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Central venous pressure (CVP) levels (mean ± SE in mmHg) at rest, exercise onset, and during upright exercise at 25 W on a cycle ergometer in normal subjects (solid circles; n = 4) and heart transplant patients (open circles; n = 6). * , values significantly different from exercise onset at p < 0.05.
Source publication
Central venous pressure (CVP) gives the integral result of changes in cardiac and peripheral factors. Thus, the sudden increase in CVP observed at the onset of dynamic exercise has been attributed to the action of the muscle pump but is also affected by reflex changes in cardiac response. To determine which predominates at the onset of exercise, we...
Contexts in source publication
Context 1
... normal heart can adjust to the increase in venous return during exercise in two ways. One is through the Frank–Starling mechanism by which the increase in the cardiac end-diastolic volume leads to an increase in stroke volume and cardiac output. This can be expressed graphically by movement upward along a cardiac function curve (Guyton 1955) ( Fig. 1). For cardiac output to increase, there must be an increase in the return of blood to the heart (i.e., venous return), which implies a change in peripheral circuit factors. Graphically, this is represented by either a shift in the venous return curve or change in its slope (Guyton 1955) (Fig. 1). The other way is through an increase in cardiac function that can be due to an increase in contractility, a decrease in afterload, or an increase in heart rate. This can be graphically represented by an upward shift of the whole cardiac function curve. Obviously, both changes in the circuit and cardiac function can occur simultaneously, but when the increase in cardiac output is predominantly due to a change in the circuit and increased cardiac filling pressures, the CVP will increase (point B in Fig. 1). On the other hand, when the increase is predominantly due to an increase in cardiac pump function, the CVP will fall (point A in Fig. 1). If cardiac output increases and CVP remains constant, adaptations must have occurred in both the heart and circuit and these changes must be of similar magnitude. The simple measurement of CVP in a condition in which cardiac output is known to increase can thus give important information about the interaction of the heart and circuit. Cardiac output increases at the start of exercise. In normal subjects this could be due to neurally mediated rapid adjustments in cardiac function as well as changes in circuit function that increase cardiac filling. A factor that recently received a lot of attention and could cause an immediate increase in venous return is the action of muscle contractions that produces an effective peripheral pump for the return of blood to the heart. This acts before neurohumoral factors and should cause an immediate rise in CVP. Patients who have undergone transplants have denervated hearts. They thus have no neural adjustment and only have a slower humoral adjustment during exercise. However, the muscle pump mechanism should be the same in heart transplant patients as in normals and CVP should also rise at the onset of exercise. The simple measurement of CVP at the onset of exercise should thus give important insight into the interaction of the heart and peripheral circuit. By comparing normal subjects to patients with heart transplants, we were able to examine the CVP change at the onset of exercise in subjects with and without cardiac innervation. This allowed a comparison of normal subjects to a group in whom there could not be an immediate cardiac neural response. If the muscle pump mechanism predominates at the onset of exercise, there should be an immediate and similar rise in CVP in normals and HT patients. However, after a few seconds, this component should be “masked” in normal but not in HT patients by the neurally mediated increase in cardiac responses. Examples of the experimental record in a normal and HT subject are shown in Fig. 2. CVP increased immediately upon commencement of pedalling in both control and transplant subjects and to a similar degree. Mean value ± SE for CVP, heart rate, minute ventilation, and oxygen consumption at rest, exercise onset, and 3 min of exercise in both groups are given in Table 2. The main effect of time on CVP was significant ( F 12.13, df = 2,6, p < 0.008) in normal subjects. CVP at exercise onset and at 3 min of exercise were not different, but both were significantly greater than rest ( p < 0.05) (Fig. 3). Heart transplant patients also had a significant main effect of time on CVP ( F = 93.89, df = 2,10, p < 0.0001). However, mean CVP at 3 min of exercise was higher than at exercise onset and