Cardiac output by rebreathing in patients with cardiopulmonary diseases.

Noninvasive estimates of cardiac output by rebreathing soluble gases (Qc) can be unreliable in patients with cardiopulmonary diseases because of uneven distribution of ventilation to lung gas volume and pulmonary blood flow. To evaluate this source of error, we compared rebreathing Qc with invasive measurements of cardiac output performed by indicator-dilution methods (COID) in 39 patients with cardiac or pulmonary diseases. In 16 patients with normal lung volumes and 1-s forced expiratory volumes (FEV1), Qc measured with acetylene [Qc(C2H2)] overestimated COID insignificantly by 2 +/- 9% (SD). In subjects with mild to moderate obstructive lung disease, Qc(C2H2) slightly overestimated COID by 6 +/- 15% (P = 0.11). In patients with restrictive disease or combined obstructive and restrictive disease, Qc(C2H2) underestimated COID significantly by 9 +/- 14% (P less than 0.04). The magnitude of the discrepancy between Qc and COID correlated with size of the volume rebreathed and an index of uneven ventilation calculated from helium mixing during rebreathing that determined a dead space to inspired volume ratio (VRD/VI). Rebreathing volumes less than 40% of the predicted FEV or VRD/VI of 0.4 or greater identified all subjects with a discrepancy between Qc(C2H2) and COID of 20% or greater.

Hemodynamic and respiratory effects of dezocine, ciramadol, and morphine.

The hemodynamic and respiratory effects of dezocine and ciramadol, two agonist-antagonist analgesics, were compared with those of morphine in 30 patients undergoing diagnostic cardiac catheterization. Each subject received a single intravenous dose of dezocine (0.125 mg/kg), ciramadol (0.6 mg/kg), or morphine (0.125 mg/kg) in a double-blind fashion. Hemodynamic and respiratory parameters were measured at baseline and 5, 10, and 20 minutes after dosing. Dezocine increased the cardiac index (CI; 2.67 to 2.92 L/min/m2), stroke volume index (SVI; 43.6 to 47.6 ml/beat/m2), left ventricular stroke work index (LVSWI; 57.4 to 64.7 gm-m/m2), and pulmonary vascular resistance (PVR; 105.6 to 154.0 dynes X sec/cm5). Ciramadol increased the CI (2.78 to 3.22 L/min/m2), SVI (40.9 to 48.2 ml/beat/m2), LVSWI (51.1 to 57.9 gm-m/m2), and mean pulmonary arterial pressure (PA; 14.7 to 18.9 mm Hg). Morphine had no effect on CI, SVI, LVSWI, PA, or PVR, but it significantly lowered systolic and diastolic blood pressures. There were no appreciable changes in heart rate, left ventricular end-diastolic pressure, mean arterial pressure, or mean pulmonary capillary wedge pressure after any of the drugs. All three drugs significantly decreased systemic vascular resistance. There were no clinically significant changes in respiratory parameters. We conclude that dezocine, ciramadol, and morphine have no clinically important adverse effects on cardiac performance.

Effect of acute hypoxia on airway and vascular exchangeable lung water spaces in dogs.

To determine if alveolar hypoxia causes subclinical noncardiogenic pulmonary edema, we measured in 8 dogs the rebreathing pulmonary tissue volume (Vt) and the pulmonary extravascular water volume using the single-pass double-indicator dilution method. After baseline measurements, the dogs were ventilated with the lowest concentration of oxygen that would not cause left ventricular failure (9 to 13% O2). One to 6 h of hypoxia had no effect on Vt, but caused a reversible 38% fall in pulmonary extravascular lung water volume by the indicator method (p less than 0.01). The ratio of the extravascular to vascular volumes estimated from the relative peak heights of the 2 indicator dilution curves did not change with hypoxia, which implies that hypoxia caused a derecruitment of pulmonary blood vessels rather than a real decrease in extra-vascular lung water volume. This conclusion is supported by our rebreathing measurement of the airway exchangeable tissue volume, which is virtually independent of tissue perfusion, and which did not fall during hypoxia. To determine if this alteration in the pulmonary circulation can cause pulmonary edema when the cardiac output is increased, we opened a femoral artery to femoral vein shunt in 9 additional dogs during ventilation with 9 to 13% oxygen. Cardiac output increased over 50% but pulmonary edema developed in only 1 dog, the dog that also had the highest mean pulmonary artery pressure of the group (35 mmHg versus group mean of 26 mmHg during hypoxia). We conclude that 1 to 6 h of alveolar hypoxia in dogs consistently decreases the volume of perfused lung tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Heart block and idiopathic pulmonary hemosiderosis.

