The Pathophysiology of Respiratory Failure: Control of Breathing, Respiratory Load, and Muscle Capacity

Abstract

The purpose of this review is to provide an overview on how interactions between control of breathing, respiratory load, and muscle function may lead to respiratory failure. The mechanisms involved vary according to the underlying pathology, but respiratory failure is most often the result of an imbalance between the muscular pump and the mechanical load placed upon it. Changes in respiratory drive and response to CO₂ seem to be important contributors to the pathophysiology of respiratory failure. Inspiratory muscle dysfunction is also frequent but is not a mandatory prerequisite to respiratory failure since increased load may also be sufficient to precipitate it. It is crucial to recognize these interactions to be able to timeously establish patients on mechanical ventilation and adapt the ventilator settings to their respiratory system physiology.

Long-Term Mechanical Ventilation: Recommendations of the Swiss Society of Pulmonology

“…Indications for long-term NIV, which have evolved over the past 30 years, are summarized in Figure 1 and Table 1 [16]. The obesity-hypoventilation syndrome (OHS), chronic obstructive pulmonary diseases (COPD; including overlap syndrome), and neuromuscular and chest wall diseases (CWD) are presently the most frequent indications for HMV.…”

Hypoxemia in COVID‐19; Comment on: “The neuroinvasive potential of SARS‐CoV2 may play a role in the respiratory failure of COVID‐19 patients”

“…Dyspnea is the subjective experience of breathing discomfort. It results from complex mechanisms, especially from a mismatch between efferent motor commands from the central nervous system (CNS) to the respiratory system, and afferent sensory informations (eg, expected airflow, cage movements) from the respiratory system to the CNS 6 . The insular cortex is essential for conscious experience of visceral perceptions elicited by interoceptive stimuli 7 .…”

“…Isolated brainstem involvement as the sole and unique center involved in COVID‐19 respiratory failure seems unconvincing. Brainstem mechanisms (necessary and sufficient to produce ventilator command and adapt it to the needs of the body) seem unaffected, as suggested by a normal to low pCO2 levels even in critically ill patients 6,14 . Nevertheless, since brainstem conveys information to higher CNS structures involved in breathing control, its dysfunction can affect this integrated system and contribute to the respiratory symptoms (or their absence) of COVID‐19 patients.…”

Oxygen Therapy: Systems and Indications in the Pediatric and Adult Population

“…These are based on the increase in heart rate and cardiac output, thus improving the V/Q ratio through an improved blood flow through pulmonary vasculature [18]. On the other hand, an increase in the renal secretion of erythropoietin causes polycythemia that increases the oxygen-carrying capacity of the blood [19]. However, these mechanisms are harmful in the medium-long term, since pulmonary vasoconstriction generates irreversible anatomical alterations such as hypertrophy of the middle muscular layer of the pulmonary arterioles and fibrosis of the intima, which leads to pulmonary hypertension and right heart failure [20].…”