Abnormal Breathing Patterns
Absence of breathing. (Ap-knee-a)
Normal breathing (Eup-knee-a)
Only able to breathe comfortable in upright position (such as sitting in chair), unable to breath laying down, (Or-thop-knee-a)
Subjective sensation related by patient as to breathing difficulty
Paroxysmal nocturnal dyspnea - attacks of severe shortness of breath that wakes a person from sleep, such that they have to sit up to catch their breath - common in patient's with congestive heart failure.
Figure 2-38 Hyperpnea: Increased depth of breathing (Hi-perp-knee-a)
Increased volume with or without and increased frequency (RR), normal blood gases present.
Figure 2-39 Hyperventilation. Increased rate (A) or depth (B), or combination of both.
"Over" ventilation - ventilation in excess of the body's need for CO2 elimination. Results in a decreased PaCO2, and a respiratory alkalosis.
Hypoventilation. Decreased rate (A) or depth (B), or some combination of both.
"Under" ventilation - ventilation that is less than needed for CO2 elimination, and inadequate to maintain normal PaCO2. Results in respiratory acidosis.
Can be a slow rate with normal tidal volumes such that the total minute ventilation is inadequate.
Can be a normal rate but with such low tidal volumes that air exchange is only in the dead space and not effective.
Increased frequency without blood gas abnormality
Kussmaul's respiration. Increased rate and depth of breathing over a prolonged period of time. In response to metabolic acidosis, the body's attempt to blow off CO2 to buffer a fixed acid such as ketones. Ketoacidosis is seen in diabetics.
Cheyne-Stokes respirations (CSR)
Gradual increase in volume and frequency, followed by a gradual decrease in volume and frequency, with apnea periods of 10 - 30 seconds between cycle. Described as a crescendo - decrescendo pattern. Characterized by cyclic waxing and waning ventilation with apnea gradually giving way to hyperpneic breathing.
Seen with low cardiac output states (CHF) with compromised cerebral perfusion
Creates lag of CSF CO2 behind arterial PaCO2 and results in characteristic cycle. Delayed sensitivity to CO2 changes- during apnea the CO2 increase above the threshold for stimulus but the brain is slow to respond, then it over shoots by hyperventilating and the signal to reduce ventilation is slow to be recognized.
Similar to CSR but VT is constant except during apneic periods. Short episodes of rapid, deep inspirations followed by 10 - 30 second apneic period.
Seen with patients with elevated ICP as seen in meningitis
Apneustic breathing (previously described)
Indicates damage to pons
Central neurogenic hyperventilation
May be caused by head trauma, severe brain hypoxia, or lack of cerebral perfusion
Mid brain and upper pons damage
Central neurogenic hypoventilation
Medulla respiratory centers are not responding to appropriate stimuli.
Associated with head trauma, cerebral hypoxia, and narcotic suppression
CO2 and Cerebral Blood Flow (CBF)
CO2 plays an important role in autoregulation of CBF mediated through its formation of H+.
Increased CO2 dilates cerebral vessels and vice versa.
In traumatic brain injury (TBI), the brain swells acutely. Head is a fixed volume container - cannot expand. When bleeding or swelling occurs in the brain pressures rapidly increase. Raising ICPs exceed cerebral arterial pressure and brain perfusion stops.
Cerebral hypoxia/ischemia - brain death
Mechanical hyperventilation can lower PaCO2, which results in vasoconstriction in cerebral vessels, reduction of swelling and ICP.
Controversial as reduces O2 and CBF to injured brain.
Only effective for the first 24 hours.
Current practice is to treat perfusion pressures pharmacologically rather then use hyperventilation.
All agree must avoid hypoventilation in TBI patients.