Effect of transmural pressure on the estimation of arterial stiffness index from the photoplethysmographic waveform.

The aim of this study was to find the effect of transmural pressure on the determination of the photoplethysmographic (PPG) waveform arterial stiffness index (PPGAI). The study was conducted on 51 subjects without diagnosis of cardiovascular disease, aged between 24 and 74 years. The relation between the transmural pressure, which is the difference between the arterial blood pressure and the PPG sensor contact pressure, and the PPGAI was determined. PPG, beat-to-beat blood pressure, and sensor contact pressure signals were recorded from the index, middle, and ring finger. The PPG sensor contact pressure of the index finger was increased from 20 to 120 mmHg. The aortic augmentation index (AIx@75) was estimated with a SphygmoCor device as a reference. High correlation coefficients r = 0.79 and r = 0.83 between PPGAI and AIx@75, and low PPGAI standard deviations were observed at the transmural pressures of 10 and 20 mmHg, respectively. Transmural pressure of 20 mmHg can be considered suitable for the PPG signal registration and PPGAI calculation for the assessment of arterial stiffness. In summary, the contact pressure of the sensor should be selected according to theblood pressure of the subject finger in order to achieve the transmural pressure suitable for the assessment of PPGAI and arterial stiffness.

Noninvasive Positive Pressure Ventilation for Acute Decompensated Heart Failure.

Noninvasive positive pressure ventilation (NIPPV), which can be applied without endotracheal airway or tracheostomy, has been used as the first-line device for patients with acute decompensated heart failure (ADHF) and cardiogenic pulmonary edema. Positive airway pressure (PAP) devices include continuous PAP, bilevel PAP, and adaptive servoventilation. NIPPV can provide favorable physiologic benefits, including improving oxygenation, respiratory mechanics, and pulmonary and systemic hemodynamics. It can also reduce the intubation rate and improve clinical symptoms, resulting in good quality of life and mortality.

Greater post-contraction hyperaemia below vs. above heart level: the role of active vasodilatation vs. passive mechanical distension of arterioles.

KEY POINTS: The immediate increase in skeletal muscle blood flow following contraction is greater when the contracting muscle is below vs. above heart level. This has been attributed to muscle pump-mediated venous emptying and subsequent widening of the arterial to venous pressure gradient, which can occur below but not above heart level. However, alternative explanations could include greater rapid onset vasodilatation and/or transmural pressure-mediated mechanical distension of resistance vessels, but these remain unexplored. We demonstrate that active vasodilatation is not responsible for greater post-contraction hyperaemia below the heart. Instead, an increased transmural pressure-mediated mechanical distension of resistance vessels is a key mechanism responsible for this phenomenon. Our findings establish the importance of considering/accounting for local mechanical arteriolar distension effects when investigating exercise hyperaemia. They also inform the application of exercise for rehabilitative purposes and prompt investigation into whether arteriolar distension accompanying vasodilatation is reduced with diseases or ageing, thereby compromising exercising muscle perfusion. ABSTRACT: We tested the hypotheses that increased post-contraction hyperaemia in higher (H; below heart) vs. lower (L; above heart) transmural pressure conditions is due to (1) greater active vasodilatation or (2) greater transmural pressure-mediated arteriolar distension. Participants (n = 20, 12 male, 8 female; combined mean age 24.5 ± 2 years) performed a 2 s isometric handgrip contraction, where arm position was maintained within or changed between H and L during contraction, resulting in four starting-finishing arm position conditions (LL, HL, LH, HH). Post-contraction forearm blood flow (echo and Doppler ultrasound) was higher with contraction release in H vs. L environments (P < 0.05). However, contraction initiated in H did not result in greater vasodilatation (forearm vascular conductance; FVC) than contraction initiated in L, regardless of contraction release condition (peak FVC: LL 217 ± 104 vs. HL 204 ± 92 ml min-1 (100 mmHg)-1 , P = 0.313, LH 229 ± 8 vs. HH 225 ± 85 ml min-1 (100 mmHg)-1 , P = 0.391; first post-contraction cardiac cycle FVC: same comparisons, both P = 0.317). However, FVC of the first post-contraction cardiac cycle was greater for contractions released in H vs. L regardless of pre-contraction condition (LL 106 ± 67 vs. LH 152 ± 76 ml min-1 (100 mmHg)-1 , P < 0.05; HL 80 ± 51 vs. HH 119 ± 58 ml min-1 (100 mmHg)-1 , P < 0.05). These findings refute the hypothesis that greater hyperaemia following a single contraction in higher transmural pressure conditions is due to greater active vasodilatation. Instead, our findings reveal a key role for increased transmural pressure-mediated mechanical distension of arterioles in creating a greater increase in vascular conductance for a given active vasodilatation following skeletal muscle contraction.

