Respiratory Monitoring

Crs=Vt/Paw-(PEEP+PEEPi)

C_dyn =  Vt/Pmax

dynamic compliance also includes the resistive (flow-dependent) component of the airways and the endotracheal tube

(erster Abfall von Pmax bis P1)

C_stat =  Vt/P2

P2 wird auch Pplat genannt

=  mirrors the elastic features of the respiratory system

Resistance is defined as Pressure divided by Flow V

Pmax – P1/V=airway flow-dependent resistance = ‘initial’ or ‘minimal’ or ‘ohmic’ resistance R_RS,init

P1 – P2/V=additional lung resistance (ΔRrs) =Pendelluft phenomenon and the visco-plasto-elastic lung and thorax behaviour

Pmax – P2/V= the sum of R_RS,init and ΔRrs.

In clinical practice, it is important to remember that the Pmax – P1 pressure gradient is flow-dependent,

whereas P2 is affected only by variations in volume and/or compliance.

Annäherungsweise über Oesophagealdruck

CL = Vt/(PAO − Pes) end-inhalation − (PAO − Pes) end-exhalation
Ccw = Vt/(Pes − Patm) end-inhalation − (Pes − Patm) end-exhalation

Wobei PAO=pressure at Airways opening

Bei ARDS ist Cl erhöht 

bei erhöhtem intraabd. Druck ist Ccw erhöht.

WOB performed by the ventilator (Wvent): measurements taken from the signals of Paw and respiratory system volume change (Vol).

work performed by the patient (Wpat).  measurement of the pressure changes generated by the respiratory muscles. Wpat can be calculated from measurements of Pes and Vol.

WOB performed by the ventilator (Wvent): measurements taken from the signals of Paw and respiratory system volume change (Vol).

work performed by the patient (Wpat).  measurement of the pressure changes generated by the respiratory muscles. Wpat can be calculated from measurements of Pes and Vol.

work = force x distance ≈ pressure x volume / 2 (Joules )
elastic work ∝ area a-b-c-a
inspiratory flow-resistive work ∝ area a-i-b-a
expiratory flow-resistive work ∝ area a-b-e-a
negative work ∝ area a-e-b-c-a (tone on inspiratory muscles during expiratory air flow)
total work ∝ Welastic + Winspiratory flow-resistive + Wnegative
passive recoil of lungs overcomes the work of expiratory flow-resistance

 is a transient increase in transpulmonary pressure intended to promote reopening of collapsed or flooded alveoli.

A sustained pressure above the range of tidal ventilation is applied, and PEEP is used to prevent derecruitment.

The result should be an increase in FRC/EELV

• Sustained high-pressure inflation of 40 cmH₂O for 40 seconds using CPAP.
• Intermittent sighs, using three consecutive sighs at 45 cmH₂O per minute for 1 hour.
• A stepwise (‘ramping’) increase in PEEP every 2 min, keeping the driving pressure constant, up to peak pressures of 45–50 cmH₂O.
• Pressure-controlled ventilation (PCV) with PEEP of 25 to 30 cmH₂O and peak inspiratory pressure of 40 to 45 cmH₂O for 2 min.

• Messung des Lungenvolumens über moderne Respiratoren
• im CT
• FRC/endexp. Lungenvolumen EELV durch N2-Washout
• EELV = ΔN₂ (ml)/ΔFiO₂

Oesophagealer Druck entspricht alveolärem Druck=PEEP=transpulmonaler Druck

Wenn der alveoläre Druck bekannt st, kann PEEP daran angepasst werden

assess the level of PEEP required to avoid over-distension. This approach uses the shape of the pressure-time curve during tidal volume delivery. Worsening compliance as the lungs are inflated (upward concavity; stress index, >1) suggests over-distension, and the recommendation is to decrease PEEP. Improving compliance as the lungs are inflated (downward concavity; stress index, <1) suggests tidal recruitment and potential for additional recruitment, thus suggesting that increased PEEP might be beneficial

assess the level of PEEP required to avoid over-distension. This approach uses the shape of the pressure-time curve during tidal volume delivery. Worsening compliance as the lungs are inflated (upward concavity; stress index, >1) suggests over-distension, and the recommendation is to decrease PEEP. Improving compliance as the lungs are inflated (downward concavity; stress index, <1) suggests tidal recruitment and potential for additional recruitment, thus suggesting that increased PEEP might be beneficial

Staphylokokken: koagul.neg.: St.aureus

                               koagul.pos.:epididermidis+saprophyticus

Streptokokken

Enterokokken

Clostridien

Listerien

Corynebakterien

Pseudomonas

Enterobacteriacea (e.coli, Enterobacter, citrobacter, Salmonellen)

Acinetobacter

Vibro

When patients begin to breathe spontaneously, intrathoracic pressure becomes negative. The consequence is that venous return and left ventricular afterload increase.

gar nicht: Anaemia does not affect the SaO₂, but only the oxygen content.

in Hämoglobin gebundenes O2 und physikalisch gebundenes O2

(SaO₂ × Hb × 1.34) + (0.003 × PaO₂ in mmHg)

  %           g/dl

1.34= Sauerstoffbindungskap.

