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RVM shows promise to be a new clinical parameter of respiratory adequacy, providing an early indication of respiratory compromise and assisting clinical decision making regarding the necessity of intubation and earlier intervention. Use of RVM could improve resuscitation protocols and patient outcomes while reducing overall health care costs.
Home Circulation Vol. Free Access article. Tools Add to favorites Download citations Track citations Permissions. Jump to. Core 4. Originally published 26 Mar Circulation. Previous Back to top. Figures References Related Details. During spontaneous breathing, P PL becomes more negative in inspiration. RAP, measured relative to the atmosphere, drops during inspiration and creates a higher pressure gradient for venous return, resulting in higher venous return.
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Accordingly, in the new state the Starling curve is shifted to the left fig. Please keep in mind that RAP TM has actually risen if P PL has been transmitted to the right atrium — we describe the function curves from a perspective outside the thorax [ 62 ]. The opposite will happen with mechanical ventilation. P PL increases with mechanical inflation of a tidal volume and is partially transmitted to the right atrium whose intracavitary pressure rises dark red dot; the transmural pressure actually falls.
The Starling curve is shifted to the right red dotted line , cardiac output and venous return decrease. Under mechanical ventilation, right ventricular preload is mainly affected by changes in P PL , whereas left ventricular preload is mainly affected by changes in P TP [ 80 ]. The same graphical analysis can be used to assess volume responsiveness.
An increase in cardiac output is considered a positive response to a volume challenge. Rapidly infusing a crystalloid solution will elevate MSFP and shift the venous return curve to the right fig. A heart with the intersection RAP of the venous return curve and the Starling curve in the steep part of Starling curve red dotted line will exhibit a profounder positive response to a volume challenge than a heart with the intersection in the flat part green dotted line. In the latter case, the volume challenge produces a considerable increase in RAP with hardly any increase in venous return or cardiac output.
It should be kept in mind that a healthy heart normally works on the steep part of the Starling curve. Volume responsiveness is therefore a normal phenomenon. The explanation is often right ventricular failure [ 82 ]. Afterload is defined as the force opposing ventricular ejection of blood [ 83 ]. Afterload can be approached by assessing ventricular wall tension or vascular resistance and impedance [ 84 ].
In order to account for the differences in geometry and muscle mass and different functions of the right and left ventricles, we discuss afterload separately for the two ventricles. The left ventricle has to generate high pressures for pulsatile ejection of blood into the arterial system. In the absence of left ventricular outflow tract obstruction or aortic valve stenosis the load on the ventricle is determined by the arterial vasculature.
The stiffer the aorta, as, for example, in older hypertensive subjects, and the higher the arterial resistance, the bigger the work the left ventricle has to deliver to maintain a certain cardiac output. P TM of the left ventricle and, to a lesser extent, of the intrathoracic part of the aorta, fall while P TM in the abdominal aorta remains higher, resulting in a net afterload reduction and facilitating blood flow from the intrathoracic to the abdominal compartment.
This seems to be mainly mediated by changes in P PL [ 80 ]. With left ventricular afterload reduction, application of continuous positive airway pressure CPAP in spontaneously breathing patients, or pressure support ventilation with PEEP in sedated patients, can be a valuable supportive measure in the treatment of acutely decompensated left ventricular failure [ 86 ].
Whereas the left ventricle pumps blood into a high pressure system with low compliance, the right ventricle ejects the same amount of blood into the highly compliant pulmonary vasculature at low pressures. The right ventricle serves, therefore, more as a flow generator than a pressure generator [ 87 , 88 ]. Alterations in right ventricular outflow are mainly mediated through changes in ITP [ 80 , 89 ].
ITP changes can strongly affect transmural pulmonary vascular pressure and PVR, and thereby right ventricular afterload. Since the right ventricle works as a pulsatile pump and the pulmonary vasculature is highly distensible, the pulmonary vascular elastance or impedance seems a more accurate measure of right ventricular afterload [ 90 , 91 ].
