Comprehensive Guide to Oxygenation in Respiratory Care

Oxygenation is a vital aspect of medical care, involving the process of delivering oxygen to the body's cells. It includes measures such as Arterial Oxygen Saturation, Oxygen Delivery, Oxygen Consumption, and Oxygen Extraction. Understanding hypoxia and hypoxemia, as well as the mechanisms of hypoxemia, is crucial in managing respiratory conditions. Various methods of oxygenation, including supplemental O2 and mechanical ventilation, play a key role in maintaining adequate oxygen levels in the body.

• Oxygenation
• Respiratory Care
• Hypoxia
• Hypoxemia
• Mechanical Ventilation

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1. METHODS OF OXYGENATION OMER MIRZA

2. INTRODUCTION MEASURES OF OXYGENATION MECHANISMS OF HYPOXEMIA EFFECTS OF HYPOXEMIA METHODS OF OXYGENATION SUPPLEMENTAL O2 MECHANICAL VENTILATION MODES OF VENTILATION

3. OXYGENATION MOVING O2 FROM THE AIR AND DELIVERING TO THE CELLS HAS A FEW STEPS A. OXYGENATION, CONTENT. OXYGEN PASSIVELY DIFFUSES FROM THE ALVEOLUS TO THE PULMONARY CAPILLARY. BINDS TO HB IN RBCS. CAO2(ML O2/DL) = 1.34 X HB X SAO2 + (0.0031 X PAO2) B. OXYGEN DELIVERY. OXYGEN TRANSPORT FROM THE LUNGS TO THE PERIPHERAL TISSUES. DO2(ML/MIN) = Q X CAO2 C. OXYGEN CONSUMPTION. RATE AT WHICH THE TISSUES REMOVE O2 FROM THE BLOOD TO USE. VO2 (ML O2/MIN) = Q X (CAO2 CVO2) D. OXYGEN EXTRACTION. RELATIONSHIP BETWEEN O2 DELIVERY (DO2) AND OXYGEN CONSUMPTION (VO2). O2 EXTRACTION RATIO = (CAO2 - CVO2)/CAO2

4. LACK OF OXYGEN HYPOXIA DEFINED AS A CONDITION WHERE THE OXYGEN SUPPLY IS INADEQUATE EITHER TO THE BODY AS A WHOLE (GENERAL HYPOXIA) OR TO A SPECIFIC REGION (TISSUE HYPOXIA). HYPOXEMIA DEFINED AS AN ABNORMALLY LOW LEVEL OF OXYGEN IN THE BLOOD.

5. MEASURES OF OXYGENATION ARTERIAL OXYGEN SATURATION (SAO2) PROPORTION OF RBC WHOSE HB IS BOUND TO O2 MEASURED BY ABG AND PULSE OXIMETRY ARTERIAL OXYGEN TENSION (PAO2) AMOUNT OF O2 DISSOLVED IN PLASMA. MEASURED BY ABG.

6. MEASURES OF OXYGENATION 2 A-A OXYGEN GRADIENT DIFFERENCE BETWEEN AMOUNT OF O2 IN THE ALVEOLI (PAO2) AND THE AMOUNT DISSOLVED IN THE PLASMA (PAO2). A-A OXYGEN GRADIENT = PAO2 PAO2 PAO2 = (FIO2 X [PATM PH2O]) (PACO2 / R) PAO2 IS MEASURED ON ABG. GRADIENT CHANGES WITH AGE. GRADIENT INCREASES WITH HIGHER FIO2, WHICH CAN BE DIFFICULT TO ESTIMATE.

7. MEASURES OF OXYGENATION 3 PAO2/FIO2 MOSTLY USED IN VENTED PATIENTS. NORMAL IS 300 500. LESS THAN 300 ABNORMAL. A-A OXYGEN RATIO PAO2 / PAO2. PREDICT CHANGE IN PAO2 WHEN FIO2 IS CHANGED. LOWER LIMIT OF NORMAL IS 0.77 0.82 OXYGENATION INDEX USED IN PEDIATRICS, HIGH OI INDICATES SEVERE HYPOXEMIC RESPIRATORY FAILURE. OI = [MEAN AIRWAY PRESSURE X FIO2 / PAO2] X 100

