Stroke Volume Response Research Articles

Longitudinal investigation of training status and cardiopulmonary responses in pre- and early-pubertal children

The presence of a maturational threshold that modulates children's physiological responses to exercise training continues to be debated, not least due to a lack of longitudinal evidence to address this question. The purpose of this study was to investigate the interaction between swim-training status and maturity in nineteen trained (T, 10 ± 1 years, -2.4 ± 1.9 years pre-peak height velocity, 8 boys) and fifteen untrained (UT, 10 ± 1 years, -2.3 ± 0.9 years pre-peak height velocity, 5 boys) children, at three annual measurements. In addition to pulmonary gas exchange measurements, stroke volume (SV) and cardiac output ([Formula: see text]) were estimated by thoracic bioelectrical impedance during incremental ramp exercise. At baseline and both subsequent measurement points, trained children had significantly (P < 0.05) higher peak oxygen uptake (year 1 T 1.75 ± 0.34 vs. UT 1.49 ± 0.22; year 2 T 2.01 ± 0.31 vs. UT 1.65 ± 0.08; year 3 T 2.07 ± 0.30 vs. UT 1.77 ± 0.16 l min(-1)) and [Formula: see text] (year 1 T 15.0 ± 2.9 vs. UT 13.2 ± 2.2; year 2 T 16.1 ± 2.8 vs. UT 13.8 ± 2.9; year 3 T 19.3 ± 4.4 vs. UT 16.0 ± 2.7 l min(-1)). Furthermore, the SV response pattern differed significantly with training status, demonstrating the conventional plateau in UT but a progressive increase in T. Multilevel modelling revealed that none of the measured pulmonary or cardiovascular parameters interacted with maturational status, and the magnitude of the difference between T and UT was similar, irrespective of maturational status. The results of this novel longitudinal study challenge the notion that differences in training status in young people are only evident once a maturational threshold has been exceeded.

Effect of Pulmonary Endarterectomy for Chronic Thromboembolic Pulmonary Hypertension on Stroke Volume Response to Exercise

In pulmonary hypertension, exercise is limited by an impaired right ventricular (RV) stroke volume response. We hypothesized that improvement in exercise capacity after pulmonary endarterectomy (PEA) for chronic thromboembolic pulmonary hypertension (CTEPH) is paralleled by an improved RV stroke volume response. We studied the extent of PEA-induced restoration of RV stroke volume index (SVI) response to exercise using cardiac magnetic resonance imaging (cMRI). Patients with CTEPH (n= 18) and 7 healthy volunteers were included. Cardiopulmonary exercise testing and cMRI were performed before and 1 year after PEA. For cMRI studies, pre- and post-operatively, all patients exercised at 40% of their preoperative cardiopulmonary exercise testing-assessed maximal workload. Post-PEA patients (n= 13) also exercised at 40% of their postoperative maximal workload. Control subjects exercised at 40% of their predicted maximal workload. Preoperatively, SVI (n= 18) decreased during exercise from 35.9 ± 7.4 to 33.0 ± 9.0ml·m(2) (p= 0.023); in the control subjects, SVI increased (46.6 ± 7.6 vs 57.9 ± 11.8ml·m(-2), p= 0.001). After PEA, the SVI response (ΔSVI) improved from-2.8 ± 4.6 to 4.0 ± 4.6ml·m(2) (p <0.001; n= 17). On exercise at 40% of the postoperative maximal workload, SVI did not increase further and was still significantly lower compared with controls. Moreover, 4 patients retained a negative SVI response, despite (near) normalization of their pulmonary hemodynamics. The improvement in SVI response was accompanied by an increased exercise tolerance and restoration of RV remodeling. In conclusion, in CTEPH, exercise is limited by an impaired stroke volume response. PEA induces a restoration of SVI response to exercise that appears, however, incomplete and not evident in all patients.

