NAVA Normal ventilation varies considerably from breath to breath, but this is lost with traditional positive pressure ventilation Neurally adjusted ventilatory assist (NAVA) uses diaphragmatic electromyography to trigger ventilation in a more natural manner
NAVA NAVA is described as a mechanical ventilation method, controlled by brain signals (i.e. vagus nerve stimulation of the diaphragm), that might help patients in critical conditions by improving the interaction between the patient and the ventilator. The technology might also have the potential to avoid diaphragm disuse atrophy in critically ill patients.
NAVA The act of breathing depends on rhythmic discharge from the respiratory center of the brain. This discharge travels along the phrenic nerve, excites the diaphragm muscle cells, leading to muscle contraction and descent of the diaphragm dome. As a result, the pressure in the airway drops, causing an inflow of air into the lungs.
NAVA Conventional mechanical ventilators sense a patient effort by either a drop in airway pressure or a reversal in flow. NAVA created and used exclusively on the Servo I ventilator With NAVA, the electrical activity of the diaphragm (Edi) is captured, fed to the ventilator and used to assist the patient’s breathing. As the ventilator and the diaphragm work with the same signal, mechanical coupling between the diaphragm and the ventilator is practically instantaneous
NAVA NAVA created to increase triggering by enhancing sensitivity to hyperinflation, intrinsic PEEP and secondary triggering problems. No current evidence to show NAVA increases clinical outcomes Increased adaptation to varying patient trigger demands has been shown
NAVA SOME OF THE POTENTIAL BENEFITS Improved synchrony: In NAVA the ventilator is cycled-on as soon as neural inspiration starts. The level of assistance provided during inspiration is determined by the patient’s own respiratory center demand. The same applies for the cycling-off phase – the ventilator cycles off inspiration the instant it is alerted to the onset of neural expiration. By utilizing the Edi signal, maintenance of synchrony between the patient and the ventilator is improved.
Lung protection: With NAVA the patient’s own respiratory demands determine the level of assistance. NAVA gives the opportunity to avoid over or under assistance of the patient. Decision support for unloading and extubation: The Edi signal can be used as an indicator to set the support level from the ventilator, and to optimize unloading. As the patient’s condition improves, Edi amplitude decreases, resulting in a reduction in ventilator-delivered pressure. This pressure drop is an indicator to consider weaning and extubation. Patient comfort: With NAVA, the respiratory muscles and the ventilator are driven by the same signal. The delivered assistance is matched to neural demands. This synchrony between patient and ventilator helps minimize patient discomfort and agitation, promoting spontaneous breathing and possible reduced sedation.
NAVA With NAVA the patient’s own respiratory demands determine the level of assistance. NAVA gives the opportunity to avoid over or under assistance of the patient. The Edi curve and its associated value can thus be used as a powerful monitoring tool in all ventilation modes, providing information on Respiratory Drive, Volume requirements and the effect of the ventilatory settings, and to gain indications for sedation and weaning.
NAVA Edi signal (Electrical activity of diaphragm) can be used in any mode Can be used to assess respiratory drive, volume requirements and the effects of the vent settings The Edi catheter picks up an esphageal ECG which can be displayed on the Servo I screen
The decrease in pressure in this particular patient is clearly visible when switching from Pressure Support to Nava (shown in red). The green value shows respiratory rate.
NAVA NAVA is as straightforward to use The only equipment required in addition to a SERVO-i ventilator is NAVA software, an Edi module with cable and an Edi catheter. The same module can be used interchangeably with different SERVO-i units. The Edi Catheter also functions as a nasogastric feeding tube, and comes in dimensions ranging from 6Fr–16Fr to cover all patient categories from neonatal to adult.
The NAVA upgrade kit installs simply on all SERVO-I ventilator configurations and is fully interchangeable with all SERVO-i units. A range of Edi catheter sizes ensures optimized signal quality across all patient categories.
NAVA The NAVA Edi catheter is as simple to apply as any standard nasogastric tube. However, positioning of the Edi catheter takes on added importance to ensure a strong Edi signal and accurate readings. With the Edi catheter inserted and positioned, all that remains is to plug the Edi module into the SERVO-i and connect the Edi catheter to its outlet. The esophageal ECG now showing on the SERVO-i screen can help confirm proper Edi catheter positioning.
The Edi catheter is inserted to the measured depth and positioned correctly.
With the catheter properly positioned, a prominent P- wave should be visible in the uppermost channel with a continued decline of P-wave amplitude in the lower leads.
PulmoVista 500 EIT monitoring involves the application of a small current and measurement of resulting voltages to determine the ventilation related impedance changes that occur in a thoracic cross-section.
PulmoVista 500 Enables the assessment of regional ventilation distribution as well as short-term changes in end-expiratory lung volumes. You can see the effects of therapeutic manoeuvres and monitor the results over time. PulmoVista 500 helps you assess conditions such as atelectasis, over- inflation, air trapping, pleural effusion or pneumothorax may have on ventilation.
PulmoVista® 500 offers: – Continuous information about regional distribution of ventilation, displayed as images, waveforms and parameters – Trend display of regional distribution of ventilation – Trend display of changes in end-expiratory lung volume
4 hrs after recruitment The same tidal volume setting was used pre and post recruitment.
PulmoVista® 500 offers: Non-invasive tomographic monitoring The regional ventilation monitoring provided by PulmoVista 500 is non-invasive and without any side-effects. Unlike chest x-rays or CT, there’s no ionizing radiation involved. EIT involves minimal preparation so monitoring is established in just a few minutes. Patient preparation only requires the positioning of a flexible non-adhesive belt around the patient’s chest.