both were greater than rest ( p < 0.05) (Fig. 3). The increase in CVP from rest to 3 min was greater than the increase at exercise onset ( t –4.87, df 5, p < 0.005). Pulmo- nary wedge pressure during the 3rd min of exercise was also significantly elevated from rest ( p < 0.001) but was not avail- able for the immediate onset of exercise. Mean values are shown in Table 2. Heart rate increased from rest to the onset of exercise in normals ( p < 0.05) but not in transplant patients (Table 2). However, heart rate increased in the transplant patients by 3 min of exercise ( p < 0.05). Heart transplant patients demonstrated an increase in cardiac output from rest to the 3rd min of exercise ( p < 0.003). The predicted cardiac output of normal subjects, calculated from the known relationship of cardiac output and V O 2 , demonstrated an appropriate rise ( p < 0.001) and the values were similar to those measured in HT (Table 2). The resting V O 2 in normals was higher than in HT, possibly due to a stronger anticipatory response. Central venous pressure increased immediately in the transition from rest to cycling exercise in both heart transplant patients and healthy normal subjects and the mean increase was of the same magnitude in both groups, approximately 4 mmHg (1 mmHg = 133.3 Pa). However, as exercise continued, central venous pressure increased further in the transplant patients, whereas it plateaued or tended to decrease in the normal subjects. Before addressing the implications of this result, we must consider some technical factors related to the measurement of central venous pressure. By measuring CVP relative to atmosphere and not intrathoracic pressure, the transmural pressure and therefore the effective filling pressure is unknown. Esophageal pressure was measured in small numbers of subjects during upright exercise to determine changes in pleural pressure (Holmgren 1956; Sprangers et al. 1991). Holmgren (1956) found no change in mean esophageal pressure during cycle exercise in 14 normal subjects but noted a small transitory increase at exercise onset in half of these subjects. Sprangers et al. (1991) showed no change in two subjects at the onset of cycle exercise and concluded that their reported change in right atrial pressure was thus equal to the change in right atrial transmural pressure. It is therefore unlikely that an increase in intrathoracic pressure explains the rise in CVP. The increase in CVP was sustained in our study. We measured central venous or right atrial pressure at the end of expiration to control for respiratory variations. Most authors have used the electronic mean value of CVP, but this depends on the magnitude of inspiratory and expiratory swings in pressure. Finally, care was taken to insure that the position of the subjects relative to the transducer was maintained to avoid movement artifacts in the pressure measurement. The lack of any discernable delay between the movement of the legs at exercise onset and the rise in CVP in both normal and transplant patients, as well as the small rise in heart rate of only 8 beats/min in the normal group, indicate that the response is unlikely to be due to neurohumoral mechanisms and is most likely due to a mechanical effect of muscle contraction on veins in exercising muscle as well as the abdomen. Sheriff et al. (1993) also found a mean increase of approximately 5 mmHg in dogs that began running on a treadmill with or without autonomic blockade. The effect of muscle contractions on veins effectively increases mean circulatory filling pressure, which increases the gradient for venous return. Guyton et al. (1973) found that the increase in average mean circulatory filling pressure during muscle stimulation in anesthetized dogs with sympathetic ganglionic blockade with hexamethonium was from 3.8 to 11.3 mmHg and did not occur when contractions were blocked by a paralytic agent. This would result in a large volume shift toward the heart from peripheral capacitance vessels at exercise onset and result in an increase in central venous pressure. If we assume a venous compliance of 2–4 mL ⋅ mmHg –1 ⋅ kg –1 (Drees 1974; Guyton et al. 1973) and no change in venous resistance such that the change in CVP in our data represents the change in mean circulatory filling pressure, we can estimate that the magnitude of volume mobilized by the muscle pump mechanism is from 8–16 mL/kg at exercise onset. This corresponds to a significant immediate volume shift of 560–1120 mL in a 70-kg person. These values are consistent with the estimate of 9.5 mL/kg made in dogs at the onset of exercise (Sheriff et al. 1993). They are also consistent with the relative increase in central blood volume with a decrease in lower extremity blood volume, measured by ...
