Changes In Cardiac Output Research Articles

Resistance training does not change glucose and cardiac autonomic function of patients with type 2 diabetes

Objective: to evaluate the influence of a RT protocol on the function autonomic heart rate and cardiovascular variables in patients with DM-2. Methods: 9 patients with DM-2 participated in the study. After initial evaluation, data collection was performed regarding the RR intervals (iR-R) of the frequency heart rate (HR) and systolic (SBP) and diastolic (DBP) blood pressures while performing Function Tests Autonomic Cardiac Respiratory Sinus Arrhythmia Accentuating Maneuver (ABR), Active Postural Maneuver (APM), Valsalva Maneuver (ValM), Handgrip Test and the HR, SBP, DBP and double product (DP) data were also analyzed under the pre and post RT. RT was applied with moderate intensity of 60% of 1RM, exercises for lower and upper limbs, twice a week for 12 weeks. Results: the variations of the calculated indices for the TFACs did not show differences significant statistics (p>0.05). PAS, PAD and FC also showed no difference However, the PD showed a decrease at rest (∆= -990.55 ±1154.91) Conclusions: the moderate RT with 12 weeks, in patients with DM-2, does not promote any change in the function autonomic cardiac output but decreases myocardial overload by attenuating PD at rest.

Physiological Effects of Centrifuge-Simulated Suborbital Spaceflight

BACKGROUND: High-G acceleration experienced during launch and re-entry of suborbital spaceflights may present challenges for older or medically susceptible participants. A detailed understanding of the associated physiological responses would support the development of an evidence-based medical approach to commercial suborbital spaceflight.METHODS: There were 24 healthy subjects recruited into 'younger' (18-44 yr), 'intermediate' (45-64 yr) and 'older' (65-80 yr) age groups. Cardiovascular and respiratory variables were measured continuously during dynamic combinations of +Gx (chest-to-back) and +Gz (head-to-foot) acceleration that simulated suborbital G profiles for spaceplane and rocket/capsule platforms. Measurements were conducted breathing air and breathing 15% oxygen to simulate a cabin pressure altitude of 8000 ft.RESULTS: Suborbital G profiles generated highly dynamic changes in heart rate, blood pressure, and cardiac output. G-induced hypoxemia was observed, with minimum arterial oxygen saturation < 80% in a quarter of subjects. Increased age was associated with greater hypoxemia and reduced cardiac output responses but did not have detrimental cardiovascular effects. ECG changes included recurrent G-induced trigeminy in one individual. Respiratory and visual symptoms were common, with 88% of subjects reporting greyout and 29% reporting blackout. There was one episode of G-induced loss of consciousness (G-LOC).DISCUSSION: Suborbital acceleration profiles are generally well tolerated but are not physiologically inconsequential. Marked hemodynamic effects and transient respiratory compromise could interact with predisposing factors to precipitate adverse cardiopulmonary effects in a minority of participants. Medically susceptible individuals may benefit from expanded preflight centrifuge familiarization that includes targeted physiological evaluation in the form of a 'G challenge test'.Smith TG, Pollock RD, Britton JK, Green NDC, Hodkinson PD, Mitchell SJ, Stevenson AT. Physiological effects of centrifuge-simulated suborbital spaceflight. Aerosp Med Hum Perform. 2022; 93(12):830-839.

The effect of various breath-hold techniques on the cardiorespiratory response to facial immersion in humans.

What is the central question of this study? What is the effect of three repeated breath-hold techniques routinely used by freedivers, thought to manipulate arterial partial pressures of O2 and CO2 , on the cardiorespiratory and haematological response to breath-holding during facial immersion? What is the main finding and its importance? All three techniques increased breath-hold by a similar duration, probably owing to the similar marked increase in end-tidal O2 and decrease in end-tidal CO2 observed in all three trials before facial immersion. These were the only cardiorespiratory changes that were consistently manipulated before the maximal breath-hold. This would suggest that pronounced bradycardia and vasoconstriction of selective vascular beds are probably not obligatory for prolonging breath-hold duration. Repeated maximal breath-holds have been demonstrated to induce bradycardia, increase haematocrit and haemoglobin and prolong subsequent breath-hold duration by 20%. Freedivers use non-maximal breath-hold techniques (BHTs) to improve breath-hold duration. The aim of this study was to investigate the cardiorespiratory and haematological responses to various BHTs. Ten healthy men (34.5±1.9 years) attended five randomized experimental trials and performed a 40min period of quiet rest or one of three BHTs followed by a maximal breath-hold challenge during facial immersion in water at 30 or 10°C. Cardiovascular and respiratory parameters were measured continuously using finger plethysmography and breath-by-breath gas analysis, respectively, and venous blood samples were collected throughout. Facial immersion in cold water caused marked bradycardia (74.1 vs. 50.2beats/min after 40 s) but did not increase breath-hold duration compared with warm water control conditions. Facial immersion breath-hold duration was 30.8-43.3% greater than the control duration when preceded by BHTs that involved repeated breath-holds of constant duration (P=0.021), increasing duration (P<0.001) or increasing frequency (P<0.001), with no difference observed between BHTs. The increased duration of apnoea across all three BHT protocols was associated with a 6.8% increase in end-tidal O2 and a 13.1% decrease in end-tidal CO2 immediately before facial immersion. There were no differences in blood pressure, cardiac output, heart rate, haematocrit or haemoglobin between each BHT and control conditions (P>0.05). In conclusion, the duration of apnoea can be extended by manipulating blood gases through repeated prior breath-holds, but changes in cardiac output and red blood cell mass do not appear essential.

