Brachial Intra-arterial Pressure Research Articles

Complications from brachial arterial pressure monitoring are rare in patients having cardiac surgery.

We would like to thank the Journal for their interest in our recent article about the use of intra-arterial brachial pressure monitoring during cardiac surgery (1).

Precision calibration of peripheral pressure waveforms using intra-arterial blood pressure reveals the need for improved ways to accurately estimate aortic blood pressure

BackgroundEstimating aortic blood pressure (BP) non-invasively requires peripheral waveform calibration using cuff systolic (SBP) and diastolic (DBP). Accuracy of estimated aortic BP has never been determined when peripheral waveforms are precision calibrated using peripheral intra-arterial SBP/DBP. This is relevant to understanding the best methods to estimate aortic BP accurately and was the aim of this study. We also determined how other calibrations influence estimated aortic BP accuracy.MethodsAscending aortic, brachial and radial artery intra-arterial BP was measured among 104 patients (61.8 ± 10 years, 66% male) undergoing coronary angiography. Intra- arterial aortic SBP was compared with estimated aortic SBP by generalised transfer function (SphygmoCor) using: (1) intraarterial brachial pressure waveforms calibrated with intra-arterial brachial SBP/DBP; (2) intra-arterial radial pressure waveforms calibrated with intra-arterial brachial SBP/DBP and (3) radial SBP/DBP and; (4) intra-arterial aortic mean arterial pressure (MAP)/DBP.ResultsAll intra-arterial SBP/DBP peripheral waveform calibrations significantly underestimated intra-arterial aortic SBP ((1) −4.5 ± 7.0 mmHg; (2) −8.8 ± 8.0 mmHg and (3) −5.4 ± 7.6 mmHg; p < 0.0001 all). Conversely, intra-arterial aortic MAP/DBP calibration (4) accurately estimated aortic SBP (0.03 ± 4.6 mmHg, p = 0.95). Underestimation of intra-arterial aortic SBP was related to lower aortic-to-brachial SBP amplification (r > 0.25, p < 0.009 all calibrations).ConclusionEven when using accurate (intra-arterial) SBP/DBP for precision peripheral waveform calibration, aortic SBP was significantly underestimated. Intra-arterial aortic MAP/DBP was the most accurate calibration, but is not feasible for non-invasive use. These findings highlight the need for improved ways to accurately estimate aortic SBP.

Endothelium-dependent vasodilatory signalling modulates α1 -adrenergic vasoconstriction in contracting skeletal muscle of humans.

'Functional sympatholysis' describes the ability of contracting skeletal muscle to attenuate sympathetic vasoconstriction, and is critical to ensure proper blood flow and oxygen delivery to metabolically active skeletal muscle. The signalling mechanism responsible for sympatholysis in healthy humans is unknown. Evidence from animal models has identified endothelium-derived hyperpolarization (EDH) as a potential mechanism capable of attenuating sympathetic vasoconstriction. In this study, increasing endothelium-dependent signalling during exercise significantly enhanced the ability of contracting skeletal muscle to attenuate sympathetic vasoconstriction in humans. This is the first study in humans to identify endothelium-dependent regulation of sympathetic vasoconstriction in contracting skeletal muscle, and specifically supports a role for EDH-like vasodilatory signalling. Impaired functional sympatholysis is a common feature of cardiovascular ageing, hypertension and heart failure, and thus identifying fundamental mechanisms responsible for sympatholysis is clinically relevant. Stimulation of α-adrenoceptors elicits vasoconstriction in resting skeletal muscle that is blunted during exercise in an intensity-dependent manner. In humans, the underlying mechanisms remain unclear. We tested the hypothesis that stimulating endothelium-dependent vasodilatory signalling will enhance the ability of contracting skeletal muscle to blunt α1 -adrenergic vasoconstriction. Changes in forearm vascular conductance (FVC; Doppler ultrasound, brachial intra-arterial pressure via catheter) to local intra-arterial infusion of phenylephrine (PE; α1 -adrenoceptor agonist) were calculated during (1) infusion of the endothelium-dependent vasodilators acetylcholine (ACh) and adenosine triphosphate (ATP), the endothelium-independent vasodilator (sodium nitroprusside, SNP), or potassium chloride (KCl) at rest; (2) mild or moderate intensity handgrip exercise; and (3) combined mild exercise + ACh, ATP, SNP, or KCl infusions in healthy adults. Robust vasoconstriction to PE was observed during vasodilator infusion alone and mild exercise, and this was blunted during moderate intensity exercise (ΔFVC: -34±4 and -34±3 vs. -13±2%, respectively, P<0.05). Infusion of ACh or ATP during mild exercise significantly attenuated PE vasoconstriction similar to levels observed during moderate exercise (ACh: -3±4; ATP: -18±4%). In contrast, infusion of SNP or KCl during mild exercise did not attenuate PE-mediated vasoconstriction (-32±5 and -46±3%). To further study the role of endothelium-dependent hyperpolarization (EDH), ACh trials were repeated with combined nitric oxide synthase and cyclooxygenase inhibition. Here, PE-mediated vasoconstriction was blunted at rest (blockade: -20±5 vs. -31±3% vs.; P<0.05) and remained blunted during exercise (blockade: -15±5 vs. -14±5%). We conclude that stimulation of EDH-like vasodilatation can blunt α1 -adrenergic vasoconstriction in contracting skeletal muscle of humans.

