Respiratory muscle fatigue: A cause of ventilatory failure in septic shock
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62 ABSTRACTS luted (P < .001) with PEmax (r- .73) and DLI (r- .64). The slope of the Pimax-DL! relationship was essentially the same in both groups of patients with COPD as it was in the normal subjects. However, at any value of DLI, Pimax was in the normal range in patients with normal PEmax, but signifi- cantly lower in patients with low PEmax (P<.001). Expressing Pimax as a combined function of PEmax and DLI yielded the highest correlation (r = .84, P < .001), with PEmax explaining 46% and DL! explaining 35% of the variance in Pimax not explained by the other variable alone (P < .001). The PaCe2 was elevated in 13 of 18 patients whose Pimax was < 55 cm tt:(3, and inversely correlated with Pimax (r = .66, P < .005). We conclude that inspiratory muscle weakness in COPD results from mechanical disad- vantage, is frequently aggravated by generalized muscle weakness, and contributes to hypercapnia. Respiratory Muscle Fatigue: A Cause of Ventilatory Failure in Septic Shock. itussain SNA. Simkus G. and Roussos C. J Appl Physiol 58:6;2033, 1985. The effect of endotoxic shock on the respiratory muscle performance was studied in spontaneously breathing dogs given Lh'cherichia coil endotoxin (Difco Laboratories, l0 mg/kg). Diaphragmatic (Edi) and parastcrnal intercostal (Eic) electromyograms were recorded using fishhook elec- trodes. The recorded signals were then rectified and electri- cally integrated. Pleural, abdominal, and transdiaphragmatic (Pdi) pressures were recorded by a balloon-catheter system, After a short control period, the cndotoxin was administered slowly intravenously (within five minutes). Death was secon- dary to respiratory arrest in all animals. All animals died within 150 to 270 minutes after onset of endotoxic shock. Within 45 to 80 minutes of the endotoxin administration, mean bh×~d pressure and cardiac output dropped to 42.1 ± 4.1% and 40.1 ± 6.0% (mean ± SE) of control values, respectively, with little change afterward. Mean inspiratory flow rate and Pdi increased front control values of 0.27 ± 0.03 I - st and 5.75 ± 0.7 cm H20 to mean values of 0.44 ± 0.03 1 • s- i and 8.70 ~_ 1.05 cm !120 and then decreased to 0.17 ± 0.03 I • s "1 and 3.90 ± 0.30 cm !-120 before the death of the animals, There were no major changes in the mechanics of the respiratory system. Edi and Eic increased progressively to mean values of 350 ± 21'?,, and 263 ± 22% of control, respectively, before the death of the animals. None of the dogs was hypoxic. Arterial PCO2 decreased from a control value of 42.9 ± 1.7 Torr to a mean value of 29.9 _+ 2.8 Torr and then increased to 51 _* 4.3 Torr before the death of the anhnals. We conclude that the vcntilatory failure of E. Coil endotoxic shock was due to fatigue of the respiratory mus- cles. Diagnostic Efficacy of Impedance Plethysmography for Clin- ically Suspected Deep-Vein Thrombosis: A Randomized Trial. Hull RD. Hirsh J. Carter CJ, el el. Ann Intern Med 102:21, 1985, Impedance plethysmography is an accurate noninvasive method to test for proximal vein thrombosis, but it is insensi- tive to calf-vein thrombi. We randomly assigned patients on referral with clinically suspected deep-vein thrombosis and normal impedance plethysmographic findings to either serial impedance plethysmography alone or combined impcdancc plethysmograhy and leg scanning (which has been shown to be essentially as sensitive as venography) and compared the long-term outcomes. During the initial surveillance, deep- vein thrombosis was detected in 6 of 311 patients (1.9%) tested by serial impedance plethysmography alone and in 30 of 323 patients (9.3%) (most with calf-vein thrombi) tested by the combined approach (P< .001). During long-term f:fllow-up, no patient died from pulmonary embolism, but six patients (1.9%; 95% confidence limits, 0.7% to 4.2%) tested by serial impedance plethysmography developed deep-vein compared with seven patients (2.2%: 95% confidence limits, 0.9% to 4.4%) tested by combined approach. Serial imped- ance plethysmography used alone is an effective strategy to evaluate such symptomatic patients. Determinants of Hypoxemia During the Acute Phase of Pulmonary Embolism in Humans. Manier G, Castait;g }: and Guenard it. Am Rev Respir Dis 132:332, 1985. The determinants of hypoxemia were studied in ten patients with acute pulmonary embolism demonstrated by pulmonary angiography. Two patients were mechanically ventilated, and in the eight who breathed room air sponta- neously, the mean arterial PO~ was 61.5 mm Hg. Measure- ments of the distributions of ventilation (VA) and perfusion (Q) against VA/Q ratios by the multiple inert gas infusion