Carotid blood flow, cardiovascular and endocrine responses during head-up tilt in patients with acute cerebrovascular diseases.

The purpose of this study was to define common carotid blood flow (CBF), cardiovascular and endocrine responses during head-up tilt (HUT) in patients with acute cerebrovascular diseases (CVD). In 31 male patients with acute CVD (damage of the supratentorial area) and 21 age-matched control male subjects, we measured CBF, mean blood pressure (MBP), heart rate, stroke volume and cardiac output responses before (baseline), during and after HUT. We also measured plasma levels of antidiuretic hormone, adrenaline, noradrenaline, aldosterone and plasma renin activity. After obtaining baseline measurements during 3-minutes horizontal position, HUT was performed for 5 minutes, followed by continuation of recording for 3 more minutes in the horizontal position. During HUT, CBF decreased significantly and equally in both groups. MBP did not change during HUT in both groups. The endocrine responses were also not different between the two groups. The results suggest that damage to the supratentorial area in patients with acute CVD do not alter the CBF, cardiovascular and endocrine responses. In other words, HUT does not predispose patients with acute CVD to serious falls in MBP and CBF at upright posture.

A prospective observational study of stroke volume responsiveness to a passive leg raise manoeuvre in healthy non‐starved volunteers as assessed by transthoracic echocardiography

Current guidelines for intra-operative fluid management recommend the use of increments in stroke volume following intravenous fluid bolus administration as a guide to subsequent fluid therapy. To study the physiological premise of this paradigm, we tested the hypothesis that healthy, non-starved volunteers would develop an increment in their stroke volume following a passive leg raise manoeuvre. Subjects were positioned supine and stroke volume was measured by transthoracic echocardiography at baseline, 30 s, 1 min, 3 min and 5 min after passive leg raise manoeuvre to 45°. Stroke volume was measured at end-expiration during quiet breathing, as the mean of three sequential measurements. Seventeen healthy volunteers were recruited; one volunteer in whom it was not possible to obtain Doppler measurements and a further five for reasons of poor Doppler image quality were not included in the study. Mean (SD) percentage difference from baseline to the largest change in stroke volume was 5.7 (9.6)% (p = 0.16). Of the 11 volunteers evaluated, five (45%) had stroke volume increases of greater than 10%. Mean (SD) maximum percentage change in cardiac index was 14.8 (9.7)% (p = 0.004). A wide variation in baseline stroke volume and response to the passive leg raise manoeuvre was seen, suggesting greater heterogeneity in the normal population than current clinical guidelines recognise.

Basic concepts of fluid responsiveness

Predicting fluid responsiveness, the response of stroke volume to fluid loading, is a relatively novel concept that aims to optimise circulation, and as such organ perfusion, while avoiding futile and potentially deleterious fluid administrations in critically ill patients. Dynamic parameters have shown to be superior in predicting the response to fluid loading compared with static cardiac filling pressures. However, in routine clinical practice the conditions necessary for dynamic parameters to predict fluid responsiveness are frequently not met. Passive leg raising as a means to alter biventricular preload in combination with subsequent measurement of the change in stroke volume can provide a fast and accurate way to guide fluid management in a broad population of critically ill patients.

