Hypoventilation Syndromes

Joyce M. Black

LEARNING OBJECTIVES

On completion of this chapter, the reader will be able to:

1. Discuss the physiology of normal ventilation and respiration.
2. Describe sleep-disordered breathing identified during sleep studies.
3. Define hypoventilation and the associated pathophysiology.
4. Discuss the clinical significance of hypoventilation.
5. Describe how hypoventilation is identified during a sleep study.

a. Explain the difference between hypopneas and hypoventilation.

b. Review the process for a diagnostic study for patients with hypoventilation.
6. Review treatments for hypoventilation.

INTRODUCTION

Hypoventilation is an impairment of the body’s ability to breathe. Chronic hypoventilation may be the result of disorders that affect any part of the respiratory system. It may be caused by congenital disorders, brainstem disorders, neurologic disorders associated with signal communication from the brain through the spinal column, or neuromuscular disorders that compromise the signals in the nerves or muscles (1).

Before delving more deeply into hypoventilation, let’s first discuss normal breathing and how the respiratory and circulatory systems work to deliver oxygen (O₂) to the cells of the body, and the other sleep-disordered breathing (SDB) events seen in the sleep laboratory during polysomnography (PSG).

PHYSIOLOGY OF NORMAL VENTILATION AND RESPIRATION

Ventilation or breathing is the process of moving air in and out of the lungs. Inhalation brings needed O₂ to the lungs and exhalation removes carbon dioxide (CO₂), the waste by-product of cell metabolism.

Inhalation is initiated when the brain signals the diaphragm (the major muscle of ventilation) to contract, making the thoracic cavity to expand. The expansion creates a pressure drop in the chest. It is a pressure gradient between the atmosphere and the chest that causes the air to pass through the nasal cavity, upper airway, bronchi and bronchioles, and ultimately to the alveoli. The alveoli are small sacks in the lungs that are surrounded by capillaries where respiration or gas exchange takes place (exchange of O₂ with CO₂).

The right side of the heart pumps blood to the lung’s capillary bed where O₂ molecules, brought to the alveoli by the inhalation process, pass through the alveolar membrane and the capillary walls into the blood. Conversely, CO₂ passes through the capillary wall and the alveolar membrane into the alveoli where it is eliminated by exhalation. It is the concentration gradient between the gases in the alveoli and the capillaries that allow this gas exchange to take place through simple diffusion. Once the blood in the capillary bed surrounding the alveoli has less CO₂ and more O₂, the oxygenated blood is then pumped by the right side of the heart to the left side of the heart. The heart’s left ventricle then pumps the oxygenated blood, through the arteries, to all the cells in the body.

The body’s motivation to breathe (contract the diaphragm) is created by the amount of CO₂ in the blood. The CO₂ molecules, pumped to the brain by the heart, pass through capillaries into the spinal fluid that bathes the brain. Through a chemical process, the CO₂ molecule is turned to hydrogen ion and water. It is the hydrogen molecule that changes the spinal fluid pH, making it more acidic. The change in spinal fluid pH is detected
in the hindbrain by the medulla oblongata and pons, which, in turn, signal the diaphragm to contract. CO₂ levels in the blood are the primary driver to breathe. This is the normal breathing process and how every cell in the body receives O₂ and maintains life (2).

Now let’s discuss what occurs during sleep that may compromise or impair this process.

KEY TAKEAWAY: Physiology of Normal Breathing

Normal breathing: CO₂ levels in the blood provide the primary drive to breathe. As CO₂ levels increase, the spinal fluid becomes more acidic and triggers the brain to send a signal to the diaphragm to contract and start the breathing process.
Air is inhaled into the body when the diaphragm contracts, creating negative pressure in the lungs. A pressure gradient causes air to pass through the respiratory system into the alveoli.
Gas exchange takes place between the alveoli and the blood in the capillary beds surrounding the alveoli—CO₂ is exchanged for O_2.
The heart pumps the blood through the arteries to the entire body exchanging the O₂ for CO₂ (a by-product of cell metabolism) to keep cells alive.
The veins carry the CO₂ from the cells back to the right side of the heart and into the lungs to exchange the CO₂ for O₂ and start the breathing process again.

Table 14-1 Description of Sleep-Disordered Breathing Categories Seen during Polysomnography

SDB Categories	Airflow	Effort	Description
Obstructive sleep apnea (OSA)/hypopnea	No airflow or reduced airflow	Effort is noted	Airway blocked, can’t get air into the lungs
Central sleep apnea (CSA)/hypopnea	No airflow or reduced airflow	No effort or reduced effort	Compromised drive to breathe
Mixed apnea	No airflow	No effort at beginning of event noted before airway opens	Starts with no drive to breathe, then airway is blocked
Cheyne-Stokes respirations (CSR)	Waxing and waning noted in the airflow channel	Waxing and waning noted in the effort channels	Drive to breathe is compromised—breathing cycles exhibit waxing and waning lasting 30 s-2 min duration
Complex sleep apnea	No airflow—central apneas appear with CPAP changes	No effort—as CPAP is increased, the obstructive apneas change to central apneas	Closure of airway is present, but the drive to breathe is compromised by the administration of CPAP, causing changes in CO₂ and decreased drive to breathe.
Hypoventilation	Airflow reduced for long periods of time—AASM rules state at least 10 min	Equal reduction in effort noted	Drive to breathe is compromised.
AASM, American Academy of Sleep Medicine; CPAP, continuous positive airway pressure; SDB, sleep-disordered breathing.