Liquid Ventilation Liquid ventilation (LV) is a technique of mechanical ventilation in which the lungs are insufflated with an oxygenated perfluorochemical liquid rather than an oxygen- containing gas mixture. The use of perfluorochemicals, rather than nitrogen, as the inert carrier of oxygen and carbon dioxide offers a number of theoretical advantages for the treatment of acute lung injury,
Liquid Ventilation Reducing surface tension by maintaining a fluid interface with alveoli Opening of collapsed alveoli by hydraulic pressure with a lower risk of barotrauma Providing a reservoir in which oxygen and carbon dioxide can be exchanged with pulmonary capillary blood Functioning as a high efficiency heat exchanger Despite its theoretical advantages, efficacy studies have been disappointing and the optimal clinical use of LV has yet to be defined
Liquid Ventilation Although total liquid ventilation (TLV) with completely liquid-filled lungs can be beneficial, the complex liquid-filled tube system required is a disadvantage compared to gas ventilation - the system must incorporate a membrane oxygenator, heater, and pumps to deliver to, and remove from the lungs tidal volume aliquots of conditioned perfluorocarbon (PFC). One research group led by Thomas H. Shaffer has maintained that with the use of microprocessors and new technology, it is possible to maintain better control of respiratory variables such as liquid functional residual capacity and tidal volume during TLV, than with gas ventilation Consequently, the total liquid ventilation necessitates a dedicated liquid ventilator similar to a medical ventilator except that it uses a breatheable liquid. (NON EXIST in USA)
Right heart effects of positive-pressure ventilation During inspiration, the positive intrathoracic pressure produced by a mechanical breath decreases venous return. An increase in intrathoracic pressure as small as 4 mm Hg is associated with a reduction in venous return by 50% for a transient period of time
Positive Pressure effects on Hemodynamics In individuals with normal cardiac function, venous return and subsequent cardiac output may be dramatically reduced with the institution of mechanical ventilation, particularly in individuals with coexisting hypovolemia or states that produce systemic vasodilation or relative hypovolemia, like septic shock In most instances, the consequences of reduced venous return are alleviated by intravenous fluid administration and adequate augmentation of blood volume Aggressive hydration during continuous positive- pressure ventilation restores atrial transmural pressure, plasma atrial natriuretic peptide concentrations, and renal function.
Positive Pressure effects on Hemodynamics Natural compensation for this hemodynamic response includes catecholamine release and secretion of arginine vasopressin and renin with subsequent increases in angiotensin II and aldosterone Natriuretic peptide hormone secretion is reduced with less cardiac chamber volume to stimulate hormone release. The net effect of these responses is sodium and water retention to support adequate preload and vasoconstriction to increase blood pressure.
Positive Pressure effects on Hemodynamics Angiotensin, a peptide hormone, causes blood vessels to constrict, and drives blood pressure up. It is part of the renin-angiotensin system, which is a major target for drugs that lower blood pressure. Angiotensin also stimulates the release of aldosterone, another hormone, from the adrenal cortex. Aldosterone promotes sodium retention in the distal nephron, in the kidney, which also drives blood pressure up.
Positive Pressure effects on Hemodynamics Patients with heart failure may actually improve cardiac function with the application of mechanical ventilation Reduction in venous return Unless optimally managed, patients with heart failure have a chronic increase in preload because of persistent stimulation of the renin angiotensin aldosterone system, reduction in natriuretic peptide release, and secretion of arginine vasopressin. Patients with heart failure also exhibit a perpetually elevated systemic vascular resistance partly because of chronic sympathetic nervous system activation. Application of mechanical ventilation reduces venous return and moderates the ventricular volume load. This reduced volume load will decrease ventricular wall tension and support the mechanical efficiency of the heart. Thus, in patients with heart failure, cardiac function may dramatically improve with the application of mechanical ventilation.
Positive Pressure effects on Hemodynamics Left heart effects of positive-pressure ventilation Several of the left ventricular effects of mechanical ventilation are directly attributed to alterations in right ventricular function, particularly the effects on left ventricular preload or end-diastolic volume Reduced venous return subsequently decreases the volume of blood the left ventricle receives. Thus, left ventricular preload is decreased and subsequent stroke volume and cardiac output are less. Increased right ventricular afterload and right ventricular dilation with shift of the interventricular septum reduces left ventricular chamber size, compliance, and filling, which also leads to reduced left ventricular preload
Positive Pressure effects on Hemodynamics Left ventricular preload may also be influenced by increased pericardial pressure Hyperinflated lungs directly compress the heart, reduce cardiac compliance, and lessen ventricular filling and end-diastolic volumes. These responses to mechanical ventilation all reduce left ventricular preload.
Positive Pressure effects on Hemodynamics Positive pressure mechanical ventilation also reduces left ventricular afterload or transmural pressure on inspiration and throughout the ventilatory cycle with the application of PEEP Transmural pressure is the pressure inside the ventricular chamber minus pressure outside the ventricle (intrathoracic pressure). Left ventricular transmural pressure is an indication of the pressure the ventricle must overcome to eject blood into the aorta. Positive intrathoracic pressure actually unloads the left ventricle by reducing transmural pressure. Consequently, the left ventricle is able to eject a greater stroke volume of blood with less pressure generation. Thus, myocardial oxygen demand is reduced and cardiac output improves. Patients with heart failure particularly benefit from mechanical ventilation by significantly increasing cardiac output with less myocardial oxygen consumption because of the combination of a reduction in ventricular volumes and a decrease in left ventricular afterload