Regional left ventricular performance during normal and obstructed spontaneous respiration

Robotham, James L.; Badke, Frederick R.; Kindred, M. K.; Beaton, M. K.

doi:10.1152/jappl.1983.55.2.569

Cited by 23 publications

(8 citation statements)

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“…This inspiratory-induced pooling of blood expands the pulmonary vasculature, which acts as a capacitance reservoir, and results in reduced LV filling [7,16]. Finally, a last possibility is that the inspiratory increase in RV volume may cause a leftward displacement of the interventricular septum, which leads to decreased LV compliance and could limit LV filling [8,10,14,30–32]. The physical constraint of the pericardium appears to contribute to this interaction as it was demonstrated that ventricular interdependence is reduced following pericardectomy in dogs [19].…”

Section: Within-breath Variation In Stroke Volume During Resting Sponmentioning

confidence: 99%

“…Moreover, pulmonary function in patients with heart failure is improved after cardiac transplant suggesting that pulmonary limitations are partly caused by the greater intrathoracic space occupied by the heart [45]. This increased heart–lung interdependence in patients with heart failure suggests that lung inflation could influence LV filling through mechanical compression of a less compliant left ventricle [30]. This possibility is also supported by findings that chest wall strapping of healthy individuals, in order to increase the competition for intrathoracic space between heart and lungs, resulted in a reduced stroke volume [15].…”

Section: Heart–lung Interdependencementioning

confidence: 99%

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Breathing strategy to preserve exercising cardiac function in patients with heart failure

Lalande¹,

Johnson²

2010

Medical Hypotheses

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SUMMARY The heart and lungs are closely linked as they lie in series, share a common surface area and compete for space within the thoracic cavity. The heart and lungs are exposed to the similar changes in intrathoracic pressure, and reflexes within one organ can influence the other (i.e. vagal influence of lung inflation on heart rate). In patients with heart failure, these cardiopulmonary interactions may be altered due to decreased lung and left ventricular compliance, increased cardiac size, high cardiac filling pressure and altered receptor sensitivity to neural activation. Exercise further affects the cardiopulmonary interactions by stimulating an increase in the depth and frequency of breathing which accentuates the fluctuations in intrathoracic pressure, and by requiring large increases in stroke volume and heart rate in order to respond to the increased metabolic demand. Previous work from our laboratory suggested that patients with heart failure avoid high lung volumes during exercise, often at the expense of unnecessary large positive expiratory intrathoracic pressures resulting in significant wasted effort. Moreover, we also observed that voluntarily increases in lung volume in patients with heart failure induced a mild relative bradycardia, a response not observed in similar aged healthy individuals. Thus, we hypothesized that the rapid shallow low lung volume breathing, in combination with positive expiratory intrathoracic pressure, often adopted by patients with heart failure during exercise is an attempt to preserve, or even enhance, the cardiac response to exercise.

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Section: Within-breath Variation In Stroke Volume During Resting Sponmentioning

confidence: 99%

Section: Heart–lung Interdependencementioning

confidence: 99%

Breathing strategy to preserve exercising cardiac function in patients with heart failure

Lalande¹,

Johnson²

2010

Medical Hypotheses

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“…Twelve healthy, adult mongrel dogs (20-35 kg) were instrumented under halothane anesthesia, through a left lateral thoracotomy, using sterile technique (Robotham et al, 1983). The instrumentation ( Fig.…”

Section: Instrumentationmentioning

confidence: 99%

Evaluation of left ventricular contractile performance utilizing end-systolic pressure-volume relationships in conscious dogs.

