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Biomedical subjects

B G Firth

Publications and source records attributed to B G Firth.

At least 37 records · Page 2Linked to original sources

Analysis of factors affecting the variability of Fick versus indicator dilution measurements of cardiac output.

This study was performed to assess the relation between Fick and indicator dilution measurements of cardiac output (CO) in a large number of subjects and to evaluate this relation in patients with a low CO, a high CO, and left-sided cardiac regurgitation. In 808 patients (428 men, 380 women, mean age 50 +/- 11), CO was measured by Fick and either thermodilution (right atrium to pulmonary artery)(n = 252) or indocyanine green dye ("dye")(pulmonary artery to systemic artery)(n = 556) within 10 minutes of each other. There was excellent agreement between Fick and both thermodilution and dye. The difference between Fick and indicator dilution measurements was 9 +/- 9%; it was 10% or less in 67% and 20% or less in 91% of patients. The disparity between Fick and indicator dilution measurements was increased in patients with a low CO (less than 2 liters/min/m2)(n = 152) (difference 14 +/- 11%, p less than 0.001) and those with aortic or mitral regurgitation (n = 83) (difference 13 +/- 11%, p less than 0.001). In these groups, the disparity between Fick and thermodilution measurements was not exaggerated, but the disparity between Fick and dye measurements was greater. Thus, although there is excellent agreement between Fick and both thermodilution and dye measurements of CO, thermodilution is preferable to dye in patients with a low CO and those with aortic or mitral regurgitation.

Adolescent↗

Measurements of left-to-right intracardiac shunting in adults: oximetric versus indicator dilution techniques.

Of the various techniques that are available to assess the presence and magnitude of intracardiac shunting, oximetry and indicator dilution are used most frequently. This study was performed to compare these methods in adult patients with pure left-to-right intracardiac shunting. In 27 patients [12 men, 15 women, aged 32 +/- 12 (mean +/- SD) years], shunt magnitude was assessed in close temporal proximity by both techniques. The oximetric percentage left-to-right shunt averaged 55 +/- 16%, whereas the indocyanine green dye percentage shunt was significantly less (36 +/- 14%, p less than 0.001). The oximetric percentage shunt exceeded the indocyanine green dye percentage shunt in 26 and did so by greater than 20% in 23 patients. Thus, there is a substantial difference in shunt magnitude between the oximetric and the indicator dilution techniques. In infants, indicator dilution yields results that are larger than those obtained with the oximetric method. Conversely, in adults, the indicator dilution technique gives results that are consistently smaller than those obtained with oximetry. As a result, the decision regarding therapy of an intracardiac shunt should be made with this in mind.

Adolescent↗

Assessment of the inotropic and vasodilator effects of amrinone versus isoproterenol.

The hemodynamic effects of graded-dose infusions of amrinone (maximal dose 30 micrograms/kg/min) (10 patients) and isoproterenol (maximum dose 4 micrograms/min) (11 patients) were assessed in patients with a range of left ventricular (LV) function. LV ejection fraction ranged from 0.13 to 0.77 (mean +/- standard deviation 0.47 +/- 0.23) among the patients who received amrinone and from 0.24 to 0.77 (mean 0.52 +/- 0.18) among those who received isoproterenol. Peak-dose amrinone produced a reduction in LV filling pressure (from 15 +/- 10 to 10 +/- 7 mm Hg, p less than 0.001), but no significant change in heart rate, cardiac output, mean aortic pressure, total systemic vascular resistance (TSVR) or LV dP/dt max. In contrast, peak-dose isoproterenol produced a similar reduction in LV filling pressure (from 17 +/- 12 to 13 +/- 13 mm Hg, p less than 0.05), but also caused increases in heart rate, cardiac output and LV dP/dt max and decreases in mean aortic pressure and TSVR (p less than 0.001). The absolute change in cardiac output and stroke volume correlated closely with the change in TSVR in response to amrinone (r = -0.90, p less than 0.001 and r = -0.84, p = 0.002, respectively), but not in response to isoproterenol. Although isoproterenol produced a marked increase in cardiac output and LV dP/dt max (not explained by heart rate changes alone) in all patients, amrinone produced an increase in cardiac output only in those with markedly elevated LV filling pressures (who had a reduction in TSVR), and an increase in LV dP/dt in a minority.