0.003= Milliliter Sauerstoff, die in 100 mL plasma bei 0.135 kPa (1 mmHg) PaO₂ gelöst sind

Normal arterial oxygen content is approximately 16 to 20 ml O₂/100 mL blood

a decrease in PaO₂

Hypoxaemia has a relatively minor impact on arterial oxygen content if the accompanying change in SaO₂ is small. PO₂ influences blood oxygen content only to the extent that it influences the saturation of haemoglobin with oxygen.  SaO₂ is a more reliable index of arterial oxygen content than PaO₂. The influence of anaemia relative to hypoxaemia on arterial oxygen content is relatively greater.

CaO2 + DO2 (Delivery, Angebot)

Cardiac index x CaO2

DO₂I = 3 × (1.34 × Hb × SaO₂) × 10(=unrechung Hb)     (presuming CI = 3 L/min/m²)

Normal range: 450−550 mL/min/m²

the deprived cells must shift from aerobic to anaerobic metabolic pathways to supply their energy needs, leading to progressive lactic acidosis.

by indirect calorimetry:

a technique that uses continuous analysis of inhaled and exhaled gas flows together with oxygen and carbon dioxide concentrations to calculate VO₂ and CO₂ production (VCO₂).

VO₂ ist die Differenz zwischen dem Produkt des inp.Volumens x FiO2 und dem expiratorischen Minutenvolumen x ausgeatemten Sauerstoffanteil

VO₂ = (Vi × FiO₂) − (Ve × FeO₂)

Umrechung der Formel durch Haldane-Umrechung auf der Grundlage dass Stickstoff ein inertes Gas ist und damit gilt:

Vi × FiN₂ = Ve × FeN₂

_{Daraus ergibt sich vereinfachte Formel, zu der nur ausgeatmeter Fluss und O2-Konzentration benötigt wird.}

Leck im Kreislauf

 FiO₂>85%

respiration rate is >35/min

during some ventilatory modes (e.g., High frequency oscillatory ventilation, HFOV; BiPAP).

indirekt duch Fick'sche Gleichung:

VO₂ = CardiacOutput × (CaO₂ − CvO₂)

The arterial–mixed venous oxygen content difference, CaO₂ − CvO₂, represents the quantity of O₂ extracted by the peripheral tissues. Because CaO₂ and CvO₂ share the same factor for haemoglobin binding (1.34 × Hb), the equation can be rearranged to isolate this term:

VO₂ = CO × 1.34 × Hb × (SaO₂ − SvO₂)

The pulse oximeter can distinguish two haemoglobin species on the basis of their different absorption of light: Oxyhaemoglobin absorbs more infrared light and less red light

deoxyhaemoglobin has an inverse pattern of absorbance.

the haemoglobin saturation is calculated as the ratio of red/infrared absorbencies.

However, not all the absorbance detected is due to arterial blood and therefore, the oximeter also determines the pulsatile component of the light absorbance signal (photoplethysmography). The change in ratio of absorption between systole and diastole can then be used to calculate the arterial saturation of haemoglobin.

Changes in pH, temperature, and 2,3-diphosphoglycerate concentration alter the PO₂–SaO₂ relationship

• Motion artefact (shivering, intra-aortic balloon pump and during transport)
• Abnormal haemoglobins (primarily COHb –falsely high SpO₂–, and MetHb – falsely low SpO₂ when SpO₂ >85% and falsely high when SpO₂ <85%)
• Exposure of probe to ambient light
• Low perfusion states
• Hypothermia
• Skin pigmentation
• Nail polish or nail coverings, when a finger probe is used
• Inability to detect saturations below 83% with the same degree of accuracy and precision seen at higher saturations, although the degree of discrepancy is not of clinical importance

At PaO₂ values greater than 12 kPa (90 mmHg), SaO₂ is nearly 100% and becomes virtually independent of PaO₂. It is important to remember this during SaO₂ monitoring; in those receiving supplemental oxygen a falling PaO₂ will not be detected until PaO₂ values less than 12 kPa (90 mmHg) are reached.

The highest value of CO₂ during the alveolar plateau is called end-tidal CO₂

Winkel zwischen Anstieg und Plateau:  which becomes wider with increasing Va/Q mismatch

Winkel zwischen Plateau und Abfall: widens as rebreathing and anatomical/apparatus dead space increases