Ετήσιο Μετεκπαιδευτικό Σεμινάριο

Παρουσίαση με θέμα: "Ετήσιο Μετεκπαιδευτικό Σεμινάριο"— Μεταγράφημα παρουσίασης:

1 Αναπνευστικές οξεοβασικές διαταραχές Σχόλια – Παραδείγματα και πολλά άλλα….
Ετήσιο Μετεκπαιδευτικό Σεμινάριο Υγρών, Ηλεκτρολυτών & Οξεοβασικής ισορροπίας 11ο Σεμινάριο Διαταραχές Υγρών & Ηλεκτρολυτών 22-23 Σεπτεμβρίου 2017, Κομοτηνή Στρογγυλό τραπέζι III: Αναπνευστικές οξεοβασικές διαταραχές Προεδρείο: Σ. Κατσούδας - Ν. Αφεντάκης Σάββατο, 23 Σεπτεμβρίου Γεώργιος Ι. Μπαλτόπουλος Ομότιμος Καθηγητής ΕΚΠΑ Πνευμονολόγος –Εντατικολόγος

2 Δήλωση συμφερόντων για τα τελευταία 4 χρόνια- Conflict of Interest
Υποστήριξη έρευνας /4ετία BIOTEST AG, Germany – Astellas Για υπηρεσίες συμβούλου (advisory board meetings ) 1/4έτη Astellas, Delta Honoraria για διαλέξεις /4ετία Baxter

3 Αναπνευστικές οξεοβασικές διαταραχές Τι αναφέρθηκε;
Παθοφυσιολογία και σημειολογία της αναπνευστικής οξέωσης Δ. Μπαχαράκη Διάγνωση και αντιμετώπιση της αναπνευστικής οξέωσης Κ. Κατωπόδης Παθοφυσιολογία και σημειολογία της αναπνευστικής αλκάλωσης Γ. Τουλκερίδης Διάγνωση και αντιμετώπιση της αναπνευστικής αλκάλωσης Κ. Κανταρτζή Σχόλια - Παραδείγματα: Γ. Μπαλτόπουλος

4 Εντός Φυσιολογικών ορίων Ι
pH:7,35 – 7,45 Μέτρο της οξεοβασικής ισορροπίας (συγκέντρωση ιόντων υδρογόνου) pCO2: mmHg Μέτρο της μερικής πίεσης του διοξειδίου στο πλάσμα, μέτρο του κατά λεπτό αερισμού, ρυθμίζεται από τον αερισμό, ανακλά την κατάσταση της αναπνευστικής οξεοβασικής ισορροπίας HCO3: mEq/L 24 mEq Μέτρο των ελεύθερων διττανθρακικών στο αίμα ανακλά την μεταβολική οξεοβασική ισορροπία που ρυθμίζεται από τους νεφρούς BE:(-2) - (+2) Δείχνει την ποσότητα του οξέως ή της βάσης που απαιτείται για να ομαλοποιηθεί το pH στο φυσιολογικό κάτω από ορισμένες συνθήκες

5 Εντός Φυσιολογικών ορίων ΙΙ
pO2: mmHg Μέτρο της μερικής πίεσης του οξυγόνου στο αρτηριακό αίμα O2 Sat: % Δείχνει το ποσοστό της αιμοσφαιρίνης που είναι δεσμευμένο με το Ο2 ΡΟ2 σε Υπερβαρικό θάλαμο O2: 2,8 atm mmHg Αέρια αίματος στα Ιμαλάια: PO2-32 mmHg, PCO2- 7 mmHg, pH- 7,70

6 Το «παραβολικό CO2 !! » PaCO2= 0,863 x VCO2 / VA
VCO2 = CO2 production VA = VE – VD=VT x f (1- VD/VT) VE = minute (total) ventilation VD = dead space ventilation 0,863 converts units to mmHg Εξίσωση του Bohr: VD/VT = PaCO2-PECO2/PaCO2

7 Evaluation of Arterial Blood Gas
Primary process Compensatory response Respiratory acidosis Respiratory alkalosis Metabolic acidosis Metabolic alkalosis

