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Biomedical subjects

R B Case

Publications and source records attributed to R B Case.

At least 37 records · Page 2Linked to original sources

Measurement of regional myocardial perfusion using collimated miniature radiation detectors and the method of 133-xenon washout.

A new approach to the measurement of local myocardial perfusion based on the application of highly-collimated miniature cadmium telluride radiation detectors to measure washout of 133-Xenon from well-defined tissue volumes is presented. Single-hole collimators with length/diameter ratios of 1 (L = 4 mm, D = 4 mm) and 4 (L = 12 mm, D = 3 mm) were employed as prototype designs. The probe field of view was characterized theoretically using a spherical model of the myocardium in conjunction with experimental point source response measurements for each collimator. Method evaluation using two medium resolution collimators (L/D = 1) was effected by performing left main and circumflex coronary artery perfusion studies at controlled but variable flows in the dog heart. An excellent correlation (r greater than 0.99) between actual and estimated perfusion determined from 65 washout curves over the flow range 0.38 to 3.18 ml/min/gm was demonstrated. The ability to resolve regional flow differences was verified by measuring tracer washout from circumflex and left anterior descending regions of the myocardium, using two high resolution collimators (L/D = 4), in a preparation where the left main coronary artery was cannulated and a snare was placed around the circumflex coronary artery to selectively reduce flow to that region.

Biomedical Engineering↗

Reduced human ventricular fibrillation threshold associated with contrast-induced Q-T prolongation.

Injection of contrast dye during selective coronary arteriography prolongs the Q-T interval well beyond that expected for the accompanying bradycardia. A case is presented in which a 5 mA stimulus delivered prematurely by an improperly sensing ventricular demand pacemaker initiated ventricular fibrillation during coronary arteriography, although no evidence of coronary or other cardiac disease was found. An analysis is made of the progressive Q-T and T changes following contrast dye injection, and their relation to the onset of ventricular fibrillation. The implications of these observations are discussed in light of existing data on human ventricular vulnerability.

Aged↗

A new thermal sensor for surface-based measurement of local myocardial perfusion.

The transient response of a new thermal sensor for continuous surface-based measurement of local tissue blood flow was evaluated in the beating dog heart. The sensor is 2.5 mm square, tests on the heart, and responds to flow changes only within a region of tissue 3-4 mm below its location on the epicardial surface. Initial studies demonstrate excellent sensitivity, good frequency response with a time constant of the order of 10-11 s, and an ability to continuously monitor changes in local myocardial blood flow during a variety of well-understood interventions, including coronary artery occlusion, reactive hyperemia, and intravenous administration of nitroglycerin and dipyridamole.

Animals↗

Lactate accumulation relative to the anaerobic and respiratory compensation thresholds.

Anaerobic thresholds of five male subjects were determined invasively (ATi), from a marked increase in plasma lactate above resting levels (delta La), and noninvasively (ATn), from a nonlinear increase in minute ventilation (VE) during incremental work (IW) leg cycling tests; work rate was increased 30 W every 2 min. Each subject also performed four constant-load work (CLW) tasks just above and just below their ATn and respiratory compensation threshold (RCT), i.e., the point expressed as O2 consumption (VO2) or work rate, at which VE increases disproportionally to CO2 output during IW. In four of the five subjects the ATn preceded the ATi during IW. Yet the ATn delineated the CLW in which marked lactate accumulation did or did not occur. During CLW just above the ATn in these same four subjects, VE/VO2 and fractional expired O2 (FEO2) peaked well before delta La plateaued. These findings suggest that exercise hyperventilation is not necessarily proportional to increases in plasma lactate.

Adult↗

Value of premature ventricular contraction morphology in the detection of myocardial infarction.

