Doppler Ultrasonic Assessment of Aortic Stenosis by Analysis of Axillary Arterial Blood Velocity Upstroke Time

CHEST Journal ◽  
1976 ◽  
Vol 70 (1) ◽  
pp. 48-50 ◽  
Author(s):  
Robert W. Barnes ◽  
Edward A. Rittenhouse ◽  
Edwin V. Miller
Keyword(s):  
Aortic Stenosis ◽  
Blood Velocity ◽  
Arterial Blood ◽  
Ultrasonic Assessment

Measurement of Phasic Scapular and Intercostal Collateral Arterial Blood Velocity in Coarctation of the Aorta

CHEST Journal ◽  
1973 ◽  
Vol 63 (6) ◽  
pp. 1015-1016 ◽  
Author(s):  
Alberto Benchimol ◽  
Jose Baldi ◽  
Kenneth B. Desser
Keyword(s):  
Coarctation Of The Aorta ◽  
Blood Velocity ◽  
Arterial Blood

Big endothelin-1 is not a predictor in aortic stenosis, but is related to arterial blood pressure

2006 ◽  
Vol 113 (2) ◽  
pp. 174-180 ◽  
Author(s):  
Jutta Bergler-Klein ◽  
Ursula Klaar ◽  
Maria Heger ◽  
Raphael Rosenhek ◽  
Harald Gabriel ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Aortic Stenosis ◽  
Arterial Blood Pressure ◽  
Endothelin 1 ◽  
Arterial Blood

scholarly journals Influence of myocardial oxygen demand on the coronary vascular response to arterial blood gas changes in humans

2018 ◽  
Vol 315 (1) ◽  
pp. H132-H140 ◽  
Author(s):  
Tyler D. Vermeulen ◽  
Lindsey M. Boulet ◽  
Mike Stembridge ◽  
Alexandra M. Williams ◽  
James D. Anholm ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Adrenergic Receptor ◽  
Blood Velocity ◽  
Rate Pressure Product ◽  
Receptor Blockade ◽  
Vascular Response ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
The Mean ◽  
Adrenergic Receptor Blockade

It remains unclear if the human coronary vasculature is inherently sensitive to changes in arterial Po2 and Pco2 or if coronary vascular responses are the result of concomitant increases in myocardial O2 consumption/demand ([Formula: see text]). We hypothesized that the coronary vascular response to Po2 and Pco2 would be attenuated in healthy men when [Formula: see text] was attenuated with β1-adrenergic receptor blockade. Healthy men (age: 25 ± 1 yr, n = 11) received intravenous esmolol (β1-adrenergic receptor antagonist) or volume-matched saline in a double-blind, randomized crossover study and were exposed to poikilocapnic hypoxia, isocapnic hypoxia, and hypercapnic hypoxia. Measurements made at baseline and after 5 min of steady state at each gas manipulation included left anterior descending coronary blood velocity (LADV; Doppler echocardiography), heart rate, and arterial blood pressure. LADV values at the end of each hypoxic condition were compared between esmolol and placebo. The rate-pressure product (RPP) and left ventricular mechanical energy (MELV) were calculated as indexes of [Formula: see text]. All gas manipulations augmented RPP, MELV, and LADV, but only RPP and MELV were attenuated (4–18%) after β1-adrenergic receptor blockade ( P < 0.05). Despite attenuated RPP and MELV responses, β1-adrenergic receptor blockade did not attenuate the mean LADV vasodilatory response compared with placebo during poikilocapnic hypoxia (29.4 ± 2.2 vs. 27.3 ± 1.6 cm/s) and isocapnic hypoxia (29.5 ± 1.5 vs. 30.3 ± 2.2 cm/s). Hypercapnic hypoxia elicited a feedforward coronary dilation that was blocked by β1-adrenergic receptor blockade. These results indicate a direct influence of arterial Po2 on coronary vascular regulation that is independent of [Formula: see text]. NEW & NOTEWORTHY In humans, arterial hypoxemia led to an increase in epicardial coronary artery blood velocity. β1-Adrenergic receptor blockade did not diminish the hypoxemic coronary response despite reduced myocardial O2 demand. These data indicate hypoxemia can regulate coronary blood flow independent of myocardial O2 consumption. A plateau in the mean left anterior descending coronary artery blood velocity-rate-pressure product relationship suggested β1-adrenergic receptor-mediated, feedforward epicardial coronary artery dilation. In addition, we observed a synergistic effect of Po2 and Pco2 during hypercapnic hypoxia.