Noninvasive measurement of blood pressure variability: accuracy of the Finometer monitor and comparison with the Finapres device

To assess the accuracy of spectral indices of arterial pressure variability and baroreflex sensitivity obtained from beat-by-beat noninvasive blood pressure recordings by the Finometer device, we compared these measures with those obtained from intra-arterial recordings. The performance of the Finometer was also compared to the traditional Finapres device. In 19 cardiac disease patients, including myocardial infarction, heart failure and cardiac transplant, we estimated the power of systolic and diastolic pressures in the VLF (0.01–0.04 Hz), LF (0.04–0.15 Hz) and HF (0.15–0.45 Hz) bands and computed absolute and percentage errors relative to intra-arterial brachial pressure. We also computed the characteristic frequency of each band (i.e. the barycentric frequency of spectral components identified in the band). The variability of systolic pressure in the VLF and LF bands was markedly overestimated by both the Finometer and Finapres (p < 0.01), with percentage median errors of respectively 130% and 103% (Finometer), and 134% and 78% (Finapres). The HF power was substantially unchanged using the Finometer and reduced using the Finapres (−28%, p < 0.05). The limits of agreement between noninvasive and invasive spectral measurements were wide. Linear system analysis showed that most (>80%) of the power of noninvasive signals was linearly related to the power of the invasive signal. The characteristic frequency of each band was substantially preserved in both noninvasive signals. The results for diastolic pressure were similar, but the Finapres errors in the VLF and LF bands were lower. Baroreflex sensitivity was significantly underestimated by both devices (Finometer: −31%, Finapres: −24%). Despite previous studies having shown that brachial artery waveform reconstruction performed by the Finometer has improved the accuracy of blood pressure measurement compared to the Finapres device, measurement of blood pressure variability in cardiac disease patients provides worse results in most spectral parameters and a better accuracy only in the HF band of systolic pressure.