A ventricular premature contraction (VCP) with a QR pattern has been associated with antecedent myocardial infarction. In order to determine the validity of this sign, we compared the presence of localized abnormal wall motion during left ventricular angiography with the morphology of VPC's induced in each patient by catheter stimulation of the left ventricular endocardium. The morphology of V1 was compared with anterior wall infarction, and of AVF with inferior wall infarction, and the specificity, sensitivity and predictive value of the QR VPC evaluated. A QR pattern VPC in V1 with a Q greater than or equal to 0.04 sec and a Q/R ratio = 0.20 had a specificity of 0.93, a sensitivity of 0.24 and a predictive value of 0.72 in the detection of anterior myocardial infarction. The detection rate was considerably increased with a Q/R ratio of greater than or equal to 0.1 and specificity remained high at 0.87. Detection of inferior infarction by use of AVF was less certain, and is probably of limited value.

Angiocardiography↗

Inlet and intrachamber concentration distributions in tracer studies of the canine central circulation and their relation to the isotope dilution residue function.

We analyzed the isotope dilution residue function from a single cardiac chamber for an arbitrary inlet distribution of tracer and arbitrary mixing within the chamber, and established a general relationship between cardiac output and the chamber residue function. In our experiments, we made simultaneous temperature measurements in three left ventricular chamber subregions of the dog subjected to left and right atrial injections of chilled saline. Flow-proportional tracer labeling always occurred at the left ventricular inlet when injection was into the right atrium. This state almost never obtained, however, with direct left atrial injection, although it was approximated most closely when multiple side hole cathers were used. We also demonstrated that imperfect tracer mixing in the normal ventricle can lead to significant regional temperature inequalities during tracer passage. These inequalities are more pronounced in the ventricle with compromised function, but in both normal and compromised ventricles they are minimal several beats after tracer concentration peaks if injection is into the right atrium.

Animals↗

A sequential angular lead presentation.

The presentation of the frontal leads was altered so that they could be displayed in sequential angular order. This was achieved by insertion of an inverting switch at the output stage of an electrocardiograph, so that the presented sequence of leads would be I, -aVR, II, aVF, III, and -aVL, corresponding to frontal plane vectors of 0 degree, 30 degrees, 60 degrees, 90 degrees, 120 degrees and 150 degrees. This form of presentation was made in normals, patients with myocardial infarction, hemiblock, and switched leads. A smooth flow of ECG information results, the extent of the disease is more easily evaluated, and the QRS, T, and P axis is more easily evaluated. The usefulness of neglected leads in diagnosis may be increased.

Heart Block↗

Measurement of myocardial PCO2 with a microelectrode: its relation to coronary sinus PCO2.

A micro-PCO2 electrode, with dimensions of 1 x 10 mm, and a 63% response time of 14 s was inserted into the left ventricular myocardium of the pentobarbital-anesthetized dog. Continuous recordings were made of myocardial PCO2 (PmCO2), arterial PCO2 (PaCO2), and coronary sinus PCO2 (CSPCO2) during variation of respiratory rate. PmCO2 and CSPCO2 were compared at varying coronary flow. PmCO2 was similar to and closely followed changes in CSPCO2. The difference between PmCO2 and CSPCO2 was -0.52 +/- 3.63 (SD) mmHg, and PmCO2 exceeded PaCO2 by 20.69 +/- 5.12 mmHg. After coronary occlusion, PmCO2, rose promptly, but CSPCO2 was only slightly elevated until the occlusion was released, when a CO2 efflux into the coronary sinus occurred. It is concluded that the electrode measures extracellular PCO2 and that extracellular and myocardial PCO2 are essentially equal. PmCO2 rises rapidly following coronary occlusion.

Animals↗

Normal left ventricular function.

The Starling relationship in the normal human ventricle may be different than usually portrayed. In normal, resting, supine man the ventricular function curve is at its peak at a left ventricular end-diastolic pressure of approximately 10 mm Hg. Below this point is a strong direct relation between filling pressure and stroke work, while at higher filling pressures, a plateau occurs. Limitation of ventricular response is related to a sharply rising ventricular pressure-volume curve at a normal level of filling pressure. Thus, in the supine position, the normal heart is not on the active portion of the ventricular function curve, but is in a unique position in which cardiac output is probably controlled by factors other than ventricular filling pressure. In ventricular failure, the peak of the ventricular function curve is displaced to a higher level.

Blood Pressure Determination↗

Rate of rise of myocardial PCO2 during early myocardial ischemia in the dog.

