DOCSLIB.ORG

A Nomogram for Obtaining the Partial Pressure of Oxygen in Alveolar Air

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
A Nomogram for Obtaining the Partial Pressure of Oxygen in Alveolar Air Thorax 1993;48:89-90 89 Technical note Thorax: first published as 10.1136/thx.48.1.89 on 1 January 1993. Downloaded from A nomogram for obtaining the partial pressure of oxygen in alveolar air Amod Karnik, Dilip R Karnad The relation between the arterial and the (which at 37°C is 47 mm Hg), Fxo2 is the alveolar partial pressure of oxygen (Po2) is fraction of oxygen in inspired air, Paco2 is the used for estimation of venous admixture in partial pressure of carbon dioxide in arterial critically ill patients,' 2 for adjusting the blood, and R is the respiratory quotient. To inspired oxygen concentration to obtain the avoid the tedious task of repeatedly calculat- required arterial Po2 in patients having ing PAO2 by solving the alveolar gas equation, mechanical ventilation,;5 as a basis for decid- we attempted to produce a nomogram that ing whether to wean a patient from mechan- takes all these variables into account. Medical Intensive ical ventilation,6 for calculating intrapulmon- Care Unit, Department of ary shunting,7 and for predicting the extent of Medicine, King hypoxaemia during an air flight in patients The nomogram Edward Memorial with chronic obstructive lung disease.8 The nomogram was drawn on the basis of the Hospital, Parel, Bombay 400 012, India Whereas the arterial Po2 is estimated by blood alveolar gas equation on the assumption that A Karnik gas analysis, the partial pressure of oxygen in the value of R is 0-8. The barometric pressure D R Karnad alveolar gas (PAo2) is obtained from the (PB) is selected on the scale at the bottom of Reprint requests to: alveolar gas equation91O: the left hand portion of the nomogram. A Dr D R Karnad vertical line is plotted upwards from this PB Received 20 August 1991 2 Returned to authors PAO2 = (PB-PH2O)x FIO2- until it intersects the desired FIo2 line. For 18 December 1991 R values of Fio2 that lie between two drawn FIo2 Revised version received 27 January 1992 where PB is the barometric pressure in lines a measured or approximate point is http://thorax.bmj.com/ Accepted 4 February 1992 mm Hg, PH2o is the water vapour pressure selected. From this point a horizontal line is Nomogram based on the 8 feet alveolar gas equationfor obtaining the alveolar Altitude 0C4 CO 350 400 450 500 550 600 650 700 750 mm Hg above l I partial pressure of oxygen sea level o PI0i-partial 0) co metresometres Alveolar Po2 (PAo2). co N F4 pressure of oxygen in %nl rfn 7Af inspired air; Pacoj- on September 28, 2021 by guest. Protected copyright. partial pressure of carbon dioxide in arterial blood. Correction for the respiratory quotient (R): The correctionfactor is obtained by rounding off 01 Paco2 in kPa to the I nearest whole number and E then dividing this by 10, or E by dividing Paco2 in mm Hg by 10 and 0v rounding this off to the nearest whole number. If R = 0-8, no change in PAo2 is required; if 0 R = 0 7,1 5 times the IC correctionfactor is subtractedfrom the PAo2; 2 if R = 0 9,1 5 times the correction factor is added to PAo2; if R = 1, twice the correction factor is E added to the PAo2- E 0 Barometric pressure Alveolar Po2 I I I I I I mm 8(00 700 600 I Hg 110 50 100 150 200 250 300 350 400 450 mm Hg 90 Karnik, Karnad plotted, extending rightwards across the nomogram values) was 7 4 mm Hg or 1 kPa vertical scale for the partial pressure of oxygen (95% CI 6-1-8 7 mm Hg or 0 8-1-2 kPa). in inspired air (PIo2, kPa) into the right hand The