DOCSLIB.ORG

The Chemoreflex Control of Breathing and Its Measurement

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Chemoreflex Control of Breathing and Its Measurement 933 Continuing Medical Education The chemoreflex control of breathing James Duffin PhD and measurement The chemoreflex control of breathing is described in terms of a Le contrrle chimiorEflexe de la respiration est dEcrit comme un graphical model. The central chemoreflex, the ventilatory modEle graphique. Le centre chimiordflexe, #1 rEponse respira- response to carbon dioxide mediated by the central chemorecep- toire au C02 mEdiEe par les chEmorEcepteurs centrmLr sont tors, is modelled as a straight-line relation between the dEcrits comme une relation directe entre la rEponse respira- ventilatory response and the arterial level of carbon dioxide. toire et les niveaux de C02 artdriels. Le chimior~flexe ptariph~- The peripheral chemoreflex, the ventilatory response to carbon rique, la r~ponse ventilatoire au C02 et I'hypoxie mddi~s par les dioxide and hypoxia mediated by the peripheral chemorecep- chEmorEcepteurs p~riph~riques sont subdivis~es en deux rela- tors, is broken into two relations. First, a straight.line relation tions. PremiErement, une relation directe entre la rdponse between the ventilatory response and the arterial level of carbon ventilatoire et le niveau artEriel de COz dont la pente (sensiti- dioxide whose slope (sensitivity) increases as the oxygen level vitE) augmente a vec les variations du niveau d' oxygEne d' hyper- varies from hyperoxic to hypoxic. Second, a rectangular oxique c} hypoxique. Deuxidmement, une relation hyperbolique hyperbolic relation between the ventilatory response and the rectangulaire entre la rdponse respiratoire et le niveau artEriel arterial level of oxygen with ventilation increasing with increas- d' oxygOne avecla ventilation augmentant avec I' augmentation ing hypoxia. The three ventilatory response relations (one de l'hypoxie. Les trois relations de la rdponse respiratoire central and two peripheral) add to produce the total chemoreflex (une centrale et deux pdriphEriques) s' ajoutent pour produire la ventilatory response which forms the feedback part of the rEponse respiratoire chEmordflexe totale qui forme la portion de respiratory regulator. The forward part consists of the relation ~,feedback ,, du r~gulateur respiratoire. L'autre partie consiste between the arterial level of carbon dioxide and ventilation dune relation entre le niveau artdriel de C02 et la ventilation when ventilation is controlled (the metabolic hyperbola). The lorsque cette dernidre est contrrlEe (l'hyperbole mdtabolique ). forward and feedback parts of the respiratory regulator can be Ces deux parties du rEgulateur respiratoire peuvent Etre combined so as to predict resting ventilation and carbon diaxide combinEes afin de pr~dire la ventilation au repos et le niveau de levels under a number of circumstances. Methods of measure. C02 dans d'autres circonstances. Des mEthodes de mesure et ment of these chemoreflex ventilatory responses are also des rdponses de ces chdmor~cepteurs respiratoires sont aussi described so as to illustrate the physiological principles in- ddcrites afin d'illustrer les principes physiologiques impliquEs volved in the model. dans ce moddle. This article presents a view of the control of breathing by the central and peripheral chemoreflexes as a graphical Key words model of this feedback regulator, and also presents REFLEXES: chemoreceptor; methods by which the regulator performance may be VENTILATION: carbon dioxide response, control, hypoxic assessed. It is not a review of the literature relating to response. either the underlying physiology or models of it, but is intended as a practical approach to understanding. For the Departments of Anaesthesia and Physiology, University of background research involved the reader is referred to the Toronto. review by Cunningham et al. Address correspondence to: Dr. J. Duffin,Department of In the awake patient, breathing is subject to conflicting Physiology, University of Toronto, Toronto, Ontario, Canada, demands and conditions. These may include diverse M5S I A8. influences such as anxiety hyperventilation, posturally CAN J ANAESTH 1990 ! 