We have investigated the rate of rise of myocardial PCO2 (PmCO2) after coronary artery occlusion using a new method for this measurement. Previous studies of PmCO2 have been limited by the slow response of the only available method, and no increase in MmCO2 prior to 3 minutes after occlusion has been found. We have implanted a miniature PCO2 electrode, with a 63% response time of 14 seconds, into the left ventricle of 14 open-chest dogs. After abrupt coronary occlusion, PmCO2 began to rise in 13.6 +/- 1.1 seconds in heparinized dogs and in 7.5 +/- 0.7 seconds in unheparinized dogs. The subsequent magnitude of the increase in PmCO2 was 24, 88, 171, and 222 mm Hg at 2, 5, 10, and 15 minutes after occlusion. The rate of rise of PmCO2 was essentially linear from 1 minute to 10 minutes at a rate of 18.3 mm Hg/min. The rate of rise was slower during the first 30 seconds after occlusion (6.1 mm Hg/min) and also from 30 seconds to 1 minute (9.7 mm Hg/min). This rate of rise is much greater than that previously observed and reflects the severe myocardial acidosis developing during ischemia. A rise in PmCO2 is one of the earliest metabolic changes that has been observed during myocardial ischemia.

Animals↗

Relative effect of CO2 on canine coronary vascular resistance.

We determined the effect of alterations in coronary arterial PCO2 on coronary vascular resistance (CVR) at a constant coronary sinus (CS) PO2 and the effect of coronary arterial PO2 variation on CVR at a constant CS PCO2. A linear but opposing effect on CVR was found for both gases. The sensitivity of CVR to O2 change, represented as CVR/CS PO2, was approximately twice that of the ratio CVR/CS PCO2. (0.0852 +/- 0.006 vs. -0.0362 +/- 0.005). The entire range of CVR variation obtainable through CO2 variation was as great as that resulting from O2 variation. During randomized variation of O2 and CO2, CVR can be mathematically related in a multiple linear expression to CS PO2 and CS PCO2.

Animals↗

The response of canine coronary vascular resistance to local alterations in coronary arterial P CO2.

The effect of hypercapnia on coronary vascular resistance (CVR) was studied in seven open-chest dogs. Coronary blood flow was supplied to the cannulated left main coronary artery from the femoral artery by a precision pump. Coronary arterial PCO2 was locally controlled with a small membrane oxygenator in the coronary perfusion circuit. Each PCO2 change was made at a constant coronary flow, and CVR was calculated from the ratio of perfusion pressure to flow. Coronary sinus (CS) PCO2 and PO2 were recorded continuously from blood withdrawn through a CS catheter. Normocapnia (PCO2 = 42.3 +/- 2.8 mm Hg) was obtained with a membrane oxygenator gas composition of 95% O2-5% CO2, and hypocapnia was produced with 100% O2-0% CO2. In addition to physiology normal coronary flow (determined by a CS PO2 of 20-30 mm Hg) relatively high and low flow states were studied. At a normal control CS PO2, a decrease in coronary arterial PCO2 from 42.3 +/- 2.8 to 23.8 +/- 1.3 mm Hg caused CVR to increase by 84.2%, from 1.27 +/- 0.06 to 2.30 +/- 0.04 units. Since pH was inversely related to PCO2, the effect on CVR may have been mediated through a pH change. CS PCO2 decreased from 65.2 +/- 1.9 to 39.4 +/- 1.3 mm Hg. myocardial oxygen consumption was unchanged. Increases in CVR of 74.5, 119.5, and 69.3% occurred during hypocapnia in three additional experiments in which control arterial PO2 was maintained at 52-90 mm Hg. When CS PO2 was greater than 30 mm Hg, the normocapnic CVR was high, and was only minimally increased by hypocapnia. When coronary flow was reduced to an ischemic level there was little response in CVR to hypocapnia. Thus the level of arterial PCO2 can have an important effect on CVR independent of changes in O2 consumption. Myocardial PCO2, derived from metabolically produced CO2 and contributed to by arterial CO2, may be a major factor in normal control of coronary flow.

Animals↗