Should we stop using the determination of central venous pressure as a way to estimate cardiac preload?

Introduction:

The determination of the values of central venous pressure has long been used as a guideline for volumetric therapy in the resuscitation of the critical patient, but the performance of such parameter is currently being questioned as an effective measurement of cardiac preload. This has aroused great interest in the search for more accurate parameters to determine cardiac preload and a patient''s blood volume.

Goals and Methods:

Based on literature currently available, we aim to discuss the performance of central venous pressure as an effective parameter to determine cardiac preload.

Results and Conclusion:

Estimating variables such as end-diastolic ventricular area and global end-diastolic volume have a better performance than central venous pressure in determining cardiac preload. Despite the best performance of these devices, central venous pressure is still considered in our setting as the most practical and most commonly available way to assess the patient''s preload. Only dynamic variables such as pulse pressure change are superior in determining an individual''s blood volume.     

慢性肺动脉高压肺血管力学特性的评价

本文以风心病二尖瓣病变合并被动性肺动脉高压为研究对象,借助右心导管技术和利用压力波形面积确定动脉顺应性的改进方法,通过测定肺血管阻力和顺应性,以评价慢性肺动脉高压肺血管力学特性的变化规律。发现慢性肺动脉高压患者肺动脉血管阻力明显升高（P＜0.01）;而反映血管壁固有结构的零压顺应性Co明显下降(P＜0.01),与术前肺动脉平均压呈显著负相关(r＝－0.745P＜0.05);扩血管药物试验提示不同程度肺动脉高压组的肺血管阻力均有显著下降(P＜0.01),轻度肺高压组零压顺应性和平均压顺应性均明显升高(P＜0.01);而重度肺高压组零压顺应性Co无明显变化(P＞0.05)。由此我们认为慢性肺高压肺血管都存在不同程度的重建,肺血管外周血管阻力和顺应性是影响其肺动脉压力水平的主要因素。     

Haemodynamic changes induced by short- and long-term sodium chloride or sodium bicarbonate intake in deoxycorticosterone-treated rats

The contribution of chloride to the haemodynamic changes of salt-dependent deoxycorticosterone (DOC) hypertension was studied in young Wistar rats subjected to dietary loading with sodium chloride (NaCl) or sodium bicarbonate (NaHCO₃). Mean arterial pressure (MAP), cardiac output, systemic resistance (TPR) and arterial rigidity (estimated from pulse pressure/stroke volume ratio, PP/SV) were determined in conscious chronically cannulated rats. DOC-induced increase of MAP and TPR appeared earlier in NaCl-loaded than in NaHCO₃-loaded rats. After 4–6 weeks of hypertensive treatment MAP, TPR and PP/SV ratio were higher in DOC-treated rats fed NaCl diet than in those fed NaHCO₃ diet. In contrast, after a long-term hypertensive regimen (lasting for 7–9 weeks) there was no significant difference in either MAP or TPR between rats loaded with NaCl or NaHCO₃. On the other hand, DOC hypertension induced by a long-term feeding of NaHCO₃ diet was not associated with an increase of arterial rigidity which was characteristic for DOC-NaCl hypertensive rats. Thus, a sufficiently long selective dietary sodium loading is capable to increase the systemic resistance but not to alter the arterial rigidity. This was also confirmed by a comparison of blood pressure-matched DOC hypertensive rats fed NaCl or NaHCO₃ diets. These animals did not differ in the degree of systemic resistance elevation but the arterial rigidity was increased only in NaCl-loaded rats.     