8. MECHANISMS OF HYPOXEMIA HYPOVENTILATION V/Q MISMATCH RIGHT TO LEFT SHUNT DIFFUSION LIMITATION REDUCED INSPIRED OXYGEN TENSION

9. HYPOVENTILATION GAS MAKES UP ALL THE CONTENTS OF THE ALVEOLUS IF PARTIAL PRESSURE OF ONE GAS RISES, OTHERS DECREASE ARTERIAL AND ALVEOLAR CO2 RISES DURING HYPOVENTILATION. SO PAO2 DECREASES PURE HYPOVENTILATION (WITHOUT AN INCREASE IN A-A GRADIENT) RESOLVES QUICKLY WITH INCREASED FIO2 UNLESS PROLONGED AND THEN ATELECTASIS CAN INCREASE THE A-A GRADIENT

10. HYPOVENTILATION 2 - CAUSES CNS DEPRESSION, SUCH AS DRUG OVERDOSE, STRUCTURAL CNS LESIONS, OR ISCHEMIC CNS LESIONS THAT IMPACT THE RESPIRATORY CENTER OBESITY HYPOVENTILATION (PICKWICKIAN) SYNDROME IMPAIRED NEURAL CONDUCTION, SUCH AS AMYOTROPHIC LATERAL SCLEROSIS, GUILLAIN-BARR SYNDROME, HIGH CERVICAL SPINE INJURY, PHRENIC NERVE PARALYSIS, OR AMINOGLYCOSIDE BLOCKADE MUSCULAR WEAKNESS, SUCH AS MYASTHENIA GRAVIS, IDIOPATHIC DIAPHRAGMATIC PARALYSIS, POLYMYOSITIS, MUSCULAR DYSTROPHY, OR SEVERE HYPOTHYROIDISM POOR CHEST WALL ELASTICITY, SUCH AS A FLAIL CHEST OR KYPHOSCOLIOSIS

11. V / Q MISMATCH REFERS TO IMBALANCE BETWEEN PERFUSION AND VENTILATION LOW V COMPARED WITH Q, LOW O2 AND HIGH CO2 HIGH V COMPARED WITH Q, LOW CO2 AND HIGH O2 IMBALANCE IS PRESENT IN NORMAL LUNGS INCREASED MISMATCH IN DISEASED LUNG. THE HETEROGENEITY OF BOTH VENTILATION AND PERFUSION WORSENS CHARACTERIZED BY A-A GRADIENT INCREASE CORRECTED WITH LOW TO MODERATE FLOW OF INCREASED O2 OBSTRUCTIVE LUNG DISEASE, PULMONARY VASCULAR DISEASE AND INTERSTITIAL LUNG DISEASE

12. RIGHT TO LEFT SHUNT BLOOD PASSES FROM THE RIGHT SIDE OF THE HEART TO THE LEFT SIDE WITHOUT BEING OXYGENATED. TWO TYPES ANATOMIC SHUNT. WHEN ALVEOLI ARE BYPASSED INTRACARDIAC SHUNT, AVMS AND HEPATOPULMONARY PHYSIOLOGIC SHUNT. NON-VENTILATED ALVEOLI ARE PERFUSED ATELECTASIS DISEASES WITH ALVEOLAR FILLING (PNEUMONIA, ARDS) CAUSES EXTREME V/Q MISMATCH. 0 IN SOME LUNG REGIONS DIFFICULT TO CORRECT WITH SUPPLEMENTAL O2 QS/QT = (CCO2 - CAO2) (CCO2 - CVO2)

