1. ACUTE RESPIRATORY FAILURE (ARF)
Alicja Sniatkowska MD, PhD
Department of Pediatric Anaesthesiology and Intensive Therapy
University of Medical Sciences in Poznan

2. Pathophysiology of Acute Respiratory Failure

3. Definition of ARF
According to the most clinicians:
Based upon the resulting abnormalities in arterial oxygen and carbon dioxide levels
arterial oxygen tension (PaO2) is less than 60 mmHg at rest breathing room air
arterial carbon dioxide (PaCO2) may be elevated, normal or low

4. Mechanisms of Abnormal Gas Exchange
Hypoventilation
Ventilation-perfusion mismatching
Shunting
Diffusion impairment
Reduction in inspired oxygen concentration
Increased venous desaturation with cardiac dysfunction plus one or more of the above 5 factors

5. Hypoventilation Characteristic abnormality in patients with
depressed central system function
inadequate chest movements
neuromuscular or skeletal diseases
If the lungs are normal or near normal the rise of PaCO2 will be accompanied by a corresponding fall in PaO2, for example:
„pure” hypoventilation is present if PaO2 is 50 and PaCO2 80 mmHg which are changed from their normal values by about 40 mmHg
but
in contrast if PaO2 is only 30 mmHg with PaCO2 of 80 mmHg in the same patient hypoventilation alone cannot explain the hypoxemia – presence of additional inadequate ventilation

6. Ventilation-Perfusion Mismatching
Alveoli that are ventilated must also be perfused !!!

7. V/Q Mismatching
V/Q mismatching is a common mechanism for both hypoxemia and carbon dioxide retention Latter effect can be minimazed or eliminated by increasing minute volume (MV) – so may result in overcompensation with a decrease in PaCO2 below normal ranges Mild V/Q – corrected by increasing the inspired oxygen concentration (FiO2) linear relationship Severe V/Q – the rate of rise in PaO2 with increasing FiO2 decreases curvilinear relationship Very severe V/Q – effect of increasing FiO2 becomes similar to that seen with shunts

8. Mild V/Q Severe V/Q Very severe V/Q
Fig. Effects on arterial PO2 of changing inspired oxygen concentration (FiO2 in the presence of increasing V/Q mismatching)
Mild V/Q
Severe V/Q
Very severe V/Q

9. Shunting
Right-to-left shunting of mixed venous blood through the lungs is the major cause of hypoxemia in patients with acute lung injury, including:
- cardiogenic pulmonary oedema - noncardiogenic pulmonary oedema
- pulmonary embolism
Normal right-to-left shunt is approximately 2 to 3 %
unoxygenated blood from the bronchial, mediastinal veins goes emptying directly into the left ventricle

10. Relationship between FiO2 and PaO2 according to severity of shunting
Extensive left-lung pneumonia caused respiratory failure; the mechanism of hypoxia is intrapulmonary shunting

11. Diffusion Impairment
Diffusion impairment is the failure of the equilibration of the pulmonary capillary blood with the alveolar gas
Normally the pulmonary capillary blood equilibrates with the alveolar gas in about 1/3 of the time it takes to pass through the alveolar capillaries
So,
***In the cases of inadequate diffusion – we have a wide margin - before the clinical symptoms of hypoxemia occurs
***Diffusing capacity must fall below 20% - before any change in PaO2 is seen

12. Abnormally rapid blood flow (e. g. in septic shock. )
Abnormally rapid blood flow (e.g. in septic shock...) ... diffusion impairment does not cause hypoxemia because... the lung can increase its diffusing capacity by recruiting additional pulmonary capillaries

13. Acid-base Disturbances in ARF
Normal regulation of acid-base balance depends on three systems in the body:
Lungs
Kidneys
Body buffer systems 3a *carbonic acid ** phosphates***protein 3b intracellular-extracellular ion shifts
Regulate
pH 7,4 PaCO2 40 mmHg bicarbonate 24mmol/l in a normal person living at sea level

