COPD und Asthma

• long expiratory phase (low RR and I:E ratio)
• low tidal volume
• permissive hypercapnia = low expired minute volume (Ve = RR × Vt) with a high inspiratory flow rate (to ensure a short inspiratory time and thus a low I:E ratio).

• Minute ventilation <115 mL/kg
• Tidal volume <8 mL/kg
• Respiratory rate 10 to 14 per minute
• Inspiratory flow 80 to 100 L/min

Führt zu gefährlicher metabolischer/resp. Alkalose

->Ziel ist die Normalisierung des pH und nicht des PaO2

end-inspiratory volume (Vei) above functional respiratory capacity (FRC).

It is measured by collecting total exhaled volume in a paralysed patient over 60 seconds of apnoea.

Vei >20 mL/kg is predictive of complications such as hypotension and barotrauma

P plateau

Intrisnsic PEEP

Ppeak steigt auch an aber wirkt sich nicht auf Alveoli aus(muss sogar hoch sein, um bei hohem Atemwegswiderstand hohen Fluss zu erreichen)

Endexpiratorische Pause-> Drücke gleichen sich im Atemwegssystem aus->mittlerer Atemwegsdruck kann gemessen werden

Druch Messung des Oesphagealdruckes Pes:

negative inflexion of Pes at the beginning of a triggered inspiration, until inspiratory flow starts (see figure below).

ΔPoe ≅ Ptrigger + PEEPi ->

PEEPi ≅ ΔPoe − Ptrigger where Ptrigger is the set trigger on the ventilator.

<30 mbar (allgemein als richtig erkannter Wert)

PEEPe etwas weniger als PEEPi weil:

• There might be a mixed picture of airflow limitation and no-airflow limitation.
• The distribution of PEEPi within a COPD or an asthmatic lung is uneven (because of inhomogeneous time constants) and therefore, in some areas, the effective PEEPi might be lower than the measured static PEEPi
• ->PEEPe 80% von PEEPi

Respirator diskonnektieren->Blutdruck wird besser

ZVD und PAOP

cardiac arrhythmias, hypokalaemia, tremor, and lactic acidosis

Ja. Prednisolon 40-50mg/d oral für 5-10 Tage. Mehr ist nicht förderlich.

Inhalative Steroide können mit dazu eingenommen werden.

Cave: Wirkung auf Mucosa in 4-6 Stunden

= Ipratropiumbromid

inhibit vagal tone and are moderately potent bronchodilators. In combination with inhaled β2-adrenergic agonists, the effect of bronchodilation will be increased and the use of an anticholinergic has been shown to lead to a faster recovery and reduce hospitalisation rates. Anticholinergic treatment is not necessary, and may not be beneficial, in less severe exacerbations of asthma or after stabilisation.

=Montelukast

They are potent mediators of inflammation and the implicated in asthma pathogenesis.

Leukotriene receptor antagonists have bronchodilator and anti-inflammatory effects

are clinically active following a single dose.

There is only sparse literature, however, suggesting that montelukast is effective in the treatment of acute asthma as an adjunct therapy to avoid intubation.

Einmalige Gabe von 2 gr hilft.

Aminophylline is an inhibitor of phosphodiesterase.

• weak bronchodilation
• dilation of the pulmonary vessels
• positive inotropic effect, especially for the right heart. The use of methylxanthines in acute asthma is not routinely recommended (no additional benefit, increased frequency of side effects).

However, some patients with near-fatal asthma or life-threatening asthma with a poor response to initial therapy may gain additional benefit from IV aminophylline, (5 mg/kg loading dose over 20 minutes, unless on maintenance oral therapy) and then by infusion (0.5–0.7 mg/kg/hr).

Toxicity should be monitored and levels checked regularly in patients on aminophylline infusions.

COPD zeigt weniger Ansprechen auf B2-Mimetika, ist aber trotzdem Standard inhalativ, nicht iv (wie bei Asthma).

Anticholinergica bei gerigem Therpieansprechen auf B2-Mimierika.

• Increased cerebral blood flow and intracranial pressure
• Increased pulmonary artery pressure and right heart failure
• Decreased peripheral vascular tone/resistance
• Increased levels of epinephrine and norepinephrine
• Increased cardiac output
• Inadequate oxygenation due to hypercapnia reducing the FAO₂
  FAO₂ = FiO₂ − FACO₂ where
  FAO₂ = alveolar fraction of O₂, FiO₂ = inspired fraction of O₂ and FACO₂ = alveolar fraction of CO₂

Überernährung führt auch zu CO2-Anstieg!

Hohe Evidenz: Inhalat. B2-mimetika und Anticholinergika, Sauerstoff, NIV

mittlere Evidenz: systemisch Steroide, Antibiotika, Sauerstoff (gut eindosiert),

keine Evidenz: Theophillin, Mukolytika

Ipratropiumbromid

Blockade von m-Cholinorezeptoren->Bronchodilatation, Protekitv gegen Reflexbronchokonstriktion

Wirkt lagsamer als b2-Mimetika (nach Minuten)

FEV1=Forciertes expir. Volumen nach einer Sekunde (Aussage über Atemwegsobstruktion)

FVC= Forcierte Vitalkapazität (Volumen nach max. Inspiration und forcierter Expiration)

FEV1/FVC>75%

Bei restriktiver Lungenerkrankung ist FEV1 und FVC reduziert

• A history of prior mechanical ventilation and intensive care unit admission
• Prescription of oral corticosteroids and theophylline
• Evidence of worsening asthma over a period of 2–7 days with increasing use of short-acting β2-adrenergic receptor agonists
• Poor compliance with inhaled corticosteroid therapy
• Altered perception of dyspnoea
• Age >40 years

• ‘Brittle’ asthma
  • Type 1: wide peak expiratory flow rate (PEFR) variability (>40% diurnal variation for >50% of the time over a period >150 days) despite intense therapy.
  • Type 2: sudden severe attacks on a background of apparently well controlled asthma.