During spontaneous breathing, inspiration associated with negative P PL distends the pulmonary vasculature and therefore reduces right ventricular afterload. During mechanical ventilation, tidal breathing increases P PL , reduces transmural pulmonary vascular pressure and consequently elevates right ventricular afterload.socialdash.inspired.lv/24195.php
Right ventricular afterload is highly sensitive to cyclic tidal inflation with positive pressure, and for this reason mechanical ventilation may elicit right ventricular failure, especially in individuals with pre-existing right ventricular dysfunction or severe hypoxic pulmonary vasoconstriction in the context of ARDS [ 80 , 89 , 92 — 95 ]. Acute elevations of afterload are poorly tolerated by the right ventricle as compared with the left ventricle, which possesses much higher contractile reserves [ 96 ].
The heart chambers lie within the pericardium, limiting the total blood volume that the heart as a whole can contain [ 19 , 22 , 88 ]. The right and left ventricles differ greatly in their anatomical structure and mode of operation. The left ventricle is spherical, with a helical arrangement of muscle fibres from the apex to the base and obliquely oriented muscle fibre bundles from the inside to the outside, which allows the generation of high pressures with good efficiency [ 97 — 99 ].
The right ventricle is partially wrapped around the left ventricle. Its anatomy, with a thin free wall, is not suitable for efficient work at high pressures, but is adapted to the low resistance pulmonary vasculature [ 88 ]. Contraction of the interventricular septum, which mostly consists of muscle fibres attributed to the left ventricle, substantially supports right ventricular ejection [ , ]. This evident structural dependency of the two ventricles is clinically relevant.
Dyssynchronous or absent contraction of the septum, as with left bundle-branch block, with right ventricular pacing or following myocardial infarction, will affect the performance of not only the left but also the right ventricle [ — ]. The right and left ventricles work as serial pumps connected by the pulmonary and systemic vasculature.
Through their electrical and mechanical synchronisation, they work in parallel within the pericardial confinement. Right ventricular stroke volume is ejected into the pulmonary vasculature and provides the left ventricular preload; hence, the left ventricle can only be as good as the right ventricle [ 87 ].
However, beyond this sequential dependency, there is also a parallel mechanical coupling of the ventricles referred to as ventricular interdependence [ ]. Because of the shared septum and the pericardial constraint, the diastolic pressure of one ventricle directly effects the diastolic filling of the other [ ]. When right ventricular volume is increased, left ventricular filling declines.
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This phenomenon can be observed in situations with right ventricular afterload elevation e. Even in healthy individuals, spontaneous respiration affects ventricular filling to a small extent, but forced breathing efforts can make ventricular interdependency overt. Under normal circumstances, end-diastolic ventricular volume EDV and pressure EDP change in opposite directions in the left and right ventricle during the respiratory cycle. Undulating ventricular filling during respiration results in changing stroke volumes of the left and right ventricles with each heartbeat, again in opposite directions.
On average, the sum of stroke volumes of the right ventricle equals left ventricular output, but beat by beat stroke volumes vary with the respiratory cycle.
This is possible because the pulmonary vasculature and venous capacitance vessels are very compliant and able to transiently accommodate volume surplus [ ]. Important clinical examples of interventricular dependence are pericardial tamponade or status asthmaticus with an exaggerated inspiratory drop in peripheral arterial pressure pulsus paradoxus during spontaneous respiration.
This drop in arterial pressure is caused by a sudden increase in right ventricular EDV during inspiration that impairs left ventricular filling and stroke volume. The complex physiology of cardiopulmonary interplay makes heart-lung interactions ever present in the ventilated patient. They are clinically relevant because mechanical ventilation can provoke cardiovascular instability [ ] and heart-lung interactions offer possibilities to predict reactions of the cardiovascular system to treatment modalities, especially volume expansion, within the framework of functional haemodynamic monitoring [ ].
