Use of Intravascular Carbon Dioxide Gas to Demonstrate Interatrial Septal Defects

1958 ◽  
Vol 195 (3) ◽  
pp. 579-585 ◽  
Author(s):  
William Winters ◽  
Michael Wilson ◽  
Dithi Chungcharoen ◽  
Herbert M. Stauffer ◽  
Thomas M. Durant ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Left Atrium ◽  
Systolic Pressure ◽  
Systemic Blood Pressure ◽  
Left Ventricular ◽  
Experimental Conditions ◽  
Ventricular Systolic Pressure ◽  
Systemic Pressure ◽  
Carbon Dioxide Gas ◽  
The Right

Carbon dioxide gas injected intravenously will safely demonstrate experimental interatrial defects using a cinefluorographic technique. Under these experimental conditions gas may be demonstrated in the left atrium and ventricle. At the time gas passes through the defect the systemic pressure rises. In the absence of a defect the systemic pressure falls. Left ventricular systolic pressure levels parallel the changes in systemic blood pressure. The presence of gas in the right atrium elevates pressure in the left atrium only a few millimeters of mercury in controls and in the presence of interatrial defects.

Cyanosis due to diastolic right-to-left shunting across a ventricular septal defect in a patient with repaired tetralogy of Fallot and pulmonary atresia

1999 ◽  
Vol 9 (5) ◽  
pp. 506-508
Author(s):  
J. D. R. Thomson ◽  
J. Forster ◽  
J. L. Gibbs
Keyword(s):  
Ventricular Septal Defect ◽  
Congenital Heart ◽  
Septal Defect ◽  
Pulmonary Atresia ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
The Right

AbstractCyanosis as a result of right-to-left shunting across a ventricular septal defect is commonly encountered in patients with congenital heart disease when systolic pressure in the right ventricle exceeds that in the left ventricle. Reported is the case of a child who remained cyanosed after surgical correction of pulmonary atresia despite right ventricular systolic pressure being lower than left ventricular pressure. Colour-flow Doppler showed a residual ventricular septal defect, with right-to-left shunting in diastole alone.

scholarly journals Right ventricular function and its coupling with the pulmonary circulation in acute heart failure

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Barki ◽  
M Losito ◽  
M.M Caracciolo ◽  
F Bandera ◽  
M Rovida ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Acute Phase ◽  
Pulmonary Circulation ◽  
Heart Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Response To Treatment ◽  
The Right ◽  
B Lines

Abstract Background The right ventricle (RV) is extremely sensitive to hemodynamic changes and increased impedance. In acute heart failure (AHF), the development of pulmonary venous congestion and the increase of left ventricular (LV) filling pressures favors pulmonary vascular adverse remodeling and ultimately RV dysfunction, leading to the onset of symptoms and to a further decay of cardiac dynamics. Purpose The aim of the study was to evaluate RV morphology and functional dynamics at admission and discharge in patients hospitalized for AHF, analyzing the role and the response to treatment of the RV and its coupling with pulmonary circulation (PC). Methods Eighty-one AHF patients (mean age 75.75±10.6 years, 59% males) were prospectively enrolled within 24–48 hours from admission to the emergency department (ED). In either the acute phase and at pre-discharge all patients underwent M-Mode, 2-Dimensional and Doppler transthoracic echocardiography (TTE), as well as lung ultrasonography (LUS), to detect an increase of extravascular lung water (EVLW) and development of pleural effusion. Laboratory tests were performed in the acute phase and at pre-discharge including the evaluation of NT-proBNP. Results At baseline we observed a high prevalence of RV dysfunction as documented by a reduced RV systolic longitudinal function [mean tricuspid annular plane systolic excursion (TAPSE) at admission of 16.47±3.86 mm with 50% of the patients exhibiting a TAPSE<16mm], a decreased DTI-derived tricuspid lateral annular systolic velocity (50% of the subjects showed a tricuspid s' wave<10 cm/s) and a reduced RV fractional area change (mean FAC at admission of 36.4±14.6%). Furthermore, an increased pulmonary arterial systolic pressure (PASP) and a severe impairment in terms of RV coupling to PC was detected at initial evaluation (mean PASP at admission: 38.8±10.8 mmHg; average TAPSE/PASP at admission: 0.45±0.17 mm/mmHg). At pre-discharge a significant increment of TAPSE (16.47±3.86 mm vs. 17.45±3.88; p=0.05) and a reduction of PASP (38.8±10.8 mmHg vs. 30.5±9.6mmHg, p<0.001) was observed. Furthermore, in the whole population we assisted to a significant improvement in terms of RV function and its coupling with PC as demonstrated by the significant increase of TAPSE/PASP ratio (TAPSE/PASP: 0.45±0.17 mm/mmHg vs 0.62±0.20 mm/mmHg; p<0.001). Patients significantly reduced from admission to discharge the number of B-lines and NT-proBNP (B-lines: 22.2±17.1 vs. 6.5±5 p<0.001; NT-proBNP: 8738±948 ng/l vs 4227±659 ng/l p<0.001) (Figure 1). Nonetheless, no significant changes of left atrial and left ventricular dimensions and function were noted. Conclusions In AHF, development of congestion and EVLW significantly impact on the right heart function. Decongestion therapy is effective for restoring acute reversal of RV dysfunction, but the question remains on how to impact on the biological properties of the RV. Funding Acknowledgement Type of funding source: None

