Combined Pre- and after-Load Reduction in Hypertensive Patients with Cardiomegaly and Normal Filling Pressure

1981 ◽  
Vol 61 (s7) ◽  
pp. 113s-116s ◽  
Author(s):  
S. N. Hunyor ◽  
G. I. Nelson ◽  
G. L. Donnelly
Keyword(s):  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Isometric Exercise ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Load Reduction ◽  
Blocking Drug ◽  
Isometric Handgrip ◽  
Hypertensive Patients

1. Twelve hypertensive patients with cardiomegaly were treated with equivalent antihypertensive doses of prazosin (11 weeks) and β-adrenoceptor-blocking drug (9 weeks) in random crossover fashion. 2. At the end of each treatment period haemodynamic assessment included the response to isometric handgrip exercise (4 min at 30% of maximum voluntary contraction). 3. Resting cardiac index and heart rate were higher on prasozin although the latter was only 65 beats/min. Systemic vascular resistance and left ventricular filling pressure were insignificantly higher on β-adrenoceptor-blocking drug. 4. During isometric handgrip the blood pressure rise was similar on the two regimens, but the mechanism whereby it was achieved was quite different. On prazosin an increase in cardiac output accounted for the pressor response with virtually no change in systemic vascular resistance, whereas on β blockade there was a flat cardiac output response with a marked increase in the systemic vascular resistance. 5. Ventricular function curves indicated a predominant utilization of the Frank-Starling mechanism during β blockade, whereas enhanced contractility played a major role during prazosin treatment. 6. The isometric exercise response pattern during prazosin treatment resembles that in normal subjects whereas in the β blockade phase it corresponded to that in untreated hypertensive patients with left ventricular hypertrophy or cardiomegaly or to that in congestive heart failure patients. 7. There was no evidence of harmful effects of combined pre- and after-load reduction in hypertensive patients with cardiomegaly and normal filling pressure, even under conditions of moderately severe cardiac loading with isometric exercise.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

Transesophageal Echocardiographic Hemodynamic Monitoring during Preoperative Acute Normovolemic Hemodilution

2000 ◽  
Vol 92 (5) ◽  
pp. 1250-1256 ◽  
Author(s):  
Zoltan Bak ◽  
Lars Abildgård ◽  
Björn Lisander ◽  
Birgitta Janerot-Sjöberg
Keyword(s):  
Cardiac Output ◽  
Transesophageal Echocardiography ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Wall Motion ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Acute Normovolemic Hemodilution ◽  
Fractional Area ◽  
Normovolemic Hemodilution

Background Preoperative acute normovolemic hemodilution may compromise oxygen transport. The aims of our study were to describe the hemodynamic effects of normovolemic hemodilution and to determine its effect on systolic and diastolic cardiac function by multiplane transesophageal echocardiography. Methods In eight anesthetized patients (aged 13-51 yr) without heart disease, hemoglobin was reduced in steps from 123 +/- 8 (mean +/- SD) to 98 +/- 3 and to 79 +/- 5 g/l. Hemodynamic measurements (intravascular pressures, thermodilution cardiac output, and echocardiographic recordings) were obtained during a stabilization period and at each level of hemodilution. Left ventricular wall motion was monitored continuously, and Doppler variables, annular motion, and changes in ejection fractional area were analyzed off-line. Results During hemodilution, cardiac output by thermodilution increased by 16 +/- 7% and 26 +/- 10%, corresponding well to the increase in cardiac output as measured by Doppler (difference, 0.32 +/- 1.2 l/min). Systemic vascular resistance fell 16 +/- 14% and 23 +/- 9% and pulmonary capillary wedge pressure increased slightly (2 +/- 2 mmHg), whereas other pressures, heart rate, wall motion, and diastolic Doppler variables remained unchanged. Ejection fractional area change increased from 44 +/- 7% to 54 +/- 10% and 60 +/- 9% as a result of reduced end-systolic and increased end-diastolic left ventricular areas. Conclusions A reduction in hemoglobin to 80 g/l during acute normovolemic hemodilution does not normally compromise systolic or diastolic myocardial function as determined by transesophageal echocardiography. Preload, left ventricular ejection fraction, and cardiac output increase with a concomitant fall in systemic vascular resistance.

