Comparison of measures of left ventricular contractile performance derived from pressure-volume loops in conscious dogs.

Little, William C.; Cheng, Che‐Ping; Mumma, Michael T.; Igarashi, Yuichi; Vinten-Johansen, J.; Johnston, William

doi:10.1161/01.cir.80.5.1378

Cited by 185 publications

(114 citation statements)

References 36 publications

(2 reference statements)

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“…In addition, with MMR activation at moderate exercise, these latter indexes tended to decrease compared with free-flow exercise. Thus our results are in support of previous investigations that found E max and PRSW to be better indexes for evaluating LV contractility (15,16,23,49). The observed changes in dP/dt max and dP/dt min may be due to alterations in loading conditions.…”

Section: Discussionsupporting

confidence: 92%

“…However, the correspondence between both techniques is extremely close, as previously shown (42). Furthermore, the SV values we obtained with the sonometric technique are highly consistent with those reported in the literature by other investigators (23,29). A possible explanation for this discrepancy in SV could be that the location and the number of crystals can impact the measurement.…”

Section: Discussionsupporting

confidence: 91%

“…Accurate evaluations of the contractile state of the heart are challenging. Different methods such as SV, ejection fraction, cardiothoracic ratio, circumferential shortening velocity, and dP/dt max , among others, are frequently used to study ventricular contractility, despite their major limitations: they are known to be sensitive not only to changes in contractility but also to loading conditions (9,23,41). Moreover, they also are influenced by changes in cardiac mass and morphology.…”

Section: Discussionmentioning

confidence: 99%

“…Ventricular contractility was assessed by employing the slope of the line intersecting the end-systolic pressure-volume relationships (E max : maximal elastance index) and preload-recruitable stroke work index (PRSW) calculated from the stroke work-end-diastolic volume relationship. Both have been shown to be sensitive to changes in ventricular contractility and relatively insensitive to loading conditions, and the latter measure (PRSW) has been shown to be independent of changes in ventricular chamber size (9,14,15,21,23,49,50). We hypothesized that in the HF state, the muscle metaboreflex-induced increase in LV contractility during mild and moderate dynamic exercise would be impaired as shown by a smaller rise or no change in E max and PRSW.…”

mentioning

confidence: 99%

“…These parameters are known to be sensitive not only to contractile state but also to loading conditions (9,23,41). To accurately evaluate the MMR effect on ventricular contractility during dynamic exercise under normal conditions, we recently investigated LV performance in the pressure-volume plane in conscious dogs during mild and moderate exercise (42).…”

mentioning

confidence: 99%

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Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise

Sala‐Mercado¹,

Hammond²,

Kim³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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DS. Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise. Am J Physiol Heart Circ Physiol 292: H2159 -H2166, 2007. First published December 22, 2006; doi:10.1152/ajpheart.01240.2006.-Underperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex (MMR). In normal dogs during mild exercise, MMR activation causes large increases in cardiac output (CO) and mean arterial pressure (MAP); however, in heart failure (HF) although MAP increases, the rise in CO is virtually abolished, which may be due to an impaired ability to increase left ventricular contractility (LVC). The objective of the present study was to determine whether the increases in LVC seen with MMR activation during dynamic exercise in normal animals are abolished in HF. Conscious dogs were chronically instrumented to measure CO, MAP, and left ventricular (LV) pressure and volume. LVC was calculated from pressure-volume loop analysis [LV maximal elastance (E max) and preload-recruitable stroke work (PRSW)] at rest and during mild and moderate exercise under free-flow conditions and with MMR activation (via partial occlusion of hindlimb blood flow) before and after rapid ventricular pacing-induced HF. In control experiments, MMR activation at both workloads [mild exercise (3.2 km/h) and moderate exercise (6.4 km/h at 10% grade)] significantly increased CO, E max, and PRSW. In contrast, after HF was induced, CO, Emax, and PRSW were significantly lower at rest. Although CO increased significantly from rest to exercise, E max and PRSW did not change. In addition, MMR activation caused no significant change in CO, E max, or PRSW at either workload. We conclude that MMR causes large increases in LVC in normal animals but that this ability is abolished in HF. pressor response; elastance; preload recruitable stroke work WHEN EXERCISING SKELETAL MUSCLE does not receive sufficient blood flow to meet the ongoing metabolic demands, by-products of metabolism such as lactic acid, H ϩ , adenosine, potassium, diprotonated phosphate, and arachidonic acid products, among others, accumulate within the muscle and stimulate group III and IV afferent neurons, which evokes a reflex response known as the muscle metaboreflex (MMR). This reflex response consists of increases in efferent sympathetic nerve activity (SNA) and mean arterial pressure (MAP) (1, 3, 11, 17, 18, 24, 31-35, 39, 40, 43, 46, 47, 52, 53). In addition, MMR activation causes increases in cardiac output (CO), heart rate (HR), and plasma levels of vasoactive hormones and produces vasoconstriction in the renal and the nonischemic active skeletal muscle vasculature to partially restore arterial O 2 delivery and blood flow to the hypoperfused muscles (25,33,36). The rise in CO likely results from increases in ventricular performance, HR, and central blood volume mobilization (32,42,43). By this means the MMR-induced increases in ventricular performance act to slightly increase or sustain stroke volume (SV) despite decreas...