Abstract 16574: Heart Failure Biomarkers (NT-proBNP, Gal-3, sST2) Correlate With Right Ventricular Systolic Pressure and Provide Insight to Poor CRT Response: A BIOCRT Substudy

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Roderick C Deaño ◽  
Jackie Szymonifka ◽  
Qing Zhou ◽  
Jigar H Contractor ◽  
Zachary Lavender ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Systolic Pressure ◽  
Fold Increase ◽  
Left Ventricular ◽  
Cardiac Resynchronization ◽  
Cardiac Transplant ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Crt Response

Objective: Patients with heart failure (HF) and pulmonary hypertension (PH) have worse outcomes after cardiac resynchronization therapy (CRT). The relationship of circulating HF biomarkers and right ventricular systolic pressure (RVSP) may provide insight to the mechanism between PH and poor CRT response. Methods: In 90 patients (age 65 ± 13, 78% male, EF 26 ± 8%, RVSP 44 ± 12 mmHg) undergoing CRT, we measured baseline RVSP by echocardiography and obtained peripheral blood samples drawn at the time of device implantation. We measured levels of established and emerging HF biomarkers (Table 1). CRT non-response was defined as no improvement of adjudicated HF Clinical Composite Score at 6 months. Major adverse cardiac event (MACE) was defined as composite endpoint of death, cardiac transplant, left ventricular assist device, and HF hospitalization within 2 years. Results: There were 34% CRT non-responders and 27% had MACE. Per 1 unit increase in log-transformed RVSP, there was an 11-fold increase risk of having CRT non-response (odd ratio [OR] 11.0, p=0.01) and over 5-fold increase of developing 2-year MACE (hazard ratio [HR] 5.8, p=0.02). When comparing patients with severe PH (RVSP>60 mmHg) to those without PH (RVSP < 35 mmHg), there was an 8-fold increase in CRT nonresponse (OR 8.4, p=0.03) but no difference in MACE (p=NS). RVSP was correlated with increased biomarker levels of myocardial stretch and fibrosis, but not myocardial necrosis (Table 1). Conclusions: Higher RVSP is associated with greater rates of CRT non-response and adverse clinical outcomes. The mechanistic association between severe PH and CRT nonresponse may be explained by the biomarker profile reflective of myocardial wall stretch and fibrosis.

Right ventricular pressure response to +GZ acceleration stress

1982 ◽  
Vol 53 (4) ◽  
pp. 908-913 ◽  
Author(s):  
J. E. Whinnery ◽  
M. H. Laughlin
Keyword(s):  
Right Ventricular ◽  
Diastolic Pressure ◽  
Vena Cava ◽  
Systolic Pressure ◽  
Ventricular Pressure ◽  
Miniature Swine ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
The Right ◽  
Acceleration Stress

Measurements of right ventricular pressure in miniature swine were made at +Gz levels from +1 through +9 Gz. Polyethylene catheters were chronically placed in the cranial vena cava of five 2-yr-old female miniature swine (35–50 kg). The catheters were large enough to allow the introduction of a Millar pressure transducer into the venous system for placement in the right heart. The animals were fitted with an abdominal anti-G suit, restrained in a fiberglass couch, and exposed to the various +Gz levels on a centrifuge while fully conscious and unanesthetized. Right ventricular pressure and heart rate were measured during and for 2 min following 30-s exposures to each level of +Gz stress. The maximum right ventricular systolic pressure observed during +Gz was 200 Torr at +5 Gz with the maximum diastolic pressure being 88 Torr observed at +5 Gz. Mean heart rates were 200–210 beats/min at all levels of +Gz greater than or equal to +3 Gz when the animal remained stable. Mean maximum right ventricular pressures during +Gz stress were observed to increase through +5 Gz (85 Torr) and to decrease at higher levels of +Gz, indicating that through +5 Gz there is at least a partial compensation during acceleration stress. Decompensation in response to the stress began to occur during acceleration above +5 Gz with all animals decompensating during +9 Gz.

