The cardiovascular thoracic air plethysmogram.
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Ballistocardiography↗
Biomedical subjects
N Westerhof
Publications and source records attributed to N Westerhof.
Calculated mean arterial blood pressure in critically ill neonates.
Mean arterial pressure (MAP) is the area under the pressure wave form averaged over the cardiac cycle. A widely used rule of thumb to estimate MAP of peripheral arterial pressure waves in adults is adding one-third of the pulse pressure (PP) to diastolic arterial pressure (DAP). However, radial artery pressure waves in newborns differ from those in adults and resemble proximal aortic pressure waves, so that the above-mentioned calculation of MAP may not be correct. The present study was set up to obtain an arithmetical approximation to derive MAP from blood pressure waves measured in the radial artery of the neonate. We accurately recorded about 300 invasively obtained blood pressure curves in the radial artery of 10 neonates admitted for intensive care. We found that MAP in the radial artery in these neonates can be well approximated by adding 46.6% PP to DAP (range 43.0-50.1%). We suggest that the rule of thumb to derive MAP from radial artery waves in the neonate to be approximately the average of systolic and diastolic pressure, as opposed to adding one-third of the pulse pressure to the diastolic value in the adult.
Blood Pressure↗
Nitric oxide is an important determinant of coronary flow in the isolated blood perfused rat heart.
Many vasoactive substances are involved in the regulation of vasomotor tone and some of them, like nitric oxide (NO), are derived from the endothelium. Nitric oxide is able to relax preconstricted coronary resistance vessels almost completely. However, it is not clear what the contribution of NO is to vasomotor tone in the intact blood perfused heart. The aim of the present study was to evaluate the contribution of NO to coronary pressure-flow relations. We used isovolumically beating, donor supported, blood perfused isolated rat hearts. We measured pressure-flow relations under control conditions, after blocking endothelial NO production with NG-nitro-L-Arginine (LNNA) and after administration of L-Arginine (L-Arg) in order to overrule the blocking effect. Administration of LNNA at a perfusion pressure of 105 mm Hg resulted, after about 40 min, in a significant (Wilcoxon's signed-rank test, (n = 8) p < 0.05) reduction of coronary flow to 47 +/- 5% (mean +/- SEM) of control and a reduction of developed isovolumic left-ventricular pressure to 62 +/- 4% of control. L-Arg returned flow to 60 +/- 7% of control which is a significant increase with respect to LNNA (p < 0.05). L-Arg did not increase the left-ventricular pressure. The entire perfusion pressure-flow relation (pressure range 65-125 mm Hg) was significantly shifted downwards after LNNA with respect to control. Pressure-flow relations after L-Arg were in between those during control and after block of NO production. L-Arg alone was found to have no effect on flow and left-ventricular pressure (n = 2) and both LNNA and L-Arg were found to have no effect on contractility of isolated trabeculae (n = 6), thus, coronary blood flow reduction after LNNA administration is mainly the result of inhibition of endothelial NO production. At a perfusion pressure of 105 mm Hg reactive hyperemia is still present after LNNA and subsequent L-Arg administration, indicating that endothelial NO is not the only factor involved in flow regulation. We conclude that endothelium-derived NO is involved in the control of coronary flow in the blood perfused rat heart.
Animals↗
Ventricular distension and diastolic coronary blood flow in the anaesthetized dog.
There appears to be no agreement as to whether or not an increase in diastolic left ventricular pressure and/or volume can cause a decrease in diastolic coronary blood flow. We investigated the problem in the anaesthetized dog using a flaccid freely distensible latex balloon inserted into the left ventricle with the animal on extracorporeal circulation and the coronary perfusion pressure constant at about 45 mm Hg. Maximal vasodilatation and suppression of autoregulation in coronary vasculature was obtained by the intracoronary infusion of dipyridamole (10-40 mg/h). Ventricular volume was changed in steps of 10 ml from 10 to 70 ml and back to 10 ml, whilst recording coronary blood flow and left ventricular pressure in the left circumflex coronary artery. Over a range of ventricular volumes from 20 to 50 ml and a concomitant rise in diastolic ventricular pressure to about 20 mm Hg there was no change in the diastolic coronary flow. Only when the ventricular volume was more than two times the control value (i.e. exceeded 50 ml) and left ventricular pressure was more than 20 mm Hg, was there a decrease in coronary flow. During the return of the volume to the control level there was a fall in diastolic flow and ventricular contractility with respect to the values obtained when the volume was increased; these two effects were transient lasting less than 10 min. It was not considered that any of the three models of the coronary circulation, waterfall, intramyocardial pump or varying elastance model could explain our results.(ABSTRACT TRUNCATED AT 250 WORDS)
Anesthesia↗
Calculated mean arterial pressure in the posterior tibial and radial artery pressure wave in newborn infants.
