scholarly journals Effects of high PEEP and fluid administration on systemic circulation, pulmonary microcirculation, and alveoli in a canine model

2019 ◽  
Vol 127 (1) ◽  
pp. 40-46
Author(s):  
Huaiwu He ◽  
Qinhe Hu ◽  
Yun Long ◽  
Xu Wang ◽  
Rui Zhang ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Systemic Circulation ◽  
Canine Model ◽  
Flow Index ◽  
High Peep ◽  
Fluid Loading ◽  
Positive End Expiratory Pressure ◽  
Septal Thickness ◽  
Pulmonary Microcirculation ◽  
Lung Microcirculation

This study aimed to determine the response of systemic circulation, pulmonary microcirculation, and alveoli to high positive end-expiratory pressure (PEEP) in a canine model. This study was conducted in nine mixed-breed dogs on mechanical ventilation under anesthesia. The PEEP was initially set at 5 cmH2O (PEEP5), the PEEP was then increased to 25 cmH2O (PEEP25), and then saline was used for fluid loading. Data were obtained at the following time points: PEEP5; PEEP25 prefluid loading; and PEEP25 postfluid loading. The images of subpleural lung microcirculation were assessed by sidestream dark-field microscopy, and the hemodynamic data were collected from pulse contour waveform-derived measurements. Compared with PEEP5, the lung microvascular flow index (MFI, 2.3 ± 0.8 versus 0.9 ± 0.8, P = 0.001), lung perfused vessel density (PVD, 4.2 ± 2 versus 1.5 ± 1.8, P = 0.004), lung proportion of perfused vessel (PPV, 93 ± 14 versus 40 ± 4, P = 0.003), cardiac output (2.5 ± 0.6 versus 1.4 ± 0.5, P = 0.001), and mean blood pressure (116 ± 24 versus 91 ± 31, P = 0.012) were significantly lower at PEEP25 prefluid loading. After fluid loading, there were no significant differences in cardiac output or mean arterial pressure between the PEEP5 and PEEP25 postfluid loading levels. However, the lung microcirculatory MFI, PVD, and PPV at PEEP25 postfluid loading remain lower than at PEEP5. A significant increase in septal thickness was found at PEEP25 postfluid loading relative to septal thickness at PEEP25 prefluid loading (25.98 ± 5.31 versus 40.76 ± 7.9, P = 0.001). Under high PEEP, systemic circulation was restored after fluid loading, but lung microcirculation was not. Moreover, the septal thickness of alveoli significantly increased after fluid loading. NEW & NOTEWORTHY An excessively high positive end-expiratory pressure (PEEP) can impair the systemic circulation and alveolar microcirculation. In the high-PEEP condition, fluid loading restored the systemic circulation but did not affect the impaired lung microcirculation. The septal thickness of the alveoli significantly increased after fluid loading in the high-PEEP condition.

ASSESSMENT OF THE MATERNAL VENOUS CIRCULATION: WHY IS IT RELEVANT?

2013 ◽  
Vol 24 (3) ◽  
pp. 194-199
Author(s):  
KATHLEEN TOMSIN ◽  
WILFRIED GYSELAERS
Keyword(s):  
Cardiac Output ◽  
Organ Dysfunction ◽  
Venous Return ◽  
Cardiovascular Disorder ◽  
Systemic Circulation ◽  
Renal Vein Thrombosis ◽  
Venous System ◽  
Total Blood ◽  
Venous Circulation ◽  
Cardiovascular Assessment

