Effects of Positive Pressure Ventilation on Intrarenal Blood Flow in Infant Primates

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.

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Pulmonary blood flow regulation: Influence of positive pressure ventilation

Respiration Physiology ◽

10.1016/0034-5687(95)00049-6 ◽

1995 ◽

Vol 102 (2-3) ◽

pp. 251-260 ◽

Cited By ~ 4

Author(s):

J.L. Theissen ◽

S.R. Fischer ◽

L.D. Traber ◽

D.L. Traber

Keyword(s):

Blood Flow ◽

Pulmonary Blood Flow ◽

Positive Pressure Ventilation ◽

Flow Regulation ◽

Positive Pressure ◽

Blood Flow Regulation

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Physiology of positive-pressure ventilation

10.1093/med/9780199600830.003.0088 ◽

2016 ◽

Author(s):

Göran Hedenstierna ◽

Hans Ulrich Rothen

Keyword(s):

Blood Flow ◽

Lung Volume ◽

Respiratory Muscle ◽

Positive Pressure Ventilation ◽

Venous Pressure ◽

Gas Absorption ◽

Positive Pressure ◽

Airway Closure ◽

Dependent Lung ◽

Oedema Formation

During positive pressure ventilation the lung volume is reduced because of loss of respiratory muscle tone. This promotes airway closure that occurs in dependent lung regions. Gas absorption behind the closed airway results sooner or later in atelectasis depending on the inspired oxygen concentration. The elevated airway and alveolar pressures squeeze blood flow down the lung so that a ventilation/perfusion mismatch ensues with more ventilation going to the upper lung regions and more perfusion going to the lower, dependent lung. Positive pressure ventilation may impede the return of venous blood to the thorax and right heart. This raises venous pressure, causing an increase in systemic capillary pressure with increased capillary leakage and possible oedema formation in peripheral organs. Steps that can be taken to counter the negative effects of mechanical ventilation include an increase in lung volume by recruitment of collapsed lung and an appropriate positive end-expiratory pressure, to keep aerated lung open and to prevent cyclic airway closure. Maintaining normo- or hypervolaemia to make the pulmonary circulation less vulnerable to increased airway and alveolar pressures, and preserving or mimicking spontaneous breaths, in addition to the mechanical breaths, since they may improve matching of ventilation and blood flow, may increase venous return and decrease systemic organ oedema formation (however, risk of respiratory muscle fatigue, and even overexpansion of lung if uncontrolled).

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Regional Organ Blood Flow during High-frequency Positive-pressure Ventilation (HFPPV) and Intermittent Positive-pressure Ventilation (IPPV)

Anesthesiology ◽

10.1097/00000542-198410000-00009 ◽

1984 ◽

Vol 61 (4) ◽

pp. 416-419 ◽

Cited By ~ 11

Author(s):

Leonid Bunegin ◽

R. Brian Smith ◽

Ulf H. Sjostrand ◽

Maurice S. Albin ◽

Maciej F. Babinski ◽

...

Keyword(s):

Blood Flow ◽

High Frequency ◽

Positive Pressure Ventilation ◽

Intermittent Positive Pressure Ventilation ◽

Positive Pressure ◽

Organ Blood Flow

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Ventilation with external high frequency oscillation around a negative baseline increases pulmonary blood flow after the Fontan operation

Cardiology in the Young ◽

10.1017/s1047951100001049 ◽

1992 ◽

Vol 2 (3) ◽

pp. 277-280 ◽

Cited By ~ 14

Author(s):

Daniel J. Penny ◽

Zamir Hayek ◽

Peter Rawle ◽

Michael L. Rigby ◽

Andrew N. Redington

Keyword(s):

Blood Flow ◽

Negative Pressure ◽

High Frequency ◽

Pulmonary Blood Flow ◽

Positive Pressure Ventilation ◽

Fontan Operation ◽

Intermittent Positive Pressure Ventilation ◽

High Frequency Oscillation ◽

Positive Pressure ◽

Frequency Oscillation

AbstractIn this prospective study, pulmonary blood flow was measured using transesophageal Doppler echocardiography to assess whether ventilation by means of external high frequency oscillation around a negative pressure baseline can increase pulmonary blood flow, compared to intermittent positive pressure ventilation, in five patients after the Fontan operation. Pulmonary blood flow was measured when patients were ventilated by means of intermittent positive pressure ventilation and again during equivalent negative pressure ventilation using the external oscillatory technique. When compared to that with intermittent positive pressure ventilation, ventilation using external high frequency oscillation increased pulmonary blood flow by 116 ±61.5% (p=0.013). These results show that ventilation using an external oscillatory device with a mean negative chamber pressure may provide hemodynamic advantages in patients requiring assisted ventilation after the Fontan operation.

