scholarly journals Validation of stroke volume and cardiac output by electrical interrogation of the brachial artery in normals: assessment of strengths, limitations, and sources of error

2015 ◽  
Vol 29 (6) ◽  
pp. 789-800 ◽  
Author(s):  
Donald P. Bernstein ◽  
Isaac C. Henry ◽  
Harry J. Lemmens ◽  
Janell L. Chaltas ◽  
Anthony N. DeMaria ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Brachial Artery ◽  
Sources Of Error

Elevated Tricuspid Regurgitation Jet Correlates with Decreased Brachial Artery Relaxivity In Sickle Cell Anemia Patients on Chronic Transfusion Therapy.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1645-1645
Author(s):  
Jon Detterich ◽  
Adam Bush ◽  
Roberta Miyeko Kato ◽  
Suvimol Sangkatumvong ◽  
Daniel Gardner ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Sickle Cell Anemia ◽  
Brachial Artery ◽  
Tricuspid Regurgitation ◽  
Reticulocyte Count ◽  
Transfusion Therapy ◽  
Plasma Hemoglobin ◽  
Hs Crp

Abstract Abstract 1645 Introduction: Vascular disease in both pulmonary and systemic vessels underlies most complications of sickle cell anemia (SCA). Multiple mechanisms contribute to this process, including inflammation, oxidative stress and decreased nitric oxide bioavailability. Chronic transfusion therapy (CTT) is thought to ameliorate some of these factors. Our goal was to determine the relationship between systemic vascular function, as indexed by flow mediated dilation (FMD), and elevated tricuspid regurgitation jet (TRJ) as a surrogate for pulmonary hypertension (PH), in chronically transfused SCA patients. Methods: 25 SCA patients on CTT were enrolled in a prospective cross sectional study between August 2008 and June 2010; the protocol was approved by our IRB. Patients were studied on the day of transfusion prior to receiving blood and then again between 24 and 120 hours post transfusion. Echocardiography, brachial artery FMD and blood sampling for CBC, reticulocyte count, LDH, plasma hemoglobin and hs-CRP were performed during each study visit. A TRJ of 2.5 m/s or higher was defined as “pulmonary hypertension” and an FMD of <8% was considered abnormal based on published data for our protocol. Pre and post transfusion data were analyzed using paired T-tests with linear regression used for univariate correlations with FMD and TRJ. Results: Table 1 summarizes pre and post transfusion results. A TRJ > 2.5 m/s was seen in 20% of patients pre-transfusion and in 12% post-transfusion, but this difference did not reach statistical significance. None of the patients with a TRJ < 2.5m/s pre transfusion had a TRJ > 2.5m/s post transfusion. FMD was significantly improved consequent to transfusion (5.4% to 6.8%, p<0.02) and was abnormal in 77% patients pre transfusion and in 64% post transfusion. As expected, transfusion increased Hb and hct and decreased %HbS, reticulocyte count and plasma hemoglobin; LDH and hs-CRP were unchanged. TRJ inversely correlated with FMD (r= -0.21, p=0.0014); all patients with TRJ > 2.5 m/s exhibited blunted FMD response. Abnormal TRJ and FMD correlated with elevated reticulocyte count, LDH, %Hb S, and prolonged left ventricular ejection time and isovolumic contraction time. FMD was directly correlated with hct and Hb and inversely correlated with stroke volume and cardiac output. There was a trend towards an inverse correlation of FMD with plasma hemoglobin, arginine/ ornithine ratio and high sensitivity CRP. Discussion: CTT offers incomplete protection from vascular disease in both the systemic and pulmonary beds. Patients with elevated TRJ > 2.5m/s also had abnormal FMD: both correlated with markers of hemolysis, increased %HbS as well as prolonged cardiac time intervals. Abnormal FMD, but not TRJ, was correlated with decreased Hb and hct and increased cardiac output and stroke volume, suggesting that worsening anemia affects FMD to a greater degree than TRJ. These data support the concept that pulmonary hypertension in SCA is only one manifestation of pan-systemic endothelial disease. Disclosures: Coates: Novartis: Research Funding, Speakers Bureau.