COMPARISON OF PORTAPRES® WITH STANDARD SPHYGMOMANOMETRY IN PREGNANCY

Background: Continuous beat-to-beat noninvasive blood pressure (BP) measurement is possible with Portapres®. It constructs finger arterial waveforms beat-to-beat. Dedicated software is used to analyze the arterial waveforms. A new technique has been developed to reconstruct brachial intra-arterial pressure that uses return to flow (RTF). This method has been validated against invasive intra-arterial measurements in nonpregnant individuals. Objectives: To validate Portapres in normal and preeclamptic pregnant women against standard anaeroid sphygmomanometry according to Riva–Rocci–Korotkoff (RRK). Methods: In 30 normotensive (10 in each trimester) and 20 preeclamptic women, two trained observers blinded from each other's results took BP measurements with a standard sphygmomanometer. These measurements were compared with sequential same-arm averaged measurements obtained during 30 sec by Portapres, following protocols from the Association for the Advancement of Medical Instrumentation (AAMI, mean accepted difference≤5 mmHg, SD≤8) and British Hypertension Society (BHS, gradings A down to D). Results: A total of 150 measurement pairs were analyzed. Cumulative percentages of absolute pressure differences for all women (BHS) and mean pressure differences (SD) for different trimesters and preeclampsia (AAMI) between sphygmomanometry and Portapres were calculated. Overall, mean difference (SD) for systolic BP was 5 (SD 8) and for diastolic BP was −3 (SD 8), although analysis of variance revealed a significant effect for preeclampsia on diastolic differences between the two methods of BP measurement (p<0.001). Conclusions: Portapres with RTF, developed to equal intra-arterial brachial pressure, compares reasonably well to RRK and overall meets the criteria set by the AAMI. According to the BHS, Portapres receives a B-grading for diastolic BP and a C-grading for systolic BP. As Portapres measures BP and calculates cardiac output continuously and noninvasively, it would appear worthwhile to further evaluate this device in pathological pregnancies.

The pulse pressure-to-stroke index ratio predicts cardiovascular events and death in uncomplicated hypertension

OBJECTIVESThe goal of this study was to assess the prognostic power of the pulse pressure-to-stroke index (PP-to-SVi) ratio for cardiovascular events and mortality in patients with uncomplicated hypertension.BACKGROUNDThe prognostic significance of pulse pressure (PP) has been studied repeatedly, but few data are available on the PP-to-SVi ratio.METHODSInvasive hemodynamic measurements, including brachial intra-arterial pressure and stroke index by the direct oxygen Fick method, were performed in the period 1972 to 1982 in 192 patients with uncomplicated hypertension; their outcome was ascertained in 1994.RESULTSAge at baseline averaged 37 ± 12 years; brachial artery pressure was 165 mm Hg ± 30/89 ± 17 mm Hg; PP averaged 76 mm Hg ± 18 mm Hg, and the PP-to-SVi ratio was 1.67 mm Hg/(ml/m2) ± 0.73 mm Hg/(ml/m2). During 3,057 patient years of follow-up, 19 patients died, and 44 experienced at least one fatal or nonfatal cardiovascular event. Cox regression analysis revealed that the PP-to-SVi ratio was a significant predictor of fatal and nonfatal cardiovascular events and of all-cause mortality after control for age and gender (p < 0.01). Its predictive power persisted after additional adjustment for mean arterial pressure and heart rate. Each 0.75-mm Hg/(ml/m2) increase in the PP-to-SVi ratio was independently associated with a 79% increase in the risk of a cardiovascular event (p = 0.01) and a 2.05-fold greater risk of all-cause mortality (p = 0.01).CONCLUSIONSThe PP-to-SVi ratio is a significant and independent predictor of cardiovascular events and mortality in selected patients with uncomplicated hypertension.

Physiological influences on continuous finger and simultaneous intra-arterial blood pressure.

Because of the clinical and experimental utility of continuous finger blood pressure measurements and the need for accuracy, we tested the performance of a new hydraulic device in 22 consecutive hypertensive subjects during physiological and pharmacological interventions. Ipsilateral brachial intra-arterial pressure was monitored during rest, Valsalva's maneuver, static handgrip, and mental arithmetic and after sublingual glyceryl trinitrate. In excess of 40,000 blood pressure values were analyzed. Average bias (intra-arterial minus finger blood pressure) was 8.2 +/- 17.0 mm Hg (mean +/- SD, P = NS) for systolic and 2.8 +/- 10.4 mm Hg (P = NS) for diastolic pressure. Two-way ANOVA of biases with subject and task factors showed a subject effect (P < .001). Intersubject and intrasubject standard deviations of bias were 13.8 and 9.8 mm Hg systolic and 8.7 and 5.7 diastolic, respectively. Linear drift (millimeters of mercury per minute) of finger pressure was greater (P < .001) for systolic than diastolic pressure during static exercise and math and after glyceryl trinitrate. Coefficients of determination for blood pressure ranged from 0.4 +/- 0.3 to 0.8 +/- 0.3 during the tasks. We conclude that (1) noninvasive finger blood pressure faithfully follows intra-arterial changes but with clinically relevant offsets, (2) this technique is best suited for assessing pressure changes, (3) physiological and pharmacological interventions do not consistently affect finger pressure accuracy, (4) many reports of finger blood pressure measuring devices are based on direct readings obtained with inadequate system response characteristics, and (5) the tested instrument falls short of the standard requirements (bias < or = 5 +/- 8 mm Hg) for devices that measure intermittently.

