2. تهيه و تنظيم : بهنام پورگرمرودى
آناتومی و فیزیولوژی
تهيه و تنظيم :
بهنام پورگرمرودى

3. آناتومى
مجاری هوايی غير تنفسی
مجاری هوايی تنفسی

12. مجاری هوايی تنفسی
برونشيولهای تنفسی
مجاری آلوئولی
آلوئولها

14. Basic Anatomy Upper Airway Lower Airway humidifies inhaled gases
site of most resistance to airflow
Lower Airway
conducting airways (anatomic dead space)
respiratory bronchioles and alveoli (gas exchange)
Remember that the upper airway is a significant site of resistance and this can be added to by iatrogenic devices (nasogastric tubes) or relieved by other devices (nasal trumpets).
When delivering a gas to any patient, give it the way nature does - give it humidified.
The lower airways can be broken down into dead space and the sites where gas exchange occurs. Anything that increases dead space (e.g., PEEP) will impact upon ventilation unless it also increases the area where gas exchange occurs.

15. Basic Physiology Negative pressure circuit
Gradient between mouth and pleural space is the driving pressure
need to overcome resistance
maintain alveolus open
overcome elastic recoil forces
Balance between elastic recoil of chest wall and the lung
During inspiration the gradient becomes more negative as you approach the alveolus. This is an active process; part of the energy used for inspiration is stored in the tissues. This is used in exhalation, which is effectively a passive process.
Recall that work = volume x pressure. For infants with their more compliant chest wall, they will have a proportionally greater work of breathing which helps predispose them to respiratory distress.
The point at which the recoil between the alveolus and the chest wall is balanced is equivalent to functional residual capacity.
I wanted to try to give some background to this slide without getting too weighed down in the physiology of breathing and respiratory failure. Besides, it always confuses me.

16. تهويه مكانيكی
تهويه مكانيكی ريه به حركت هوا به داخل و خارج ريه اطلاق ميشود كه توسط فعاليت ماهيچه های تنفسی ايجاد ميشود.

17. Basic Physiology http://www.biology.eku.edu/RITCHISO/301notes6.htm

18. Ventilation Carbon Dioxide
PaCO2= k * metabolic production alveolar minute ventilation
Alveolar MV = resp. rate * effective tidal vol.
Effective TV = TV - dead space
Dead Space = anatomic + physiologic
The partial pressure of carbon dioxide in the arterial blood is directly related to metabolic production and indirectly related to minute ventilation. To be accurate, it is alveolar minute ventilation that matters. When a child is tachypneic, the minute ventilation may not change since the increase in rate is balanced by a decrease in tidal volume. However, the amount of dead space has not changed so the effective tidal volume will decrease and hence the effective minute ventilation and thus PaCO2 will increase despite the increased respiratory rate. Likewise, any process that increases dead space without changing minute ventilation will result in an increase in PaCO2 .

19. تنفس
تنفس در واقع به معنای تبادل اكسيژن و دی اكسيد كربن بين سلول ها و محيط خارج است.
اگر تبادلات اكسيژن و دی اكسيد كربن در سطح سلولی باشد تنفس داخلی Respiration Internal ناميده ميشود
و اگر تبادلات گازی در سطح آلوئولهای ريوی ،انجام گيرد تنفس خارجی External Respiration ناميده ميشود.

20. PHYSIOLOGY Respiration
Ventilation: air entering and leaving the alveoli.
Transfer through the alveolo-capillary membrane: exchange of O2 and CO2 between the blood in the capillaries and the gases in the alveoli.
Perfusion - Circulation: transfer of O2 from the pulmonary capillaries to the cells of the body and transfer of CO2 from the cells to the pulmonary capillaries.
Cellular respiration: transfer of O2 in the blood to the cells and CO2 from the cells to the blood. 1

21. Alveolar/capillary membrane
Alveolus O2 O2 O2 O2 O2
CO2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2
CO2
CO2 O2
CO2 O2 O2 O2
CO2
CO2
CO2
CO2
The transfer of gases between the alveoli and the blood takes place through the alveolar/capillary membrane. Transfer and diffusion occur due to the partial pressure gradient of each gas. O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2 O2
CO2 O2
CO2
CO2 O2 O2
CO2
CO2
CO2
Membrane 2