Aminopyridines↗

Limitations of qualitative angiographic grading in aortic or mitral regurgitation.

This study was performed to assess the accuracy of qualitative angiographic grading in persons with aortic regurgitation (AR) or mitral regurgitation (MR) and to determine the factors that may influence the reliability of such grading. In 230 patients (152 men, 78 women, aged 52 +/- 14 years) with AR or MR, forward cardiac index was measured by the Fick and indicator dilution techniques and left ventricular (LV) angiographic index by the area-length method, from which the regurgitant volume index was calculated. In 124 other patients (89 men, 35 women, aged 52 +/- 11 years) without regurgitation, there was good agreement between forward and angiographic cardiac indexes (r = 0.87, p less than 0.001). In the 83 patients with AR, the regurgitant volume indexes in those with 1+ (0.87 +/- 0.57 liters/min/m2) and 2+ (1.72 +/- 1.19 liters/min/m2) angiographic regurgitation were not significantly different from one another, but were significantly different from those with 3+ (3.0 +/- 1.42 liters/min/m2) and 4+ (4.80 +/- 2.25 liters/min/m2) regurgitation; at the same time, the regurgitant volume indexes of patients with 3+ and 4+ AR were not significantly different from one another. In the 147 patients with MR, the regurgitant volume indexes in patients with 1+ regurgitation (0.61 +/- 0.64 liters/min/m2) were significantly lower than other grades, but the regurgitant volume indexes of 2+ (1.14 +/- 0.85 liters/min/m2) vs 3+ (2.14 +/- 1.37 liters/min/m2) and of 3+ vs 4+ (4.60 +/- 2.31 liters/min/m2) were not significantly different. With AR and MR, regurgitant flow within each angiographic grade varied widely, especially in grades 3+ and 4+, and there was considerable overlap of regurgitant volume indexes between grades.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Pathophysiologic mechanisms of cardiac tamponade and pulsus alternans shown by echocardiography.

A pericardial effusion is easily recognized by echocardiography, but the diagnosis of cardiac tamponade by echocardiography is controversial. Recently, several reports have indicated that right ventricular (RV) or right atrial (RA) diastolic collapse represent highly specific and sensitive signs of a hemodynamically significant pericardial effusion. This report evaluates the pathophysiologic significance of these findings in 3 patients. One patient had classic clinical and hemodynamic features of tamponade without typical echocardiographic features; 1 had typical echocardiographic features of tamponade without the characteristic clinical or hemodynamic features; and 1 had all the findings characteristic of tamponade, including mechanical and electrical alternans. The first patient had increased right-sided cardiac pressures and RV hypertrophy, which prevented RV or RA collapse. The second patient had low right-sided intracardiac pressures, which allowed RV and RA diastolic compression to occur during early and mid-diastole. In the third patient, severe holodiastolic impairment of right-sided filling, and presumed decreased pulmonary venous and pericardial compliance, in the setting of tamponade produced a beat-to-beat alternation of RV and left ventricular filling with associated electrical and mechanical alternans. RV or RA collapse during diastole occurs when intrapericardial pressure equals or exceeds intracardiac pressure. Increases in wall stiffness of chamber pressures may prevent diastolic collapse in the setting of tamponade. Conversely, extremely low intracardiac pressures may allow diastolic collapse to occur in the absence of overt cardiac tamponade. The extent and timing of the RA or RV collapse, rather than its mere occurrence, are important in the diagnosis of cardiac tamponade by echocardiography.

Adolescent↗

Left ventricular volumes by single-plane cineangiography: in vivo validation of the Kennedy regression equation.