Management of pregnant patients with pulmonary arterial hypertension.

Pregnant individuals with pulmonary arterial hypertension (PAH) have significantly high risks of maternal and perinatal mortality. Profound changes in plasma volume, cardiac output and systemic vascular resistance can all increase the strain being placed on the right ventricle, leading to heart failure and cardiovascular collapse. Given the complex network of opposing physiological changes, strict contraception and reduction of hemodynamic fluctuations during pregnancy are important methods of minimizing the risk of maternal mortality and improving the outcomes following pregnancy. In this review, we discuss the recent research progress into pre-conception management and the various therapeutic strategies for pregnant individuals with PAH.

Abstract 12774: Detecting Change in Cardiopulmonary Bypass Blood Flow Rate With a Novel, Wireless, Wearable Doppler Ultrasound Patch: A Pilot Study

Introduction: Assessing preload reserve (PR) is important when managing cardiac surgery patients. Typically, a 10% change in cardiac output is used as a reference standard to gauge PR; how this change in cardiac output translates to common carotid artery (CCA) velocity is unknown. In this pilot study, we compared known changes in cardiopulmonary bypass (CPB) flow rate to those measured by a novel wireless, wearable Doppler ultrasound placed over the CCA. Methods: A sample of 14 adult patients undergoing elective CABG was studied. While on CPB, at least two changes in blood flow (one negative, one positive) were made. The corresponding change in CCA velocity was measured by a wearable continuous wave (CW) Doppler ultrasound patch. For each subject, CPB flow changes were determined from the displayed spectrogram by the peristaltic pulsation frequency and CCA velocity changes were calculated from the automated maximum velocity trace. 5-10s windows pre- and post-CPB speed changes were selected, with sufficient signal quality to determine both relative CPB flow and CCA velocity. A “dose-response” curve was fitted to the relative changes in flow and velocity for each subject, as shown in Fig. 1, and the CCA velocity change corresponding to a 10% change in CPB flow was calculated. Results: CPB flows ranged from 0.5-6.3L/min. Mean relative flow changes were -58 and 179%, corresponding to mean CCA velocity changes of -43 and 107%. A mean CCA velocity change of 14% was found to correspond to 10% CPB flow change, ranging from 1.5-27.8%. Conclusions: CCA velocity measured with the Doppler patch successfully tracked changes in CPB flow. A CCA velocity change of &gt;14% suggests a &gt;10% change in cardiac output. Although preliminary, these results provide another important parameter for predicting the response to preload using a novel, easy-to-use, wireless Doppler device.

Abstract 15256: Treatment With Ketone Ester in Patients With Cardiogenic Shock Improves Cardiac Performance

