Increase In Diastolic Pressure Research Articles

Assessment of Modified Ultrafiltration Hemodynamic Impact by Pressure Recording Analytical Method During Pediatric Cardiac Surgery

Modified ultrafiltration is commonly used in pediatric cardiac surgery. Although its clinical benefits are currently debated, modified ultrafiltration has proved to improve mean arterial pressure in the first postoperative hours. Aim of our study was to measure cardiac index, stroke volume index, and mean arterial pressure modification before and after modified ultrafiltration by means of Pressure Recording Analytical Method. Single-center prospective observational cohort study. Pediatric cardiac surgery operating room. Children below 20 kg that are included in the "pediatric" mode of Pressure Recording Analytical Method. Forty patients were enrolled in this study. Median age, weight, and body surface area at surgery were 3 months (interquartile range, 10 days to 3.5 yr), 5.6 (3.1-15) kg, and 0.31 (0.21-0.56), respectively. During the modified ultrafiltration procedure, a median volume of 17 mL/kg (11-25) was ultrafiltered and a median volume of 11 mL/kg (6-17) was reinfused with a median final modified ultrafiltration balance of -0.15 mL/kg (-4.0 to 0.1). By univariate analyses, there was a 10% increase in postmodified ultrafiltration mean, systolic and diastolic pressures (p = 0.01), stroke volume index (p = 0.02), and cardiac index (p = 0.001) without significant changes in heart rate, central (left and right) venous pressures, stroke volume variation, and inotropic score. By multivariate analysis, when controlling for cardiopulmonary bypass time and age at surgery, cardiac index variation was independently associated with lower preoperative body surface area (beta coefficient -5.5, p = 0.04). According to Pressure Recording Analytical Method assessment, modified ultrafiltration acutely improves myocardial function, as shown by a 10% increase of systemic arterial pressure, stroke volume index, and cardiac index. This effect is more pronounced in smaller sized patients.

Abstract P394: Impact of Caffeinated Versus Decaffeinated Energy Shots on Blood Pressure

Introduction: Energy drinks are commonly used to boost cognitive performance. However, this is paralleled with a significant increase in systolic and diastolic blood pressures. No studies have evaluated these changes with energy “shots” and whether these effects are driven solely by the caffeine component in energy drinks or a multitude of ingredients remains unknown. The purpose of this study was to determine if the effects of regular (caffeinated) 5-Hour Energy® shot differ from that of decaffeinated 5-Hour Energy® (decaf) shot as assessed by changes in systolic (SBP) and diastolic blood pressure (DBP). Methods: This was a randomized, double-blind, crossover study conducted at a university campus. Healthy subjects, between 18-40 years of age with a blood pressure less than 140/90 and not on any medications were eligible for inclusion. Participants were randomized into either the regular 5-Hour Energy® drink or the decaf 5-Hour Energy® drink study arms with blood pressure recorded at baseline, 1, 3 and 5 hours. Following a washout period of at least 6 days, the same was performed giving the alternate study drink. Additionally, heart rate, adverse events and energy score (1-5 scale) were also assessed. Results: Ten males and 10 females were enrolled in the study with 90% (18 of 20) being of Asian race. Average age was 23.3±2.7 years, weighing 149.1±31.7 pounds with SBP of 114±11.3 mmHg and DBP of 69.5±7.6 mmHg. Baseline coffee consumption was less than 2 cups per week in 11 subjects and at least 1 cup per day in the remainder. The maximum SBP increase from baseline in the regular arm was 7.8±6.5 mmHg versus 2.8±5.6 mmHg in the decaf arm (p = 0.046). Maximum DBP increase was 6.3±3.7mmHg and 1.0±5.4 mmHg (p = 0.003) in the regular and decaf arms, respectively. Significant increases in systolic and diastolic pressures were evident at 1 and 3 hours post consumption (p ≤ 0.027) but not at 5 hours. Maximum heart rate or energy levels between the two groups were not significantly different (p ≥ 0.436). In subgroup analysis, regular energy drinks invoked a significantly higher increase in systolic and diastolic blood pressures (p ≤ 0.003) 1 hour post consumption in caffeine naïve subjects (n=11). Conclusion: Regular energy drinks available in the form of a “shot” increase both systolic and diastolic blood pressures by approximately 5mmHg. This effect appears to be exaggerated in caffeine naïve subjects.