13. DIFFUSION LIMITATION MOVEMENT OF OXYGEN FROM THE ALVEOLUS TO THE PULMONARY CAPILLARY IS IMPAIRED. IT IS USUALLY A CONSEQUENCE OF ALVEOLAR AND/OR INTERSTITIAL INFLAMMATION AND FIBROSIS, SUCH AS THAT DUE TO INTERSTITIAL LUNG DISEASE. IN SUCH DISEASES, DIFFUSION LIMITATION USUALLY COEXISTS WITH V/Q MISMATCH, WHICH MAKES THE RELATIVE CONTRIBUTION OF EACH TO THE PATIENT'S HYPOXEMIA UNCERTAIN DIFFUSION LIMITATION IS CHARACTERIZED BY EXERCISE-INDUCED OR -EXACERBATED HYPOXEMIA. THIS IS ILLUSTRATED BY THE FOLLOWING DURING REST, BLOOD TRAVERSES THE LUNG RELATIVELY SLOWLY. THUS, THERE IS USUALLY SUFFICIENT TIME FOR OXYGENATION TO OCCUR EVEN IF DIFFUSION LIMITATION EXISTS DURING EXERCISE, CARDIAC OUTPUT INCREASES AND BLOOD TRAVERSES THE LUNG MORE QUICKLY. AS A RESULT, THERE IS LESS TIME FOR OXYGENATION IN THE HEALTHY INDIVIDUALS, SEVERAL COMPENSATORY MECHANISMS OCCUR. PULMONARY CAPILLARIES DILATE, WHICH INCREASES THE SURFACE AREA AVAILABLE FOR GAS EXCHANGE BY PERFUSING ADDITIONAL REGIONS OF LUNG. PAO2 ALSO INCREASES, WHICH PROMOTES OXYGEN DIFFUSION BY INCREASING THE OXYGEN GRADIENT FROM THE ALVEOLUS TO THE ARTERY. THE NET EFFECT IS THAT FULL OXYGENATION IS SUSTAINED IN PATIENTS WITH DIFFUSION LIMITATION (SUCH AS WITH PULMONARY FIBROSIS), THERE IS INSUFFICIENT TIME FOR OXYGENATION TO OCCUR. IN ADDITION, MOST SUCH PATIENTS HAVE PARENCHYMAL DESTRUCTION, WHICH RENDERS IT IMPOSSIBLE TO RECRUIT ADDITIONAL SURFACE AREA FOR GAS EXCHANGE. THE NET EFFECT IS MEASURABLE HYPOXEMIA

14. REDUCED INSPIRED OXYGEN TENSION THE INSPIRED OXYGEN TENSION (PIO2) IS A COMPONENT OF THE ALVEOLAR GAS EQUATION THAT WAS DESCRIBED ABOVE. IT CAN BE DETERMINED BY THE EQUATION: PIO2 = FIO2 X (PATM - PH2O) WHERE FIO2 IS THE FRACTION OF INSPIRED OXYGEN (0.21 AT ROOM AIR), PATM IS THE ATMOSPHERIC PRESSURE (760 MMHG AT SEA LEVEL), AND PH2O IS THE PARTIAL PRESSURE OF WATER (47 MMHG AT 37 DEGREES C) REDUCTION OF THE PIO2 WILL DECREASE THE PAO2. THIS IMPAIRS OXYGEN DIFFUSION BY DECREASING THE OXYGEN GRADIENT FROM THE ALVEOLUS TO THE ARTERY. THE NET EFFECT IS HYPOXEMIA. A REDUCED PIO2 IS MOST COMMONLY ASSOCIATED WITH HIGH ALTITUDE

15. EFFECTS OF HYPOXEMIA ADVERSELY EFFECTS EVERY TISSUE OF THE BODY CAUSES CELLULAR HYPOXIA. INSUFFICIENT O2 TO MEET THE NEEDS OF ANY GIVEN TISSUE CELLULAR HYPOXIA CAN BE DUE TO DIMINISHED O2 CONTENT (ANEMIA OR HYPOXEMIA) OR PERFUSION ABNORMALITY (ISCHEMIA) DIFFERENT TISSUES ARE AFFECTED DIFFERENTLY BY REDUCTION OF OR LACK OF O2

16. CELLULAR HYPOXIA MECHANISM OF INJURY DEPLETION OF ATP DEVELOPMENT OF INTRACELLULAR ACIDOSIS INCREASED CONCENTRATION OF METABOLIC BY-PRODUCTS GENERATION OF OXYGEN FREE RADICALS DESTRUCTION MEMBRANE PHOSPHOLIPIDS INCREASE OF INTRACELLULAR CALCIUM DIRECT DAMAGE TO CYTOSKELETON INDUCTION OF GENES CONTRIBUTING TO APOPTOSIS INFLAMMATORY REACTION NEUTROPHILIC INFILTRATION ISCHEMIA DUE TO DISRUPTION OF MICROCIRCULATION AND RELEASE OF O2 FREE RADICALS AS WELL AS CYTOKINE MEDIATORS