14. The accurate interpretation of a patient’s acid-base balance requires integration of information from several different sources, incl.:
clinical history
physical examination
arterial blood gas analysis
Measurements of electrolites

15. Acid-base Normogram
The nomogram rates values of pH, pCO2 and HCO3 that would be expectated for simple respiratory and metabolic acid-base disturbances. Values lying out-side the bands suggest the presence of mixed disorder

16. Oxygen Delivery
Adequate systemic oxygen delivery depends on : Cardiac output (Q) Level of hemoglobin Saturation system cardiovascular hematologic respiratory

17. 100ml of arterial blood contains about 20 ml of oxygen
Normal resting cardiac output (CO) – 6 L/min
It means 1200ml of oxygen is delivered per minute
Normal resting consumption is about 300 ml/min
900 ml remains in the mixed venous blood (CvO2)
1g of hemoglobim carries 1,34 ml of oxygen when fully saturated
The ability of hemoglobin to bind oxygen at normal PaO2 levels and to give it up at lower levels is described by the:
oxyhemoglobin disociation curve (fig.)

18. The normal oxyhemoglobin dissociation curve at pH 7,4 and 37oC
Fig.
Hypothermia and alkalemia shift the curve to the left
Fever and acidemia shift the curve to the right

19. Oxygen Delivery Estimation
The adequacy of oxygen delivery could be estimate by measuring the mixed venous PO2 – PvO2 PvO2 – about 40 mmHg PvO2 < 30 mmHg – anaerobic cellular metabolism with lactic acid production Abnormalities of arterial oxygen content (CaO2), oxygen consumption (VO2) and cardiac output (CO) are common in critically ill patients

20. Macrocirculation vs Ovygenation
Oxygen extraction in the lungs SaO2, PaO2, PCO2
Oxygen transport from the lungs to the organs BP, MAP, CVP, HR,CO, CI, SVI, SVR HB/Htk, CRT
Oxygen extraction in the tissues O2ER, ScvO2, SvO2, lactate clearance
OXYGENATION
MACROHAEMODYNAMICS
CONSUMPTION
Każdy z tych trzech etapów wymaga spełnienia warunków, aby możliwe było osiągnięcie optymalnego stanu.
W płucach – konieczna jest prawidłowa ekstrakcja tlenu, wyrazem czego będzie prawidłowa saturacja tętnicza
W krążeniu systemowym – ważne są właściwe parametry hemodynamiczne ale także prawidłowy poziom hemoglobiny koniecznej dla transportu tlenu z płuc do tkanek obwodowych
W tkankach i narządach z kolei – właściwa ekstrakcja tlenu, ale też klirens mleczanów i ocena saturacji żylnej centralnej jako wykładników konsumpcji tlenu w tkankach obwodowych

21. DO2 (Oxygen Delivery) VO2 : DO2 CO x (CaO2 – CvO) : CO x CaO2
Extraction
in the lungs
Transport from the lungs into the tissues
Extraction in the tissues
We wstrząsie utrzymanie dostarczania tlenu na poziomie co najmniej minimalnym zależy od procesów, w których istotne są trzy elementy: ekstrakcja tlenu w płucach, następnie jego transport z płuc do tkanek i ekstrakcja tlenu w komórkach i tkankach.
Istotnym jest utrzymanie optymalnego balansu pomiędzy zużyciem tlenu a jego dostawą, które jak wiadomo zależą z kolei od całkowitej zawartości tlenu w organizmie jak i wysokości rzutu serca.
VO2 : DO2 CO x (CaO2 – CvO) : CO x CaO2