The right ventricle is particularly strained by mechanical ventilation, as venous return and its preload are reduced, mediated by elevation of P PL , while afterload is mechanically increased as reduction of the P TM of the pulmonary vasculature increases resistance [ 89 ]. In patients with ARDS, these effects are aggravated by hypoxic or hypercapnic pulmonary vasoconstriction, pulmonary microthrombosis, changes in West zones and lung derecruitment [ ], all leading to pulmonary hypertension and a worse prognosis [ ].
The risk for developing acute cor pulmonale becomes higher with worse oxygenation, hypercapnia, high ventilator pressures and pneumonia as the cause of ARDS [ ]. Prone positioning can lead to improved right ventricular function via recruitment of dorsal lung areas and vasculature, resulting in reduced right ventricular afterload [ , ]. Mechanical ventilation is a lifesaving procedure in ARDS. Besides the negative effects discussed, it may improve pulmonary vasoconstriction by improving gas exchange and recruitment.
The effects of mechanical ventilation are often unpredictable and highly dynamic. The ventilator strategy should not be set by guidelines or gas exchange alone, but needs to take into account right ventricular function in order to determine the optimal cardiopulmonary functional state. Ventilated patients prone to right ventricular failure need advanced monitoring in order to recognise cardiopulmonary deterioration early. An arterial and central venous line are mandatory.
Clinical awareness of right ventricular failure needs to be high. Measurements of mixed venous oxygenation allow assessment of pulmonary shunting and adequacy of oxygen delivery despite impaired oxygenation through the lung [ ]. Optimal lung recruitment can lower right ventricular afterload and improve oxygenation, and can be optimised by measuring oesophageal pressure as a surrogate of P PL [ ].
Patients with exacerbations of COPD or status asthmaticus are also prone to develop acute cor pulmonale during mechanical ventilation. The high C L facilitates pressure transmission from the lung to the pulmonary vasculature. The high airway resistance leads to incomplete exhalation with air trapping, dynamic overinflation and auto-PEEP [ , ], resulting in reduced right ventricular preload and elevated afterload. Auto-PEEP is primarily independent of mechanical ventilation and is caused by the narrowed airway and tachypnoea.
It can be minimised by careful ventilator settings. Low tidal volume and low respiratory rates with small inspiration to expiration ratios may prevent auto-PEEP. Often, sedation and tolerance of respiratory acidosis are necessary and monitoring of cardiopulmonary function is needed as described for ARDS. Recognition of right ventricular failure and afterload dependence during mechanical ventilation is of paramount importance, as it can lead to left ventricular preload dependence with pulse pressure variation PPV, see below [ , ]. In such a context, volume therapy may be detrimental owing to ventricular interdependence if the cause PPV is not carefully looked for.
The extent of heart-lung interactions and cardiovascular compromise is comparable between different modes of ventilation, in the case of similar mean airway pressures and tidal volumes [ — ]. We have recently shown beneficial effects on right ventricular function for neurally adjusted ventilatory assist [ 92 ] in comparison with pressure support ventilation for patients at the transition from controlled to assisted ventilation.
Heart-lung interactions have been used for preload assessment based on dynamic indices in three different approaches: i PPV and its variants, ii echocardiographic assessment of the caval veins, iii estimation of MSFP with ventilator manoeuvres. Volume therapy must be guided by clinical signs of inadequate tissue perfusion, such as low urinary output, altered mentation, clammy periphery and mottled skin, elevated lactate levels and the need for vasopressor agents.
Positive indicators of fluid responsiveness do not justify fluid therapy by themselves [ ]. Even though central venous pressure itself is a bad indicator of volume responsiveness [ ], observing its reaction to a volume bolus holds valuable information about the ability of the right heart to handle volume expansion, similar to the hepatojugular reflux test. The cyclic change in P PL during respiration causes RAP to rise during mechanical inspiration and fall with exhalation fig. Venous return and right ventricular stroke volume therefore drop with mechanical inspiration and rise with exhalation.
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