Effect of pulsatile flow during cardiopulmonary bypass.
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A method is described for measuring the mean pressure gradient that occurs across a prosthetic heart valve over the forward flow phase in a simulated cardiac pumping cycle. The procedure is to simultaneously gate both the pressure signal and a manually controlled reference voltage of opposite polarity. The gated pressure signal is used to charge up a capacitor, while at the same time the gated reference signal is used to remove charge from the capacitor. The reference voltage is equal to the mean value of the pressure gradient voltage when there is zero net voltage on the capacitor. The gating procedure is simple and straightforward. Sample results for the system, which has been used extensively to study valve performance in vitro, are given.
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Pulsatile cerebral blood flow reflects characteristics of arterial blood pressure as well as the structure and mechanical properties of the cerebrovascular network. Although the effects of changes in systemic blood gases and blood pressure on mean cerebral flow are established, their effects on pulsatile cerebral blood flow are unknown. These studies assessed the effects of hypoxia-hypercapnia (combined; both arterial PO2 and PCO2 approximately 55 Torr) and acute hypertension (+30-35 mmHg by aortic occlusion) on pulsatile cerebral blood flow in ketamine-anesthetized rabbits. We characterized the relationship between pulsatile systemic blood pressure (Millar catheter) and cerebral cortical capillary blood-flow (laser-Doppler) by calculating the transfer function, a frequency-domain expression that relates amplitudes and phase angles of flow output to those of the pressure input. During hypoxia-hypercapnia, mean flow increased 17% (P < 0.001), but the amplitude and contour of pulsatile cortical blood flow were unchanged (P > 0.10). Although aortic occlusion, during hypoxia-hypercapnia as well as during normoxia-normocapnia, increased systemic pulse pressure by 40%, the amplitude of cortical flow pulsations was unaffected. Changes in dynamic properties of the cerebral vasculature (P < 0.0001 by analysis of the transfer function) minimized alterations in pulsatile cortical blood flow and thus intrabeat vessel wall stress during acute hypertension; on the basis of analysis of an electrical analogue, we propose that these changes reflect alterations in both resistance and compliance.
The mechanism of ventilatory stimulation that accompanies increases in cardiac output is unknown. Previous studies addressing this issue have been inconclusive. However, only steady pulmonary blood flow was used. The effect of flow pulsatility merits consideration, because increasing cardiac output raises not only mean pulmonary arterial pressure but also pulse pressure; mechanoreceptors with an important dynamic component to their responses may cause a response to pulsatile, but not steady, flow. Studies were done on anesthetized cats (n = 4) and dogs (n = 4). The right pulmonary artery was cannulated within the pericardium, and systemic blood was pumped from the left atrium to the right pulmonary artery. The right pulmonary circulation was perfused at different levels of flow, which was either steady or pulsatile. Steady-state flow of up to 150 ml.kg-1.min-1 (270 ml.kg-1.min-1 when corrected for the proportion of lung tissue perfused) did not affect breathing pattern. When high pulmonary flow was made pulsatile (pulse pressure approximately 23 mmHg), breath duration decreased from 3.7 +/- 0.72 to 3.4 +/- 0.81 (SD) s (P less than 0.01), representing a change in frequency of only 9%. There was no change in peak inspiratory activity. It was concluded that pulmonary vascular mechanoreceptors are not likely to contribute significantly to the increase in ventilation in association with increases in cardiac output.
OBJECTIVE: The aim of this study was to determine the efficacy of color Doppler sonography in the diagnosis of portal vein thrombosis in patients with primary hepatocellular carcinoma. The findings on angiography were used as the gold standard for diagnosis. SUBJECTS AND METHODS: We compared the findings on color Doppler sonograms and hepatic angiograms in 18 patients with hepatocellular carcinoma and portal vein thrombosis and in 22 patients with hepatocellular carcinoma without portal vein thrombosis. In most patients, tumor-related thrombus of the portal vein was confirmed by autopsy or surgery. The sonographic criteria for diagnosing portal vein thrombosis included nonvisualization of portal vein flow, pulsatile flow in the thrombus, arterioportal shunts, and cavernous transformation of the portal vein. RESULTS: Nonvisualization of portal vein flow was the predominant color Doppler finding in all patients with portal vein thrombosis. Other flow abnormalities overlapped the finding of nonvisualization of portal vein flow in 10 of 18 patients with portal vein thrombosis. The sensitivity of color Doppler sonography was 100% for nonvisualization of portal vein flow, 89% for detection of pulsatile flow in the thrombus, 60% for detection of arterioportal shunts, and 100% for detection of cavernous transformation. Among these findings, pulsatile flow in the thrombus was diagnostic for pathologically proved neoplastic thrombi in the main portal vein; sensitivity and specificity were 89% and 100%, respectively, and accuracy was 96%. No portal vein that appeared normal on color Doppler sonograms was thrombosed on arteriograms. CONCLUSION: We conclude that color Doppler sonography is a useful means of imaging the vascular extension of a tumor-based thrombus and an accurate means of screening for portal vein thrombosis.
