Increase In Total Peripheral Resistance Index Research Articles

Non‐invasive measurement of cardiac output by whole‐body bio‐impedance during dobutamine stress echocardiography: Clinical implications in patients with left ventricular dysfunction and ischaemia

To compare non-invasive determination of cardiac index (CI) by whole body electrical bioimpedance using the NICaS apparatus and Doppler echocardiography, and the role of cardiac power index (Cpi) and total peripheral resistance index (TPRi) calculation during dobutamine stress echocardiography (DSE). We enrolled 60 consecutive patients undergoing DSE. Patients were prospectively divided into 3 groups: Group 1 (n = 20): normal DSE (control). Group 2 (n = 20): EF<40% without significant ischaemia. Group 3 (n = 20): patients with significant ischaemia on DSE. Measurements of CI were performed at the end of each stage of DSE by both echocardiographic left ventricular outflow track flow and the NICaS apparatus, using whole-body bio-impedance. MAP was measured simultaneously and TPRi and Cpi were calculated. The correlation between non-invasive CI as determined by NICaS and echocardiography was 0.81, although Echocardiographic readings of CI were higher during administration of higher doses of dobutamine. Lower EF correlated with lower Cpi, especially stress induced Cpi. Hence, patients with reduced EF (group 2) had a blunted increase in Cpi during stress. Patients with ischaemia (group 3) had a blunted increase in Cpi as well as a decrease in Cpi and increase in TPRi during the last stages of DSE. Measurement of CI by NICaS correlated well with Doppler derived CI. The calculation of Cpi and TPRi changes during dobutamine stress may provide important clinical information.

Hypotension during hemodialysis results from an impairment of arteriolar tone and left ventricular function

Hypotensive episodes are a major complication of hemodialysis. Hypotension during dialysis could be directly related to a reduction in blood volume or to a decrease in cardiovascular activation as a response to decreased cardiac filling. A decreased cardiovascular activation could be due to patient-related or to dialysis-related factors. In order to study the isolated effect of a reduction in filling pressure, lower body negative pressure (LBNP) causes activation of the cardiovascular reactivity with a decrease in cardiac filling, but without the influence of the dialysis procedure that could affect cardiovascular reactivity. We studied the relationship between relative blood volume (RBV), central venous pressure (CVP), systolic arterial pressure, heart rate, stroke volume index (SI), and total peripheral resistance index (TPRI) during a combined dialysis/ultrafiltration and during LBNP to -40 mmHg in 21 hemodialysis patients with a high incidence of hypotension. Systolic arterial pressure, heart rate, SI and TPRI were measured by Finapres. CVP was measured after cannulation of the jugular vein. During dialysis RBV was measured by a blood volume monitor (BVM). In order to study the conditions in which hypotension occurred after dialysis, we divided the patients into 2 groups: hypotensive (H) and non-hypotensive (NH) during dialysis. Baseline levels did not show any significant differences. During dialysis systolic arterial pressure declined gradually in the H group from 30 minutes before the onset of hypotension. There was a similar decrease of RBV and increase of heart rate in both groups with a large interindividual variation. At hypotension, H patients showed a significantly smaller increase in TPRI as compared to NH patients. The reduction in SI tended to be greater at hypotension, while CVP decreased to a similar extent in both groups. Moreover, during LBNP, a similar reduction in CVP resulted in a much smaller decrease in SI. Systolic arterial pressure was only slightly lowered due to a much greater increase in TPRI. We conclude that dialysis-related hypotension in our patient group did not result from an inability to maintain blood volume or from decreased cardiac filling. Hypotension appeared to result from the inability to adequately increase arteriolar tone and a reduction in left ventricular function. Both vascular tone and left ventricular function appeared to be impaired by the dialysis procedure.

Hemodynamic mechanism of the elevation in blood pressure following the improvement of anemia with recombinant human erythropoietin.

Following the administration of recombinant human erythropoietin (rHuEPO) to 18 patients undergoing hemodialysis, the hematocrit (Ht) increased from 19.7 +/- 1.8 to 31.0 +/- 2.0%. The incidence of hypertension according to the criteria of WHO was 11.1%. The systolic blood pressure (SBP) increased significantly from 120 +/- 21 to 129 +/- 26 mmHg (p less than 0.01) and diastolic blood pressure (DBP) increased from 67 +/- 14 to 73 +/- 12 mmHg (p less than 0.05). The cardiac index (CI) decreased significantly from 4.07 +/- 1.13 to 3.56 +/- 0.88 L/min/m2 (p less than 0.05). Total peripheral resistance index (TPRI) and blood volume (BV) increased significantly from 1,725 +/- 406 to 2,170 +/- 643 dynes/sec/cm-5/m2 (p less than 0.001) and from 78.9 +/- 11.2 to 87.8 +/- 14.8 ml/kg (p less than 0.005) respectively. Pulse rate (PR) decreased significantly from 73.0 +/- 10.7 to 65.9 +/- 7.8 beats/min (p less than 0.01). Patients who developed a blood pressure (BP) elevation of 10% or more for the mean blood pressure (MBP) showed a slight and insignificant decrease in CI from 3.65 +/- 1.12 to 3.49 +/- 1.06 L/min/m2, which clearly contrasted to that in another group of patients who showed a reduced increase in MBP and a significant reduction in CI from 4.50 +/- 1.03 to 3.63 +/- 0.72 L/min/m2 (p less than 0.05). Stroke volume index (SVI) was unchanged in both groups but PR decrease significantly in the latter group. A significant increase in TPRI or BV was observed equally in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The role of multiple action agents in hypertension

