We conclude that S delivered with an MDI and a spacer device induces significant bronchodilation in mechanically ventilated patients with COPD, the magnitude of which is not affected by at least a 50% increase in VT. These results do not support the VT manipulations when bronchodilators are administered in adequate doses during controlled mechanical ventilation.

Background: Proportional assist ventilation (PAV) has been shown to maintain better patient-ventilator synchrony than pressure support ventilation (PSV); however, its clinical advantage regarding invasive ventilation of COPD patients has not been clarified. Objectives: To compare the effect of PAV and PSV on respiratory parameters of hypercapnic COPD patients with acute respiratory failure (ARF). Methods: Nine intubated hypercapnic COPD patients were placed on the PAV or PSV mode in random sequence. For each mode, four levels (L₁–L₄) of support were applied. At each level, blood gases, flow, tidal volume (V_T), airway pressure (Paw), esophageal pressure (Pes) (n = 7), patient respiratory rate (fp), ventilator rate (fv), missing efforts (ME = fp – fv) were measured. Results: We found increases in ME with increasing levels of PSV but not with PAV. PO₂ and V_T increased whereas PCO₂ decreased significantly with increasing levels of PSV (p < 0.05). With PAV, PCO₂ decreased and V_T increased significantly only at L₄ whereas PO₂ increased from L₁ to L₄. Runaways were observed at L₃ and L₄ of PAV. The pressure-time product (PTP) was determined for effective and missing breaths. The mean total PTP per minute (of effective plus missing breaths) was 160 ± 57 cm H₂O/s·min in PSV and 194 ± 60 cm H₂O/s·min in PAV. Conclusion: We conclude that in COPD patients with hypercapnic ARF, with increasing support, PSV causes the appearance of ME whereas PAV develops runaway phenomena, due to the different patient-ventilator interaction; however, these do not limit the improvement of blood gases with the application of both methods.

Recent studies suggest that, in the presence of heart failure, the capability of skeletal muscle to utilize delivered flow may be impaired due to maldistribution of blood flow within working muscle. Similarly, this mechanism could explain the failure of drugs to improve maximal oxygen consumption (VO2max) immediately. Accordingly, we assessed muscular blood flow distribution (ml/min/g, radioactive microspheres, 15 + 5 gm) among and within working muscle, V02max, and arterial lactate in a rat preparation of myocardial infarction and heart failure (infarct size 36.0 ± 3.3% of the left ventricle, n = 9), and in sham-operated animals (n = 1 1). Data were obtained at maximal treadmill exercise during alternate infusions of milrinone and saline. Total skeletal muscle blood flow during exercise was significantly lower in the infarction group (p < .05 vs sham); reduced blood flow was primarily attributed to decreased flow to oxidative working muscle such as soleus and the red portion of gastrocnemius, whereas blood flow to glycolytic muscle portions (e.g., gastrocnemius white, vastus lateralis white) was similar in the infarction and sham-operated groups. Milrinone increased flow to the glycolytic working muscle portions in sham-operated animals (e.g., vastus lateralis white, 0.23 vs 0.29, p < .05); by contrast, blood flow to the oxidative muscle fibers was increased in the infarction group (e.g., gastrocnemius red, 1.45 vs 1.87, p < .05). Arterial lactate levels at similar workloads during exercise were higher in the infarction group (p < .05). Neither lactate nor VO2max were significantly altered with milrinone in either group. We conclude that (1) skeletal muscle underperfusion in heart failure emerges predominantly in oxidative working muscle and therefore early recruitment of glycolytic fibers may increase lactate levels in the early stages of exercise, (2) significant blood flow redistribution (e.g., that induced by drugs) within working muscle may be present without changes in total muscular blood flow, and (3) milrinone increased blood flow to glycolytic fibers in sham-operated animals, suggesting functional shunt, but caused possibly beneficial redistribution of blood flow to more oxidative working muscle in the presence of heart failure.

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To characterize the systemic and regional vascular effects of atrial natriuretic peptide (ANP) in chronic heart failure, central hemodynamics, regional blood flow and plasma ANP levels were determined in a rat model of myocardial infarction and failure and in sham-operated animals. Measurements were made in the conscious state before and after intravenous rANP [99-126] (8 micrograms bolus followed by continuous infusion of 1.0 microgram/kg/min). With this protocol, ANP significantly decreased cardiac output, right atrial, left ventricular end-diastolic and arterial pressures and there were increases in heart rate, systemic and intestinal vascular resistances in sham animals. Renal blood flow per gram of tissue was unchanged with ANP, but when expressed as a percentage of cardiac output, increased significantly, indicating a preferential renal vasodilatory effect of ANP. In rats with infarction and failure, this dose did not alter cardiac output or arterial pressure, but decreased right atrial and left ventricular blood flow. Although significantly reduced as compared to the control group, renal blood flow was not improved with ANP in the heart failure group. ANP plasma levels of the heart failure group were elevated at baseline (p less than 0.01), and increased 5-10 times after infusion of rANP. Thus, in rats with chronic heart failure, the renal vascular effects of ANP are blunted, which may, in part, explain the failure of ANP to restore the altered volume homeostasis in heart failure despite elevated ANP plasma levels. However, the effects on venous return were preserved which, in turn, improved cardiac performance via a reduction of preload.