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Respiratory Failure: Concepts and Sample MCQs

(For NEET PG, USMLE, PLAB, FMGE /MCI Screening Entrance Exams)

Overview :

Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, it may be classified as either hypoxemic or hypercapnic.

Hypoxemic respiratory failure (type I) is characterized by an arterial oxygen tension (Pa O2) lower than 60 mm Hg with a normal or low arterial carbon dioxide tension (Pa CO2). This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.

Hypercapnic respiratory failure (type II) is characterized by a PaCO2 higher than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma and chronic obstructive pulmonary disease [COPD]).

Respiratory failure may be further classified as either acute or chronic. Although acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.

Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH is less than 7.3. Chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased.

The distinction between acute and chronic hypoxemic respiratory failure cannot readily be made on the basis of arterial blood gases. The clinical markers of chronic hypoxemia, such as polycythemia or cor pulmonale, suggest a long-standing disorder.

Arterial blood gases should be evaluated in all patients who are seriously ill or in whom respiratory failure is suspected. Chest radiography is essential. Echocardiography is not routine but is sometimes useful. Pulmonary functions tests (PFTs) may be helpful. Electrocardiography (ECG) should be performed to assess the possibility of a cardiovascular cause of respiratory failure; it also may detect dysrhythmias resulting from severe hypoxemia or acidosis. Right-sided heart catheterization is controversial (see Workup).

Hypoxemia is the major immediate threat to organ function. After the patient’s hypoxemia is corrected and the ventilatory and hemodynamic status have stabilized, every attempt should be made to identify and correct the underlying pathophysiologic process that led to respiratory failure in the first place. The specific treatment depends on the etiology of respiratory failure (see Treatment).

For patient education resources, see the Lung and Airway Center, as well as Acute Respiratory Distress Syndrome.

Pathology :

Respiratory failure can arise from an abnormality in any of the components of the respiratory system, including the airways, alveoli, central nervous system (CNS), peripheral nervous system, respiratory muscles, and chest wall. Patients who have hypoperfusion secondary to cardiogenic, hypovolemic, or septic shock often present with respiratory failure.

Ventilatory capacity is the maximal spontaneous ventilation that can be maintained without development of respiratory muscle fatigue. Ventilatory demand is the spontaneous minute ventilation that results in a stable Pa CO2.

Normally, ventilatory capacity greatly exceeds ventilatory demand. Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both). Ventilatory capacity can be decreased by a disease process involving any of the functional components of the respiratory system and its controller. Ventilatory demand is augmented by an increase in minute ventilation and/or an increase in the work of breathing.

Respiratory physiologyThe act of respiration engages 3 processes:

Transfer of oxygen across the alveolus

Transport of oxygen to the tissues

Removal of carbon dioxide from blood into the alveolus and then into the environmentRespiratory failure may occur from malfunctioning of any of these processes. In order to understand the pathophysiologic basis of acute respiratory failure, an understanding of pulmonary gas exchange is essential.

Gas exchange

Respiration primarily occurs at the alveolar capillary units of the lungs, where exchange of oxygen and carbon dioxide between alveolar gas and blood takes place. After diffusing into the blood, the oxygen molecules reversibly bind to the hemoglobin. Each molecule of hemoglobin contains 4 sites for combination with molecular oxygen; 1 g of hemoglobin combines with a maximum of 1.36 mL of oxygen.

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www.medicoapps.orgThe quantity of oxygen combined with hemoglobin depends on the level of blood Pa O2. This relationship, expressed as the oxygen hemoglobin dissociation curve, is not linear but has a sigmoid-shaped curve with a steep slope between a Pa O2 of 10 and 50 mm Hg and a flat portion above a Pa O2 of 70 mm Hg.

The carbon dioxide is transported in 3 main forms: (1) in simple solution, (2) as bicarbonate, and (3) combined with protein of hemoglobin as a carbamino compound.

During ideal gas exchange, blood flow and ventilation would perfectly match each other, resulting in no alveolar-arterial oxygen tension (PO2) gradient. However, even in normal lungs, not all alveoli are ventilated and perfused perfectly. For a given perfusion, some alveoli are underventilated, while others are overventilated. Similarly, for known alveolar ventilation, some units are underperfused, while others are overperfused.