Validity of the Water Hammer Formula for Determining Regional Aortic Pulse Wave Velocity: Comparison of One-Point and Two-Point (Foot-to-Foot) Measurements Using a Multisensor Catheter in Human

Lack of high-fidelity simultaneous measurements of pressure and flow velocity in the aorta has impeded the direct validation of the water-hammer formula for estimating regional aortic pulse wave velocity (AO-PWV1) and has restricted the study of the change of beat-to-beat AO-PWV1 under varying physiological conditions in man. Aortic pulse wave velocity was derived using two methods in 15 normotensive subjects: 1) the conventional two-point (foot-to-foot) method (AO-PWV2) and 2) a one-point method (AO-PWV1) in which the pressure velocity-loop (PV-loop) was analyzed based on the water hammer formula using simultaneous measurements of flow velocity (Vm) and pressure (Pm) at the same site in the proximal aorta using a multisensor catheter. AO-PWV1 was calculated from the slope of the linear regression line between Pm and Vm where wave reflection (Pb) was at a minimum in early systole in the PV-loop using the water hammer formula, PWV1 = (Pm/Vm)/ρ, where ρ is the blood density. AO-PWV2 was calculated using the conventional two-point measurement method as the distance/traveling time of the wave between 2 sites for measuring P in the proximal aorta. Beat-to-beat alterations of AO-PWV1 in relationship to aortic pressure and linearity of the initial part of the PV-loop during a Valsalva maneuver were also assessed in one subject. The initial part of the loop became steeper in association with the beat-to-beat increase in diastolic pressure in phase 4 during the Valsalva maneuver. The linearity of the initial part of the PV-loop was maintained consistently during the maneuver. Flow velocity vs. pressure in the proximal aorta was highly linear during early systole, with Pearson's coefficients ranging from 0.9954 to 0.9998. The average values of AO-PWV1 and AO-PWV2 were 6.3 ± 1.2 and 6.7 ± 1.3 m/s, respectively. The regression line of AO-PWV1 on AO-PWV2 was y = 0.95x + 0.68 (r = 0.93, p <0.001). This study concluded that the water-hammer formula (one-point method) provides a reliable and conventional estimate of beat-to-beat aortic regional pulse wave velocity consistently regardless of the changes in physiological states in human clinically. (English Translation of J Jpn Coll Angiol 2011; 51: 215-221).

Resistance Training Controls Arterial Blood Pressure in Rats with L-NAME- Induced Hypertension

Arterial hypertension is a multifactorial chronic condition caused by either congenital or acquired factors. To evaluate the effects of Resistance Training (RT) on arterial pressure, and on vascular reactivity and morphology, of L-NAME-treated hypertensive rats. Male Wistar rats (200 - 250 g) were allocated into Sedentary Normotensive (SN), Sedentary Hypertensive (SH) and Trained Hypertensive (TH) groups. Hypertension was induced by adding L-NAME (40 mg/Kg) to the drinking water for four weeks. Arterial pressure was evaluated before and after RT. RT was performed using 50% of 1RM, 3 sets of 10 repetitions, 3 times per week for four weeks. Vascular reactivity was measured in rat mesenteric artery rings by concentration-response curves to sodium nitroprusside (SNP); phenylephrine (PHE) was also used for histological and stereological analysis. Resistance training inhibited the increase in mean and diastolic arterial pressures. Significant reduction was observed in Rmax (maximal response) and pD2 (potency) of PHE between SH and TH groups. Arteries demonstrated normal intima, media and adventitia layers in all groups. Stereological analysis demonstrated no significant difference in luminal, tunica media, and total areas of arteries in the SH and TH groups when compared to the SN group. Wall-to-lumen ratio of SH arteries was significantly different compared to SN arteries (p<0.05) but there was no difference when compared to TH arteries. RT was able to prevent an increase in blood pressure under the conditions in this study. This appears to involve a vasoconstrictor regulation mechanism and maintenance of luminal diameter in L-NAME induced hypertensive rats.

Temporary Percutaneous Left Ventricular Support for Ablation of Untolerated Ventricular Tachycardias

Catheter ablation is increasingly recognized as an important option for the treatment of ventricular tachycardia (VT) in the serious clinical settings of frequent implantable cardioverter defibrillator shocks, and arrhythmia storms, in a variety of structural heart diseases.1 The high incidence of VTs that are not hemodynamically tolerated forces challenges to the traditional approaches of using activation and entrainment mapping to localize the ablation target area, in favor of a strategy of substrate modification that can be performed during sinus rhythm. In some patients, however, a clear target cannot be detected during sinus rhythm; this frequently occurs in some forms of nonischemic cardiomyopathies. More recently, interest is growing in the possibility of making VT tolerable through cardiopulmonary support. Article see p 1202 In this issue of Circulation: Arrythmia and Electrophysiology , Ostadal et al2 provide experimental data on the different capabilities offered by 3 commercially available support systems. It should be kept in mind, however, that these systems are Food and Drug Administration–approved only to support temporary high-risk situations. The data offered in this study are limited in that they provide only information related to systemic arterial pressure in healthy animals and do not allow any evaluation of the different levels of perfusion attained at individual critical organs, ie, brain or kidney. The study does, however, offer a comparative evaluation of the performances of these different systems and offers the opportunity to discuss advantages and limitation of their use. Percutaneous left ventricular assist devices (pLVAD) are increasingly used in few high-volume and skilled centers around the world in an attempt to achieve hemodynamic support during previously nontolerated ventricular arrhythmias to allow use of electrophysiological maneuvers to identify the critical isthmus of the circuit where an effective ablation will produce a permanent interruption of the VT. It is hoped that …