Context 2
... normal heart can adjust to the increase in venous return during exercise in two ways. One is through the Frank–Starling mechanism by which the increase in the cardiac end-diastolic volume leads to an increase in stroke volume and cardiac output. This can be expressed graphically by movement upward along a cardiac function curve (Guyton 1955) ( Fig. 1). For cardiac output to increase, there must be an increase in the return of blood to the heart (i.e., venous return), which implies a change in peripheral circuit factors. Graphically, this is represented by either a shift in the venous return curve or change in its slope (Guyton 1955) (Fig. 1). The other way is through an increase in cardiac function that can be due to an increase in contractility, a decrease in afterload, or an increase in heart rate. This can be graphically represented by an upward shift of the whole cardiac function curve. Obviously, both changes in the circuit and cardiac function can occur simultaneously, but when the increase in cardiac output is predominantly due to a change in the circuit and increased cardiac filling pressures, the CVP will increase (point B in Fig. 1). On the other hand, when the increase is predominantly due to an increase in cardiac pump function, the CVP will fall (point A in Fig. 1). If cardiac output increases and CVP remains constant, adaptations must have occurred in both the heart and circuit and these changes must be of similar magnitude. The simple measurement of CVP in a condition in which cardiac output is known to increase can thus give important information about the interaction of the heart and circuit. Cardiac output increases at the start of exercise. In normal subjects this could be due to neurally mediated rapid adjustments in cardiac function as well as changes in circuit function that increase cardiac filling. A factor that recently received a lot of attention and could cause an immediate increase in venous return is the action of muscle contractions that produces an effective peripheral pump for the return of blood to the heart. This acts before neurohumoral factors and should cause an immediate rise in CVP. Patients who have undergone transplants have denervated hearts. They thus have no neural adjustment and only have a slower humoral adjustment during exercise. However, the muscle pump mechanism should be the same in heart transplant patients as in normals and CVP should also rise at the onset of exercise. The simple measurement of CVP at the onset of exercise should thus give important insight into the interaction of the heart and peripheral circuit. By comparing normal subjects to patients with heart transplants, we were able to examine the CVP change at the onset of exercise in subjects with and without cardiac innervation. This allowed a comparison of normal subjects to a group in whom there could not be an immediate cardiac neural response. If the muscle pump mechanism predominates at the onset of exercise, there should be an immediate and similar rise in CVP in normals and HT patients. However, after a few seconds, this component should be “masked” in normal but not in HT patients by the neurally mediated increase in cardiac responses. Examples of the experimental record in a normal and HT subject are shown in Fig. 2. CVP increased immediately upon commencement of pedalling in both control and transplant subjects and to a similar degree. Mean value ± SE for CVP, heart rate, minute ventilation, and oxygen consumption at rest, exercise onset, and 3 min of exercise in both groups are given in Table 2. The main effect of time on CVP was significant ( F 12.13, df = 2,6, p < 0.008) in normal subjects. CVP at exercise onset and at 3 min of exercise were not different, but both were significantly greater than rest ( p < 0.05) (Fig. 3). Heart transplant patients also had a significant main effect of time on CVP ( F = 93.89, df = 2,10, p < 0.0001). However, mean CVP at 3 min of exercise was higher than at exercise onset and both were greater than rest ( p < 0.05) (Fig. 3). The increase in CVP from rest to 3 min was greater than the increase at exercise onset ( t –4.87, df 5, p < 0.005). Pulmo- nary wedge pressure during the 3rd min of exercise was also significantly elevated from rest ( p < 0.001) but was not avail- able for the immediate onset of exercise. Mean values are shown in Table 2. Heart rate increased from rest to the onset of exercise in normals ( p < 0.05) but not in transplant patients (Table 2). However, heart rate increased in the transplant patients by 3 min of exercise ( p < 0.05). Heart transplant patients demonstrated an increase in cardiac output from rest to the 3rd min of exercise ( p < 0.003). The predicted cardiac output of normal subjects, calculated from the known relationship of cardiac output and V O 2 , demonstrated an appropriate rise ( p < 0.001) and the values were similar to those measured in HT (Table 2). The resting V O 2 in normals was higher than in HT, possibly due to a stronger anticipatory response. Central venous pressure increased immediately in the transition from rest to cycling exercise in both heart transplant patients and healthy normal subjects and the mean increase was of the same magnitude in both groups, approximately 4 mmHg (1 mmHg = 133.3 Pa). However, as exercise continued, central venous pressure increased further in the transplant patients, whereas it plateaued or tended to