22. Oxygenation
Oxygen:
Minute ventilation is the amount of fresh gas delivered to the alveolus
Partial pressure of oxygen in alveolus (PAO2) is the driving pressure for gas exchange across the alveolar-capillary barrier
PAO2 = ({Atmospheric pressure - water vapor}*FiO2) - PaCO2 / RQ
Match perfusion to alveoli that are well ventilated
Hemoglobin is fully saturated 1/3 of the way thru the capillary
To be simplistic, oxygenation involves getting enough oxygen to an alveolus that is perfused. The more volume of gas that can be delivered for exchange, the better. The higher the driving pressure for that gas exchange, the better. Ideally, ventilation (V) and perfusion (Q) are matched so that oxygen is where the blood is (V/Q = 1).
When gas exchange does take place, it is so rapid that a hemoglobin molecule passing through an alveolar capillary is fully saturated before it is one third of the way across. The rest of the capillary represents a reserve for when transit time is increased (e.g., tachycardia) or for when diffusion is slowed (e.g., pulmonary edema, fibrosis) so that hemoglobin still may be fully saturated when it exits the capillary.
[I made this slide to replace the old one that listed factors that affect the rate of gas exchange. I agree that V/Q mismatch will be hard to do well but it is important. I can’t believe that I never realized it wasn’t in my original set of slides. I tell residents that saying “V/Q mismatch” in response to any respiratory question in the ICU will usually be right………What I would like to try to do is to link the physiology of normal gas exchange to abnormal gas exchange and then link that to what we do with the vent…..I.e., increase PEEP to increase area for gas exchange and improve oxygenation, etc etc. This will be tough to do without discussing V/Q mismatch. For what it is worth, here is my attempt at this….]

23. The alveolus PalvCO2 = % CO2 x Palv e.g. 5 % x 760 = 38 mm Hg
PalvO2 = % O2 x PALV
e.g % x 760 = 101 mm Hg
e.g. 50 % x 760 = 380 mm Hg
e.g. 50 % x ( ) = 393 mm Hg
(25 mm Hg = 33 cm H2O)
PalvCO = 5 % x 760 = 38 mm Hg
PalvO2 = 45 % x 760 = 342 mm Hg
PalvN2 = 50 % x 760 = 380 mm Hg
760 mm Hg 4

24. Partial oxygen pressures in the blood
Gaseous exchange
Partial oxygen pressures in the blood
% SAT O2
O2-Hb- O2 O2 xx O2 O2 O2
O2-Hb- O2 O2
O2-Hb- O2 O2 O2
The quantity of oxygen contained in the blood = O2 fixed by hemoglobin + O2 dissolved in the blood.
There is a dynamic balance between fixed O2 and dissolved O2, illustrated by the oxygen dissociation curve.
PO2 is the quantity of O2 dissolved in the blood, expressed as partial pressure.
The % SaO2 represents the percentage of sites in the hemoglobin molecule that have fixed a molecule of oxygen (max. HbO2/HbO2). O2 O2
PaO2
Fixed and dissolved oxygen
Oxygen dissociation curve 5

25. Oxygenation http://www.biology.eku.edu/RITCHISO/301notes6.htm
The sigmoidal shape of the oxygen disassociation curve is of critical importance. Hemoglobin can only carry so much oxygen (1.34 ml per gram of hemoglobin) regardless of high the PaO2 may be. Furthermore, dissolved oxygen contributes very little to oxygen content (0.003 ml oxygen/dL/mmHg PaO2 ). As a result, increasing the PaO2 oxygen in oxygenated blood cannot overcome the effect of shunted blood that is deoxygenated and the patient will be desaturated to a degree proportional to the magnitude of the shunt.
I am going to see if I can scan the curve for carbon dioxide and put it after this slide…..This would be the text for that slide…...

26. Hemoglobin dissociation curve
Gaseous exchange
Hemoglobin dissociation curve
100 20 80 16
Veinous
PO2 = 40
Arterial
PO2 = 100
Sat = 75
Sat = 97 60 12
HEMOGLOBIN SATURATION
O2 CONTENT IN ml/100ml 40 8 20 4 20 40 60 80
100
PO2 mm Hg 7

27. Correspondence between PaO2 and SaO2 at normal pH
Gaseous exchange
Correspondence between PaO2 and SaO2 at normal pH
PaO2
mm Hg
96-105
86-95
76-85
66-75
56-65
46-55
35-45
SaO2 % 98 97 95 93 89 84 75 8