This study was performed to assess the accuracy and reliability of the regression equations of Kennedy et al and Wynne et al in the quantitation of single plane left ventricular (LV) volumes. In 15 patients with normal LV function and without intracardiac shunting or valvular insufficiency, gated equilibrium blood pool scintigraphy was performed simultaneously with the measurement of cardiac output (by thermodilution), after which left ventriculography was performed in the 30 degrees right anterior oblique (RAO) projection. From the scintigraphically determined LV ejection fraction (EF) and the thermodilution-measured stroke volume (SV), absolute LV volumes were calculated. The cineangiographic LV volumes obtained with the regression equation of Kennedy et al closely approximated those calculated by scintigraphy/thermodilution, whereas the volumes determined using the regression equation of Wynne et al were larger (p less than 0.05) than the calculated volumes. In 204 patients without intracardiac shunting or valvular insufficiency, SV was measured by the Fick or indicator dilution methods, after which single-plane left ventriculography was performed in the 30 degrees RAO projection. In the 83 patients without coronary artery disease with normal (n = 69) or depressed (n = 14) LVEF, cineangiographic SV (obtained using the regression equation of Kennedy et al) closely approximated forward SV. Similarly, this relation was excellent in the 142 patients whose LVEFs were greater than or equal to 0.50.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Acute systemic and coronary hemodynamic and serologic responses to cigarette smoking in long-term smokers with atherosclerotic coronary artery disease.

Previous studies suggested that cigarette smoking 1) inhibits an increase in coronary blood flow that should occur with increased myocardial oxygen demands, and 2) alters thromboxane and prostacyclin production, causing vasoconstriction and platelet aggregation. In 38 smokers (26 men and 12 women, aged 50 +/- 8 years [mean +/- standard deviation] ) with coronary artery disease, systemic and coronary hemodynamic and serologic variables were measured before and after smoking two cigarettes (in 8 to 10 minutes) (21 patients) or 8 to 10 minutes without smoking (17 patients; control group). No variable changed in the control group. Smoking increased (p less than 0.05) heart rate-systolic pressure product, cardiac output and maximal first derivative of left ventricular pressure (dP/dt) without significantly changing the coronary sinus concentrations of thromboxane B2 or 6-keto-prostaglandin F1 alpha (the stable metabolites of thromboxane A2 and prostacyclin, respectively). Smoking did not increase coronary flow in 6 of 11 patients with greater than 70% stenosis of the proximal left anterior descending or circumflex coronary artery, or both, whereas it caused an increase in coronary flow in all 10 patients without proximal stenoses (p = 0.006). To determine if smoking altered the response of coronary flow to increased myocardial oxygen demands, 10 smokers (5 men and 5 women, aged 48 +/- 9 years) underwent atrial pacing for 5 minutes followed 15 minutes later by atrial pacing for 5 minutes during smoking. In the five patients without proximal left coronary artery stenoses, coronary flow increased 26 +/- 29 ml/min with pacing and 45 +/- 21 ml/min with pacing/smoking (p = 0.018).(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

The value of rest and exercise radionuclide ventriculography as compared to echocardiography and angiography in the detection of left ventricular dysfunction in patients with chronic aortic regurgitation.

Symptomatic patients with chronic aortic regurgitation and a left ventricular ejection fraction greater than 0.50, or forward cardiac index greater than 2.5 l/min/m2 at rest, have a much better survival rate than those with a depressed ejection fraction or cardiac index following aortic valve replacement. The annual mortality rate is approximately 2% for those with well preserved ventricular function versus 10% for those with depressed ventricular function at rest. This is in striking contrast to the situation that exists in patients with aortic stenosis, where the long-term survival is similar for those with a normal or depressed left ventricular ejection fraction or cardiac index at rest. Therefore, it would seem to be important to detect incipient left ventricular failure in patients with chronic aortic regurgitation and to intervene surgically before the left ventricular dysfunction becomes irreversible. In patients with a normal left ventricular ejection fraction at rest, maximal supine bicycle exercise testing with radionuclide ventriculography defines a group of patients with truly normal ventricular function (ejection fraction increases by greater than 0.05 ejection fraction units at peak exercise), and a group with incipient left ventricular dysfunction earlier than previously described variables (i.e., left ventricular ejection fraction at rest less than 0.50, left ventricular end-systolic volume index greater than 90 ml/m2, left ventricular end-systolic dimension greater than or equal to 5.5 cm, left ventricular shortening fraction less than or equal to 25%), and generally before the onset of symptoms.

