Pattern of blood flow in the pulmonary veins of the dog

1965 ◽  
Vol 20 (6) ◽  
pp. 1118-1128 ◽  
Author(s):  
Eugene Morkin ◽  
John A. Collins ◽  
Harold S. Goldman ◽  
Alfred P. Fishman
Keyword(s):  
Blood Flow ◽  
Pulmonary Circulation ◽  
Pulmonary Veins ◽  
Electromagnetic Flowmeter ◽  
Sine Wave ◽  
Left Ventricular ◽  
Mean Flow ◽  
Venous Flow ◽  
Pulmonary Venous Flow ◽  
Atrial Contraction

The pattern of blood flow in the large pulmonary veins was studied in dogs by chronic implantation of sine-wave electromagnetic flowmeters and cineangiographic observations. These revealed that: 1) pulmonary venous flow is continuous and pulsatile with peak rate of flow of approximately twice the mean flow; 2) the initial rapid increase in venous flow occurs 0.10 sec after the onset of ventricular systole, reaching a peak at the time of closure of the A-V valves; 3) left atrial contraction produces a fleeting slowing or reversal of flow; and 4) respiratory variations in pulmonary venous flow follow those in pulmonary arterial flow, beat by beat. The genesis of phasic pulmonary venous flow was investigated by analysis of pressure and flow curves from the two sides of the heart, by consideration of the energy required for left ventricular filling, and by reconstruction of the pulmonary venous flow pulse using a mathematical model of the pulmonary circulation. These three lines of evidence are consistent in indicating that the transmitted right ventricular pressure is the major determinant of the pulmonary venous flow pattern in the dog. pulsatile pulmonary venous flow; pulmonary venous flow; pulmonary circulation; ventricular suction; respiration on pulmonary circulation; pulmonary venous angiography; pulmonary veno-atrial junctions; electromagnetic flowmeter; cineangiography Submitted on November 16, 1964

Physical and physiological determinants of pulmonary venous flow: numerical analysis

1997 ◽  
Vol 272 (5) ◽  
pp. H2453-H2465 ◽  
Author(s):  
J. D. Thomas ◽  
J. Zhou ◽  
N. Greenberg ◽  
G. Bibawy ◽  
P. M. McCarthy ◽  
...  
Keyword(s):  
Systolic Function ◽  
Systolic Dysfunction ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Lumped Parameter Model ◽  
Physiological Data ◽  
Venous Flow ◽  
Pulmonary Venous Flow ◽  
Atrial Contraction ◽  
Before And After

To study the physical and physiological determinants of transmitral and pulmonary venous flow, a lumped-parameter model of the cardiovascular system has been created, modeling the instantaneous pressure, volume, and influx/efflux of the pulmonary veins, left atrium and ventricle, systemic arteries and veins. right atrium and ventricle, and pulmonary arteries. Initial validation has been obtained by direct comparison with transesophageal echocardiographic recordings of mitral and pulmonary venous velocity for the following clinical situations: normal diastolic function, delayed ventricular relaxation, restrictive filling due to severe systolic dysfunction, severe mitral regurgitation before and after valve repair surgery, and premature atrial contraction occurring during ventricular systole. Sensitivity analysis has been performed with a Jacobian matrix, representing the proportional change in a group of output indexes (yi) in response to isolated changes in input parameters (xj), [(delta yi/yi)/ ([delta xj/xj)], demonstrating the complementary nature of mitral and pulmonary venous A-wave velocity for predicting ventricular stiffness and atrial systolic function. This unified numerical-experimental programming environment should facilitate model refinement and physiological data exploration, in particular guiding more accurate interpretations of Doppler echocardiographic data.

scholarly journals Assessment of Left Ventricular Diastolic Pressures with Pulmonary Venous Flow and Transmitral Inflow by Doppler Echocardiography

1997 ◽  
Vol 27 (3) ◽  
pp. 312
Author(s):  
Dongsoo Kim ◽  
Namsik Chung ◽  
Se Joong Rim ◽  
June Kwon ◽  
Hyuck-Moon Kwon ◽  
...  
Keyword(s):  
Doppler Echocardiography ◽  
Left Ventricular ◽  
Venous Flow ◽  
Pulmonary Venous Flow