Effect of coronary stenosis on phasic pattern of septal artery in dogs

1992 ◽  
Vol 262 (6) ◽  
pp. H1690-H1698 ◽  
Author(s):  
A. Kimura ◽  
O. Hiramatsu ◽  
T. Yamamoto ◽  
Y. Ogasawara ◽  
T. Yada ◽  
...  
Keyword(s):  
Coronary Stenosis ◽  
Coronary Perfusion Pressure ◽  
Blood Velocity ◽  
Arterial Stenosis ◽  
Coronary Perfusion ◽  
Retrograde Flow ◽  
Complete Occlusion ◽  
Arterial Blood ◽  
Before And After ◽  
Adenosine Administration

To analyze the effect of coronary stenosis on the phasic pattern of blood flow velocity into the myocardium, we measured septal artery blood velocities under control conditions, i.e., no stenosis (N), with moderate (S1) and severe (S2) proximal coronary arterial stenosis, and during complete occlusion. In eight anesthetized open-chest dogs, the blood velocity measurements were performed using our 20-MHz multichannel pulsed Doppler method before and after intracoronary adenosine administration. Under N, the coronary perfusion pressure was set to approximately 100 mmHg, with S1 the poststenotic pressure was approximately 60 mmHg, and with S2 it was decreased to 35 mmHg. Septal arterial blood velocity area, which is the time-integrated envelope of the velocity, was divided into three components; systolic retrograde velocity area, systolic anterograde velocity area, and diastolic anterograde velocity area. There were no significant changes from N to S1 in any of the three velocity areas, which is a measure of the flow. Total inflow decreased from N to S2 by 52% (P less than 0.05). Diastolic anterograde flow decreased from N to S2 by 32% (P less than 0.05). Systolic retrograde flow increased from N to S2 by 75% (P less than 0.05). Systolic anterograde flow was almost unchanged by increasing stenosis. After complete occlusion, the septal artery exhibited a to-and-fro flow pattern. Adenosine-induced vasodilation reduced poststenotic pressure (P less than 0.05) and enhanced systolic retrograde flow without a significant increase in diastolic anterograde flow. Systolic retrograde flow increased at S1 by 49% (P less than 0.05) and at S2 by 27% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Augmented cerebral blood velocity in response to isometric handgrip exercise in women with a history of preeclampsia

2019 ◽  
Vol 317 (6) ◽  
pp. R834-R839
Author(s):  
Kathleen B. Miller ◽  
Virginia M. Miller ◽  
Ronée E. Harvey ◽  
Sushant M. Ranadive ◽  
Michael J. Joyner ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Recovery Period ◽  
Blood Velocity ◽  
Hypertensive Disorder ◽  
Isometric Handgrip ◽  
Arterial Blood ◽  
Increased Risk ◽  
Cerebral Blood Velocity ◽  
History Of ◽  
Isometric Handgrip Exercise

Preeclampsia (PE) is a hypertensive disorder of pregnancy described as a condition of excessive sympathoexcitation. PE places a woman at increased risk for lifelong hypertension and cognitive impairment. Cerebral blood velocity is blunted in response to a vasoactive stimulus in women with a history of PE. This study investigated how a sympathoexcitatory stimulus affects cerebral blood velocity in women with a history of PE. Middle cerebral artery blood velocity (MCAv) and beat-to-beat mean arterial blood pressure (MAP) were measured in postmenopausal women with a history of PE ( n = 21; age = 59 ± 5 yr) and a history of a normotensive pregnancy (NP; n = 27; age = 58 ± 4 yr), at baseline, during isometric handgrip to fatigue (IHG) followed by postexercise ischemia (PEI), and a recovery period (REC). Baseline MAP and MAP responses to IHG and PEI did not differ between groups. MCAv at baseline and throughout the stimulus was lower in PE women compared with NP women ( P < 0.05 for all). MCAv increased during IHG in both groups ( P < 0.05). This increase in MCAv was greater in PE compared with NP women during IHG and REC (IHG: PE 13 ± 2% vs. NP 9 ± 2%; REC: PE 3 ± 2% vs. NP −2 ± 2%; P < 0.05 for both). Thus, a history of PE is associated with low baseline cerebral blood velocity but an augmented response to a sympathoexcitatory stimulus. These changes in cerebral blood flow regulation may lead to an increased risk for cognitive impairment in women with a history of PE.