8 1037 consecutive admissions
Acid-Base Disorders in the Emergency Department: Incidence, Etiologies and Outcomes 1037 consecutive admissions 736 (71%) showed an acid base disturbance 74 acidosis respiratory 22 /74 (30%) / 736 (3%) /1037 (2%) metabolic 52 99 alkalosis respiratory 74 /99 (75%) /736 (10%) /1037 (7%) metabolic 25 563 mixed Figure 1. Outcomes of the blood gas drawn in the study and types of ABDs Abstract Objective: Acid-base disorders (ABDs) are usually correlated with high rates of morbidity and mortality. The objective of this study was to analyze the causes, outcomes, types and incidences of ABDs in patients presenting at the emergency department (ED). Material and Methods: We prospectively analyzed data from patients who presented between January 2011 and May Data on age, gender, chief complaint, and diagnosis in the ED were collected for ABD cases. Results: Of the 736 cases with an ABD, 173 patients (23.5%) had simple ABD and 563 patients (76.5%) had mixed ABD. The most common ABD was a mixed metabolic acidosis and respiratory alkalosis (MACRAL) (n=408, 55.4%). All ABD types were most commonly observed in patients over 65 years of age. Dyspnea was the most common complaint among ABD patients who presented at the ED (44.4%). In cases of ABD, pneumonia was the most common diagnosis (16.3%). Of the ABD cases, 379 patients (51.6%) were discharged, while 318 patients (43.2%) were hospitalized. Death was more commonly observed in cases with mixed metabolic and respiratory acidosis (MRAC) (n=6) and MACRAL (n=11). Conclusion: ABDs are quite common in patients presenting at the ED, especially among patients in a critical condition (71%). Mixed MACRAL was the most commonly noted ABD. Dyspnea and pneumonia were the most common diagnoses in ABD patients. Mortality was more common in cases with a mixed MRAC and MACRAL. This knowledge may provide important information concerning the diagnosis, treatment and early prognosis of patients. (JAEM 2014; 13: 4-9) Ataman Köse, Erol Armağan, Nuran Öner, Özlem Köksal, Dilek Kostak Mert, Fatma Özdemir, Şule Akköse Aydın. Acid-Base Disorders in the Emergency Department:Incidence, Etiologies and Outcomes. JAEM 2014; 13: 4-9

9 Acid-Base Disorders in the Emergency Department: Incidence, Etiologies and Outcomes
Figure 2. Distribution of ABDs according to age Abstract Objective: Acid-base disorders (ABDs) are usually correlated with high rates of morbidity and mortality. The objective of this study was to analyze the causes, outcomes, types and incidences of ABDs in patients presenting at the emergency department (ED). Material and Methods: We prospectively analyzed data from patients who presented between January 2011 and May Data on age, gender, chief complaint, and diagnosis in the ED were collected for ABD cases. Results: Of the 736 cases with an ABD, 173 patients (23.5%) had simple ABD and 563 patients (76.5%) had mixed ABD. The most common ABD was a mixed metabolic acidosis and respiratory alkalosis (MACRAL) (n=408, 55.4%). All ABD types were most commonly observed in patients over 65 years of age. Dyspnea was the most common complaint among ABD patients who presented at the ED (44.4%). In cases of ABD, pneumonia was the most common diagnosis (16.3%). Of the ABD cases, 379 patients (51.6%) were discharged, while 318 patients (43.2%) were hospitalized. Death was more commonly observed in cases with mixed metabolic and respiratory acidosis (MRAC) (n=6) and MACRAL (n=11). Conclusion: ABDs are quite common in patients presenting at the ED, especially among patients in a critical condition (71%). Mixed MACRAL was the most commonly noted ABD. Dyspnea and pneumonia were the most common diagnoses in ABD patients. Mortality was more common in cases with a mixed MRAC and MACRAL. This knowledge may provide important information concerning the diagnosis, treatment and early prognosis of patients. (JAEM 2014; 13: 4-9) Ataman Köse, Erol Armağan, Nuran Öner, Özlem Köksal, Dilek Kostak Mert, Fatma Özdemir, Şule Akköse Aydın. Acid-Base Disorders in the Emergency Department:Incidence, Etiologies and Outcomes. JAEM 2014; 13: 4-9