Human pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) after repeated doses taken 2 h apart

3,4-methylenedioxymethamphetamine (MDMA, ecstasy) is one of the most abused recreational drugs. Its usual pattern of misuse includes repeated doses taken over a short time period that could influence MDMA pharmacology and toxicity. This study aims to evaluate the pharmacokinetics and pharmacologically induced effects of two MDMA consecutive doses separated by 2 h. A randomized, double-blind, crossover, and placebo-controlled trial included ten male volunteers participating in two experimental sessions. MDMA was administered as a single 100-mg dose or as a repeated dose (50 mg followed by 100 mg, administered at 2 h apart). Outcome variables included pharmacokinetics, physiological, subjective, and psychomotor effects. Following the repeated doses, plasma concentrations of MDMA were higher than those expected by simple dose accumulation (+16.2 % AUC; +12.8 % C (max)), but those of HMMA and HMA were significantly lower (-29.8 % AUC; -38.2 % C (max)). After the second dose, physiological effects, psychomotor performance, and subjective effects were lower than expected especially for euphoria and stimulation. MDMA-induced increases in diastolic and systolic arterial pressure and body temperature were in the range of those expected following MDMA concentrations. MDMA pharmacokinetics and metabolic disposition following two doses separated by 2 h show that the contribution of the first dose to the MDMA-induced mechanism-based metabolic inhibition was already apparent. The concentrations of MDMA after the second dose were slightly higher than expected. The effects on blood pressure and temperature after the second administration were slightly higher than those following the first, but for heart rate and subjective variables these were lower than expected considering the MDMA concentrations achieved, suggesting a possible tolerance phenomenon.

Choroidal Thickness Change after Water Drinking Is Greater in Angle Closure than in Open Angle Eyes

To study change in choroidal thickness (CT) after water drinking test (WDT), comparing angle closure (AC) to open angle (OA) eyes. Before and 30 minutes after drinking 1 L of water, 88 glaucoma subjects underwent measurements of CT by spectral domain-optical coherence tomography, IOP, blood pressure (BP), axial length (AL), and anterior chamber depth (ACD). Baseline CT was significantly greater in AC than in OA eyes (P = 0.002). After WDT, BP, IOP, and AL increased significantly (all P ≤ 0.0001). Mean CT increased significantly in the AC group (5.6 μm, P = 0.04, n = 40) and among 80 subjects whose IOP rose > 2 mm Hg (responders; 3.2 μm, P = 0.048), but not in the OA group or among all subjects (2.5 μm increase overall, <1% of baseline CT, P = 0.10). ACD decreased in AC (-18 μm, P = 0.07), but not in OA eyes (+3 μm, P = 0.74). AC eyes had a significantly greater IOP increase after WDT than OA eyes (P = 0.002, multivariate regression). Among responders, CT increased more in those with larger diastolic perfusion pressure increase and in AC compared to OA eyes (P = 0.04 and P = 0.053, respectively, multivariate regression). A significant increase in CT and a decrease in ACD after WDT were observed in AC but not in OA eyes, and IOP increased significantly more in AC than in OA eyes, suggesting that the dynamic behavior of the choroid may play a role in the AC process. IOP increase after the WDT was not fully explained by CT increase.

Association of blood cadmium with hypertension in the Korean general population: Analysis of the 2008–2010 Korean national health and nutrition examination survey data

We present data from the Korean National Health and Nutrition Examination Survey 2008-2010 regarding the association between blood cadmium levels and blood pressure in a representative sample of the adult South Korean population. We restricted the analysis to participants ≥20 years of age who completed the health examination survey, including blood cadmium measurements (n = 5,919). We performed multivariate linear regression analyses to estimate adjusted mean differences in diastolic and systolic blood pressure associated with doubling of, or quartiles of, cadmium levels after covariate adjustment. We calculated odds ratios (ORs) for hypertension and prehypertension for log-transformed blood cadmium levels and quartiles thereof after covariate adjustment. We observed a twofold increase in blood cadmium associated with 0.755 and 1.007 mmHg increases in diastolic pressure in women and men, respectively. We observed 2.243 and 1.975 mmHg increases in diastolic pressure in women and men, respectively, in the highest compared with the lowest quartile of blood cadmium. Systolic pressure showed results similar to those of diastolic pressure. Based on ORs, a doubling of blood cadmium resulted in 18.6% and 31.5% increases in the risk of hypertension in women and men, respectively. Doubling of blood cadmium resulted in a 23.5% and 22.9% increase in the risk of prehypertension in women and men, respectively. We found a significant association between blood cadmium levels and elevated blood pressure regardless of the type of variable (continuous or categorical) in women and men with a lower blood cadmium level compared to previous Korean studies. This study also showed that blood cadmium levels were robust risk factors for prehypertension in both women and men.