Role of cardiac structural and functional abnormalities in the pathogenesis of hyperdynamic circulation and renal sodium retention in cirrhosis

1999 ◽  
Vol 97 (3) ◽  
pp. 259-267 ◽  
Author(s):  
Florence WONG ◽  
Peter LIU ◽  
Lesley LILLY ◽  
Arieh BOMZON ◽  
Laurence BLENDIS
Keyword(s):  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Left Ventricular ◽  
Contractile Dysfunction ◽  
Sodium Retention ◽  
Sodium Load ◽  
Volume Relationship ◽  
Pressure Volume Relationship ◽  
Cirrhotic Patients

The aim of this study was to assess the relationship between subtle cardiovascular abnormalities and abnormal sodium handling in cirrhosis. A total of 35 biopsy-proven patients with cirrhosis with or without ascites and 14 age-matched controls underwent two-dimensional echocardiography and radionuclide angiography for assessment of cardiac volumes, structural changes and systolic and diastolic functions under strict metabolic conditions of a sodium intake of 22 mmol/day. Cardiac output, systemic vascular resistance and pressure/volume relationship (an index of cardiac contractility) were calculated. Eight controls and 14 patients with non-ascitic cirrhosis underwent repeat volume measurements and the pressure/volume relationship was re-evaluated after consuming a diet containing 200 mmol of sodium/day for 7 days. Ascitic cirrhotic patients had significant reductions in (i) cardiac pre-load (end diastolic volume 106±9 ml; P < 0.05 compared with controls), due to relatively thicker left ventricular wall and septum (P < 0.05); (ii) afterload (systemic vascular resistance 992±84 dyn·s·cm-5; P < 0.05 compared with controls) due to systemic arterial vasodilatation; and (iii) reversal of the pressure/volume relationship, indicating contractility dysfunction. Increased cardiac output (6.12±0.45 litres/min; P < 0.05 compared with controls) was due to a significantly increased heart rate. Pre-ascitic cirrhotic patients had contractile dysfunction, which was accentuated when challenged with a dietary sodium load, associated with renal sodium retention (urinary sodium excretion 162±12 mmol/day, compared with 197±12 mmol/day in controls; P < 0.05). Cardiac output was maintained, since the pre-load was normal or increased, despite a mild degree of ventricular thickening, indicating some diastolic dysfunction. We conclude that: (i) contractile dysfunction is present in cirrhosis and is aggravated by a sodium load; (ii) an increased pre-load in the pre-ascitic patients compensates for the cardiac dysfunction; and (iii) in ascitic patients, a reduced afterload, manifested as systemic arterial vasodilatation, compensates for a reduced pre-load and contractile dysfunction. Cirrhotic cardiomyopathy may well play a pathogenic role in the complications of cirrhosis.

scholarly journals Pharmacodynamics and Cardiopulmonary Side Effects of CW002, a Cysteine-reversible Neuromuscular Blocking Drug in Dogs

2010 ◽  
Vol 112 (4) ◽  
pp. 910-916 ◽  
Author(s):  
Paul M. Heerdt ◽  
Jaideep K. Malhotra ◽  
Brian Y. Pan ◽  
Hiroshi Sunaga ◽  
John J. Savarese
Keyword(s):  
Cardiac Output ◽  
Side Effects ◽  
Histamine Release ◽  
Vascular Resistance ◽  
Onset Time ◽  
Left Ventricular ◽  
Neuromuscular Blocking ◽  
Blocking Drug ◽  
Volume Data ◽  
Neuromuscular Blocking Drug