decrease in the normal subjects. Before addressing the implications of this result, we must consider some technical factors related to the measurement of central venous pressure. By measuring CVP relative to atmosphere and not intrathoracic pressure, the transmural pressure and therefore the effective filling pressure is unknown. Esophageal pressure was measured in small numbers of subjects during upright exercise to determine changes in pleural pressure (Holmgren 1956; Sprangers et al. 1991). Holmgren (1956) found no change in mean esophageal pressure during cycle exercise in 14 normal subjects but noted a small transitory increase at exercise onset in half of these subjects. Sprangers et al. (1991) showed no change in two subjects at the onset of cycle exercise and concluded that their reported change in right atrial pressure was thus equal to the change in right atrial transmural pressure. It is therefore unlikely that an increase in intrathoracic pressure explains the rise in CVP. The increase in CVP was sustained in our study. We measured central venous or right atrial pressure at the end of expiration to control for respiratory variations. Most authors have used the electronic mean value of CVP, but this depends on the magnitude of inspiratory and expiratory swings in pressure. Finally, care was taken to insure that the position of the subjects relative to the transducer was maintained to avoid movement artifacts in the pressure measurement. The lack of any discernable delay between the movement of the legs at exercise onset and the rise in CVP in both normal and transplant patients, as well as the small rise in heart rate of only 8 beats/min in the normal group, indicate that the response is unlikely to be due to neurohumoral mechanisms and is most likely due to a mechanical effect of muscle contraction on veins in exercising muscle as well as the abdomen. Sheriff et al. (1993) also found a mean increase of approximately 5 mmHg in dogs that began running on a treadmill with or without autonomic blockade. The effect of muscle contractions on veins effectively increases mean circulatory filling pressure, which increases the gradient for venous return. Guyton et al. (1973) found that the increase in average mean circulatory filling pressure during muscle stimulation in anesthetized dogs with sympathetic ganglionic blockade with hexamethonium was from 3.8 to 11.3 mmHg and did not occur when contractions were blocked by a paralytic agent. This would result in a large volume shift toward the heart from peripheral capacitance vessels at exercise onset and result in an increase in central venous pressure. If we assume a venous compliance of 2–4 mL ⋅ mmHg –1 ⋅ kg –1 (Drees 1974; Guyton et al. 1973) and no change in venous resistance such that the change in CVP in our data represents the change in mean circulatory filling pressure, we can estimate that the magnitude of volume mobilized by the muscle pump mechanism is from 8–16 mL/kg at exercise onset. This corresponds to a significant immediate volume shift of 560–1120 mL in a 70-kg person. These values are consistent with the estimate of 9.5 mL/kg made in dogs at the onset of exercise (Sheriff et al. 1993). They are also consistent with the relative increase in central blood volume with a decrease in lower extremity blood volume, measured by radionuclide techniques, reported by Flamm et al. (1990) at the transition from rest to zero-load cycling in normal exercising humans. Others have reported a significant decrease in venous pressure in the lower limbs as a result of a single muscle ...
Citations
... Other studies reported no influence of compression garments on lactate levels (Hamner et al., 2010;Sugiyama et al., 2013). Potential explanations for the lactate variations are that, during recovery, skeletal muscles facilitate blood return by rhythmic muscle contractions that create oscillations in intramuscular pressure, which increases blood flow and venous return (Notarius and Magder, 1996). Likewise, increased blood flow is thought to enhance lactate removal from exercising muscles, which facilitates faster redistribution to alternative sites such as the heart, liver, and non-working muscles (Menzies et al., 2010). ...
Background: The use of elastomeric technology in sports garments is increasing in popularity; however, its specific impact on physiological and psychological variables is not fully understood. Thus, we aimed to analyze the physiological (muscle activation of the pectoralis major, triceps brachii, anterior deltoid, and rectus abdominis, capillary blood lactate, systolic and diastolic blood pressure, and heart rate) and psychological (global and respiratory rating of perceived exertion [RPE]) responses during an incremental treadmill test wearing a new sports garment for the upper body that incorporates elastomeric technology or a placebo garment.
Methods: Eighteen physically active young adults participated in two randomized sessions, one wearing the elastomeric garment and the other wearing a placebo. Participants performed in both sessions the same treadmill incremental test (i.e., starting at 8 km/h, an increase of 2 km/h each stage, stage duration of 3 min, and inclination of 1%; the test ended after completing the 18 km/h Stage or participant volitional exhaustion). The dependent variables were assessed before, during, and/or after the test. Nonparametric tests evaluated differences.
