Optimal matching between canine left ventricle and afterload

1988 ◽  
Vol 254 (6) ◽  
pp. H1051-H1058
Author(s):  
E. S. Myhre ◽  
A. Johansen ◽  
H. Piene
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Stroke Work ◽  
External Work ◽  
Volume Load ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Pressure Volume Relationship ◽  
Optimal Values

A parabolic relationship exists between ventricular external work and arterial load at given preload and contractility. Previous data indicate that the working point falls close to the parabola optimum. By combining the left ventricular (LV) end-systolic pressure-volume relationship (ESPVR) and an equation describing external stroke work, optimum values of stroke volume (SV), the slope (Emax) of the ESPVR, and arterial resistance (Rp) corresponding with the optimum (i.e., mSV, mEmax, mRp) were obtained. Experiments in anesthetized dogs were performed to test whether mSV, mEmax, and mRp also correspond to observed SV, Emax, and Rp at three different levels of volume load (right atrial pressure, RAP) before and after acute depression of LV contractility. Comparisons of observed and optimal values of SV, Emax, and Rp were made before and after LV depression. Before embolization, the ratios were SV/mSV 1.10–1.20 (RAP 5–15 mmHg); Emax/mEmax 1.21–1.41; and Rp/mRp 0.84–0.69. After LV depression, SV/mSV was 0.80–0.83, Emax/mEmax was 0.78–0.71, and Rp/mRp was 1.56–1.46. The ratios were all significantly changed (P less than 0.01) by the induced LV depression. The present analysis may offer a new tool to detect nonoptimal relations between cardiac and arterial functions.

scholarly journals Altered LV inotropic reserve and mechanoenergetics early in the development of heart failure

2000 ◽  
Vol 278 (3) ◽  
pp. H698-H705 ◽  
Author(s):  
Sumanth D. Prabhu ◽  
Gregory L. Freeman
Keyword(s):  
Heart Failure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Short Term ◽  
Before And After ◽  
Autonomic Blockade ◽  
Anesthetized Dogs ◽  
Rapid Ventricular Pacing ◽  
Volume Relation

To test the hypothesis that alterations in left ventricular (LV) mechanoenergetics and the LV inotropic response to afterload manifest early in the evolution of heart failure, we examined six anesthetized dogs instrumented with LV micromanometers, piezoelectric crystals, and coronary sinus catheters before and after 24 h of rapid ventricular pacing (RVP). After autonomic blockade, the end-systolic pressure-volume relation (ESPVR), myocardial O2 consumption (MV˙o 2), and LV pressure-volume area (PVA) were defined at several different afterloads produced by graded infusions of phenylephrine. Short-term RVP resulted in reduced preload with proportionate reductions in stroke work and the maximum first derivative of LV pressure but with no significant reduction in baseline LV contractile state. In response to increased afterload, the baseline ESPVR shifted to the left with maintained end-systolic elastance ( E es). In contrast, after short-term RVP, in response to comparable increases in afterload, the ESPVR displayed reduced E es ( P < 0.05) and significantly less leftward shift compared with control ( P< 0.05). Compared with the control MV˙o 2-PVA relation, short-term RVP significantly increased the MV˙o 2 intercept ( P< 0.05) with no change in slope. These results indicate that short-term RVP produces attenuation of afterload-induced enhancement of LV performance and increases energy consumption for nonmechanical processes with maintenance of contractile efficiency, suggesting that early in the development of tachycardia heart failure, there is blunting of length-dependent activation and increased O2requirements for excitation-contraction coupling, basal metabolism, or both. Rather than being adaptive mechanisms, these abnormalities may be primary defects involved in the progression of the heart failure phenotype.

