Acute Dyspnea in Critically Ill Patient

Abstract

The respiratory system is dependent upon adequate ventilation to supply oxygen, remove carbon dioxide, and help maintain acid-base homeostasis. Ventilation responds to changes in the arterial carbon dioxide tension (PaCO2), arterial oxygen tension (PaO2), and pH and may be modified in response to a number of mechanical and irritant stimuli arising from various structures within the thoracic cage, and probably from within muscles and joints during exercise. Broadly viewed, the respiratory control mechanisms respond to input from neural and chemical receptors. Respiratory centers in the brain integrate these inputs and provide neuronal drive to the respiratory muscles, which maintain upper airway patency and drive the thoracic bellows to determine the level of ventilation. Acute hypercapnia: While acute hypercapnia typically leads to brisk increases in ventilation, dyspnea can result from hypercapnia among ventilator-dependent C1-2 quadriplegics who lack functioning respiratory muscles, and in normal subjects paralyzed with neuromuscular blocking agents.