37: S / pp933-42 934 CANADIAN JOURNAL OF ANAESTHESIA FORWARD LOOP 24 Pco2 Pulmonary and [H +1 Cardiovascular [HCO3"] Systems where: is the Hydrogen ion concentration [H +] in nanomoles per litre Peripheral 1~ and Central Pco 2 is the partial pressure of Carbon Chemorcnexes Dioxide In mm Hg FEEDBACK LOOP is the Bicarbonate ion eoHeentration [HCO3-] in millimoles per litre FIGURE I A block diagram of the control of breathing by the chemoreflexes. FIGURE 2 The linear form of Ihe Henderson-Hasselbalch equation. Normal resting values are: hydrogen ion concentration = 40 nmol. L -j, partial pressure of carbon dioxide = 40 mmHg, and induced changes in pulmonary mechanics, and metabolic bicarbonate ion concentration = 24 mmol. L -j. requirements. While the control of breathing in the anaesthetized patient is somewhat simplified by the elimination or suppression of many of these infuences, arterial blood, but the partial pressure of carbon dioxide the physiology of breathing will be further simplified in does. In addition, the bicarbonate ion concentration this article by assuming that breathing is under the sole within the tissues of the central chemoreceptors may alter control of the respiration chemoreflexes. over time and differ from that of arterial blood; usually in The term chemoreflexes refers to the effects of the such a way as to restore central nervous system hydrogen central and peripheral chemoreceptors on pulmonary ion concentration to normal values. 4 For these reasons, ventilation. The chemoreflexes form the feedback portion the hydrogen ion concentration sensed by the central of a control loop. The forward portion, which completes chemoreceptors is likely to be more closely related to the the control loop, refers to the effects that changing arterial partial pressure of carbon dioxide than to the pulmonary ventilation has upon the stimuli sensed by the arterial hydrogen ion concentration in the short term chemoreceptors and is usually termed the metabolic (minutes), and furthermore that relationship may be hyperbola because of its shape. The complete control loop altered by changes in central nervous system bicarbonate is the classical, negative feedback regulator which main- ion concentration (hours). tains respiratory homeostasis, pictured in Figure I. The second consequences of the location of the central chemoreceptors concerns the time course for changes in The central chemoreflex the partial pressure of carbon dioxide at the central The central chemoreceptors respond only to the hydrogen chemoreceptors, relative to such changes in arterial ion concentration of their environment, and therefore this blood. chemoreflex might be expected to be relatively simple to Because the central chemoreceptors are located in brain understand. However, the complexities associaled with tissue which is supplied with blood at a flow of about 0.01 the central chemoreflex are due to the location of the ml. sec- ~for every ml of tissue, the changes in the partial central chemoreceptors, somewhere within the brain pressure of carbon dioxide at the central chemoreceptors tissue in the medulla. 2 This location has three conse- lag behind those in arterial blood. In experiments where quences for the operation of the central chemoreflex. the arterial level of the partial pressure of carbon dioxide The first consequence concerns the relation between is abruptly increased (a step change), the partial pressure hydrogen ion concentration and the partial pressure of of carbon dioxide at the central chemoreceptors gradually carbon dioxide. This relation can be expressed as the increases to a new level following the time course of a linear form of the Henderson-Hasselbalch equation wash-in exponential function. 5 The time constant of this shown in Figure 2 (but also see an alternative approach to exponential function can be estimated as the reciprocal of acid-base chemistry using fundamental physical and the blood perfusion per volume of chemoreceptor tissue, chemical principles). 