OBJECTIVES: We hypothesized that recognition of systolic flow reversal (pulsatile flow) after thrombolytic administration on coronary angiography is associated with angiographic and electrocardiogram findings reflecting impaired myocardial perfusion, as well as poorer clinical outcomes. BACKGROUND: Reversal of systolic flow on Doppler velocity wire recordings has been associated with impaired tissue perfusion on myocardial contrast echocardiography in the setting of myocardial infarction (MI). METHODS: Patients (n = 1,062) with a patent infarct-related artery were drawn from the Thrombolysis In Myocardial Infarction (TIMI) 10, TIMI 14, and Integrillin and Tenecteplase acute MI trials. RESULTS: Pulsatile flow (systolic flow reversal with cessation of antegrade contrast-dye motion or frank reversal of contrast-dye motion during systole) at 60 min after fibrinolytic administration was present in 11.0% of patients. Pulsatile flow was associated with higher corrected TIMI frame counts (slower epicardial flow) (median 40.1 frames, IQ 30 of 63 vs. 30 frames, interquartile 22 of 42, p < 0.0001), a closed microvasculature (TIMI myocardial perfusion grades 0 of 1, 57.1% vs. 37.8%, p = 0.03) and less complete (> or =70%) ST-segment resolution (23.5% vs. 58.9%, p = 0.008). Patients with pulsatile flow had a higher risk of death or reinfarction at 30 days (10.3% vs. 5.0%, p = 0.019). After controlling for age, pulse, blood pressure, anterior MI location, epicardial flow, and creatine kinase, pulsatile flow remained associated with an increased risk of death/MI (odds ratio 3.1, p = 0.006). CONCLUSIONS: A pulsatile pattern of flow is associated with impaired myocardial perfusion and poorer clinical outcomes independent of the velocity of antegrade flow in the epicardial artery. This simple and easily identifiable angiographic flow pattern may be useful in clinical risk stratification.
BACKGROUND: Many advances have been made in left ventricular assist device (LVAD) development including the introduction of smaller, non-pulsatile pumps. However, controversy exists over the potential significance of non-pulsatile blood flow. In addition, some newer LVADs incorporate descending aortic anastomosis (and therefore retrograde ascending aortic flow) for outflow rather than the traditional ascending aortic anastomosis. This, combined with non-pulsatile flow, may significantly increase the risks of ascending aortic thrombus formation, especially if native cardiac function is negligible and the aortic valve remains closed. The purpose of this study was to compare pulsatile and non-pulsatile flow generated by LVADs with outflow to the ascending aorta and descending aorta. METHODS: An in vitro mock circulatory loop, driven by either a pulsatile or a non-pulsatile LVAD, was anastomosed to transparent aortic models at either the ascending or descending aortic position. The aortic valve was kept closed, modeling no native cardiac output. Normal saline was used as a blood analog. Methylene blue dye was injected into the ascending aorta and aortic arch to demonstrate flow patterns. Dye washout time (in seconds) was used as a marker of flow stagnation and potential thrombogenicity. LVAD flow, rate, after-load and coronary flow were measured. RESULTS: Dye washout times at a flow rate of 5 liters/min were 1.7 +/- 0.75, 2.1 +/- 0.71, 4.7 +/- 0.82 and 9.9 +/- 4.4 seconds for pulsatile ascending (PA), non-pulsatile ascending (NPA), pulsatile descending (PD) and non-pulsatile descending flow (NPD), respectively. Coronary flow averaged 294 ml/min over all set-ups. Dye washout times at a flow rate of 4-liters/min were 3.0 +/- 1.0, 3.0 +/- 0.8, 14.0 +/- 3.8 and 25.0 +/- 9.1 seconds for PA, NPA, PD and NPD, respectively. Coronary flow averaged 227 ml/min over all set-ups. Ascending aortic anastomoses were associated with shorter dye washout times compared with descending aortic anastomoses, regardless of flow type (p < 0.001). There was no difference in washout time between pulsatile and non-pulsatile flow in the ascending aortic position (p = 0.23 and 0.12 for 5 and 4 liters/min, respectively). Pulsatile flow in the descending aorta had shorter washout times than non-pulsatile flow in the descending aorta (p < 0.001 and p = 0.004 for 5 and 4 liters/min, respectively). CONCLUSIONS: LVAD descending aortic anastomosis and retrograde aortic flow is associated with increased flow stagnation in the ascending aorta. This may increase the risk for thrombus formation in patients relying solely on retrograde aortic flow, especially if cardiac function and antegrade blood flow returns.
