C. Roussos

Clinical manifestations of inspiratory muscle fatigue

Twelve patients exhibiting difficulties during discontinuation of artificial ventilation permitted us to investigate physical examination techniques used in diagnosing inspiratory muscle fatigue. Diaphragmatic and intercostal electromyographic tracings, arterial blood gases, rate and depth of ventilation, and thoracoabdominal motion were monitored during spontaneous breathing. Six patients showed electromyographic evidence of inspiratory muscle fatigue. A sequence of events leading to respiratory acidemia emerged--namely electromyographic evidence of fatigue, accompanied or followed by an increased respiratory rate, in turn followed by alternation between abdominal and rib cage breathing (respiratory alternans), paradoxical inward abdominal motion during inspiration (abdominal paradox), and finally an increase in PaCO2 associated with a fall in minute ventilation and respiratory rate, and worsening of respiratory acidemia. The abnormalities of respiratory movements may be reliable clinical signs of inspiratory muscle fatigue, particularly when accompanied by tachypnea and hypercapnia.

The effects of ischemia, lactic acid and hypertonic sodium chloride on phrenic afferent discharge during spontaneous diaphragmatic contraction

In 9 sodium pentobarbital anaesthetized cats, 50 single-unit phrenic afferent recordings were determined during spontaneous ventilation, retrograde carotid arterial injection of lactic acid (LA, 0.1 N) and NaCl (5%), and a 2-min occlusion of the superior thoracic aorta. Fifty percent of the units had tonic low-frequency spontaneous discharge; 50% had phasic high-frequency discharge. Tonic fiber activity increased significantly with LA, NaCl and occlusion, while phasic fiber activity decreased in all 3 conditions. These results suggest that the diaphragm contains sensory endings sensitive to ischemia and extracellular metabolic changes.

The failing ventilatory pump

Respiratory failure may be categorized into non-hypercapnic and hypercapnic (venti lator) . Ventilatory failure is due to failure o f the thorax i, (ventilatory pump) to generate the pressure required for ventilation (Schema A). This failure may be due to ei ther high opposing forces from the lung and airways (e.g. airways obstruction) or to low driving forces (weakness) as a result of a defect in the chest wall (e.g. flail chest) or a failure in the neural and /o r muscular apparatus. In this review, I will focus on situations resulting from a compromised ventilatory pump due to low driving force (weakness) of the respiratory system. This failure may stem from any

Influence of immersion to the neck in water on airway closure and distribution of perfusion in man.

We measured closing volume (CV), expiratory reserve volume (ERV) regional distribution of lung volume (Vr) and perfusion in 7 normal subjects in air and during immersion to the neck in water. In four subjects immersion resulted in a CV greater than ERV and the normal perfusion distribution became inverted. In the other subjects, ERV remained larger than CV and perfusion distribution during immersion was uniform, not inverted. In 5 subjects closing volume increased and in 3 of them, the ratio of apical/basal Vr increased significantly during immersion. One subject had nomeasurable CV and in the other it was not measured. The data suggest: (1) that when CV is greater than ERV during immersion there is an inversion of the normal perfusion distribution, caused by hypoxia and/or an increase in mean alveolar pressure in the alveoli beyond the closed airways, and (2) that an increase in pleural pressure gradient during immersion may contribute to the increase in C.V.

Effects of neostigmine and salbutamol on diaphragmatic fatigue

We studied the effects of neostigmine and salbutamol on the force generated by the fatigued diaphragm in anesthetized dogs. Mechanically ventilated animals were prepared with an open thorax. A thin-walled latex balloon was positioned beneath the diaphragm to measure transdiaphragmatic pressure (Pdi) and a rigid cast was fixed around the abdomen to limit changes in diaphragmatic length and geometry during contractions. Pdi was the index of force generated by the diaphragm. We measured Pdi during supramaximal phrenic stimulation at different frequencies and during spontaneous inspiratory efforts. The diaphragm was fatigued by repeated phrenic stimulation. Fatigue significantly reduced Pdi at all frequencies of stimulation and during spontaneous contractions (P less than 0.05). The reduction in Pdi was associated with a decrease in peak twitch tension (PTT) to 50% of control (P less than 0.05). Infusion of neostigmine restored PTT to values equivalent with or greater than control (P less than 0.05) and improved Pdi at low stimulation frequencies (P less than 0.05) and during spontaneous inspiratory efforts (P less than 0.05). Infusion of salbutamol had no effect on PTT, but did significantly shortened twitch half relaxation time (P less than 0.05). Salbutamol also had no effect on Pdi during stimulated and spontaneous contractions. We conclude that neostigmine improves force generated by the fatigued diaphragm by increasing twitch amplitude while salbutamol did not have a positive inotropic effect.

The geometry of the microvascular bed of the diaphragm: Comparison to intercostals and triceps

The diaphragm may differ from other skeletal muscles in certain blood flow characteristics. We attempted to determine if this could be accounted for by structural differences in the microvasculature. We compared coded specimens of the diaphragm to the intercostals and triceps in rats by a cast corrosion, scanning electron microscopic study. For the comparison we first quantitatively described the vasculature by measuring the angles, distances, and diameters. We also tabulated subjective, descriptive, recurring patterns. We then performed frequency analysis by vessel diameter, correlation, and factor analysis to obtain the description. Arteries and veins of greater than 50 microns diameter have structural characteristics of a conducting system, namely, infrequent, single branching at obtuse angles whereas the vessels from about 15 to 50 microns in diameter have greater branching and frequently splay into many smaller streams. The capillaries form arcades and dichotomize with Y- and psi-shaped branches. The best predictor of branching (distance, angle, and pattern) is the trunk diameter. Individual and combinations of measurements and patterns comparing the diaphragm to the triceps and intercostals pointed out no convincing difference in these structural aspects of microvasculature of these muscles.

Maintenance of circulation without chest compression during CPR

Abstract To test the “thoracic-pump” model of CPR we tightly casted the thorax and abdomen of dogs and inflated the lungs with a specially designed ventilator to determine if we could produce blood flow without any chest compression. We observed the relationship between common carotid blood flow (CCBF) as measured by an electromagnetic flow probe, and intrathoracic abdominal pressures measured in the esophagus and abdomen as well as intravascular pressures in the thoracic and abdominal aorta and veins. We also studied the effects of changes in the frequency of ventilation, duty cycle, and blood volume on generated blood flows. Maximum mean CCBF by this method was 26.2 ± 11.1 mL/min or 1.1 ± 0.4 mL/min/kg, which was 30.1 % of control CCBF and occurred at a mean airway pressure (Paw) of 64.7 ± 20.8 mmHg. Further increases in Paw thereafter did not produce further increases in CCBF and even resulted in decreases in CCBF which suggests that either aortic collapse occurred or possibly lung inflation trapped blood in the lungs. Variations in duty cycle from 0.3 to 0.8, and frequency of ventilation from 15 to 55 breaths/min, had no significant effect. Volume infusion (500cc of 6% dextran) increased maximum CCBF to 38.6 ± 20.0 ml/min. In conclusion, changes in intrathoracic pressure alone without any chest compression can produce blood flow when the circulation is arrested.