3 Because of the blood-brain barrier i.e., 100 sec. Since a wash-in exponential process is for polar solutes, hydrogen ion concentration does not almost complete in about three time constants, it therefore easily equilibrate between the central chemoreceptors and takes five minutes for the partial pressure of carbon Duffin: CHEMOREFLEX CONTROL 935 rVENTILATION litres/minute Vcos 50 Paco~ - PIco 2 VA 4O where: 30 is the arterial partial pressure of Paco= Carbon Dioxide in turn Hg 20 is the inspired partial pressure of P[co~ Carbon Dioxide in mm Hg 10 V is the rate of Carbon Dioxide 0 CO s output in litres per minute 30 40 610 is the alveolar ventilation in Pco~ mm Hg VA litres per minute FIGURE 4 The metabolic hyperbola, the relation between ventilation FIGURE 3 The alveolar ventilation response to arterial carbon and carbon dioxide when ventilation is controlled. dioxide mediated by the central chemoreceptors. dioxide at the central chemoreceptors to reach its new The relationship between the partial pressure of carbon level. dioxide in arterial blood and alveolar ventilation is that It should be understood that the partial pressure of shown in Figure 3, when only the central chemoreflex is carbon dioxide at the central chemoreceptors is not the operating. This straight-line relationship with a threshold same as that of arterial blood, even when equilibration is of approximately 5.3 kPa (40 mmHg) partial pressure of complete, but is close to
Load more

Recommended publications
  • Chapter 22 We Won't Do Much Anatomy Here (Left Column; 22.1-22.3)
    Chapter 22 Marieb & Hoehn (2019), p. 8181 We won’t do much anatomy here (left column; 22.1-22.3). Main issues (in lecture and lab): mechanics and measurement of breathing (22.4-22.5), chemoreceptor control of ventilation (22.8), and a few respiratory disorders (22.10). *** Sections 22.6-22.7 were briefly covered in Chapter 17. 1 Ch. 22: Test Question Templates • Q1. If given an appropriate graph of volume of air in lung vs. time, estimate or calculate FEV1/FVC ratio, FVC, residual volume, TLC, tidal volume, and/or minute ventilation. • Example (from Winter 2019 exam): 2 Q1. There are multiple ways to do this. The key is to choose a respiratory rate (breaths per minute) and a tidal volume (milliliters of air per breath) that, when multiplied together, give you 4000 mL air/minute. For example, I can draw a curve to show a tidal volume of 400 mL and a respiratory rate of 10 breaths/minute. Minute ventilation = (tidal volume)*(respiratory rate) = (400 mL air/breath)*(10 breaths/min) = 4000 mL air/min. 2 • Q2. If given two of the three values, calculate the third one: minute ventilation, respiratory rate, and tidal volume. • Example: Lola takes 10 breaths per minute, and her minute ventilation is 6000 mL air per minute. What is her tidal volume? • Q3. If given spirometry data and reference values, determine whether the data are consistent with obstructive pulmonary disease, restrictive pulmonary disease, both, or neither. • Example [from Fall 2019 test]: Rik is put through various pulmonary function tests. At time 0 in the table below, he begins deflating his fully inflated lungs as forcefully and rapidly as he can.
    [Show full text]
  • Cardiovascular System 9
    Chapter Cardiovascular System 9 Learning Outcomes On completion of this chapter, you will be able to: 1. State the description and primary functions of the organs/structures of the car- diovascular system. 2. Explain the circulation of blood through the chambers of the heart. 3. Identify and locate the commonly used sites for taking a pulse. 4. Explain blood pressure. 5. Recognize terminology included in the ICD-10-CM. 6. Analyze, build, spell, and pronounce medical words. 7. Comprehend the drugs highlighted in this chapter. 8. Describe diagnostic and laboratory tests related to the cardiovascular system. 9. Identify and define selected abbreviations. 10. Apply your acquired knowledge of medical terms by successfully completing the Practical Application exercise. 255 Anatomy and Physiology The cardiovascular (CV) system, also called the circulatory system, circulates blood to all parts of the body by the action of the heart. This process provides the body’s cells with oxygen and nutritive ele- ments and removes waste materials and carbon dioxide. The heart, a muscular pump, is the central organ of the system. It beats approximately 100,000 times each day, pumping roughly 8,000 liters of blood, enough to fill about 8,500 quart-sized milk cartons. Arteries, veins, and capillaries comprise the network of vessels that transport blood (fluid consisting of blood cells and plasma) throughout the body. Blood flows through the heart, to the lungs, back to the heart, and on to the various body parts. Table 9.1 provides an at-a-glance look at the cardiovascular system. Figure 9.1 shows a schematic overview of the cardiovascular system.