Introduction: Cardiogenic shock is a life-threatening condition but no medical therapy has been documented to improve outcome. Recent evidence suggests that the ketone body 3-hydroxybutyrate (3-OHB) has favorable hemodynamic effects in patients with stable chronic heart failure. However, the hemodynamic effects of exogenous ketone supplements to patients with cardiogenic shock remains unknown. Hypothesis: In patients hospitalized with cardiogenic shock, acute treatment with a ketone ester has beneficial hemodynamic effects. Methods: In a randomized, double-blind, crossover study, we included 12 patients with cardiogenic shock who were treated with inotropes and/or vasopressors. In random order, patients received an enteral bolus of 500 mg/kg ketone ester (KetoneAid Inc.) and isocaloric, isovolemic placebo containing maltodextrin. Each study period lasted for three hours and was separated by a 3-hour washout period. The primary endpoint was change in cardiac output expressed as area under curve (AUC). Secondary endpoints were recorded at the end of each study period and included mixed venous saturation (SVO 2 ), pulmonary capillary wedge pressure, and echocardiographic measures of contractile function. Results: The ketone ester increased circulating 3-OHB significantly vs. placebo (peak: 3.7±0.5 mmol/L vs. 0.3±0.1 mmol/L, AUC: 6.0±0.9 mmol/L x hour vs. 0.3±0.1 mmol/L x hour, all p&lt;0.001). This was accompanied by an increase in cardiac output (5.1±0.3 L/min vs. 4.4±0.3 L/min, p=0.043; AUC of relative change: 61±22 L vs. 1±18 L, p=0.044), primarily due to a higher stroke volume (53±4 mL vs. 47±4 mL, p=0.048). Ketone ester increased SVO 2 vs. placebo (61±2% vs. 57±3%, p=0.035) whereas heart rate, mean arterial, pulmonary arterial, and pulmonary capillary wedge pressures did not differ between study periods. Ketone ester increased left ventricular ejection fraction (32±3% vs. 28±3%, p=0.005) and global longitudinal strain (-7.3±0.7% vs. -6.5±0.6%, p=0.01) as compared with placebo. Conclusions: Treatment with ketone ester has beneficial hemodynamic effects in patients with cardiogenic shock by increasing cardiac output and left ventricular function.

Stress-induced pulmonary hypertension: definition and diagnosis

The first hemodynamic definition of pulmonary hypertension (PH) was given at the World Symposium on PH (WSPH, 1973) in Geneva as an increasebin resting mean pulmonary artery pressure (mPAP) &gt;25 mm Hg by heart chamber catheterization. Since 2004, in the definition of PH, in addition to an increase in resting mPAP, an 'exercise' criterion has also been included: mPAP at the peak of exercise &gt;30 mm Hg. However, at the 4th WSPH Symposium in 2008, due to uncertainty of the relationship between age-related changes in cardiac output (CO) and pulmonary vascular physiology, in particular pulmonary vascular resistance (PVR) under exercise, this criterion was excluded.Resting PH manifests only at the absence of ≥50 % of pulmonary microcirculation, so for the earliest diagnosis of the disease, it’s necessary to use factors that provoke an increase in CO and PVR. Moreover, in clinical practice, manifestations of PH are not uncommon on exercise. In the absence of consensus the definition of stress- induced PH is defined in individuals with normal mPAP (&lt; 25 mm Hg) at rest and elevated mPAP (&gt;30 mm Hg) and PVR&gt; 3 WU at the peak of exercise.

Is pulmonary artery wedge pressure a reliable surrogate of left ventricular end-diastolic pressure during exercise for diagnosing HFpEF in patients with unexplained dyspnea?

Abstract Background Left ventricular end-diastolic pressure (LVEDP) is the gold-standard for the assessment of LV filling pressure. For practical reasons, pulmonary artery wedge pressure (PAWP) is used as a surrogate for LVEDP. However, the interposition of the left atrium (LA) may account discrepancies between LVEDP and PAWP. The imprecision of both end-diastolic (or mid-A) and mean PAWP estimates for LVEDP has been widely described for cardiac catheterization at rest. PAWP measurement during exercise has been advocated to discriminate heart failure with preserved ejection fraction (HFpEF) from non-cardiac dyspnea, with an end-expiratory pathologic threshold ≥25 mmHg. However, a formal comparison of PAWP (either mid-A or mean PAWP) vs LVEDP during exercise has never been performed. Aim To compare LVEDP and PAWP during exercise. Methods We retrospectively analyzed consecutive patients with unexplained dyspnea and a normal LV ejection fraction, who had a clinical indication of right and left heart catheterization at rest and during exercise to assess unexplained dyspnea. Patients with mitral regurgitation ≥ moderate were excluded. Hemodynamic measurements were always taken at end-expiration. Results Forty-six consecutive patients were included in the analysis (80% with a peak mean PAWP ≥25 mmHg). We found a good correlation between both mid-A and mean PAWP on one side, and LVEDP on the other side (R2&amp;gt;0.55). At peak exercise, mid-A PAWP had no bias as compared with LVEDP, while mean PAWP slightly overestimated LVEDP by 1–2 mmHg. However, confidence intervals were quite large (Figure 1), suggesting imprecision of PAWP estimates for LVEDP in the individual patient. A disagreement between mean PAWP and LVEDP, using a threshold of ≥25 mmHg for both variables at peak exercise, was found in 11% of patients. In 4% of them, mean PAWP was ≥25 but LVEDP &amp;lt;25 mmHg, due to the appearance of tall V waves in the PAWP position (LA stiffness), increasing PAWP above LVEDP. In the remaining 7%, LVEDP was ≥25 but PAWP &amp;lt;25 mmHg. The latter patients, in whom HFpEF would have not been diagnosed based on peak PAWP alone, showed a PAWP increase during exercise relative to cardiac output changes (PAWP/CO slope) &amp;gt;2 mmHg/L/min, as an alternative parameter suggesting HFpEF. Conclusions In patients with unexplained exertional breathlessness, both mid-A and mean PAWP showed good correlation with LVEDP during exercise with minimal average bias, but their ability to estimate LVEDP was burdened by a relevant imprecision. Therefore, when in these patients peak PAWP is &amp;lt;25 mmHg, its assessment might need to be complemented by additional measurements (including LVEDP or PAWP/CO slope) to maximize the diagnostic power of exercise cardiac catheterization in identifying HFpEF. Funding Acknowledgement Type of funding sources: Private grant(s) and/or Sponsorship.

