Central Hemodynamics and Cardiac Output Control in Essential Hypertensive Patients

2015 ◽  
pp. 109-116 ◽  
Author(s):  
N. P. Chau ◽  
M. E. Safar ◽  
Y. A. Weiss ◽  
G. M. London ◽  
A. C. Simon ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Central Hemodynamics ◽  
Output Control ◽  
Hypertensive Patients

P3.21 CENTRAL HEMODYNAMICS PARAMETERS IN BLACK HYPERTENSIVE PATIENTS BORN AND LIVING IN SUB-SAHARAN AFRICA

2013 ◽  
Vol 7 (3-4) ◽  
pp. 132
Author(s):  
M.K. Kamdem ◽  
E.A. Birinus ◽  
D. Lemougoum ◽  
B.C. Anisiuba ◽  
J. Kaptue ◽  
...  
Keyword(s):  
Sub Saharan Africa ◽  
Central Hemodynamics ◽  
Hypertensive Patients ◽  
Sub Saharan

Cardiovascular System in the Critically Ill Patient

2019 ◽  
pp. 26-34
Author(s):  
Juan G. Ripoll Sanz ◽  
Norlalak Jiramethee ◽  
Jose L. Diaz-Gomez
Keyword(s):  
Cardiac Output ◽  
Cardiovascular System ◽  
Critically Ill ◽  
Fluid Responsiveness ◽  
Critically Ill Patients ◽  
Integrated System ◽  
Critically Ill Patient ◽  
Cardiovascular Disorders ◽  
Output Control ◽  
System 2

This chapter provides an overview of fundamental pathophysiologic concepts for the diagnosis and management of cardiovascular disorders in critically ill patients. Three major topics are presented: 1) the importance of vascular–cardiac pump coupling as an integrated system, 2) practical considerations of ventricular dysfunction, and 3) systemic vessels as a crucial factor for cardiac output control and fluid responsiveness.

Cardiovascular and Sympatho-Adrenal Responses to Mental Stress in Primary Hypertension

1993 ◽  
Vol 85 (4) ◽  
pp. 401-409 ◽  
Author(s):  
Madeleine Lindqvist ◽  
Thomas Kahan ◽  
Anders Melcher ◽  
Paul Hjemdahl
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Neuropeptide Y ◽  
Mental Stress ◽  
Forearm Blood Flow ◽  
Primary Hypertension ◽  
Hypertensive Patients ◽  
Control Subjects ◽  
Venous Plasma

1. Eleven untreated men with mild to moderate primary hypertension and 10 normotensive control subjects were studied at rest and during a mental stress test (Stroop colour word conflict test), which has previously been used in studies of hypertensive patients with regard to non-invasive cardiovascular variables and venous plasma catecholamine concentrations. 2. Heart rate, central cardiovascular pressures, cardiac output (thermodilution) and forearm blood flow (strain gauge plethysmography) were determined. Systemic and forearm vascular resistances were calculated. Arterial and venous plasma adrenaline and noradrenaline concentrations were measured by h.p.l.c., and arterial noradrenaline spillover and noradrenaline overflow from the forearm were assessed by isotope methodology ([3H]noradrenaline). Neuropeptide Y-like immunoreactivity was measured by radioimmunoassay. 3. In hypertensive patients heart rate, arterial blood pressure, cardiac output and forearm blood flow increased by 28%, 13%, 37% and 115%, respectively, and forearm and systemic vascular resistances decreased by 48% and 21%, respectively (P <0.001 for all responses), during stress. These responses were not different from those of the control group. 4. Arterial noradrenaline spillover rose by 63% and noradrenaline overflow from the forearm rose by 150% in the hypertensive patients in response to mental stress (P <0.001); no significant group differences could be demonstrated. However, the forearm noradrenaline overflow response to stress tended to be greater in the hypertensive group (P = 0.11). Arterial adrenaline concentrations doubled in both groups (P <0.001). 5. Arterial neuropeptide Y-like immunoreactivity increased slightly and similarly in the two groups (+7% in hypertensive patients and +9% in control subjects, P <0.05 for both) in response to mental stress. No net overflow of neuropeptide-Y-like immunoreactivity could be detected over the forearm. 6. It is concluded that the cardiovascular and sympatho-adrenal responses to mental stress evaluated in this study are similar in hypertensive patients and control subjects. Stress-induced vasodilatation occurs in the forearm despite signs of increased local sympathetic activity, indicating that powerful neurohormonal vasodilator mechanisms are activated by mental stress.

scholarly journals Relation between Oscillometric Measurement of Central Hemodynamics and Left Ventricular Hypertrophy in Hypertensive Patients

