A condition marked by an unusually high concentration of carbon dioxide in the blood as a result of hypoventilation.

 Respiratory acidosis:  an acid - base disturbance characterized by reduced alveolar ventilation and manifested by hypercapnia (an excess of carbon dioxide in the blood), respiratory acidosis can be acute ( from a sudden failure in ventilation ) or chronic ( as in long term pulmonary disease ). 
Respiratory acidosis can result from: 

 * Central nervous system (CNS) trauma,
 * Chronic Obstructive Pulmonary  Disease (COPD),
 * Drugs such as narcotics, anesthetics, hypnotics, and sedatives
 * Chronic metabolic alkalosis with respiratory compensatory mechanisms
 * Neuromuscular disease, such as myasthenia gravis, Guillain - Barre` syndrome, and poliomyelitis
 * Airway obstruction
 * Severe Adult respiratory distress syndrome (ARDS)
 * Extensive pneumonia
 * Large pneumothorax
 * Pulmonary edema
Prognosis depends on the severity of the underlying disturbance as well as on the patient's general clinical condition.
 

Symptoms: 

CNS effects include:
Restlessness
Confusion
Apprehension
Unnatural drowsiness (somnolence)
Motor disturbance (asterixis)

Cardiovascular effects include:
 * Possible tachycardia
 * hypertension
 * Possible atrial and ventricular dysrythmias 
 * In severe acidosis, possible hypotension with vasodilation (bounding pulse)
 

Treatment: 

Effected treatment aims to correct the underlying source of alveolar hypoventilation.
Treatment for underlying conditions includes:

 * Bronchodilators,
 * Oxygen
 * Antibiotics/Drug therapy
 * Dialysis - to remove toxic drugs, and correction of metabolic alkalosis

BIPAP

NPPV decreases the work of breathing and thereby improves alveolar ventilation while simultaneously resting the respiratory musculature. The improvement in gas exchange with BIPAP occurs because of an increase in alveolar ventilation. Externally applied expiratory pressure (eg, positive end-expiratory pressure [PEEP]) decreases the work of breathing by partially overcoming the auto-PEEP, which is frequently present in these patients. The patients generate a less negative inspiratory force to initiate a breathing cycle.

Inhalation and exhalation

In spontaneous mode, upon detection of inspiration, higher pressure is delivered until the flow rate falls below the threshold level. The expiratory pressure with bilevel pressure support is equivalent to the PEEP, and the inspiratory pressure is equivalent to the sum of the PEEP and the level of pressure support. In timed mode, biphasic positive airway pressure ventilation alternates between the inspiratory and expiratory pressures at fixed time intervals, which allows unrestricted breathing at both pressures. This differs from the spontaneous mode of BIPAP, which cycles on the basis of the flow rates of the patient's own breathing.

Supplemental oxygen can be connected to the device, but a higher flow of oxygen therapy is usually required.

 

Major mechanisms that can cause or contribute to hypercapnia are insufficient respiratory drive, a defective ventilatory pump, a workload so great that respiratory muscle fatigue develops, and intrinsic lung disease with severe / mismatching. The last two mechanisms often coexist.

Although an increase in the partial pressure of inspired CO2 (eg, in proximity to an indoor fire or with deliberate inhalation of CO2) may occasionally cause hypercapnia, hypercapnia almost always indicates ventilatory insufficiency or failure.

The PaCO2 is proportional to CO2 production (CO2) and is inversely proportional to alveolar ventilation (A) according to the standard equation (where k = a constant)



An increase in CO2 due to fever, seizures, agitation, or other factors is usually compensated for by an immediate increase in A. Hypercapnia develops only if the increase in A is inappropriately low.

Hypoventilation is the most common cause of hypercapnia. In addition to an elevated PaCO2, respiratory acidosis is present in proportion to the extent of tissue and renal buffering.

A reduced A can be due to a decrease in total minute ventilation (E)--often called global hypoventilation--or to an increase in dead space ventilation per minute (D). (E equals exhaled volume per breath [tidal volume] times respiratory rate per minute.)



A drug overdose with suppression of the brain stem respiratory centers is one cause of global hypoventilation.

Dead space (VD), or wasted ventilation, occurs when lung regions are well ventilated but underperfused or, conversely, when well-perfused alveoli are ventilated with gas that contains a high fraction of CO2. Such regions eliminate less than their normal share of CO2. The fraction of each tidal breath not involved in CO2 exchange (VD/VT), called the physiologic dead space fraction, can be estimated as follows:



(PECO2 = mixed expired concentration of CO2.) An alternative equation shows how an elevation in dead space contributes to hypercapnia; CO2, E, and VT are assumed to be constant.



Etiology Respiratory failure (resulting in hypoxemia and/or hypercapnia) may be caused by airway obstruction; dysfunction of lung parenchyma but not of the airways; and ventilatory pump failure.

For effective ventilation, negative pleural pressure must be generated by the respiratory muscles acting in a coordinated fashion on an intact rib cage. Ventilatory pump failure may be caused by primary dysfunction of the CNS respiratory centers, dysfunction of the ventilatory neuromuscular apparatus, or structural abnormalities of the chest wall that prevent effective transmission of respiratory muscle forces. The airways and lung parenchyma may be anatomically normal. For example, disorders (eg, flail chest, kyphoscoliosis) that alter the structure of the chest wall can cause inefficient coupling of muscle contraction and pleural pressure generation. Hypoventilation can also occur when the inspiratory muscles of the diaphragm and rib cage contract asynchronously (eg, during diaphragmatic paralysis, quadriplegia, or acute stroke).

Often, the primary reason for pump dysfunction is reduced muscular power. The endurance of muscle fibers is determined by the balance of nutritional supply and demand. Therefore, respiratory muscles deprived of nutrients because of hypotension or hypoxemia perform inefficiently and become fatigued.

Acute hyperinflation severely reduces the efficiency of the ventilatory pump even when the strength of individual muscle fibers remains normal. Not only are the inspiratory muscle fibers foreshortened so that they produce less force, but also the work that the muscles must do is increased because of residual end-expiratory alveolar recoil tension and reduced compliance of the lung's connective tissue at high lung volumes. Furthermore, altered geometry (eg, flattened diaphragm, expanded rib cage) limits the pleural pressure change that can be generated during forceful contraction. During positive pressure ventilation, acute hyperinflation is associated with a positive end-expiratory difference between alveolar and central airway pressures (auto-PEEP).