10 Acid-Base Disorders in the Emergency Department: Incidence, Etiologies and Outcomes
Figure 3. Distribution of ABD types according to case outcome Abstract Objective: Acid-base disorders (ABDs) are usually correlated with high rates of morbidity and mortality. The objective of this study was to analyze the causes, outcomes, types and incidences of ABDs in patients presenting at the emergency department (ED). Material and Methods: We prospectively analyzed data from patients who presented between January 2011 and May Data on age, gender, chief complaint, and diagnosis in the ED were collected for ABD cases. Results: Of the 736 cases with an ABD, 173 patients (23.5%) had simple ABD and 563 patients (76.5%) had mixed ABD. The most common ABD was a mixed metabolic acidosis and respiratory alkalosis (MACRAL) (n=408, 55.4%). All ABD types were most commonly observed in patients over 65 years of age. Dyspnea was the most common complaint among ABD patients who presented at the ED (44.4%). In cases of ABD, pneumonia was the most common diagnosis (16.3%). Of the ABD cases, 379 patients (51.6%) were discharged, while 318 patients (43.2%) were hospitalized. Death was more commonly observed in cases with mixed metabolic and respiratory acidosis (MRAC) (n=6) and MACRAL (n=11). Conclusion: ABDs are quite common in patients presenting at the ED, especially among patients in a critical condition (71%). Mixed MACRAL was the most commonly noted ABD. Dyspnea and pneumonia were the most common diagnoses in ABD patients. Mortality was more common in cases with a mixed MRAC and MACRAL. This knowledge may provide important information concerning the diagnosis, treatment and early prognosis of patients. (JAEM 2014; 13: 4-9) Ataman Köse, Erol Armağan, Nuran Öner, Özlem Köksal, Dilek Kostak Mert, Fatma Özdemir, Şule Akköse Aydın. Acid-Base Disorders in the Emergency Department:Incidence, Etiologies and Outcomes. JAEM 2014; 13: 4-9

11 General hospital: Incidence of acid-base disturbances
110 consecutive admissions 62 (56%) showed a disturbance in acid base equilibrium 21 acidosis respiratory 15 /21 (71%) /62 (24%) /110 (14%) metabolic 6 30 alkalosis respiratory 21 /30 (70%) /62 (34%) /110 (19%) metabolic 9 11 mixed Format: AbstractSend to Recenti Prog Med Dec;81(12): Incidence of acid-base and electrolyte disturbances in a general hospital: a study of 110 consecutive admissions. Palange P1, Carlone S, Galassetti P, Felli A, Serra P. Author information Abstract To establish the overall frequency distribution and combination of acid-base and electrolyte disturbances as they occur in a general population requiring hospital care, we studied arterial blood gases and plasma electrolytes (sodium, potassium and chloride) in 110 consecutive patients (age = 68 +/- 8 SE; 64 M, 46 F) at the time of admission to a general medical ward. Disturbances were defined on the basis of the standard pH/pCO2 plot and the normal (mean +/- 2 SD) electrolyte range for our laboratory. Sixty-two patients (56%) showed a disturbance in acid base equilibrium: acidosis: respiratory 16, metabolic 6; alkalosis: respiratory 26, metabolic 10; in 4/62 the acid base disturbance was mixed. In 47 of the 62 patients, the acid base imbalance were associated with electrolyte derangements (low PNa+, 12; high PNa+, 1; low PK+, 10; high pK+, 7; increased anion gap, 17). Electrolyte disturbances with a normal acid base status were detected in only 2 patients. Of significance, in 7 of the 58 individuals considered to have a "pure" acid base disturbance on the basis of the pH/pCO2 plot (5 respiratory alkalosis; 1 respiratory acidosis; 1 metabolic alkalosis), a widened anion gap revealed that the acid-base change was mixed, i.e. there was a concomitant component of metabolic acidosis. Thus, the total number of mixed acid base equilibrium disorders were eleven. This study emphasizes the frequent incidence of acid base and electrolyte disorders, very often in combination, among unselected adult patients admitted to a general medical ward. In addition it reinforces that a high prevalence of hidden cases of mixed acid base disturbances can be recognized by concomitant analysis of acid base and electrolyte parameters, including anion gap calculation. Recenti Prog Med Dec;81(12): Incidence of acid-base and electrolyte disturbances in a general hospital: a study of 110 consecutive admissions.

12 The prevalence of acid-base disturbances (%) at zero, six, 12 hrs after ICU admission
213 patients post operatively admitted in ICU 123 male and 90 female (age yrs) 18 pts (8.5%)  normal ABG 195 pts (91.5%)  acid-base dysfunction (metabolic acidosis & alkalosis:67.1%) Taghavi Gilani M, Razavi M, Peivandi Yazdi A. Incidence of Postoperative Acid-Base Disturbances in Abdominal Surgery. Patient Saf Qual Improv. 2014; 2(2):82-85.