A young woman with idiopathic pulmonary hemosiderosis (IPH) and advanced heart block below the atrioventricular node requiring pacemaker therapy is discussed. Thirteen years after the onset of IPH she is free of pulmonary symptoms despite having never received steroid or antimetabolite therapy.

False aneurysm and pseudo-false aneurysm of the left ventricle: etiology, pathology, diagnosis, and operative management.

Four patients are presented in whom either a false aneurysm or a "pseudo-false" aneurysm of the left ventricle developed following a myocardial infarction. False aneurysms of the left ventricle are unusual and are distinctly different from the more common true aneurysms. A false aneurysm is the result of a contained hematoma dissecting, into a transmural infarct. It communicates with the left ventricle through a small orifice. Previous descriptions of false aneurysms have stressed that their wall consists of pericardium and mural thrombus and lack identifiable epicardial or myocardial elements. Two pseudo-false aneurysms are described. They communicated with the left ventricle through a small orifice but their wall contained myocardial tissue. False aneurysms have a tendency to rupture and therefore their presence alone is an indication for operation. One of the pseudo-false aneurysms discussed ruptured into the right ventricle. The operation for false aneurysm may be simpler than that for true aneurysm since it might be possible to close the small communication into the left ventricle without resecting the entire aneurysm wall.

Surgical management of an aneurysm of the left main coronary artery.

A 28-year-old woman underwent cardiac catheterization three months after sustaining an acute anterolateral myocardial infarct. An aneurysm of the left main coronary artery was found at angiography and also was visualized by two-dimensional echocardiography. The patient had no evidence of atherosclerotic vascular disease. At operation, vein grafts were placed to bypass the aneurysm and the orifice of the left coronary artery was oversewn to exclude the aneurysm from the coronary circulation.

Delayed appearance of left-to-right shunt following aortic valvular replacement. Report of two cases.

Two cases are presented in which a left-to-right shunt occurred late following aortic valvular replacement. In one patient a fistula was found between the aortic root and the right atrium and ventricle. In the second patient a defect developed in the membranous septum, allowing shunting from the left ventricle to both the right atrium and right ventricle.

Pulmonary tissue volume in dogs during pulmonary edema.

Pulmonary tissue volume (Vt) and pulmonary capillary blood flow (Qc) were measured in anesthetized dogs by analyzing end-expiratory concentrations of dimethyl ether (DME), acetylene (C2H2), and sulfur hexafluoride during a 30-s rebreathing maneuver. Vt was compared to the postmortem lung weight of control dogs and dogs with hemodynamic and nonhemodynamic (alloxan) pulmonary edema. Qc was compared to the cardiac output measured by dye dilution. A 100-ml increase in alveolar volume (VA) in the range of 1-2 liters resulted in a 9 +/- 3 ml increase in Vt. Vt measured at a VA of 1.9 liters measures 114 +/- 18% of the postmortem lung weight in 20 control dogs and in 6 dogs with moderate edema (lung weight < 250% of predicted). Vt measured only 53 +/- 14% of the lung weight in 11 dogs with more severe edema. DME and C2H2 gave the smae mean values of Vt, but the reproducibility of a series of 3-7 measurements was greater with DME (coefficient of variation was 5% with DME and 8% C2H2). Qc measured 96 +/ 15% of the cardiac output during the rebreathing maneuver, but the maneuver caused a 4-40% fall in the cardiac output. These data show that Vt determined by rebreathing DME is between 86% and 135% of the lung weight in dogs with pulmonary edema until the lung weight is greater than 250% of the predicted value.