nomogram is suitable for use up to an portion of the nomogram. The PIo2 value may altitude of 11 000 feet (3353 metres). We Thorax: first published as 10.1136/thx.48.1.89 on 1 January 1993. Downloaded from be read off this vertical (kPa) scale or off the recommend that users draw a vertical line vertical scale on the right in mm Hg if corresponding to the barometric pressure at desired, but is not essential for obtaining the the altitude at which they are working. The PAO2. The horizontal line that is being plotted line for use at sea level is the one already is extended until it intersects the desired drawn at 760 mm Hg. Plotting values on a Paco2 line. A vertical line through this point line that is already drawn increased accuracy. of intersection, drawn upwards (if the Our nomogram therefore gives fairly horizontal line is in the upper half of the accurate values of PAO2 within a reasonable nomogram) or downwards (if the horizontal time. Moreover, its ease of use makes it a line is in the lower half of the nomogram) will convenient alternative to a pocket calculator. give the PAO2 value in kPa and mm Hg. In most clinical circumstances the res- We are grateful to the resident doctors from the department of piratory quotient is assumed to be 0 837; we medicine for their cooperation, and to Peter Gonsalves for therefore assumed this value when preparing helping us to prepare this nomogram. the nomogram. If, however, in a particular patient the respiratory quotient is measured and is not 0-8, a correction is provided (see 1 Nunn JF. Applied respiratory physiology. London: Butter- legend below figure). worths, 1977:274-310. 2 West JB. Ventilation-perfusion relationship. Am Rev Respir Dis 1977;116:919-43. 3 Bone RC, Stober G. Mechanical ventilation in respiratory Validation failure. Med Clin North Am 1983;67:599-619. After some practice in using the nomogram 4 Benator FR, Hewlett AM, Nunn JF. The use of isoshunt lines for control ofoxygen therapy. Br J Anaesthesiol 1973; and a non-programmable pocket calculator, 45:711-8. 20 resident doctors were given 10 problems; 5 Gilbert R, Keighley JF. The arterial/alveolar oxygen tension in each case values were provided for PB, FIO2, ratio. An index of gas exchange applicable to varying inspired oxygen concentration. Am Rev Respir Dis and Paco2, from which the PAO2 had to be 1974;109: 142-5. derived first with the calculator and then with 6 Balk RA, Bone RC. Mechanical ventilation. In: Bone RC, In 1-5 there was a George RB, Hudson LD, eds. Acute respiratory failure. the nomogram. problems New York: Churchill Livingstone, 1987:213-38. constant PB of 760 mm Hg, so these values 7 Shapiro BA, Harrison RA, Walton JR. Clinicalapplication of could be plotted on the vertical line already blood gases. 3rd ed. Chicago: Year Book Medical Pub- drawn on the nomogram at 760 mm In lishers, 1982:209-27. Hg. 8 Apte NM, Karnad DR. Altitude hypoxia and the arterial to http://thorax.bmj.com/ problems 6-10 the PB varied from 500 to alveolar oxygen ratio (letter). Ann Intern Med 1990; an 112:547-8. 800 mm Hg. These doctors took average of 9 George RB. Pathophysiology ofacute respiratory failure. In: 13 seconds (95% CI 8-07-18-03 seconds) lon- Bone RC, George RB, Hudson LD, eds. Acute respiratory ger over each problem with the nomogram failure. New York: Churchill Livingstone, 1987:1-9. 10 Riley RL, Cournand A. Ideal alveolar air and the analysis of than with the calculator. The mean of the ventilation perfusion relationships in the lung. J Appl residuals (difference between actual and Physiol 1949;1:825-47. on September 28, 2021 by guest. Protected copyright..