28. Oxygen transfer Gaseous exchange PO2 kPa AIR INHALED 20.9 Alveoli
1 mmHg = 1,359 cmH2O
1 cmH2O = 0,735 mmHg
1 hPa = 1 cmH2O = 1 mbar
AIR INHALED
20.9
Alveoli
ALVEOLAR GAS
13.3 O2
The consumption of O2 by the cells reduces the partial pressure (2.7 kPa).
O2 is diffused in the arterial blood to the cells due to the significant difference in partial pressure (10.0 vs. 2.7). Passage of the blood through the cells reduces its O2 content, veinous blood only containing 5.3 kPa.
In the alveoli the veinous blood also picks up the O2 from the alveolar gas by diffusion (13.3 vs. 5.3)
ARTERIEL BLOOD
10.0 O2 O2 O2 O2 O2
VEINOUS BLOOD
5.3 O2 O2
TISSUE
2.7
Cells 9

29. Transfer of carbon dioxide
Gaseous exchange
Transfer of carbon dioxide
PCO2
kPa
Tissue
TISSUE
6.7
CO2
The creation of CO2 by the tissue cells increases the partial CO2 pressure in the tissue (6.7 kPa). CO2 is diffused between the tissue and the arteriel blood due to the significant difference in partial pressure (6.7 vs. 5.3). The passage of blood through the cells increases its CO2 content to 6.1 kPa. The veinous blood comes into contact with the alveoli that only contain 2.7 kPa of CO2. The difference in partial pressure (2.7 vs. 6.1) causes diffusion of CO2 from the blood to the alveoli, reducing the CO2 content.
VEINOUS BLOOD
6.1
CO2
ARTERIAL BLOOD
5.3
CO2
CO2
EXHALED AIR
2.7
Alveoli
CO2 10

30. تغييرات پاتولوژيك در روابط بين تهويه به پرفيوژن شامل:
تغييرات پاتولوژيك در روابط بين تهويه به پرفيوژن شامل:
شنت (Shunt)گردش خون مناسب اما تهويه آلوئولی ناكافی مثل: ادم ريه وARDS آتلكتازی و پنومونی
SHUNT ZONE
NORMAL UNIT

31. تغييرات پاتولوژيك در روابط بين تهويه به پرفيوژن شامل:
تغييرات پاتولوژيك در روابط بين تهويه به پرفيوژن شامل:
فضای مرده آلوئولی (Dead Space) تهويه مناسب اما گردش خون ناكافی مثل: آمبولی ريه
DEAD SPACE
NORMAL UNIT

32. تغييرات پاتولوژيك در روابط بين تهويه به پرفيوژن شامل:
تغييرات پاتولوژيك در روابط بين تهويه به پرفيوژن شامل:
فاز خاموشی (Silent) زمانيكه گردش خون و تهويه هر دو ناكافی باشد مثل: پنومونكتومی
NORMAL UNIT
SILENT ZONE

33. Abnormal Gas Exchange Hypoxemia can be due to: hypoventilation
V/Q mismatch
shunt
diffusion impairments
Hypercarbia can be due to:
hypoventilation
V/Q mismatch
As outlined in the preceding slides, hypoxemia (not hypoxia) can be the result of hypoventilation (not enough delivered) or not matching the delivery to the loading sites (V/Q mismatch). Shunt, whether intracardiac or intrapulmonary, is the ultimate form of V/Q mismatch (V/Q = ). Diffusion impairments must be significant to result in hypoxemia and are rarely of clinical relevance in pediatrics. Hypoventilation is the primary cause of hypercarbia. V/Q mismatch must be profound before hypercarbia results for the reasons discussed in the previous slide.
Due to differences between oxygen and CO2 in their solubility and respective disassociation curves, shunt and diffusion impairments do not result in hypercarbia

34. Gas Exchange
Hypoventilation and V/Q mismatch are the most common causes of abnormal gas exchange in the PICU
Can correct hypoventilation by increasing minute ventilation
Can correct V/Q mismatch by increasing amount of lung that is ventilated or by improving perfusion to those areas that are ventilated
Maneuvers designed to improve V/Q are beyond the scope of this introductory lecture. Suffice to say, it is hard to selectively manipulate one area of the lung without affecting the entire system. For example, inhaled bronchodilators improve ventilation by relieving bronchospasm; they can also improve perfusion by producing vasodilatation in the alveolar capillary and thereby improve V/Q mismatch. However, there can be systemic absorption of these bronchodilators; this can lead to vasodilatation of vessels that were vasoconstricted secondary to hypoxia. The result is worsening V/Q mismatch and hypoxemia.
The last sentence is awkward on the slide …..as you said, V/Q will be tough to do……I would also like to try and get the topic of proning in briefly later on…the whole idea of “good lung down” or is that up? I think would be hard to do if we want to keep this at slides…..should we just mention it but not discuss it ?