Evaluation of non-invasive blood pressure measurement by the Finapres method at rest and during dynamic exercise in subjects with cardiovascular insufficiency

The accuracy and precision of the Finapres in recording rest and exercise blood pressure compared with the intra-arterial (aortic and branchial) and random-zero sphygmomanometer methods was assessed in 84 ischaemic patients in three different studies. Firstly, comparison at rest with the aortic intra-arterial pressure in 50 ischaemic patients demonstrated that the Finapres systolic (136.5 +/- 21.1 vs. 129.3 +/- 19.0 mmHg; p < 0.001) and mean (92.4 +/- 13.4 vs. 90.7 +/- 11.4 mmHg; p < 0.001) arterial pressures were higher and diastolic pressures lower (70.4 +/- 11.5 vs. 71.5 +/- 9.8 mmHg; p < 0.001). The reproducibility of the Finapres and invasive method was similar for systolic (4.6% vs. 4.0%), diastolic (2.8% vs. 2.7%) and mean (3.3% vs. 3.0%) blood pressures. Second, in seven subjects studied twice at rest and during 4 min supine bicycle exercise, the exercise increase in blood pressure was greater on the Finapres compared with the brachial intra-arterial pressure (systolic +10.2 +/- 6.3 vs. +3.6 +/- 9.8 mmHg; diastolic +9.6 +/- 11.1 vs. +0.2 +/- 2.1 mmHg; p = 0.02 for each); however, at steady-state the peak/trough differences in pressure between the methods were similar. Thirdly, compared under rest conditions, to random zero sphygmomanometer (RZO), the Finapres systolic pressure was higher (6.8 +/- 3.5 mmHg) and diastolic pressure lower (-6.0 +/- 1.9 mmHg). During upright bicycle exercise, the difference between the Finapres and RZO in systolic blood pressure increased at each level of exercise (+14.3 +/- 4.2, +17.9 +/- 4.0 and +22.2 +/- 4.1 mmHg respectively at each exercise stage: p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Impairment of left ventricular function during maximal isometric dead lifting

High-intensity short-duration lifting is frequently performed by athletes and laborers. Little is known about the magnitude and pattern of blood pressure response and resultant effects on left ventricular (LV) function during this form of intense isometric exercise. We monitored brachial intra-arterial pressure and LV ejection fraction (LVEF) during upright isometric dead lifting performed on a force platform. Fourteen healthy male subjects (age 27 yr) maintained maximal sustained isometric dead lift (140 +/- 34 kg) for 32 s. LVEF was measured by 99mTc first-pass radionuclide ventriculography. Mean arterial pressure increased from 107 +/- 15 mmHg at rest to a peak of 174 +/- 28 mmHg and fell precipitously to 88 +/- 13 mmHg within 10 s after release of the dead lift. LVEF decreased from 63 +/- 8 to 51 +/- 14% (P less than 0.02) in seven subjects with technically acceptable ventriculograms. We conclude that maximal upright isometric dead-lift exercise produces a marked increase in arterial pressure and corresponding LV afterload that is associated with a transient reduction in LVEF in normal men.

Maximal aerobic power in essential hypertension.

