Pulmonary Vascular Impedance Research Articles

Effects of Breathing 10 Per Cent Carbon Dioxide on the Pulmonary Circulation of Human Subjects

The effects on the pulmonary circulation of breathing 10% CO 2 for 10 to 20 min were studied in five eucapnic and 11 convalescing hypercapnic patients to recreate the CO 2 tensions which they had experienced during respiratory failure. Right heart catheterization permitted measurements of pulmonary arterial and wedge pressures and obtaining samples of mixed venous blood. Breathing CO 2 increased mean pulmonary arterial pressures from 33 to 50 mm Hg (52%); pulmonary arterial wedge pressures were unchanged, and cardiac output increased only 22%. In three hypercapnic and two eucapnic subjects reduction of blood hydrogen ion levels by rapid infusion of 120 to 135 mEq NaHCO 3 during CO 2 breathing did not lower pulmonary arterial pressure significantly, nor raise cardiac output. Neither vascular pressures nor cardiac outputs changed during oxygen breathing. Larger increases in cardiac output, which were produced by exercise, raised pulmonary artery pressure only half as much as breathing 10% CO 2 did. Therefore, pulmonary vascular resistance (PVR) that was elevated to an average of 4.8 mm Hg/L/min at rest while breathing air was increased to 6.5 mm Hg/L/min during CO 2 breathing ( P <0.01). In contrast, PVR was unchanged (4.6 mm Hg/L/min) during exercise. This difference between PVR while breathing CO 2 and during exercise was statistically significant ( P <0.02). Restoration of the pH of the blood toward normal by the infusion of bicarbonate during breathing of CO 2 raised the pulmonary arterial pressure. The five eucapnic subjects showed similar changes during CO 2 breathing and exercise, although their base-line values were significantly different. The differences were due, at least in part, to lower Paco 2 . This evidence suggests that CO 2 acts on pulmonary arterioles and capillaries that are exposed to alveolar gases to increase the pulmonary vascular impedance.

Impact pressure, lateral pressure, and impedance in the proximal aorta and pulmonary artery.

ArticleImpact pressure, lateral pressure, and impedance in the proximal aorta and pulmonary artery.M F O'RourkeM F O'RourkePublished Online:01 Nov 1968https://doi.org/10.1152/jappl.1968.25.5.533MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByBernoulli’s Equation15 September 2018Hemodynamic Monitoring and Resuscitation9 October 2016High Flow Velocity and Low Systolic PressureJournal of the American College of Cardiology, Vol. 66, No. 5Ventricular kinetic energy may provide a novel noninvasive way to assess ventricular performance in patients with repaired tetralogy of FallotThe Journal of Thoracic and Cardiovascular Surgery, Vol. 149, No. 5Quantification of left and right ventricular kinetic energy using four-dimensional intracardiac magnetic resonance imaging flow measurementsM. Carlsson, E. Heiberg, J. Toger, and H. Arheden15 February 2012 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 302, No. 4The Mean Machine; Accurate Non-invasive Blood Pressure Measurement in the Critically Ill Patient12 August 2009 | Journal of Clinical Monitoring and Computing, Vol. 23, No. 5Measuring Vascular Function and Ventricular/Arterial Coupling Dynamics18 April 2009Genesis of the normal and abnormal arterial pulseCurrent Problems in Cardiology, Vol. 25, No. 5An ultrasonic method for noninvasive estimation of vascular impedance to an absolute level: in vitro validation of the relationship between impedance and phase velocityIEEE Transactions on Biomedical Engineering, Vol. 47, No. 4Arterial Pulse Transmission CharacteristicsSubaortic septal bulge simulates hypertrophic cardiomyopathy by angulation of the septum with age, independent of focal hypertrophy. An echocardiographic studyJournal of the American Society of Echocardiography, Vol. 10, No. 5Mean outflow resistance as a marker of left ventricular afterloadBasic Research in Cardiology, Vol. 82, No. 3Input impedance of the pulmonary arterial system in normal man. Effects of respiration and comparison to systemic impedance.Circulation Research, Vol. 54, No. 6Physiological and pathophysiological implications of ventricular/vascular couplingAnnals of Biomedical Engineering, Vol. 12, No. 2Normal rate of ventricular emptying in valvular aortic stenosis.Heart, Vol. 46, No. 4Comments on "pulmonary vascular impedance analysis of adaptation to chronically elevated blood flow in the awake dog.Circulation Research, Vol. 46, No. 5Venous return more than cardiac output?Circulation Research, Vol. 46, No. 5Influence of central and peripheral changes on the hydraulic input impedance of the systemic arterial treeMedical & Biological Engineering, Vol. 11, No. 6Hemodynamics of counterpulsation: The study of a lumped-parameter computer modelJournal of Biomechanics, Vol. 5, No. 5Comparative Pathophysiology of Pulmonary Hypertension: Development of a Model25 February 2012Vascular Input ImpedanceThe arterial pulse in health and diseaseAmerican Heart Journal, Vol. 82, No. 5Arterial elasticity and fluid dynamicsProgress in Biophysics and Molecular Biology, Vol. 22Hemodynamics of the ventricular outflow tractJournal of Biomechanics, Vol. 3, No. 4Influence of Sympathetic Nerve Stimulation on Right Ventricular Outflow-Tract Pressures in Anesthetized DogsCirculation Research, Vol. 24, No. 3 More from this issue > Volume 25Issue 5November 1968Pages 533-41 https://doi.org/10.1152/jappl.1968.25.5.533PubMed5687359History Published online 1 November 1968 Published in print 1 November 1968 Metrics

Pulse wave velocity in the main pulmonary artery of the dog.