The Effect of Gypenosides on Cardiac Function and Expression of Cytoskeletal Genes of Myocardium in Diabetic Cardiomyopathy Rats

2009 ◽  
Vol 37 (06) ◽  
pp. 1059-1068 ◽  
Author(s):  
Min Ge ◽  
Shanfeng Ma ◽  
Liang Tao ◽  
Sudong Guan
Keyword(s):  
Cardiac Function ◽  
Diabetic Cardiomyopathy ◽  
Diastolic Pressure ◽  
Pure Water ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Sprague Dawley ◽  
Gene Expressions ◽  
Ventricular Systolic Pressure

The relationship between changes of cardiac function and the gene expressions of two major myocardial skeleton proteins, titin and nebulin, and the effect of gypenosides on these gene expressions in diabetic cardiomyopathy rat were explored in the present study. Forty Sprague-Dawley rats were randomly divided into three groups: control group, diabetic cardiomyopathy group and gypenosides-treated diabetic cardiomyopathy group. The diabetic cardiomyopathy was induced in rats by injecting streptozotocin (STZ, 55 mg/kg) intraperitoneally. Seven weeks after the rats suffered from diabetes, the rats were treated with gypenosides 100 mg/kg per day orally for six weeks in gypenosides-treated group. In the meanwhile, the pure water was given to diabetic cardiomyopathy and the control groups. Subsequently, the cardiac functions, including left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), ± dP/dtmax and t–dP/dmaxt, as well as the mRNA content and proteins of titin and nebulin in myocardium were determined. The results indicated that (1) the diabetic cardiomyopathy rats had decreased LVSP and ± dP/dtmax, increased LVEDP, and prolonged t–dP/dtmax than normal rats; (2) LVSP and ± dP/dtmax in diabetic cardiomyopathy rats treated with gypenosides were significantly higher and LVEDP and t–dP/dtmax were significantly lower than those without giving gypenosides; (3) the mRNA contents and proteins of titin and nebulin in diabetic cardiomyopathy rats were remarkably lower than those in the control rats and gypenosides had no effect on mRNA and protein expression levels of titin and nebulin in diabetic cardiomyopathy rats. We conclude that (1) the cardiac function as well as the mRNA expressions of titin and nebulin decreased in diabetic cardiomyopathy rats; (2) gypenosides secure cardiac muscles and their function from diabetic impairment and these beneficial effects of gypenosides are not by changing the expressions of titin and nebulin.

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

Effect of human urotensin-II infusion on hemodynamics and cardiac function

2003 ◽  
Vol 81 (2) ◽  
pp. 125-128 ◽  
Author(s):  
Ghada S Hassan ◽  
Fazila Chouiali ◽  
Takayuki Saito ◽  
Fu Hu ◽  
Stephen A Douglas ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Diastolic Pressure ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Urotensin Ii ◽  
Ventricular Systolic Pressure ◽  
Wide Range ◽  
Dose Dependent Decrease

Recent studies have shown that the vasoactive peptide urotensin-II (U-II) exerts a wide range of action on the cardiovascular system of various species. In the present study, we determined the in vivo effects of U-II on basal hemodynamics and cardiac function in the anesthetized intact rat. Intravenous bolus injection of human U-II resulted in a dose-dependent decrease in mean arterial pressure and left ventricular systolic pressure. Cardiac contractility represented by ±dP/dt was decreased after injection of U-II. However, there was no significant change in heart rate or diastolic pressure. The present study suggests that upregulation of myocardial U-II may contribute to impaired myocardial function in disease conditions such as congestive heart failure.Key words: urotensin-II, rat, infusion, heart.

Abstract P144: Effects of Alamandine in Post-ischemic Function

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Jonathas F Almeida ◽  
Robson A Santos
Keyword(s):  
Ischemia Reperfusion ◽  
Systolic Pressure ◽  
Baseline Period ◽  
Left Ventricular ◽  
Biologically Active ◽  
Ventricular Systolic Pressure ◽  
Infarcted Area ◽  
Rat Hearts ◽  
Ischemic Period ◽  
Isolated Rat