Vascular adaptations to 8-week cycling training in older men

Aim: Because age‐related changes in the large conduit arteries (increased wall thickness, and attenuated arterial compliance and endothelial function) are associated with cardiovascular pathology, prevention is of paramount importance. The effects of endurance training (i.e. walking or cycling) in older humans are assessed in cross‐sectional studies, examining the brachial and carotid arteries (supplying non‐trained areas). The purpose of this study was to assess the effects of 8‐week endurance training in older men on conduit artery characteristics in the trained and non‐trained vascular beds. Methods: In eight healthy sedentary older men (70 ± 3 years), characteristics of the large conduit arteries [common femoral (CFA), superficial femoral (SFA), carotid (CA), and brachial artery (BA)] were measured before and after 8‐week cycling training. Functional [arterial compliance and flow‐mediated dilation (FMD)] and structural (diameter and intima‐media thickness) conduit artery properties were measured using echo‐Doppler. Peak blood flow, representing structural peripheral adaptations, was measured using venous occlusion plethysmography. Results: After training, peak leg blood flow was increased (P < 0.01) and baseline diameter and flow were increased in the CFA (P < 0.05). Cycling training enhanced arterial compliance of the SFA (P = 0.03), but did not affect the FMD (P = 0.32) or the intima‐media thickness of the SFA. Exercise training did not alter characteristics of the BA or CA. Conclusion: Eight weeks of endurance training in older men altered functional and structural characteristics of the lower extremity vasculature, whereas no changes are reported for the conduit arteries in the non‐trained areas (BA or in the CA).     

Contribution of oxygen extraction fraction to maximal oxygen uptake in healthy young men

We analysed the importance of systemic and peripheral arteriovenous O₂ difference ( difference and a‐v_fO₂ difference, respectively) and O₂ extraction fraction for maximal oxygen uptake ( ). Fick law of diffusion and the Piiper and Scheid model were applied to investigate whether diffusion versus perfusion limitations vary with . Articles (n = 17) publishing individual data (n = 154) on , maximal cardiac output ( ; indicator‐dilution or the Fick method), difference (catheters or the Fick equation) and systemic O₂ extraction fraction were identified. For the peripheral responses, group‐mean data (articles: n = 27; subjects: n = 234) on leg blood flow (LBF; thermodilution), a‐v_fO₂ difference and O₂ extraction fraction (arterial and femoral venous catheters) were obtained. and two‐LBF increased linearly by 4.9‐6.0 L · min^–1 per 1 L · min^–1 increase in (R² = .73 and R² = .67, respectively; both P < .001). The difference increased from 118‐168 mL · L^–1 from a of 2‐4.5 L · min^–1 followed by a reduction (second‐order polynomial: R² = .27). After accounting for a hypoxemia‐induced decrease in arterial O₂ content with increasing (R² = .17; P < .001), systemic O₂ extraction fraction increased up to ~90% ( : 4.5 L · min^–1) with no further change (exponential decay model: R² = .42). Likewise, leg O₂ extraction fraction increased with to approach a maximal value of ~90‐95% (R² = .83). Muscle O₂ diffusing capacity and the equilibration index Y increased linearly with (R² = .77 and R² = .31, respectively; both P < .01), reflecting decreasing O₂ diffusional limitations and accentuating O₂ delivery limitations. In conclusion, although O₂ delivery is the main limiting factor to , enhanced O₂ extraction fraction (≥90%) contributes to the remarkably high in endurance‐trained individuals.     

Forearm plethysmography in the assessment of vascular tone and resistance vasculature design: new methodological insights

Aim: High peripheral resistance and structural alteration in resistance arteries are central phenomena in essential hypertension and have been widely examined by forearm venous occlusion plethysmography; at rest for studying vascular tone, and during reactive hyperaemia for studying vascular structure. This work concerns the influence of venous pressure on hyperaemic vascular resistance (R_min), the reproducibility of hyperaemic and resting vascular resistances (R_rest) and the relation between forearm and total peripheral vascular resistance (TPR). Methods: In four healthy subjects, intravenous and intra‐arterial blood pressures were measured simultaneously with plethysmographic recordings of hyperaemic and resting forearm blood flows. Reproducibility was examined in 15 young and 14 middle‐aged healthy subjects and in 21 untreated hypertensive patients. Results: R _min remained low in the first recorded cardiac cycle, but rose in the second, even though corrected for the venous pressure rise, suggesting vascular tone recovery along with venous congestion. Between‐day reproducibility of R_min was high in middle‐aged normotensive (8.7%) and hypertensive subjects (10.6%), but R_min fell significantly between successive days in the young subjects. R_rest correlated with TPR, but required up to 40 min to reach steady state and showed high day‐to‐day variation in young (21.8%) and hypertensive subjects (16.2%). Conclusions: During hyperaemia, vascular resistance should be measured in the first cardiac cycle following venous occlusion to minimize influences of venous pressure rise and possible tone recovery. R_rest seems to reflect TPR. About 20 subjects may be needed to detect 15% changes between days in R_rest, fewer when concerning R_min and TPR.     