Fifty untreated male patients aged 32 +/- 10 (s.d.) years, referred for hypertension, in whom organ damage was limited to WHO stages I and II, without underlying disease, performed a graded, uninterrupted exercise on a bicycle ergometer up to exhaustion. Mean brachial intra-arterial pressure at rest ranged from 74 to 152 mmHg. Maximal voluntary oxygen uptake was independently and negatively related to resting blood pressure (P less than 0.05), age (P = 0.05), and positively to body weight (P less than 0.05). Pulmonary wedge pressure and the components of the Fick equation--heart rate, stroke volume and arteriovenous oxygen difference--were measured in order to study the mechanisms involved. Stroke volume at peak exercise was inversely (P less than 0.05), and pulmonary wedge pressure positively (P less than 0.01), related to mean brachial artery pressure at rest. Peak heart rate was not significantly related to the severity of hypertension, but was inversely related to age (P less than 0.01). Stroke volume and pulmonary wedge pressure at the end of exercise were both similar in older and younger patients. Arteriovenous oxygen difference at peak exercise was not related either to blood pressure or to age. In conclusion, both high blood pressure and age reduce maximal voluntary oxygen uptake independently of each other by separate mechanisms; the former by an impairment of cardiac function, the latter by the limitation of peak heart rate.

The pulmonary circulation in essential systemic hypertension

Seventy-one men, ages 16 to 59 years, were referred for systemic hypertension, which was without detectable cause and with limited organ damage (World Health Organization stages I to II). They performed a graded exercise test on the bicycle ergometer in the sitting position. Mean brachial intraarterial pressure, mean pulmonary artery and wedge pressures and cardiac output (Fick method) were measured. At rest mean brachial artery pressure ranged from 72 to 168 mm Hg. Mean pulmonary wedge pressure was significantly (p < 0.05) related to mean brachial artery pressure at rest, at submaximal work (50 watts) and at the end of exercise (161 ± 42 [standard deviation] watts). In each subject pulmonary vascular resistance was calculated as the slope of the relation between the pressure gradient across the pulmonary circulation and cardiac output from data at rest, at 50 watts and at the end of exercise; mean critical closing pressure was calculated as the intercept of this relation. Pulmonary vascular resistance averaged 0.63 ± 0.37 mm Hg/liter/min and was significantly related to age (r = 0.28, p < 0.05) but not to rest brachial artery pressure (r = 0.14) or pulmonary wedge pressure (r = 0.09, difference not significant for both). The mean critical closing pressure averaged 6.1 ± 4.0 mm Hg and was not related to brachial artery pressure (r = −0.08) or to age (r = −0.18, difference not significant for both). It is concluded that there is neither a primary nor a secondary effect of systemic hypertension on the pulmonary vasculature in patients with World Health Organization stages I to II essential hypertension.

Hemodynamic effects of verapamil in essential hypertension at rest and during exercise.

In recent years the calcium antagonist verapamil has been used in the treatment of essential hypertension. Relatively little work has been done to elucidate its long-term haemodynamic effects at rest and during exercise. Ten males with previously untreated essential hypertension in WHO stage I, aged 35-55 years, were studied on an outpatient basis. Oxygen consumption, heart rate, cardiac output ( Cardiogreen ) and intra-arterial brachial pressure were recorded at rest in the supine and sitting position and during steady state work at 50, 100 and 150 W. As expected, the hypertension was associated with an increase in total peripheral resistance. The subjects were treated with verapamil 120-240 mg daily as the sole drug for one year. The haemodynamic study was then repeated. One subject demonstrated a slight increase in blood pressure at rest and during exercise, while there was a blood pressure reduction in the other 9. The nonresponding patient was excluded from the statistical evaluation. The main results were as follows: There was a statistically significant reduction in systolic, diastolic and mean arterial pressure at rest as well as during exercise. The reductions reached about 10% at rest, slightly less during exercise. The blood pressure reduction was associated with a statistically significant reduction in total peripheral resistance at rest only. During exercise, the reduction in resistance was modest (about 5%). The heart rate was practically unchanged during supine rest, but decreased about 8% at rest sitting and during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

New oscillometric method for indirect measurement of systolic and mean arterial pressure in the human finger. Part 2: correlation study.