LINKS BETWEEN CORONARY MICROVASCULAR DYSFUNCTION AND EVIDENCE OF HEART FAILURE WITH PRESERVED EJECTIVE FRACTION

BackgroundIt has been hypothesized that coronary microvascular dysfunction (CMD) may be associated with the development of myocardial abnormalities associated with heart failure with preserved ejective fraction (HFpEF). Making a diagnosis of HFpEF is aided by exercise right heart catheterization (RHC) based on an abnormal pulmonary artery wedge pressure (PAWP) response during exercise. An exercise-associated increase in PAWP adjusted for the change in cardiac output (ΔPAWP/ΔCO) greater than 2 mmHg/L/min is a clinical predictor for HF outcomes and predicts exercise capacity. Although there is speculation that CMD may play a role in the development of early HFpEF, there is limited evidence that directly links CMD as assessed by an invasive coronary physiology study (ICPS) with HFpEF as measured by an exercise RHC.Methods and ResultsThis study was an exploratory, retrospective cohort analysis. The study population included patients experiencing unexplained cardiovascular symptoms including chest pain and dyspnea who were referred to our institution for a RHC with exercise who had also undergone an ICPS. Patients were classified hemodynamically based on a ΔPAWP/ΔCO ≤ or > 2 with exercise. Coronary physiology interventions included Doppler flow assessment after administration of intracoronary adenosine and acetylcholine, where coronary flow reserve (CFR) and the index of microvascular resistance (IMR) were quantified during hyperemia. To date, we identified a cohort of 20 patients who met the study’s inclusion criteria. Of these, 19 completed a RHC exercise study from which 9/19 (47%) had a ΔPAWP/ΔCO > 2. Characteristics of the patients are shown in Table 1. The mean index of microvascular resistance (IMR) for patients with abnormal exercise hemodynamics was 32.6 versus 20.9 (p=0.08).Conclusion BackgroundIt has been hypothesized that coronary microvascular dysfunction (CMD) may be associated with the development of myocardial abnormalities associated with heart failure with preserved ejective fraction (HFpEF). Making a diagnosis of HFpEF is aided by exercise right heart catheterization (RHC) based on an abnormal pulmonary artery wedge pressure (PAWP) response during exercise. An exercise-associated increase in PAWP adjusted for the change in cardiac output (ΔPAWP/ΔCO) greater than 2 mmHg/L/min is a clinical predictor for HF outcomes and predicts exercise capacity. Although there is speculation that CMD may play a role in the development of early HFpEF, there is limited evidence that directly links CMD as assessed by an invasive coronary physiology study (ICPS) with HFpEF as measured by an exercise RHC. It has been hypothesized that coronary microvascular dysfunction (CMD) may be associated with the development of myocardial abnormalities associated with heart failure with preserved ejective fraction (HFpEF). Making a diagnosis of HFpEF is aided by exercise right heart catheterization (RHC) based on an abnormal pulmonary artery wedge pressure (PAWP) response during exercise. An exercise-associated increase in PAWP adjusted for the change in cardiac output (ΔPAWP/ΔCO) greater than 2 mmHg/L/min is a clinical predictor for HF outcomes and predicts exercise capacity. Although there is speculation that CMD may play a role in the development of early HFpEF, there is limited evidence that directly links CMD as assessed by an invasive coronary physiology study (ICPS) with HFpEF as measured by an exercise RHC. Methods and ResultsThis study was an exploratory, retrospective cohort analysis. The study population included patients experiencing unexplained cardiovascular symptoms including chest pain and dyspnea who were referred to our institution for a RHC with exercise who had also undergone an ICPS. Patients were classified hemodynamically based on a ΔPAWP/ΔCO ≤ or > 2 with exercise. Coronary physiology interventions included Doppler flow assessment after administration of intracoronary adenosine and acetylcholine, where coronary flow reserve (CFR) and the index of microvascular resistance (IMR) were quantified during hyperemia. To date, we identified a cohort of 20 patients who met the study’s inclusion criteria. Of these, 19 completed a RHC exercise study from which 9/19 (47%) had a ΔPAWP/ΔCO > 2. Characteristics of the patients are shown in Table 1. The mean index of microvascular resistance (IMR) for patients with abnormal exercise hemodynamics was 32.6 versus 20.9 (p=0.08). This study was an exploratory, retrospective cohort analysis. The study population included patients experiencing unexplained cardiovascular symptoms including chest pain and dyspnea who were referred to our institution for a RHC with exercise who had also undergone an ICPS. Patients were classified hemodynamically based on a ΔPAWP/ΔCO ≤ or > 2 with exercise. Coronary physiology interventions included Doppler flow assessment after administration of intracoronary adenosine and acetylcholine, where coronary flow reserve (CFR) and the index of microvascular resistance (IMR) were quantified during hyperemia. To date, we identified a cohort of 20 patients who met the study’s inclusion criteria. Of these, 19 completed a RHC exercise study from which 9/19 (47%) had a ΔPAWP/ΔCO > 2. Characteristics of the patients are shown in Table 1. The mean index of microvascular resistance (IMR) for patients with abnormal exercise hemodynamics was 32.6 versus 20.9 (p=0.08). Conclusion