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise

Sala‐Mercado¹,

Hammond²,

Kim³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Cardiovascular Responses During Sepsis

Pecchiari

Pontikis

Alevrakis

et al. 2021

Comprehensive Physiology

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Sepsis is the life-threatening organ dysfunction arising from a dysregulated host response to infection.Although the specific mechanisms leading to organ dysfunction are still debated, impaired tissue oxygenation appears to play a major role, and concomitant hemodynamic alterations are invariably present. The hemodynamic phenotype of affected individuals is highly variable for reasons that have been partially elucidated. Indeed, each patient's circulatory condition is shaped by the complex interplay between the medical history, the volemic status, the interval from disease onset, the pathogen, the site of infection and the attempted resuscitation. Moreover, the same hemodynamic pattern can be generated by different combinations of various pathophysiological processes, so the presence of a given hemodynamic pattern cannot be directly related to a unique cluster of alterations. Research based on endotoxin administration to healthy volunteers and animal models compensate, to an extent, for the scarcity of clinical studies on the evolution of sepsis hemodynamics. Their results, however, cannot be directly extrapolated to the clinical setting, due to fundamental differences between the septic patient, the healthy volunteer and the experimental model. Numerous microcirculatory derangements might exist in the septic host, even in the presence of a preserved macrocirculation. This dissociation between the macro-and the micro-circulation might account for the limited success of therapeutic interventions targeting typical hemodynamic parameters, such as arterial and cardiac filling pressures, and cardiac output. Finally, physiological studies point to an early contribution of cardiac dysfunction to the septic phenotype, however our defective diagnostic tools preclude its clinical recognition.) to anesthetized, vagotomized and mechanically ventilated Sprague-Dawley rats on the operating point of the baroreflex using a baroreflex diagram (SNA: sympathetic nervous activity; CSP: carotid sinus pressure; AP: arterial pressure). As time passes after lipopolysaccharide injection, the neural arc 9 progressively shifts rightwards, and the peripheral arc downwards, so the operating point moves from a (baseline) to b at 1 hour and to c at 2 hours, showing a progressive increase of SNA with little change of AP. From (523), with permission under the terms of the Creative Commons Attribution License. significantly (from 1.7±0.5 to 1.4±0.2 mmHg ml -1 min) (313). In the same preparation N w -nitro-L-methyl ester (L-NAME) increases SVR more than R VR both in the presence (+294 and +129%, respectively) and in the absence (+196 and +107%, respectively) of fluid-loading. In another study from the same group, L-NAME elicited similar effects (117). Overall, these experimental studies warn against the assumption that changes of SVR are always paralleled by similar changes of R VR .

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Magnetic resonance imaging analysis of left ventricular pressure‐volume relations: Validation with the conductance method at rest and during dobutamine stress

Pattynama

Roos

Velde

et al. 1995

Magnetic Resonance in Med

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The accuracy of magnetic resonance (MR) imaging was assessed for in vivo measurement of the ventricular end-systolic pressure-volume relation (ESPVR) and preload recruitable stroke work (PRSW). The conductance catheter was used as reference. In 10 pigs, ventricular volumes were measured with both methods under different loading conditions at two levels of contractility. Increased contractility resulted in a significant leftward shift of the ESPVR and PRSW for both methods. The magnitude of these shifts was on average similar for the two methods; MR imaging, 6.9 ml for ESPVR, 9.3 ml for PRSW; and the conductance catheter, 7.4 ml for ESPVR, 9.1 ml for PRSW. It was concluded that MR imaging may be used for in vivo analysis of pressure-volume relations, and that its sensitivity for detecting contractility changes is similar to that of the conductance catheter method.

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Comparison of measures of left ventricular contractile performance derived from pressure-volume loops in conscious dogs.

Cited by 185 publications

References 36 publications

Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise

Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise

Cardiovascular Responses During Sepsis

Magnetic resonance imaging analysis of left ventricular pressure‐volume relations: Validation with the conductance method at rest and during dobutamine stress

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