Stroke Volume Response to Liver Graft Reperfusion Stress in Cirrhotic Patients

In patients with advanced cirrhosis, stressful stimuli may reveal a silent reduced cardiac performance. During liver transplantation (LT), graft reperfusion strongly stresses the heart and may unmask latent myocardial dysfunction. The objective of this study was to assess heart response to acutely increased preload after liver graft reperfusion and correlate this response with preoperative data and outcome. Preoperative clinical, echocardiographic, and hemodynamic data, and patient outcome were retrospectively recorded for 235 liver recipients who had no known cardiac disease. Myocardial dysfunction was defined as less than 10 % increase of stroke volume after graft reperfusion (non-responder). We found 84 (35.7 %) non-responder patients. The non-responders showed higher Model for end-stage liver disease scores (p = 0.046), left atrial diameter (LAD) (p = 0.040), hepatic vein pressure gradient (p = 0.055), and hyperdynamic state than responders. The percentages of patients with hyponatremia (p = 0.048) and alcohol etiology (p = 0.025) were also higher among non-responders. Independent predictors of inadequate cardiac response in the multivariate analysis were low preoperative systemic vascular resistance (SVRI) [odds ratio (OR) 3.09, 95 % CI 1.15-4.82; p = 0.027] and enlargement of LAD (OR 2.08, 95 % CI 1.49-2.74; p = 0.044). Non-response was associated with higher rates of early cardiovascular events [hazard ratio (HR) 2.84, 95 % CI 1.09-4.22; p = 0.039] and higher length of intensive care unit stay (p = 0.038). No differences were found in 1-year survival rates. Latent cardiac dysfunction among LT recipients, considered to be abnormal stroke volume response to unclamping of portal vein, is very prevalent. SVRI and LAD were independent predictors of inadequate responses. This condition deserves special attention since it may aggravate the early postoperative course of LT.

Sildenafil: a definitive NO in COPD

Several studies have shown that chronic obstructive pulmonary disease (COPD) patients have a low stroke volume at rest and an impaired stroke volume response during exercise [1, 2]. As a consequence, oxygen delivery to the tissues is impaired. Since oxygen delivery is critical for maintenance and growth of muscles, the systemic effects of COPD might, in part, be attributed to the lowered stroke volume. Therefore, restoring the stroke volume response would not only improve oxygen delivery capacity, but may also have beneficial effects at the muscle level. Improving muscle strength may, in turn, enhance exercise tolerance by reducing negative feedback from lower limb sensory muscle afferents and by reducing ventilatory responses and dyspnoea during exercise [3]. Since increased right ventricular afterload is considered the most likely explanation for the impaired stroke volume response, reducing pulmonary artery pressure is the key to restore stroke volume. Although pulmonary hypertension is present in 50% of the patients with severe COPD, pulmonary hypertension is usually mild-to-moderate [4]. However, exercise will induce a steep increase in pulmonary artery pressure in these patients [5, 6 …

Effects of acute vasodilation on the hemodynamic response to muscle metaboreflex

The aim of the present study was to test the contribution of stroke volume (SV) in hemodynamic response to muscle metaboreflex activation in healthy individuals. We hypothesized that an acute decrease in cardiac afterload and preload due to the administration of a vasodilating agent could reduce postexercise muscle ischemia (PEMI)-induced SV response. Ten healthy males (age 33.6 ± 1.3 yr) were enrolled and randomly assigned to the following study protocol: 1) PEMI session, 2) control exercise recovery (CER) session, 3) PEMI after sublingual administration of 5 mg of isosorbide dinitrate (ISDN), and 4) CER after ISDN. Central hemodynamics were evaluated by means of impedance cardiography. The main findings were a blunted SV response during metaboreflex following acute arterial and venous vasodilation, associated with a reduction in cardiac diastolic time and filling, and a decrement of systemic vascular resistance. These hemodynamic changes restrain blood pressure response during metaboreflex activation. Our results indicate that hemodynamic response to metaboreflex activation is a highly integrated phenomenon encompassing complex interplay between heart rate, cardiac performance, preload, and afterload and that impairment of one or more of these parameters leads to altered hemodynamic response to metaboreflex.