Load more

Recommended publications
  • The Oxyhaemoglobin Dissociation Curve in Critical Illness
    Basic sciences review The Oxyhaemoglobin Dissociation Curve in Critical Illness T. J. MORGAN Intensive Care Facility, Division of Anaesthesiology and Intensive Care, Royal Brisbane Hospital, Brisbane, QUEENSLAND ABSTRACT Objective: To review the status of haemoglobin-oxygen affinity in critical illness and investigate the potential to improve gas exchange, tissue oxygenation and outcome by manipulations of the oxyhaemoglobin dissociation curve. Data sources: Articles and published peer-review abstracts. Summary of review: The P50 of a species is determined by natural selection according to animal size, tissue metabolic requirements and ambient oxygen tension. In right to left shunting mathematical modeling indicates that an increased P50 defends capillary oxygenation, the one exception being sustained hypercapnia. Increasing the P50 should also be protective in tissue ischaemia, and this is supported by modeling and experimental evidence. Most studies of critically ill patients have indicated reduced 2,3-DPG concentrations. This is probably due to acidaemia, and the in vivo P50 is likely to be normal despite low 2,3-DPG levels. It may soon be possible to achieve significant P50 elevations without potentially harmful manipulations of acid-base balance or hazardous drug therapy. Conclusions: Despite encouraging theoretical and experimental data, it is not known whether manipulations of the P50 in critical illness can improve gas exchange and tissue oxygenation or improve outcome. The status of the P50 may warrant more routine quantification and consideration along with the traditional determinants of tissue oxygen availability. (Critical Care and Resuscitation 1999; 1: 93-100) Key words: Critical illness, haemoglobin-oxygen affinity, ischaemia, P50, tissue oxygenation, shunt In intensive care practice, manipulations to improve in the tissues.
    [Show full text]
  • Oxygenation and Oxygen Therapy
    Rules on Oxygen Therapy: Physiology: 1. PO2, SaO2, CaO2 are all related but different. 2. PaO2 is a sensitive and non-specific indicator of the lungs’ ability to exchange gases with the atmosphere. 3. FIO2 is the same at all altitudes 4. Normal PaO2 decreases with age 5. The body does not store oxygen Therapy & Diagnosis: 1. Supplemental O2 is an FIO2 > 21% and is a drug. 2. A reduced PaO2 is a non-specific finding. 3. A normal PaO2 and alveolar-arterial PO2 difference (A-a gradient) do NOT rule out pulmonary embolism. 4. High FIO2 doesn’t affect COPD hypoxic drive 5. A given liter flow rate of nasal O2 does not equal any specific FIO2. 6. Face masks cannot deliver 100% oxygen unless there is a tight seal. 7. No need to humidify if flow of 4 LPM or less Indications for Oxygen Therapy: 1. Hypoxemia 2. Increased work of breathing 3. Increased myocardial work 4. Pulmonary hypertension Delivery Devices: 1. Nasal Cannula a. 1 – 6 LPM b. FIO2 0.24 – 0.44 (approx 4% per liter flow) c. FIO2 decreases as Ve increases 2. Simple Mask a. 5 – 8 LPM b. FIO2 0.35 – 0.55 (approx 4% per liter flow) c. Minimum flow 5 LPM to flush CO2 from mask 3. Venturi Mask a. Variable LPM b. FIO2 0.24 – 0.50 c. Flow and corresponding FIO2 varies by manufacturer 4. Partial Rebreather a. 6 – 10 LPM b. FIO2 0.50 – 0.70 c. Flow must be sufficient to keep reservoir bag from deflating upon inspiration 5.
    [Show full text]
  • Respiratory Support
    Intensive Care Nursery House Staff Manual Respiratory Support ABBREVIATIONS FIO2 Fractional concentration of O2 in inspired gas PaO2 Partial pressure of arterial oxygen PAO2 Partial pressure of alveolar oxygen PaCO2 Partial pressure of arterial carbon dioxide PACO2 Partial pressure of alveolar carbon dioxide tcPCO2 Transcutaneous PCO2 PBAR Barometric pressure PH2O Partial pressure of water RQ Respiratory quotient (CO2 production/oxygen consumption) SaO2 Arterial blood hemoglobin oxygen saturation SpO2 Arterial oxygen saturation measured by pulse oximetry PIP Peak inspiratory pressure PEEP Positive end-expiratory pressure CPAP Continuous positive airway pressure PAW Mean airway pressure FRC Functional residual capacity Ti Inspiratory time Te Expiratory time IMV Intermittent mandatory ventilation SIMV Synchronized intermittent mandatory ventilation HFV High frequency ventilation OXYGEN (Oxygen is a drug!): A. Most infants require only enough O2 to maintain SpO2 between 87% to 92%, usually achieved with PaO2 of 40 to 60 mmHg, if pH is normal. Patients with pulmonary hypertension may require a much higher PaO2. B. With tracheal suctioning, it may be necessary to raise the inspired O2 temporarily. This should not be ordered routinely but only when the infant needs it. These orders are good for only 24h. OXYGEN DELIVERY and MEASUREMENT: A. Oxygen blenders allow O2 concentration to be adjusted between 21% and 100%. B. Head Hoods permit non-intubated infants to breathe high concentrations of humidified oxygen. Without a silencer they can be very noisy. C. Nasal Cannulae allow non-intubated infants to breathe high O2 concentrations and to be less encumbered than with a head hood. O2 flows of 0.25-0.5 L/min are usually sufficient to meet oxygen needs.
