scholarly journals Cardiopulmonary Interactions during Positive Pressure Ventilation

1996 ◽  
Vol 3 (6) ◽  
pp. 380-385
Author(s):  
John Granton
Keyword(s):  
Cardiac Output ◽  
Left Ventricle ◽  
Positive Pressure Ventilation ◽  
Contractile Function ◽  
Cardiac Performance ◽  
Positive Pressure ◽  
Loading Conditions ◽  
Cardiopulmonary Interactions ◽  
The Right ◽  
Cardiocirculatory Effects

Positive pressure ventilation (PPV) may lead to significant hemodynamic alterations. The cardiocirculatory effects of PPV occur through alterations in the loading conditions of the right and left ventricle and are mediated by changes in intrathoracic pressures and in lung volume. However, the net effect of PPV on cardiac output and hemodynamics is not always predictable. PPV may lead to either a decrease or an increase in cardiac performance. The cardiac consequences of PPV are also dependent on baseline loading conditions and contractile function of the heart.

Haemodynamic assessments in mechanically ventilated patients

2020 ◽  
pp. 321-326
Author(s):  
Antoine Vieillard-Baron
Keyword(s):  
Pulse Pressure ◽  
Positive Pressure Ventilation ◽  
Superior Vena ◽  
Vena Cava ◽  
Positive Pressure ◽  
Mechanically Ventilated ◽  
Mechanically Ventilated Patients ◽  
Pulmonary Capillaries ◽  
The Right ◽  
Ventilated Patients

Knowledge of heart–lung interactions is key to manage haemodynamics in mechanically ventilated patients (see also Chapter 5). It allows intensivists to understand the meaning of blood and pulse pressure respiratory variations (PPV). Unlike spontaneous breathing, positive pressure ventilation increases blood pressure and pulse pressure during inspiration following by a decrease during expiration. This is called reverse pulsus paradoxus and includes a ‘d-down’ and a ‘d-up’ effect. No variation means no effect of mechanical ventilation on the heart and especially on the right heart. In case of significant PPV, tidal volume usually reduces right ventricular stroke volume by way of reducing preload where systemic venous return is decreased (fluid expansion is useful to restore haemodynamics, when impaired) or increasing afterload (obstruction of pulmonary capillaries due to alveolar inflation and, in this case, fluid expansion is useless or even sometimes deleterious). Clinical examination as well as evaluation of respiratory variations of superior vena cava by echo, helps to distinguish between these two situations. By studying the beat-by-beat changes in echo parameters induced by positive pressure ventilation heartbeat by heartbeat, echocardiography is perfectly suited to study heart–lung interactions and then to propose an appropriate optimization in case of haemodynamic impairment.

CARDIAC PERFORMANCE IN HEART–LUNG PREPARATIONS OF RATS WITH EXPERIMENTAL CARDIAC HYPERTROPHY

1966 ◽  
Vol 44 (1) ◽  
pp. 21-27 ◽  
Author(s):  
B. Korecky ◽  
M. Beznak ◽  
M. Korecka
Keyword(s):  
Cardiac Output ◽  
Left Ventricle ◽  
Arterial Pressure ◽  
Cardiac Hypertrophy ◽  
Cardiac Performance ◽  
Aortic Constriction ◽  
Chronic Anemia ◽  
Stepwise Increase ◽  
Thyroxine Treatment ◽  
Made In

Heart-lung preparations (h.l.p.) were made in normal rats and in rats with cardiac hypertrophy produced by aortic constriction, thyroxine treatment, or chronic anemia. In the h.l.p., arterial pressure was kept constant at 100 mm Hg, and maximum cardiac output (m.c.o.) was measured by stepwise increase in the inflow of blood until no further rise in cardiac output occurred. The m.c.o. of enlarged hearts was above normal, but not if it was expressed per gram of left ventricle weight. This latter value was not above normal in any of the enlarged hearts, contrary to earlier findings in whole animals. In fact, in one group of severely anemic rats it was significantly below normal.

Continuous positive-pressure ventilation does not alter ventricular pressure-volume relationship

1981 ◽  
Vol 240 (6) ◽  
pp. H821-H826 ◽  
Author(s):  
J. E. Fewell ◽  
D. R. Abendschein ◽  
C. J. Carlson ◽  
E. Rapaport ◽  
J. F. Murray
Keyword(s):  
Mechanical Properties ◽  
Positive Pressure Ventilation ◽  
Venous Return ◽  
Intermittent Positive Pressure Ventilation ◽  
Left Ventricular ◽  
Positive Pressure ◽  
Volume Relationship ◽  
Pressure Volume Relationship ◽  
The Right ◽  
Continuous Positive Pressure

To determine whether alterations in the mechanical properties (i.e., stiffening) of the right and left ventricles contribute to the decrease in right and left ventricular end-diastolic volumes during continuous positive-pressure ventilation (CPPV), we studied six dogs anesthetized with chloralose urethane and ventilated with a volume ventilator. We varied ventricular volumes by withdrawing or infusing blood. Pressure-volume curves, constructed by plotting transmural ventricular end-diastolic pressures against ventricular end-diastolic volumes, did not change during CPPV (12 cmH2O positive end-expiratory pressure) compared to intermittent positive-pressure ventilation (IPPV, 0 cmH2O end-expiratory pressure). We conclude that decreased ventricular end-diastolic volumes during CPPV result primarily from a decrease in venous return. Alterations in the mechanical properties of the ventricles do not play a significant role in this response.

scholarly journals Genomic modulation of mitochondrial respiratory genes in the hypertrophied heart reflects adaptive changes in mitochondrial and contractile function