17. HOW TO DELIVER OXYGEN NASAL CANNULA VENTURI MASK NON REBREATHER NON INVASIVE VENTILATION HIGH FLOW NASAL CANNULA INTUBATION AND MECHANICAL VENTILATION ECMO

18. NASAL CANNULA LOW FLOW NASAL CANNULA USED WHERE LOWER FLOW RATES AND FIO2 IS NEEDED FLOW RATES OF 1 TO 5 L/MIN DIFFICULT TO ESTIMATE WHAT FIO2 IS. MIX OF ROOM AIR AND O2 HEATED HUMID HIGH FLOW NASAL CANNULA USED INCREASINGLY IN PLACE OF CPAP/ BIPAP USES A HIGH FLOW OR AIR AND OXYGEN TO WASHOUT THE UPPER AIRWAY MAY NOT BE EFFECTIVE AS PRIMARY RESPIRATORY SUPPORT STUDIES SUGGESTING EQUIVALENCE WITH NIV MAY BE OF LOWER QUALITY HUMIDIFICATION MAY AID SECRETION CLEARANCE

19. MASKS VENTURI MASK AIR-ENTRAINMENT SYSTEM HIGH-FLOW OXYGEN THERAPY USUALLY LIMITS O2 FLOW TO 12 -15 L/MIN AT HIGHER FIO2, FLOW REDUCES NON REBREATHER MASK USES A RESERVOIR BAG MAY BE ABLE TO DELIVER 60 80% UNLESS BAG DEFLATES PARTLY, ONLY FLOW RATE AS DETERMINED BY THE FLOW METER IS DELIVERED

20. NON-INVASIVE VENTILATION POSITIVE PRESSURE VENTILATION DELIVERED THROUGH A NONINVASIVE INTERFACE (NASAL MASK, FACEMASK, OR NASAL PLUGS) INDICATIONS EXACERBATIONS OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) THAT ARE COMPLICATED BY HYPERCAPNIC ACIDOSIS (ARTERIAL CARBON DIOXIDE TENSION [PACO2] >45 MMHG OR PH <7.30) CARDIOGENIC PULMONARY EDEMA ACUTE HYPOXEMIC RESPIRATORY FAILURE CONTRAINDICATION CARDIAC OR RESPIRATORY ARREST INABILITY TO COOPERATE, PROTECT THE AIRWAY, OR CLEAR SECRETIONS SEVERELY IMPAIRED CONSCIOUSNESS NONRESPIRATORY ORGAN FAILURE THAT IS ACUTELY LIFE THREATENING FACIAL SURGERY, TRAUMA, OR DEFORMITY HIGH ASPIRATION RISK PROLONGED DURATION OF MECHANICAL VENTILATION ANTICIPATED RECENT ESOPHAGEAL ANASTOMOSIS

21. INTUBATION AND MECHANICAL VENTILATION EXTENSIVE TOPIC VENTILATION STRATEGIES LOW TIDAL VOLUMES HIGH PEEP AND RECRUITMENT MANEUVERS HIGH FREQUENCY OSCILLATORY VENTILATION ADJUNCTIVE STRATEGIES PRONE POSITION PARTIAL OR TOTAL EXTRACORPOREAL SUPPORT PHARMACOLOGIC INTERVENTIONS. NEUROMUSCULAR BLOCKING AGENTS ANTI-INFLAMMATORY AGENTS AND STEM CELLS

22. HIGH PEEP AND RECRUITMENT MANEUVERS PULMONARY EDEMA AND END-EXPIRATORY ALVEOLAR COLLAPSE CHARACTERIZE SEVERAL FORMS OF RESPIRATORY FAILURE LOW PEEP. INSUFFICIENT TO STABILIZE ALVEOLI AND KEEP OPEN. INCREASING RISK OF VILI FROM ATELECTRAUMA HIGHER PEEP, IMPAIRMENT OF VENOUS RETURN, PULMONARY OVERDISTENSION IN ARDS PATIENTS, WITH WORSE OXYGENATION(P/F =< 200), HIGHER PEEP WAS ASSOCIATED WITH 5% REDUCTION IN RATE OF DEATH RECRUITMENT MANEUVERS SHOULD THEORETICALLY REDUCE VILI IN CLINICAL PRACTICE ROLE IS UNCERTAIN RISKS INCLUDE HEMODYNAMIC COMPROMISE AND PNEUMOTHORAX