With a new oscillometric method equipped with a transmittance infrared photoelectric plethysmograph, indirect systolic, and mean arterial pressures were measured in 12 normotensive and hypertensive subjects with systolic and mean arterial pressures ranging from 55 to 163 mmHg and from 95 to 200 mmHg, respectively. The pressure values obtained by this method were compared with direct measurements of the brachial intra-arterial pressure recorded simultaneously. A fairly good correlation between the pairs of simultaneous data from these two methods were obtained.

Hemodynamic response to captopril at rest and during exercise in hypertensive patients

Captopril in 20 hypertensive patients acutely reduced brachial intraarterial pressure at rest and during exercise, based on a reduction in systemic vascular resistance. Heart rate increased slightly whereas stroke volume was not affected. Plasma angiotensin II was significantly reduced whereas plasma renin activity increased.

Hemodynamic consequences of long-term beta-blocker therapy: a 5-year follow-up study of atenolol.

The long-term hemodynamic effects of atenolol were studied in 10 patients with previously untreated essential hypertension in WHO stage I. Oxygen consumption, heart rate, cardiac output, and intra-arterial brachial pressure were recorded at rest in supine and sitting positions and during steady-state work at 50, 100, and 150 W. The patients were treated with 100 mg atenolol daily (200 mg in 1 patient) as the sole antihypertensive drug and were restudied after 1 and 5 years. After 1 year the blood pressure was reduced approximately 18% both at rest and during exercise, and the heart rate about 25%. The cardiac output was reduced 16% at rest supine, 27% at rest sitting, and about 20% during exercise. The calculated total peripheral resistance was not decreased compared to pretreatment values. After 5 years on treatment, the hemodynamic parameters were almost identical to those seen after 1 year. There was no increase in stroke volume or cardiac output and no decrease in the total peripheral resistance. Thus prolonged beta-blocker treatment over several years does not seem to normalize hemodynamics in patients with mild to moderate essential hypertension.

Haemodynamic effects and plasma concentrations of labetalol during long-term treatment of essential hypertension.

Abstract 1 Fifteen men with untreated essential hypertension in WHO stage 1 were studied on an outpatient basis to evaluate the haemodynamic long-term effect of a new α- and β-adrenergic receptor blocker, labetalol. 2 Oxygen consumption, heart rate, cardiac output (Cardiogreen) and intraarterial brachial pressure were recorded at rest in a supine and sitting position, and during steady state work at 300, 600 and 900 kpm/min. 3 The subjects were treated with labetalol (dose 200-800 mg/day) as the sole drug for 1 year. The haemodynamic study was then repeated and the concentration of labetalol in plasma 2-2.5 h after the morning dose was measured. 4 Mean arterial blood pressure was reduced approximately 23% at rest and 21% during exercise. The heart rate was decreased 15% at rest and 16% during exercise. There was a compensatory increase in the stroke volume and consequently the cardiac index was reduced less than the heart rate, 7% at rest supine and 10% during exercise. There was a significant decrease in total peripheral resistance at rest supine (16%) and during exercise (12%). 5 No serious side-effects were seen, but two subjects almost syncopated in the sitting position after the 900 kpm/min work load at the restudy. 6 There was no correlation between the plasma concentration and the effect of labetalol. 7 The haemodynamic changes differ from those seen after long-term therapy with drugs possessing only β-adrenoceptor blocking properties, and agree well with what should be expected with a drug which possesses both α- and β-adrenoceptor blocking properties.

Haemodynamic long-term effects of prazosin plus tolamolol in essential hypertension.