Effect of Pneumothorax-lnduced Systemic Blood Pressure Alterations on the Cerebral Circulation in Newborn Dogs

PEDIATRICS ◽  
1984 ◽  
Vol 74 (3) ◽  
pp. 350-353
Author(s):  
Daniel G. Batton ◽  
Jonathan Hellmann ◽  
Elizabeth E. Nardis
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Premature Infants ◽  
Mean Arterial Blood Pressure ◽  
Cerebral Circulation ◽  
Intraventricular Hemorrhage ◽  
Blood Velocity ◽  
Arterial Blood ◽  
Cerebral Blood Velocity ◽  
Rapid Evacuation

Pneumothorax has been associated with intraventricular hemorrhage in premature infants, although the mechanism for this relationship is not clear. Because alterations in cerebral blood flow are believed to be important in the pathogenesis of intraventricular hemorrhage, the effect of induced pneumothorax and subsequent evacuation on the cerebral circulation in 16 newborn dogs was evaluated. Continuous Doppler ultrasound was used to monitor changes in cerebral blood velocity. Pneumothorax was induced by slow infusion (5 cc/kg/min) or rapid infusion (5 to 10 seconds) of air to reduce mean arterial blood pressure to half of base-line levels. Both methods of pneumothorax induction resulted in significant elevations of central venous pressure and intrapleural pressure, whereas mean arterial blood pressure and cerebral blood velocity decreased significantly. In each group, the pneumothorax was evacuated either by slow withdrawal of air (10 cc/kg/min) or as rapidly as possible. Rapid evacuation of air resulted in an immediate increase in mean arterial blood pressure and cerebral blood velocity to supranormal levels. Slow evacuation led to a more gradual normalization of mean arterial blood pressure and cerebral blood velocity. It is suggested that the precipitous increases in mean arterial blood pressure and cerebral blood velocity following rapid evacuation of a tension pneumothorax may account for the observed association between pneumothorax and intraventricular hemorrhage in premature infants.

Effect of CO2 on the ventilatory sensitivity to rising body temperature during exercise

2011 ◽  
Vol 110 (5) ◽  
pp. 1334-1341 ◽  
Author(s):  
Keiji Hayashi ◽  
Yasushi Honda ◽  
Natsuki Miyakawa ◽  
Naoto Fujii ◽  
Masashi Ichinose ◽  
...  
Keyword(s):  
Body Temperature ◽  
Prolonged Exercise ◽  
Minute Ventilation ◽  
Regression Line ◽  
Cycle Ergometer ◽  
Blood Velocity ◽  
Esophageal Temperature ◽  
Arterial Blood ◽  
End Tidal ◽  
Respiratory Gases

We examined the degree to which ventilatory sensitivity to rising body temperature (the slope of the regression line relating ventilation and body temperature) is altered by restoration of arterial Pco2 to the eucapnic level during prolonged exercise in the heat. Thirteen subjects exercised for ∼60 min on a cycle ergometer at 50% of peak O2 uptake with and without inhalation of CO2-enriched air. Subjects began breathing CO2-enriched air at the point that end-tidal Pco2 started to decline. Esophageal temperature (Tes), minute ventilation (V̇e), tidal volume (VT), respiratory frequency ( fR), respiratory gases, middle cerebral artery blood velocity, and arterial blood pressure were recorded continuously. When V̇e, VT, fR, and ventilatory equivalents for O2 uptake (V̇e/V̇o2) and CO2 output (V̇e/V̇co2) were plotted against changes in Tes from the start of the CO2-enriched air inhalation (ΔTes), the slopes of the regression lines relating V̇e, VT, V̇e/V̇o2, and V̇e/V̇co2 to ΔTes (ventilatory sensitivity to rising body temperature) were significantly greater when subjects breathed CO2-enriched air than when they breathed room air (V̇e: 19.8 ± 10.3 vs. 8.9 ± 6.7 l·min−1·°C−1, VT: 18 ± 120 vs. −81 ± 92 ml/°C; V̇e/V̇o2: 7.4 ± 5.5 vs. 2.6 ± 2.3 units/°C, and V̇e/V̇co2: 7.6 ± 6.6 vs. 3.4 ± 2.8 units/°C). The increase in V̇e was accompanied by increases in VT and fR. These results suggest that restoration of arterial Pco2 to nearly eucapnic levels increases ventilatory sensitivity to rising body temperature by around threefold.

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