SLEEP-DISORDERED BREATHING

A PSG monitors how well a person sleeps and how well the body functions while he or she is asleep. A PSG records the patient’s brain activity using a modified electroencephalogram (EEG), eye movement using electrooculogram (EOG), muscle tone using electromyogram (EMG), and the heart and heart rate via a modified electrocardiogram (ECG). SDB is identified by monitoring airflow, respiratory effort, oxygen saturation, and, if possible, CO₂ levels in the blood (3).

SDB disrupts the normal breathing process during sleep. This may be caused by air not getting into the lungs because of airway obstructions, the drive to breathe being affected due to the diaphragm not receiving the signal to contract or it cannot contract, or a combination of both.

Table 14-1 summarizes the categories of SDB and how they are monitored, and includes short descriptions (4).

The treatment for SDB caused by airway blockage is continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BPAP) if CPAP is not tolerated, applied to the airway via a mask to keep the airway open. The treatment for a patient who has diminished drive to breathe or no drive to breathe is usually a BPAP device that includes a spontaneous/timed backup mode (BPAP S/T) or more sophisticated noninvasive ventilation (NIV) if needed (5).

Cheyne-Stokes Respirations (CSR) are characterized by the appearance of a crescendo-decrescendo (waxing and waning) of the breathing pattern caused by changes in the partial pressures of oxygen and carbon dioxide. CSR may be caused by cardiac failure, renal failure, narcotic poisoning, and raised intracranial pressures. CSR displays periods of increased tidal volumes and respiratory rate (blowing off CO₂) caused by increases in CO₂ and a decrease in volume and rate often resulting in central apnea caused by decreases in CO₂.

Treating CSR and complex sleep apnea with conventional BPAP S/T may overventilate the patient and knock out the drive to breathe even more. Servo-ventilation is the treatment of choice for these patients. By identifying the patient’s peak flow or minute ventilation and applying supplemental pressure support, the patient gets only the flow that he or she needs without overventilation (8).

KEY TAKEAWAY: Sleep-Disordered Breathing

PSG monitors and records how well the body is working during rest and while asleep.
SDB is identified during a PSG using airflow, effort, oximetry, and, in some cases, CO₂ monitors.
The most common SDB identified during PSG is obstructive sleep apnea (OSA), which does not let air enter the lungs. The treatment of choice for OSA is CPAP therapy.
Other types of SDB may be secondary to a diminished or absent drive to breathe. This can be caused by compromises in the signal to breathe: the brain not identifying the need to breathe, the signal being interrupted and not reaching the lungs, or the muscles not responding to the signal. The most common therapy is some form of BPAP or, if necessary, NIV.

HYPOVENTILATION AND ASSOCIATED PATHOPHYSIOLOGY

Hypoventilation is a state in which there is a reduced amount of air entering the alveoli that causes an increase in CO₂ levels in the blood. The primary function of the lungs is to inhale O₂ and exhale CO₂. When we discuss the needed amount of air that a person breathes, we often refer to it in terms of tidal volume (Vt) or minute ventilation (MV). The Vt is the amount of air inhaled or exhaled during a normal breathing cycle. In a normal young adult, it is approximately 500 mL per inspiration or 7 mL per kg of body mass. The MV is found by multiplying the Vt by the respiratory rate (Fig. 14-1).

Some normal variables influence our Vt and therefore our MV—issues such as stress, exercise, and sympathetic nervous system activation (fight or flight). These can cause Vt and respiratory rates to increase. Conversely, when we relax by reading a book or watching TV, our Vt and respiratory rate may decrease and still be able to maintain adequate oxygenation for the body.

Another variable is the normal increase in CO₂ retention that occurs when we transition from wakefulness to sleep. There is an additional increase in CO₂ retention when we transition from nonrapid eye movement to rapid eye movement (REM) sleep. All of these are normal occurrences that elicit a decrease or increase in Vt, and all are done without conscious effort (1).

The body uses the Vt to adequately oxygenate and eliminate CO₂. In normal adults, it is not unusual for the CO₂ level to increase by 7 mm Hg from wake to sleep and to fluctuate by 10 mm Hg throughout the sleep stages. These variables should still be no higher than 50 mm Hg. This normal variability is maintained by the body taking deeper or shallower breaths as well as increasing or decreasing the respiratory rate. In addition, diminished muscle tone develops during REM sleep, which may further exacerbate hypoventilation secondary to reduced respiratory effort.

Now let’s discuss what happens when the body can’t maintain adequate ventilation. A very short and concise definition of hypoventilation is an increase in CO₂ and decrease in O₂. Hypoventilation is a complicated breathing pattern caused by breathing that is too shallow, too slow, or has diminished lung function.

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