Mean arterial pressure (MAP) is the area under the pressure wave averaged over the cardiac cycle, and therefore depends on pressure wave contour. A generally used rule of thumb to estimate MAP of peripheral arteries in adults is adding one-third of the arterial pulse pressure (PP) to diastolic arterial pressure (DAP). As peripheral pressure wave forms in neonates do not resemble adult peripheral wave forms, it may be expected that this rule of thumb does not hold for neonates. Previously, we found that MAP can be calculated by adding 50% PP to DAP in radial artery waves in neonates. In the present study, we investigated in neonates how MAP in the posterior tibial artery depends on systolic and diastolic pressure and we compared these findings to those found in the radial artery. Forty infants admitted for intensive care were studied. We analyzed 5000 invasively and accurately obtained blood pressure waves in the posterior tibial artery of 20 neonates and another 5000 waves similarly obtained from the radial artery in another group of 20 neonates. We found that MAP in posterior tibial artery waves is well approximated by adding 41.5 +/- 2.0% of PP to DAP, whereas MAP in radial artery waves can be calculated by adding 46.7 +/- 1.7% of PP to DAP. These values are significantly different (p < 0.0001). In conclusion, the rule of thumb as used in the adult to find MAP, where 33% PP is added to DAP, does not hold for the newborn. We recommend to calculate MAP in the tibial artery by adding 40% of PP to DAP and in the radial artery by adding 50% of PP to DAP.
Blood Pressure↗
Physiological hypotheses--intramyocardial pressure. A new concept, suggestions for measurement.
Intramyocardial pressure is supposed to play a major role in systolic coronary flow impediment. Via its assumed relation with radial wall stress it is supposed to be similar to ventricular pressure at the endocardium and decreases linearly to negligible values epicardially. Many attempts to measure intramyocardial pressure have been reported in the literature with rather different results. For instance, with most of the various methods, intramyocardial pressures both higher and lower than left ventricular pressure have been obtained and intramyocardial pressures of more than 125 mm Hg have been found in low-loaded isobaric beats (negligible pressure development in systole). In this "physiological hypotheses paper" I suggest left ventricular pressure and intramyocardial pressure both to result from the varying stiffness of cardiac muscle over the heart cycle. For any intramuscular cavity a time varying pressure-volume (P-V) relation results from the changes in muscle stiffness, the so-called time varying elastance defined as E(t) = P(t)/V(t), and with maximal or systolic elastance called Emax. For a constant contractile state the time varying elastance (E(t)) is suggested to be almost independent of preload and afterload. This concept has been well established for the ventricular cavities, but is here proposed to hold for the interstitial space as well. If a cavity is subject to isovolumic conditions the pressure will be high, but when volume in systole decreases (ventricular ejection or squeezing out of interstitial fluid) pressures will be lower. Thus for constant load on the interstitial cavities, but different loads on the ventricle, left ventricular pressure will vary while intramyocardial pressure remains the same. For low-loaded isobaric beats where left ventricular pressure is minimal intramyocardial pressure will remain the same as during normal ventricular loads and isovolumic beats. Augmented contractility will increase Emax and this will increase left ventricular and intramyocardial pressure only by the same amount if loading conditions of both cavities remain the same. Both ventricular pressure and intramyocardial pressure arise from varying stiffness of cardiac muscle and intramyocardial pressure does not result from left ventricular pressure. A proportionality of left ventricular and intramyocardial pressure is therefore not to be expected. The results on intramyocardial pressure obtained by the different methods used in the literature should be re-interpreted taking this concept into account.
Animals↗
Can coronary systolic-diastolic flow differences be predicted by left ventricular pressure or time-varying intramyocardial elastance?