13 Acid-Base Disorders: Τοπογραφία!!
In the Emergency Department 71% Total 23,5% Respiratory On Hospital Admission 56%Total 82% Respiratory On ICU admission postoperatively 91.5% 32,9%

14 Compensatory increase Respiratory alkalosis Compensatory decrease
Compensation Primary Disturbance pH HCO3- PCO2 Compensation Respiratory acidosis <7.35 Compensatory increase Primary increase Acute: 1-2 mEq/L increase in HCO3- for every 10 mm Hg increase in PCO2 Chronic: 3-4 mEq/L increase in HCO3- for every 10 mm Hg increase in PCO2 Respiratory alkalosis >7.45 Compensatory decrease Primary decrease Acute: 1-2 mEq/L decrease in HCO3- for every 10 mm Hg decrease in PCO2 Chronic: 4-5 mEq/L decrease in HCO3- for every 10 mm Hg decrease in PCO2 Metabolic acidosis 1.2 mm Hg decrease in PCO2 for every 1 mEq/L decrease in HCO3- Metabolic alkalosis mm Hg increase in PCO2 for every 1 mEq/L increase in HCO3- , PCO2 should not rise above 55 mm Hg in compensation

15 PCO2 greater than expected
Respiratory acidosis PCO2 greater than expected Acute or chronic Causes excess CO2 in inspired air rebreathing of CO2-containing expired air addition of CO2 to inspired air insufflation of CO2 into body cavity decreased alveolar ventilation central respiratory depression & other CNS problems nerve or muscle disorders lung or chest wall defects airway disorders external factors (Lung-protective MV with permissive hypercapnia) increased production of CO2 hypercatabolic disorders

16 Acute Respiratory Acidosis- No renal compensation 65-yr ♂ with a BMI 30 kg/m2
3-hour history of shortness of breath + feeling ill for the past week Temp 38.3°C, HR 96/min, RR 20/min and shallow, BP 145/90 mm Hg Hhypoventilation : History/Physical Exam + increased PCO2 and (A-a)PO2 difference Na+ 138 mEq/L pH 7,33 K+ 4,2 mEq/L PCO2 50 mm Hg Cl- 101 mEq/L PO2 67 mm Hg CO2, total 28 mEq/L HCO3- 26 mEq/L 1-2 mEq/L increase in HCO3- for every 10 mm Hg increase in PCO2 PCO2 increase = = 10 mm Hg HCO3- increase predicted = (1-2) x (10/10) = 1-2 mEq/L add to 24 mEq/L (reference point) = mEq/L (A-a)PO2 difference = 0.21(760 – 47) -50/ = 20 mm Hg

17 Chronic Respiratory Acidosis - Renal compensation 56-yr ♀ with COPD
3-hour history of shortness of breath. Temp 37°C, HR 90/min, RR 22/min and shallow, BP 135/80 mmHg V/Q imbalance: History/PE + increased PCO2 and (A-a)PO2 difference Na+ 145 mEq/L pH 7,33 K+ 4.5 mEq/L PCO2 62 mmHg Cl- 99 mEq/L PO2 32 mmHg CO2, total 34 mEq/L HCO3- 32 mEq/L 3-4 mEq/L increase in HCO3- for every 10 mm Hg increase in PCO2. PCO2 increase = = 22 mmHg HCO3- increase predicted = (3-4) x (22/10) = 7-9 mEq/L add to 24 mEq/L (reference point) = mEq/L (A-a)PO2 difference = 0.21(760 – 47) – 62/0.8 – 32 = 41 mm Hg

18 Respiratory alkalosis
PCO2 less than expected Acute or chronic Causes increased alveolar ventilation central causes, direct action via respiratory center Head Injury-Stroke Anxiety-hyperventilation syndrome (psychogenic) Other 'supra-tentorial' causes (pain, fear, stress, voluntary) Various drugs (eg analeptics, propanidid, salicylate intoxication) Various endogenous compounds (eg progesterone during pregnancy, cytokines during sepsis, toxins in patients with chronic liver disease) hypoxaemia, act via peripheral chemoreceptors pulmonary causes, act via intrapulmonary receptors Pulmonary Embolism Pneumonia Asthma- Pulmonary oedema (all types) iatrogenic, act directly on ventilation) Excessive controlled ventilation Examples: Central causes (direct action via respiratory center) - various drugs (eg, analeptics, propanidid, salicylate intoxication) Hypoxaemia (act via peripheral chemoreceptors) - respiratory stimulation via peripheral chemoreceptors Pulmonary causes (act via intrapulmonary receptors) – pulmonary embolism Iatrogenic (act directly on ventilation)– excessive controlled ventilation see for more examples.