22. SpO2, SaO2, PaO2 CaO2 = SaO2 x Hb x 1,34 CvO2 = SvO2 x Hb x 1,34
DO2 = CO x CaO2 ml/min x m2
CO x (SaO2 x Hb x 1,34) + (0,003 x PaO2) ml/min
DO2Index = DO2/BSA ml/min/m2
VO2 CO x (CaO2 – CvO2) – 270 ml/min (4 - 8 ml/min/kg) VO2Index = VO2/BSA ml/min/m2
O2ER = VO2 / DO2 = (SatO2 – ScvO2):SatO2 0,2 – 0,3 (śr. 24%) > 0,5 = kwasica
ScvO2 / SvO2 > 70% / > 65%
Zatem, które z parametrów można mierzyć i monitorować już we wczesnej fazie wstrząsu lub jeszcze wcześniej?
Które z nich oceniać?
Po pierwsze – wymianę gazową w płucach, tak kluczową w ocenie całkowitej zawartości tlenu w organizmie. Można ją ocenić pośrednio poprzez pomiar saturacji przezskórnej lub gazometrii krwi tętniczej
Po drugie – transport tlenu z płuc do tkanek obwodowych. Wymaga to dodatkowo pomiaru rzutu serca poprzez zastosowanie nieinwazyjnej lub inwazyjnej metody monitorowania. Tej drugiej metody nie zawsze łatwo udaje się implementować do dziecięcych oddziałów intensywnej terapii ze względu na ograniczenia sprzętowe z jednej strony jak i rozmiary pacjenta z drugiej.
Można w zastępstwie zastosować ciągły pomiar saturacji żylnej lub (znacznie rzadziej) mieszanej żylnej oczywiście u dzieci bez współistniejących wad serca . Echokardiografia bywa zawodna, zwłaszcza że nawet w rękach doświadczonych sonografistów nie udaje się uniknąć błędów pomiarowych, nie mniej może być również stosowana
3. Trzecim istotnym parametrem jest ocena zużycia tlenu przez organizm dziecka we wstrząsie.
4. I na koniec pomiar współczynnika ekstrakcji tlenu, korelującego ściśle ze stanem metabolicznym.

23. Comparison of variables
Vincent JL. Crit Care Clin. 1996;12(4): Review.
Comparison of variables
W literaturze powszechnie znany jest wykres przedstawiający wzajemna zależność wszystkich istotnych zmiennych, koniecznych do oceny dostarczania tlenu.
W momencie zmniejszenia DO2 dzięki zwiększeniu współczynnika ekstrakcji tlenu dochodzi do zwiększenia zużycia tlenu. Pozwala to jednocześnie na zwiększenie klirensu mleczanów.
Jeżeli redukcji DO2 towarzyszy zmniejszenie VO2 dochodzi do transwersji metabolizmu do beztlenowego, aby zabezpieczyć choć minimalne zapotrzebowanie energetyczne. Jeżeli jednocześnie zwiekszona ekstrakcja tlenu nie jest wystarczająca DO2 osiąga wartość krytyczną.
Zaburzenie O2ER we wstrząsie prowadzi do tzw. luki tlenowej „pO2 gap”, gdy pcapO2 osiąga wartości niższe niż pvO2, stanowiąc wykładnik wielkości przecieku. Zjawisko to jest bardziej nasilone w sepsie niż we wstrząsie krwotocznym.
I jest bezspornym dowodem na to, że monitorowanie tylko parametrów hemodynamicznych czy dostawy tlenu jest niewystarczające w ocenie krążenia młośniczkowego.
O2ER disorder in the shock leads to the „pO2 gap”, when pcapO2 achieve the level lower then pvO2,e.g. Shunting
„pO2 gap” – higher in sepsis in comparison to hypovolemic shock

24. DO2 CO fluids, inotropes Hb RBC SO2 oxygenation/mechanical ventilation
Utrzymanie prawidłowej podaży tlenu do tkanek i komórek determinują trzy główne komponenty:
Rzut serca
Stężenie hb
I stopień jej utlenowania, a także zdolność przenikania tlenu z najmniejszych arterioli i kapilar do komórek.
Każdy z tych elementów można korygować poprzez odpowiednie postępowanie terapeutyczne.

