with Respiratory Failure

Type

Cause

Respiratory drive

Pharmacological

Drug overdose, anesthesia

Congenital

Central hypoventilation syndrome

Acquired

Cerebrovascular accident

Neuromuscular

Cervical spinal cord injury

Trauma

Chronic inflammatory demyelinating polyneuropathy

Guillain–Barré syndrome

Anterior horn disease

Poliomyelitis

Phrenic nerve injury

Trauma, cardiac surgery

Muscles of respiration

Pharmacological

Neuromuscular blocks

Congenital

Hypophosphatemia

Acquired

Kyphoscoliosis, trauma

Rib cage

Decreased mobility

Alt. Pleura

Extrapulmonary restriction

Pneumothorax, pleural effusion

Airway

Upper airway obstruction

Epiglottitis, foreign body

Lower airway obstruction

Asthma

Increase in dead space

Increased ventilation/perfusion ratio

Emphysema

Decreased ventilation/perfusion ratio

Acute respiratory distress syndrome

General pulmonary hypoperfusion

Hypovolemia, cardiogenic shock

Localized hypoperfusion

Thromboembolism

Physiopathology

There are five physiopathological mechanisms that can alter the homeostasis of gases and lead to respiratory insufficiency: (1) an alteration in the alveolar ventilation and pulmonary perfusion ratio (V/Q ratio); (2) a shunt (short circuit); (3) hypoventilation; (4) an alteration in the diffusion of gases in the alveolocapillary membrane; and (5) a decrease in the concentration of inhaled oxygen. The three most important are the V/Q ratio, hypoventilation, and a shunt, with a decrease in inhaled O₂ being considered a minor clinical implication of acute respiratory insufficiency.

Ventilation/Perfusion Alterations

An alteration in the V/Q ratio is the most common cause of arterial hypoxemia. The concentration of O₂ in the alveoli and capillary blood depends on the relative concentrations of inhaled O₂ and unsaturated blood in the pulmonary artery, which is termed the ventilation/perfusion ratio. The same applies to CO₂. While it could be expected that there is an adequate ratio for every alveolar unit, the lung does not act as a multitude of identical gas exchange units; rather, it acts as a multitude of parallel and serial perfusion and ventilation units, which vary, even in healthy individuals, because of age, physical activity, bodily posture, and other factors, with some poorly ventilated but well perfused areas, and other areas that are well ventilated but poorly perfused (Fig. 17.1).

../images/441522_1_En_17_Chapter/441522_1_En_17_Fig1_HTML.png — Fig. 17.1
Ventilation distribution, blood flow, and ventilation/perfusion (V/Q) ratio

Alveolar oxygen pressure (P_aO₂ ) is determined by the pressure of inhaled oxygen, the pressure of alveolar carbon dioxide (P_aCO₂ ), and the respiratory quotient, while P_aCO₂ is determined by alveolar ventilation (V_A) and the range of corporeal CO₂ production. When the pulmonary blood flow of the unit decreases (i.e., the V/Q ratio increases), P_aO₂ and the capillary oxygen pressure approach the partial inhaled oxygen pressure. When the ventilation of the unit decreases (i.e., the V/Q ratio decreases), P_aO₂ and PcO₂ approximate the P_aO₂ of mixed venous blood. In the normal lung, the V/Q ratio ranges between 0/6 and 3.0, concentrated mostly at 1.0. Hypoxemia occurs when perfusion exceeds ventilation—that is, when the V/Q ratio is <1 (Fig. 17.2).

../images/441522_1_En_17_Chapter/441522_1_En_17_Fig2_HTML.png — Fig. 17.2
Ventilation/perfusion alteration

In a person who is breathing spontaneously, there are compensatory mechanisms to correct hypoxia and/or hypercarbia. In the context of hypoxemia, pulmonary vascular vasoconstriction consists of the alveolar units with better V/Q ratios an excluding those that are poorly ventilated, while the increase in V_A as a response to hypoxia prevents an increase in PcO₂, including lowering it to below normal levels.

Hypoventilation

P_aO₂ is determined by the balance between oxygen provided by V_A (which provides oxygen from inhaled air) and the extraction of oxygen by capillary blood. Consequently, when V_A decreases significantly, P_aO₂ decreases and PcO₂ increases, which are the fundamental characteristics of hypoventilation.

PcO₂ is determined by V_A and the production of CO₂ (VCO₂), multiplied by the K constant, as is seen in the formula P_aCO₂ = (VCO₂/V_A) × K, from which it can be deduced that increased CO₂ production or a decrease in V_A increases P_aCO₂. As the compensatory renal response to hypercarbia is slow (bicarbonate retention), there is an acute fall in arterial pH.

Given that minute ventilation includes both V_A and dead space, its reduction or increase implies an increase or decrease in V_A. The ratio between the decrease in P_aO₂ and the increase in PcO₂ that occurs in hypoventilation can be calculated by the alveolar gas equation, (P_aO₂ = PIo₂ − (P_aCO₂/R) + F, where PIo₂ is the inhaled oxygen fraction multiplied by barometric pressure, minus water vapor; R is the gas exchange ratio (CO₂ production/oxygen consumption), which is determined by the metabolic state of the tissue; and F is a minimal correction. This formula makes it clear that hypoventilation responds to the contribution of oxygen without necessarily decreasing PcO₂. The effects of the equation at the arterial level can be seen in Fig. 17.3.