Exercise on land or in water?

We have read with interest the study published in the International Journal of General Medicine entitled “Hypotensive response after water-walking and land walking exercise sessions in healthy trained and untrained women” by Rodriguez et al.1 In this study, the authors investigated cardiovascular changes induced by walking in water in comparison with walking on land. Water exercises are commonly used in rehabilitation programs, particularly patients with mobility problems. Recently, some studies have suggested that exercise performed in water could improve cardiovascular function.2 Thermoneutral headout water immersion leads to important hemodynamic alterations, such as increases in both cardiac preload and cardiac output and a decrease in peripheral vascular resistance.3 An increase in cardiac output induces an increase in peripheral blood flow and subsequently an increase in endothelial shear stress. This mechanism could be responsible for greater improvement in endothelial function after water gymnastics in comparison with land exercise. Consequently, water exercises might be of particular interest for patients with endothelial dysfunction. However, clinical interest in water exercise for the treatment of cardiovascular disease remains to be established. Further studies are needed to compare the cardiovascular effects of exercises performed in water and on land. We have some concerns about the methods used in the study reported by Rodriguez et al1 whereby all subjects were immersed in a bath and remained standing for 60 minutes before the exercise period. The temperature of the water was adjusted to 30°C ± 1°C. The thermoconductivity of water is 25 times greater than that of air. Consequently, the loss of body heat in water requires that thermal conditions be rigorously controlled. In the study by Rodriguez et al1 the suitability of the water temperature is debatable. Previous studies have determined that for subjects at rest, to provide thermoneutral conditions in water, the temperature of the bath should be maintained between 34°C and 35°C. In exercising volunteers, a thermoneutral water temperature was found to be around 32°C. To accommodate these conditions, some authors have investigated resting volunteers during headout immersion in water at temperatures between 34°C and 35°C. Subsequently, to provide thermoneutral water temperature during exercise, water temperature was progressively cooled to 32.5°C.4,5 These water temperature conditions produced a pulmonary arterial temperature in water similar to that on land at any exertion level from 40% to 100% of maximal oxygen consumption.5 In the work performed by Rodriguez et al the water temperature was below thermoneutrality both at rest and during exercise. It has been documented by Park et al6 that headout water immersion at a temperature below 34°C or 35°C modifies hemodynamic status in comparison with both thermoneutral water immersion and ambient air. During headout water immersion at thermoneutral temperature, cardiac output and stroke volume increased compared with levels in air. At a lower temperature, the increased stroke volume tended to be higher, whereas the heart rate decreased. Furthermore, the decrease in peripheral vascular resistance, commonly observed in thermoneutral water immersion, was attenuated when the temperature was decreased down from 34.5°C to 30°C. Arterial pressure was also altered, and an increase in diastolic arterial pressure was recorded at temperatures lower than 34.5°C. Lastly, it has been demonstrated that autonomic control of the cardiovascular system is variously affected depending on water temperature. During thermoneutral headout water immersion, decreased sympathetic activity (both cardiac and vascular) and a shift towards cardiac parasympathetic predominance have been recorded.7 In contrast, immersion in slightly cold water (temperature 25°C–30°C), leads to sympathetic vascular and parasympathetic cardiac hyperactivity. 8 Despite these limitations, the findings of Rodriguez et al are interesting. The greater post exercise decrease in blood pressure recorded in untrained healthy women after walking in chest-deep water in comparison with walking on land suggests an enhancement of the cardiovascular outcomes of exercise in water. Furthermore, this study can be considered to be relevant to assessments made in real clinical practice. Indeed, rehabilitation programs are frequently performed in swimming pools at water temperatures below thermoneutral conditions (between 28°C and 31°C). Further studies are needed to assess the benefit of water exercises in the management of cardiac patients.

