Responses to continuous negative-pressure breathing in man at rest and during exercise

1980 ◽  
Vol 48 (6) ◽  
pp. 977-981 ◽  
Author(s):  
H. Bjurstedt ◽  
G. Rosenhamer ◽  
C. M. Hesser ◽  
B. Lindborg
Keyword(s):  
Negative Pressure ◽  
Venous Pressure ◽  
Intrathoracic Pressure ◽  
Carbon Dioxide Tension ◽  
Minute Volume ◽  
Left Ventricular ◽  
Circulatory Effects ◽  
Ventricular Afterload ◽  
Negative Pressure Breathing ◽  
The Right

We studied the respiratory and circulatory effects in six healthy supine volunteers of continuous negative-pressure breathing (CNPB) at -15 and -30 cmH2O at rest and during dynamic leg exercies at 50% of individual working capacity. CNPB had no significant effects on respiratory minute volume, tidal volume, or arterial carbon dioxide tension. Mean arterial pressure remained essentially unchanged both at rest and during exercise, signifying that the reductions in intrathoracic pressure caused corresponding increases in left ventricular afterload. Nevertheless, cardiac output increased significantly in both conditions, causing reductions of mean central venous pressure that were considerably greater during exercise than at rest. These responses were reflected by increments in left ventricular work, amounting to 24 and 20% at rest and during exercise, respectively, at -30 cmH2O. We conclude that in CNPB at rest the increased activity of the left ventricle with associated juxtathoracic venous collapse protects the right heart and pulmonary circulation from congestion and that it does so even more effectively during exercise.

Effect of continuous pressure breathing on right ventricular volumes

1967 ◽  
Vol 22 (6) ◽  
pp. 1053-1060 ◽  
Author(s):  
Maylene Wong ◽  
Edgardo E. Escobar ◽  
Gilberto Martinez ◽  
John Butler ◽  
Elliot Rapaport
Keyword(s):  
Right Ventricular ◽  
Negative Pressure ◽  
Atmospheric Pressure ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Intrathoracic Pressure ◽  
Transmural Pressure ◽  
Positive Pressure ◽  
End Diastolic Volume ◽  
Negative Pressure Breathing

We measured the end-diastolic volume (EDV) and stroke volume (SV) in the right ventricle of anesthetized dogs during continuous pressure breathing and compared them to measurements taken during breathing at atmospheric pressure. During intratracheal positive-pressure breathing, EDV, and SV decreased and end-diastolic pressure became more positive relative to atmospheric pressure. During intratracheal negative-pressure breathing, EDV enlarged and SV tended to increase; end-diastolic pressure became more negative. During extrathoracic negative-pressure breathing SV decreased, EDV fell, though not significantly, and end-diastolic pressure rose, but insignificantly. Changes in EDV observed during intratracheal positive-pressure breathing and intratracheal negative-pressure breathing were associated with minor shifts in transmural pressure (end-diastolic pressure minus intrapleural pressure) in the expected directions, but during extrathoracic negative-pressure breathing a large increase in transmural pressure took place with the nonsignificant reduction in EDV. We believe that intrathoracic pressure influences right ventricular filling by changing the peripheral-to-central venous pressure gradient. The cause of the alteration in diastolic ventricular distensibility demonstrated during extra-thoracic negative-pressure breathing remains unexplained. positive-pressure breathing; negative-pressure breathing; extrathoracic negative-pressure breathing Submitted on August 16, 1966

Cardiac adjustments to left-side inotropic stimulation of in situ pig hearts

1987 ◽  
Vol 252 (6) ◽  
pp. H1164-H1174
Author(s):  
O. A. Vengen ◽  
K. Lande ◽  
O. Ellingsen ◽  
A. Ilebekk
Keyword(s):  
Right Ventricular ◽  
Systemic Circulation ◽  
Left Ventricular ◽  
Segment Length ◽  
Ventricular Afterload ◽  
Computer Based ◽  
The Right ◽  
Isoproterenol Infusion ◽  
Inotropic Stimulation ◽  
Stimulation Of

Cardiac adjustments to inotropic stimulation of the left side of the heart by continuous infusions of isoproterenol (0.6-0.8 microgram/min) and calcium chloride (240 mumol/min) into the left coronary artery were examined in open-chest pigs (17-36 kg) anesthetized with pentobarbital sodium. Both agents caused a reduction in the left ventricular (LV) preload and preejection segment length (PESL). Stroke volume (SV) rose by only 1.2 ml from 15.9 ml (P less than 0.01) during isoproterenol infusion, but when the reduction in LV PESL of 3.2% (P less than 0.01) was restored by saline infusion, SV increased by 27%. The LV PESL reduction was less at hypervolemia than at normovolemia. A computer-based model of the circulation predicted most of these changes and suggested redistribution of blood from the pulmonary to the systemic circulation. During isoproterenol infusion, the pulmonary arterial pressure fell, and the right ventricular end-ejection segment length declined. Reduced right ventricular afterload thus appears to be an important mechanism by which right ventricular output is increased during a selective increase in LV inotropy.