technique demonstrated an increase in VA/Q inequality. The major part of pulmonary blood ftow was distributed in a mode near to, or slightly above, a VA/Q ratio of I. The cumulative fraction of blood in true shunt and low VA/Q mode (VA/ Q < .01) was 9.1%. For a small part ofthe AaDO2 (13%),an oxygen diffusional component was found. The remaining hypoxemia was due to the fall in the mixed venous PO 2 (PVOz), irrespective of its cause: low cardiac output, low hemoglobin concentration, high oxygen consumption, low P~o. The fall in PVO2 led to a fall in endeapillary blood PO2 in both shunt or ventilated and perfused units. We conclude that the major determinant of hypoxemia in these patients suffer- ing from acute pulmonary embolism is the fall in PVOv This is enhanced by a moderate increase in the fraction of blood flowing through low VA/Q units. Diffusion impairment plays only a minor role. Transpulmonary Passage of Venous Air Emboli. Butler BD and Itills BA. J Appl Physiol 59:2;543.1985. Twenty-seven paralyzed ano,~hctizcd dogs were embolized with venous air to determine the effectiveness of the pulmo- nary vasculature for bubble filtration or trapping. Air doses ranged from 0.05 to 0.40 mL • kg -~ • min -~ in 0.05-mL increments with ultrasonic Doppler monitors placed over arterial vessels to detect an), microbubbl,-.s that crossed the lungs. Pulmonary vascular filtration of the venous air infu- sions was complete for the lower air doses ranging from 0.05 to 0.30 mL • kd- ~ • min - t. When the air doses were increased to 0.35 mL • kg -t • rain -t. the filtration threshold was exceeded with arterial spillover of bubbles occurring in 50% of the animals and reaching 71% for 0.40 mL • kg -t. Significant elevations were observed in pulmonary arterial pressure and pulmonary vascular resistance. Systemic blood pressure and cardiac output decreased, whereas left ventricu-
Transcript of Respiratory muscle fatigue: A cause of ventilatory failure in septic shock
62 ABSTRACTS
luted (P < .001) with PEmax ( r - .73) and DLI ( r - .64). The slope of the Pimax-DL! relationship was essentially the same in both groups of patients with COPD as it was in the normal subjects. However, at any value of DLI, Pimax was in the normal range in patients with normal PEmax, but signifi- cantly lower in patients with low PEmax ( P < . 0 0 1 ) . Expressing Pimax as a combined function of PEmax and DLI yielded the highest correlation (r = .84, P < .001), with PEmax explaining 46% and DL! explaining 35% of the variance in Pimax not explained by the other variable alone (P < .001). The PaCe2 was elevated in 13 of 18 patients whose Pimax was < 55 cm tt:(3, and inversely correlated with Pimax (r = .66, P < .005). We conclude that inspiratory muscle weakness in COPD results from mechanical disad- vantage, is frequently aggravated by generalized muscle weakness, and contributes to hypercapnia.
Respiratory Muscle Fatigue: A Cause of Ventilatory Failure in Septic Shock. itussain SNA. Simkus G. and Roussos C. J Appl Physiol 58:6;2033, 1985.
The effect of endotoxic shock on the respiratory muscle performance was studied in spontaneously breathing dogs given Lh'cherichia coil endotoxin (Difco Laboratories, l0 mg/kg). Diaphragmatic (Edi) and parastcrnal intercostal (Eic) electromyograms were recorded using fishhook elec- trodes. The recorded signals were then rectified and electri- cally integrated. Pleural, abdominal, and transdiaphragmatic (Pdi) pressures were recorded by a balloon-catheter system, After a short control period, the cndotoxin was administered slowly intravenously (within five minutes). Death was secon- dary to respiratory arrest in all animals. All animals died within 150 to 270 minutes after onset of endotoxic shock. Within 45 to 80 minutes of the endotoxin administration, mean bh×~d pressure and cardiac output dropped to 42.1 ± 4.1% and 40.1 ± 6.0% (mean ± SE) of control values, respectively, with little change afterward. Mean inspiratory flow rate and Pdi increased front control values of 0.27 ± 0.03 I - s t and 5.75 ± 0.7 cm H20 to mean values of 0.44 ± 0.03 1 • s- i and 8.70 ~_ 1.05 cm !120 and then decreased to 0.17 ± 0.03 I • s "1 and 3.90 ± 0.30 cm !-120 before the death of the animals, There were no major changes in the mechanics of the respiratory system. Edi and Eic increased progressively to mean values of 350 ± 21'?,, and 263 ± 22% of control, respectively, before the death of the animals. None of the dogs was hypoxic. Arterial PCO2 decreased from a control value of 42.9 ± 1.7 Torr to a mean value of 29.9 _+ 2.8 Torr and then increased to 51 _* 4.3 Torr before the death of the anhnals. We conclude that the vcntilatory failure of E. Coil endotoxic shock was due to fatigue of the respiratory mus- cles.