1 Twelve men with untreated essential hypertension in WHO stage I were studied on an outpatient basis to evaluate the haemodynamic long-term effects of a combination of prazosin and a β-adrenoceptor blocker, tolamolol. 2 Oxygen consumption, heart rate, cardiac output (Cardiogreen) and intra-arterial brachial pressure were recorded at rest in a supine and sitting position and during steady state work at 300, 600 and 900 kpm/min. 3 The subjects were treated with the combination of prazosin (dose 3-6 mg daily) plus tolamolol (150-300 mg daily) for 7-12 months and the haemodynamic study was repeated. 4 The blood pressure was reduced approximately 18% at rest and during exercise. The pressure reduction was due to a combination of reduction in cardiac index and total peripheral resistance. During hard exercise the cardiac index was almost unchanged, the pressure reduction being almost entirely due to reduction in total peripheral resistance. The heart rate was reduced significantly, but less than what is seen by β-adrenoceptor-blockers alone. 5 One subject demonstrated the `first dose reaction' of prazosin with syncope. During the study tolamolol was withdrawn from clinical trials due to possible side-effects in long-term high dose studies in animals. After the haemodynamic study was completed, tolamolol was replaced by timolol without changes in the blood pressure. 6 The combination of prazosin and a β-adrenoceptor blocking drug is very effective in most patients with mild and moderate essential hypertension. The blood pressure reduction is due to a combination of reduction in total peripheral resistance and in cardiac index, the latter being only slightly decreased during severe muscular exercise.

Haemodynamic long-term effects of metoprolol at rest and during exercise in essential hypertension.

1 Twelve men with untreated essential hypertension in WHO stage I were studied on an outpatient basis to evaluate the haemodynamic long-term effect of a new beta-adrenoceptor blocker, metoprolol. 2 Oxygen consumption, heart rate, cardiac output (Cardiogreen) and intraarterial brachial pressure were recorded at rest in a supine and sitting position and during steady state work at 300, 600 and 900 kpm/min. 3 The subjects were treated with metoprolol (dose 50-250 mg/day) as the sole drug for 1 year and the haemodynamic study was repeated. 4 Mean arterial blood pressure was reduced about 12% at rest and 9% during exercise. The heart rate was decreased about 22% at rest and 20% during exercise. There was no significant compensatory increase in the stroke volume and consequently the cardiac index was reduced about 22% at rest sitting and about 17% during exercise. There was no decrease in total peripheral resistance. 5 No side-effects were seen. 6 The major haemodynamic long-term effects of metoprolol in mild and moderate essential hypertension resemble those seen by other beta-adrenoceptor blockers like alprenolol, atenolol and timolol. The study has not given support to the assumption that metoprolol should cause less depression in cardiac output than other beta-adrenoceptor blockers.

Hemodynamic long-term effects of timolol at rest and during exercise in essential hypertension.

Sixteen men with previously untreated essential hypertension in WHO stage I have been studied as out-patients. Oxygen consumption, heart rate (HR), cardiac output (Q) (Cardiogreen) and intraarterial brachial pressure were recorded at rest in supine and sitting position and during steady state work at 300, 600 and 900 kpm/min. The subjects were treated with timolol as the sole drug for one year and the hemodynamic study was repeated. BP was reduced approximately 18% at rest and 14% during exercise, HR approximately 26% and the cardiac index 28% at rest supine and 32% at rest sitting. During exercise the reductions in Q were 25-30%. The calculated total peripheral resistance was significantly increased at rest as well as during exercise. The product of mean arterial pressure and HR was reduced about 40%. No severe side-effects were seen.

Hemodynamic changes at rest and during exercise in long-term clonidine therapy of essential hypertension.

Abstract. Thirteen men with untreated essential hypertension in WHO stage I, all working, have been studied ambulatorily. Oxygen consumption, heart rate, cardiac output (Cardiogreen) and intraarterial brachial pressure were recorded at rest in supine and sitting position and during steady state work at 300, 600 and 900 kpm/min. The subjects were treated with Clonidine as the sole drug for one year and the hemodynamic study was repeated. The reduction in the intraarterial pressure was usually due to a decrease in cardiac output which again was due to a reduction in heart rate. The calculated total peripheral resistance did not change significantly. The pressure reduction was greatest at rest. During submaximal exercise the differences between the hemodynamic parameters before and after therapy were small.