A 20-year follow-up study of central hemodynamics in essential hypertension at rest and during exercise in 61 men with uncomplicated essential hypertension has clearly shown that hemodynamic disturbances depend on the age of the subjects and the severity of the hypertensive state and that a shift in the hemodynamic alterations take place over time. During 10- and 20-year follow-up, central hemodynamics changed towards a low cardiac-index (CI)-high total peripheral-resistance index (TPRI) pattern. With increasing age there was a gradual reduction in CI as well as stroke index (SI). The arteriovenous oxygen difference increased, particularly during exercise. The 20-year treatment with conventional drugs (beta-blockers and/or diuretics) did not prevent a marked increase in TPRI and a marked reduction in CI and SI in subjects initially 40-49 years of age. In recent years, beta-blockers with vasodilating activity have been introduced in the treatment of hypertension (labetalol, prizidilol, dilevalol and carvedilol). The hemodynamic effects of these compounds clearly differ from the changes induced during acute and chronic conventional beta-blocking treatment. In contrast to usual beta-blockers, these drugs reduce TPRI acutely and the reductions they produce in heart rate (HR) and CI are considerably lower. Our long-term data on labetalol (n = 15), prizidilol (n = 15) and dilevalol (n = 17) indicate a persistent reduction in TPRI and little or no decrease in exercise CI. Long-term data on carvedilol are not yet available. Approximately 70% of patients with mild to moderately severe essential hypertension achieved normal blood pressure during chronic treatment on beta-blockers with vasodilating activity.

Acute arteriolar vasoconstriction following furosemide in conscious spontaneously hypertensive rats

In a previous study in conscious spontaneously hypertensive rats (SHR), we observed an immediate decrease in the cardiac index (CI) and an increase in the total peripheral resistance index (TPRI) following the administration of furosemide. The present study was designed to evaluate the regional hemodynamic effects and the involvement of sinoaortic baroreceptors in the increase in TPRI. In SHR instrumented for the measurement of central hemodynamics, 8 mg·kg −1 furosemide decreased CI from 31.0 ± 2.5 ml · min −1 · 100 g bw −1 by 9.5 ± 1.3 ml · min −1 · 100 g bw −1 (n = 7). TPRI increased maximally from 5.7 ± 0.8 by 2.7 ± 0.5 mm Hg · min · 100 g bw · ml −1. The effect on TPRI was not affected by sinoaortic denervation (SAD) to abolish arterial baroreflexes. However, furosemide induced a significantly greater decrease in CI (−12.6 ± 1.2 ml · min −1 · 100 g bw −1; n =7) after SAD, Furosemide effectively reduced the mean arterial pressure in SAD SHR (−21 ± 9 mm Hg) but not in sham-denervated SHR. Furosemide (8 mg · kg −1) reduced renal, mesenteric and hindquarter blood flow to a comparable extent (approximately 20%) in intact SHR. The reduction in renal flow at 3.5 min after injection (−17.9 ± 4.1%; n = 8) was significantly greater than the reduction in mesenteric (−7.1 ± 4.7%) and hindquarter blood flow (−4.2 ± 3.7%), suggesting that the renal bed responds faster. Thereafter, the flow reductions in the three beds were not different. The results show that furosemide causes a general vasoconstriction in conscious SHR. Renal vasodilatation, which has been suggested to occur and to contribute to the diuretic response, was never observed. Sinoaortic baroreceptor reflexes prevent the blood pressure from falling in the face of a reduced cardiac output and do so by limiting the cardiac effect, rather than affecting the total peripheral resistance.