Abstract P065: Standing Echocardiogram For Orthostatic Hypotension: A Feasibility Study

Background: Orthostatic hypotension (OH) is associated with cardiovascular disease, particularly in older adults. While standing transthoracic echocardiography (TTE) could identify changes in cardiac output to diagnose OH, no established protocols exist, and its feasibility is unknown. Objective: Determine the feasibility of standing TTE on adults in the outpatient setting. Methods: We recruited 72 adults scheduled for elective TTE. Consenting participants underwent recumbent TTE, followed by a focused standing TTE within 1-2 minutes of standing. The focused standing TTE used apical windows to measure left ventricular outflow tract velocity time integral, subsequently used to determine stroke volume and cardiac output. Standing blood pressure and heart rate were taken concurrently, and patients were monitored for symptoms. Results: Of the 72 enrolled participants, 60 (over 80%) completed the standing TTE. Mean age was 63 years (49% were ≥70 years), 49% were women, 42% had a BMI ≥30 kg/m 2 , and 18% had OH. The average duration of the study in the standing position was 127 seconds. Doppler quality was good-to-excellent in 87% of all our completing participants, 54% in those ≥70 years, and 86% in those with obesity. Only 5% of the participants experienced discomfort, and 9% experienced dizziness. There was no significant association between standing blood pressure and standing cardiac output. Conclusions: Standing focused TTE is safe, well-tolerated, and feasible in the ambulatory setting. While this clinical assessment is promising for identifying cardiogenic OH, further work is needed in larger at-risk cohorts to determine its clinical utility.

Acute Effects Of The Passive Static Stretching On Central And Peripheral Hemodynamics

Acute one-legged intermittent static stretching reduces arterial stiffness only in the stretched leg. Continuous high shear stress (e.g., shear rate) on endothelial cells induces vasodilation with increased endothelial-derived relaxation factor. Our recent study showed that shear rate and blood flow in the posterior tibial artery of the stretched leg was increased after acute passive one-legged calf intermittent stretching. Thus, the static stretching increases shear rate after stretching and may consequently decreases arterial stiffness. However, it remains unclear whether changes in central and peripheral circulation are related to a mechanism of static stretching-induced decrease in arterial stiffness. PURPOSE: This study aimed to clarify the time-course of changes in central and peripheral circulation on the acute static stretching-induced increase in shear rate. METHODS: The changes in cardiac output as central hemodynamics and blood flow and shear rate in the posterior tibial artery as peripheral hemodynamics by using echocardiography and doppler ultrasound, and blood volume in the calf muscle as peripheral hemodynamics by using near-infrared spectrophotometer were measured during recovery (0-60s) from a single bout of one-legged passive calf stretching (0-30s) in 12 healthy young men (22.8 ± 1.1 years). Blood pressure was measured before and after stretching session. RESULTS: The stretched leg’s blood flow and shear rate in posterior tibial artery significantly increased from 0 to 10th s after stretching (each P < 0.05). The muscle blood volume in the stretched leg significantly reduced during stretching, and then significantly increased during the recovery period after stretching (each P < 0.05); however, blood pressure and cardiac output remained unchanged during stretching and recovery. CONCLUSION: These findings indicate that mild ischemia-reperfusion was caused mechanically by the stretching calf muscles rather than by central hemodynamics, and consequently, it may have induced the increases in blood flow and shear rate in the posterior tibial artery of the stretched leg.