25. ScvO2 Edwards LifeSciences SaO2 Cardiac output Dobutamine
Normal ≥ 70%
Do nothing
Low ≤ 70%
SaO2
Low (hypoxemia)
Oxygen therapy, increased PEEP
Normal ≥ 95%
Cardiac output
High >2,5 L/min/m2
hemoglobin
> 8 g/dl stress, anxiety, pain high VO2
Analgesia,sedation
< 8 g/dl anemia
Blood transfusion
Low <2,5 L/min/m2
SVV
< 12% myocardial dysfunction
Dobutamine
> 12% hypovolemia
Fluid challenge

26. de Oliveira CF et al. Intensive Care Med. 2008 Jun;34(6):1065-75.
We conclude that goal-oriented resuscitation with the current ACCM/PALS guidelines can improve morbidity and mortality when supplemented by ScvO2monitoring.
These findings may have a significant impact on the outcome of children and adolescents with septic shock.

27. Lemson J et al. J Crit Care. 2011 Aug;26(4):432.e7-12.
EVLWI (Extravascular Lung Water Index) GEDVI (Global End-Diastolic Volume Index)
Jeszcze innym parametrem służącym do oceny wypełnienia łożyska systemowego jest ilość poznaczyniowej wody płucnej, który podobnie jak wartości hemodynamiczne serca wykazują duże zróżnicowanie w zależności od wieku dziecka.
U niemowląt i dzieci przedszkolnych wartości indeksu wody pozanaczyniowej są dużo wyższe, podczas gdy wskażnik objętości końcowo-rozkurczowej dużo niższy.
Zmiany te wynikają ze stosunku masy płuc w odniesieniu do masy ciała (3 rys.), który najwiekszy jest w pierwszym roku życia. Ilość wody w płucach determinuje sama w spbie masa płuc, która przeliczona na masę ciala, daje wartości największe własnie w pierwszym roku życia dziecka.
Ponieważ zależności te maja charakter nielinearny, stąd konieczność indeksowania ich u dzieci w odniesieniu do masy ciała bądź jego powierzchni.
Z tych też róznic wynika brak jednolitego stanowiska a co gorsze brak wartości referencyjnych w pediatrii.

28. EVLWI vs Chest X-Ray Lemson J et al. Crit Care. 2010;14(3):R105.
Wydaje się jednak, że parametr ten nie ma wiekszego znaczenia klinicznego u małych dzieci, gdyż wykazuje słabą korelację zarówno z obrazem radiologicznym, jak i indeksem tlenowym.
Dodatkowo wartości uzyskane w tym badaniu wykazywały bardzo duży rozrzut od 13 do 120 ml/kg m.c. U dorosłych wartości powyżej 20 ml.kg m.c. Zwiększają istotnie śmiertelność chorych we wstrząsie i ARDS.
• Extravascular lung water index measured in critically ill children using the transpulmonary thermodi- lution technique does not correlate with a chest x-ray score of pulmonary edema.
• Extravascular lung water in critically ill children does not correlate with parameters of oxygenation.
• A chest x-ray score of pulmonary edema in critically ill children does not correlate with parameters of oxygenation.

29. Pediatric considerations

30. The respiratory pump includes: 1
The respiratory pump includes: 1. the nervous system with central control (ie, cerebrum, brainstem, spinal cord, peripheral nerves) 2. respiratory muscles 3. chest wall.

31. Differences among pediatric children include the following:
Infants and young children have fewer alveoli than do adults. The number dramatically increases during childhood, from approximately 20 million after birth to 300 million by 8 years of age. Therefore, infants and young children have a relatively small area for gas exchange.
The alveolus is small. Alveolar size increases from to µm during childhood.
Collateral ventilation is not fully developed; therefore, atelectasis is more common in children than in adults. During childhood, anatomic channels form to provide collateral ventilation to alveoli. These pathways are between adjacent alveoli (pores of Kohn), bronchiole and alveoli (Lambert channel), and adjacent bronchioles. This important feature allows alveoli to participate in gas exchange even in the presence of an obstructed distal airway.
Smaller intrathoracic airways are more easily obstructed than larger ones. With age, the airways enlarge in diameter and length.
Infants and young children have relatively little cartilaginous support of the airways. As cartilaginous support increases, dynamic compression during high expiratory flow rates is prevented.

