a. Inspiratory termination ends when the inspiratory time is up.

b. Current goes to zero before inspiration ends. The pressure remains constant during the set inspiratory period. Since the pressure-controlled mode is a time-cycle mode, the current will decrease to zero just before or after the inspiratory time runs out. The tidal volume delivered depends on the characteristics of the lung.

        Functional Residual Capacity

It is the lung volume at the moment when the forces that force the lungs to come back and the forces of the chest wall trying to keep the lungs open are in balance. The pressure at this point is called distending pressure.

        Pressure-Volume Cycle

Cdinamik toatal = ΔTidal volume / ΔPressure

Expiratory infection: sudden alveolar degree

Inspiratory infection: sudden alveolar recurrence

It is generally elliptical. The upper point (x) of the ellipse gives the total dynamic compliance. It is found by dividing the volume at this point by pressure (Tidal volume / Ppeak) (if there is no PEEP).

Expiratory And Inspiratory Infection Points

 Each cycle has at least two infection points (inspiratory and expiratory), but can be more. A decrease in FRK causes a decrease in distending pressure. The reduction in distending pressure decreases functional residual capacity and compliance, thereby increasing respiratory work. Airway obstructions reduce maximal expiratory flow. Insufficient expiratory time and early closure of small airways cause air arrest.

        Mean Airway Pressure (Pmean)

 In normal spontaneous breathing, intrathoracic pressure is negative throughout the breathing cycle. Intrapleural pressure ranges from -5 (in expiratory) and -8 (in inspirium) cmH2O. Alveolar pressure varies between +1 (in expiratory) and -1 (in inspirium) cmH₂O. The decrease of intrapleural pressure during inhalation facilitates lung inflation and venous return. The maximal static transpulmonary pressure (= intraalveolar pressure - intrplevral pressure) that may occur during spontaneous inspirium is 35 cmH₂O. In positive pressure ventilation, intrathoracic pressure increases in inspirium and decreases in expiratory. If the expiration time is too short or if the alveolar pressure is too high in the expiration, venous return decreases.

Pmean is the average pressure applied to the airways during the ventilatory cycle. It relates to the size and duration of the pressure applied. Influencing factors:

a. Inspiratory pressure level: The mean pressure increases as the peak pressure increases. In volume cycle ventilation, the peak pressure adjusted tidal volume, inspiratory flow, resistance, compliance and PEEP affect. Peak pressure is set in ventilation with pressure cycle.

b. Expiratory pressure level: The airway pressure during expiration is determined by PEEP.

c. I / E ratio: mean pressure increases as inspiratory time increases. End-inspiratory hold mean increases pressure.

d. If inspiratory pressure is kept constant and inspiratory flow is increased, mean pressure increases.

e. Square wave current creates more mean pressure than descending ramp currents.

Shunt (perfusion-free ventilation):

Total shunt = capillary shunt + anatomical shunt

Blood passing through the capillary shunt nonventile area (atelectasis, ARDS, Pneumonia)

Anatomical shunt: Blood bypassing the lungs (congenital heart disease, deep bronchial veins pouring into pulmonary veins, thabesian circulation of the heart)

Inspiratory pressure that exceeds the opening pressure of the alveolar opening in the inspiration and the application of more pressure than the closing pressure of the alveoli at the end of expiration reduces the shunts by preventing the collapse of the alveoli. However, overdistation in a region may direct the blood flow to nonventile areas from here and cause the shunt rate to increase. Positive pressure ventilation can reduce the rate of capillary shunt while increasing pulmonary vascular resistance and increasing blood flow through anatomical shunts. Mean pressure should be kept as low as possible in the presence of anatomic right-left shunt.

As with airway diseases, poor distribution of ventilation causes the relative shunt effect:

a. Some alveoli are relatively less ventilated than perfusion (shunt-like effect and low V / P ratio)

b. Some alveoli are more ventilated than perfusion (dead space effect, high V / P ratio)

       Ventilation

It is the inward-outward movement of gas within the lungs.

Minute ventilation (VE) = tidal volume (Vt) x frequency

VE = dead space ventilation (VD) + alveolar ventilation (VA)

VD / Vt ~ 1/3

                                                               i. dead space: ventilation without perfusion

                                                             ii. anatomical dead space: volume of transmitting airways (~ 2 ml / kg)

                                                           iii. alveolar dead space: conditions that reduce pulmonary perfusion

                                                           iv. mechanical dead space: this is the breathing volume of the breathing circuit, increasing the anatomical dead space.

Since the anatomical dead space is constant, low tidal volume increases the dead space fraction and reduces alveolar ventilation. That is, a decrease in tidal volume increases the dead space ratio (VD / Vt). Increased dead space fraction in this case requires more minute ventilation for continuity of alveolar ventilation.

The required ventilation level depends on the intended PaCO2, alveolar ventilation and CO2 production .;

PaCO2 α CO2 production (VCO2) / VA

PaCO2 = (VCO2 x 0.863) / (VE x [1 - VD / Vt])

Mechanical ventilation can produce alveolar dead space effect with alveolar overdistension. Mechanical ventilation can increase anatomical dead space by creating distention in the airways.

Alveolar overdistension causes barotrauma. Alveolar rupture air enters the bronchovascular sheath;

a. pulmonary interstitial emphysema

b. systemic air embolism

c. pneumomediastinum

d. A pneumothorax

e. pneumopericardium

f. pnomoretroperitoniu

g. pneumoperitoneum

h. It can cause subcutaneous emphysema.