    [Show full text]
  • Respiratory Therapy Pocket Reference
    Pulmonary Physiology Volume Control Pressure Control Pressure Support Respiratory Therapy “AC” Assist Control; AC-VC, ~CMV (controlled mandatory Measure of static lung compliance. If in AC-VC, perform a.k.a. a.k.a. AC-PC; Assist Control Pressure Control; ~CMV-PC a.k.a PS (~BiPAP). Spontaneous: Pressure-present inspiratory pause (when there is no flow, there is no effect ventilation = all modes with RR and fixed Ti) PPlateau of Resistance; Pplat@Palv); or set Pause Time ~0.5s; RR, Pinsp, PEEP, FiO2, Flow Trigger, rise time, I:E (set Pocket Reference RR, Vt, PEEP, FiO2, Flow Trigger, Flow pattern, I:E (either Settings Pinsp, PEEP, FiO2, Flow Trigger, Rise time Target: < 30, Optimal: ~ 25 Settings directly or by inspiratory time Ti) Settings directly or via peak flow, Ti settings) Decreasing Ramp (potentially more physiologic) PIP: Total inspiratory work by vent; Reflects resistance & - Decreasing Ramp (potentially more physiologic) Card design by Respiratory care providers from: Square wave/constant vs Decreasing Ramp (potentially Flow Determined by: 1) PS level, 2) R, Rise Time (­ rise time ® PPeak inspiratory compliance; Normal ~20 cmH20 (@8cc/kg and adult ETT); - Peak Flow determined by 1) Pinsp level, 2) R, 3)Ti (shorter Flow more physiologic) ¯ peak flow and 3.) pt effort Resp failure 30-40 (low VT use); Concern if >40. Flow = more flow), 4) pressure rise time (¯ Rise Time ® ­ Peak v 0.9 Flow), 5) pt effort (­ effort ® ­ peak flow) Pplat-PEEP: tidal stress (lung injury & mortality risk). Target Determined by set RR, Vt, & Flow Pattern (i.e. for any set I:E Determined by patient effort & flow termination (“Esens” – PDriving peak flow, Square (¯ Ti) & Ramp (­ Ti); Normal Ti: 1-1.5s; see below “Breath Termination”) < 15 cmH2O.
    [Show full text]
  • Respiratory Equations – Behind the Numbers
    Southern African Journal of Anaesthesia and Analgesia. 2020;26(6 Suppl 3):S90-93 https://doi.org/10.36303/SAJAA.2020.26.6.S3.2546 South Afr J Anaesth Analg Open Access article distributed under the terms of the ISSN 2220-1181 EISSN 2220-1173 Creative Commons License [CC BY-NC 3.0] © 2020 The Author(s) http://creativecommons.org/licenses/by-nc/3.0 FCA 1 REFRESHER COURSE Respiratory equations – behind the numbers T Leonard Department of Anaesthesia, School of Clinical Medicine, Faculty of Health Sciences, Chris Hani Baragwanath Academic Hospital, University of the Witwatersrand, South Africa Corresponding author, email: [email protected] Summary Candidates for the FCA 1 exam will come across dozens of equations that eventually all merge into something complicated and daunting. The purpose of this review is to highlight some of the respiratory equations that are important and that candidates find confusing and explain the mathematical and physiological principles behind them. Keywords: equations, respiratory physiology, ventilation, perfusion, dead space Introduction VD / VT = (PACO2 – PECO2) / PACO2 P CO partial pressure of CO in alveolar gas There are many equations that candidates will come across in A 2 2 their study of respiratory physiology. These equations describe PECO2 partial pressure of CO2 in the total mixed principles of ventilation, perfusion and diffusion within the res- exhaled breath piratory system. This review attempts to explain the origins and A further modification was made by Henrik Enghoff due to make sense
    [Show full text]