Comparison of stroke volume and fluid responsiveness measurements in commonly used technologies for goal-directed therapy

Study ObjectiveTo compare stroke volume (SV) and preload responsiveness measurements from different technologies with the esophageal Doppler monitor (EDM). DesignProspective measurement study. SettingOperating room. Patients20 ASA physical status 3 patients undergoing vascular, major urological, and bariatric surgery. InterventionsSubjects received fluids using a standard Doppler protocol of 250 mL of colloid administered until SV no longer increased by >10%, and again when the measured SV decreased by 10%. MeasurementsSimultaneous readings of SV, stroke volume variation (SVV) and pulse pressure variation (PPV) from the LiDCOrapid, and SVV from the FloTrac/Vigileo were compared with EDM measurements. The pleth variability index (PVI) also was recorded. Main ResultsNo correlation was seen in percentage SV change as measured by either the LiDCOrapid (r=0.05, P=0.616) or FloTrac (r=0.09, P= 0.363) systems compared with the EDM. Correlation was present between the LiDCOrapid and FloTrac (r=0.515, P<0.0001). Percentage error compared with the EDM was 81% for the FloTrac and 90% for the LiDCOrapid. SVV as measured by LiDCOrapid differed for fluid responders and nonresponders (10% vs 7%; P=0.021). Receiver operator curve analysis to predict a 10% increase in SV from the measured variables showed an area under the curve of 0.57 (95% CI 0.43-0.72) for SVVFloTrac, 0.64 (95% CI 0.52-0.78) for SVVLiDCO, 0.61 (95% CI 0.46 -0.76) for PPV, and 0.59 (95% CI 0.46 -0.71) for PVI. ConclusionsStroke volume as measured by the FloTrac and LiDCOrapid systems does not correlate with the esphageal Doppler, has poor concordance, and a clinically unacceptable percentage error. The predictive value of the fluid responsiveness parameters is low, with only SVV measured by the LiDCOrapid having clinical utility.

Comparison of optimised stroke volume and fluid responsiveness measurements from commonly used technologies for perioperative goal directed fluid therapy

Comparison of optimised stroke volume and fluid responsiveness measurements from commonly used technologies for perioperative goal directed fluid therapy

Familial Hypertrophic Cardiomyopathy

Building on work by Otto Frank in the late 19th century, Ernest Starling described in the early 20th century the ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return, which has been called the Frank–Starling law of the heart in honor of these 2 physiologists. The Frank–Starling effect enables the heart to match cardiac output to venous return on a beat-to-beat basis.1 A major mechanism responsible for the Frank–Starling effect and hence the beat-to-beat autoregulation of cardiac output is the sarcomere length-dependent activation of force development.2 Article, see p 1491 In this issue of Circulation Research , Sequeira et al3 investigate both the Ca- and length-dependent regulation of force development in cardiomyocytes harvested from patients with hypertrophic cardiomyopathy (HCM), a familial disorder commonly associated with mutations in genes encoding sarcomeric proteins.4 Consistent with previous animal and human studies,5 myofilament Ca sensitivity was increased in all 38 HCM patient samples compared with 12 nonfailing donor hearts. Notable, the authors observed that length-dependent activation was impaired, which, unlike the Ca sensitivity increase, seemed to be a primary effect of the mutant sarcomeric proteins because (1) it could not be rescued by increasing protein kinase A (PKA) phosphorylation and (2) was normalized when mutant troponin (Tn) proteins were replaced with wild-type protein. These new results suggest that impaired length-dependent activation and hence a defective Frank–Starling effect importantly contribute to the pathogenesis of HCM (Figure). HCM is a familial disorder commonly associated with mutations in genes encoding sarcomeric proteins. Mutation carriers develop progressive heart hypertrophy and fibrosis and are at a high risk for sudden death because of ventricular arrhythmia. More than 1000 mutations in >11 genes have been identified, which can lead to this disease. …

Prediction of stroke volume response to fluid bolus in 100 children

Fluid overload is associated with poor outcome in the critically ill. Thus, an accurate predictor of a positive haemodynamic response (increase in stroke volume) to fluid challenge is vital.

