiratory failure

• Pulmonary: pulmonary embolism, pulmonary fibrosis, complications secondary to the use of mechanical ventilator
• Cardiovascular: hypotension, reduced cardiac output, cor pulmonale, arrythmias, pericarditis and acute myocardial infarction
• Gastrointestinal :haemorrhage, gastric distention, ileus, diarrhoea, pneumoperitoneum and duodenal ulceration- caused by stress is common in patients with acute respiratory failure
• Infectious: noscomial- pneumonia, urinary tract infection and catheter related sepsis. Usuallly occur with use of mechanical devices.
• Renal: acute renal failure, abnormalities of electrolytes and acid-base balance.
• Nutritional: malnutrition and complications relating to parenteral or enteral nutrition and complications associated with NG tube- abdominal distention and diarrhea

Outcome Measures

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Management / Interventions

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Differential Diagnosis

• Acute Respiratory Distress Syndrome
• Angina Pectoris
• Aspiration Pneumonitis
• Asthma
• Atelectasis
• Cardiogenic shock
• Obstructive sleep apnea
• Myocardial infarction
• Pulmonary embolism

Prognosis

Respiratory failure is associated with poor prognosis but advances in mechanical ventilation and airway management have improved prognosis. It is dependent on the underlying cause of the respiratory failure. Mortality rates of approximately 40-45% occurs for acute respiratory distress syndrome(ARDS) with younger patients(< 60 years) having better survival rates. About two-thirds of the patients who survive an episode of ARDS show some impairment of pulmonary function one or more years post recovery. For COPD and acute respiratory failure. overall mortality has reportedly declined from 26% to 10%. Also, significant mortality occurs in patients with hypercapnic respiratory failure due to associated co-morbidities and poor nutritional status. Noveanu et al's study shows a strong association between preadmission use of beta-blockers and in-hospital and 1-year mortality among patients with acute respiratory failure.

Key Evidence

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Resources

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