Results: The elastomeric garment led to a greater muscle activation (p < 0.05) in the pectoralis major at 16 km/h (+33.35%, p = 0.01, d = 0.47) and 18 km/h (+32.09%, p = 0.02, d = 0.55) and in the triceps brachii at 10 km/h (+20.28%, p = 0.01, d = 0.41) and 12 km/h (+34.95%, p = 0.04, d = 0.28). Additionally, lower lactate was observed at the end of the test (−7.81%, p = 0.01, d = 0.68) and after 5 min of recovery (−13.71%, p < 0.001, d = 1.00) with the elastomeric garment. Nonsignificant differences between the garments were encountered in the time to exhaustion, cardiovascular responses, or ratings of perceived exertion.
Conclusion: These findings suggest that elastomeric garments enhance physiological responses (muscle activation and blood lactate) during an incremental treadmill test without impairing physical performance or effort perception.
... However, our notion is supported by most previous findings that the exercise pressor reflex does not suppress cardiac baroreflex sensitivity Murata et al., 2004;Potts & Mitchell, 1998;Smith et al., 2003). (Notarius & Magder, 1996;Sprangers et al., 1991). However, Faris et al. (1983) performed careful experiments to avoid several confounding factors and found that in conscious rabbits, the baroreflex sensitivity for HR was not affected by hypervolaemia or by 20% hypovolaemia; the baroreflex sensitivity for systemic vascular resistance was reduced by hypervolaemia and increased by 20% ...
It remains unclear whether cardiac baroreflex function is preserved or suppressed at the onset of standing up. To answer the question and, if cardiac baroreflex is suppressed, to investigate the mechanism responsible for the suppression, we compared the sensitivity of the arterial cardiac baroreflex at the onset of voluntary and passive hindlimb standing in conscious cats. Cardiac baroreflex sensitivity was estimated from the maximal slope of the baroreflex curve between the responses of systolic arterial blood pressure and heart rate to a brief occlusion of the abdominal aorta. The systolic arterial blood pressure response to standing up without aortic occlusion was greater in the voluntary case than in the passive case. Cardiac baroreflex sensitivity was clearly decreased at the onset of voluntary standing up compared with rest (P = 0.005) and the onset of passive standing up (P = 0.007). The cardiac baroreflex sensitivity at the onset of passive standing up was similar to that at rest (P = 0.909). The findings suggest that central command would transmit a modulatory signal to the cardiac baroreflex system during the voluntary initiation of standing up. Furthermore, the present data tempt speculation on a close relationship between central inhibition of the cardiac baroreflex and the centrally induced tachycardiac response to standing up.
... In this model, cardiovascular function is predominantly determined by intrinsic factors (such as myocardial contractility) and by extrinsic factors that alter the preload and afterload of the heart (i.e., venous return, mean arterial pressure and peripheral vascular resistance). Venous flow (venous return to the pump) is also driven by a pressure gradient between the venous vasculature of peripheral tissues and the right atrium, and is facilitated by the action of the skeletal muscle pump [180][181][182][183][184]. Experimental findings will be interpreted in the context of this paradigm to answer whether the function of the heart itself is compromised during exercise with and without environmental stress. ...
Claude Bernard’s milieu intérieur (internal environment) and the associated concept of homeostasis are fundamental to the understanding of the physiological responses to exercise and environmental stress. Maintenance of cellular homeostasis is thought to happen during exercise through the precise matching of cellular energetic demand and supply, and the production and clearance of metabolic by-products. The mind-boggling number of molecular and cellular pathways and the host of tissues and organ systems involved in the processes sustaining locomotion, however, necessitate an integrative examination of the body’s physiological systems. This integrative approach can be used to identify whether function and cellular homeostasis are maintained or compromised during exercise. In this review, we discuss the responses of the human brain, the lungs, the heart, and the skeletal muscles to the varying physiological demands of exercise and environmental stress. Multiple alterations in physiological function and differential homeostatic adjustments occur when people undertake strenuous exercise with and without thermal stress. These adjustments can include: hyperthermia; hyperventilation; cardiovascular strain with restrictions in brain, muscle, skin and visceral organs blood flow; greater reliance on muscle glycogen and cellular metabolism; alterations in neural activity; and, in some conditions, compromised muscle metabolism and aerobic capacity. Oxygen supply to the human brain is also blunted during intense exercise, but global cerebral metabolism and central neural drive are preserved or enhanced. In contrast to the strain seen during severe exercise and environmental stress, a steady state is maintained when humans exercise at intensities and in environmental conditions that require a small fraction of the functional capacity. The impact of exercise and environmental stress upon whole-body functions and homeostasis therefore depends on the functional needs and differs across organ systems.