Alamandine, a biologically active peptide of the renin-angiotensin system (RAS), was recently described and characterized. Further it has been shown to present effects similar to those elicited by Ang-(1-7). It has been described that Ang-(1-7) decreases the incidence and duration of ischemia-reperfusion arrhythmias and improved the post-ischemic function in isolated perfused rat hearts. In this study we aimed to evaluate the effects of Alamandine in isolated rat hearts subjected to myocardial infarction (MI). Wistar rats weighing between 250-300g were euthanized and their hearts were placed on Langendorff apparatus to evaluate the cardiac parameters. Hearts were submitted to 30min of stabilization, 30min of partial ischemia by occlusion of the left descending coronary artery and 30min of reperfusion. Drugs (alamandine 22pM, d-pro7-ang-(1-7) 220pM) were added to the perfusion setting from the beginning of the experiment until the end. 2,3,5-trypheniltetrazolium chloride were used to evaluate the extension of infarcted area. In control hearts (CON), there was a decrease on the left ventricular systolic pressure (LVSP) on ischemic period (54,6 ± 6,9mmHg) compared to the baseline period (84,6 ± 11,6mmHg). Alamandine (ALA) attenuated that decrease in the ischemic period (66,9 ± 7,9mmHg) vs (82,3 ± 8,9mmHg). Further, ischemia led to a decrease in the left ventricular developed pressure (dLVP), dP/dt maximum and minimum when compared to baseline values. ALA, once more, kept the ischemic parameters of dLVP and dP/dt max and min (58,9 ± 8mmHg; 1629 ± 202,2mmHg/s; 1101 ± 130mmHg/s, respectively) similar to those of baseline period (68,9 ± 8,92; 1682 ± 248,8; 1179 ± 118,6 mmHg, respectively). Ischemia/reperfusion induced an arrhythmia severity index (ASI) in control hearts (4,9 ± 1,26) higher than in hearts treated with ALA (1,10 ± 0,58). ALA also reduced infarcted area (19,64 ± 2,61%) compared with CON (33,85 ± 4,55%). All those effects were blocked by D-PRO7-Ang-(1-7). In conclusion, our data shown that Alamandine exert cardioprotective effects in post-ischemic function in isolated rat hearts by preventing LVSP, dLVP , dP/dt max and min decrease. Furthermore it reduced the infarcted area and I/R arrhythmias, apparently involving MrgD receptor participation.

Role of reflexes following myocardial necrobiosis

1965 ◽  
Vol 209 (6) ◽  
pp. 1081-1088 ◽  
Author(s):  
G. Ascanio ◽  
F. Barrera ◽  
E. V. Lautsch ◽  
M. J. Oppenheimer
Keyword(s):  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Hemodynamic Changes ◽  
Ventricular Systolic Pressure ◽  
Arterial Blood ◽  
Bilateral Vagotomy ◽  
Left Ventricular Systolic Pressure

Intracoronary administration of hexachlorotetrafluorobutane (Hexa) into non-thoracotomized dogs produced a statistically significant decrease in left ventricular systolic pressure (LVSP), mean femoral arterial blood pressure (MFAP), first derivative of left ventricular pressure pulse (dP/d t), total peripheral resistance (TPR), and cardiac output (C.O.) lasting up to 1 hr after injection. Femoral vascular resistance decreased during the first 3 min after production of necrobiosis. Fifty percent of the dogs died of ventricular fibrillation (VF) after Hexa infarction. Prereserpinized dogs did not show significant changes in the parameters which were significantly changed in normal dogs after Hexa necrobiosis except in the case of VF which was almost absent in this group. Bilateral vagotomy prior to Hexa administration prevented most hemodynamic changes after necrobiosis whereas atropine did not. Bilateral vagotomy and atropine 1 hr after necrobiosis increased MFAP, dP/d t, LVSP, C.O., and TPR. Apparently excitatory efferent sympathetic activity on heart and femoral arterial vessels is reflexly inhibited by the effects of intracoronary injection of Hexa. The afferent pathway is via the vagus nerve.

Effects of alpha-adrenergic blockade on cardiovascular responses to static exercise in cats

1986 ◽  
Vol 250 (1) ◽  
pp. R1-R4
Author(s):  
T. G. Waldrop ◽  
M. Bielecki ◽  
W. J. Gonyea ◽  
J. H. Mitchell
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Static Exercise ◽  
Ventricular Systolic Pressure ◽  
Pressure Transducers ◽  
Adrenergic Mechanism ◽  
Alpha Blockade

Static exercise performed by conscious cats elicits increases in heart rate (HR), left ventricular systolic pressure (LVSP), and the maximal rate of left ventricular pressure development [LV(dP/dt)max]. The increased HR is mediated primarily by withdrawal of parasympathetic tone, whereas a beta-adrenergic mechanism is responsible for the LV(dP/dt)max increase. In the present study the cardiovascular responses to static exercise in awake cats was recorded before and after alpha-adrenergic blockade. Pressure transducers were implanted into the left ventricle of cats who had been trained operantly to perform static exercise. Significant increases in LVSP, LV(dP/dt)max and HR occurred in all cats during static exercise before blockade. In contrast, alpha-adrenergic blockade (phentolamine, 2.5 mg/kg iv) abolished the exercise-induced increase in LVSP but did not prevent increases in HR and LV(dP/dt)max. The cats performed fewer exercise bouts per day during alpha-blockade than when unblocked. We conclude that an alpha-adrenergic mechanism mediates the increase in LVSP in response to static exercise in conscious cats.

Sign in / Sign up

Export Citation Format

Share Document