Apparent phase velocities in the main pulmonary artery were calculated from simultaneous measurements of pressure at two sites in 11 anesthetized, open-chest dogs, at heart rates ranging from 24 to 240 beat/min. The distribution of apparent phase velocity with harmonic frequency was similar to that reported previously for input impedance and frequency. Phase velocity in the absence of reflections, estimated by averaging apparent phase velocities at frequencies from 9 to 23 cycle/sec, averaged 275 cm/sec in the control state and 417 cm/sec during the infusion of 5-hydroxytryptamine (serotonin). The elastic modulus of the pulmonary arterial wall implied by these velocities was calculated to be approximately 1.2 x 10 6 dyne/cm 2 in the controls and 2.7 x 10 6 dyne/cm 2 during serotonin. These results are consistent with previous observations on normal pulmonary vascular input impedance in the dog under these conditions, and with the relationships predicted by the Womersley equations, and suggest that the effects of serotonin on the input impedance spectrum are due in part to an increase in pulse wave velocity.

Hydraulic power associated with pulmonary blood flow and its relation to heart rate.

Pulmonary vascular input impedance and hydraulic power were measured at various heart rates in 29 anesthetized and 5 unanesthetized dogs. Hydraulic power at the pulmonary veno-atrial junction was measured in 5 dogs. The pulmonary vascular impedance spectrum in the unanesthetized dogs did not differ significantly from that in the anesthetized dogs. Average pulmonary arterial power in the anesthetized dogs was 157 milliwatts (mw), of which 108 mw was associated with mean pressure and flow, and 49 mw with the pulsations around these means. Seventy-eight per cent of this input power was dissipated in passage through the pulmonary bed. Kinetic energy accounted for 7% of the total input power. Because of a steep fall in impedance between zero and 3 cycles/sec, and a rate-dependent change in the harmonic structure of flow pulsations, there was an inverse relationship between heart rate and the input power for a given mean flow, up to 180 beats/min. Pulmonary vascular dimensions and elasticity, which determine impedance, thus embody a mechanism whereby tachycardia can increase pulmonary blood flow by as much as 35% with an increase in pulmonary arterial input power of less than 5%, without the intervention of vasomotor activity.

Stroke volume in conscious dogs; effect of respiration, posture, and vascular occlusion.

Right and left ventricular stroke volumes were measured beat by beat in tranquil, conscious, healthy dogs by electromagnetic flowmeter transducers implanted around the roots of the aorta and main pulmonary artery. The onset and time courses of stroke volume changes of each ventricle differed in response to respiration, passive change of posture, application and release of positive pressure, and occlusion of the inferior cava; the two ventricles were always out of phase and balance, and only appeared to be in phase when changes of heart rate dominated the picture. The immediate response to these events was probably determined by alterations in systemic venous return which changed end-diastolic fiber length and so altered stroke volume by the Frank-Starling mechanism. Changes of vagal tone might have played a small part by altering atrial contractility but sympathetic activity did not seem to be involved. The initial backflow in the pulmonary artery was taken as an index of the level of pulmonary vascular impedance and increased only when the transpulmonary pressure increased. ventricular stroke volume; electromagnetic flowmeter; Frank-Starling mechanism; autonomic tone; backflow pulmonary vascular impedance Submitted on December 3, 1964

PULMONARY VASCULAR IMPEDANCE IN THE DOG.

Pulmonary vascular hydraulic input impedance was measured in 13 anesthetized openchest dogs with normal sinus rhythm, and 2 dogs with surgically induced atrioventricular block, by means of electromagnetic flowmeters and strain gauge manometers of known frequency response. The linearity of the pulmonary bed was evaluated by measuring impedance while the heart rate, and hence the pulsatile input to the bed, was varied. The pulmonary bed behaved as a quasilinear system, within the limits of accuracy of the methods employed and the range of frequencies tested. The use of input impedance, or oscillatory pressure/flow ratio, to describe some characteristics of the bed is therefore justifiable, and analogies with linear models like the simple transmission line are not unreasonable. The characteristic input impedance averaged 3,094 dyne sec cm -5 kg, or about one-third the magnitude of the pulmonary vascular resistance, and was therefore a significant part of the total opposition that must be overcome in moving blood through the lungs. This impedance to pulsatile flow is not included in calculations of resistance from mean pressure and flow measurements. The pattern of the impedance spectrum suggested that reflections originating from arteries 1.0 mm and less in diameter play a large role in determining input impedance and its variations with frequency. Pulmonary vasoconstriction by 5-hydroxytryptamine (serotonin) altered the impedance pattern in a manner consistent with increased wave reflection and displacement of the dominant reflecting sites to positions nearer the main pulmonary artery. Capillary compression by increased intra-alveolar pressure also increased reflection, but did not alter the sites of reflection significantly, providing further evidence that the normal impedance pattern and its modification by serotonin are both determined by the characteristics of the arterial part of the bed.