The optimally ventilated alveoli that are not perfused well have a large ventilation-to-perfusion ratio (V/Q) and are called high-V/Q units (which act like dead space). Alveoli that are optimally perfused but not adequately ventilated are called low-V/Q units (which act like a shunt).

Alveolar ventilation

At steady state, the rate of carbon dioxide production by the tissues is constant and equals the rate of carbon dioxide elimination by the lung. This relation is expressed by the following equation:

VA = K × VCO2/ Pa CO2

where K is a constant (0.863), VA is alveolar ventilation, and VCO2 is carbon dioxide ventilation. This relation determines whether the alveolar ventilation is adequate for metabolic needs of the body.

The efficiency of lungs at carrying out of respiration can be further evaluated by measuring the alveolar-arterial PO2 gradient. This difference is calculated by the following equation:

PA O2 = FI O2 × (PB – PH2 O) – PA CO2/R

where PA O2 is alveolar PO2, FI O2 is fractional concentration of oxygen in inspired gas, PB is barometric pressure, PH2 O is water vapor pressure at 37°C, PA CO2 is alveolar PCO2 (assumed to be equal to Pa CO2), and R is respiratory exchange ratio. R depends on oxygen consumption and carbon dioxide production. At rest, the ratio of VCO2 to oxygen ventilation (VO2) is approximately 0.8.

Even normal lungs have some degree of V/Q mismatching and a small quantity of right-to-left shunt, with PA O2 slightly higher than Pa O2. However, an increase in the alveolar-arterial PO2 gradient above 15-20 mm Hg indicates pulmonary disease as the cause of hypoxemia.

Hypoxemic respiratory failureThe pathophysiologic mechanisms that account for the hypoxemia observed in a wide variety of diseases are V/Q mismatch and shunt. These 2 mechanisms lead to widening of the alveolar-arterial PO2 gradient, which normally is less than 15 mm Hg. They can be differentiated by assessing the response to oxygen supplementation or calculating the shunt fraction after inhalation of 100% oxygen. In most patients with hypoxemic respiratory failure, these 2 mechanisms coexist.

V/Q mismatch

V/Q mismatch is the most common cause of hypoxemia. Alveolar units may vary from low-V/Q to high-V/Q in the presence of a disease process. The low-V/Q units contribute to hypoxemia and hypercapnia, whereas the high-V/Q units waste ventilation but do not affect gas exchange unless the abnormality is quite severe.

The low V/Q ratio may occur either from a decrease in ventilation secondary to airway or interstitial lung disease or from overperfusion in the presence of normal ventilation. The overperfusion may occur in case of pulmonary embolism, where the blood is diverted to normally ventilated units from regions of lungs that have blood flow obstruction secondary to embolism.

Administration of 100% oxygen eliminates all of the low-V/Q units, thus leading to correction of hypoxemia. Hypoxemia increases minute ventilation by chemoreceptor stimulation, but the Pa CO2 generally is not affected.

Shunt

Shunt is defined as the persistence of hypoxemia despite 100% oxygen inhalation. The deoxygenated blood (mixed venous blood) bypasses the ventilated alveoli and mixes with oxygenated blood that has flowed through the ventilated alveoli, consequently leading to a reduction in arterial blood content. The shunt is calculated by the following equation:

QS/QT = (CC O2 – Ca O2)/CC O2 – Cv O2)

where QS/QT is the shunt fraction, CC O2 is capillary oxygen content (calculated from ideal PA O2), Ca O2 is arterial oxygen content (derived from Pa O2 by using the oxygen dissociation curve), and Cv O2 is mixed venous oxygen content (assumed or measured by drawing mixed venous blood from a pulmonary arterial catheter).

Anatomic shunt exists in normal lungs because of the bronchial and thebesian circulations, which account for 2-3% of shunt. A normal right-to-left shunt may occur from atrial septal defect, ventricular septal defect, patent ductus arteriosus, or arteriovenous malformation in the lung.