Increased myocardial contractility during endotoxin shock in dogs

1985 ◽  
Vol 249 (4) ◽  
pp. H715-H722 ◽  
Author(s):  
P. M. Kober ◽  
J. X. Thomas ◽  
R. M. Raymond
Keyword(s):  
Myocardial Contractility ◽  
Salmonella Enteritidis ◽  
Systolic Pressure ◽  
Systemic Arterial Pressure ◽  
Endotoxin Shock ◽  
Left Ventricular ◽  
Terminal Phase ◽  
Endotoxin Administration ◽  
Before And After ◽  
Anesthetized Dogs

The slope of the left ventricular (LV) end-systolic pressure-diameter relationship (Ees) was analyzed in open-chest, pentobarbital-anesthetized dogs before and after endotoxin administration. A lead II electrocardiogram, systemic arterial pressure, LV pressure, LV dP/dt, and LV minor axis diameter were measured. After control measurements were taken, dogs were given either 1 mg/kg Salmonella enteritidis endotoxin (n = 5) or an equivalent volume of saline (n = 4). Control dogs were followed for 240 min. Endotoxic dogs were monitored until death (246 +/- 44 min). There were no significant changes in Ees in control dogs (17 +/- 3 mmHg/mm), which were hemodynamically stable for 4 h. Ees was significantly increased in endotoxic dogs even into the late stages of shock (41 +/- 11 mmHg/mm, P less than 0.01). Only during the terminal phase did Ees fall significantly below control (11 +/- 2 mmHg/mm, P less than 0.05). End-diastolic diameter decreased following endotoxin administration (P less than 0.05) but returned toward control by the terminal stage. Peak + LV dP/dt was depressed following endotoxin injection. Myocardial contractility was not depressed except as a terminal event. Early depression of cardiovascular performance in endotoxic dogs was therefore due to decreased preload and not cardiac dysfunction.

Effects of hypertonic saline and dextran 70 on cardiac functions after burns

1995 ◽  
Vol 268 (2) ◽  
pp. H856-H864 ◽  
Author(s):  
K. Suzuki ◽  
R. Ogino ◽  
M. Nishina ◽  
A. Kohama
Keyword(s):  
Hypertonic Saline ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Sudden Increase ◽  
Stroke Work ◽  
End Diastolic Volume ◽  
Significant Difference ◽  
Volume Relationship ◽  
Pressure Volume Relationship

The effects of hypertonic saline-dextran (HSD) on cardiac contractility and hemodynamics after burns were studied in anesthetized animals with full-thickness 50% total body surface area burns that were resuscitated with HSD or lactated Ringer solution (LR) alone. No significant difference in cardiac contractility during 6 h postburn was observed between the two groups, as assessed by the end-systolic pressure-volume relationship and the stroke work-end-diastolic volume relationship. An additional bolus of HSD at 6 h postburn caused no significant changes in the end-systolic pressure-volume relationship and stroke work-end-diastolic volume relationship in the burned and sham-burned animals, both of which were resuscitated with HSD. Ten minutes of hemodynamic changes following HSD infusion at 30 min postburn revealed a sudden increase in stroke volume with biphasic responses in left ventricular systolic pressure, which first decreased, then increased, and finally returned to the pre-HSD value. End-diastolic volume was maintained at approximately 110% of the pre-HSD value during this period. We concluded that HSD does not enhance cardiac contractility after severe burns but does produce direct effects on postburn circulation to reduce afterload and augment preload, resulting in a short-lived increase in cardiac output.

Pulmonary injury depresses cardiac systolic function through Starling mechanism

1986 ◽  
Vol 251 (4) ◽  
pp. H722-H733 ◽  
Author(s):  
J. E. Calvin ◽  
R. W. Baer ◽  
S. A. Glantz
Keyword(s):  
Diastolic Pressure ◽  
Systolic Function ◽  
Left Ventricular ◽  
Stroke Work ◽  
Volume Loading ◽  
Lung Hyperinflation ◽  
Microvascular Injury ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Heart Size

To determine whether pulmonary microvascular injury or lung hyperinflation changes left ventricular (LV) performance and whether ventricular interaction plays a role in mediating such changes, we studied seven open-chest, closed-pericardium, anesthetized dogs before and after right ventricular (RV) injections of 150- to 200-micron glass beads. Because people with pulmonary disease are often treated with positive end-expiratory pressure, we also hyperinflated the lungs before and after creating the pulmonary microvascular injury. Measurements of LV and RV pressures and dimensions were taken at end expiration during the basal state, during lung hyperinflation, and after microvascular injury at RV end-diastolic pressures of 5, 10, and 15 mmHg produced by volume loading. Acute volume loading produced upward shifts in the LV diastolic pressure-size curve both before and after microvascular injury. Neither microvascular injury nor lung hyperinflation substantially affected the LV diastolic pressure-size relationship. LV end-diastolic size determined LV stroke work with no consistent independent influence of microvascular injury or lung hyperinflation. Neither microvascular injury nor lung hyperinflation depressed systolic performance beyond that associated with changes in end-diastolic heart size.