Different patterns of pulmonary vascular disease induced by type 1 diabetes and moderate hypoxia in rats

Although type 1 and type 2 diabetes are strongly associated with systemic cardiovascular morbidity, the relationship with pulmonary vascular disease had been almost disregarded until recent epidemiological data revealed that diabetes might be a risk factor for pulmonary hypertension. Recent experimental studies suggest that diabetes induces changes in lung function insufficient to elevate pulmonary pressure. The aim of this study was to assess the effects of diabetes on the sensitivity to other risk factors for pulmonary hypertension. We therefore analysed the effects of the combination of diabetes with exposure to moderate hypoxia on classical markers of pulmonary hypertension. Control (saline-treated) and diabetic (70 mg kg(-1) streptozotocin-treated) male Wistar-Kyoto rats were followed for 4 weeks and exposed to normoxia or moderate normobaric hypoxia (14%) for another 2 weeks. Hypoxia, but not diabetes, strongly reduced voltage-gated potassium currents, whereas diabetes, but not hypoxia, induced pulmonary artery endothelial dysfunction. Both factors independently induced pulmonary vascular remodelling and downregulated the lung bone morphogenetic protein receptor type 2. However, diabetes, but not hypoxia, induced pulmonary infiltration of macrophages, which was markedly increased when both factors were combined. Diabetes plus hypoxia induced a modest increase in diastolic and mean pulmonary artery pressure and right ventricular weight, while each of the two factors alone had no significant effect. The pattern of changes in markers of pulmonary hypertension was different for moderate hypoxia and diabetes, with no synergic effect except for macrophage recruitment, and the combination of both factors was required to induce a moderate elevation in pulmonary arterial pressure.

Can ambulatory blood pressure serve as a biomarker for presence of chronic kidney disease?

Can ambulatory blood pressure serve as a biomarker for presence of chronic kidney disease?

IPLA2β Overexpression in Smooth Muscle Exacerbates Angiotensin II-Induced Hypertension and Vascular Remodeling

ObjectivesCalcium independent group VIA phospholipase A2 (iPLA2β) is up-regulated in vascular smooth muscle cells in some diseases, but whether the up-regulated iPLA2β affects vascular morphology and blood pressure is unknown. The current study addresses this question by evaluating the basal- and angiotensin II infusion-induced vascular remodeling and hypertension in smooth muscle specific iPLA2β transgenic (iPLA2β -Tg) mice.Method and ResultsBlood pressure was monitored by radiotelemetry and vascular remodeling was assessed by morphologic analysis. We found that the angiotensin II-induced increase in diastolic pressure was significantly higher in iPLA2β-Tg than iPLA2β-Wt mice, whereas, the basal blood pressure was not significantly different. The media thickness and media∶lumen ratio of the mesenteric arteries were significantly increased in angiotensin II-infused iPLA2β-Tg mice. Analysis revealed no difference in vascular smooth muscle cell proliferation. In contrast, adenovirus-mediated iPLA2β overexpression in cultured vascular smooth muscle cells promoted angiotensin II-induced [3H]-leucine incorporation, indicating enhanced hypertrophy. Moreover, angiotensin II infusion-induced c-Jun phosphorylation in vascular smooth muscle cells overexpressing iPLA2β to higher levels, which was abolished by inhibition of 12/15 lipoxygenase. In addition, we found that angiotensin II up-regulated the endogenous iPLA2β protein in-vitro and in-vivo.ConclusionThe present study reports that iPLA2β up-regulation exacerbates angiotensin II-induced vascular smooth muscle cell hypertrophy, vascular remodeling and hypertension via the 12/15 lipoxygenase and c-Jun pathways.

The role of Na+/H+ exchanger in Ca2+ overload and ischemic myocardial damage in hearts from type 2 diabetic db/db mice

BackgroundA higher increase in intracellular Na+ via Na+/H+ exchanger (NHE) during ischemia has been reported in type 2 diabetic mouse hearts. We investigated the role of NHE in inducing changes in cytoplasmic Ca2+ concentration ([Ca2+]i) and alterations in ventricular function during ischemia-reperfusion in type 2 diabetic mouse hearts.MethodsHearts from male type 2 diabetic db/db (12-15 weeks old) and age-matched control db/+ mice were subjected to Langendorff perfusion and loaded with 4μM of the Ca2+ indicator fura-2. The hearts were exposed to no-flow ischemia for 15 minutes and then reperfused. [Ca2+]i was measured by monitoring fura-2 fluorescence at 500 nm (excitation wavelengths of 340 and 380 nm), while left ventricular (LV) pressure was simultaneously measured.Resultsdb/db hearts exhibited a lower recovery of LV developed pressure than db/+ hearts during reperfusion following ischemia. Diastolic [Ca2+]i was increased to a greater level in diabetic hearts than in the control hearts during ischemia and reperfusion. Such an increase in cytoplasmic Ca2+ overload during ischemia-reperfusion in diabetic hearts was markedly reduced in the presence of the NHE inhibitor cariporide. This was accompanied by a significantly improved recovery of ventricular function on reperfusion, as shown by a lower increase in diastolic pressure and increased recovery of developed pressure.ConclusionNHE plays a key role in enhancing cytoplasmic Ca2+ overload during ischemia-reperfusion and severely impairing post-ischemic cardiac function in hearts from type 2 diabetic db/db mice.