Parental history of hypertension and cardiovascular response to stress in black and white men

White offspring of hypertensives typically exhibit an elevated cardiovascular response to stress. Studies of Black offspring of hypertensives have been fewer, with inconsistent results. This may be due, in part, to incomplete characterizations of hemodynamic responses. This study examines cardiovascular reactivity in Black and White offspring of hypertensives with a particular focus on vascular resistance responses. A total of 62 healthy normotensive men, 41 with a parental history of hypertension (PH+: 21 Blacks, 20 Whites), and 21 without parental hypertension (PH-: 7 Blacks, 14 Whites) engaged in a series of laboratory tasks. Both Black and White PH+ participants exhibited elevated diastolic blood pressure (DBP) responses, but to different patterns of stressor tasks. Familial differences in total peripheral resistance response were also obtained for Black and White participants in a comparison across all tasks, but were particularly evident in tasks when PH+ participants had elevated DBP responses. These results suggest that a parental history of hypertension is an important moderator of cardiovascular, and in particular peripheral vascular, responses to stress in Black and White individuals. This research was supported in part by National Institutes of Health Grants HL31533 and RR00046. We thank Doris Murrell, Antonia Vincent, Nancy Pettee, and Deborah Jansen for their technical assistance.     

Adaptation of the cardiovascular system to weightlessness: Surprises,paradoxes and implications for deep space missions

Weightlessness in space induces a fluid shift from the dependent to the cephalad parts of the body leading to distension of the cardiac chambers and an accumulation of blood in the veins of the head and neck. Surprisingly, central venous pressure (CVP) during the initial hours of spaceflight decreases compared to being horizontal supine on the ground. The explanation is that the thorax is expanded by weightlessness leading to a decrease in inter‐pleural pressure (IPP), which exceeds the measured decrease in CVP. Thus, transmural CVP (TCVP = CVP ? IPP) is increased indicating an augmented cardiac preload. Simultaneously, stroke volume and cardiac output (CO) are increased by 18%‐26% within the initial weeks and more so by 35%‐56% during the subsequent months of flight relative to in the upright posture on the ground. Mean arterial pressure (MAP) is decreased indicating a lower systemic vascular resistance (MAP/CO). It is therefore a surprise that sympathetic nerve activity is not suppressed in space and thus cannot be a mechanism for the systemic vasodilation, which still needs to be explored. Recent observations indicate that the fluid shift during long duration (months) flights is associated with increased retinal thickness that sometimes leads to optical disc oedema. Ocular and cerebral structural changes, increases in left atrial size and decreased flows with thrombi formation in the left internal jugular vein have also been observed. This is of concern for future long duration deep space missions because the health implications are unknown.     

Local vascular responses to elevation of an organ above the heart

Elevation of an organ above the heart reduces the arterial and venous hydrostatic pressures in proportion to the height of elevation. Intact autoregulation protects organs, such as the brain and skeletal muscle, from significant alterations in blood flow and hydrostatic capillary pressure due to the decrease in arterial inflow pressure during such a manoeuvre. However, the consequences of the decreased hydrostatic pressure on the venous side are far from clarified. The present study analyses the local haemodynamic effects of the decrease in arterial and venous hydrostatic pressures that occur during vertical elevation of an organ above the heart at atmospheric and raised tissue pressures (0, 10 and 30 mmHg). A sympathectomized cat skeletal muscle enclosed in a plethysmograph and perfused from the animal was used as the experimental model. The results show that elevation of the muscle above the heart at atmospheric tissue pressure created a variable vascular resistance starting at the venous outlet of the organ, and related to the difference between tissue pressure and venous outflow pressure. This resistance completely protects the organ from the hydrostatic pressure alterations on the venous side. The results also show that arterial pressure variations will exert the same haemodynamic influences on the organ as tissue pressure variations, except for the formation of the venous outflow resistance at raised tissue pressure. The application of these results to normal and injured organs, e.g. normal and injured skeletal muscle and brain, with various tissue pressures, is discussed.     