Effects of increased afterload on left ventricular function in closed-chest dogs

1990 ◽  
Vol 259 (2) ◽  
pp. H619-H625 ◽  
Author(s):  
G. L. Freeman
Keyword(s):  
Mechanical Response ◽  
Systolic Pressure ◽  
Circulatory System ◽  
Left Ventricular ◽  
Stroke Work ◽  
Closed Chest ◽  
End Diastolic Volume ◽  
Before And After ◽  
Pressure Development ◽  
Integrated Response

Mechanical response of the left ventricle (LV) in an intact circulatory system to steady-state increases in afterload may differ from that of an isolated LV, because secondary hemodynamic changes cannot be independently manipulated when the circulation is intact. To evaluate the integrated response of the LV in closed-chest dogs to sustained increases in afterload, six animals chronically instrumented with three orthogonal diameter gauges and LV manometers were studied after autonomic blockade and fentanyl-droperidol anesthesia. End-systolic pressure-volume (PES-VES) and stroke work end-diastolic volume (SW-EDV) relations and the relations between pressure-volume area (PVA, area bounded by PV loop and PES-VES relation) and EDV were quantified. Balloon inflation (BI) in the proximal descending aorta increased LV PES from 100.7 +/- 13.4 to 140.2 +/- 19.3 mmHg (P less than 0.002) and LVEDV from 39.1 +/- 11.3 to 43.3 +/- 12.2 ml (P less than 0.01). The slope of the PES-VES relation was not significantly changed, whereas V100, a volume intercept in the common range of pressures, was reduced from 27.5 +/- 7.3 to 23.7 +/- 6.1 ml (P less than 0.005). PVA-EDV relation was highly linear; its slope was increased after BI. Comparison of beats with matched LVEDV before and after BI showed significant increases in maximum rate of pressure development and PVA; the change in SW after BI was modest and not significant. The efficiency of energy transfer from PVA to SW (TransPVA, SW/PVA X 100) decreased from 52.5 +/- 8.6 to 42.6 +/- 6.3% (P less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of the right ventricle on canine left ventricular function with PEEP

1982 ◽  
Vol 52 (1) ◽  
pp. 254-259 ◽  
Author(s):  
S. M. Scharf ◽  
R. Brown
Keyword(s):  
Pulmonary Arterial Pressure ◽  
Arterial Occlusion ◽  
Left Ventricular ◽  
Right Atrial ◽  
Lv Function ◽  
Stroke Work ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
The Right ◽  
Extracorporeal Bypass

In anesthetized dogs we evaluated the influence of increased right ventricular (RV) pressures on left ventricular (LV) function by comparing the hemodynamic effects of increases in RV afterload (pulmonary arterial pressure) produced by positive end-expiratory pressure (PEEP) with those due to pulmonary arterial occlusion (PAO). Left atrial (Pla) and right atrial (Pra) pressures increased with PEEP and PAO [for Pla: 3.1 +/- 0.7 Torr (PEEP), 2.4 +/- 0.9 Torr (PAO); for Pra: 2.9 +/- 0.4 Torr (PEEP), 3.1 +/- 1.2 Torr (PAO)]. RV septal-free wall dimension (RVD) increased, and LV septal-posterolateral dimension (L2) decreased with both conditions [increases in RVD: 1.9 +/- 0.3 mm (PEEP), 2.2 +/- 0.5 mm (PAO); decrease in L2: 1.1 +/- 0.4 mm (PEEP), 0.9 +/- 0.3 mm (PAO)]. Extracorporeal bypass of the great veins did not alter these findings. LV function curves showed less stroke work at any Pla during PEEP, this being unaffected by vagotomy. When the RV was bypassed, there were no PEEP or PAO related changes in Pla or LV function. Thus diminished LV function with PEEP is probably due to the influence on the LV of a stressed RV in this situation.