Transmural pressure drives proliferation of human arterial smooth muscle cells via mechanism associated with NADPH oxidase and Survivin.

Proliferation of vascular smooth muscle cells (VSMCs) plays an important role in various vascular diseases. Abnormal hemodynamic factors are important stimulus for promoting proliferation of VSMCs. In this study, we show that transmural pressure (TP) promotes the proliferation of human arterial smooth muscle cells (HASMCs) and its related mechanism. HASMCs were treated with different TPs (0,100,120,140,160,180 and 200 mmHg) in a custom-made pressure loading apparatus for 6 h. Results showed that proliferation of HASMCs was significantly promoted when the TP was over 160 mmHg compared with 0 mmHg (atmosphere pressure). In like manner, the expressions of NADPH oxidase 2(Nox2) and Survivin (SVV) and production of intracellular reactive oxygen species (ROS) were all elevated distinctly when TP exceeded 160 mmHg. Moreover, ROS scavenger NAC reduced TP-induced proliferation of HASMCs and expression of SVV largely, and slightly down-regulated expression of NOX2. NOX inhibitor apocynin (Apo) also significantly reduced TP-induced proliferation of HASMCs and expression of SVV and almost completely eliminated TP-induced production of ROS. These results demonstrate that TP drives proliferation of HASMCs via mechanism associated with NOX and SVV.

Interacciones cardiopulmonares: de la fisiología a la clínica / Cardiopulmonary Interactions: from Physiology to Clinic

Resumen: Las Interacciones Cardiopulmonares (ICP) corresponden al conjunto de interrelaciones entre el sis tema respiratorio y el cardiovascular, durante el ciclo respiratorio y cardíaco. Estas interacciones varían dependiendo de si el paciente se encuentra en ventilación espontánea o mecánica, afectando en distintos grados la precarga y postcarga, tanto del ventrículo derecho e izquierdo. El entender estas interacciones, resulta esencial al momento de manejar pacientes críticamente enfermos, en donde las manipulaciones de la precarga y postcarga, son de especial importancia al momento de optimizar el débito cardíaco y la entrega de oxígeno a los tejidos. En este artículo se presentan los principios fisiológicos que permiten entender las interacciones cardiopulmonares en ventilación espontánea y en ventilación mecánica, aplicadas a situaciones clínicas específicas, lo que nos ayudará a utilizarlas como herramientas en el manejo de los pacientes.

Abstract: Cardiopulmonary Interactions (CPI) refer to the interplay between the respiratory and cardiovascu lar systems during the respiratory and cardiac cycle. These interactions vary depending on whether the patient is in spontaneous or mechanical ventilation and affect the preload and afterload of both ventricles at different levels. Understanding CPI is essential to the management of critically ill pa tients, where preload and afterload manipulations are specialy important to optimize cardiac output and oxygen delivery to the periphery. The present article reviews the physiological principles required to understand CPI in patients both in spontaneous and mechanical ventilation using specific clinical scenarios to facilitate its use as part of day to day clinical practice.

Active Expiration and the Measurement of Central Venous Pressure.

PURPOSE: To obtain a point prevalence estimate of alterations in central venous pressure (CVP) produced by active expiration in a consecutive series of intensive care patients. METHODS: We evaluated CVP tracings taken by the nurses at their morning shift change in a consecutive series of 60 cardiac surgery and 59 noncardiac surgery patients. We also assessed change in values due to the change in transducer level. Three physicians and a nurse instructor independently reviewed the tracings and determined whether there was evidence of forced expiration and whether it was type A, defined by decreasing CVP during expiration, or type B, defined by increasing CVP during expiration. RESULTS: Agreement for CVP value was 96% between a physician and a bedside nurse. Twenty-nine percent of participants had active expiration, evenly distributed between A and B types. Active expiration was not related to the type of surgery, use of bronchodilators, and the presence of chronic obstructive lung disease or abdominal distention. Active expiration was more common in nonventilated patients and patients not receiving vasopressor drugs, suggesting they were more awake. CONCLUSION: Active expiration is common in critically ill patients. Failure to recognize it can result in important errors in the estimation of CVP and other hemodynamic measurements.

Measurement of pleural pressure swings with a fluid-filled esophageal catheter vs pulmonary artery occlusion pressure.