Influence Of Cardiac Output Response To The Onset Of Exercise On Cerebral Blood Flow

It is reported that the changes in cardiac output (Q) contribute to cerebral blood flow (CBF) regulation at rest and even during steady-state exercise. At the onset of cycling exercise, cardiac output (Q) increases acutely and largely via muscle pump, which may cause a larger elevation in CBF than an adequate value. However, the relationship between Q and CBF at the onset of exercise remains unknown. PURPOSE: The purpose of the present study was to examine whether onset exercise-induced large increase in Q contributes to CBF regulation at the onset of exercise. METHODS: In 11 young healthy participants, Q, mean arterial pressure (MAP), and mean blood velocities of middle and posterior cerebral arteries (MCA Vm and PCA Vm, respectively) were continuously measured during a 3-min light cycling exercise at 20 W on the ergometer. RESULTS: At the onset of exercise, Q increased acutely to the peak (P < 0.001), while MCA Vm and PCA Vm had two nadir and peak responses, but these CBF changes were not significant (MCA Vm and PCA Vm; P = 0.461 and P = 0.125, respectively). The change in Q was correlated with that of MCA Vm or PCA Vm from resting baseline to the steady-state exercise (r = 0.371, P = 0.008 and r = 0.418, P = 0.003, respectively). However, interestingly, the change in Q was not correlated with that of MCA Vm or PCA Vm at the onset of exercise (P = 0.223 and P = 0.151, respectively). CONCLUSION: These findings indicate that the change in Q does not contribute to CBF regulation at the onset of exercise for protecting cerebral vasculature against a large and acute elevation in Q at the onset of exercise.

Pressure–flow responses to exercise in aortic stenosis, mitral regurgitation and diastolic dysfunction

BackgroundHaemodynamic exercise testing is important for evaluating patients with dyspnoea on exertion and preserved ejection fraction. Despite very different pathologies, patients with pressure (aortic stenosis (AS)) and volume (mitral regurgitation...

Mechanisms for blood pressure reduction following isometric exercise training: a systematic review and meta-analysis.

Isometric exercise training (IET) is established as an effective antihypertensive intervention. Despite this, the physiological mechanisms driving blood pressure (BP) reductions following IET are not well understood. Therefore, we aimed to perform the first meta-analysis of the mechanistic changes measured following IET. PubMed, Cochrane library and SPORTDiscus were systematically searched for randomized controlled trials published between January 2000 and December 2021 reporting the effects of IET on resting BP and at least one secondary mechanistic parameter following a short-term intervention (2-12 weeks). Eighteen studies with a pooled sample size of 628 participants were included in the final analysis. IET produced significant reductions in resting systolic and diastolic BP of 9.35 mmHg (95% confidence interval [CI] = -7.80 to -10.89, P < 0.001) and 4.30 mmHg (CI = -3.01 to -5.60, P < 0.001), respectively. Mechanistically, IET produced a statistically significant reduction in resting heart rate (mean difference [MD]: -1.55 bpm, CI = -0.14 to -2.96, P = 0.031) and a significant increase in stroke volume (MD: 6.35 ml, CI = 0.35 to 12.60, P = 0.038), with no significant change in cardiac output. Conversely, total peripheral resistance (TPR) significantly decreased following IET (MD: -100.38 dyne s -1 cm 5 , CI = -14.16 to -186.61, P = 0.023), with significant improvements in the low frequency to high frequency heart rate variability ratio (MD: -0.41, CI = -0.09 to -0.73, P = 0.013) and baroreceptor reflex sensitivity (MD: 7.43 ms/mmHg, P < 0.001). This work demonstrates that a reduction in TPR, potentially mediated through enhanced autonomic vasomotor control, is primarily responsible for BP reductions following IET. Furthermore, this novel analysis suggests wall squat interventions to be the most effective IET mode, with clinically relevant differences in BP reductions compared to handgrip and leg extension IET; although future direct comparative research is required.

Effect of inotropic agents on oxygenation and cerebral perfusion in acute brain injury.