Left ventricular contractility and diastolic properties in anesthetized dogs after severe burns

1991 ◽  
Vol 260 (5) ◽  
pp. H1433-H1442 ◽  
Author(s):  
K. Suzuki ◽  
M. Nishina ◽  
R. Ogino ◽  
A. Kohama
Keyword(s):  
Diastolic Pressure ◽  
Total Body Surface Area ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Control Group ◽  
Stroke Work ◽  
Ventricular Contractility ◽  
Volume Curve ◽  
Volume Relationship ◽  
Anesthetized Dogs

To clarify the mechanisms of a prompt decrease in cardiac output following burns, we studied left ventricular (LV) contractility and distensibility after full-thickness 50% total body surface area burns in anesthetized dogs during a 6-h postburn period. Contractility was assessed from the end-systolic pressure-volume relationship (ESPVR) and the stroke work-end-diastolic volume relationship (the preload recruitable stroke work relationship; PRSW). LV chamber distensibility was also assessed from the end-diastolic pressure-volume curve. The PRSW slopes in the burn group showed a significant decrease compared with those in the control group (P less than 0.05), indicating burn-impaired contractility. The ESPVR shifted significantly rightward without changes in its slope after burns (P less than 0.02). This also suggested that contractility was depressed by burns. On the other hand, there was no significant change in the indexes of chamber distensibility between the two groups. We therefore concluded that burns decreased contractility as well as preload but did not change end-diastolic distensibility during this early postburn period.

Left ventricular pressure-volume relationship in conscious mice

2007 ◽  
Vol 292 (1) ◽  
pp. H369-H377 ◽  
Author(s):  
Shuji Joho ◽  
Shinji Ishizaka ◽  
Richard Sievers ◽  
Elyse Foster ◽  
Paul C. Simpson ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Conscious State ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
Polyethylene Tube ◽  
End Diastolic Volume ◽  
Volume Relationship ◽  
Pressure Volume Relationship

With the availability of transgenic models, the mouse has become an increasingly important subject for genetic-hemodynamic studies. Recently, we developed a technique to measure left ventricular (LV) pressure in conscious mice with an implanted LV polyethylene tube. We extended our new method by evaluating the LV pressure-volume relationship and examined the feasibility of this method in this study. We studied 17 male mice (age, 11–20 wk) with a conductance catheter inserted into the LV through the polyethylene tube. Load-independent parameters of contractility derived from pressure-volume relationship [slope of the end-systolic pressure-volume relationship ( Ees), slope of the maximum first derivative of LV pressure (dP/d tmax)-end-diastolic volume (EDV) relation, and preload-recruitable stroke work (PRSW)] were evaluated by inferior vena caval occlusion with an implanted snare. LV function assessed by this technique on two different days showed that the parameters were very similar, indicating reproducibility. Both linear and nonlinear regression analyses were performed for Ees. Contractility was enhanced by isoproterenol ( Ees, 13.1 ± 6.6 to 20.8 ± 8.7 mmHg/μl; dP/d tmax-EDV, 496 ± 139 to 825 ± 178 mmHg·s−1·μl−1; and PRSW, 110 ± 23 to 127 ± 21 mmHg), depressed by atenolol ( Ees, 14.5 ± 6.1 to 4.6 ± 2.0 mmHg/μl; dP/d tmax-EDV, 543 ± 188 to 185 ± 94 mmHg·s−1·μl−1; and PRSW, 117 ± 20 to 70 ± 15 mmHg) and isoflurane ( Ees, 12.3 ± 6.0 to 5.7 ± 2.1 mmHg/μl; dP/d tmax-EDV, 528 ± 172 to 164 ± 68 mmHg/s·μl; and PRSW, 124 ± 19 to 48 ± 10 mmHg), significantly. In conclusion, this is the first description of the LV pressure-volume relationship in conscious mice. These findings suggest that this method is feasible to detect changes of contractility in the conscious state, allowing serial assessment of pressure-volume-derived cardiac function indexes over time without anesthesia or repeated surgery.