The venous system is considered the main capacitor of the human body. Approximately 70% of the total blood volume resides in the venous bed, half of which circulates as venous return whereas the other half functions as reserve volume in the splanchnic veins. These veins are richly innervated and highly compliant, and communicate with the systemic circulation via capillaries (entrance) and portal vein and liver (exit). This constitution allows the venous compartment to balance circulating and stored blood volumes, and thus control cardiac output. Clinical conditions with reduced cardiac output are often associated with hampered venous return, resulting in visceral oedema, ascites or organ dysfunction. Organ dysfunction or failure may also result from (sub)obstructed venous outflow, as is illustrated in renal vein thrombosis or in the Nutcracker syndrome. Recently, the application of Doppler ultrasonography in the study of the maternal venous system illustrated that preeclampsia is another cardiovascular disorder with dysfunctional venous haemodynamics. In this opinion paper, we summarise results from Doppler studies of the maternal venous compartment, illustrating that performing venous haemodynamics function tests is to become a fundamental part of an integrated cardiovascular assessment of women with hypertension in pregnancy, facilitating an individualised diagnostic and therapeutic approach for every woman at risk for gestational hypertensive disease.

Lingual, splanchnic, and systemic hemodynamic and carbon dioxide tension changes during endotoxic shock and resuscitation

2005 ◽  
Vol 98 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Jorge A. Guzman ◽  
Mathew S. Dikin ◽  
James A. Kruse
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Endotoxic Shock ◽  
Mucosal Blood Flow ◽  
Canine Model ◽  
Endotoxin Shock ◽  
Carbon Dioxide Tension ◽  
Systemic Hemodynamic ◽  
Hemodynamic Variables ◽  
Blood Flow Patterns

Sublingual and intestinal mucosal blood flow and Pco2 were studied in a canine model of endotoxin-induced circulatory shock and resuscitation. Sublingual Pco2 (PsCO2) was measured by using a novel fluorescent optrode-based technique and compared with lingual measurements obtained by using a Stowe-Severinghaus electrode [lingual Pco2 (PlCO2)]. Endotoxin caused parallel changes in cardiac output, and in portal, intestinal mucosal, and sublingual blood flow (Q̇s). Different blood flow patterns were observed during resuscitation: intestinal mucosal blood flow returned to near baseline levels postfluid resuscitation and decreased by 21% after vasopressor resuscitation, whereas Q̇s rose to twice that of the preshock level and was maintained throughout the resuscitation period. Electrochemical and fluorescent Pco2 measurements showed similar changes throughout the experiments. The shock-induced increases in PsCO2 and PlCO2 were nearly reversed after fluid resuscitation, despite persistent systemic arterial hypotension. Vasopressor administration induced a rebound of PsCO2 and PlCO2 to shock levels, despite higher cardiac output and Q̇s, possibly due to blood flow redistribution and shunting. Changes in PlCO2 and PsCO2 paralleled gastric and intestinal Pco2 changes during shock but not during resuscitation. We found that the lingual, splanchnic, and systemic circulations follow a similar pattern of blood flow variations in response to endotoxin shock, although discrepancies were observed during resuscitation. Restoration of systemic, splanchnic, and lingual perfusion can be accompanied by persistent tissue hypercarbia, mainly lingual and intestinal, more so when a vasopressor agent is used to normalize systemic hemodynamic variables.

Pulmonary microvascular response to prostacyclin (PGI2) infusion in unanesthetized sheep

1982 ◽  
Vol 52 (5) ◽  
pp. 1338-1342 ◽  
Author(s):  
R. Gunther ◽  
C. Zaiss ◽  
R. H. Demling
Keyword(s):  
Cardiac Output ◽  
Aortic Pressure ◽  
Base Line ◽  
Fluid Exchange ◽  
Protein Ratio ◽  
Microvascular Response ◽  
Pulmonary Arterial ◽  
Pulmonary Microcirculation ◽  
Rebound Increase ◽  
Mean Aortic Pressure