    [Show full text]
  • Human Physiology an Integrated Approach
    Gas Exchange and Transport Gas Exchange in the Lungs and Tissues 18 Lower Alveolar P Decreases Oxygen Uptake O2 Diff usion Problems Cause Hypoxia Gas Solubility Aff ects Diff usion Gas Transport in the Blood Hemoglobin Binds to Oxygen Oxygen Binding Obeys the Law of Mass Action Hemoglobin Transports Most Oxygen to the Tissues P Determines Oxygen-Hb Binding O2 Oxygen Binding Is Expressed As a Percentage Several Factors Aff ect Oxygen-Hb Binding Carbon Dioxide Is Transported in Three Ways Regulation of Ventilation Neurons in the Medulla Control Breathing Carbon Dioxide, Oxygen, and pH Infl uence Ventilation Protective Refl exes Guard the Lungs Higher Brain Centers Aff ect Patterns of Ventilation The successful ascent of Everest without supplementary oxygen is one of the great sagas of the 20th century. — John B. West, Climbing with O’s , NOVA Online (www.pbs.org) Background Basics Exchange epithelia pH and buff ers Law of mass action Cerebrospinal fl uid Simple diff usion Autonomic and somatic motor neurons Structure of the brain stem Red blood cells and Giant liposomes hemoglobin of pulmonary Blood-brain barrier surfactant (40X) From Chapter 18 of Human Physiology: An Integrated Approach, Sixth Edition. Dee Unglaub Silverthorn. Copyright © 2013 by Pearson Education, Inc. All rights reserved. 633 Gas Exchange and Transport he book Into Thin Air by Jon Krakauer chronicles an ill- RUNNING PROBLEM fated trek to the top of Mt. Everest. To reach the summit of Mt. Everest, climbers must pass through the “death zone” T High Altitude located at about 8000 meters (over 26,000 ft ). Of the thousands of people who have attempted the summit, only about 2000 have been In 1981 a group of 20 physiologists, physicians, and successful, and more than 185 have died.
    [Show full text]
  • Mechanisms of Pulmonary Gas Exchange Abnormalities During Experimental Group B Streptococcal Infusion
    003 I -3998/85/1909-0922$02.00/0 PEDIATRIC RESEARCH Vol. 19, No. 9, I985 Copyright 0 1985 International Pediatric Research Foundation, Inc. Printed in (I.S. A. Mechanisms of Pulmonary Gas Exchange Abnormalities during Experimental Group B Streptococcal Infusion GREGORY K. SORENSEN, GREGORY J. REDDING, AND WILLIAM E. TRUOG ABSTRACT. Group B streptococcal sepsis in newborns obtained from GBS (5, 6). Arterial Poz fell by 9 torr in association produces pulmonary arterial hypertension and hypoxemia. with the increase in pulmonary arterial pressure (4). In contrast, The purpose of this study was to investigate the mecha- the neonatal piglet infused with GBS demonstrated both pul- nisms by which hypoxemia occurs. Ten anesthetized, ven- monary arterial hypertension and profound arterial hypoxemia tilated piglets were infused with 2 x lo9 colony forming (7). These results suggest that the neonatal pulmonary vascula- unitstkg of Group B streptococci over a 30-min period. ture may respond to bacteremia differently from that of adults. Pulmonary arterial pressure rose from 14 ? 2.8 to 38 ? The relationship between Ppa and the matching of alveolar 6.7 torr after 20 min of the bacterial infusion (p< 0.01). ventilation and pulmonary perfusion, a major determinant of During the same period, cardiac output fell from 295 to arterial oxygenation during room air breathing (8), has not been 184 ml/kg/min (p< 0.02). Arterial Po2 declined from 97 studied in newborns. The predictable rise in Ppa with an infusion 2 7 to 56 2 11 torr (p< 0.02) and mixed venous Po2 fell of group B streptococcus offers an opportunity to delineate the from 39.6 2 5 to 28 2 8 torr (p< 0.05).