        Ventilator Induced Lung Injury (Vili)

 High peak inflation volumes (volutrauma) cause alveolar overdistension. Alveolar overdistension is associated with high alveolar pressure. Since localized overdis- tations are difficult to monitor, overdistation is estimated from peak alveolar pressure (end-inspiratory plateau pressure). Pplato should be kept below 30 cmH2O, and alveolar overdistension can be minimalized with low tidal volume (6ml / kg).

VILI may also occur due to alveolar collapse (atelectasis). The pressure on the contact surfaces of open and collapsed alveoli can reach 100 cmH₂O. Cyclic opening and closing of the alveoli is harmful and can be prevented by providing optimal recruitment and avoiding degree growth.Alveolar overdistention and degree enhances inflammation in the lungs (biotrauma). Inflammatory mediators (cytokines, chemokines) can switch to the pulmonary circulation and cause SIRS.

        Ventilator Induced Pneumonia (Vip)

 The agent is usually Gram - bacteria originating from the oropharynx and gastrointestianal system. Frequent replacement of ventilator circuits does not affect VIP development, while ulcer prophylaxis, subglottic aspiration, cuff pressure (20-25mmHg) that prevents aspiration, and elevation of the head reduce VIP frequency.

       Hyperventilation

 Barotrauma causes VLI, causing overdistension. Overdistation lowers cardiac output. Respiratory alkalosis hypokalemia caused by hyperventilation causes lowering of ionized calcium and separation of oxygen from hemoglobin (left shift). Hyperventilation lowers arterial carbon dioxide pressure in COPD and causes alkalinity of blood pH.

        Hypoventilation

 50-70 mmHg arterial partial oxygen pressure and blood pH above 7.2 are generally well tolerated.

Oxygen Toxicity

 FiO2 values higher than 0.6 for a period longer than 48 hours should be avoided. The lowest FiO2 (<0.6) that will hold PaO2 between 60-80 mmHg should be targeted. The oxygen-related sebaceous radicals cause ultrastructural changes in the lung tissue.High PaO2 values increase partial arterial carbon dioxide pressure due to Halden effect (carbon dioxide is separated from hemoglobin), blood flow to low ventilated areas due to inhibition of hypoxic pulmonary vasoconstriction and inhibition of ventilation.

Cardiac Effects

 Increased mean airway pressure and lung compliance and hypovolemia lowers cardiac output. Increasing intrathoracic pressure decreases venous return and reduces right heart filling pressure. The increased alveolar pressure in positive pressure ventilation increases the transpulmonary pressure, thereby increasing pulmonary vascular resistance, thereby decreasing left ventricular filling pressure and increasing right ventricular afterload, thereby assisting interventricular septal cipher. It decreases.

  In positive pressure ventilation, decreasing cardiac output and atrial natriuretic peptide and increasing antitidiuretic hormone decrease urine flow. Cuff leak and aerophagia cause meteorism.

        Nutrition

 In malnutrition, respiratory muscles break down, the risk of pulmonary infection and edema increases. In overfeeding, the need for ventilation increases.

Excessive daytime insomnia and cognitive impairment cause delirium, patient ventilator dissynchronization and sedation-related ventilator dependence.

 Causes of patient ventilator dissynchronization:

                                                               i. poor trigger sensitivity

                                                             ii. incorrect inspiratory flow and time setting

                                                           iii. inappropriate tidal volume

                                                           iv. inappropriate mode

                                                             v. otopeep

        Barotrauma

 Tearing of the alveolar capillary membrane causes dissection of air in the facial plane and accumulation in the pleural and other cavities. Although barotrauma is thought to be related to high alveolar pressure, it should not be forgotten that the volume and pressure causing barotrauma are patient-specific.

        Volutrauma

 Early ARDS-like table occurs.

                                                               i.      Alveolo-capillary membrane permeability increases

                                                             ii.      Pulmonary edema development increases

                                                           iii.      Neutrophils and proteins accumulate in alveoli

                                                           iv.      Surfactant construction decreases

                                                             v.      Hyalen membrane development increases

Pulmonary compliance decreases

it called on to be the primary cause of overdistansiyon. The risk of VILI increases when the plateau pressure is above 30 cm H2O.

 If there is overdistation in a lung unit, the transpulmonary pressure is high (intra-alveolar pressure-non-alveolar pressure). As the difference between alveolar and pleural pressures increases, distension of the lungs increases. The chest wall plays an important role in determining alveolar overdistension pressures. As the chest wall compliance increases, the transpulmonary pressure increases and the volume of the lungs increases for the given unit pressure.

Transpulmonary pressure = alveolar pressure - pleural pressure

When the chest wall is solid (abdominal distension excess fluid resuscitation, deformity, etc.), transpulmonary pressure drops. So that a higher pressure is combined with an alveolar less alveolar distension. The solid chest wall does not allow overdistation, protecting the lungs from VILI. In these cases, plateau pressures of more than 30 cm H2O can be applied with less risk.

       Atelectotrauma

 Cyclic opening and closing of unstable atelectatic alveoli is the cause of VILI. It is the stress that occurs between alveoli, the mechanism of which is stable and not. Stress pressure exceeding 100 cmH2O occurs on the surface of the alveolar when tension pressure of 30 cm H2O is applied.

Biotrauma

 Overdistension, cyclic opening and closings would be attempted by the release of proinflammatory mediators. As a result, pulmonary edema, neutrophil accumulation increases, and vascular smooth muscles relax. PEEP protects from inflammatory damage. With proper PEEP and low tidal volume, bacterial translocation from the lungs is reduced.High vascular volume, rapid respiratory rate, and high body temperature also increase the risk of VILI. To protect from VILI, the tidal volume should be 4-8 ml / kg, the plateau pressure should be less than 30 cm H2O and the degree should be prevented by PEEP (10-15 cm H₂O).