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Atelectatic lobe blood flow: open vs. closed chest, positive pressure vs. spontaneous ventilation

Journal of Applied Physiology ◽

10.1152/jappl.1981.50.5.1022 ◽

1981 ◽

Vol 50 (5) ◽

pp. 1022-1026 ◽

Cited By ~ 28

Author(s):

A. F. Pirlo ◽

J. L. Benumof ◽

F. R. Trousdale

Keyword(s):

Blood Flow ◽

Positive Pressure Ventilation ◽

Hypoxic Pulmonary Vasoconstriction ◽

Transpulmonary Pressure ◽

Spontaneous Ventilation ◽

Positive Pressure ◽

Closed Chest ◽

Pulmonary Vasoconstriction ◽

Anesthetized Dogs ◽

Percent Decrease

We measured lobar hypoxic pulmonary vasoconstriction (HPV) caused by both absorption atelectasis (AA) and nitrogen ventilation (N2) during conditions of a) open chest and positive-pressure ventilation (PPV), b) closed chest ad PPV, and c) closed chest and spontaneous ventilation (SV) and compared conditions a with b and b with c. In eight pentobarbital-anesthetized dogs we found that selective hypoxia of the left lower loe (LLL) caused by either AA or N2 resulted in the same percent decrease in the electromagnetically measured LLL blood flow whether the ches was open or closed to whether ventilation was by PPV or SV (range 58.3-65.0%). Whether the chest was open or closed and whether ventilation was by PPV or SV, reexpansion and ventilation of LLL AA with LLL N2 did not change LLL blood flow and indicated that there were no mechanical forces responsible for the decreased LLL AA blood flow. Differences in the degree of hypoxia, magnitude of transpulmonary pressure, and absolute pulmonary vascular pressure between LLL AA and N2 were considered to be minor. We conclude that the mechanism of decreased blood flow to an atelectatic lobe, whether the chest is open or closed and whether ventilation is by PPV or SV, is entirely due to HPV.

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Cardiac Output and Organ Blood Flow in Young Rabbits during Intermittent Positive-Pressure Ventilation

Neonatology ◽

10.1159/000241696 ◽

1983 ◽

Vol 44 (1) ◽

pp. 58-64 ◽

Cited By ~ 3

Author(s):

Elizabeth John ◽

Michael McDevitt ◽

George Cassady

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Positive Pressure Ventilation ◽

Intermittent Positive Pressure Ventilation ◽

Positive Pressure ◽

Organ Blood Flow

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Evidence for cardiac volume-receptor regulation of feline jejunal blood flow and fluid transport

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1984.246.4.g401 ◽

1984 ◽

Vol 246 (4) ◽

pp. G401-G410 ◽

Cited By ~ 3

Author(s):

H. Sjovall ◽

S. Redfors ◽

B. Biber ◽

J. Martner ◽

O. Winso

Keyword(s):

Blood Flow ◽

Fluid Transport ◽

Positive Pressure Ventilation ◽

Intestinal Secretion ◽

Vagal Afferents ◽

Positive Pressure ◽

Cardiac Volume ◽

Jejunal Segment ◽

Inspiratory Resistance

The aim of the study was to investigate the role of cardiac mechanoreceptors in the reflex regulation of intestinal blood flow and fluid transport. Feline cardiac mechanoreceptor activity was modified with two noninvasive techniques: positive-pressure ventilation (PPV) and inspiratory resistance breathing (IRB). A jejunal segment with intact vascular and nervous supply was isolated and exposed to cholera toxin as a model for intestinal secretion. The results revealed that PPV induced a pronounced intestinal vasoconstriction and a marked inhibition of choleraic secretion. IRB had the opposite effects. The responses were well correlated with changes in central blood volume and either markedly reduced or abolished by vagotomy, intestinal alpha-adrenoreceptor blockade, or postganglionic mesenteric denervation. The results indicate that cardiac mechanoreceptors with vagal afferents may mediate the observed reflex responses, and hence this receptor station may be of importance in the normal reflex control of intestinal hemodynamics and fluid transport.

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