what is intrathoracic pressure

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The heart and lungs work closely to meet the oxygen needs of the tissues. If the balance between oxygen demand and supply is disturbed during a critical illness, tissue hypoxia and cell death can rapidly occur. An essential part of critical care is maintaining cardiopulmonary function through medication, fluid management, and respiratory support. Paradoxically, interventions that improve the function of one system can sometimes have undesirable effects on another, and although the pulmonary impact of heart disease is well known, The impact of changes in pulmonary physiology on cardiac function has been less well appreciated.

What Is Intrathoracic Pressure

Cardiopulmonary interactions (circulatory effects of spontaneous and mechanical ventilation) were first documented in 1733, when Stephen Hales showed that blood pressure in healthy subjects decreased with spontaneous inspiration.1Read More A century later, Kussmaul described the pulse paradox (not breathing). radial pulse) in patients with tuberculous pericarditis.2

Intrathoracic Pressure Regulation Therapy Device May Help Save Lives On The Battlefield > Joint Base San Antonio > News

Cardiopulmonary interactions occur in health and can be exaggerated or abnormal in disease. This article provides an overview of this broad topic. By emphasizing the underlying physiological principles and the influence of disease status on these, we hope that respiratory support will then be tailored to the individual patient.

Spontaneous and mechanical ventilation induces changes in pleural or thoracic pressure and lung volume, which can independently affect key factors of cardiovascular function: atrial filling or preload; ventricular emptying impedance or afterload; heart rate and myocardial contractility. Changes in thoracic pressure are transmitted to the internal structures of the chest: namely the heart and pericardium, the great arteries and veins. Spontaneous inspiration causes a negative pleural pressure and a decrease in thoracic pressure is transmitted to the right atrium. In contrast, intermittent positive pressure ventilation (IPPV) increases inspiratory pressure and thus right atrial pressure (P

), and if positive expiratory pressures (PEEP) are added, these pressures remain greater than atmospheric pressure throughout the respiratory cycle. In addition, changes in thoracic pressure and lung volume may be of other significance in patients with interstitial or vascular lung disease or congenital heart disease, all of which are seen quite frequently in children. .

Cardiovascular effects of intrathoracic pressure changes

Constrictive Pericarditis & Severe Mitral Regurgitation

The Valsalva phenomenon, a physiological response to a persistent increase in airway pressure when the larynx is closed, is characterized by an early rise in arterial pressure and a decrease in cardiac output due to decreased venous return. Although the Valsalva phenomenon is not an exact physiological "model" of PPV, it clearly demonstrates the important effect of increased thoracic pressure on the right heart. One of the first and most important physiological studies on the effects of PPV on cardiac function was by Cournand's group, who in the late 1940s demonstrated variable decreased cardiac output in healthy volunteers. strongly received "masked" PPV.3 4 Cournand showed that the right ventricle (RV) is inversely proportional to thoracic pressure, and as this becomes more aggressive, the RV preload decreases, causing a possible decrease detected in cardiac output.

View the circulation as a three-chamber model (Figure 1): thoracic, abdominal, and peripheral, where P

Thoracic pressure directly affects intra-abdominal pressure, lowering the diaphragm and peripheral venous pressure in relation to barometric pressure.5 P

Decreases during inspiration and intra-abdominal pressure increases as the inspiratory diaphragm descends, while peripheral venous pressure remains constant throughout the respiratory cycle. Systemic venous return, which is often the major contributor to cardiac output, depends on the pressure difference between the extrathoracic veins (push pressure) and P.

Ventilation In Patients With Intra Abdominal Hypertension: What Every Critical Care Physician Needs To Know

(back pressure). Spontaneous inspiration increases this gradient and thus accelerates venous return. Thus, RV preload and stroke volume both increase during spontaneous inspiration2 (or even negative pressure6-8). In contrast, increasing P

During the Valsalva or positive pressure maneuver, inspiration slows venous return; therefore, RV preload and thus cardiac output may decrease as thoracic pressure becomes more positive.9 10 PEEP prevents intrathoracic pressure from returning to barometric pressure during expiration, and to a level sufficient to May decrease cardiac output during the respiratory cycle. 11 12

Circulatory model showing factors affecting systemic venous outflow. Right heart (RH) and great intrathoracic veins are exposed to pleural pressure (P

), changes throughout the respiratory cycle. Intra-abdominal pressure increases as the inspiratory diaphragm descends and normalizes to barometric pressure (P

How We Breathe

) expired. The peripheral venous pressure is unaffected by respiration so it remains at atmospheric pressure throughout the respiratory cycle. Systemic venous drainage (broken arrow) depends on the pressure difference between the great extrathoracic veins (EGV) and the right atrium, so during spontaneous breathing it is maximized during Inspiratory inspiration as pleural (and right atrium) pressure decreases and intra-abdominal (and thus EGV pressure) increases.