Background CW002 is a novel neuromuscular blocking drug with a duration dependent on the rate of cysteine adduction to the molecule. The current study characterized the pharmacodynamics and cardiopulmonary side effects of CW002 in dogs. Methods In eight beagles, the dose required to produce 95% neuromuscular blockade (ED95) for CW002 was first determined and cysteine reversibility was confirmed. Five to 7 days later, incrementally larger doses were injected starting with 6.25 x ED95 and doubling the dose every 15 min. Before and after injection, blood was obtained for histamine analysis. Systemic and pulmonary arterial pressures, cardiac output, and left ventricular pressure and volume were recorded along with inspiratory pressure and pulmonary compliance. Ventricular contractility and lusitropy were indexed from pressure and volume data. Results The ED95 for CW002 from pooled data was 0.009 mg/kg. At 3 x ED95, onset time was 2.6 +/- 0.9 min and duration was 47 +/- 9 min. The duration was shortened to 3.7 +/- 0.6 min by 50 mg/kg L-cysteine injected 1 min after CW002. At 25 x ED95, CW002 reduced mean arterial pressure with concomitant decreases in systemic vascular resistance, mean pulmonary artery pressure, cardiac output, contractility, and lusitropy, beginning at 50 x ED95. However, even at a dose of 100 x ED95, the average change in any variable was less than 20%. There were no changes in pulmonary vascular resistance or ventilation mechanics at any dose, and histamine release occurred in only two of eight animals. Conclusions CW002 is a potent neuromuscular blocking drug that at doses up to 100 x ED95 produces modest hemodynamic effects that are not associated with bronchoconstriction or consistent histamine release.

Abstract 323: Acute Reduction of Ambient Air Pressure Lowers Systemic Vascular Resistance and Improves Cardiac Output in Mice in-vivo

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Anmol Shahid ◽  
Vaibhav B Patel ◽  
Gavin Y Oudit ◽  
Michael S McMurtry
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Atmospheric Pressure ◽  
Arterial Compliance ◽  
Ambient Air ◽  
Left Ventricular ◽  
Air Pressure

Background: Humans have lower risk for myocardial infarction and stroke at higher altitudes. The mechanism is unknown. We previously demonstrated that acute reductions in ambient air pressure result in enhanced arterial vasodilation ex vivo using a myograph model of murine resistance arteries. Enhanced vasodilation might increase effective arterial compliance in vivo , thus we further hypothesized a reduction in systemic vascular resistance in vivo as a result of lowered ambient air pressure. Methods: In-vivo Pressure Volume Loops: A novel hypobaric chamber was designed and constructed with the capacity to hold a single anaesthetized mouse and simulate a variety of lowered air pressures within the chamber. The design of the chamber allowed for monitoring of murine heart rate, respiratory rate, & blood oxygen saturation at all times. Using inhaled isoflurane to anesthetize the animal, a closed-chest left-ventricular catheterization procedure was performed within the chamber on free-breathing adult male C57-WT mice (n=8) during consecutive acute exposures to the three air pressure steps: 754 mmHg (control or room atmospheric pressure), 714 mmHg (p1) and 674 mmHg (p2). Results: In-vivo : Total systemic vascular resistance was reduced by acute exposure to lower air pressure (10.09±0.15 mmHg*min/μL at control vs. 8.11±1.45 and 8.18±1.24 mmHg*min/μL at p1 and p2, respectively; p<0.05). Cardiac output was significantly improved by lowering atmospheric pressure below room pressure (7.36±0.15 mL/min at control versus 9.71±1.45 mL/min and 9.59±1.77 mL/min at p1 and p2, respectively; p<0.05). Significant increases in stroke volume with a reduction in air pressure were also observed (p<0.05 for p1 and p2 vs. control). We did not note significant changes in heart rate, mean arterial pressure, or contractility of the mice with lowered atmospheric pressure. Conclusion: Acute reductions in ambient air pressure lower systemic vascular resistance, and increase cardiac output and stroke volumes in vivo .