The relationships among arterial oxygen flow rate, oxygen binding by hemoglobin, and oxygen utilization in chronic cardiac decompensation.

We have examined the interrelationships among CaO2, blood flow, oxygen binding by hemoglobin, and VO2 in cardiac patients with and without chronic cardiac decompensation. We have quantified the role that decreased oxygen-binding to hemoglobin may play in maintaining VO2 in the presence of low systemic blood flow rates. The volume rate of oxygen delivery to tissues was expressed as the OFIa, the product of CO2 and blood flow. OFIa varied from 738 to 262 ml/min/m2, whereas VO2 varied from 170 to 117 ml/min/m2. Thus, in the patients with lowest OFIa (63% below the highest OFIa), VO2 was only down 19%. VO2 was maintained because the extraction of oxygen rose from about 20% to 50% in close association with the decrease in OFIa. Oxygen binding to hemoglobin was lower in patients with the lowest OFIa--and therefore, at in vivo conditions of pH, PCO2, and temperature, P50 in vivo was higher. The resulting facilitation of oxygen release at the PO2 of tissue capillaries could explain about one third of the observed increment in oxygen extraction in patients with low OFIa. An alternative interpretation is that a high P50 in vivo minimizes the reduction in PVO2 needed to maintain VO2 when increased proportional extraction of O2 compensates for decreased OFIa.

Hemodynamic and respiratory effects of morphine and butorphanol.

The hemodynamic effects of butorphanol, a potent synthetic narcotic-antagonist analgesic, were investigated and compared with those of morphine. A total of 20 patients were studied (8 butorphanol, 12 morphine) at the time of diagnostic cardiac catheterization. Butorphanol decreased pH, PCO2, and systemic artery pressure and increased PCO2, cardiac index, and pulmonary artery pressure. Morphine caused similar changes in pH, PO2, systemic artery pressure, and PCO2 but much smaller changes in cardiac index and no change in pulmonary artery pressure. The clinical implications and possible mechanisms are discussed.

Spectral energy of the first heart sound in acute myocardial ischemia. A correlation with electrocardiographic, hemodynamic, and wall motion abnormalities.

First heart sound (S1) energy spectra in isovolumic systole, hemodynamics, and angiographic left ventricular wall motion (LVWM) at rest and with atrial pacing were compared in 27 patients who underwent diagnostic cardiac catheterization and angiography because of chest pain. Eighteen patients were found to have coronary artery disease (CAD) and nine patients, normal coronary arteries. Eleven of the 18 CAD patients (61%) had a mean reduction in the spectral energy of S1 of 6.5 +/- 1.4 (SEM) dB below control (-52%), during interruption of ischemic stress of rapid atrial pacing, compared to only one of nine patients without CAD (P less than 0.05). Only five CAD patients (28%) had an abnormal rise (greater than or equal to 5 mm) in left ventricular end-diastolic pressure (LVEDP) either during or upon interruption of pacing, and six (33%) had ischemic ST-segment depression greater than or equal to mv in the ECG. Similarly two patients free of CAD (22%) had an abnormal increase in LVEDP, and none had ECG evidence of ischemia. Seventeen CAD patients (94%) had segmental LVWM abnormalities at rest or with interruption of pacing, while three patients with normal coronary arteries (33%) had abnormal angiographic LVWM (P less than 0.01). Thus, reduction is S1 spectral energy is a common accompaniment of myocardial ischemia. In the present study, it was more frequently observed than abnormalities in either the ECG or LVEDP, but was not was consistently seen as segmental left ventricular wall motion abnormalities.

Underestimation of true pulmonary blood volume by the pulmonary artery wedge injection technique in cardiac patients.

Pulmonary blood volume measurements were made comparing pulmonary artery with pulmonary artery wedge and left atrial dye dilution curves in 32 patients with cardiac disease. Mean transit times across the lungs were underestimated by the PAW curve technique. Hence calculated PBV by the right heart injections alone underestimates true PBV.