  • 5. Oxygen Transport
    Introductory Human Physiology ©copyright Jennifer Carbrey & Emma Jakoi 5. Oxygen transport Partial Pressures of Alveolar Gases In the alveoli, the partial pressures of oxygen and carbon dioxide vary during the respiratory cycle. As gas exchange occurs, the alveolar partial pressure of carbon dioxide will rise and the alveolar partial pressure of oxygen will fall. Because these fluctuations are small (a few mm Hg) as compared with the 3000 ml present at the end of tidal exhalation, they are generally ignored and only mean values PO2 and PCO2 are considered. The relationship between PO2 and PCO2 in the alveoli is described by the alveolar gas equation: PAO2 = (Patm- PH2O) x FiO2 – PACO2/RQ Because diffusion is so rapid and complete in the lung, the PACO2 and PAO2 in the alveoli normally determine these gas pressures in arterial blood (PaCO2 and PaO2). But there is a slight difference between alveolar and arterial gas pressures even in normal subjects such that PAO2 and PaO2 differ by 5-15 mm Hg. This difference is due to anatomical shunting of blood (reduced perfusion) and to the mismatch between ventilation and perfusion that exists even in normal lungs. Both of these conditions will be discussed later in detail. Normal values for arterial PaO2 and PaCO2 are: PaO2 = 100 mm Hg PaCO2= 40 mm Hg. The PaO2 and PaCO2 can be measured directly from arterial blood draws. PAO2 is calculated by the alveolar gas equation. For a patient breathing room air at sea level, this equation simplifies to: PAO2 = 150 - PaCO2/0.8 Notice that alveolar PO2 is determined by three factors: 1.
    [Show full text]
  • Gas Exchange and Ventilation–Perfusion Relationships in the Lung
    ERJ Express. Published on July 25, 2014 as doi: 10.1183/09031936.00037014 REVIEW IN PRESS | CORRECTED PROOF Gas exchange and ventilation–perfusion relationships in the lung Johan Petersson1,2 and Robb W. Glenny3,4 Affiliations: 1Section of Anaesthesiology and Intensive Care Medicine, Dept of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. 2Dept of Anaesthesiology, Surgical Services and Intensive Care, Karolinska University Hospital, Stockholm, Sweden. 3Dept of Medicine, Division of Pulmonary and Critical Care Medicine, University of Washington, Seattle, WA, USA. 4Dept of Physiology and Biophysics, University of Washington, Seattle, WA, USA. Correspondence: Johan Petersson, Dept of Anaesthesiology, Surgical Services and Intensive Care, Karolinska University Hospital, 17176 Stockholm, Sweden. E-mail: [email protected] ABSTRACT This review provides an overview of the relationship between ventilation/perfusion ratios and gas exchange in the lung, emphasising basic concepts and relating them to clinical scenarios. For each gas exchanging unit, the alveolar and effluent blood partial pressures of oxygen and carbon dioxide (PO2 and PCO2) are determined by the ratio of alveolar ventilation to blood flow (V9A/Q9) for each unit. Shunt and low V9A/Q9 regions are two examples of V9A/Q9 mismatch and are the most frequent causes of hypoxaemia. Diffusion limitation, hypoventilation and low inspired PO2 cause hypoxaemia, even in the absence of V9A/Q9 mismatch. In contrast to other causes, hypoxaemia due to shunt responds poorly to supplemental oxygen. Gas exchanging units with little or no blood flow (high V9A/Q9 regions) result in alveolar dead space and increased wasted ventilation, i.e. less efficient carbon dioxide removal.