Arterial pulsatile hemodynamic load induced by isometric exercise strongly predicts left ventricular mass in hypertension

2010 ◽  
Vol 298 (2) ◽  
pp. H320-H330 ◽  
Author(s):  
Julio A. Chirinos ◽  
Patrick Segers ◽  
Amresh Raina ◽  
Hassam Saif ◽  
Abigail Swillens ◽  
...  
Keyword(s):  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Interindividual Variability ◽  
Augmentation Index ◽  
Arterial Compliance ◽  
Characteristic Impedance ◽  
Isometric Exercise ◽  
Left Ventricular ◽  
Applanation Tonometry ◽  
Wave Reflections

Although resting hemodynamic load has been extensively investigated as a determinant of left ventricular (LV) hypertrophy, little is known about the relationship between provoked hemodynamic load and the risk of LV hypertrophy. We studied central pressure-flow relations among 40 hypertensive and 19 normotensive adults using carotid applanation tonometry and Doppler echocardiography at rest and during a 40% maximal voluntary forearm contraction (handgrip) maneuver. Carotid-femoral pulse wave velocity (CF-PWV) was measured at rest. Hypertensive subjects demonstrated various abnormalities in resting and induced pulsatile load. Isometric exercise significantly increased systemic vascular resistance, aortic characteristic impedance (Zc), induced earlier wave reflections, increased augmentation index, and decreased total arterial compliance (TAC; all P ≤ 0.01). In hypertensive subjects, CF-PWV was the strongest resting predictor of LV mass index (LVMI) and remained an independent predictor after adjustment for age, gender, systemic vascular resistance, reflection magnitude, aortic Zc, and TAC (β = 2.52 m/s; P < 0.0001). Age, sex, CF-PWV, and resting hemodynamic indexes explained 48% of the interindividual variability in LVMI. In stepwise regression, TAC (β = −17.85; P < 0.0001) during handgrip, Zc during handgrip (β = −150; P < 0.0001), and the change in the timing of wave reflections during handgrip (β = −0.63; P = 0.03) were independent predictors of LVMI. A model that included indexes of provoked hemodynamic load explained 68% of the interindividual variability in LVMI. Hemodynamic load provoked by isometric exercise strongly predicts LVMI in hypertension. The magnitude of this association is far greater than for resting hemodynamic load, suggesting that provoked testing captures important arterial properties that are not apparent at rest and is advantageous to assess dynamic arterial load in hypertension.

Hypertension and Sports

PEDIATRICS ◽  
1979 ◽  
Vol 64 (5) ◽  
pp. 693-695
Author(s):  
William B. Strong
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Exercise Testing ◽  
Isometric Exercise ◽  
Exercise Stress ◽  
Additional Information ◽  
Wide Range

The article "Response of Hypertensive Adolescents to Dynamic and Isometric Exercise Stress" which appears in this issue of Pediatrics (p 579) raises a number of interesting and practical questions for pediatricians. For example, What is hypertension? What does hypertension mean to the child or youth? Should the youth with hypertension be allowed to participate in competitive athletics? What is the role of exercise testing in the evaluation of hypertension? What additional information does it provide? WHAT IS HYPERTENSION? Blood pressure (BP) is the resultant of cardiac output (CO), and systemic vascular resistance (SVR). Because CO and SVR vary from one person to another, it is not surprising that there is a wide range of normal BP values.

Haemodynamic Effects of Captopril in Hypertensive Patients: Comparison with Saralasin

1979 ◽  
Vol 57 (s5) ◽  
pp. 131s-134s ◽  
Author(s):  
R. Fagard ◽  
A. Amery ◽  
P. Lijnen ◽  
T. Reybrouck
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Chronic Administration ◽  
Plasma Renin ◽  
Acute Administration ◽  
Ang Ii ◽  
Hypertensive Patients ◽  
Plasma Angiotensin