The acute hemodynamic effects of ethacrynic acid and furosemide in patients with chronic postcapillary pulmonary hypertension.

The acute hemodynamic effects of either ethacrynic acid or furosemide were studied in 27 patients who underwent diagnostic right and transseptal left heart catheterization. Twenth-three patients had postcapillary pulmonary hypertension secondary to isolated or predominant mitral stenosis. Of these, 21 patients were in New York Heart Association functional class III, and one each in class II and IV. In the remaining four patients pulmonary artery pressures were normal. Two patients had aortic stenosis and one each coronary artery disease and nonobstructive cardiomyopathy. All four patients were in class II. Cardiac index, pressures, and pulmonary blood volume (PBV) were measured in the control state and 20, 40, and 60 min after diuretic administration. Pulmonary extravascular fluid volume (PEV) was measured in the control state and at 60 min post drug infusion. A similar hemodynamic response was observed for each drug. Significant reductions in pulmonary artery and left atrial mean pressures, cardiac index, and plasma volume occurred over the one hour observation period and were accompanied by a significant duiresis. However, despite recutions in central pressures and blood flow, PBV, ev, and PEV/PBV remained unchanged, as did systemic arterial pressure. Since 23 of the subjects had postcapillary pulmonary hypertension it is postulated that the failure of PBV to decrease significantly despite significant decreases in pulmonary artery mean pressure is related to altered pressure volume characteristics in the pulmonary vascular bed in which the lung is operating on a steep portion of its pressure volume curve. The failure of the PEV to decrease supports the concept that the pulmonary extravascular space is relatively resistant to early decreases in pulmonary capillary pressure induced acutely. The failure of the pulmonary extravascular fluid volume to decrease despite a fall in plasma volume and pressures corresponds to the well recognized delay in resolution of radiologic evidence of pulmonary congestion.

Acute effects of increase in pulmonary vascular distending pressures on pulmonary blood volume and pulmonary extravascular fluid volume in man.

The acute hemodynamic effects of supine leg exercise or atrial pacing were studied in 114 patients undergoing right and either transseptal (87 cases) or retrograde (27 cases) left heart catheterization. Seventy-one patients - 15 with coronary artery disease, 22 with aortic valve disease, and 34 with mitral valve disease - performed exercise on a bicylce ergometer. Forty-three patients, of whom 22 had coronary artery disease, nine aortic valve disease and 12 mitral valve disease, were studied during rapid atrial pacing. Cardiac index (CI), pulmonary artery mean (PAm), and left atrial mean (LAm) pressure, pulmonary blood volume (PBV) and pulmonary extravascular volume (PEV) were measured during the control state and during acute intervention. Both exercise and pacing resulted in significant elevations in PAm (range 37-65%) and LAm (range 36-43%) mean pressures in all patients. Cardiac index rose between 34 and 58% in the exercise groups, but did not change in those who were paced. During intervention both PBV and PEV increased significantly in all but the nine patients with aortic valve disease who were paced. Although volume increased occurred, they did not achieve the 5% significanc- level. For all patients the mean increment in PBV ranged between 37 and 123 ml/m2 over control, while PEV rose between 15 and 35 ml/m2. In each group the increases in PEV and PBV were proporationate, so that the ratio of PEV/PBV DID NOT CHANGE SIGNIFICANTLY BETWEEN THE CONTROL AND INTERVENTION STATES. Thus PEV and PBV increases occurred with elevations in pulmonary vascular pressures whether or not blood flow increased. Our data in patients with normal pulmonary vascular beds (i.e., coronary artery disease and aortic valve disease) strongly support the hypothesis that recruitment of vascular channels accounts for the acute changes in PEV and PBV and that the changes in PEV over a brief period of time do not necessarily reflect a "true" increase in extravascular lung water. Although pressures are higher in the lungs of patients with mitral valve disease, the data also suggest that recruitment is likely to be the mechanism for the observed proportionate increase in pulmonary extravascular volume and pulmonary blood volume.