MECHANISMS OF ADAPTATION OF THE LEFT VENTRICLE TO MUSCULAR EXERCISE

PEDIATRICS ◽  
1963 ◽  
Vol 32 (4) ◽  
pp. 660-670
Author(s):  
Jere H. Mitchell
Keyword(s):  
Cardiac Output ◽  
Left Ventricle ◽  
Stroke Volume ◽  
Pulse Rate ◽  
Individual Factors ◽  
Normal Male ◽  
Oxygen Intake ◽  
Mechanisms Of Adaptation ◽  
Male Subjects ◽  
Oxygen Difference

THE mechanisms of adaptation of the left ventricle to the demands of muscular exercise have intrigued cardiovascular physiologists for many years. Although highly complex, these adaptive mechanisms are more and more susceptible to analysis and quantification. In this presentation I will attempt to identify some of the individual factors which appear to be important in the response of the left ventricle to exercise, beginning with data obtained from experiments on conscious normal male subjects and proceeding to experiments performed on dog preparations in which individual factors were controlled and analyzed. The changes in oxygen intake, cardiac output, estimated arteriovenous oxygen difference, pulse rate and estimated mean stroke volume were determined in 15 normal male subjects during rest in the standing position and during treadmill exercise at the maximal oxygen intake level. Oxygen intake was obtained from the volume and composition of expired air, cardiac output by the dye dilution technique, and pulse rate from the electrocardiogram. Estimated arteriovenous oxygen difference was obtained by dividing the oxygen intake by the cardiac output (Fick principle) and estimated mean stroke volume by dividing the cardiac output by the heart rate. The data are shown in Figure 1. Oxygen intake increased from a mean value of 0.34 at rest to a maximal value of 3.22 L./min. The corresponding mean values for cardiac output were 5.4 and 23.4 L./min. and for arteriovenous oxygen difference were 6.5 and 14.3 ml./100 ml. Thus, as oxygen intake increased 9.5 times, the cardiac output increased 4.3 times and the arterio venous oxygen difference 2.2 times.

Cardiac Output Changes in Newborns With Hyperbilirubinemia Treated With Phototherapy

PEDIATRICS ◽  
1985 ◽  
Vol 76 (6) ◽  
pp. 918-921
Author(s):  
Frans J. Walther ◽  
Paul Y. K. Wu ◽  
Bijan Siassi
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Skin Blood Flow ◽  
Peripheral Blood ◽  
Cardiovascular Effects ◽  
Tissue Perfusion ◽  
Peripheral Blood Flow ◽  
Limb Blood Flow ◽  
Term Infants

Phototherapy is known to increase peripheral blood flow in neonates, but information on the associated cardiovascular effects is not available. Using pulsed Doppler echocardiography we evaluated cardiac output and stroke volume in 12 preterm and 13 term neonates during and after phototherapy. We concomitantly measured arterial limb blood flow by strain gauge plethysmography and skin blood flow by photoplethysmography. Cardiac output decreased by 6% due to reduced stroke volume during phototherapy, whereas total limb blood flow and skin blood flow increased by 38% and 41%, respectively. Peripheral blood flow increments tended to be higher in the preterm than in the term infants. The reduced stroke volume during phototherapy may be an expression of reduced activity of the newborn during phototherapy. For healthy neonates the reduction in cardiac output is minimal, but for sick infants with reduced cardiac output, this reduction may further aggravate the decrease in tissue perfusion.

Long-term hemodynamic actions of atrial natriuretic factor (99-126) in conscious sheep

1988 ◽  
Vol 254 (4) ◽  
pp. H811-H815 ◽  
Author(s):  
D. G. Parkes ◽  
J. P. Coghlan ◽  
J. G. McDougall ◽  
B. A. Scoggins
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Blood Volume ◽  
Total Peripheral Resistance ◽  
Atrial Natriuretic Factor ◽  
Peripheral Resistance ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The hemodynamic and metabolic effects of long-term (5 day) infusion of human atrial natriuretic factor (ANF) were examined in conscious chronically instrumented sheep. Infusion of ANF at 20 micrograms/h, a rate below the threshold for an acute natriuretic effect, decreased blood pressure by 9 +/- 1 mmHg on day 5, associated with a fall in calculated total peripheral resistance. On day 1, ANF reduced cardiac output, stroke volume, and blood volume, effects that were associated with an increase in heart rate and calculated total peripheral resistance and a small decrease in blood pressure. On days 4 and 5 there was a small increase in urine volume and sodium excretion. On day 5 an increase in water intake and body weight was observed. No change was seen in plasma concentrations of renin, arginine vasopressin, glucose, adrenocorticotropic hormone, or protein. This study suggests that the short-term hypotensive effect of ANF results from a reduction in cardiac output associated with a fall in both stroke volume and effective blood volume. However, after 5 days of infusion, ANF lowers blood pressure via a reduction in total peripheral resistance.