32. Features of note in pediatric patients
The respiratory center is immature in infants and young children and leads to irregular respirations and an increased risk of apnea.
The ribs are horizontally oriented. During inspiration, a decreased volume is displaced, and the capacity to increase tidal volume is limited compared with that in older individuals.
The small surface area for the interaction between the diaphragm and thorax limits displacing volume in the vertical direction.
The musculature is not fully developed. The slow-twitch fatigue-resistant muscle fibers in the infant are underdeveloped.
The soft compliant chest wall provides little opposition to the deflating tendency of the lungs. This leads to a lower functional residual capacity (FRC) in pediatric patients than in adults, a volume that approaches the pediatric alveolus critical closing volume.

33. ARF / ARDS

34. Definition of Acute Respiratory Failure (ARF)
The term of ARF is defined very various by many authors:
Primary disorder in gas exchange (in contrast to acute ventilatory failure)
Any disruption in the function of the respiratory system (which is consist of the central nerwous system control center, efferent and afferent nervous pathways, as well as muscles, lungs, pleura)
The best def. described ARF as condition resulting in an abnormally low arterial oxygen tension with or without an abnormally high arterial carbon dioxide tension

35. Two types of ARF
Type 1 (termed nonventilatory, hypocapnic or normocapnic) - is manifested by an abnormally low PaO2 with PaCO2 either low or normal - disease process involving the lungs: *acute lung injury **ARDS (adult resipratory distress syndrome)
Type 2 (ventilatory or hypercapnic) - is manifested by hypoxemia as well as hypercapnia - failure of alveolar ventilation decrease in minute ventilation increase in total dead space *depression of CNS control of ventilation **exacerbations of chronic obstructive pulmonary disease (COPD)

36. Ventilation – perfusion relationships change during the course of the illness, so the type of respiratory failure may change
Remember – type1 and type2 do not represent specific disease entities but rather two manifestations of ARF

37. Assessment of Severity
Respiratory rate
Tachypnoe is the usual response to the respiratory difficulty but is also seen with metabolic acidosis and psychological disturbances tab. normal respiratory rates
Age
Breaths/minute
<1
1-5
5-12
>12
30-40
20-30
15-20
12-16

38. Increased work of respiration
Recession in younger children and infants the increased compliance of the chest will make the recession a common sign, in older children (>7 years) it signifies severe respiratrpy problems
Use of accessory muscles nasal flaring may indicate mild increase in work of breathing while sternomastoid and ather muscles use indicates increased and severe respiratory effort
Grunting Is due to decreased lower airway compliances - characteristically seen in infants - sign of severe respiratory difficulties - may disappear in a fatigued child

39. Effectiveness of breathing
The colour of skin and mucus membrane gives a subjective assessment od cyanosis.
Anaemia, poor perfusion, hypercapnia and poor lighting can complicate the assessment
Effect of respiration on other organs
Cardiovascular system – hypoxia initially causes a tachycardia which leads to bradycardia (more severe and pre-terminal)
CNS – hypoxia leads to drowsiness and eventually coma

40. Lower Airway and Alveoli
Etiologies of ARF
Brain
Spinal cord
Neuromuscular system
Disruption of any link in the chain may lead to the development of acute respiratory failure
Thorax and Pleura
Upper airway
Cardiovascular
Lower Airway and Alveoli

41. Etiology of ARF

42. Examination
LOOK colour, sweating, distress, high respiratory rate, use of accessory muscles, evidence of exhaustion, chest wall movements, jugular venous pulsation
FEEL tracheal position, chest expansion, percussion, subcutaneous ephysema
LISTEN breath sounds, vocal resonance will help
ACT identify and treat immediately, life threatening problems that are within your capacity or call early for appropiate assistance

43. Adult Respiratory Distress Syndrome (ARDS)
Common cause of Acute Respiratory Failure
There are similarities to Infant Respiratory Distress Syndrome
Originally we thought that a lack of surfactant played an etiologic role but later the defect of surfactant was found
They were also the first groups describing the beneficial effect of positive end-expiratory pressure (PEEP) in the treatment
ARDS is associated with the high mortality 150,000 patients per year and more than 75% need greater than 50% FiO2

