Serial study of factors influencing changes in cardiac output during human pregnancy

1989 ◽  
Vol 256 (4) ◽  
pp. H1060-H1065 ◽  
Author(s):  
S. C. Robson ◽  
S. Hunter ◽  
R. J. Boys ◽  
W. Dunlop

Serial hemodynamic measurements were performed in 13 women on two occasions before conception and then at monthly intervals throughout pregnancy. Cardiac output (CO) was measured by Doppler and cross-sectional echocardiography at the aortic, pulmonary, and mitral valves. Cardiac chamber size and ventricular function were investigated by M-mode echocardiography. CO increased from a mean of 4.88 l/min before the conception to a maximum of 7.21 l/min at 32 wk, the increase being significant by 5 wk after the last menstrual period. Heart rate and left ventricular performance increased during the first trimester. Heart rate increased further during the second trimester, during which left atrial and left ventricular end-diastolic dimensions increased, suggesting an increase in venous return. Derived values of total peripheral vascular resistance fell during the first 20 wk. These changes were associated with a progressive increase in valve orifice area and left ventricular wall thickness during pregnancy.

1990 ◽  
Vol 258 (3) ◽  
pp. H625-H633 ◽  
Author(s):  
T. J. Stahl ◽  
P. B. Alden ◽  
W. S. Ring ◽  
R. C. Madoff ◽  
F. B. Cerra

A chronic canine model of hyperdynamic sepsis was achieved by cecal ligation and puncture (SEP) in conjunction with continuous high-volume fluid resuscitation. Cardiac function was evaluated using ultrasonic cardiac crystals placed across the major, minor, and wall thickness axes of the left ventricle, together with simultaneous arterial and ventricular pressure measurement. Seven to 10 days after crystal implantation, animals were randomized to either SEP (n = 10) or sham laparotomy control (n = 7). SEP dogs became febrile and lethargic, with elevated leukocyte counts and positive blood cultures for enteric organisms. They were also hyperdynamic, with significant increases in heart rate and cardiac output and a fall in systemic vascular resistance. Systolic blood pressure, stroke volume, and ejection fraction remained stable. Relative to control, the SEP group demonstrated a significant reduction in intrinsic contractility during systole, as measured by the heart rate and load-independent index of left ventricular performance Emax (P less than 0.01), confirming the observations of others. In addition, however, diastolic function also became markedly abnormal with a progressive increase in unstressed and end-diastolic ventricular volumes (P less than 0.05) and a significant decrease in myocardial compliance as quantitated by transmural pressure vs. volume-strain analysis. It is hypothesized that this increase in diastolic volume helps to maintain global cardiac performance during the hyperdynamic response to sepsis in the presence of adequate volume support.


1986 ◽  
Vol 14 (6) ◽  
pp. 289-298
Author(s):  
U Abshagen ◽  
E von Möllendorff

Mean arterial pressure is determined primarily by cardiac output and total peripheral resistance, in addition to blood volume and compliance of the arterial system. The regulation of these determinants occurs via reflex neurogenic mechanisms and metabolic or humoral mechanisms. The haemodynamic situation in the early stages of arterial hypertension is characterized by a slight hypercirculatory state due to a moderate increase in heart rate and cardiac output, whereas the total peripheral resistance is increased only moderately, if at all. In later stages, however, a progressive increase in total peripheral resistance prevails, accompanied by a decrease in left ventricular performance due to the development of left ventricular hypertrophy, changes in ventricle geometry and coronary heart disease. A pharmacologically-induced decrease of total peripheral resistance by means of vasodilators, therefore, represents a logical approach to therapy, at least of advanced hypertension. Vasodilators can be classified into three categories: (1) those with preferential activity on the arterial resistance vessels, eg hydralazine, diazoxide, minoxidil; (2) those with preferential activity on venous capacitance vessels, eg organic nitrates; and (3) those with activities on both branches, eg sodium nitroprusside, urapidil, prazosin and other α-blockers. Brief reference is made to new and possibly more acceptable vasodilators – in particular carvedilol and prizidilol.