... The advantage of having opposite processes active at the same time is that it allows a more rapid change. For example, at the start of exercise, the parasympathetic output is quickly withdrawn and the sympathetic output increased so that there is a rapid acceleration of the heart rate which then can accommodate a rapid increase in venous return (Notarius and Magder 1996). ...
... Sympathetic activity to peripheral resistance vessels also increases and maintains the increased arterial pressure. As originally proposed by Bainbridge, the reflex allows the heart rate to respond faster to a sudden increase in venous return as occurs at the onset of exercise as discussed under the rapid vagal withdrawal at the onset of exercise (Notarius and Magder 1996;Fagraeus and Linnarsson 1976;Linnarsson 1974). As will be seen later, the consequent shortened diastolic time also limits the distension of the right heart. ...
Changes in heart rate are a major regulator of normal cardiac output, and thus a key component of adaptations in the cardiovascular system. The direct regulation of heart rate at the cellular level has evolved with a complex system of processes that regulate the currents across the cardiac membranes. These set spontaneous cyclic activation and lengths of the action potential which determine the lengths of systole and diastole. This cyclic nature of cardiac output creates important limitations on the circulation because it sets the time available for filling and the time available for ejection. These limits affect the maximum possible outputs from the heart and can lead to pathological processes. Heart rate is regulated by intrinsic processes in the membranes of the pacemaker of the heart (sinoatrial node), the conducting system of the heart, and neural and humoral regulating factors. Heart rate normally increases in proportion to what is called the relative workload but also can be altered by many factors not directly related to metabolic needs. The interplay of all these factors need to be considered by critical care physicians managing patients at the bedside.
... Applied Computational Intelligence and Soft Computing pump [22]. erefore, systemic venous pressure increases for healthy subjects (see Figure 11(b)). ...
The prediction of cardiac conditions can be done through comparison and analysis of parameters transformed into mathematical model equations. This paper aims to present the design of a web-based graphical user interface of mathematical model of cardiovascular-respiratory system (ICRSMM) as an appropriate displaying tool. The designed system offers an easy way of recording and storing parameters in a database. Those parameters are computerized to generate automatic results in a graphic representation, which is an effective way used in medicine to allow physicians, nurses, and other experienced health personnel to analyze and discuss results. The designed solution provides an adequate and friendly environment that eases the task of recording the results in a graphic representation. This gives a clear picture of analysis to determine a healthy or unhealthy cardiovascular-respiratory system of a person exercising. However, such a complex design solution comes in to put an accent of consideration to an area of research that still needs more discoveries and exploration.
... 31 The right atrial pressure was set at 5 mmHg according to previous studies, and it may be significantly increased under high workload, particularly in HF patients. 32 This may cause underestimation of exercise RVSP. Further large-scale trials evaluating the favorable effects of dapagliflozin under exercise conditions in chronic HF patients, including a heterogeneous population, may be required. ...
Background:
This prospective randomized multicenter open-label trial evaluated whether sodium-glucose cotransporter-2 inhibitor (SGLT2-i) improves left ventricular (LV) pump function and suppresses elevation of LV filling pressure (LVFP) and right ventricular systolic pressure (RVSP) during exercise in type 2 diabetes mellitus (T2DM) patients.Methods and Results:Based on HbA1c and LV ejection fraction, 78 patients with poorly controlled T2DM were randomly assigned to D-group (dapagliflozin 5 mg/day add-on) or C-group (conventional therapy add-on). Physical examination, home and office blood pressure examination, blood tests, and echocardiography at rest and during ergometer exercise were performed at baseline and at 1.5 and 6 months after treatment. The primary endpoint was defined as the change in RVSP (mmHg) between baseline and 6-month follow up. The secondary endpoints were changes in LVFP (ratio), stroke volume index (SVi; mL/m2), and cardiac index (CI; L/min/m2). Both RVSP and LVFP during exercise significantly decreased from baseline to 6 months after starting treatment in the D-group (P<0.001). No changes to either parameter was observed in the C-group. The SVi and CI did not improve in either group. Both home and office blood pressure significantly decreased in the D-group. Decreases in HbA1c were somewhat greater in the C-group.