In six isolated rabbit hearts perfused with a pressure source and Krebs-Henseleit as the perfusion medium, the effect of left ventricular pressure on coronary inflow in the maximally vasodilated bed was studied. This effect was determined from isovolumic beats, low afterloaded isobaric beats (afterload maintained at values below 10 mm Hg) and during cardiac arrest. For isovolumic beats end-diastolic left ventricular pressure was varied by means of an intraventricular balloon between 0-40 mm Hg and systolic left ventricular pressure varied between 90-130 mm Hg. In these ranges diastolic inflow decreased significantly 18 +/- 6% (mean +/- SD) with increasing pressure and systolic inflow could not be shown to depend on pressure (n = 6). For isobaric beats, diastolic and systolic inflow remained at values similar to those found for the isovolumic beats (n = 6). In the arrested heart inflow diminished 8 +/- 2% when the pressure in the left ventricle was increased from 0 to 40 mm Hg (n = 3). We conclude that systolic coronary inflow is hardly affected by left ventricular pressure. Systolic inflow decreased by the same amount in the isovolumically and isobarically beating heart, when cardiac contractility was enhanced by epinephrine infusion. We suggest the results can be explained on the basis of the time-varying elastance concept: systolic elastance is the same for isovolumic and isobaric beats but depends on contractility. Models that relate coronary inflow impediment to left ventricular pressure should therefore be reevaluated.
Animals↗
Simple and accurate way for estimating total and segmental arterial compliance: the pulse pressure method.
We derived and tested a new, simple, and accurate method to estimate the compliance of the entire arterial tree and parts thereof. The method requires the measurements of pressure and flow and is based on fitting the pulse pressure (systolic minus diastolic pressure) predicted by the two-element windkessel model to the measured pulse pressure. We show that the two-element windkessel model accurately describes the modulus of the input impedance at low harmonics (0-4th) of the heart rate so that the gross features of the arterial pressure wave, including pulse pressure, are accounted for. The method was tested using a distributed nonlinear model of the human systemic arterial tree. Pressure and flow were calculated in the ascending aorta, thoracic aorta, common carotid, and iliac artery. In a linear version of the systemic model the estimated compliance was within 1% of the compliance at the first three locations. In the iliac artery an error of 7% was found. In a nonlinear version, we compared the estimates of compliance with the average compliance over the cardiac cycle and the compliance at the mean working pressure. At the first three locations we found the estimated and "actual" compliance to be within 12% of each other. In the iliac artery the error was larger. We also investigated an increase and decrease in heart rate, a decrease in wall elasticity and exercise conditions. In all cases the estimated total arterial compliance was within 10% of mean compliance. Thus, the errors result mainly from the nonlinearity of the arterial system. Segmental compliance can be obtained by subtraction of compliance determined at two locations.
Aorta↗
Rate of the myogenic response increases with the constriction level in rabbit femoral arteries.
The myogenic response forms an important aspect of blood flow regulation and is usually quantified by the steady-state relation between pressure and diameter. The aim of the present study is to analyze the dynamics of the myogenic response. In six isolated rabbit femoral arteries, the time course of the active part of the diameter response to a pressure step from 95 to 110 cm H2O (from 9.5 to 11 kPa), at two levels of norepinephrine (NE)-induced constriction, was fitted to a monoexponential curve to obtain the time constant. The NE concentrations used in the superfusion solution were between 0.8 and 1.5 microM for high constriction and between 0.2 and 0.6 microM for low constriction. Acetylcholine (1 microM in perfusion) was used to check endothelial function. The respective median values of the time constants with and without endothelium, are 13.2 and 15.5 sec (NS) for the high level of constriction and 49.5 and 58.5 sec (NS) for the low constriction level. Time constants at the two constriction levels were significantly different (p = 0.002). In seven separate experiments using 40 mM KCl, in the superfusion fluid, to constrict femoral arteries to the same level as during the high level of NE constriction, it was found that the amplitude of the myogenic response was much smaller, compared with the norepinephrine experiments, and the time constant was significantly longer (median: 80.8 sec). We conclude that the dynamics of the myogenic response in the rabbit femoral artery is independent of the endothelium, but is dependent on the constriction level and type of constricting agent.
Animals↗
Hemodynamic effects of intermittent manual lung hyperinflation in patients with septic shock.