IntroductionTissue hypoxia and insufficient energy delivery is one of the mechanisms behind the occurrence of several complications in acute brain injured patients. Several interventions can improve cerebral oxygenation; however, the effects of inotropic agents remain poorly characterized.MethodsRetrospective analysis including patients suffering from acute brain injury and monitored with brain oxygen pressure (PbtO2) catheter, in whom inotropic agents were administered according to the decision of the treating physician's decision; PbtO2 values were collected before, 1 and 2 h after the initiation of therapy from the patient data monitoring system. PbtO2 “responders” were patients with a relative increase in PbtO2 from baseline values of at least 20%.ResultsA total of 35 patients were included in this study. Most of them (31/35, 89%) suffered from non-traumatic subarachnoid hemorrhage (SAH). Compared with baseline values [20 (14–24) mmHg], PbtO2 did not significantly increase over time [19 (15–25) mmHg at 1 h and 19 (17–25) mmHg at 2 h, respectively; p = 0.052]. A total of 12/35 (34%) patients were PbtO2 “responders,” in particular if low PbtO2 was observed at baseline. A PbtO2 of 17 mmHg at baseline had a sensibility of 84% and a specificity of 91% to predict a PbtO2 responder. A significant direct correlation between changes in PbtO2 and cardiac output [r = 0.496 (95% CI 0.122 to 0.746), p = 0.01; n = 25] and a significant negative correlation between changes in PbtO2 and cerebral perfusion pressure [r = −0.389 (95% CI −0.681 to −0.010), p = 0.05] were observed.ConclusionsIn this study, inotropic administration significantly increased brain oxygenation in one third of brain injured patients, especially when tissue hypoxia was present at baseline. Future studies should highlight the role of inotropic agents in the management of tissue hypoxia in this setting.

Invasive and non-invasive assessment of macro- and micro-circulatory effects of vasopressors during sevoflurane anesthesia in a pediatric experimental model: A randomized trial.

While non-invasive assessment of macro- and micro-circulation has the promise to optimize anesthesia management, evidence is lacking for the relationship between invasive and non-invasive measurements of cardiac output and microcirculatory indices. We aimed to compare the abilities of non-invasive techniques to detect changes in macro- and micro-circulation following deep anesthesia and subsequent restoration of the compromised hemodynamic by routinely used vasopressors in a randomized experimental study. A 20%-25% drop in mean arterial pressure was induced by sevoflurane in anesthetized mechanically ventilated just-weaned piglets (n=12) prior to the administration of vasopressors in random order (dopamine, ephedrine, noradrenaline, and phenylephrine). Simultaneous transpulmonary thermodilution cardiac output assessment with the invasive pulse index continuous contour (PiCCO) method was compared with non-invasive estimates obtained with electrical conductivity (ICON) and echo Doppler (Cardio Q). Changes in microcirculation were characterized by sublingual red blood cell velocity, jugular cerebral venous oxygen saturation, and arterial lactate. Cardiac output indices obtained by invasive and non-invasive methods. Changes in cardiac output measured invasively and non-invasively correlated significantly after sevoflurane (r=.78, p=.003 and r=.76, p=.006 between PiCCO and ICON or Cardio Q, respectively). Following the administration of vasopressors, invasive and non-invasive cardiac output assessments were unrelated with significant correlations observed only between PiCCO and ICON after dopamine and ephedrine. Sevoflurane-induced hypotension decreased jugular cerebral venous oxygen saturation significantly and was recovered by all vasopressors. Sevoflurane and vasopressors had no effect on red blood cell velocity, which increased only after dopamine. No consistent changes in lactate were observed during the study period. The results of this study suggest that non-invasive cardiac output measurements may not accurately reflect changes in macrocirculation after hemodynamic optimization by vasopressors. Due to the incoherence between macro- and micro-circulation, monitoring microcirculation is essential to guide patient management.

Influence of cardiac output response to the onset of exercise on cerebral blood flow.

Change in cardiac output (Q) contributes to cerebral blood flow (CBF) regulation at rest and even during steady-state exercise. At the onset of cycling exercise, Q increases acutely and largely via muscle pump. The purpose of the present study was to examine whether onset exercise-induced a large increase in Q contributes to CBF regulation at the onset of exercise. In 20 young healthy participants (10 males and 10 females), Q, mean arterial pressure (MAP), and mean blood velocities of middle and posterior cerebral arteries (MCA Vm and PCA Vm) were continuously measured during light cycling exercise for 3min. At the onset of exercise, Q increased acutely to the peak (P < 0.001), while the CBF peak responses were not significantly higher than the values during the steady-state exercise (MCA Vm and PCA Vm; P = 0.183 and P = 0.101, respectively). The change in Q was correlated with that of MCA Vm or PCA Vm from resting baseline to the steady-state exercise (r = 0.404, P < 0.001 and r = 0.393, P < 0.001, respectively). However, the change in Q was not correlated with that of MCA Vm or PCA Vm at the onset of exercise (P = 0.853 and P = 0.893, respectively). Any sex differences in the onset response of peripheral and cerebral hemodynamics to exercise were not observed. These findings suggest that the acute change in Q does not contribute to CBF regulation at the onset of exercise for protecting cerebral vasculature against a large and acute elevation in Q at the onset of exercise.