Diagnostic Efficacy of Impedance Plethysmography for Clin- ically Suspected Deep-Vein Thrombosis: A Randomized Trial. Hull RD. Hirsh J. Carter CJ, el el. Ann Intern Med 102:21, 1985,
Impedance plethysmography is an accurate noninvasive method to test for proximal vein thrombosis, but it is insensi- tive to calf-vein thrombi. We randomly assigned patients on referral with clinically suspected deep-vein thrombosis and normal impedance plethysmographic findings to either serial
impedance plethysmography alone or combined impcdancc plethysmograhy and leg scanning (which has been shown to be essentially as sensitive as venography) and compared the long-term outcomes. During the initial surveillance, deep- vein thrombosis was detected in 6 of 311 patients (1.9%) tested by serial impedance plethysmography alone and in 30 of 323 patients (9.3%) (most with calf-vein thrombi) tested by the combined approach ( P < .001). During long-term f:fllow-up, no patient died from pulmonary embolism, but six patients (1.9%; 95% confidence limits, 0.7% to 4.2%) tested by serial impedance plethysmography developed deep-vein compared with seven patients (2.2%: 95% confidence limits, 0.9% to 4.4%) tested by combined approach. Serial imped- ance plethysmography used alone is an effective strategy to evaluate such symptomatic patients.
Determinants of Hypoxemia During the Acute Phase of Pulmonary Embolism in Humans. Manier G, Castait;g } : and Guenard it. Am Rev Respir Dis 132:332, 1985.
The determinants of hypoxemia were studied in ten patients with acute pulmonary embolism demonstrated by pulmonary angiography. Two patients were mechanically ventilated, and in the eight who breathed room air sponta- neously, the mean arterial PO~ was 61.5 mm Hg. Measure- ments of the distributions of ventilation (VA) and perfusion (Q) against VA/Q ratios by the multiple inert gas infusion technique demonstrated an increase in V A / Q inequality. The major part of pulmonary blood ftow was distributed in a mode near to, or slightly above, a VA/Q ratio of I. The cumulative fraction of blood in true shunt and low V A / Q mode ( V A / Q < .01) was 9.1%. For a small part ofthe AaDO2 (13%),an oxygen diffusional component was found. The remaining hypoxemia was due to the fall in the mixed venous PO 2 (PVOz), irrespective of its cause: low cardiac output, low hemoglobin concentration, high oxygen consumption, low P~o. The fall in PVO2 led to a fall in endeapillary blood PO2 in both shunt or ventilated and perfused units. We conclude that the major determinant of hypoxemia in these patients suffer- ing from acute pulmonary embolism is the fall in PVOv This is enhanced by a moderate increase in the fraction of blood flowing through low VA/Q units. Diffusion impairment plays only a minor role.
Transpulmonary Passage of Venous Air Emboli. Butler BD and Itills BA. J Appl Physiol 59:2;543.1985.
Twenty-seven paralyzed ano,~hctizcd dogs were embolized with venous air to determine the effectiveness of the pulmo- nary vasculature for bubble filtration or trapping. Air doses ranged from 0.05 to 0.40 mL • kg -~ • min -~ in 0.05-mL increments with ultrasonic Doppler monitors placed over arterial vessels to detect an), microbubbl,-.s that crossed the lungs. Pulmonary vascular filtration of the venous air infu- sions was complete for the lower air doses ranging from 0.05 to 0.30 mL • kd- ~ • min - t. When the air doses were increased to 0.35 mL • kg -t • rain -t. the filtration threshold was exceeded with arterial spillover of bubbles occurring in 50% of the animals and reaching 71% for 0.40 mL • kg -t. Significant elevations were observed in pulmonary arterial pressure and pulmonary vascular resistance. Systemic blood pressure and cardiac output decreased, whereas left ventricu-