    [Show full text]
  • Oxygen Concentration of Blood: PO
    Oxygen Concentration of Blood: PO2, Co-Oximetry, and More Gary L. Horowitz, MD Beth Israel Deaconess Medical Center Boston, MA Objectives • Define “O2 Content”, listing its 3 major variables • Define the limitations of pulse oximetry • Explain why a normal arterial PO2 at sea level on room air is ~100 mmHg (13.3 kPa) • Describe the major features of methemogobin and carboxyhemglobin O2 Concentration of Blood • not simply PaO2 – Arterial O2 Partial Pressure ~100 mm Hg (~13.3 kPa) • not simply Hct (~40%) – or, more precisely, Hgb (14 g/dL, 140 g/L) • not simply “O2 saturation” – i.e., ~89% O2 Concentration of Blood • rather, a combination of all three parameters • a value labs do not report • a value few medical people even know! O2 Content mm Hg g/dL = 0.003 * PaO2 + 1.4 * [Hgb] * [%O2Sat] = 0.0225 * PaO2 + 1.4 * [Hgb] * [%O2Sat] kPa g/dL • normal value: about 20 mL/dL Why Is the “Normal” PaO2 90-100 mmHg? • PAO2 = (FiO2 x [Patm - PH2O]) - (PaCO2 / R) – PAO2 is alveolar O2 pressure – FiO2 is fraction of inspired oxygen (room air ~0.20) – Patm is atmospheric pressure (~760 mmHg at sea level) o – PH2O is vapor pressure of water (47 mmHg at 37 C) – PaCO2 is partial pressure of CO2 – R is the respiratory quotient (typically ~0.8) – 0.21 x (760-47) - (40/0.8) – ~100 mm Hg • Alveolar–arterial (A-a) O2 gradient is normally ~ 10, so PaO2 (arterial PO2) should be ~90 mmHg NB: To convert mm Hg to kPa, multiply by 0.133 Insights from PAO2 Equation (1) • PaO2 ~ PAO2 = (0.21x[Patm-47]) - (PaCO2 / 0.8) – At lower Patm, the PaO2 will be lower • that’s
    [Show full text]
  • Effects of Lethal Levels of Environmental Hypercapnia on Cardiovascular and Blood-Gas Status in Yellowtail, Seriola Quinqueradiata
    ZOOLOGICAL SCIENCE 20: 417–422 (2003) 2003 Zoological Society of Japan Effects of Lethal Levels of Environmental Hypercapnia on Cardiovascular and Blood-Gas Status in Yellowtail, Seriola quinqueradiata Kyoung-Seon Lee1, Jun Kita2 and Atsushi Ishimatsu1* 1Marine Research Institute, Nagasaki University, Tairamachi, Nagasaki 851-2213, Japan 2Research Institute of Innovative Technology for the Earth (RITE), Kizucho, Kyoto 619-0209, Japan ABSTRACT—The cardiorespiratory responses were examined in yellowtail, Seriola quinqueradiata exposed to two levels of hypercapnia (seawater equilibrated with a gas mixture containing 1% CO2 (water PCO2 = 7 mmHg) or 5% CO2 (38 mmHg)) for 72 hr at 20°C. Mortality was 100% within 8 hr at 5% CO2, while no fish died at 1% CO2. No cardiovascular variables (cardiac output, Q;˙ heart rate, HR; stroke volume, SV and arterial blood pressure, BP) significantly changed from pre-exposure values during exposure to 1% CO2. Arterial CO2 partial pressure (PaCO2) significantly increased (P < 0.05), reaching a new steady- state level after 3 hr. Arterial blood pH (pHa) decreased initially (P < 0.05), but was subsequently restored – by elevation of plasma bicarbonate ([HCO3 ]). Arterial O2 partial pressure (PaO2), oxygen content (CaO2), and hematocrit (Hct) were maintained throughout the exposure period. In contrast, exposure to 5% CO2 dramatically reduced Q˙ (P < 0.05) through decreasing SV (P < 0.05), although HR did not change. BP was transiently elevated (P < 0.05), followed by a precipitous fall before death. The pHa was restored – incompletely despite a significant increase in [HCO3 ]. PaO2 decreased only shortly before death, whereas CaO2 kept elevated due to a large increase in Hct (P < 0.05).