Physiological factors associated with the lower maximal oxygen consumption of master runners

1989 ◽  
Vol 66 (2) ◽  
pp. 949-954 ◽  
Author(s):  
A. M. Rivera ◽  
A. E. Pels ◽  
S. P. Sady ◽  
M. A. Sady ◽  
E. M. Cullinane ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Maximal Oxygen Consumption ◽  
Maximal Heart Rate ◽  
Distance Runners ◽  
Physiological Factors ◽  
Factors Associated ◽  
Older Athletes ◽  
Maximal Cardiac Output

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.

Genome-wide linkage scan for exercise stroke volume and cardiac output in the HERITAGE Family Study

2002 ◽  
Vol 10 (2) ◽  
pp. 57-62 ◽  
Author(s):  
Tuomo Rankinen ◽  
Ping An ◽  
Louis Pérusse ◽  
Treva Rice ◽  
Yvon C. Chagnon ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Black Family ◽  
Potential Candidate ◽  
Nuclear Families ◽  
Sibling Pairs ◽  
Suggestive Evidence ◽  
Genome Wide ◽  
A Genome ◽  
Analytical Strategies

A genome-wide linkage scan was performed for genes affecting submaximal exercise cardiac output (Q) and stroke volume (SV) in the sedentary state and their responses to a standardized 20-wk endurance training program. A total of 509 polymorphic markers were used, and 328 pairs of siblings from 99 white nuclear families and 102 sibling pairs from 105 black family units were available. Q and SV were measured in relative steady state during exercise at 50 W (Q50 and SV50, respectively). Baseline phenotypes were adjusted for age, sex, and body surface area (BSA), and the training responses (post-training − baseline, Δ) were adjusted for age, sex, baseline BSA, and baseline value of the phenotype. Three analytical strategies were used: a multipoint variance components linkage analysis using all the family data, and regression-based single- and multipoint linkage analyses using pairs of siblings. In whites, baseline SV50 and ΔSV50 showed promising linkages ( P < 0.0023) with markers on chromosomes 14q31.1 and 10p11.2, respectively. Suggestive evidence of linkage (0.01 > P > 0.0023) for ΔSV50 and Δ Q50 was detected on chromosome 2q31.1 and for baseline SV50 and Q50 on chromosome 9q32-q33. In blacks, markers on 18q11.2 showed promising linkages with baseline Q50. Suggestive evidence of linkage was found in three regions for baseline SV50 (1p21.3, 3q13.3, 12q13.2) and one for baseline SV50 and Q50 (10p14). All these chromosomal regions include several potential candidate genes and therefore warrant further studies in the HERITAGE cohort and other studies.

Breathing through an inspiratory threshold device improves stroke volume during central hypovolemia in humans

2008 ◽  
Vol 104 (5) ◽  
pp. 1402-1409 ◽  
Author(s):  
Kathy L. Ryan ◽  
William H. Cooke ◽  
Caroline A. Rickards ◽  
Keith G. Lurie ◽  
Victor A. Convertino
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Lower Body Negative Pressure ◽  
Systolic Arterial Pressure ◽  
Intrathoracic Pressure ◽  
Subsequent Increase ◽  
Arterial Blood ◽  
Threshold Device ◽  
Inspiratory Resistance

Inspiratory resistance induced by breathing through an impedance threshold device (ITD) reduces intrathoracic pressure and increases stroke volume (SV) in supine normovolemic humans. We hypothesized that breathing through an ITD would also be associated with a protection of SV and a subsequent increase in the tolerance to progressive central hypovolemia. Eight volunteers (5 men, 3 women) were instrumented to record ECG and beat-by-beat arterial pressure and SV (Finometer). Tolerance to progressive lower body negative pressure (LBNP) was assessed while subjects breathed against either 0 (sham ITD) or −7 cmH2O inspiratory resistance (active ITD); experiments were performed on separate days. Because the active ITD increased LBNP tolerance time from 2,014 ± 106 to 2,259 ± 138 s ( P = 0.006), data were analyzed (time and frequency domains) under both conditions at the time at which cardiovascular collapse occurred during the sham experiment to determine the mechanisms underlying this protective effect. At this time point, arterial blood pressure, SV, and cardiac output were higher ( P ≤ 0.005) when breathing on the active ITD rather than the sham ITD, whereas indirect indicators of autonomic activity (low- and high-frequency oscillations of the R-to-R interval) were not altered. ITD breathing did not alter the transfer function between systolic arterial pressure and R-to-R interval, indicating that integrated baroreflex sensitivity was similar between the two conditions. These data show that breathing against inspiratory resistance increases tolerance to progressive central hypovolemia by better maintaining SV, cardiac output, and arterial blood pressures via primarily mechanical rather than neural mechanisms.

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