2007 ◽  
Vol 293 (5) ◽  
pp. H2819-H2825 ◽  
Author(s):  
Makhosazane Zungu ◽  
Maria Pilar Alcolea ◽  
Francisco José García-Palmer ◽  
Martin E. Young ◽  
M. Faadiel Essop
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Respiratory Function ◽  
Hypobaric Hypoxia ◽  
Contractile Function ◽  
Left Ventricular ◽  
Transcript Levels ◽  
Mitochondrial Number ◽  
The Right ◽  
Mitochondrial Respiratory

We hypothesized the coordinate induction of mitochondrial regulatory genes in the hypertrophied right ventricle to sustain mitochondrial respiratory capacity and contractile function in response to increased load. Wistar rats were exposed to hypobaric hypoxia (11% O2) or normoxia for 2 wk. Cardiac contractile and mitochondrial respiratory function were separately assessed for the right and left ventricles. Transcript levels of several mitochondrial regulators were measured. A robust hypertrophic response was observed in the right (but not left) ventricle in response to hypobaric hypoxia. Mitochondrial O2 consumption was increased in the right ventricle, while proton leak was reduced vs. normoxic controls. Citrate synthase activity and mitochondrial DNA content were significantly increased in the hypertrophied right ventricle, suggesting higher mitochondrial number. Transcript levels of nuclear respiratory factor-1, peroxisome proliferator-activated receptor-γ-coactivator-1α, cytochrome oxidase (COX) subunit II, and uncoupling protein-2 (UCP2) were coordinately induced in the hypertrophied right ventricle following hypoxia. UCP3 transcript levels were significantly reduced in the hypertrophied right ventricle vs. normoxic controls. Exposure to chronic hypobaric hypoxia had no significant effects on left ventricular mitochondrial respiration or contractile function. However, COXIV and UCP2 gene expression were increased in the left ventricle in response to chronic hypobaric hypoxia. In summary, we found coordinate induction of several genes regulating mitochondrial function and higher mitochondrial number in a model of physiological right ventricular hypertrophy, linking the efficiency of mitochondrial oxidative phosphorylation and respiratory function to sustained contractile function in response to the increased load.

scholarly journals Alterations in the expression of genes related to contractile function and hypertrophy of the left ventricle in chronically paced patients from the right ventricular apex

EP Europace ◽  
2015 ◽  
Vol 17 (10) ◽  
pp. 1563.1-1570 ◽  
Author(s):  
Eva G. Arkolaki ◽  
Emmanuel N. Simantirakis ◽  
Joanna E. Kontaraki ◽  
Stavros I. Chrysostomakis ◽  
Alexandros P. Patrianakos ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Right Ventricular ◽  
Contractile Function ◽  
Expression Of Genes ◽  
Right Ventricular Apex ◽  
The Right

Effect of positive-pressure ventilatory frequency on regional pleural pressure

1988 ◽  
Vol 65 (3) ◽  
pp. 1314-1323 ◽  
Author(s):  
R. Novak ◽  
G. M. Matuschak ◽  
M. R. Pinsky
Keyword(s):  
Positive Pressure Ventilation ◽  
Lung Ventilation ◽  
Pleural Pressure ◽  
Positive Pressure ◽  
Ventilatory Frequency ◽  
Balloon Catheters ◽  
Airflow Distribution ◽  
Pleural Surface ◽  
The Right ◽  
Phase Differences

Regional lung ventilation is modulated by the spatiotemporal distribution of alveolar distending forces. During positive-pressure ventilation, regional transmission of airway pressure (Paw) to the pleural surface may vary with ventilatory frequency (f), thus changing interregional airflow distribution. Pendelluft phenomena may result owing to selective regional hyperventilation or phase differences in alveolar distension. To define the effects of f on regional alveolar distension during positive-pressure ventilation, we compared regional pleural pressure (Ppl) swings from expiration to inspiration (delta Ppl) and end-expiratory Ppl over the f range 0-150 min-1 in anesthetized, paralyzed, close-chested dogs with normal lungs. We inserted six pleural balloon catheters to analyze Ppl distribution along three orthogonal axes of the right hemithorax. Increases in regional Ppl were synchronously coupled with inspiratory increases in Paw regardless of f. However, at a constant tidal volume and percent inspiratory time, end-expiratory Paw and Ppl increased in all regions once a f threshold was reached (P less than 0.01). Supradiaphragmatic delta Ppl were less than in other regions (P less than 0.05), but thoracoabdominal binding abolished this difference by decreasing thoracoabdominal compliance. We conclude that the distribution of forces determining dynamic regional alveolar distension are temporally synchronous but spatially asymmetric during positive-pressure ventilation at f less than or equal to 150/min.

scholarly journals Influence of Cimetidine on Cardiovascular Parameters in Man

1979 ◽  
Vol 72 (12) ◽  
pp. 898-901 ◽  
Author(s):  
I O Samuel ◽  
J W Dundee
Keyword(s):  
Blood Pressure ◽  
Intensive Care Unit ◽  
Cardiac Output ◽  
Positive Pressure Ventilation ◽  
Intermittent Positive Pressure Ventilation ◽  
Positive Pressure ◽  
Dilution Method ◽  
Depressant Effect ◽  
Average Blood Pressure ◽  
Before And After

Cardiac output was measured in 10 patients using the dye dilution method, before and after the intravenous injection of 400 mg cimetidine. The subjects were in the intensive care unit and required intermittent positive pressure ventilation. There was no change in the average blood pressure, heart rate and cardiac output during the 60 minutes following the cimetidine, although one patient showed a marked fall in cardiac output. The results suggest that cimetidine is without a marked depressant effect on cardiovascular system.

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