44. ARDS
Bilateral airspace infiltrates on chest radiograph film secondary to acute respiratory distress syndrome that resulted in respiratory failure

45. Criteria for Diagnosing of ARDS

46. The new Berlin definition of ARDS - 2012
Ioannis Pneumatikos1, MD, PhD, FCCP
Vasilios Ε. Papaioannou2, MD, MSc, PhD
PNEUMON Number 4, Vol. 25, October - December 2012

47. LIS score score 0: no lung injury
Parameter Finding Value
Rx.Torax no alveolar consolidation 0
alveolar consolidation de 1 quadrant 1
alveolar consolidation de 2 quadrant 2
alveolar consolidation de 3 quadrant 3
alveolar consolidation de 4 quadrant 4
Hypoxemia  PaO2/FIO2 >
PaO2/FIO
PaO2/FIO
PaO2/FIO
PaO2/FIO2 <
PEEP  PEEP <= 5 cm H2O
PEEP cm H2O
PEEP cm H2O
PEEP cm H2O
PEEP >= 15 cm H2O
Pulmonary Compliance 
compliance >= 80 mL/cm H2O 0
compliance mL/cm H2O 1
compliance mL/cm H2O 2
compliance mL/cm H2O 3
compliance <= 19 mL/cm H2O 4
LIS score
score 0: no lung injury
score : mild-to-moderate lung injury
score > 2.5: severe lung injury (ARDS)

48. Causes of ARDS

49. Clinical stages of ARDS
Four phases
Injury
Apparent stability
Respiratory insufficiency
Terminal stage

50. Injury (1) Usually no evident clinical signs
Chest roentgenogram may be clear
Up to 6 hours

51. Apparent stability (2) Hyperventilation
Abnormalities in chest roentgenogram reticular infiltrates representing perivascular fluid accumulation and interstitial oedema
12-24 hours

52. Respiratory insufficiency (3)
Next hours
X-ray – five-lobed alveolar and interstitial infiltrate „snow storm” picture
Tachypnoe, crackles
Severe reduction in PaO2 even high oxygen concentration is given

53. Terminal stage (4)
Persistent severe hypoxemia despite the administration of 100 percent oxygen
High carbon dioxide retention
The occurence of multiorgan dysfunction syndrome (MODS)

54. Pathophysiology of ARDS
Primary site of injury in ARDS – alveolar-capillary membrane
Swelling and retraction of the capillary endothelial cells leads to increased alveolar permeability and interstitial oedema
Increased interstitial fluid produces noncompliant lungs
Continuating process leads to alveolar oedema and alveolar collapse
Microatelectasis and alveolar disruptions and haemorrhagic oedema
Surfactant (phospholipoprotein produced by 2 types of pneumocyte) has decreased activity
ARDS

55. Mechanism of Lung Injury
Mediators characteristic and responsible for producing and sustaining the intense inflammatory response
Arachidonic acid and its metabolites such as prostaglandins, leukotriens, tromboxane A2
Serotonin
Histamine
ß-endorfin
Fibrin and fibrin degradation products (FDP)
Superoxides
Polymorphonuclear lukocytes
Platelets
Free fatty acids
Bradykinin
Proteolytic enzymes
Lysosomes

56. There is no specific therapy for ARDS!!!
Treatment
There is no specific therapy for ARDS!!!

57. 
Treatment of ARDS must be individualized as a variety of causes may produce this syndrome

58. Directions of treatment of ARDS
Maintainence adequate tissue oxygenation of vital organs, particularly the brain and heart
Treatment of underlying cause of lung damage

59. Treatment of ARDS Mechanical ventilation non-invasive and invasive
small volumes 5-6 ml/kg b.w.
PEEP
Appropriate antibiotic therapy when infection is present and severe sepsis or septic shock is responsible for ARDS
Immunologic therapy
Proper fluid balance
Haemofiltration or haemodiafiltration
Prevention and control of multiorgan dysfunction or failure
Proper and good nursing care

