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Biomedical subjects

P N Yu

Publications and source records attributed to P N Yu.

At least 37 records · Page 2Linked to original sources
PubMed1976

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.

Adult↗
PubMed1976

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.

Adult↗
PubMed1976

ST-segment variations after acute myocardial infarction. Relationship to clinical status.

The degree of vectorcardiographic ST-segment elevation was employed as an index of myocardial ischemic injury in a study of 27 patients after acute myocardial infarction (AMI). The ST-segment vector magnitude (STVM) was derived from the continuously recorded modified Frank vectorcardiogram and was plotted serially by hours after onset of AMI. The STVM in normal subjects was 51.1 +/- 7.1 muV (mean +/- SE). A standard deviation of the pooled variance of 15.2 muV was obtained in a group of control patients and a change of more than 2 SD (greater than 30 muV) in an individual STVM was considered to be significant. The STVM progressively decreased in patients who survived without clinical complications while it remained elevated in those with congestive heart failure. A modest, sustained re-elevation of STVM was observed in patients who developed pericarditis, and a significant late average increase of 64 muV occurred in survivors with infarct extension. In contrast, STVM underwent a major increase in patients who died. In five of these six patients without associated pericarditis a mean increase of 164 muV was recorded in the last 5-12 hours of life. While death was clinically predictable in two patients with cardiogenic shock, it was not so for the four other patients who died. Thus, major increases in STVM frequently suggested significant new ischemic injury and were often premonitory to sudden death after AMI. The increases preceding death implied that not only ventricular extopy but also lethal conduction abnormalities after AMI might be ischemia-related.

Acute Disease↗
PubMed1976

Early care of acute myocardial infarction.

A fixed life support station (LSS) was established in the emergency department of a community hospital in order to provide early care for patients with suspected acute myocardial infarction (MI). Prospective studies were conducted on 154 patients with verified acute MI. Median time from onset of symptoms to electrocardiographic monitoring was 164 minutes. Overall hospital mortality for these patients was 15.6%. Of 112 patients less than 70 years old, 51 arrived within two hours; only three (6%) of the 51 died. Patients arriving within two hours of the onset of symptoms in clinical class I had an incidence of cardiogenic shock (CS) of 2%, while those arriving two hours or more after the onset of symptoms in clinical class II had an incidence of CS of 26% (P less than .005). A fixed LSS in a community hospital is feasible and effective for early care of patients with acute MI and may facilitate identification of patients at highest risk for development of CS.

Acute Disease↗
PubMed1975

The acute phase of myocardial infarction.

During the acute phase of myocardial infarction, two groups of patients are observed. Patients in the first group have no significant complications, and approximately 95 per cent of these patients recover fully without any specific therapy. Patients in the second group may have various complications, some of which are benign, whereas others may lead to a fatal outcome. The complications may be divided into four major types: 1. Cardiac arrhythmias and conduction defects. The tachyarrhythmias and bradyarrhythmias are the most frequently encountered complications in patients with acute myocardial infarction. Tachyarrhythmias include ventricular premature beats, ventricular tachycardia, ventricular fibrillation, supraventricular tachycardia, atrial flutter, and atrial fibrillation. Bradyarrhythmias include sinus and junctional bradycardia and various degrees of heart block. Those patients who are unable to reach a hospital and die suddenly presumably succumb to ventricular fibrillation. 2. Left ventricular failure and cardiogenic shock. In more than 33 per cent of patients with acute myocardial infarction, a third heart sound and pulmonary rales may be heard. If they are present for only 24 hours, the physical findings may indicate an alteration of left ventricular failure. However, if they persist for a few days and disappear after medical therapy, mild left ventricular failure may be present. About 12 per cent of patients have acute pulmonary edema, and 10 per cent of patients develop cardiogenic shock. These two complications carry a high mortality rate (40 per cent and nearly 100 per cent respectively). 3. Rupture of the heart. Cardiac rupture may occur in the free wall, ventricular septum, and papillary muscles. These complications, although less frequently encountered, cause a number of deaths in patients with acute myocardial infarction. 4. Thromboembolism. Under this category are included pulmonary embolism, systemic arterial embolism, and systemic venous thrombosis.

Acute Disease↗
PubMed1973

Interrelation between alterations in pulmonary mechanics and hemodynamics in acute myocardial infarction.

Pulmonary mechanics were evaluated in 30 patients with acute myocardial infarction by measuring forced expiratory flow rates and total pulmonary resistance (R(T)) with the oscillometric method at the resonant frequency of the chest (6-8) cycle/s). During the first 3 days after infarction, forced expiratory volume (FEV) and forced mid-expiratory flow rate (FEF(25-75%)) were 69% and 60% of predicted values, respectively. 10 or more wk later these values were 95% and 91%. Initially, R(T) was 52% greater than predicted, but was only 4% greater 10 or more wk later. In 11 patients R(T) was measured at both resonant frequency and at 3 cycle/s. Five of these patients had no clinical signs of heart failure, but nine had abnormally high values of pulmonary artery pressure, "wedge" pressure and pulmonary extravascular water volume. All of these patients recovered. Initially, R(T) at resonance was 50% and R(T) at 3 cycle/s was 130% greater than predicted values. 2-3 wk later these figures were -3% and +6% of those predicted, respectively. At 10 wk or more, significant frequency dependence of R(T) had disappeared (R(T) at 3 cycle/s was 7% greater than R(T) at resonance). Isoproterenol inhalation in six patients caused no change in flow rates, R(T) at resonance, or R(T) at 3 cycle/s. R(T) at resonance and at 3 cycle/s, FEV, and FEF(25-75%) correlated significantly with the pulmonary vascular pressures. Patients with more marked arterial hypoxia and larger values for extravascular water volume had greater elevations of R(T) and depression of FEF(25-75%), but linear correlations were not significant. Clinical signs of congestive heart failure significantly correlated with a fall in FEV and FEF(25-75%), the development of frequency dependence of R(T), and elevation of the pulmonary wedge pressure. The initial elevation of R(T) and low flow rates indicate a modest degree of airway obstruction in acute myocardial infarction. Lack of response to isoproterenol suggests that bronchial muscular constriction is not a major factor. Frequency dependence of R(T) accompanied by elevated pulmonary vascular pressures and extravascular water volume indicates that pulmonary congestion causes the development of uneven time constants in the airways. Vascular engorgement and interstitial edema from elevated vascular pressures causing narrowing of the peripheral airways and closure of collateral airways could account for the above findings.

Acute Disease↗