35. Mechanical Ventilation
What we can manipulate……
Minute Ventilation (increase respiratory rate, tidal volume)
Pressure Gradient = A-a equation (increase atmospheric pressure, FiO2, increase ventilation, change RQ)
Surface Area = volume of lungs available for ventilation (increase volume by increasing airway pressure, i.e., mean airway pressure)
Solubility = ?perflurocarbons?
We can manipulate the same things a patient does - increase the respiratory rate and tidal volume for each breath. We can also try to keep alveoli from collapsing (as a baby does when they grunt)with positive end expiratory pressure. Unlike patients, we can manipulate the FiO2 or even the atmospheric pressure.
We can also try to open up collapsed areas by applying increased positive pressure. Remember that an alveolus that has collapsed will require a greater amount of pressure for a given change in volume than an alveolus that starts at FRC (see the section on compliance). Increasing the area available for gas exchange improves oxygenation and ventilation.
Perflurocarbons are experimental drugs; they are liquids through which oxygenation and ventilation can occur; one of their advantages is that oxygen is more soluble in perflurocarbons than it is in air. A full discussion of perflurocarbons is beyond the scope of this lecture.
Use this slide to bride pathophsy and vents…..

36. كمپليانس ريه(Compliance)
قابليت اتساع ريه ها و قفسه سينه را كمپليانس يا پذيرش ريه مي نامند كه عبارت از افزايش حجم ريه ها به ازای يك واحد افزايش فشار در داخل آلوئولها ست.

37. Mechanical Ventilation
If volume is set, pressure varies…..if pressure is set, volume varies…..
….according to the compliance…...
COMPLIANCE =
 Volume /  Pressure
If one parameter is set, then the other will vary as dictated by the patient’s compliance. The parameter that varies can be followed as an index of the patient’s compliance.

38. Compliance
Ref: Burton SL and Hubmayr RD: Determinants of Patient-Ventilator Interactions: Bedside Waveform Analysis,s in Tobin MJ (ed): Principles and Practice of Intensive Care Monitoring. New York, McGraw-Hill, Inc, 1998, p. 656.
Note that the FRC rests on a favorable part of the compliance curve. Small changes in pressure result in large changes in volume. If a patient’s compliance is on this part of the curve, then a given tidal volume will result in low peak pressures. If the compliance worsens (i.e., moves to the left or far right) then the pressure needed to deliver that same tidal volume will increase and the PIP will increase. The same is true if a set pressure is delivered - as compliance improves, the tidal volume will increase. If compliance worsens then a smaller tidal volume will result for the same PAP. Ideally, you want the alveolus to be at the bottom inflection point (FRC) at the beginning of each breath (end of each breath).
Burton SL & Hubmayr RD: Determinants of Patient-Ventilator Interactions: Bedside Waveform Analysis, in Tobin MJ (ed): Principles & Practice of Intensive Care Monitoring

39. مقاومت ريه :(Resistance)
مقاومت عبارت از اندازه گيری موانع موجود برای جريان گاز در كل راههای هوايی است.

41.   حجمها و ظرفيتهای ريوی :
حجم جاری (VT : Tidal volume)
حجمی از هواست كه با يك دم عادی به ريه ها وارد و با يك بازدم معمولی از ريه ها خارج می شود. مقدار آن 6-8 ML/Kg يا در حدود 500 ML است.

43. حجم ذخيره دمی IRV: Inspiratory Reserve Volume
  حجمها و ظرفيتهای ريوی
حجم ذخيره دمی IRV: Inspiratory Reserve Volume
حجم هوای اضافی دمی است كه می توان به دنبال يك دم عادی، با يك دم عميق وارد ريه ها نمود. مقدار آن در حدود 3000ميلی ليتر است.

45.   حجمها و ظرفيتهای ريوی
حجم ذخيره بازدمی (ERV : Expiratory Reserve Volume)
حجمی از هواست كه می توان بعد از پايان يك بازدم عادی ، با يك بازدم قوی از ريه ها خارج كرد. مقدار آن در حدود 1100 ميلی ليتر است.

47. حجم باقيمانده (RV : Residual Volume)
  حجمها و ظرفيتهای ريوی
حجم باقيمانده (RV : Residual Volume)
حجمی از هواست كه حتی با شديدترين بازدم نيز در ريه ها باقی می ماند و مانع از كلاپس آلوئولها می گردد. مقدار تقريبی آن 1200 ميلی ليتر است.

49. IC : Inspiratory capacity=VT+IRV) ظرفيت دمی (FRC : Functional Residual Capacity=ERV+RV) ظرفيت باقيمانده عملی (VC = Vital Capacitity)= IRV+VT+ERV) ظرفيت حياتی

50. به اميد ديدار در جلسه بعد