60. Tracheal intubation - MSOAPP
M = Monitors (heart rate, blood pressure, pulse oximetry, capnography for CO2 detection) S = Suction and catheters O = Oxygenation with a bag-valve mask A = Apparatus (laryngoscope, endotracheal tubes appropriate for the patient's age and endotracheal tubes 0.5 size smaller and larger, stylets, oral airways) P = Pharmacy (medications for amnesia and paralysis) P = People (respiratory therapist, nurse, a skilled set of hands)

61. Oxygen Therapy
The initial treatment for hypoxemia is to provide supplemental oxygen. High-flow (>15 L/min) oxygen delivery systems include a Venturi-type device that places an adjustable aperture lateral to the stream of oxygen. Oxygen is mixed with entrained room air, and the amount of air is adjusted by varying the aperture size. The oxygen hoods and tents also supply high gas flows. Low-flow (<6 L/min) oxygen delivery systems include the nasal cannula and simple face mask.

62. Humidified high-flow nasal cannula (HHFNC)
Although no single universally accepted definition is available for what constitutes HHFNC therapy in neonates, a widely used and reasonable definition is optimally warmed (body temperature) and humidified respiratory gases delivered by nasal cannula at flow rates of 2-8 L/min.[2 ] In 2004, the US Food and Drug Administration (FDA) approved a device specifically for the provision of HHFNC in neonates: Vapotherm 2000i (Vapotherm, Inc, Stevensville, MD). This devices delivered molecular vapor with % relative humidity at body temperature through nasal cannula at flow rates between 5-40 L/min.

63. Continuous positive airway pressure (CPAP)
CPAP may be indicated if lung disease results in severe oxygenation abnormalities such that an FiO2 greater than 0.6 is needed to maintain a PaO2 greater than 60 mm Hg.
CPAP in pressures from 3-10 cm H2 O is applied to increase lung volume and may redistribute pulmonary edema fluid from the alveoli to the interstitium.
CPAP enhances ventilation to areas with low V/Q ratios and improves respiratory mechanics.
If a high concentration of FiO2 is needed and if the patient does not tolerate even short periods of discontinued airway pressure, positive-pressure ventilation should be administered.

64. Noninvasive positive-pressure ventilation (NPPV)
Noninvasive mechanical ventilation refers to assisted ventilation provided with nasal prongs or a face mask instead of an endotracheal or tracheostomy tube.
This therapy can be administered to decrease the work of breathing and to provide adequate gas exchange.
NPPV can be given by using a volume ventilator, a pressure-controlled ventilator, or a device for bilevel positive airway pressure (BIPAP or bilevel ventilator).

65. Mechanical ventilation
A primary strategy for mechanical ventilation should be the avoidance of high peak inspiratory pressures and the optimization of lung recruitment.
In adults with acute respiratory distress syndrome (ARDS), a strategy to provide low tidal volume (6 mL/kg) with optimized positive end-expiratory pressure (PEEP) offers a substantial survival benefit compared with a strategy for high tidal volume (12 mL/kg).
According to the permissive hypercapnia strategy in ARDS, arterial CO2 is allowed to rise to levels as high as 100 mm Hg while the blood pH is maintained at greater than 7.2 by means of the intravenous administration of buffer solutions. This is done to limit inspiratory airway pressure to values less than 35 cm H2 O.
PEEP should be applied to a point above the inflection pressure such that alveolar distention is maintained throughout the ventilatory cycle.

66. PEEP as Method of Therapy in ARDS
PEEP (Positive End-Expiratory Pressure)
Indications:
to obtain optimal distention of alveoli
to reverse alveolar collapse
to increase the FRC (Functional Residual Capacity)
to correct the progressive atelectasis
it allows to maintenance of adequate oxygenation with a decrease in required oxygen concentration – help tp minimaze the potential toxic effect of high oxygen tension
to stabilize fluid-filled alveoli
to improve ventilation of alveoli which were previosly sites of shunting or low ventilation in reltion to perfusion
there is no evidence that use of PEEP decreases extravascular lung water (in fact high lung volumes may it increase...)