Continuous cardiac output measured with a Swan‐Ganz catheter reacts too slowly in animal experiments with sudden circulatory failure

BackgroundIn many animal experiments, it is vital to detect sudden changes in cardiac output (CO). This porcine study compared CO that was measured with a Swan‐Ganz pulmonary catheter with the gold standard (which was a transit‐time flow probe around the pulmonary artery) during interventions that caused hemodynamic instability.MethodsIn one series, 7 pigs were exposed to sudden changes in CO. In another series, 9 pigs experienced more prolonged changes in CO. All the pigs had a Swan‐Ganz catheter placed into the pulmonary artery and a flow probe around the pulmonary artery. Adrenaline infusion and controlled hemorrhage were used to increase and decrease CO, respectively. The measurements of CO before and after each intervention were compared for correlation, agreement, and the time delay that it took each method to detect at least a 30% change in CO. A Bland–Altman test was used to identify correlations and agreements between the methods.ResultsIn the first series, there was a delay of 5–7 min for the Swan Ganz catheter to register a 30% change in cardiac output, compared with the flow probe. However, during prolonged changes in CO in the second series, there was a good correlation between the 2 methods. Mixed venous oxygen saturation reacted faster to changes than did CO; both were measured via the Swan‐Ganz catheter.ConclusionsIn many animal studies, the use of Swan‐Ganz catheters is suitable; however, in experiments with sudden hemodynamic instability, the flow probe is the most advantageous method for measuring CO.

Pulmonary Vasculature Responsiveness to Phosphodiesterase-5A Inhibition in Heart Failure With Reduced Ejection Fraction: Possible Role of Plasma Potassium.

IntroductionPhosphodiesterase-5a inhibition (PDE5i) leads to favorable changes in pulmonary hemodynamic and cardiac output (CO) in patients with advanced heart failure (HF) and reduced ejection fraction (HFrEF). The hemodynamic response to PDE5i could be heterogeneous and the clinical variables associated with these changes are scarcely investigated.Materials and MethodsOf 260 patients with advanced HFrEF referred for advanced therapies [cardiac transplant/left ventricular assist device (LVAD)], 55 had pulmonary hypertension (PH) and fulfilled the criteria for the PDE5i vasoreactivity test. Right heart catheterization (RHC) was performed as a part of clinical evaluation before and after 20-mg intravenous sildenafil. Absolute and relative changes in pulmonary vascular resistance (PVR) were evaluated to assess hemodynamic response to PDE5i. Clinical, biochemical, and hemodynamic factors associated with PVR changes were identified.ResultsSildenafil administration reduced PVR (− 45.3%) and transpulmonary gradient (TPG; − 34.8%) and increased CO (+ 13.6%). Relative change analysis showed a negative moderate association between baseline plasma potassium and changes in PVR (r = − 0.48; p = 0.001) and TPG (r = − 0.43; p = 0.005) after PDE5i. Aldosterone concentration shows a direct moderate association with PVR changes after PDE5i. A significant moderate association was also demonstrated between CO improvement and the severity of mitral (r = 0.42; p = 0.002) and tricuspid (r = 0.39; p = 0.004) regurgitation.ConclusionWe identified plasma potassium, plasma aldosterone level, and atrioventricular valve regurgitations as potential cofounders of hemodynamic response to acute administration of PDE5i. Whether modulation of potassium levels could enhance pulmonary vasoreactivity in advanced HFrEF deserves further research.

Dynamic and Hybrid Extracorporeal Membrane Oxygenation Configurations Require Greater Involvement of Vascular Surgeons

The use of extracorporeal membrane oxygenation (ECMO) for adult patients with refractory cardiac, pulmonary, or cardiopulmonary shock has increased dramatically in the past decades. A substantial and understudied subset of these patients will require reconfiguration of their ECMO circuit. The indications for reconfiguration include escalation or de-escalation of arterial support for changes in native cardiac output, anatomic considerations for limb compromise or thrombus formation, and transition to long-term support involving ventricular-assist devices.