Shunt as a cause of hypoxemia is observed primarily in pneumonia, atelectasis, and severe pulmonary edema of either cardiac or noncardiac origin. Hypercapnia generally does not develop unless the shunt is excessive (> 60%). Compared with V/Q mismatch, hypoxemia produced by shunt is difficult to correct by means of oxygen administration.

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Hypercapnic respiratory failureAt a constant rate of carbon dioxide production, Pa CO2 is determined by the level of alveolar ventilation according to the following equation (a restatement of the equation given above for alveolar ventilation):

Pa CO2 = VCO2 × K/VA

where K is a constant (0.863). The relation between Pa CO2 and alveolar ventilation is hyperbolic. As ventilation decreases below 4-6 L/min, Pa CO2 rises precipitously. A decrease in alveolar ventilation can result from a reduction in overall (minute) ventilation or an increase in the proportion of dead space ventilation. A reduction in minute ventilation is observed primarily in the setting of neuromuscular disorders and CNS depression. In pure hypercapnic respiratory failure, the hypoxemia is easily corrected with oxygen therapy.

Hyperventilation is an uncommon cause of respiratory failure and usually occurs from depression of the CNS from drugs or neuromuscular diseases affecting respiratory muscles. Hypoventilation is characterized by hypercapnia and hypoxemia. Hypoventilation can be differentiated from other causes of hypoxemia by the presence of a normal alveolar-arterial PO2 gradient.

Etiology

These diseases can be grouped according to the primary abnormality and the individual components of the respiratory system (eg, CNS, peripheral nervous system, respiratory muscles, chest wall, airways, and alveoli).

A variety of pharmacologic, structural, and metabolic disorders of the CNS are characterized by depression of the neural drive to breathe. This may lead to acute or chronic hypoventilation and hypercapnia. Examples include tumors or vascular abnormalities involving the brain stem, an overdose of a narcotic or sedative, and metabolic disorders such as myxedema or chronic metabolic alkalosis.

Disorders of the peripheral nervous system, respiratory muscles, and chest wall lead to an inability to maintain a level of minute ventilation appropriate for the rate of carbon dioxide production. Concomitant hypoxemia and hypercapnia occur. Examples include Guillain-Barré syndrome, muscular dystrophy, myasthenia gravis, severe kyphoscoliosis, and morbid obesity.

Severe airway obstruction is a common cause of acute and chronic hypercapnia. Examples of upper-airway disorders are acute epiglottitis and tumors involving the trachea; lower-airway disorders include COPD, asthma, and cystic fibrosis.

Diseases of the alveoli are characterized by diffuse alveolar filling, frequently resulting in hypoxemic respiratory failure, although hypercapnia may complicate the clinical picture. Common examples are cardiogenic and noncardiogenic pulmonary edema, aspiration pneumonia, or extensive pulmonary hemorrhage. These disorders are associated with intrapulmonary shunt and an increased work of breathing.

Common causes of type I (hypoxemic) respiratory failure include the following:

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

Common causes of type II (hypercapnic) respiratory failure include the following:

COPD

Severe asthma

Drug overdose

Poisonings

Myasthenia gravis

Polyneuropathy

Poliomyelitis

Primary muscle disorders

Porphyria

Cervical cordotomy

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Primary alveolar hypoventilation

Obesity-hypoventilation syndrome

Pulmonary edema

ARDS

Myxedema

Tetanus

Acute respiratory failure is defined as hypoxemia, which i.e; PaO2 of <50mmHg. This type of respiratory failure also consists of marked V/Q abnormalities and shunting occurring within a lung.

 Classification :Type 1 respiratory failure occurs in the following clinical settings;

Acute respiratory distress syndrome

Fat embolism

Pulmonary edema

Type 2 respiratory failure is a ventillatory failure having V/Q imbalance and inadequate alveolar ventilation. Patients with type 2 respiratory failures are divided in to categories, namely

Patients with inherent lung disease (ex; include cystic fibrosis, emphysema, etc.)

Patients with normal inherent lungs, but having inadequate ventilation (ex; include CNS disease, drug overdose and trauma.