23. HIGH FREQUENCY OSCILLATORY VENTILATION METHOD INVOLVES VERY SMALL TIDAL VOLUMES, MAY BE LASS THAN ANATOMIC DEAD SPACE HIGH FREQUENCIES. UPTO 15 PER SECOND THEORETICAL BENEFIT. MINIMIZING VILI MIXED DATA META-ANALYSIS OF 8 RCT WITH ARDS. SIGNIFICANTLY LOWER MORTALITY. 2 LARGE MULTICENTER TRIALS. DID NOT SHOW IMPROVED OUTCOMES. NOT RECOMMENDED AS FIRST LINE THERAPY.

24. ADJUNCTIVE THERAPIES REDUCING PATIENTS METABOLIC DEMANDS DECREASING REQUIRED MINUTE VENTILATION AND DECREASING BREATHING EFFORTS BOTH OF ABOVE WOULD RESULT FROM REDUCING METABOLIC DEMANDS AND MAY LIMIT VENTILATOR INDUCED LUNG INJURY. PRONE POSITION PARTIAL OR TOTAL EXTRACORPOREAL SUPPORT

25. PRONE POSITION ESTIMATED 70% OF ARDS PATIENTS WITH ARDS AND HYPOXEMIA HAVE IMPROVED OXYGENATION IN A PRONE POSITION POSSIBLE MECHANISMS INCREASED END-EXPIRATORY LUNG VOLUME BETTER VENTILATION-PERFUSION MATCHING LESS EFFECT OF MASS OF HEART ON THE LOWER LOBES IMPROVED REGIONAL VENTILATION SHOULD MINIMIZE LUNG INJURY BY INCREASING HOMOGENEITY OF VENTILATION META-ANALYSIS OF 7 TRIALS. 1724 ARDS PATIENTS PRONE POSITIONING LOWERED ABSOLUTE MORTALITY BY 10% POINTS IN SUBGROUP OF ARDS PATIENTS WITH SEVERE HYPOXEMIA. (P/F <100) INCREASED POTENTIALLY REVERSIBLE COMPLICATIONS RECENT TRIAL. 456 ARDS PATIENTS. (P/F < 150 AND FIO2 >0.6 RATE OF DEATH AT 28 DAYS. 32.8% IN SUPINE AND 16% IN PRONED PATIENTS

26. PARTIAL OR TOTAL EXTRACORPOREAL SUPPORT AVOID MECHANICAL VENTILATION RISKS AVOIDS VILI USE FULL ECMO HYBRID. POSSIBLE TO COMBINE MECHANICAL VENTILATION WITH PARTIAL EXTRACORPOREAL SUPPORT PRELIMINARY DATA SUPPORTIVE. FURTHER STUDIES REQUIRED TO DEFINE WHICH MODE OF EXTRACORPOREAL SUPPORT TO USE, WHEN TO USE IT AND ON WHICH PATIENT POPULATION

27. PHARMACOLOGIC INTERVENTIONS NEUROMUSCULAR BLOCKING AGENTS DYSPNEA IN ARDS AND VENTILATOR DYSSYNCHRONY AMELIORATED FACILITATE LIMITATIONS ON TIDAL VOLUMES AND PRESSURE BLOCKING AGENT USED IN PATIENT WITH POOR OXYGENATION IN ARDS (P/F < 150) LOWER 90 DAY ADJUSTED MORTALITY, WITHOUT INCREASE IN MUSCULAR WEAKNESS PRECISE MECHANISM IS UNCLEAR. PREVIOUS STUDY SUGGESTED LOWER CYTOKINES IN PATIENTS WITH NEUROMUSCULAR BLOCKERS. SO POSSIBLY LESS MULTIORGAN FAILURE WITH LOWER CYTOKINES, LESS BIOTRAUMA ANTI-INFLAMMATORY AGENTS AND STEM CELLS INVESTIGATED IN ANIMALS POSSIBILITY OF REDUCING CONSEQUENCES OF VILI BY ADMINISTRATION BEFORE INCITING AGENT (INTUBATION) EXPERIMENTAL. UNPROVEN BENEFIT.

28. QUESTIONS?