Effect of forward acceleration and negative pressure breathing on pulmonary diffusion

1962 ◽  
Vol 17 (6) ◽  
pp. 909-912
Author(s):  
Fred Zechman ◽  
Gustave Mueller
Keyword(s):  
Negative Pressure ◽  
Technical Assistance ◽  
Human Subjects ◽  
Pulmonary Ventilation ◽  
Pressure Curve ◽  
Experimental Conditions ◽  
Lung Volumes ◽  
Control Value ◽  
Negative Pressure Breathing ◽  
The Right

Forward acceleration decreases lung volumes, resembling negative pressure breathing (NPB). At 4 g the relaxation pressure curve is shifted downward and to the right 15 mm Hg. Pulmonary gas exchange and diffusion capacity were measured in nine human subjects during NPB (-15 mm Hg) and forward acceleration (4 g). Pulmonary ventilation increased approximately 40% in each condition. The O2 uptake increased with NPB (from 261 to 293 ml/min) and was slightly decreased or unchanged at 4 g. Carbon dioxide elimination increased in both experimental conditions. The apparent steady-state Dco was unchanged by NPB but decreased from an average control value of 21 to 12 ml/min mm Hg at 4 g. Since lung volumes are decreased by comparable amounts in both conditions, it is believed that the deleterious effects observed with forward acceleration are associated with the increased hydrostatic gradient from chest to back. Note: (With the Technical Assistance of Justin Taylor) Submitted on June 4, 1962

scholarly journals Novel Point-of-Care Ultrasound (POCUS) Technique to Modernize the JVP Exam and Rule out Elevated Right Atrial Pressures

2021 ◽  
Author(s):  
Larry Istrail ◽  
Maria Stepanova
Keyword(s):  
Right Atrium ◽  
Point Of Care ◽  
Venous Pressure ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Right Atrial ◽  
Point Of Care Ultrasound ◽  
Status Assessment ◽  
Left Ventricular Outflow ◽  
The Right

Accurate assessment of the jugular venous pressure (JVP) and right atrial pressure (RAP) has relied on the same bedside examination method since 1930. While this technique provides a rough estimate of right-sided pressures, it is limited by poor sensitivity and overall diagnostic inaccuracy. The internal jugular vein (IJV) is difficult to visualize in many patients and relies on an incorrect assumption that the right atrium lies 5 centimeters below the sternum. Point-of-care ultrasound (POCUS) offers an alternative method for more precisely estimating JVP and RAP. We propose a novel method of measuring the right atrial depth (RAD) using a sonographic measurement of the depth of the posterior left ventricular outflow tract as a surrogate landmark to the center of the right atrium when viewed in the parasternal long axis view. This is combined with determination if JVD was present at the supraclavicular point. Sensitivity, specificity, PPV, NPV of JVD at the supraclavicular point was 70%, 76%, 59%, 91% respectively. These values were confounded by the lack of standardization of zero reference landmarks (ZRLs) used during the right heart catheterizations. When the RAD estimate was adjusted to account for measurement error the sensitivity of JVD at supraclavicular point for elevated RAP improved to 90% with negative predictive value of 96%. This may offer a rapid and reliable method for ruling out elevated RAP and increase objectivity in our volume status assessment.

Cardiovascular interactions in respiratory failure

2016 ◽  
Author(s):  
Jae Myeong Lee ◽  
Michael R. Pinsky
Keyword(s):  
Respiratory Failure ◽  
Gas Exchange ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Work Of Breathing ◽  
Intrathoracic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Left Ventricular Ejection ◽  
Positive Pressure ◽  
Ventricular Afterload

Acute respiratory failure not only impairs gas exchange, but also stresses cardiovascular reserve by increasing the need for increased cardiac output (CO) to sustain O2 delivery in the face of hypoxaemia, increased O2 demand by the increased work of breathing and inefficient gas exchange, and increased right ventricular afterload due to lung collapse via hypoxic pulmonary vasoconstriction. Mechanical ventilation, though often reversing these processes by lung recruitment and improved arterial oxygenation, may also decrease CO by increasing right atrial pressure by either increasing intrathoracic pressure or lung over-distention by excess positive end-expiratory pressure or inadequate expiratory time causing acute cor pulmonale. Finally, spontaneous negative swings in intrathoracic pressure also increase venous return and impede left ventricular ejection thus increasing intrathoracic blood volume and often precipitating or worsening hydrostatic pulmonary oedema. Positive-pressure breathing has the opposite effects.