Conclusions:
Dapagliflozin significantly improved RVSP and LVFP during exercise in patients with T2DM and cardiovascular risk, which may contribute to favorable effects on heart failure.
... For example, it has been shown that a single muscle contraction is capable of inducing an intramuscular pressure that effectively translocates more than 40% of the intra-muscular blood volume to the central venous pool (Stewart et al. 2004). Furthermore, it has been reported that the increase in filling volume during the first minute of exercise can be attributed to the regulation of the central venous pressure by the muscle pump (Notarius and Magder 1996). In the current study, LV filling in the non-disabled subjects was malleable to changes in workloads, despite the elicitation of exercise-induced tachycardia whereas neither EDV nor EDFR changed with exercise in the subjects with icSCI. ...
Purpose
To characterize left ventricular diastolic function during an exertional challenge in adults with incomplete cervical spinal cord Injury (icSCI).
Methods
In this cross-sectional study, a two-group convenience sample was used to compare left ventricular LV diastolic performance during a 5–10 W·min⁻¹ incremental arm ergometer exercise protocol, using bioimpedance cardiography. Subjects were eight males with cervical incomplete spinal cord injury (icSCI; C5-C7: age 39 ± 14 years) versus eight able-bodied males (CON: age 38 ± 13 years). Left ventricular (LV) diastolic indices included end-diastolic volume (EDV) and early diastolic filling ratio (EDFR). LV ejection time (LVET), inotropic index (dZ/dT²) and stroke volume (SV) were compared between the groups at peak exercise, and maximum workload for the icSCI group (isomax).
Results
EDV (at peak exercise:131.4 ± 7.3 vs 188.78 ± 9.4, p < 0.001; at isomax: 131.4 ± 7.3 vs 169 ± 23, p = 0.0009) and EDFR (at peak exercise 73 ± 14% vs 119 ± 11%, p = 0.006; at isomax 94 ± 10; p = 0.009) were significantly reduced in icSCI compared to CON, respectively. Significant differences in LVET (icSCI: 273 ± 48 vs CON: 305 ± 68; p = 0.1) and dZ/dT² (icSCI: 0.64 ± 0.11 vs CON: 0.85 ± 0.31; p = 0.1) were not observed at isomax, despite a significant decrease in SV in the subjects with icSCI (77.1 ± 6.05 mL vs 105.8 ± 9.2 mL, p < 0.00)
Conclusion
Left ventricular filling was impaired in the subjects with icSCI as evidenced at both peak exercise and isomax. It is likely that restrictions on the skeletal muscle pump mechanized the impairment but increased left ventricular wall stiffness could not be excluded as a mediator.
... The volume shift has been estimated to be of the order of 500e1100 ml (8e16 ml kg À1 ); a similar autotransfusion during anaphylaxis could explain observed clinical improvements. 71 Reversal of neuromuscular block by sugammadex in anaphylaxis, regardless of the trigger, would be expected to similarly increase muscular tone and cause a reduction in venous capacitance. ...
Perioperative hypersensitivity reactions (POH) constitute a clinical and diagnostic challenge, a consequence of heterogeneous clinical presentations, and multiple underlying pathomechanisms. POH do not necessarily involve an allergen-specific immune response with cross-linking of specific immunoglobulin E (sIgE) antibodies on mast cells and basophils. POH can also result from alternative specific and non-specific effector cell activation/degranulation such as complement-derived anaphylatoxins and off-target occupancy of mast cell, basophil, or both surface receptors. Moreover, POH and anaphylaxis can occur independent from mast cell and basophil degranulation. The manifestations of POH primarily affect the cardiovascular, respiratory, and integumentary systems. POH present within the context of surgical or procedural pathology and the effects of surgical and anaesthetic techniques on pre-existing physiological reserve. The majority of cases of appropriately-treated intraoperative anaphylaxis can be considered a compensated cardiovascular anaphylaxis. With increasing severity of anaphylaxis, maldistribution and hypovolaemia lead to reduced venous return and circulatory failure. Treatment with a combination of epinephrine and i.v. fluid is critical for successful resuscitation, although the excessive use of epinephrine without adequate volume expansion may be deleterious. Neural control of the airways is important in the pathophysiology of bronchospasm. Anticholinergic drug premedication is beneficial in patients with hyperreactive airways. Pulmonary oedema can result from a combination of pulmonary capillary hypertension, incompetence of the alveolocapillary membrane, or both. Angioedema can be distinguished mechanistically into histaminergic and non-histaminergic (e.g. bradykinin-mediated). An understanding of the molecular mechanisms and pathophysiology of POH are essential for the immediate management and subsequent investigation of these cases.