Type 1 Respiratory Failure Type 2 Respiratory Failure Type 3 Respiratory Failure

 Oxygenation Failuree.g. V/Q mismatch / shunt

 Ventilation Failure e.g hypoventilation

 Respiratory or Combined Failuree.g. combination

Low PO2 Low PO2 Low PO2

Normal / Elevated PCO2 Elevated PCO2 Elevated PCO2

Elevated A-a Gradient Normal A-a Gradient Elevated A-a Gradient

1.

Which of the following statements are true about Flail chest?

1. Fracture of 3 or 4th ribs2. Mechanical ventilation always needed3. Mediastinal shift4. Inward movement of chest wall during inspiration5. Ultimately leads to Respiratory failure

a.3,4,5 True & 1,2 False

b. 3,4,5 False & 1,2 True

c.1,4,5 True & 2,3 False

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d.1,2,4 False & 3,5 True

Fracture of 3 or 4th ribs and inward movement of chest wall during inspiration are seen in Flail chest. It will ultimately leads to respiratory failure.

2.

Which of the following is a false statement about Type I respiratory failure:

a.Decreased Pa02

b.Decreased PaC02

c.Normal PaC02

d.Normal A-a gradient

A-a Gradient is the difference between the Alveolar PO2 (A) and arterial PO2 (a). The a-a gradient indicates how well O2 is equilibrating across the blood air barrier.

Acute respiratory failure is defined as a lung disorder, wherein adequate functioning of lung, to meet the necessary demands of an individual is not met. It is unable to maintain normal levels of arterial gas in the blood. Respiratory failure is of 3 types, namely

Type 1 respiratory failure or Oxygenation FailureType 2 respiratory failure or Ventilation FailureType 3 respiratory failure or Combined Respiratory Failure

3.

All of the following agents cause respiratory failure due to central inhibition of respiratory centre, EXCEPT:

a.Opium

b.Strychnine

c.Barbiturate

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d.Gelsemium

Strychnine:It competitively antagonizes glycine, an inhibitory neurotransmitter released by postsynaptic inhibitory neurons in the spinal cord.It also binds to the chloride ion channel, causing increased neuronal excitability and exaggerated reflex arcs.This results in generalized seizure-like contraction of skeletal muscles.Death usually is caused by respiratory arrest that results from intense contraction of the respiratory muscles.

4.

Pneumatoceles in chest X-ray in an infant with breathlesness, tachycardia, fever and respiratory failure suggests a diagnosis of:

a. S.aureus

b.Klebsiella

c. Pneumothorax

d. Air embolism

Respiratory tract infections caused by S. aureusA) In children, it can cause serious respiratory tract infections in newborns and infants; these infections present as shortness of breath, fever, and respiratory failure. Chest x-ray may reveal pneumatoceles (shaggy, thin-walled cavities).

B) In adults, nosocomial S. aureus pulmonary infections are commonly seen in intubated patients in intensive care units. Patients produce increased volumes of purulent sputum and develop respiratory distress, fever, and new pulmonary infiltrates. Distinguishing bacterial pneumonia from respiratory failure of other causes or new pulmonary infiltrates in critically ill patients is often difficult and relies on a constellation of clinical, radiologic, and laboratory findings.

MUST KNOW:Community-acquired respiratory tract infections due to S. aureus usually follow viral infections—most commonly influenza. Patients may present with fever, bloody sputum production, and mid lung-field pneumatoceles or multiple, patchy pulmonary infiltrates.

5.

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The antibiotic which can cause respiratory failure when used in patients with myasthenia gravis is:

a.Telithromycin

b.Clindamycin

c.Linezolid

d.Tetracycline

Telithromycin may lead to respiratory failure.

6.

Most common contributory factor to respiratory failure in patients with cystic fibrosis is:

a.H.Influenzae infection

b.Pseudomona infection

c.Associated heart failure

d.Hypokalemia

P. aeruginosa is the most common cause of gram-negative bacteremia in neutropenic patients and it is the most common contributing factor to respiratory failure in cystic fibrosis and is responsible for the majority of deaths among them. P. aeruginosa infection in burns is no longer a major problem.

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