    [Show full text]
  • The Alveolar Gas Equation: Do Lessons from WW2 Research Into High Flying Pilots Provide Insights Into the Adaptation to High Altitude Flight in Birds?
    bioRxiv preprint doi: https://doi.org/10.1101/2020.05.13.093740; this version posted May 15, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. The alveolar gas equation: do lessons from WW2 research into high flying pilots provide insights into the adaptation to high altitude flight in birds? Seear, Michael, FRCPC From the Centre for Wildlife Ecology, Simon Fraser University, Burnaby, BC, Canada. Correspondence to: Dr. Michael Seear, Centre for Wildlife Ecology, Simon Fraser University, 8888 University Drive, Burnaby, BC, V5A 1S6 Phone: 604 737 7751. Fax: 604 875 3293. Email: [email protected] Running title: alveolar gas equation Key words: alveolar gas equation, high altitude adaptation, hypoxic hyperventilation. 4,500 words, 2 tables, 6 figures, 40 references. bioRxiv preprint doi: https://doi.org/10.1101/2020.05.13.093740; this version posted May 15, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Authors’ contributions. The author, Dr Seear, is solely responsible for the analysis of relevant publications, development of models and manuscript preparation. Conflicts of interest. The author, Dr Seear, has no personal or financial conflicts of interest with any aspect of this research study. Ethical approval. The study is based on a review of existing literature and subsequent generation of mathematical models of high altitude physiology. No animals were involved and no treatments or procedures were administered. Given these study conditions, our Institutional and University research ethics committees waived the need for ethical approval.
    [Show full text]
  • Rebeka Wright
    Recognition and Treatment of the Critically Unwell Patient Rebeka Wright PA-R, BSc (Hons), PgDip (Physician Associate studies), PGCert (Critical Care) Physician Associate Critical Care – Guys and St Thomas’ Hospital NHS Foundation Trust No conflict of interests Introduction History of critical care Correcting abnormal physiology in first instance Recognising the unwell diagnostic considerations patient second Respiratory failure Many simple interventions to correct abnormal Shock physiology can occur in ward setting Renal Failure Critical Care “care for patients who have potentially recoverable conditions who can benefit from more detailed observation ( with or without invasive treatments) then can be provided safely in an ordinary ward”. Intensive Care Society Level 2 – single organ failure, post op, stepdown from higher levels Level 3 – advanced respiratory support alone of monitoring or support two or more organ systems History of Critical Care Florence Nightingale in her observation of recovery areas near the operating theatre 1923 – Johns Hopkins Hospital USA – post op neurosurgical patients WWII and Korean and Vietnam wars Modern concept after Poli epidemic in 1952 Copenhagen positive pressure ventilation from ‘iron lung’ Further expansion in 1960s 1992 First formation of advisory committee for intensive care medicine 2001 First ICM training programme launched 2010 Faculty of ICM training Very heterogeneous – variable care nationwide Recognising the Unwell Patient Essential to recognise to Airway initiate immediate
    [Show full text]
  • The Respiratory System - 5 Oxygen Transport
    The Respiratory System - 5 Oxygen transport Jennifer Carbrey Ph.D. Department of Cell Biology image by OCAL, http://www.clker.com/clipart-26501.html, public domain Respiratory System 1. Anatomy and mechanics 2. Lung volumes and compliance 3. Pressure changes and resistance 4. Pulmonary function tests and alveolar ventilation 5. Oxygen transport 6. CO2 transport and V/Q mismatch 7. Regulation of breathing 8. Exercise and hypoxia Alveolar gas equation CO produced RQ = 2 O2 consumed Ventilation & Alveolar Gas Pressure Hypoventilation: CO2 production > alveolar ventilation (increased PCO in O2 2 arterial blood). 100 mm Hg Hyperventilation: CO2 production < alveolar ventilation (decreased PCO2 in arterial blood). 40 mm Hg CO alveolar partial pressure 2 hypoventilation hyperventilation O2 Transport 100 healthy O2 80 diseased 60 40 Pulmonary capillary Pulmonary P capillary 20 0 20 40 60 80 100 Normally, diffusion of O2 across pulmonary capillaries is always sufficient, even with exercise. % of capillary length PAO2 determines the diffusion gradients throughout the cardio-pulmonary system. Hemoglobin PO2 = PO2 PO2 < PO2 PO2 = PO2 O2 O2 O O2 O2 O2 O2 O2 O 2 O O 2 2 O2 O2 2 O2 O2 O2 O2 O2O O2 O2 O 2 O O2 2 2 O2 O2 O2 O2 O2 O O O 2 2 2 O2 O2 O2 O2 Total amount of O2 in blood depends on PO2 and amount of Hb in blood! 98-99% is O2-Hb in RBC, 1-2% is free in plasma Hemoglobin HbO2 HbO2 O2 O2 O2 O2 lung tissues O2 O2 O2-Hb Dissociation Curve arterial PO2 venous PO2 Arterial blood is 100% Saturated Venous blood is 75% saturated exercising muscle O2-Hb Binding Cooperativity: even at high altitude where PO2 = 60 mmHg Hb is 90% saturated! image by Diberri (modified), http://commons.wikimedia.org/wiki/File:Hb_saturation_curve.png, Creative Commons Attribution-Share Alike 3.0 Unported license.