PURPOSE: To compare the hemodynamics and wall mechanics of swine iliac arteries after placement of six types of stent. MATERIALS AND METHODS: Stents were placed in the iliac artery of 18 pigs (three pigs each underwent placement with one of six types of stent); 16 untreated pigs served as control animals. Iliac arterial hemodynamics and wall mechanics were measured 4 days after placement. RESULTS: Four stents (Palmaz-Schatz, Cordis, Warren, NJ; and Strecker, Cragg, and Symphony, Boston Scientific/Vascular, Natick, Mass) caused decreased pulsatile flow rate in the treated and contralateral iliac arteries; one (Memotherm; Bard, Covington, Ga) caused increased flow pulsatility; and one (Wallstent; Schneider, Plymouth, Minn) had no effect. No compliance mismatching was noted for the Cragg, Symphony, and Memotherm stents, whereas a decrease in compliance was noted for the Palmaz-Schatz, Strecker, and Wallstent designs. The Palmaz-Schatz and Strecker stents caused increased arterial wall rigidity, the Symphony and Wallstent designs had no effect, and the Memotherm and Cragg stents caused decreased wall rigidity. Stents made of stiff metal yielded different early results than did stents made of the less rigid nitinol. CONCLUSION: Soon after implantation, the six stent designs elicited varying changes in blood flow, arterial compliance, and arterial wall mechanics. Contralateral arterial flow also was affected.
We have investigated the role of Ca(2+)- and ATP-sensitive K+ channels (KCa and KATP, respectively) in flow- and agonist-stimulated release of endothelium-derived relaxing factor (EDRF). Segments of rabbit abdominal aorta, perfused at constant flow with buffer containing indomethacin, were used as a source of EDRF in cascade bioassay, and responses to endothelium-dependent agonists were studied isometrically in rings of the same tissue in the absence of flow. Apamin, charybdotoxin (ChTX), and tetraethylammonium (TEA) were used to block a variety of low, medium, and high conductance KCa channels, and glibenclamide was used to block KATP channels. The effects of flow pulsatility were studied at pulse frequencies ranging from 0.15 to 9.75 Hz, and time-averaged shear stress was manipulated by adding dextran (80,000 mol wt) to the perfusate to increase its viscosity. Frequency-related EDRF release was maximal at approximately 5 Hz and attenuated by apamin, TEA, and ChTX, but not by glibenclamide. EDRF release stimulated by increased viscosity was attenuated by TEA, ChTX, and glibenclamide, but not by apamin. In marked contrast, EDRF release stimulated by acetylcholine and ATP was unaffected by blockade of either KCa or KATP channels. We conclude that a spectrum of KCa channel subtypes mediates endothelial transduction of the oscillatory component of pulsatile flow and that KATP channels may be additionally involved in the transduction of time-averaged shear stress. In contrast, agonist-stimulated endothelium-dependent relaxation is independent of K+ channel activation in rabbit aorta.