Relation between NT‐proBNP Levels, Iron Overload, and Early Stage of Myocardial Dysfunction in β‐Thalassemia Major Patients

Heart failure (HF) secondary to myocardial iron loading remains the leading cause of death in β-thalassemia major (β-TM) patients. The early diagnosis and treatment of HF in these patients is related to survival. We aimed to evaluate myocardial performance using conventional and tissue Doppler echocardiography and its relation to plasma NT-proBNP levels and iron overload indices in β-TM patients with preserved systolic function. The study population included 49 β-TM patients (24.0 ± 4.2 years) and 48 age-matched healthy controls. Doppler-echocardiographic study was performed and blood samples for NT-proBNP measurements were drawn on the third day following blood transfusion. Patients were divided as group-1, without diastolic dysfunction: E/E' ratio < 9 and group-2, with suspected diastolic dysfunction: E/E' ratio ≥ 9. NT-proBNP levels and E/E' ratio were increased in patients compared with controls (P < 0.001 and P < 0.001) but did not correlate with each other. A strong positive correlation was detected between NT-proBNP levels and mean ferritin levels in β-TM patients (r(s) = 0.939; P < 0.001). Median NT-proBNP levels were significantly higher in group-1 in comparison to controls [51.2 (41.51-113.5) vs 30.1 (17.97-68.16) ng/mL, P < 0.01]. NT-proBNP levels were also increased in group-2 in comparison to group-1 but this increase was not statistically significant. NT-proBNP secretion begins in the early phase of the disease before the increase in diastolic pressure becomes overt. While there was a strong correlation between the plasma NT-proBNP levels and iron overload, there was no correlation between NT-proBNP levels and diastolic dysfunction parameters in patients in the third decade of life.

Impact of central hypovolemia on photoplethysmographic waveform parameters in healthy volunteers. Part 1: time domain Analysis

Our study sought to explore changes in photoplethysmographic (PPG) waveform param- eters, during lower body negative pressure (LBNP) which simulated hypovolemia, in spontaneously breathing volunteers. We hypothesize that during progressive LBNP; there will be a preservation of ear PPG parameters and a decrease in finger PPG parameters. With IRB approval, 11 volunteers underwent a LBNP protocol at baseline, 30, 75, and 90 mm Hg (or until the subject became symptomatic). Subjects were monitored with finger and ear pulse oximeter probes, an ECG, and a finger arterial blood pressure monitor. The square root of the mean of the squared differences between adjacent NN intervals (RMSSD) which is the time domain analysis of the heart rate variability (HRV) was measured. PPG waveforms were analyzed for height, area, width 50, maximum and minimum slope. Data are presented as median and inter-quartile range. Friedman ANOVA and Wilcoxon tests were used to identify changes in hemo- dynamic and PPG parameters, P < 0.017 was considered statistically significant. There were no significant changes in the blood pressure variables at LBNP(30), but at and beyond LBNP(75), the decreases in systolic, mean and pulse pressure were significant as was the increase in diastolic pressure. Heart rate increased significantly at LBNP(30), reaching a maximum of 75.4% above baseline at the symptomatic phase while RMSSD showed significant reduction at LBNP(75). Finger PPG height, area, width 50, and maximum slope decreased significantly at LBNP(30) and during symptomatic phase they showed a reduction of 59.4, 76.9, 27.4 and 51.6%, respectively. Ear PPG height, area, width 50 and maximum slope did not change significantly until the LBNP(75), reached. During symptomatic phase, the respective declines reached 39.3, 61.0, 21.4 and 34.9%. PPG waveform parameters may prove to be sensitive and specific as early indicators of blood loss. These PPG changes were observed before profound decreases in arterial blood pressure. The relative sparing of central cutaneous blood flow is consistent with the increased parasympathetic innervation of central structures.