    [Show full text]
  • Pulmonary Blood Flow Distribution and Hypoxic Pulmonary Vasoconstriction in Pentobarbital-Anesthetized Horses
    PULMONARY BLOOD FLOW DISTRIBUTION AND HYPOXIC PULMONARY VASOCONSTRICTION IN PENTOBARBITAL-ANESTHETIZED HORSES DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Phillip Lerche, BVSc MS ***** The Ohio State University 2006 Dissertation Committee: Approved by Dr William W Muir III, Adviser Dr Robert L Hamlin ________________________ Dr John AE Hubbell Adviser Graduate Program in Veterinary Clinical Sciences ABSTRACT Anesthetized horses commonly develop undesirable hypoxemia when dorsally recumbent. The major reason for this is development of ventilation/perfusion (V/Q) mismatching associated with atelectasis of dependent lung tissue. Improving ventilation frequently does not improve oxygenation, suggesting that pulmonary blood flow distribution is abnormal during anesthesia. Perfusion is normally matched to ventilation by hypoxic pulmonary vasoconstriction (HPV). This mechanism causes pulmonary arterioles to constrict in areas where alveolar oxygen (O 2) tension is low, redirecting blood flow to better-ventilated alveoli, and is believed to be modulated by nitric oxide (NO). The purpose of this study was to evaluate blood flow distribution in the anesthetized horse and to investigate the role of NO as a regulator of HPV in the anesthetized dorsally recumbent adult horse. Six adult horses anesthetized with pentobarbital were intubated via tracheostomy with a double-lumen tube, which separated gas flow to left and right lungs. Each lung was individually ventilated via a dual-lung ventilator, and 100% O 2 was delivered to both lungs. A hypoxic/hyperoxic state was then induced by ventilating the left lung with 100% nitrogen (N 2) while 100% O 2 was delivered to the right lung.
    [Show full text]
  • Ventilation and Perfusion in Health and Disease
    VENTILATION AND PERFUSION IN HEALTH AND DISEASE Dr.HARIPRASAD VS Ventilation Total ventilation - total rate of air flow in and out of the lung during normal tidal breathing. Alveolar ventilation -represents the amount of fresh inspired air available for gas exchange in alveolar gas compartment VA=VE-VD VA x n=VT x n-VD x n Also; VCO2= VAxFCO2 VA = VCO2/PCO2 Alveolar gas equation pAO2 The alveolar partial pressure of 107 mmHg oxygen FIO2 The fraction of inspired gas that is .21 oxygen PATM The prevailing atmospheric 760 mmHg pressure pH2O The saturated vapour pressure of 47 mmHg water at body temperature paCO2 The arterial partial pressure of 40 mmHg carbon dioxide (pCO2) RER The respiratory exchange ratio 0.8 Anatomical Dead space Volume of the conducting airways. Usually 150 Ml. Increases with large breath. Measured by fowler’s or N2 wash out method. .Subject breaths though a valve box •N2 concentration at the mouth is analyzed •Following a single breath of pure O2,N2 conc increases as dead space gas is washed out by the alveolar gas, finally reaching a plateau. Physiologic dead space Physiologic dead space is the volume of lung that does not eliminate CO2 •In normal subjects, Anatomical D.S = Physiological DS •patients with lung disease, the physiologic DS > Anatomical D.S •inequality of blood flow and ventilation within the lung Dead space ventilation Pulmonary embolism Vascular obliteration ex. PAH Emphysema Regional Differences in Ventilation “change in volume per unit resting volume” ! lower regions of the lung ventilate better than do the upper zones.
    [Show full text]