We studied the effect of prostacyclin (PGI2) infusion and cessation of infusion on the pulmonary microcirculation. We used lung lymph flow (QL) and the lymph to plasma protein ratio as sensitive indices of net fluid (QF) and protein flux (CP). After a 4-h base line period, we infused PGI2 (0.2 micrograms . kg(-1).min(-1) into eight unanesthetized sheep for 2 h. We monitored vascular pressures and lymph during infusion and for another 18 h after PGI2. During infusion, QL and cardiac output increased by 75 and 50%, respectively, over base line, whereas the lymph-to-plasma ratio (L/P) remained constant for both albumin and globulin. This resulted in a significant increase in both fluid and protein flux. Pulmonary vascular pressures remained unchanged, whereas mean aortic pressure decreased. The increase in QF and CP was felt to be due to an increase in the surface area of fluid exchange vessels rather than increased permeability. After infusion, cardiac output rapidly returned to base line, whereas mean QL remained increased by 70% over base line for 2–8 h. Mean L/P decreased from 0.65 to 0.53. Pulmonary arterial pressure and pulmonary vascular resistance increased. The increase in QL and decrease in L/P indicate a rebound increase in pulmonary microvascular pressure in the postperfusion period.

Dynamic Hyperinflation and Intrinsic Positive End-Expiratory Pressure

2017 ◽  
Author(s):  
John W. Kreit
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Adverse Effects ◽  
Obstructive Lung Disease ◽  
Airflow Obstruction ◽  
Intrinsic Peep ◽  
Dynamic Hyperinflation ◽  
Positive End Expiratory Pressure ◽  
Inspiratory Time ◽  
Pulmonary Barotrauma

Dynamic hyperinflation and intrinsic PEEP almost always occur in patients with severe obstructive lung disease, in whom slowing of expiratory flow prevents complete exhalation. Occasionally, patients without airflow obstruction develop dynamic hyperinflation when expiratory time, is excessively shortened by a rapid respiratory rate, a long set inspiratory time (TI), or both. Dynamic Hyperinflation and Intrinsic Positive End-Expiratory Pressure describes the causes of dynamic hyperinflation and the mechanisms of its adverse effects, including reduced cardiac output and blood pressure, pulmonary barotrauma, and ineffective ventilator triggering. The chapter also describes how to screen for and measure intrinsic PEEP, and how to reduce or eliminate its adverse effects.

Atrial and pulmonary endothelin mRNA is increased in a canine model of chronic low cardiac output

1997 ◽  
Vol 273 (2) ◽  
pp. R838-R844 ◽  
Author(s):  
C. M. Wei ◽  
A. L. Clavell ◽  
J. C. Burnett
Keyword(s):  
Cardiac Output ◽  
Immunohistochemical Staining ◽  
Canine Model ◽  
Pulmonary Tissue ◽  
Low Cardiac Output ◽  
Inferior Vena Caval ◽  
Pulmonary Epithelial Cells ◽  
Key Sites ◽  
Potent Vasoconstrictor ◽  
Paracrine Actions

Chronic thoracic inferior vena caval constriction (TIVCC) is a model of low-cardiac output congestive heart failure (CHF), in which pulmonary and atrial as well as circulating endothelin (ET) are increased. ET is a potent vasoconstrictor and mitogenic peptide whose circulating concentrations are increased in severe human and experimental CHF. To date, an increase in ET production at key sites in CHF remains controversial. Therefore, the current study was designed to determine cardiac and pulmonary ET-1 mRNA in an experimental model of CHF produced by TIVCC in which avid sodium retention, intense vasoconstriction, and elevation of circulating ET-1 occur as in human CHF. Experiments were conducted in normal dogs and dogs with 7 days of TIVCC. Cardiac and pulmonary ET-1 mRNA were measured by quantified densitometry of Northern blots. Plasma and tissue (cardiac and pulmonary) ET-1 immunoreactivity were determined by radioimmunoassay. Cardiac and pulmonary tissue localization of ET-1 were determined by immunohistochemical staining. Plasma ET-1 was significantly increased in TIVCC compared with normal dogs. ET-1 mRNA was detectable in normal canine atria, ventricle, and lung. ET-1 mRNA was significantly increased in TIVCC compared with normal dogs in both atrial and pulmonary tissues without alternations in ventricular ET mRNA. Atrial and pulmonary tissue concentrations of ET-1 also were markedly elevated in TIVCC compared with normal dogs. Immunohistochemical staining of atrial and pulmonary tissues for ET-1 demonstrated that the increased ET immunoreactivity was localized to atrial myocytes and pulmonary epithelial cells. These studies support a role for the heart and lung in the increased production of ET-1 in CHF. The current studies also suggest that ET-1 may have important autocrine and paracrine actions in cardiopulmonary regulation in experimental CHF.