Pulse ◽  
2021 ◽  
pp. 1-9
Author(s):  
Masakazu Obayashi ◽  
Shigeki Kobayashi ◽  
Takuma Nanno ◽  
Yoriomi Hamada ◽  
Masafumi Yano
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Augmentation Index ◽  
Characteristic Curve ◽  
Left Ventricular ◽  
Applanation Tonometry ◽  
Central Hemodynamics ◽  
Prognostic Information ◽  
Hypertensive Patients ◽  
Significant Difference

<b><i>Introduction:</i></b> The augmentation index (AIx) or central systolic blood pressure (SBP), measured by radial applanation tonometry, has been reported to be independently associated with left ventricular hypertrophy (LVH) in Japanese hypertensive patients. Cuff-based oscillometric measurement of the AIx using Mobil-O-Graph® showed a low or moderate agreement with the AIx measurement with other devices. <b><i>Methods:</i></b> The AIx measured using the Mobil-O-Graph was validated against the tonometric measurements of the radial AIx measured using HEM-9000AI in 110 normotensive healthy individuals (age, 21–76 years; 50 men). We investigated the relationship between the central hemodynamics assessed using the Mobil-O-Graph and LVH in 100 hypertensive patients (age, 54–75 years; 48 men), presenting a wall thickness of ≥11 mm and ≥10 mm in men and women, respectively. <b><i>Results:</i></b> Although the Mobil-O-Graph-measured central AIx showed no negative values, it correlated moderately with the HEM-9000AI-measured radial AIx (<i>r</i> = 0.602, <i>p</i> &#x3c; 0.001) in the normotensive individuals. The hypertensive patients did not show a significant difference in the central SBP between the sexes, but the central AIx was lower in men than in women. The independent determinants influencing left ventricle (LV) mass index (LVMI) (<i>R</i><sup>2</sup> = 0.362; adjusted <i>R</i><sup>2</sup> = 0.329, <i>p</i> &#x3c; 0.001) were heart rate (β = −0.568 ± 0.149, <i>p</i> &#x3c; 0.001), central SBP (β = 0.290 ± 0.100, <i>p</i> = 0.005), and aortic root diameter (β = 1.355 ± 0.344, <i>p</i> = 0.001). Age (β = −0.025 ± 0.124, <i>p</i> = 0.841) and the central AIx (β = 0.120 ± 0.131, <i>p</i> = 0.361) were not independently associated with the LVMI. The area under the receiver operator characteristic curve to evaluate the diagnostic performance of the central AIx for the presence of LVH (LVMI &#x3e;118 g/m<sup>2</sup> in men or &#x3e;108 g/m<sup>2</sup> in women) was statistically significant in men (0.875, <i>p</i> &#x3c; 0.001) but not in women (0.622, <i>p</i> = 0.132). In men, a central AIx of 28.06% had a sensitivity of 83.3% and specificity of 80.0% for detecting LVH. <b><i>Conclusions:</i></b> AIx measurement in men provided useful prognostic information for the presence of LVH. Pulse-wave analysis assessed using the Mobil-O-Graph may be a valuable tool for detecting LVH in hypertensive patients.

Haemodynamic Profile of Angiotensin II Antagonism in Essential Hypertensive Patients

1979 ◽  
Vol 57 (s5) ◽  
pp. 119s-121s
Author(s):  
S. N. Hunyor ◽  
H. Larkin ◽  
Janet Rowe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Salt Intake ◽  
Peripheral Resistance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
Heart Rate Effect

1. The haemodynamic response to antagonistic (10 μg min−1 kg−1) and agonistic (40 μg min−1 kg−1) doses of saralasin was studied in young essential hypertensive patients. Blood pressure behaviour alone was thought to be inadequate to describe the response pattern. 2. Pre-saralasin setting of the renin-angiotensin axis was varied with salt intake (15 and 290 mmol of Na+/day) each for 10 days. This failed to influence blood pressure or plasma volume. 3. Antagonist blockade after low salt lowered blood pressure in three patients with the highest plasma renin values. Cardiac output rose in two of these, but it dropped in all others. 4. Decreases in cardiac output occurred with both doses of saralasin and even with suppression of the renin-angiotensin axis. This response is therefore unlikely to be due to removal of myocardial or venous angiotensin effects. 5. The renin-angiotensin system played a part in maintenance of blood pressure only with severe salt restriction and in a small proportion of cases. 6. No heart rate effect was seen with saralasin. 7. Blood pressure and total peripheral resistance responses were dependent on pre-(antagonist/ agonist) setting, but heart rate and cardiac output were not influenced by this factor.

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