Modification of cardio-vascular responses to hemorrhage by induced hyperosmolality in the rat

Starved rats sedated with a neurolept analgesic were subjected to hemorrhagic hypotension while receiving infusions of iso-osmolar and hyperosmolar solutions. The hemorrhage model used resulted in similar residual blood volumes and hematocrits in all groups. The non-metabolizable pentose, xylose, and glucose were used to induce a state of hyperosmolality, which was absent in those animals which received iso-osmolar infusions (0.29 M xylose). After 45 mins hemorrhagic hypotension and a blood loss equal to 40% of the initial blood volume, the animals receiving the hyperosmolar infusions had a better cardiovascular status compared to those which received the iso-osmolar infusions. The cardiac outputs and stroke volumes were higher and heart rate lower in the hyperosmolar groups. Evidence of better tissue perfusion was obtained in those animals with the induced state of hyperosmolality.     

Acute effects of pulmonary artery banding in sheep on right ventricle pressure–volume relations: relevance to the arterial switch operation

The first stage of the two‐stage arterial switch operation (ASO) for transposition of the great arteries (TGA) is associated with depressed ventricular function and an unstable immediate post‐operative course. It is unclear if this is because of the acute increase in afterload of the thin‐walled, low‐pressure ventricle by pulmonary artery banding (PAB). To determine the acute effects of afterload increase on the contractile function of thin‐walled ventricles, we studied the right ventricular pressure–volume relations of seven sheep before and 30 min after PAB using combined pressure–conductance catheters during inflow reduction. Load independent indices of systolic and diastolic performance were derived from these relations. Pulmonary artery banding increased the mean ratio between right and left ventricular systolic pressure from 0.34 ± 0.05 to 0.64 ± 0.10, P < 0.05 (mean ± SD). There were no significant changes in heart rate and end‐systolic volume after banding although there was an incremental trend in the end‐diastolic volume and stroke volume. Right ventricular output (530 ± 163–713 ± 295 mL min^–1, P < 0.05), slope of the end‐systolic pressure–volume relation (ESPVR) (3.7 ± 2.8–10.0 ± 4.8 mmHg mL^–1, P < 0.05) and slope of the pre‐load recruitable stroke work (PRSW) relation (9.6 ± 1.8–15.0 ± 3.1 mmHg, P < 0.05) were significantly increased indicating improved contractile state after banding. The diastolic function curve was unchanged after banding although the right ventricle (RV) was operating at a larger end‐diastolic volume. Hence, the RV of sheep responded to acute pressure overload by demonstrating enhanced contractility and evidence of the Frank–Starling mechanism without associated change in right ventricular diastolic performance.     

Bronchial response to histamine after inhaled propranolol and atropine in monkeys

To investigate the nature of the variable response to inhaled histamine in monkeys, we performed dose-response curves in a group of 10 anesthetized Macaca mulatta monkeys before and after administration of propranolol and atropine in inhaled doses sufficient to produce significant beta-adrenergic and cholinergic blockade of airway smooth muscle. Animals were studied in a volume-displacement body plethysmograph and changes in pulmonary resistance (RL), dynamic compliance (Cdyn), frequency (f) and tidal volume (VT) were plotted against inhaled histamine concentration (0.016 to 64 mg/ml). Sensitivity to histamine was assessed by the concentrations producing a 50% increase in RL and a 50% decrease in Cdyn. A wide range of sensitivity (0.44 to 3.3 mg/ml for RL, 0.47 to 11.3 mg/ml for Cdyn) was found in this small group of animals, and this was not influenced by prior inhalation of propranolol. Atropine inhalation resulted in a marked decrease in sensitivity in all animals but did not reduce the variability of response.     