PURPOSE: Pleural pressure measured with esophageal balloon catheters (Peso) can guide ventilator management and help with the interpretation of hemodynamic measurements, but these catheters are not readily available or easy to use. We tested the utility of an inexpensive, fluid-filled esophageal catheter (Peso) by comparing respiratory-induced changes in pulmonary artery occlusion (Ppao), central venous (CVP), and Peso pressures. METHODS: We studied 30 patients undergoing elective cardiac surgery who had pulmonary artery and esophageal catheters in place. Proper placement was confirmed by chest compression with airway occlusion. Measurements were made during pressure-regulated volume control (VC) and pressure support (PS) ventilation. RESULTS: The fluid-filled esophageal catheter provided a high-quality signal. During VC and PS, change in Ppao (∆Ppao) was greater than ∆Peso (bias = -2 mm Hg) indicating an inspiratory increase in cardiac filling. During VC, ∆CVP bias was 0 indicating no change in right heart filling, but during PS, CVP fell less than Peso indicating an inspiratory increase in filling. Peso measurements detected activation of expiratory muscles, development of non-west zone 3 lung conditions during inspiration, and ventilator-triggered inspiratory efforts. CONCLUSIONS: A fluid-filled esophageal catheter provides a high-quality, easily accessible, and inexpensive measure of change in pleural pressure and provided insights into patient-ventilator interactions.

Effect of External Positive and Negative Pressure on Venous Flow in an Experimental Model.

OBJECTIVE: Positive external pressure is said to decrease transmural pressure; negative pressure in the pleural cavity is widely believed to result in negative pressure in systemic chest veins. The discrepancy between erect column height and foot venous pressure has been explained on this basis. METHODS: These core concepts rest on static closed models that may not be appropriate. This study examined the effects of external pressures in a dynamic open model that may better reflect in vivo conditions. Flow in a Penrose drain enclosed in a chamber that could be positively or negatively pressurized was used. Input and output reservoirs with pressures in the physiological range provided flow. Flow and pressure were monitored in horizontal and erect models with modifications to suit particular experiments. RESULTS: The discrepancy between foot venous pressure and erect venous column height was shown in this experimental model to be a result of two flows in opposite directions (superior and inferior vena cavae) meeting at the zero reference level at the heart; the upper column pressure therefore does not register at the foot. Positive external pressure results in slowing of velocity with conversion to pressure. Internal and transmural pressures therefore do not decrease. Negative external pressure has only a marginal effect on flow; importantly, internal pressure does not become negative. In an experimental set-up it was shown that negative pressure in chest veins was not necessary for air embolism to occur. CONCLUSION: Persistent negative pressure in systemic chest veins probably does not occur. The reason for the discrepant foot venous pressure is likely to be a result of dynamic flow and not negative pressure in chest veins. External positive pressure results in slowing of velocity but the transmural pressure remains largely unchanged.

A pilot application of Korotkoff sound delay time in evaluating cardiovascular status.

BACKGROUND: Korotkoff sounds have been used to measure systolic and diastolic arterial blood pressures noninvasively for over 100 years. However, most of the research concerning the Korotkoff sound were focused on the origin and frequency component analyzing the Korotkoff sound signal. OBJECTIVE: To show that the occurrence time of the Korotkoff sounds for each cardiac cycle demonstrates a characteristic value during the cuff deflating process of blood pressure measurement. METHODS: The Korotkoff sound delay time (KDT) decreases as the cuff pressure P deflates and KDT is a function of arterial transmural pressure. In the present research, an experiment system was established to explore the relationship between the KDT and the cuff pressure in different subjects. RESULTS: A pilot experiment was conducted to obtain different subjects' KDTs and investigate the relationship between KDT and cuff pressure. CONCLUSION: The relationship between KDT and invasive blood pressure was also studied and its potential application in detection of cardiovascular status was discussed.

In aged men, central vessel transmural pressure is reduced by brief Valsalva manoeuvre during strength exercise.

A brief Valsalva manoeuvre, lasting 2-3 s, performed by young healthy men during strength exercise reduces transmural pressure acting on intrathoracic arteries. In this study, we sought to verify this finding in older men. Twenty normotensive, prehypertensive and moderately hypertensive otherwise healthy men 46-69 years old performed knee extensions combined with inspiration or with brief Valsalva manoeuvre performed at 10, 20 and 40 mmHg mouth pressure. Same respiratory manoeuvres were also performed at rest. Non-invasively measured blood pressure, knee angle, respiratory airflow and mouth pressure were continuously registered. In comparison to inspiration, estimated transmural pressure acting on thoracic arteries changed slightly and insignificantly during brief Valsalva manoeuvre at 10 and 20 mmHg mouth pressure. At 40 mmHg mouth pressure, transmural pressure declined at rest (-8·8 ± 11·4 mmHg) and during knee extension (-12·1 ± 11·9 mmHg). This decline ensued, as peak systolic pressure increase caused by this manoeuvre, was distinctly <40 mmHg. Only a main effect of mouth pressure was revealed (P<0·001) and neither exercise nor interaction between these factors, what suggests that transmural pressure decline, depended mainly on intrathoracic pressure developed during brief Valsalva manoeuvre. Resting blood pressure did not influence the effect of brief Valsalva manoeuvre on transmural pressure.