Ultra-Small Intravenous Bolus of 7.5% NaCl/Mg2+ With Adenosine and Lidocaine Improves Early Resuscitation Outcome in the Rat After Severe Hemorrhagic Shock In Vivo

Much controversy exists over the fluid composition for hypotensive resuscitation. We previously showed that addition of 6% Dextran-70 or hetastarch to 7.5% NaCl led to heart instability and mortality. Our aim was to examine the early resuscitative effects of 7.5% NaCl with adenosine, lidocaine, and magnesium (ALM) on hemodynamics and mortality in a rat model of severe hemorrhagic shock. Male fed Sprague-Dawley rats (300-450 g, n = 48) were anesthetized and randomly assigned to one of six groups (n = 8): (1) Untreated, (2) 7.5% saline, (3) 7.5% NaCl/Mg²⁺, (4) 7.5% NaCl with adenosine/Mg²⁺, (5) 7.5% NaCl with lidocaine/Mg²⁺, and (6) 7.5% NaCl/ALM. Hemorrhagic shock was induced by phlebotomy until mean arterial pressure (MAP) was 35 mm Hg to 40 mm Hg and continued for 20 minutes (40% blood loss). Animals were left in shock for 60 minutes at 34°C. 0.3 mL (~3.5% of shed blood) was injected as a 10-second bolus into the femoral vein. Lead II electrocardiography, arterial pressures, MAP, heart rate, and rate-pressure product were monitored. Untreated rats experienced severe arrhythmias and 38% mortality. There were no other deaths. 7.5% NaCl alone failed to maintain MAP after 5 minutes and was significantly improved with Mg²⁺. At 60 minutes, the MAP for 7.5% NaCl alone was 36 mm Hg compared with 48 mm Hg for the magnesium group. 7.5% NaCl/ALM led to a significantly higher MAP (57-60 mm Hg at 45-60 minutes). The higher MAP was associated with up to a 2-fold increase in arterial diastolic pressure. Both 7.5% NaCl with adenosine/Mg²⁺ and lidocaine/Mg²⁺ were mildly bradycardic but not when combined as ALM. A few arrhythmias occurred in 7.5% NaCl group with or without Mg, but no arrhythmias occurred in the other treatment groups. Ultra-small intravenous bolus of 7.5% NaCl with ALM led to a significantly higher MAP, higher diastolic rescue, and higher rate-pressure product compared with other treatment groups. The possible clinical and military applications for permissive hypotensive resuscitation are discussed.

Hemodynamic and Arrhythmogenic Effects of Cocaine in Hypertensive Individuals

Despite the increased risk of myocardial infarction, aortic dissection, and arrhythmias in patients with hypertension who use cocaine, the hemodynamic and arrhythmogenic effects of cocaine use have not been well characterized in this population. The authors hypothesized that patients with hypertension demonstrate extreme, transient changes in arterial pressures as well as new arrhythmic activity during cocaine use. Ambulatory blood pressures, heart rates, and electrocardiograms (AECGs) were recorded for 48 hours in 10 patients with a history of hypertension who smoke cocaine. Active cocaine use was identified through patient diaries and manual activation of the blood pressure cuff. Of the 10 patients studied (6 men, 7 African Americans, age 49±8 years), 8 were taking antihypertensive medications. The mean blood pressure prior to cocaine use was 126/77 mm Hg and average increase in systolic, diastolic, and mean arterial pressure after use was 74 mm Hg, 30 mm Hg, and 45 mm Hg, respectively (P<.0001 for all). There was no significant change in heart rate. AECGs demonstrated arrhythmic activity during cocaine use, including 6 patients with increased atrial and ventricular ectopy, 2 patients with episodes of nonsustained atrial tachycardia, and 1 patient with 3 episodes of nonsustained monomorphic ventricular tachycardia. Cocaine use resulted in extreme elevations in arterial pressures in patients with hypertension taking medication. Cocaine use was also associated with an increase in arrhythmic activity. These findings may underlie the heightened risk of myocardial infarction, aortic dissection, and potentially lethal arrhythmias in patients with hypertension who use cocaine.

Intuitive visualization and quantification of intraventricular convection in acute ischemic left ventricular failure during early diastole using color Doppler-based echocardiographic vector flow mapping