OBJECTIVE: The purposes of this study were to investigate the hemodynamic changes induced by intermittent manual lung hyperinflation (MHI) and to assess if these changes are adverse enough to warrant prohibition of MHI as a routine procedure in the care of patients with septic shock. DESIGN: The study's design was experimental prospective. SETTING: The settings were university hospital intensive care units. PATIENTS: Subjects included 13 consecutive mechanically ventilated patients with septic shock who met the inclusion criteria. MEASUREMENTS AND RESULTS: Phasic MHI-related increments in mean inspiratory airway pressure were concordant to changes in mean pulmonary artery pressure (MPAP) (r(2) = 0.67) with a 0.6 mm Hg rise in MPAP per cm H(2)O airway pressure. The magnitude of MPAP changes was not reflected in magnitude of stroke volume index (SVI) (r(2) = 0.06). On average, MHI did not induce statistically significant hemodynamic changes and mean values returned to baseline level within 15 minutes. SVI during MHI increased slightly in 9 patients, from 37 +/- 15 (mean +/- SD) to 41 +/- 17 mL/m(2) (P <.05), and decreased in 4, from 60 +/- 10 to 50 +/- 14 mL/m(2) (not significant). Patients with an increase in SVI had lower baseline values for SVI, cardiac index, and left ventricular stroke work index (P <.05) and higher values for systemic vascular resistance index compared with patients with a decrease in SVI (P <.05). Left ventricular stroke work index was higher in patients with a decrease in SVI than in patients with an increase in SVI (52 +/- 9 vs 34 +/- 8; P <.05). Tidal volume increased from 499 +/- 176 mL before MHI to 587 +/- 82 mL, 5 minutes after MHI (P <.05) with a return to baseline values within 15 minutes after the procedure. CONCLUSION: The hemodynamic effects of intermittent MHI in patients with septic shock are relatively small and insignificant and seem to be related to the cardiovascular state before the procedure. The risk of inducing hemodynamic changes with MHI should not be considered as a contraindication in patients with septic shock who are mechanically ventilated.
Adult↗
Alpha-1-adrenoceptor stimulation induces nitric oxide release in rat pulmonary arteries.
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Adrenergic alpha-Agonists↗
Endothelium function is protected by albumin and flow-induced constriction is independent of endothelium and tone in isolated rabbit femoral artery.
To investigate the preservation of endothelial function, we perfused two segments of one rabbit femoral artery (n = 8) in a pressure myograph in parallel, both with Tyrode, but one with 0.6% albumin added. The change in the outer diameter of the vessels [preconstricted with norepinephrine (NE) to 70%] in response to acetylcholine as an indicator of the endothelial function, was repeatedly measured over 5 h after the equilibration. The difference between the acetylcholine responses of the two vessel segments was significant (p < 0.05) after a perfusion period of 4 h. We also investigated whether flow-induced constriction is dependent on (1) the presence of endothelium and (2) the level of preconstriction. We therefore perfused segments of rabbit femoral arteries (n = 5) with Tyrode with 0.6% albumin. If acetylcholine-induced dilatation was present, a flow-diameter relation was determined at two constriction levels: about 60% (high) and 90% (low) of the passive outer diameter. Both determinations were repeated after mechanical endothelium removal (checked functionally and histologically). A similar decrease in diameter (about 7%) with an increase in flow ranging from 0 to 1,330 microliters/min was found in all conditions. We conclude that the addition of (0.6%) albumin protects endothelial function in the rabbit femoral artery when perfused in the low-flow range for a period longer than 4 h. We also found that flow-dependent constriction is neither influenced by the presence of the endothelium nor by the level of tone induced with NE.
Animals↗
Vasoactive properties of rat coronary artery: in the tissue and isolated.
Perfusion of the heart takes place mainly in diastole. It is therefore important to study the factors that affect coronary diastolic flow. One of the factors that may limit coronary artery vasoactive responses is the surrounding cardiac tissue. We have therefore studied the intramyocardial septal artery, both when still embedded in the diastolic, unstretched myocardial tissue and after complete dissection (n = 6). In situ, the average external diameter was 351 +/- 21 microns; after dissection, it was 362 +/- 21 microns. These values were not significantly different. The average response of the vessel to KCl (125 mM, receptor-independent constriction) reduced the diameter to 56.1 +/- 5.0% and 69.4 +/- 3.7% of the maximal diameter for in situ and dissected vessels, respectively. The reduction in diameter after dissection was significantly less than the reduction in situ. The response to vasopressin (1,000 microU/ml, a receptor-dependent constrictor) was a reduction to 62.6 +/- 4.7% and 70.4 +/- 4.5%, respectively. The reduction in diameter of the dissected vessel is significantly smaller than that of the in situ vessel. The average values of the ratios of the diameter reductions for vasopressin and KCl were 0.85 +/- 0.06 in the in situ condition and 0.95 +/- 0.08 after dissection and were not significantly different (paired t-test). The results show that the dilated diameter and the diameter responses of intramyocardial conduit arteries are not affected by the surrounding diastolic cardiac tissue.
Animals↗