I got it! Transient cardiovascular response to the perception of humor

The aim of the present study was to examine the transient cardiovascular response to the perception of humor, that is, the impact of the cognitive process of insight as well as the modulation of the response by the affective appraisal of the humor. To this end transient heart rate, stroke volume, cardiac output, and blood pressure responses were obtained in the immediate context of detecting the punch line in cartoons. Fine-grained analysis of the transient behavior of cardiovascular variables during viewing the cartoons was contrasted to non-humorous cartoon-like pictures. The detection of a punch line was accompanied by relative heart rate acceleration in conjunction with increased cardiac output, which was more pronounced the more amusing the cartoons were perceived. These results provide first evidence of the usefulness of cardiovascular variables for detecting the moment of insight and the quantification of the size of the emotional response accompanying it.

Use of Noninvasive Gas Exchange to Track pulmonary Vascular Responses to exercise in Heart Failure

We determined whether a non-invasive gas exchange based estimate of pulmonary vascular (PV) capacitance [PVCAP = stroke volume (SV) × pulmonary arterial pressure (Ppa)] (GXCAP) tracked the PV response to exercise in heart-failure (HF) patients. Pulmonary wedge pressure (Ppw), Ppa, PV resistance (PVR), and gas exchange were measured simultaneously during cycle exercise in 42 HF patients undergoing right-heart catheterization. During exercise, PETCO2 and VE/VCO2 were related to each other (r = −0.93, P < 0.01) and similarly related to mean Ppa (mPpa) (r = −0.39 and 0.36; P < 0.05); PETCO2 was subsequently used as a metric of mPpa. Oxygen pulse (O2 pulse) tracked the SV response to exercise (r = 0.91, P < 0.01). Thus, GXCAP was calculated as O2 pulse × PETCO2. During exercise, invasively determined PVCAP and non-invasive GXCAP were related (r = 0.86, P < 0.01), and GXCAP correlated with mPpa and PVR (r = −0.46 and −0.54; P < 0.01). In conclusion, noninvasive gas exchange measures may represent a simple way to track the PV response to exercise in HF.

Lessons from liver transplantation

Lessons from liver transplantation

Central versus peripheral control of cardiac output in humans: insight from atrial pacing

Central <i>versus</i> peripheral control of cardiac output in humans: insight from atrial pacing

Ontogeny of hypoxic modulation of cardiac performance and its allometry in the African clawed frog Xenopus laevis

The ontogeny of cardiac hypoxic responses, and how such responses may be modified by rearing environment, are poorly understood in amphibians. In this study, cardiac performance was investigated in Xenopus laevis from 2 to 25 days post-fertilization (dpf). Larvae were reared under either normoxia or moderate hypoxia (PO₂ = 110 mmHg), and each population was assessed in both normoxia and acute hypoxia. Heart rate (f(H)) of normoxic-reared larvae exhibited an early increase from 77 ± 1 beats min⁻¹ at 2 dpf to 153 ± 1 beats min⁻¹ at 4 dpf, followed by gradual decreases to 123 ± 3 beats min⁻¹ at 25 dpf. Stroke volume (SV), 6 ± 1 nl, and cardiac output (CO), 0.8 ± 0.1 μl min⁻¹, at 5 dpf both increased by more than 40-fold to 25 dpf with rapid larval growth (~30-fold increase in body mass). When exposed to acute hypoxia, normoxic-reared larvae increased f(H) and CO between 5 and 25 dpf. Increased SV in acute hypoxia, produced by increased end-diastolic volume (EDV), only occurred before 10 dpf. Hypoxic-reared larvae showed decreased acute hypoxic responses of EDV, SV and CO at 7 and 10 dpf. Over the period of 2-25 dpf, cardiac scaling with mass showed scaling coefficients of -0.04 (f(H)), 1.23 (SV) and 1.19 (CO), contrary to the cardiac scaling relationships described in birds and mammals. In addition, f(H) scaling in hypoxic-reared larvae was altered to a shallower slope of -0.01. Collectively, these results indicate that acute cardiac hypoxic responses develop before 5 dpf. Chronic hypoxia at a moderate level can not only modulate this cardiac reflex, but also changes cardiac scaling relationship with mass.