Influence of adenosine on left ventricular performance in conscious dogs

1990 ◽  
Vol 258 (2) ◽  
pp. H424-H430
Author(s):  
G. L. Freeman ◽  
J. T. Colston ◽  
J. Hultman
Keyword(s):  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Controlled Hypotension ◽  
Ventricular Performance ◽  
Systolic Volume ◽  
End Diastolic Volume ◽  
Before And After ◽  
Lv Volume

Adenosine, a potent vasodilator of both the peripheral and coronary vasculature, is increasingly used to produce controlled hypotension in the clinical and experimental setting. To define the influence of adenosine on left ventricular (LV) performance in conscious closed-chest dogs were studied six chronically instrumented autonomically blocked animals before and after the administration of 0.3, 0.6, and 1.2 microM.kg-1.min-1 infusions of adenosine. Systolic performance was quantified by the end-systolic pressure-volume (Pes-Ves) and stroke work end-diastolic volume (SW-EDV) relations. Active diastolic performance was quantified by the time constant of LV relaxation (T), whereas passive diastolic properties were assessed by comparing LV pressures at a common LV volume. Despite a decrease of mean arterial pressure of 51 mmHg, adenosine did not change the slope of the Pes-Ves relation or the end-systolic volume at a pressure of 100 mmHg. The slope of the SW-EDV relation was also unchanged, and its volume axis intercept was slightly reduced. There were no differences in T or in the diastolic pressure at a common LV volume. Thus adenosine appears to have little influence on systolic or diastolic LV performance aside from its marked affect on afterload, indicating it is a useful agent for producing controlled hypotension.

Abstract 17266: Right Atrial Volumes Changes in Tetralogy of Fallot

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Ashish Patel ◽  
Divya Shakti ◽  
Chad Blackshear
Keyword(s):  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Tetralogy Of Fallot ◽  
Surgical Repair ◽  
Left Ventricular ◽  
Right Atrial ◽  
Before And After ◽  
Ventricular Diastolic Dysfunction ◽  
And Function ◽  
Averaged Model

Introduction & Hypothesis: There is limited information on right atrial (RA) function in the congenital heart defects. RA volume and function may give insight into the right ventricle (RV) diastolic function. We sought to assess RA function in tetralogy of Fallot (TOF) patients prior to and after complete surgical repair. Methods: Infants with TOF prior to complete repair were included for retrospective chart review and offline analysis of 2-dimensional echocardiograms (echo) before and after surgical repair. RA phasic volumes and stroke volumes were calculated. All volumes were indexed to body surface area. Results: There were 40 infants with TOF (45% females), of which 70% had pulmonary stenosis, 30% pulmonary atresia. Roughly 85% and 60% had 3, or more, echo available pre- and postoperatively. Table 1 (attached) shows the patient characteristics and phasic RA volumes. The indexed RA phasic volumes were in normal range in initial echo prior to surgery. We used normal index RA phasic volumes published by European Society of Echocardiography. There was the increasing trend of indexed RA phasic volume on follow up echo immediately before TOF repair. These phasic volumes continued to remain elevated after complete surgical repair (Table 1). Trends in RA stroke volumes for all available echos before and after surgery were modeled using a population-averaged model with an exchangeable within-panel correlation structure (Figure 2), showing no statistically significant difference after surgery. But there was statistical significance noted in RA ejection fraction. Please see attached image for statistical analysis and results of the study. Conclusions: The indexed RA phasic volumes in children with TOF are normal initially and increases before TOF repair and it continued to increase after TOF repair. The increase RA phasic volumes suggest RV diastolic dysfunction similar to the findings of LA phasic volumes and left ventricular diastolic dysfunction. Our findings indicate slow worsening RV diastolic function in patients with TOF after surgical repair. RA volume and function can be the novel marker to diagnose and monitor right ventricular diastolic dysfunction.

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