2021 ◽  
pp. 75-79
Author(s):  
Munesh Tomar ◽  
Tanvi goel ◽  
Raza Faizan ◽  
Vijay Jaiswal

Background:There are wide number of diseases of almost every system in the body which can affect heart in a number of different ways including increasing demands on the heart ,ventricular dysfunction ,rhythm abnormalities ,valve abnormalities ,pulmonary pressures and lot more.Cardiac involvement in systemic diseases is usually silent or oligosymptomatic and includes different pathophysiological mechanisms such as myocardial inflammation, infarction ,subendocardial vasculitis,valvular disease and different patterns of fibrosis. Objective : To study association between systemic illnesses (hematological, endocrinal , renal) and cardiac function abnormalities as ventricular function,cardiac dimensions ,pulmonary artery pressure and pericardial effusion,for early diagnosis and treatment to decrease morbidity and mortality in patient with systemic illness. Design/Method:It was a cross sectional,descriptive study The present study was conducted in the Department of Pediatrics, LLRM Medical College,Meerut,Uttar Pradesh over a period of 1 year (June 2019-June 2020) Results: Cardiac findings in all three groups show ECG abnormalities and echocardiographic changes compared to general population. ECG abnormalities were prolonged PR interval and sinus tachycardia while echocardiographic changes mainly left ventricular(LV) dilatation and hypertrophy ,increased cardiac output ,ventricular dysfunction and pulmonary arterial hypertension(PAH),were noted in a significant proportion of patients. Conclusion:Systemic illnesses affect cardiac parameters in various ways including prolonged PR interval,cardiac dilatation,chamber hypertrophy ,high cardiac output,high cardiac index ,PAH and ventricular dysfunction.


2021 ◽  
pp. 1-20
Author(s):  
Yume Imahori ◽  
Davide L. Vetrano ◽  
Petter Ljungman ◽  
Chengxuan Qiu

Background: Markers of altered cardiac function might predict cognitive decline and dementia. Objective: This systematic review aims to review the literature that examines the associations of various electrocardiogram (ECG) markers with cognitive decline and dementia in middle-aged and elderly populations. Methods: We searched PubMed, Embase, and Web of Science through 1 July 2020 for literature and conducted a systematic literature review. We included studies examining the associations of ECG markers (e.g., left ventricular hypertrophy [LVH], spatial QRS-T angle, and QT prolongation) with cognitive function and dementia in adult populations regardless of study setting and design, but excluded studies examining atrial fibrillation and heart rate variability. Results: Fourteen community-based cross-sectional and longitudinal studies were identified. ECG markers were investigated in association with dementia in four prospective studies, and with cognitive decline in ten prospective studies. ECG-assessed LVH was associated with dementia in one study while five heterogeneous prospective studies yielded inconsistent associations with cognitive decline. Regarding ventricular repolarization markers, spatial QRS-T angle was associated with cognitive decline in one study while another study found no association between QT prolongation and cognitive decline. High resting heart rate was associated with both dementia and cognitive decline in one study but not associated with dementia in another study. P-wave abnormality was significantly associated with incident dementia and cognitive decline in one prospective study. Conclusion: Some ECG markers were associated with incident dementia and cognitive decline. However, limited number of heterogeneous studies did not allow us to make firm conclusions. Further studies are needed.


2011 ◽  
pp. 42-47
Author(s):  
James R. Munis

We've already looked at 2 types of pressure that affect physiology (atmospheric and hydrostatic pressure). Now let's consider the third: vascular pressures that result from mechanical events in the cardiovascular system. As you already know, cardiac output can be defined as the product of heart rate times stroke volume. Heart rate is self-explanatory. Stroke volume is determined by 3 factors—preload, afterload, and inotropy—and these determinants are in turn dependent on how the left ventricle handles pressure. In a pressure-volume loop, ‘afterload’ is represented by the pressure at the end of isovolumic contraction—just when the aortic valve opens (because the ventricular pressure is now higher than aortic root pressure). These loops not only are straightforward but are easier to construct just by thinking them through, rather than by memorization.