Adolescent↗

Hemodynamic effects of intravenous prostacyclin in stable angina pectoris.

Prostacyclin (PGI2) is a naturally occurring vasodilator and inhibitor of platelet aggregation that produces vasodilatation of the systemic, pulmonary and coronary vascular beds in animal models. Because the endogenous production of PGI2 is reduced in those with coronary arterial disease (CAD), it may have a therapeutic role in patients with ischemic heart disease. To assess its safety and efficacy in this clinical setting, 17 patients with stable angina and CAD received an incremental intravenous infusion of either PGI2 (n = 10) to a maximum dose of 10 ng/kg/min (average 9.8 +/- 0.8 [mean +/- standard deviation]), or diluent buffer solution (placebo) (n = 7). All patients who received PGI2 became flushed, but experienced no other adverse effects PGI2 caused an increase in heart rate (66 +/- 11 to 80 +/- 11 beats/min, p less than 0.001) and cardiac index (2.88 +/- 0.65 to 3.97 +/- 1.17 liters/min/m2, p less than 0.001) and a decrease in mean femoral arterial pressure (96 +/- 18 to 86 +/- 11 mm Hg, p less than 0.001), but no change in mean pulmonary arterial or capillary wedge pressure. Total systemic and pulmonary vascular resistance decreased significantly (p less than 0.001). In response to PGI2, mean coronary sinus blood flow did not change significantly (100 +/- 40 to 121 +/- 52 ml/min), but coronary vascular resistance decreased (1.07 +/- 0.40 to 0.83 +/- 0.36 U, p less than 0.001). No variable was altered by placebo infusion. PGI2 caused a marked increase in 6-keto PGF1 alpha (the stable metabolite of PGI2) concentrations in both arterial (42 +/- 29 to 567 +/- 216 pg/ml, p less than 0.001) and venous (46 +/- 31 to 604 +/- 229 pg/ml, p less than 0.001) blood but no demonstrable change in plasma renin activity. Thus, intravenous PGI2 to a dosage of 10 ng/kg/min is a safe and effective systemic, pulmonary and coronary arterial vasodilator in patients with CAD and stable angina pectoris.

6-Ketoprostaglandin F1 alpha↗

Efficacy of prazosin in the management of chronic congestive heart failure: a 6-month randomized, double-blind, placebo-controlled study.

The beneficial effects of acute prazosin therapy in patients with congestive heart failure (CHF) have been well documented; however, its chronic efficacy over several months has not previously been evaluated in a placebo-controlled manner. Therefore, an assessment was made by radionuclide ventriculography of the effect of prazosin, 20 mg/day, on left ventricular ejection fraction and end-systolic and end-diastolic volumes at rest and on peak upright bicycle exercise, as well as its effect on right ventricular ejection fraction at rest, exercise time and work load, and standard clinical variables in 23 patients with stable class III symptoms of CHF. The study consisted of a 6-month randomized, double-blind, controlled evaluation of prazosin versus placebo in patients receiving a stable dose of digitalis and diuretics for at least 1 month. At entry, the prazosin and placebo groups did not differ in any respect. Prazosin caused no demonstrable effect on clinical variables such as status of symptoms, heart rate, mean arterial pressure, and cardiothoracic ratio when compared with placebo. Prazosin also caused no demonstrable effect compared with placebo on absolute or percent changes in radionuclide variables at rest or on peak exercise, or on exercise time or exercise work load. In addition, prazosin had no consistent effect compared with placebo on plasma renin activity or plasma catecholamine levels. However, there was a slight but significant increase in weight (p less than 0.0001) and in plasma renin activity in the upright position (p less than 0.002) with time, as well as a tendency for the diuretic dose to increase with time in both groups. Thus, long-term prazosin therapy generally produces no demonstrable subjective or objective improvement in patients with stable, chronic class III CHF receiving digitalis and diuretic therapy.

Adult↗