67. The goal of PEEP is to allow a reduction in the FiO2 to 50% or less
Non-positive effects and consequences of using PEEP
Impaired venous return
Increased pulmonary vascular resistance
Reduced left ventricular afterload
Altered right and left ventricular geometry
Altered compliance
Optimal level of PEEP ?!
Controversial opinions (.... 5 cm H2O)
The goal of PEEP is to allow a reduction in the FiO2 to 50% or less

68. Haemodynamic effects of positive pressure ventilation on cardiac output
Likely effect on cardiac output
Haemodynamic effect of positive pressure ventilation
Preload dependent
Afterload dependent
RV preload ↓ ↓ ↑
RV afterload ↑
LV preload ↓
LV afterload ↓

69. Prone positioning
Prone positioning reduces compliance of the thoracoabdominal cage by impeding the compliant rib cage. Gases should distribute toward the sternal and anterior diaphragmatic regions that become dependent on prone positioning. Improved homogeneity of ventilation improves oxygenation. This measure may cause a redistribution of blood flow, improving the V/Q match. Researchers in a multicenter randomized controlled clinical trial concluded that prone positioning did not significantly reduce ventilator-free days, mortality, or time to recovery in pediatric patients with acute lung injury. but…………

70. Prone positioning in ARDS

71. Extracorporeal life support (ECLS)
ECLS: blood is removed from the patient, passed through an artificial membrane where gas exchange occurs, and is returned to the body by either the arterial (venoarterial [VA]) or venous (venovenous [VV]) system.
VV ECLS has become the preferred method for patients of all age groups who do not require cardiac support.
From at the University of Michigan, 586 neonatal, 132 pediatric, and 146 adult patients were given ECLS for respiratory failure, with survival rates of 88%, 70%, and 56%, respectively.

72. Complications Associated with the ARDS

73. History of mechanical ventilation
1928r. First „iron lungs”, Boston, creator - Emerson
1948r. Ventilator Bennett in the USA
1950r. Ventilator Engström in Sweden
1952r. Epidemy of poliomyelitis, Kopenhagen, dr Björn Ibsen
cause – respiratory insufficiency among 11% of pts
mortality among them 90%!!!

74. New Techniques of Mechanical Ventilation
Pressure Support Ventilation (PSV)
Pressure Support Ventilation Back Up Rate (PSV BUR)
Pressure Controlled Ventilation (PCV)
Pressure Assisted Controlled Ventilation (PACV)
Controlled Volume (CV)
Assisted Controlled Volume (ACV)
Synchronous Intermittent Mandatory Ventilation (SIMV)

75. High Frequency Ventilation (HFV)
HFO High Frequency Oscillation Ventilation
rates up to 6,000bpm
HFJV High Frequency Jet Ventilation rates up to 600 bpm the tidal volumes are usually smaller than dead space volume and much faster rates are utilized

76. Potential Uses for High-Frequency Ventilation
HFOV combines small tidal volumes (smaller than the calculated airway dead space) with frequencies of more than 1 Hz to minimize the effects of elevated peak and mean airway pressures.
HFOV has proven benefit in improving the occurrence and treatment of air-leak syndromes associated with neonatal and pediatric acute lung injury.

77. Prognosis
The prognosis depends on the underlying etiology leading to acute respiratory failure.
The prognosis can be good when the respiratory failure is not very very severe event and not associated with prolonged hypoxemia.
The prognosis may be fair when a new process is associated with chronic respiratory failure secondary to a neuromuscular disease or thoracic deformity. This may herald the need for long-term mechanical ventilation.
The prognosis can vary when respiratory failure is associated with a chronic disease with acute exacerbations.
Respiratory failure may be the sign of an irreversible progressive disease that leads to death.

80. THANK YOU FOR
YOUR ATTENTION