1989 ◽  
Vol 257 (4) ◽  
pp. H1062-H1067 ◽  
Author(s):  
R. W. Lee ◽  
R. G. Gay ◽  
S. Goldman

To determine whether atrial natriuretic peptide (ANP) can reverse angiotensin (ANG II)-induced venoconstriction, ANP was infused (0.3 micrograms.kg-1.min-1) in the presence of ANG II-induced hypertension in six ganglion-blocked dogs. ANG II was initially administered to increase mean arterial blood pressure (MAP) 50% above control. ANG II did not change heart rate or left ventricular rate of pressure development (LV dP/dt) but increased total peripheral vascular resistance (TPVR) and left ventricular end-diastolic pressure (LVEDP). Mean circulatory filling pressure (MCFP) increased, whereas cardiac output and venous compliance decreased. Unstressed vascular volume did not change, but central blood volume increased. ANP infusion during ANG II-induced hypertension resulted in a decrease in MAP, but TPVR did not change. There were no changes in heart rate or LV dP/dt. ANP decreased cardiac output further. LVEDP returned to base line with ANP. ANP also decreased MCFP and normalized venous compliance. There was no significant change in total blood volume, but central blood volume decreased. In summary, ANP can reverse the venoconstriction but not the arterial vasoconstriction produced by ANG II. The decrease in MAP was due to a decrease in cardiac output that resulted from venodilatation and aggravation of the preload-afterload mismatch produced by ANG II alone. Because TPVR did not change when MAP fell, we conclude that the interaction between ANG II and ANP occurs primarily in the venous circulation.


1995 ◽  
Vol 78 (5) ◽  
pp. 1793-1799 ◽  
Author(s):  
M. Kamitomo ◽  
T. Ohtsuka ◽  
R. D. Gilbert

We exposed fetuses to high-altitude (3,820 m) hypoxemia from 30 to 130 days gestation, when we measured fetal heart rate, right and left ventricular outputs with electromagnetic flow probes, and arterial blood pressure during an isoproterenol dose-response infusion. We also measured the distribution of cardiac output with radiolabeled microspheres during the maximal isoproterenol dose. Baseline fetal arterial blood pressure was higher in long-term hypoxemic fetuses (50.1 +/- 1.3 vs. 43.4 +/- 1.0 mmHg) but fell during the isoproterenol infusion to 41.3 +/- 1.4 and 37.5 +/- 1.4 mmHg, respectively, at the highest dose. Heart rate was the same in both groups and did not differ during isoproterenol infusion. Baseline fetal cardiac output was lower in the hypoxemic group (339 +/- 18 vs. 436 +/- 19 ml.min-1.kg-1) due mainly to a reduction in right ventricular output. During the isoproterenol infusion, right ventricular output increased to the same extent in both hypoxemic and normoxic fetuses (approximately 35%); however, left ventricular output increased only approximately 15% in the hypoxemic group compared with approximately 40% in the normoxic group. The percent change in individual organ blood flows during isoproterenol infusion in the hypoxemic groups was not significantly different from the normoxic group. All of the mechanisms that might be responsible for the differential response of the fetal left and right ventricles to long-term hypoxia are not understood and need further exploration.


1997 ◽  
Vol 273 (6) ◽  
pp. H2919-H2925 ◽  
Author(s):  
Dierk E. Remmers ◽  
Ping Wang ◽  
William G. Cioffi ◽  
Kirby I. Bland ◽  
Irshad H. Chaudry