Effect of lung inflation on lung blood volume and pulmonary venous flow

1985 ◽  
Vol 58 (3) ◽  
pp. 954-963 ◽  
Author(s):  
R. Brower ◽  
R. A. Wise ◽  
C. Hassapoyannes ◽  
B. Bromberger-Barnea ◽  
S. Permutt
Keyword(s):  
Blood Volume ◽  
Transpulmonary Pressure ◽  
Left Ventricular ◽  
Respiratory Cycle ◽  
Pulmonary Vasculature ◽  
Venous Flow ◽  
Lung Inflation ◽  
Pulmonary Venous Flow ◽  
Respiratory Wave ◽  
Left Ventricular Preload

Phasic changes in lung blood volume (LBV) during the respiratory cycle may play an important role in the genesis of the respiratory wave in arterial pressure, or pulsus paradoxus. To better understand the effects of lung inflation on LBV, we studied the effect of changes in transpulmonary pressure (delta Ptp) on pulmonary venous flow (Qv) in eight isolated canine lungs with constant inflow. Inflation when the zone 2 condition was predominant resulted in transient decreases in Qv associated with increases in LBV. In contrast, inflation when the zone 3 condition was predominant resulted in transient increases in Qv associated with decreases in LBV. These findings are consistent with a model of the pulmonary vasculature that consists of alveolar and extra-alveolar vessels. Blood may be expelled from alveolar vessels but is retained in extra-alveolar vessels with each inflation. The net effect on LBV and thus on Qv is dependent on the zone conditions that predominate during inflation, with alveolar or extra-alveolar effects being greater when the zone 3 or zone 2 conditions predominate, respectively. Lung inflation may therefore result in either transiently augmented or diminished Qv. Phasic changes in left ventricular preload may therefore depend on the zone conditions of the lungs during the respiratory cycle. This may be an important modulator of respiratory variations in cardiac output and blood pressure.

Mechanisms of blood flow during pneumatic vest cardiopulmonary resuscitation

1991 ◽  
Vol 70 (1) ◽  
pp. 454-465 ◽  
Author(s):  
C. Beattie ◽  
A. D. Guerci ◽  
T. Hall ◽  
A. M. Borkon ◽  
W. Baumgartner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiopulmonary Resuscitation ◽  
Positive Pressure Ventilation ◽  
Pulmonary Veins ◽  
Left Ventricular ◽  
Aortic Flow ◽  
Positive Pressure ◽  
Compression Rate ◽  
Compression Phase ◽  
Cardiac Compression

Mechanisms of blood flow during cardiopulmonary resuscitation (CPR) were studied in a canine model with implanted mitral and aortic flow probes and by use of cineangiography. Intrathoracic pressure (ITP) fluctuations were induced by a circumferential pneumatic vest, with and without simultaneous ventilation, and by use of positive-pressure ventilation alone. Vascular volume and compression rate were altered with each CPR mode. Antegrade mitral flow was interpreted as left ventricular (LV) inflow, and antegrade aortic flow was interpreted as LV outflow. The pneumatic vest was expected to elevate ITP uniformly and thus produce simultaneous LV inflow and LV outflow throughout compression. This pattern, the passive conduit of "thoracic pump" physiology, was unequivocally demonstrated only during ITP elevation with positive-pressure ventilation alone at slow rates. During vest CPR, LV outflow started promptly with the onset of compression, whereas LV inflow was delayed. At compression rates of 50 times/min and normal vascular filling pressures, the delay was sufficiently long that all LV filling occurred with release of compression. This is the pattern that would be expected with direct LV compression or "cardiac pump" physiology. During the early part of the compression phase, catheter tip transducer LV and left atrial pressure measurements demonstrated gradients necessitating mitral valve closure, while cineangiography showed dye droplets moving from the large pulmonary veins retrograde to the small pulmonary veins. When the compression rate was reduced and/or when intravascular pressures were raised with volume infusion, LV inflow was observed at some point during the compressive phase. Thus, under these conditions, features of both thoracic pump and cardiac pump physiology occurred within the same compression. Our findings are not explained by the conventional conceptions of either thoracic pump or cardiac compression CPR mechanisms alone.

Sign in / Sign up

Export Citation Format

Share Document