• Failure to attend appointments
• Self-discharge from hospital
• Psychosis, depression, other psychiatric illness or deliberate self-harm
• Alcohol or drug abuse
• Obesity
• Employment and income problems
• Social isolation

A good predictor of impending respiratory exhaustion is the occurrence of uncompensated respiratory acidosis (pH <7.35), and in particular its progression over time.

• PEFR <60% of predicted normal or of best normal if known; or<100 L/min, if not known

the initial response to therapy is an important prognostic indicator

- patient fulfils the criteria for a severe exacerbation

- does not improve rapidly, i.e. within 1–2 hours,

Improvement:  blood gases (decreasing pCO₂) and changes in lung mechanics (i.e. PEFR).

COPD

• Inadequate response to initial therapy (persistent severe dyspnoea, altered mental status)
• Persistent or worsening hypoxaemia (PaO₂ <5.3 kPa/40 mmHg) despite supplemental oxygen and non-invasive ventilation
• Persistent or worsening respiratory acidosis (pH <7.25) despite non-invasive ventilation
• Need for invasive mechanical ventilation
• Haemodynamic instability requiring vasopressors.

Asthma

• Poor response to initial 1 to 2 hours of treatment
• Risk factors for near-fatal asthma
• Persistent or worsening clinical signs and symptoms (respiratory distress, decreased mental status)
• PEFR <30%
• PaO₂ <8 kPa/60 mmHg or rising PaCO₂
• PaCO₂ >6 kPa/45 mmHg.

Increased airway resistance, which impedes airflow and can lead to so-called dynamic hyperinflation if expiratory time is too short to exhale the whole tidal volume (a prominent feature of asthma). = without expiratory flow limitation (without EFL)

Distal airway collapse, leading to cessation of airflow and distal ‘gas trapping’ is an important feature of COPD. =‘with expiratory flow limitation’ (with EFL)

Bei no EFL (ohne expiratorische Flusseinschränkung) summieren sich  Atemwegswiderstände auf und PEEPe würde die überblähung verstärken

Bei "with EFL" wird der Fluss nach den kollabierten Atemwegen(COPD) oder dem Schleimpropf(Asthma) bei Expiration unterbrochen. Deswegen hat jeder weitere Widerstand danach keinen Einfluss und PEEPe kann verwendet werden, solange PEEPe<PEEPi

Inhalierte Noxen/Gase ->Inflammation-> excessive mucus secretion, inflammatory mucosal oedema, increased fluid and cell exudation in the airways. These phenomena are reversible and are the target of therapy.

structural remodelling of the airway wall caused by the repeated injury and repair process, which leads to irreversible airway obstruction (decreased diameter caused by increased fibrous wall thickness).

Besonders in den kleinen Atemwegen <2mm

1. Es muss mehr Druck aufegbaut werden um den gleichen Fluss bei erhöhtem Flusswiderstand aufrecht zu erhalten (ΔP = Airway resistance × Airflow)

2. Überblähung ist zwar gut gegen erhöhten Widerstand durch Vergrösserung des Atemwegsdurchmessers aber sie reduziert gleichzeitig die Compliance des Atemwegssystems durch Rechtsverschiebung der Lungen-Druckvolumen-Kurve

3.Überblähung führt zu mehr Totraumventilation->mehr Atemminutenvolumen nötig

4.Durch Auto-PEEP =PEEPi muss bei Inspiration dieser erst überwunden werden, bis Fluss entsteht (sowohl in Spotantamung als auch am Ventiator (vermehrte Triggerwork)

• The altered geometry of chest wall and diaphragm (flattened diaphragm, shortened diaphragm and intercostal muscles with ‘horizontal ribs’) decrease the efficiency of respiratory muscles.
• Hypoxaemia and respiratory acidosis disturb muscle energetics.
• Respiratory muscle cachexia, as seen in severe COPD, also impairs muscle strength.

asthma:inflammatory process is quite different. In asthma, a chronic inflammatory disorder of the airways, many cells (mast cells, eosinophils, …) and cellular elements (cytokines, histamine, …) play a central role.

This chronic inflammation causes structural changes in the airways including hypertrophy and hyperplasia of smooth muscle, goblet cells and submucosal glands for instance (see figure 1-7 p. 8 GINA 2011).

Acute exacerbations: exposure to risk factors for asthma symptoms or triggers such as exercise, air pollutants or allergens, for instance. Occasionally infections can trigger an acute exacerbation (mostly viral).

Chronic inflammation is also associated with airway hyperresponsiveness that leads to recurrent episodes of obstructive symptoms, particularly at night or in the early morning.

These episodes are usually associated with widespread, but variable, airflow obstruction within the lung that is often reversible (in contrast to COPD).

• Exaggerated and abnormal contraction of airway smooth muscle cells (predominant and reversible mechanism)
• Airway oedema (important component during exacerbation)
• Mucus hypersecretion (airway plugging)
• Airway thickening (due to structural changes, not fully reversible)

Increased hyperinflation → decreased compliance → increased minute ventilation and tachypnoea → increased auto-PEEP → increased hyperinflation