Although studies have shown that testosterone receptor blockade with flutamide after hemorrhage restores the depressed immune function, it remains unknown whether administration of flutamide following trauma and hemorrhage and resuscitation has any salutary effects on the depressed cardiovascular and hepatocellular functions. To study this, male rats underwent a laparotomy (representing trauma) and were then bled and maintained at a mean arterial pressure (MAP) of 40 mmHg until the animals could not maintain this pressure. Ringer lactate was given to maintain a MAP of 40 mmHg until 40% of the maximal shed blood volume was returned in the form of Ringer lactate. The rats were then resuscitated with four times the shed blood volume in the form of Ringer lactate over 60 min. Flutamide (25 mg/kg) or an equal volume of the vehicle propanediol was injected subcutaneously 15 min before the end of resuscitation. Various in vivo heart performance parameters (e.g., maximal rate of the pressure increase or decrease), cardiac output, and hepatocellular function (i.e., the maximum velocity and the overall efficiency of indocyanine green clearance) were determined at 20 h after resuscitation. Additionally, hepatic microvascular blood flow (HMBF) was determined using a laser Doppler flowmeter. The results indicate that left ventricular performance, cardiac output, HMBF, and hepatocellular function decreased significantly at 20 h after the completion of trauma, hemorrhage, and resuscitation. Administration of the testosterone receptor blocker flutamide, however, significantly improved cardiac performance, HMBF, and hepatocellular function. Thus flutamide appears to be a novel and useful adjunct for improving cardiovascular and hepatocellular functions in males following trauma and hemorrhagic shock.


1984 ◽  
Vol 247 (1) ◽  
pp. H1-H7 ◽  
Author(s):  
C. F. Pilati ◽  
M. B. Maron

The effect of histamine on coronary vascular permeability was assessed under conditions of elevated venous pressure in the spontaneously beating, isolated canine heart perfused with autologous blood. The apparent volume of fluid filtered from the vasculature to the interstitium (VF) was calculated from the increase in plasma protein concentration and also from the increase in hematocrit. The ratio of the protein-filtered volume to the hematocrit-filtered volume (VF,Pr/VF,Hct) was used to evaluate changes in permeability. In the absence of histamine, the VF,Pr/VF,Hct was near unity (1.05 +/- 0.11), which indicated that the blood proteins and the red blood cells had concentrated equally. Thus the transudate was essentially protein free. On exposure to histamine (3.8 +/- 0.3 microgram base/ml blood), VF,Pr/VF,Hct decreased to 0.37 +/- 0.06 (P less than 0.001), which indicated that coronary vascular permeability had increased. This value remained constant throughout the 60 min of histamine exposure. Aortic perfusion pressure decreased significantly (P less than 0.05) from 111 +/- 11 to 84 +/- 5 mmHg during the 1st min of histamine exposure and rose slowly thereafter. In four of the seven hearts, concomitant increases in left ventricular isovolumic pressure development (13-31 mmHg) and heart rate (4-29 beats/min) were observed. In the remaining hearts, neither variable was affected by histamine. We conclude that histamine causes an increase in the permeability of the canine coronary microvasculature but fails to increase heart rate or left ventricular performance consistently.


1996 ◽  
Vol 91 (3) ◽  
pp. 275-281 ◽  
Author(s):  
Paolo Palatini ◽  
Pieralberto Visentin ◽  
Gianluigi Nicolosi ◽  
Vincenzo Mione ◽  
Paolo Stritoni ◽  
...  

1. To assess the clinical significance of supernormal left ventricular systolic function in the initial phase of hypertension, 635 never-treated 18–45-year-old borderline to mild hypertensive subjects (477 males, 158 females) were studied. All subjects underwent echocardiography, 24 h ambulatory blood pressure monitoring and 24 h urine collection for catecholamine dosage. 2. Subjects whose left ventricular shortening-stress relationship was above the 95% confidence intervals of 50 normotensive subjects of similar age and sex distribution were defined as having supernormal function. 3. Age, duration of hypertension and left ventricular mass were similar in the hypertensive subjects with normal (85%) and supernormal (15%) ejective performance. Subjects with supernormal function showed higher office systolic blood pressure (P < 0001), office heart rate (P = 0.03) and cardiac index (P < 0001). Conversely, 24 h systolic blood pressure, 24 h heart rate and 24 h catecholamine output did not differ according to left ventricular function. 4. In conclusion, the greater white-coat effect and the normal baseline sympathetic tone exhibited by the patients with increased performance suggest that supernormal left ventricular pump function is only a marker of the alerting reaction elicited by the echocardiographic examination.


Sign in / Sign up

Export Citation Format

Share Document