... This mechanism has been demonstrated in crocodilians (34) and other reptiles (16,35). Venous return may also be facilitated by the skeletal muscle pump during locomotion (26) and the respiratory pump generating negative intrathoracic pressures (16,22), as ventilation increases during exercise (24). Finally, local sympatholytic vasodilatation in active muscle appears to be a potent mediator to elevate Q in humans (3,8). ...
In most vertebrates, increases in cardiac output result from increases in heart rate (fH) with little or no change in stroke volume (Vs), and maximum cardiac output (Q̇) is typically attained at or close to maximum fH. We therefore tested the hypothesis that increasing maximum fH may increase maximum Q̇. To this end, we investigated the effects of elevating fH with right atrial pacing on Q̇ in the American alligator (Alligator mississippiensis) at rest and whilst swimming. During normal swimming, Q̇ increased entirely by virtue of a tachycardia (29 {plus minus} 1 to 40 {plus minus} 3 beats min-1) whilst Vs remained stable. In both resting and swimming alligators, increasing fH with right atrial pacing resulted in a parallel decline in Vs that resulted in an unchanged cardiac output. In swimming animals, this reciprocal relationship extended to supraphysiological fH (up to ~ 72 beats min-1), which suggests that maximum fH does not limit maximum cardiac output and that fH changes are secondary to the peripheral factors (for example vascular capacitance) that determine venous return at rest and during exercise.
... Early increases in pressure have been attributed in part to an initial mobilisation of venous return, 18 driven by sympathetic activation and the activity of the skeletal muscle pump at the onset of exercise. 19 The mechanisms by which PAWP and mPAP subsequently decayed during sustained exercise were not elucidated in this study, but a time-varying accommodation via augmented LV diastolic function, such as enhanced relaxation and early diastolic suction, 20 may contribute. The current study recorded a measurable interval over which both PAWP and PA pressures declined, suggesting there may be a delay in recruitment of LV diastolic reserve 21 in response to exercise within this age group. ...
Objectives:
The clinical and prognostic significance of 'exaggerated' elevations in pulmonary artery wedge pressure (PAWP) during symptom-limited exercise testing is increasingly recognised. However, the paucity of normative data makes the identification of abnormal responses challenging. Our objectives was to describe haemodynamic responses that reflect normal adaptation to submaximal exercise in a group of community-dwelling, older, non-dyspnoeic adults.
Methods:
Twenty-eight healthy volunteers (16 men/12 women; 55±6 years) were studied during rest and two consecutive stages of cycle ergometry, at targeted heart rates of 100 bpm (light exercise) and 120 bpm (moderate exercise). Right-heart catheterisation was performed to measure pulmonary artery pressures, both early (2 min) and after sustained (7 min) exercise at each intensity.
Results:
End-expiratory PAWP at baseline was 11±3 mm Hg and increased to 22±5 mm Hg at early-light exercise (p<0.01). At sustained-light exercise, PAWP declined to 17±5 mm Hg, remaining elevated versus baseline (p<0.01). PAWP increased again at early-moderate exercise to 20±6 mm Hg but did not exceed the values observed at early-light exercise, and declined further to 15±5 mm Hg at sustained-moderate exercise (p<0.01 vs baseline). When analysed at 30 s intervals, mean and diastolic pulmonary artery pressures peaked at 180 (IQR=30) s and 130 (IQR=90) s, respectively, and both declined significantly by 420 (IQR=30) s (both p<0.01) of light exercise. Similar temporal patterns were observed at moderate exercise.
Conclusions:
The range of PAWP responses to submaximal exercise is broad in health, but also time-variant. PAWP may routinely exceed 20 mm Hg early in exercise. Initial increases in PAWP and mean pulmonary artery pressures do not necessarily reflect abnormal cardiopulmonary physiology, as pressures may normalise within a period of minutes.