1. Captopril (25 mg) reduced plasma angiotensin II (ANG II) by 53% (P &lt; 0·001) and mean brachial artery pressure (MBAP) by 18·7 mmHg (P &lt; 0·001) within 75 min in 26 hypertensive patients. After 2 months (on 150–600 mg/day) MBAP had decreased by 27·1 mmHg (n = 18) with no further change of plasma ANG II. δMBAP was significantly related to control log plasma renin (PRA) and log ANG II in both conditions. 2. The acute depressor response to captopril was 11·2 mmHg greater (P &lt; 0·001) than δMBAP during saralasin infusion (n = 12). 3. Heart rate slightly increased after acute administration of captopril (+ 3·3 beats/min; P &lt; 0·005), but cardiac output was not significantly affected; systemic vascular resistance decreased by 10% (P &lt; 0·01) with unchanged pulmonary vascular resistance. 4. During chronic administration, oxygen consumption, cardiac output and stroke volume increased by 15% (P &lt; 0·01), with unchanged heart rate; systemic vascular resistance had dropped by 30% (P &lt; 0·001). 5. Plasma ANG II and plasma aldosterone decreased, and PRA and ANG I increased acutely, with no further changes during chronic treatment.

scholarly journals Empagliflozin does not change cardiac index nor systemic vascular resistance but rapidly improves left ventricular filling pressure in patients with type 2 diabetes: a randomized controlled study

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Matthias Rau ◽  
Kirsten Thiele ◽  
Niels-Ulrik Korbinian Hartmann ◽  
Alexander Schuh ◽  
Ertunc Altiok ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Left Ventricular ◽  
Volume Index ◽  
Hemodynamic Parameters ◽  
Mitral Inflow ◽  
Ventricular Filling Pressure

Abstract Background In the EMPA-REG OUTCOME trial (Empagliflozin Cardiovascular Outcome Event Trial) treatment with the sodium-glucose cotransporter-2 (SGLT2) inhibitor empagliflozin significantly reduced heart failure hospitalization (HHF) in patients with type 2 diabetes mellitus (T2D) and established cardiovascular disease. The early separation of the HHF event curves within the first 3 months of the trial suggest that immediate hemodynamic effects may play a role. However, hitherto no data exist on early effects of SGLT2 inhibitors on hemodynamic parameters and cardiac function. Thus, this study examined early and delayed effects of empagliflozin treatment on hemodynamic parameters including systemic vascular resistance index, cardiac index, and stroke volume index, as well as echocardiographic measures of cardiac function. Methods In this placebo-controlled, randomized, double blind, exploratory study patients with T2D were randomized to empagliflozin 10 mg or placebo for a period of 3 months. Hemodynamic and echocardiographic parameters were assessed after 1 day, 3 days and 3 months of treatment. Results Baseline characteristics were not different in the empagliflozin (n = 22) and placebo (n = 20) group. Empagliflozin led to a significant increase in urinary glucose excretion (baseline: 7.3 ± 22.7 g/24 h; day 1: 48.4 ± 34.7 g/24 h; p < 0.001) as well as urinary volume (1740 ± 601 mL/24 h to 2112 ± 837 mL/24 h; p = 0.011) already after one day compared to placebo. Treatment with empagliflozin had no effect on the primary endpoint of systemic vascular resistance index, nor on cardiac index, stroke volume index or pulse rate at any time point. In addition, echocardiography showed no difference in left ventricular systolic function as assessed by left ventricular ejections fraction and strain analysis. However, empagliflozin significantly improved left ventricular filling pressure as assessed by a reduction of early mitral inflow velocity relative to early diastolic left ventricular relaxation (E/eʹ) which became significant at day 1 of treatment (baseline: 9.2 ± 2.6; day 1: 8.5 ± 2.2; p = 0.005) and remained apparent throughout the study. This was primarily attributable to reduced early mitral inflow velocity E (baseline: 0.8 ± 0.2 m/s; day 1: 0.73 ± 0.2 m/sec; p = 0.003). Conclusions Empagliflozin treatment of patients with T2D has no significant effect on hemodynamic parameters after 1 or 3 days, nor after 3 months, but leads to rapid and sustained significant improvement of diastolic function. Trial registration EudraCT Number: 2016-000172-19; date of registration: 2017-02-20 (clinicaltrialregister.eu)

Sign in / Sign up

Export Citation Format

Share Document