Perfusion technique for treatment of right heart failure

Perfusion ◽  
1995 ◽  
Vol 10 (5) ◽  
pp. 323-326 ◽  
Author(s):  
James R Beck ◽  
Linda B Mongero ◽  
Daniel J Goldstein ◽  
Mehmet C Oz
Keyword(s):  
Femoral Vein ◽  
Venous Pressure ◽  
Venous Blood ◽  
Right Heart Failure ◽  
Systemic Blood Pressure ◽  
Left Ventricular ◽  
Circulatory Failure ◽  
Ventricular Assist ◽  
Pump Head ◽  
The Right

A simple heparin-bonded circuit to facilitate a femoral vein to femoral artery shunt for the treatment of right-sided circulatory failure is proposed. Desaturated venous blood is shunted to the left-sided circulation to increase systemic blood pressure at the expense of saturation. The circuit comprised ¼ inch x 3/32 inch tubing with a paediatric Bio-Medicus centrifugal pump head allowing adequate regulation of flow. Paediatric Bio- Medicus cannulae provide flows between 500 and 2000 ml/min. Measurements of pulmonary artery pressure, central venous pressure, arterial pressure, arterial saturation and cardiac output were recorded. In the four case studies presented, the treatment included unloading of the right ventricle with venous to arterial shunting. Likewise, eight Holstein calves underwent shunt utilization after placement of a left ventricular assist device and induction of right ventricular failure. The future use of this device may be instrumental in aiding the cardiothoracic surgical team in the treatment of right-sided circulatory failure.

FAILURE OF THE HEART AFTER UNDUE ASPHYXIA AT BIRTH

PEDIATRICS ◽  
1961 ◽  
Vol 28 (4) ◽  
pp. 545-565
Author(s):  
E. D. Burnard ◽  
L. S. James
Keyword(s):  
Venous Pressure ◽  
Left Ventricular ◽  
Left Ventricular Failure ◽  
Transverse Diameter ◽  
Ventricular Failure ◽  
Healthy Infants ◽  
Vascular Congestion ◽  
Wide Range ◽  
The Right ◽  
Cardiac Enlargement

Thirty-three mature infants became ill in the neonatal period after suffering undue asphyxiation at birth. Dyspnea was a prominent symptom. Nineteen died and 14 recovered. The transverse diameter of the cardiac silhouette in most cases was greater than the average in healthy infants. The progressively increasing size of the heart between 1) healthy infants, 2) those who appeared healthy, but had suffered undue asphyxiation at birth, and 3) those in whom signs of illness developed after asphyxia, indicated that the illness and cardiac enlargement were related. Dilatation rather than hypertrophy was the likely cause of the greater roentgenographic size. This was most obvious on the right. There was also evidence suggestive of left ventricular dilatation. The size of the heart diminished as the infants recovered. In three infants who died serial films showed that enlargement remained or increased, and hypertrophy of both ventricles was present at necropsy in the one who survived the longest time. Roentgenographic changes in the lungs did not correlate well with either the signs of illness or with the presence of cardiac enlargement. The possibility existed that vascular congestion and transudation could be responsible for abnormal appearances in the lungs, when these were present. Biochemical changes resulting from severe asphyxia were observed soon after birth in four cases, and their presence in the others at this time was inferred from the depressed state of the infant as judged by the Apgar score. The quick recovery of the deranged acid base status which occurs after normal birth was not seen in most of the patients. Exceptions were those in whom the illness was brief. The abnormal biochemical status was characterized by arterial hypoxia and metabolic acidosis. The partial pressure of arterial carbon dioxide was distributed over a wide range. These findings are compatible with the presence of left ventricular failure. The left atrial pressure was high in comparison with that of healthy newborn infants. Venous pressure was also increased on the right. Consideration of the results of the three different kinds of investigation led to the suggestion that left ventricular failure occurred early in the illness. Disproportion between different signs in individual cases might have been related to attempted compensation by the heart and to the rate at which failure of the right heart might follow, as well as to the severity of the illness and the rate of recovery. While atelectasis and infection may have been present, there was evidence that heart failure could be the explanation of dyspnea in life and pulmonary vascular congestion at necropsy. The cause of failure is not known. It is related to the metabolic disorder from undue birth asphyxia. A disturbance in hemodynamics that requires more investigation is present.