Quantification of blood flow in vessels provides valuable information that aids management decisions in a variety of cardiac conditions. Current flow measurement techniques are often limited by accuracy, time resolution, convenience, or anatomic localization. This study examined the accuracy of a commercially available phase-velocity cine magnetic resonance imaging (PVC MRI) technique to quantify flow rate in a pulsatile flow phantom. In addition, the equivalence of PVC MRI measurements of pulmonary and systemic flow was evaluated in children and adults without any pathologic shunt. Using a pulsatile flow phantom, volume flow rates measured by PVC MRI were compared to those by a transit-time ultrasound flowmeter over a range of flow rates (1.25-3.5 L/min, 13 trials). Close agreement was found between these techniques (y = 1.02x - 0.02, r = 0.99, Bland-Altman bias = -0.045 L/min, 95% limits of agreement = -0. 19-0.10 L/min). Twenty subjects (median age 12.8 years, range 0.7-49 years) with no pathologic shunt underwent PVC MRI measurement of blood flow in the main pulmonary artery (Q(p)) and the ascending aorta (Q(s)). Data processing time for each location was 20 minutes. The Q(p)/Q(s) ratio closely approximated unity (mean = 0.99, SD = 0. 10, range 0.85-1.19). Interobserver agreement was excellent (Bland-Altman bias = 0.09 L/min, 95% limits of agreement = 0.15-0.33 L/min). PVC MRI is an accurate technique to quantify pulsatile blood flow at a specific location. It can be used to noninvasively calculate Q(p) and Q(s) under normal flow conditions.
To realize a totally implantable total artificial heart (TAH), a new pulsatile TAH, the flow-transformed pulsatile TAH (FTPTAH), was developed. The system was composed of a single centrifugal pump (CFP) and two three-way valves. One port of each three-way valve was connected to the inlet and outlet of a CFP. The other two ports of each valve were connected to the right and left atrium, and the pulmonary artery and aorta. The CFP can perfuse the pulmonary and systemic circulation alternately with pulsatile flow by switching the two three-way valves. A prototype and the secondary model in which the solenoid valves and a spool valve were included, respectively, were connected to a mock circulatory unit with the results that a pulsatile TAH with physiological flow wave form could be obtained from a single CFP, about 5 L/min of pulsatile output could be obtained alternately on the right and left side by switching the solenoid valves or a spool valve, and flow balance between the right and left could be easily controlled by the switching duration. The system is feasible for a totally implantable TAH because it does not need a compliance chamber and can be miniaturized.
The pH, oxygen tension, and carbon dioxide tension of canine brain tissue were experimentally examined during profoundly hypothermic cardiopulmonary bypass. After core cooling, a 60-minute period of circulatory arrest was performed in group 1 (n = 8), a 120-minute nonpulsatile low-flow perfusion (25 ml/kg/min) in group 2 (n = 8), and a 120-minute pulsatile low-flow perfusion (25 ml/kg/min) in group 3 (n = 8). When the animal was rewarmed, the core temperature was raised to 32 degrees C. Brain tissue pH kept decreasing in group 1, but it showed a delayed recovery in group 2 and a rapid recovery in group 3 during core rewarming. Brain tissue oxygen tension decreased significantly in group 1. Brain tissue carbon dioxide tension increased irreversibly in group 1, increased to about 100 mm Hg and recovered to 89.9 +/- 15.3 mm Hg in group 2, and reached a plateau of about 85 mm Hg and recovered to 55.4 +/- 6.7 mm Hg in group 3. We concluded that a 120-minute period of nonpulsatile low-flow perfusion provides more protection from brain damage than a 60-minute period of circulatory arrest. Furthermore, pulsatile flow will increase the safety margin of cardiopulmonary bypass even if the flow rate is reduced to 25 ml/kg/min.
BACKGROUND: To determine the effect of pulsatility during cardiopulmonary bypass (CPB) on cerebral oxygenation, we measured oxyhaemoglobin (HbO2), deoxyhaemoglobin (Hb) and oxidised cytochrome aa3 (CtO2) with near-infrared spectroscopy (NIRS) in 14 patients electively scheduled for cardiac surgery. METHODS: Cerebral oxygenation was measured during steady state CPB at a core temperature of 32 degrees C. Non-pulsatile flow and pulsatile flow were performed for 10 min each. RESULTS: After 14 min of CPB, HbO2, Hb and CtO2 were significantly below prebypass values. HbO2 and CtO2 did not alter with changing flow patterns. Hb significantly increased both during the period of nonpulsatile (median: -0.7 vs. 0.25 micromol/l; P<0.05) and pulsatile flow (median: 0.25 vs. 0.5 micromol/l; P<0.001). This increase was independent of flow pattern. CONCLUSIONS: Neither oxygenated haemoglobin, nor intracellular oxygenation, represented by CtO2, indicated a beneficial effect of pulsatile perfusion during hypothermic CPB. These results, however, are only valid for short time effects within 10 min before rewarming from CPB and patients without flow-limiting stenoses of the carotid artery.