19 Acute Respiratory Alkalosis-no renal compensation 17-yr ♀ with epigastric pain & nausea for 3-hrs
She admits taking a large dose of aspirin. RR 20/min- full range Hyperventilation:History/PE + decreased PCO2 Na+ 136 mEq/L pH 7,55 K+ 3.7 mEq/L PCO2 25 mmHg Cl- 101 mEq/L PO2 104 mmHg CO2, total 23 mEq/L HCO3- 22 mEq/L 1-2 mEq/L decrease in HCO3- for every 10 mm Hg decrease in PCO2. PCO2 decrease = = 15 mmHg HCO3- decrease predicted = (1-2) x (15/10) = 2-3 mEq/L subtract from 24 mEq/L (reference point) = mEq/L (A-a)PO2 difference = 0.21(760 – 47) – 25/0.8 – 104 = 15 mm Hg

20 Chronic Respiratory Alkalosis-Renal compensation 81-yr ♀ Living at 2743m for the past 1 month + anxiety 2-day history of shortness of breath. RR 20/min full range Hyperventilation:History/PE + decreased PCO2 Na+ 133 mEq/L pH 7.48 K+ 4.9 mEq/L PCO2 22 mmHg Cl- 105 mEq/L PO2 69 mmHg CO2, total 17 mEq/L HCO3- 16 mEq/L 4-5 mEq/L decrease in HCO3- for every 10 mm Hg decrease in PCO2 PCO2 decrease = = 18 mmHg HCO3- decrease predicted = (4-5) x (18/10) = 7-9 mEq/L subtract from 24 mEq/L (reference point) = mEq/L (A-a)PO2 difference = 0.21(760 – 47) – 22/0.8 – 69 = 54 mm Hg

21 Respiratory Alkalosis: Hysterical Hyperventilation
Charlotte Lind, a 55-year-old interior designer, has been terrified of flying ever since she had a "bad" experience on a commuter flight. Nevertheless, she and her husband planned a trip to Paris to celebrate their thirtieth wedding anniversary. As the time for the trip approached, Charlotte had what she called "anxiety attacks." One evening, a few days before the scheduled flight to Paris, Charlotte started hyperventilating uncontrollably. She became light-headed, and her hands and feet were numb and tingling. She thought she was having a stroke. Her husband rushed her to the local emergency department, where a blood sample was drawn immediately PH 7.56 (normal, 7.4) PCO2 23 mm Hg (normal, 40 mm Hg) HCO3– 20 mEq/L (normal, 24 mEq/L) The emergency department staff asked Charlotte to breathe into and out of a paper bag. A second blood sample was drawn. pH 7.41 (normal, 7.4) PCO2 41 mm Hg (normal, 40 mm Hg) HCO3- 25 mEq/L (normal, 24 mEq/L) Charlotte was pronounced "well," and she returned home that evening.

22 Ο κύκλος της Αναπνευστικής Αλκάλωσης και η σακούλα!!!
Ο κύκλος της Αναπνευστικής Αλκάλωσης και η σακούλα!!!

