Respiratory complications of obesity

Obesity has significant effects upon the pulmonary mechanics. BMI has

a direct relationship with the degree of airways resistance and

work of breathing, and is inversely correlated with thoracic lung

volumes.

Specifically, the reductions in functional residual capacity (FRC)

and expiratory reserve volume are associated with early airway

closure and resultant gas trapping, causing ventilation-perfusion mismatching and subsequent

hypoxia.

Obesity also imposes a restrictive defect due to the mass loading on the chest wall, with resultant reduction in chest wall compliance. Studies in

anaesthetised obese patients have demonstrated a direct relationship between the degree of obesity and

static lung compliance because of the reduction in FRC. Finally, breathing at low lung volumes causes expiratory

flow limitation due to early airway closure with the generation of intrinsic positive end-expiratory pressure,

again resulting in an increased work of breathing .

All these changes are further exaggerated during sleep due to

the negative impact on the pulmonary mechanics of obese

patients adopting the supine position.

Pulmonary complications of obesity present significant risks to the critically ill individual. Duration

of mechanical ventilation and weaning times were found to be

significantly longer for these patients, as well as oxygen

requirements during hospitalization.

Deposition of adipose tissue in the abdomen, on the diaphragm, and in

intercostal muscles impairs respiratory system function and decreases lung

expansion. These alterations, along with the increased weight of excess adipose

tissue on the chest wall, lead to decreased functional residual capacity,

expiratory reserve volume, forced expiratory reserve volume, and minute

ventilation.

Vital capacity and total lung volume generally remain in the normal range

but may be reduced by ≥ 30% in a severely obese individual .

Multiple factors such as abnormal chest wall resistance, abnormal

diaphragmatic position, increased airway resistance, and/or the need to eliminate higher daily levels of carbon

dioxide contribute to an increased .breathing effort

Because of alveolar collapse and airway closure at the lung bases, obese individuals have widened

alveolar-arterial oxygen gradients and ventilation-perfusion

mismatching .

Arterial hypoxemia associated with the ventilation-perfusion

abnormality puts the obese individual at increased risk

for .sudden death

Obese individuals are also at increased risk of developing OSAS and/or OHS. These syndromes lead to chronic hypoxia, hypercapnia, and sleep

fragmentation, which ultimately results in hypoventilation, episodic hypoapnea, apnea, and arousal from sleep. These problems, when combined with the increased work of breathing in inefficient and

fatigued respiratory muscles, hamper the ability of the severely obese individual to recover from periods of apnea due to hyperventilation, which leads to worsening arterial blood gas abnormalities. A vicious cycle develops wherein chronic hypoxemia and hypercarbia further

exacerbate the condition

Clinically, these individuals exhibit daytime sleepiness, fatigue, irritability,

and personality changes associated with the chronic sleep deprivation and

nocturnal oxyhemoglobin desaturation, which puts them at

increased risk for arrhythmias, including tachy-brady syndrome, atrial fibrillation, sinus arrest, and second-

degree heart blocks

Gastroesophageal reflux disease is also common in the obese individual,which occurs because obese individuals have higher

volumes of gastric fluid and increased intraabdominal pressures, which predispose them to an increased incidence of aspiration.

The incidence of developing postoperative pulmonary complications is double that of nonobese individuals.In addition,

thoracic and upper abdominal incisions may exacerbate pulmonary dysfunction

Alterations in the hematologic system, immobility, and venous stasis place the critically ill obese patient at increased risk of thrombus

formation. Because increased adipose tissue may mask swelling in the patient who develops deep vein thrombosis, routine assessment of

circulation and pain or warmth in the extremities is essential .

Obesity also impacts assessment of the pulmonary system, which

includes the ability to auscultate breath sounds, monitor oxygen status with pulse oximetry, and

assess respiratory rate and character.

As with heart sounds, auscultating breath sounds may be impaired by excess adipose

tissue.

Continuous monitoring of arterial oxygen saturation with pulse oximetry may be negatively effected if adipose tissue prevents adequate penetration

of light. Poor tissue perfusion and poor probe placement may exacerbate

the problem; therefore, specially adapted probes should be used at

alternate placement sites, such as the nose or earlobe.

Sleep-disordered breathing is common in obese patients, with

studies estimating the prevalence of OSA as 2–24% of the population

OSA is defined as recurrent partial or complete upper airway obstruction during sleep .

The diagnostic gold-standard for sleep-disordered breathing is nocturnal multichannel

respiratory polysomnography .