Sodums¹,

Badke²,

Starling³

et al. 1984

Circulation Research

151

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SUMMARY. The relationship between left ventricular end-systolic pressure and volume has been proposed as a model of left ventricular contraction which may be useful for quantifying inotropic state independent of preload and afterload. Although the model has been well-validated in isolated hearts, systematic evaluation in conscious animals with an intact peripheral circulation has been limited. Accordingly, we derived end-systolic pressure-volume relationships in twelve conscious dogs, chronically instrumented to measure left ventricular pressure and dimensions from endocardial ultrasonic crystals in three orthogonal axes. We examined the linearity of the end-systolic pressure-volume relationship, its response to alterations of inotropic state and the peripheral circulation, and the influence of /?-adrenergic reflexes. End-systolic pressure-volume relationships were constructed by linear regression of end-systolic pressure-volume coordinates produced by transient inferior vena caval occlusions during atrial pacing. The relations were highly linear; of 127 inferior vena caval occlusions, the correlation coefficient was 0.96 ± 0.05 (mean ± SD). The slope of the end-systolic pressure-volume relationship was not significantly altered either by a moderate resistive afterload induced by angiotensin II infusion, or by a moderate increase in preload produced by dextran, but was increased from 4.7 ± 2.3 to 6.5 ± 2.2 mm Hg/ml (P < 0.05) in response to the positive inotropic stimulus of dobutamine. The volume intercept at zero end-systolic pressure was unaffected by dextran or dobutamine, but was decreased from 12 ± 8 to 5 ± 11 ml (P < 0.01) by angiotensin II infusion, indicating a leftward shift of the end-systolic pressure-volume relationship. Pretreatment with propranolol to block fimediated adrenergic reflexes did not affect the response to angiotensin or dextran. We conclude that linear end-systolic pressure-volume relationships can be derived in conscious dogs with intact sympathetic reflexes. The slope appears to reflect left ventricular contractile function and is indepednent of the level of afterload and preload. However, the relation is shifted leftward by high levels of arterial resistance, indicating that end-systolic pressure is a function, not only of end-systolic volume and inotropic state, but also of the peripheral circulation, in this intact animal model. (CircRes 54: 731-739, 1984) THE assessment of ventricular contractile function remains an important problem in clinical practice and in physiological investigation (Ross and Peterson, 1973;Sagawa et al., 1977;Sagawa, 1978;Weber et al., 1982). Because traditional isovolumic and ejection phase indices of ventricular performance are variably affected by preload and afterload, as well as by inotropic state (Mahler et al., 1975a), the search has continued for a load-independent measure of contractile function. In isolated hearts, Suga and Sagawa (1974) have demonstrated that the relation between end-systolic pressure and volume (P-V) is an index of contract...

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“…During spontaneous inspiration, a decrease in the left ventricular septal-lateral dimension consistent with compression of the heart in the lateral direction has been reported [18]. However, SCHARF et al [19] showed that the compressive effect of lung inflation probably plays a less important role during spontaneous inspiration than during mechanical ventilation with positive end-expiratory pressure.…”

Section: Effects On Left Ventricular Afterloadmentioning

confidence: 91%

Pulsus paradoxus

2012

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Systolic blood pressure normally falls during quiet inspiration in normal individuals. Pulsus paradoxus is defined as a fall of systolic blood pressure of .10 mmHg during the inspiratory phase. Pulsus paradoxus can be observed in cardiac tamponade and in conditions where intrathoracic pressure swings are exaggerated or the right ventricle is distended, such as severe acute asthma or exacerbations of chronic obstructive pulmonary disease. Both the inspiratory decrease in left ventricular stroke volume and the passive transmission to the arterial tree of the inspiratory decrease in intrathoracic pressure contribute to the occurrence of pulsus paradoxus. During cardiac tamponade and acute asthma, biventricular interdependence (series and parallel) plays an important role in the inspiratory decrease in left ventricular stroke volume.Early recognition of pulsus paradoxus in the emergency room can help to diagnose rapidly cardiac tamponade. Measurement of pulsus paradoxus is also useful to assess the severity of acute asthma as well as its response to therapy. Recent development of noninvasive devices capable of automatic calculation and display of arterial pressure variation or derived indices should help improve the assessment of pulsus paradoxus at the bedside.

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Regional left ventricular performance during normal and obstructed spontaneous respiration

Cited by 23 publications

References 0 publications

Breathing strategy to preserve exercising cardiac function in patients with heart failure

Breathing strategy to preserve exercising cardiac function in patients with heart failure

Evaluation of left ventricular contractile performance utilizing end-systolic pressure-volume relationships in conscious dogs.

Pulsus paradoxus

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