5‐Nitro‐2‐(3‐Phenylpropylamino) Benzoic Acid Induced Drug Resistance to Cisplatin in Human Erythroleukemia Cell Lines

Mechanisms of cisplatin resistance in cancer cells are not fully understood. Here, we showed a critical role for the chloride channel‐3 (ClC‐3) in cisplatin resistance in human erythroleukemia K562 and RK562 cells. We found that a chloride channel blocker 5‐nitro‐2‐(3‐phenylpropylamino) benzoic acid (NPPB) could protect cells from cisplatin‐induced apoptosis. NPPB treatment decreased the mRNA and the protein expression of Bax/Bcl‐2, decreased the protein expressions of cytochrome C and caspase‐3, and increased the mRNA expressions of cyclin D1 and ClC‐3 in cells treated with cisplatin. The caspase‐3 activity was decreased significantly and the rate of cell apoptosis was decreased. NPPB treatment increased CIC‐3 expression, which could increase acidification of intracellular compartments, and increased sequestration of cisplatin, inducing decreased effective drug concentrations, and subsequently cell death. Collectively, our data indicate that NPPB can induce drug resistance to cisplatin by upregulating the expression of CIC‐3. NPPB‐induced CIC‐3 expression facilitates acidification of sequestrated cisplatin, and plays an important role in preventing cisplatin‐induced apoptosis in human erythroleukemia K562 and RK562 cells. Anat Rec,, 2011. © 2011 Wiley‐Liss, Inc.     

Central and Regional Circulatory Effects of Adding Arm Exercise to Leg Exercise

7 young, healthy, male subjects performed exercise on bicycle ergometers in two 20 min periods with an interval of 1 h. The first 10 min of each 20 min period consisted of arm exercise (38–62% of Vdot;o₂ max for arm exercise) or leg exercise (58–78% of Vdot;o₂ max for leg exercise). During the last 10 min the subjects performed combined arm and leg exercise (71–83% of Vdot;o₂ max for this type of exercise). The following variables were measured during each type of exercise: oxygen uptake, heart rate, mean arterial blood pressure, cardiac output, leg blood flow (only during leg exercise and combined exercise), arterio-venous concentration differences for O₂ and lactate at the levels of the axillary and the external iliac vessels. Superimposing a sufficiently strenuous arm exercise (oxygen uptake for arm exercise 40% of oxygen uptake for combined exercise) on leg exercise caused a reduction in blood flow and oxygen uptake in the exercising legs with unchanged mean arterial blood pressure. Superimposing leg exercise on arm exercise caused a decrease in mean arterial blood pressure and an increased axillary arterio-venous oxygen difference. These findings indicate that the oxygen supply to one large group of exercising muscles may be limited by vasoconstriction or by a fall in arterial pressure, when another large group of muscles is exercising simultaneously.     

Improved aorto-ventricular matching in ischemic dilated cardiomyopathy patients after surgical ventricular restoration

Scope

This paper contains (i) derivation of the aorto-ventricular matching (AVM) index in terms of the ratio of aortic elastance and LV end-systolic elastance, E_aorta/E_es; (ii) procedure for determination of this index, by means of non-invasive measurements of auscultatory pressures, time-variation of blood volume ejected into the aorta, stroke volume and ejection fraction; (iii) results of improved AVM index evaluation in ischemic dilated cardiomyopathy (IDCM) patients following surgical ventricular restoration (SVR), as a result of reduced end-diastolic and end-systolic LV volumes and increased LV E_es.

Methodology

Among the ten recruited IDCM patients, four of them underwent surgical ventricular restoration (SVR) and coronary artery bypass graft (CABG), while six of them underwent CABG alone. All patients were studied by echocardiography pre- and 4 months post-operatively; LV volumes were determined by echo Doppler. LV end-systolic elastance E_es was determined from a derived expression, by employing blood pressure, stroke volume, ejection fraction, pre-ejection and systolic periods, and estimated normalized ventricular elastance at end-diastole, based on single-beat measurements. Aortic elastance E_aorta was determined by means of our modified single-beat method for determining aortic pressure profile.

Results

In the CABG plus SVR group, the AVM index E_aorta/E_es was reduced by 35% from 0.93 ± 0.32 to 0.60 ± 0.33, consistent with improved aorto-ventricular matching. However, in the CABG alone group, the AVM index E_aorta/E_es decreased only 11% from 1.02 ± 0.24 to 0.91 ± 0.29.

Conclusion

There is shown to be increased value of LV E_es and a more favorable decreased value of AVM index in those IDCM patients who underwent SVR.