Divergence of Intracranial and Central Venous Pressures in Lightly Anesthetized, Tracheally Intubated Dogs That Move in Response to a Noxious Stimulus

1996 ◽  
Vol 84 (3) ◽  
pp. 605-613 ◽  
Author(s):  
William L. Lanier ◽  
Ronald F. Albrecht ◽  
Paul A. Iaizzo
Keyword(s):  
Central Venous Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Superior Vena ◽  
Venous Pressure ◽  
Intrathoracic Pressure ◽  
Noxious Stimulus ◽  
Central Venous ◽  
Superior Vena Caval ◽  
The Right

Background Intracranial pressure (ICP) may increase in tracheally intubated subjects during periods of movement (e.g, "bucking" and coughing). Recent research has suggested that factors other than passive congestion of the cerebral vessels, resulting from increases in central venous pressure, may contribute to the ICP response. The current study evaluated this issue in a canine model of intracranial hypertension and additionally evaluated the relationship between ICP and static increases in superior vena caval pressure. Methods Six dogs were lightly anesthetized with 0.65% end-expired halothane in oxygen and nitrogen, and ventilation was mechanically controlled. Intracranial pressure was increased to a stable baseline of 15-20 mmHg using a subarachnoid infusion of warm 0.9% saline solution. The following variables were quantified before, and for 6 min after, initiating a 1-min noxious stimulus to the trachea and skin: ICP, central venous pressure, electromyograms (masseter, deltoid, and intercostal muscles), intrathoracic pressure, and cerebral perfusion pressure (defined as mean arterial pressure -- ICP). Later, the protocol was repeated in the presence of neuromuscular block with pancuronium. Finally, in the same dogs, occlusion of the superior vena cava at its junction with the right atrium was used to increase superior vena caval pressure in 5-mmHg increments, from 5 to 30 mmHG, so that the resulting increases in ICP could be quantified. Results In unparalyzed dogs whose heads were maintained at the level of the right atrium, there was a 22-mmHg increase in ICP at 1 min after initiating the noxious stimulus (P<0.05). The ICP increase was related to electromyogram activation and a 6-mmHg increase in central venous pressure; however, it was not associated with significant increases in intrathoracic pressure or cerebral perfusion pressure. Treatment with pancuronium abolished the electromyographic, ICP, and central venous pressure responses to noxious stimulus. When superior vena caval pressure was statically manipulated, the resulting ICP increase was only one half the magnitude of the superior vena caval pressure increase. After elevating the head 14 cm, the ratio of ICP to superior vena pressure increases was reduced to one third. Conclusions If these results apply to humans, it was concluded that increases in ICP that accompany movement in tracheally intubated patients may arise from two complementary factors: (1) cerebrovascular dilation that correlates with electromyographic activity and is mediated by ascending neural pathways that transmit proprioreceptive information, and (2) passive venous congestion that results from any increase in central venous pressure. The influence of the latter factor can be reduced by elevating the head. (Key words: Blood pressure, venous pressure; mean arterial pressure. Muscle: afferent activity; electromyograms, skeletal. Neuromuscular relaxants: pancuronium.)

scholarly journals Comparison of Doppler Flow Tei-Indexes With Pulmonary Artery Thermodilution Measurement of Cardiac Output in an Experimental Porcine Model

2011 ◽  
pp. 483-492 ◽  
Author(s):  
J. KOBR ◽  
V. TŘEŠKA ◽  
J. MOLÁČEK ◽  
V. KUNTSCHER ◽  
V. LIŠKA ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Average Weight ◽  
Ventricular Afterload ◽  
Echocardiographic Examination ◽  
The Right ◽  
Right Ventricular Preload ◽  
Thermodilution Measurement

The objective of our study was to compare Doppler echocardiography imaging with pulmonary artery thermodilution measurement during mechanical ventilation. Total 78 piglets (6 weeks old, average weight 24 kg, under general anesthesia) were divided into 4 groups under different cardiac loading conditions (at rest, with increased left ventricular afterload, with increased right ventricular preload, and with increased afterload of both heart ventricles). At 60 and 120 min the animals were examined by echocardiography and simultaneously pulmonary artery thermodilution was used to measure cardiac output. Tei-indexes data were compared with invasively monitored hemodynamic data and cardiac output values together with calculated vascular resistance indices. A total of 224 parallel measurements were obtained. Correlation was found between values of right Tei-index of myocardial performance and changes in right ventricular preload (p<0.05) and afterload (p<0.01). Significant correlation was also found between left index values and changes of left ventricular preload (p<0.001), afterload (p<0.001), stroke volume (p<0.01), and cardiac output (p<0.01). In conclusion, echocardiographic examination and determination of the global performance selectively for the right and left ventricle can be recommended as a suitable non-invasive supplement to the whole set of methods used for monitoring of circulation and cardiac performance.

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