23 14♂ & 6 ♀ young healthy volunteers Hyperventilation to a mean ETCO2: 21.6 mmHg Rebreathe.. paper bag… 30 seconds O2: −15.9 (SD, 4.6) CO2: 38.7 (SD, 6.2) 60 seconds O2: −20.5 (6.0), CO2:40.2 (6.4); 90 seconds O2:−22 (6.8) CO2:40.5 (6.4) 120 seconds O2: −23.6 (6.8) CO2:40.7 (6.5) 150 seconds O2: −25.1 (1.2) CO2: 41 (7.3) 180 seconds O2: −26.6 (8.4) CO2: 41.3 (7.5) A few subjects achieved CO2 levels as high as 50, but many never reached 40. The mean maximal drop in O2 was 26 (8.8); seven subjects had drops in oxygen of 26 mm Hg at three minutes, four had drops of 34 mm Hg, and one had a drop of 42 mm Hg. Three subjects rebreathed into an 18-L plastic bag filled with 100% O2, but although CO2 rapidly exceeded 40, O2 levels reached 21% within two to four minutes and continued to decline to less than 10% at 15 minutes. Paper bag rebreathing decreases inspired oxygen sufficiently to endanger hypoxic patients. Paper bag rebreathing should never be administered unless myocardial ischemia can be ruled out and the patient's oxygenation has been directly measured by arterial blood gases or pulse oximetry Since these conditions are impossible to achieve outside the hospital, its recommendation and use by prehospital personnel should be abandoned, and its use in hospital probably should be diminished. rebreathe into a brown paper bag three cases in which this treatment, erroneously applied to patients who were hypoxemic or had myocardial ischemia, resulted in death. Callaham M .Hypoxic hazards of traditional paper bag rebreathing in hyperventilating patients. Annals of Emergency Medicine, 1989; 18: DOI:

24 Signs & Symptoms

25 Βασικές αρχές Ακραίες τιμές pH: 6,8-7,8 ( nmol/L) Οι μεταβολές του pH αντιμετωπίζονται με ταχείς και βραδείς μηχανισμούς Κάθε λεπτό χωρίς αναπνοή αυξάνει το CO2 στο αίμα κατά 3 mmHg Κάθε μεγάλη αναπνοή μειώνει το CO2 κατά 3 mmHg Στο σχεδιασμό μας είμαστε αλκαλικά όντα (pH=7,37-7,43), στη λειτουργία όμως είμαστε παραγωγοί οξέων

26 PaCO2-pH-Apnea in 11 Neurosurgery pts BENZEL EC,MASHBURN JP, CONRAD S, MODLING D. J. Neurosurg. 1992; 76: FIG. 1. Graph showing the rate of PaCO2 elevation during apnea. The closed boxes represent the average for Group I (patients with a baseline PaCO2 between 40 and 45 mm Hg) and the open boxes represent the average for Group II (patients with a baseline PaCO2 above 45 mm Hg). FIG. 3. Graph showing the rate of pO2 decrease during apnea. The closed boxes represent the average for Group I (patients with a baseline PaCO2 between 40 and 45 mm Hg) and the open boxes represent the average for Group II (patients with a baseline PaCO2 above 45 mm Hg). FIG. 2. Graph depicting the rate of pH decrease during apnea. The closed boxes represent the average for Group I (patients with a baseline PaCO: between 40 and 45 mm Hg) and the open boxes represent the average for Group I1 (patients with a baseline PaCO2 above 45 mm Hg). FIG. 4. Graph depicting the rate of PaCO2 elevation during apnea companng mean changes for four different PaCO2 baseline levels. The upper two curves represent data presented here and the lower two curves represent previously published data.

27 5 ενήλικα άλογα και ένα πουλάρι για ευθανασία- median values plotted
Αναισθησία: Xylazine–midazolam–ketamine Ευθανασία: atlanto-occipital intrathecal lidocaine injection Guedes Α, Aleman M, Davis E, Tearney C. Cardiovascular, respiratory and metabolic responses to apnea induced by atlanto-occipital intrathecal lidocaine injection in anesthetized horses.Veterinary Anaesthesia and Analgesia, 2016, 43, 590–598

28 Apnea Test Personal case

29 Same case-Post Apnea test

30 Same case-Post Apnea test

31 Same case-Post Apnea test

32 Ευχαριστώ για την προσοχή σας
Συμπεράσματα Οι αναπνευστικές οξεοβασικές διαταραχές είναι συνηθισμένες στα επείγοντα, στις πτέρυγες και στη ΜΕΘ, με μικρότερη όμως συχνότητά σε σχέση με τις υπόλοιπες οξεοβασικές διαταραχές Η αντιρρόπηση του οργανισμού μας ακολουθεί συγκεκριμένο μοτίβο Επί κατάργησης της αναπνευστικής λειτουργίας οι αναπνευστικές οξεοβασικές μεταβολές είναι προβλέψιμες είτε χωρίς καθόλου αερισμό είτε με μηχανική υποστήριξη της αναπνοής Ευχαριστώ για την προσοχή σας