Impaired stroke volume response after liver graft reperfusion as a predictor of early major cardiovascular events and outcome in cirrhotic patient undergoing liver transplantation

Cubas Quiroga, M. G.; De Vargas, I.; Rivas, E.; Martin, N.; Blasi, A.; Taura, P. Author Information

Signal‐morphology impedance cardiography during incremental cardiopulmonary exercise testing in pulmonary arterial hypertension

Haemodynamic responses to exercise are related to physical impairment and worse prognosis in patients with pulmonary arterial hypertension (PAH). It is clinically relevant, therefore, to investigate the practical usefulness of non-invasive methods of monitoring exercise haemodynamics in this patient population. Using a novel impedance cardiography (ICG) approach that does not require basal impedance estimations and relies on a morphological analysis of the impedance signal (Signal-Morphology-ICG(™)), stroke volume (SV) and cardiac index (CI) were evaluated in 50 patients and 21 age-matched controls during a ramp-incremental cardiopulmonary exercise testing. Technically unacceptable readings were found in 12 of 50 (24%) patients. In the remaining subjects, early decrease (N = 9) or a 'plateau' in SV (N = 8) and Δ (peak-unloaded exercise) SV <10 ml were markers of more advanced PAH (P<0.05). ΔCI ≤ 1.5-fold and early estimated lactate threshold were the only independent predictors of a severely reduced peak oxygen uptake (VO(2)) in patients (R(2) = 0.71, P<0.001). The finding of ΔCI ≤ 1.5-fold plus peak VO(2) < 50% predicted was associated with a number of clinical and functional markers of disease severity (P<0.001). In addition, abnormal SV responses and ΔCI ≤ 1.5-fold were significantly related to 1-year frequency of PAH-related adverse events (death and balloon atrial septostomy, N = 8; P<0.05). 'Qualitative' and 'semi-quantitative' signal-morphology impedance cardiography(™) (PhysioFlow(™)) during incremental exercise provided clinically useful information to estimate disease severity and short-term prognosis in patients with PAH in whom acceptable impedance signals could be obtained.

Effect of age on exercise capacity and cardiac reserve in patients with pulmonary atresia with intact ventricular septum after biventricular repair

OBJECTIVESIn patients with pulmonary atresia with intact ventricular septum (PAIVS), biventricular repair is considered to be the optimal treatment option in the absence of significant right ventricular (RV) hypoplasia. However, long-term clinical outcome studies are limited. We evaluated exercise capacity and cardiac function during pharmacological stress in children and young adults with PAIVS after biventricular repair.METHODSTen PAIVS patients after biventricular repair, with a median age of 12 years (range 9-42 years), underwent a cardiopulmonary exercise test, dobutamine stress magnetic resonance imaging (DS-MRI) and delayed contrast enhancement (DCE) MRI.RESULTSThe patients' ages negatively correlated with exercise capacity (r = -0.72, P = 0.01) as well as left (LV) and RV stroke volume (SV) response to pharmacological stress (r = -0.72, P = 0.02; and r = -0.64, P = 0.04; respectively), Furthermore, older age was associated with decreased RV E/A volume ratio and increased pulmonary late diastolic forward flow percentage (r = 0-0.65, P = 0.04, r = 0.66, P = 0.03, respectively). RV E/A volume ratio positively correlated with RV-SV response to DS-MRI (r = 0.77, P = 0.009). and O(2)-pulse during physical stress correlated with biventricular SV response to DS-MRI. No RV or LV ventricular myocardial fibrosis was detected.CONCLUSIONSIn PAIVS patients after biventricular repair exercise capacity and cardiac reserve decrease with age. These findings appear to be related to impaired diastolic RV function and decreased RV filling, indicating that the function of the relatively small RV deteriorates with time