Ventilatory limitation

Dyspnea upon exertion Exercise-induced bronchospasm Suspected arterial desaturation with exercise Evaluation of ventilatory limitations to exercise Evaluation of cardiac limitations to exercise Assessment of general fitness or conditioning Evaluation of cardiopulmonary disability Establishment of safe levels for exercise Evaluation of drug therapy... 

Alterations in cardiopulmonary exercise tests (CPET) have been noted in 28% to 47% of patients with sarcoidosis (6,63,65,66). Typical findings include ventilatory limitation or increased dead space/tidal volume ratio (Vd/Vx) or widened alveolar-arterial O2 (A-a O2) gradient with exercise (63,65). CPET may be abnormal when static PFTs are normal (63,67). Exercise-induced desaturation correlated with reductions in DLco (63,68-70), whereas lung volumes and expiratory flow rates did not (70). 

Exercise limitation and functional disability in COPD have a complex, multifactorial basis. Ventilatory limitation is caused by increased airways resistance, static and dynamic hyperinflation, increased elastic load to breathing, gas exchange disturbances, and mechanical disadvantage and/or weakness of the respiratory muscles (4-6). Car-diocirculatory disturbances (7,8), nutritional factors (9), and psychological factors, such as anxiety and fear, also contribute commonly to exercise intolerance. Skeletal muscle dysfunction is characterized by reductions in muscle mass (10,11), atrophy of type I (slow twitch, oxidative, endurance) (12,13) and type Ila (fast twitch) muscle fibers (14), altered myosin heavy chain expression (15), as well as reductions in fiber capillarization (16) and oxidative enzyme capacity (17,18). Such a dysfunction is another key factor that contributes... 

O Donnell DE. Ventilatory limitations in chronic obstructive pulmonary disease. Med Sci Sports Exerc 2001 33(suppl 7) S 647-655. 

Doxapram increases the tidal volume and respiratory rate by stimulating carotid chemoreceptors. Its use has been limited since the introduction of non-invasive ventilatory techniques for respiratory failure. 

Supporting this view is a report from the Tokyo subway terrorist incident of 1995. One hospital received two casualties who were apneic with no heartbeat. With vigorous resuscitation, cardiac activity was established in both. One resumed spontaneous respiration and walked out of the hospital several days later, and the other did not start breathing spontaneously and died days later. These anecdotes suggest that when circumstances permit, resuscitation should be attempted. In a contaminated area where resources, including personnel, are limited, the use of ventilatory support and closed chest cardiac compression must be balanced against other factors (see above), but the immediate administration of diazepam and additional atropine requires little effort and can be very rewarding in the casualty who still has apparent cardiopulmonary function. Cyanide... 

Casualties of phosgene or vesicant agents who have moderate or severe respiratory distress should be placed in the immediate group when intense ventilatory and other support are immediately available. In a BAS or other unit-level MTF, these support systems will not be available immediately and probably will not be available during the hours required to transport this casualty to a large medical facility. In general, limited assets would best be used for other casualties more likely to benefit from them. Delayed... 

Energetics of breathing is only one of many constraints that conflict with the metabolic cause of respiration. Another is the sensation of dyspnea which may be a limiting factor at high ventilatory levels [Oku et al., 1993]. A general optimization criterion may therefore include both energetic and dyspneic penalties as follows ... 

The respiratory system is responsible for generating and regulating the transpulmonary pressures needed to inflate and deflate the lung. Normal gas exchange between the lung and blood requires breathing patterns that ensure appropriate alveolar ventilation. Ventilatory disorders that alter alveolar ventilation are defined as hypoventilation or hyperventilation syndromes. Hyperventilation results in an increase in the partial pressure of arterial CO2 above normal limits and can lead to acidosis, pulmonary hypertension, congestive heart failure, headache, and disturbed sleep. Hypoventilation results in a decrease in the partial pressure of arterial CO2 below normal limits and can lead to alkalosis, syncope, epileptic attacks, reduced cardiac output, and muscle weakness. 

The measurements of rates, volumes, and capacities provided by plethys-mograph measurements have a limited ability to detect and evaluate some ventilatory disorders [16,25]. 

Several studies have shown that changes in Penh and respiratory resistance sometimes do not correlate (Adler et al. 2004 DeLorme and Moss 2002 Handle et al. 2003). Investigators have presented mathematical and theoretical arguments that the WBP waveform and parameters derived from Penh are dominated by conditioning, primarily related to ventilatory timing and unrelated to airway resistance (Lundblad et al. 2002 Mitzner and Tankersley 2003) however, it may be the nature of the restrictive changes anatomically and physiologically that limit the sensitivity and specificity of the Penh analysis. 

FIGURE 11.4 (a) Optimal waveforms for respiratory muscle driving pressure, P(t) respiratory airflow, V and respired volume, R, during normal breathing (NL) or under various types of ventilatory loads IRL and ERL, inspiratory and expiratory resistive load lEL and CEL, inspiratory and continuous elastic load, (b) Optimal waveforms for P(t) under increasing respiratory muscle fatigue (amplitude limited upper panel) and muscle weakness (rate limited lower panel). (From Poon and coworkers [1992]. With permission.)... 

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