Cournand proposes the following strategies to protect the cardiovascular system in PPV: the maximal pressure rises slowly during inspiration should decrease rapidly afterwards; The mean "mask pressure" should be as close to atmospheric pressure as possible, and the exhalation time should be at least equal to the inhalation time. If we apply these principles, the body's baroreceptor response, in which the sympathetic system responds by increasing heart rate, systemic vascular tone, and myocardial contractility, can often be minimized. Cardiovascular injury due to changes in thoracic pressure in PPV.13

Clearly, there are a number of clinical situations in which the impact of positive intrathoracic pressure can exert a major influence on cardiac output by preventing venous return. These include hypovolemia, septic shock, gas accumulation associated with obstructive airway disease, and obstructive lesions of the right heart with pulmonary venous involvement. In these situations, we usually compensate by using right cardiac volume loading to increase venous return,11 12 cautiously use α-adrenergic agonists or inotropes and minimize the effects of positive intrathoracic pressure using the ventilation strategies recommended by Cournand 50 years ago. .

To understand the complex effects of changes in intrathoracic pressure on the left ventricle (LV), it is necessary to understand the concept of transmural pressure (the difference between the pressure inside the ventricles or blood vessels and the pressure inside the ventricles). power around it). When we invasively monitor peripheral arterial pressure, we measure intravascular pressure relative to barometric pressure. However, the thoracic aorta, located in the thorax, is subject to changes in pleural pressure rather than atmospheric pressure. Trans-wall pressure (P

Ventilation And Cardiovascular Support: The Heart Lung Connection

Aorta) is therefore the difference between intravascular pressure and pleural pressure (P

And decreased aortic intravascular pressure, but the decrease in pleural pressure was more proportional than the decrease in aortic pressure. So, P.

Actually increase, increase LV afterload and decrease LV stroke volume. The effect of spontaneous and negative pressure breathing on LV afterload is negligible in healthy and functional patients when right-heart effects predominate. However, in patients with acute asthma or in children with acute airway obstruction, the inspiratory pleural pressure was significantly negative and the LV afterload increased significantly. In this situation, a minimal negative "oscillation" in thoracic pressure can cause a sudden increase in afterload and lead to pulmonary edema even in a previously healthy heart.14 15

Changes in thoracic pressure can also have clinically significant effects on LV afterload in patients with heart failure. Negative fluctuations in intrathoracic pressure16 17 – eg, in the Mueller maneuver (closed glottis) or PPV interruption 18 can cause acute afterload if LV function is poor. Conversely, PPV and PEEP can reduce or correct "negative inspiratory fluctuations" in thoracic pressure and, by reducing afterload, potentially return hemodynamics to a more favorable position in the curve. Starling.19

Optimizing The Respiratory Pump: Harnessing Inspiratory Resistance To Treat Systemic Hypotension

Pulmonary vascular resistance (PVR) is a major determinant of RV afterload and is directly affected by changes in lung volume.20 Total pulmonary vascular resistance depends on two of its components, vascularity. lungs and extra-alveolar or parenchymal blood vessels. PVR can be increased at both poles of lung volume (Figure 2).21 When the lungs are inflated above functional residual capacity (FRC), alveolar blood vessels are compressed due to alveolar distension. As lung volume decreases from FRC to residual volume, two events can occur, both of which can independently increase PVR. First, the extra-alveolar blood vessels become increasingly tortuous and tend to collapse. Second, and perhaps more importantly, end-stage airway collapse when lung volumes are low can cause alveolar hypoxia, and at oxygen pressures less than 60 mm Hg, this leads to pulmonary vasoconstriction. lack of oxygen.

Schematic representation of the relationship between lung volume and pulmonary vascular resistance (PVR). As lung volume increases from residual volume (RV) to total lung capacity (TLC), alveolar blood vessels become increasingly compressed.