Age Hemodynamics and Exercise in Essential Hypertension

The hemodynamic disturbances behind increased blood pressure (BP) differ widely and depend on the patient's age as well as on the severity of the hypertensive state. During the last 20 years we have studied central hemodynamics with the same invasive methods in groups of hypertensive patients at rest and exercising. [BP recorded intra-arterially in the brachial artery and cardiac output (CO) measured by dye dilution method, Cardiogreen.] In elderly hypertensive subjects (60-69 years) with almost the same mean resting arterial BP [mean arterial pressure (MAP) = 113 mm Hg] as a young group (17-29 years, MAP = 114.1 mm Hg) cardiac index (CI) was 2.17 L/min m2 (or 42% lower), and total peripheral resistance index (TPRI) was 4,223 dyn/s cm-5m2 (or 69% higher). The increase in MAP during exercise was much steeper in the older group. During 150 W exercise TPRI was about twice as high whereas CI was only about half of that in the younger group. Arteriovenous oxygen (AVO2) difference was markedly increased and stroke index fell when subjects were in transition from submaximal to maximal work, probably early markers of incipient heart insufficiency during work. Most data on drug effects are based on studies in middle aged subjects. The typical response to nonselective or selective beta-blockers without intrinsic sympathomimetic activity (ISA) (agents such as propranolol, timolol, atenolol and metoprolol) is a BP reduction through a fall in CI and heart rate (HR) of approximately 20-25% when subjects were at rest and exercising. Initially there is an increase in TPRI that prevents BP from falling, but with time TPRI is downregulated, and BP falls.(ABSTRACT TRUNCATED AT 250 WORDS)

β遮断薬ｂｉｌｉｓｏｌｏｌおよびα遮断薬ｄｏｘａｚｏｓｉｎの本態性高血圧の循環動態におよぼす影響

To investigate the hemodynamic effects of tilisolol (N-696), a new β-blocking agent with vasodilating property, and doxazosin, a new α-blocking agent, cardiac performance by RI angiocardiography using 99mTc in vivo-labelled red cells was studied by introducing the drugs orally to 22 outpatients with essential hypertension.These two drugs reduced blood pressure significantly (P<0.005) with different changes in heart rate; tilisolol reduced heart rate, though doxazosin did not. Cardiac index decreased in the tilisolol-treated group (3.28±0.15to2.85±0.09l/min/m2, P<0.01), but the change was not significant in the doxazosin-treated group.Tilisolol and doxazosin induced no significant change in left ventricular ejection fraction . Total peripheral resistance index (TPRI) stayed at pretreatment level in the tilisolol-treated group (3, 161±194 to 3, 167±89 dyn·sec·cm-5·m2);however, TPRI decreased in the doxazosin-treated group (3, 072±166 to 2, 546±207dyn·sec·cm-5·m2, P<0.01).These two drugs did not induce any significant change in circulating blood volume evaluated by 131I-labelled human serum albumin.Tilisolol a non-selective β-blocking agent with vasodilating property, reduced cardiac output without any significant change in TPRI . As tilisolol was reported to have no in trinsic sympathomimetic activity (ISA) on vascular β2-receptors in animal experiments, its direct vasodilating property was assumed to counteract and minimize an increase in TPRI induced by vascular β2-receptor blocking action and reduced cardiac pump function .Hemody namic effiects induced by doxazosin may be explained mainly by its vascular α1-receptor blockade with a resultant decrease in TPRI .

Hemodynamic characterization of hypertension induced by chronic intrarenal or intravenous infusion of norepinephrine in conscious rats.

The present study was designed to determine the hemodynamic changes underlying the hypertension induced by chronic intrarenal infusion of norepinephrine (NE) in conscious rats. NE was infused for a 5-day period intrarenally with osmotic minipumps via a chronic catheter in the right suprarenal artery at rates of 4 and 36 micrograms . kg-1 . hr-1 or intravenously at a rate of 36 micrograms . kg-1 . hr-1. Control rats received a 1 microliter . hr-1 intrarenal infusion of pyrogen-free 0.9% NaCl. In separate experiments, short-term effects were measured continuously during a 22- to 24-hour intrarenal infusion of 4 and 36 micrograms NE . kg-1 . hr-1 or intravenous infusion of 36 micrograms NE . kg-1 . hr-1. Intrarenal infusion of NE produced a more pronounced long-term hypertensive effect than infusion of the same dose intravenously. This hypertension was characterized by a rapid and sustained increase in total peripheral resistance index (TPRI). Despite of the initial renal vasoconstriction, specifically produced during the first 24 hours of intrarenal NE application, cardiac index (CI) in parallel to stroke volume index (SVI) decreased significantly during intrarenal as well as during intravenous NE infusion. Furthermore, no signs of sodium retention were observed. Both rates of intrarenal NE infusion have been shown previously to produce a significant long-term increase in plasma potassium concentration, and the present study indicates that this is presumably the result of decreased urinary potassium output. It is concluded that chronic hypertension produced by intrarenal or intravenous infusion is not volume-dependent. The relatively greater increase in TPRI during intrarenal NE infusion is attributed to vascular wall receptor sensitization by increased plasma potassium levels resulting from effects of intrarenally present NE on tubular cation exchange mechanisms.