Effect of PEEP on discharge of pulmonary C-fibers in dogs

1985 ◽  
Vol 59 (4) ◽  
pp. 1085-1089 ◽  
Author(s):  
M. P. Kaufman ◽  
G. A. Ordway ◽  
T. G. Waldrop
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Impulse Activity ◽  
Vena Cava ◽  
Laboratory Animals ◽  
Positive End Expiratory Pressure ◽  
Firing Rates ◽  
C Fibers ◽  
Anesthetized Dogs ◽  
Stimulation Of

Although positive end-expiratory pressure (PEEP) is believed to depress cardiac output and arterial pressure by compressing the vena cava and the heart, it is unclear whether PEEP also depresses these variables by a reflex arising from an inflation-induced stimulation of pulmonary C-fibers. We therefore recorded the impulse activity of 17 pulmonary C-fibers in barbiturate-anesthetized dogs with closed chests, while we placed the expiratory outlet of a ventilator under 5–30 cmH2O. Increasing PEEP in a ramp-like manner stimulated 12 of the 17 pulmonary C-fibers, with activity increasing from 0.0 +/- 0.1 to 0.9 +/- 0.2 imp/s when end-expiratory pressure equaled 15 cmH2O. When PEEP was increased in a stepwise manner to 15–20 cmH2O and maintained at this pressure for 15 min, pulmonary C-fibers increased their firing rates, but the effect was small averaging 0.2–0.3 imp/s after the 1st min of this maneuver. We conclude that pulmonary C-fibers are unlikely to be responsible for causing much of the decreases in cardiac output and arterial pressure evoked by sustained periods of PEEP in both patients and laboratory animals. These C-fibers, however, are likely to be responsible for causing the reflex decreases in these variables evoked by sudden application of PEEP.

Positive end-expiratory pressure shifts left ventricular diastolic pressure-area curves

1980 ◽  
Vol 48 (4) ◽  
pp. 670-676 ◽  
Author(s):  
J. B. Haynes ◽  
S. D. Carson ◽  
W. P. Whitney ◽  
G. O. Zerbe ◽  
T. M. Hyers ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Positive End Expiratory Pressure ◽  
Pressure Area ◽  
Radiopaque Markers ◽  
Peep Ventilation ◽  
Volume Characteristics ◽  
Area Data

Positive end-expiratory pressure (PEEP) ventilation is frequently associated with reduction in cardiac output despite unchanged transmural left ventricular (LV) end-diastolic pressure. These findings have been interpreted to indicate decreased contractility, but could also be explained by altered LV diastolic pressure-volume characteristics. To study this possibility, radiopaque markers were inserted into a plane of the LV in nine dogs. Transmural pressure (LV-pericardial) was synchronized with LV area during ventilation with zero end-expiratory pressure and with 15 cmH2O PEEP. Mean polynomial curves derived from the diastolic pressure-area data demonstrated that PEEP shifted the curves upward so that a given diastolic area was associated with a higher transmural LV pressure (P less than 0.0001). PEEP decreased end-diastolic area and stroke area, both of which were normalized with dextran volume expansion. Restoration of stroke area by normalizing end-diastolic area with volume expansion suggests the initial changes with PEEP were due to a decrease in preload rather than in contractility.

Sign in / Sign up

Export Citation Format

Share Document