The aim of this study was to make an intuitive visualization of intraventricular convection (IC) and quantification of intraventricular convection velocity (ICV) in acute ischemic left ventricular (LV) failure of open-chest canines during early diastole contrast to the baseline conditions using color Doppler-based echocardiographic vector flow mapping (VFM). The animal care committee approved this prospective study. In 6 anesthetized open-chest beagle models, the emergence time and the emergence sites of IC in the LV cavity during early diastole were visualized at the standard apical 3-chamber (AP3c) views with the VFM at baseline conditions and after coronary artery ligation. The global ICV and the ICV at the basal, middle and apical levels of LV at the AP3c views at T1, T2, T3, T4, and T5 between both states were compared respectively (T1: the beginning of LV rapid filling period; T2: the middle of LV rapid filling period; T3: the peak of LV rapid filling period; T4: the middle of period of reduced filling; T5: the end of early diastole.). Acute ischemic LV failure with a marked increase in LV end diastolic volume and LV minimal diastolic pressure was induced by coronary artery ligation. The IC appeared only during the period of reduced filling at baseline conditions, and limited to the basal level of LV cavity. But the IC appeared throughout all the early diastole, and was seen almost occupying whole LV cavity during ischemia. The peak of the global ICV for both states appeared at T4. The global ICV at the AP3c views in acute ischemic failure LV cavity increased than those of baseline conditions at the T1 (6.593 ± 0.834 cm(2)/s vs. 0.000 ± 0.000 cm(2)/s, P < 0.001), T2 (9.457 ± 0.852 cm(2)/s vs. 0.000 ± 0.000 cm(2)/s, P < 0.001), T3 (14.765 ± 1.791 cm(2)/s vs. 2.030 ± 0.502 cm(2)/s, P < 0.001), T4 (25.392 ± 4.640 cm(2)/s vs. 6.688 ± 1.343 cm(2)/s, P < 0.001), and T5 (15.890 ± 3.159 cm(2)/s vs. 2.518 ± 0.869 cm(2)/s, P < 0.001). And the ICV at the basal, middle and apical levels at AP3c views in acute ischemic failure LV cavity also increased than those of baseline conditions at the same phase of early diastole (P < 0.01), except for the ICV at the LV basal level at T1. VFM is a powerful tool for visualization IC and quantification of ICV on profiles of LV flow fields, which can give intriguing insights into the subtle, flow-associated LV fluid dynamics of normal and abnormal cardiac function. It will be of great practical importance to elucidate the accurate physiological and the pathophysiological significance of the IC in further studies, so as to determine whether the cardiac function can be precisely evaluated with IC related index, and to incorporate VFM into clinical routine practice in the future.

Evolution of volume sensitivity during hemodialysis and ultrafiltration

This study aimed at assessing the evolution of cardiovascular characteristics during hemodialysis and ultrafiltration by a perturbation accurately defined in its magnitude and directly relevant to the problem of volume adjustment in stable hemodialysis patients. Excess fluid volume was removed by constant ultrafiltration-rate as prescribed. Hemodynamic variables were continuously measured throughout treatments using non-invasive finger plethysmography. In addition to ongoing volume reduction by ultrafiltration (long-term perturbation), well-defined magnitudes of intravascular volume were transiently and reversibly sequestered (short-term perturbation) into the extracorporeal circulation at hourly intervals. Sensitivities of hemodynamic variables and of the baroreflex to the acute change in intravascular volume (volume sensitivities) were analyzed. Eight stable patients were assessed during two subsequent treatments. Treatments were accompanied by a decrease in cardiac output (p<0.05) and stroke volume (p<0.01), and by an increase in peripheral resistance (p<0.05) and diastolic pressure (p<0.05). Mean arterial pressure remained unchanged for the whole group but correlated with the change in total peripheral resistance in individual treatments (p<0.01). The average volume sensitivity of mean arterial pressure was 11.9±9.9 mmHg/L and increased (p<0.01) during treatments, while the average volume sensitivity of heart rate remained unchanged at -7.9±8.58 1/(min L). The corresponding volume sensitivity of the baroreflex was -0.81±1.5 1/(min mmHg) and remained unchanged for the whole group, but the change correlated with the change in mean arterial pressure in individual treatments (p<0.05). The changes in arterial pressures during hemodialysis appear to relate to an unbalanced response of barocontrol mechanisms characterized by a compromised chronotropy and vascular over-reactivity.

Invariable susceptibility to blockade by nifedipine of vasoconstriction to various alpha 2-adrenoceptor agonists in pithed rats.

The sensitivity of the increase in diastolic pressure brought about by the selective agonists of alpha 2-adrenoceptors, B-HT 920, B-HT 933, xylazine, UK-14,304, M-7, TL-99 and DP-6, 7-ADTN in pithed normotensive rats to blockade by the calcium entry inhibitor nifedipine has been investigated. To exclude any participation of vascular alpha 1- and beta 2-adrenoceptors, as well as cardiac beta 1-adrenoceptors, in the pressor responses, the study was made after treatment of the pithed rats with prazosin (0.1 mg kg-1) and (-)-propranol (1 mg kg-1). Without exception, the preferential agonists of alpha 2-adrenoceptors elicited vasoconstrictor responses which were susceptible to inhibition by nifedipine (0.03-1 mg kg-1) in a dose-dependent manner regardless of the differences in intrinsic activity of the compounds. The pressor activity was almost completely abolished after 1 mg kg-1 of nifedipine. The results show that vasoconstriction induced in pithed rats by various selective stimulating agents of postjunctional vascular alpha 2-adrenoceptors is invariably and equally sensitive to attenuation by nifedipine. This susceptibility of alpha 2-adrenoceptor-mediated vasoconstriction to impairment by blockade of calcium entry is not dependent on the nature, the potency or the efficacy of the agonist.