    [Show full text]
  • Physiologic Effects of Noninvasive Ventilation
    Physiologic Effects of Noninvasive Ventilation Neil R MacIntyre Introduction NIV Can Augment Minute Ventilation NIV Unloads Ventilatory Muscles NIV Resets the Ventilatory Control System Alveolar Recruitment and Gas Exchange Other Physiologic Effects of NIV: Intended and Unintended Maintaining Upper-Airway Patency Reducing Imposed Triggering Loads From Auto-PEEP Cardiac Interactions: Both Beneficial and Harmful Ventilator-Induced Lung Injury Production of Auto-PEEP Patient-Ventilator Interactions Summary Noninvasive ventilation (NIV) has a number of physiologic effects similar to invasive ventilation. The major effects are to augment minute ventilation and reduce muscle loading. These effects, in turn, can have profound effects on the patient’s ventilator control system, both acutely and chron- ically. Because NIV can be supplied with PEEP, the maintenance of alveolar recruitment is also made possible and the triggering load imposed by auto-PEEP can be reduced. NIV (or simply mask CPAP) can maintain upper-airway patency during sleep in patients with obstructive sleep apnea. NIV can have multiple effects on cardiac function. By reducing venous return, it can help in patients with heart failure or fluid overload, but it can compromise cardiac output in others. NIV can also increase right ventricular afterload or function to reduce left ventricular afterload. Potential det- rimental physiologic effects of NIV are ventilator-induced lung injury, auto-PEEP development, and discomfort/muscle overload from poor patient–ventilator interactions. Key words: invasive ventilation; noninvasive ventilation; minute and alveolar ventilation; ventilation distribution; ventilation-perfusion match- ing; control of ventilation; ventilatory muscles; work of breathing; patient–ventilator interactions; ventilator- induced lung injury. [Respir Care 2019;64(6):617–628.
    [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]
  • Arterial Blood Gases During Treatment of Congestive Heart Failure
    University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1969 Arterial blood gases during treatment of congestive heart failure John B. Byrd University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Byrd, John B., "Arterial blood gases during treatment of congestive heart failure" (1969). MD Theses. 77. https://digitalcommons.unmc.edu/mdtheses/77 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. ARTERIAL BLOOD GASES DURING TREATMENT OF CONGESTIVE HEART FAILURE By John B~ Byrd A THESIS Presented to the Faculty of The CollsQs of Medicine in the Universi,!;v of Ne.braska In Partial Fulfillment of Requirements For the Degree of Doctor of Medicine Under the Supervision of John R. Jones, MO Omaha, Nebraska February 3, 1969 CONTENTS Introduction 1 Methods 4 Results 6 Discussion 7 Summary 9 References 10 ARTERIAL BLOOD GASES DURING TREATMENT OF CONGESTIVE HEART FAILURE The congestive syndromes of heart failure are classified as 1) acute pulmonary edema (acute left ventricular failure) and 2) chronic heart failure in Principles of Internal Medicine e d ~'t e d'oy H'arr~son, ea.tIll Acute left ventricular failure is characterized oy paroxysmal dyppnea. It may be caused by an elevated filling load (most common), acute myocardial infarction, ectopic tachycardia or fulminant myocarditis--th8 first causing a high-output syndrome with cardiogenic shock occurring late; the remaining causes characterized by an abrupt declir~in cardiac output.
    [Show full text]
  • Control of Respiration Central Control of Ventilation
    Control of Respiration Control of Respiration Bioengineering 6000 CV Physiology Central Control of Ventilation • Goal: maintain sufficient ventilation with minimal energy – Ventilation should match perfusion • Process steps: – Ventilation mechanics + aerodynamics • Points of Regulation – Breathing rate and depth, coughing, swallowing, breath holding – Musculature: very precise control • Sensors: – Chemoreceptors: central and peripheral – Stretch receptors in the lungs, bronchi, and bronchioles • Feedback: – Nerves – Central processor: • Pattern generator of breathing depth/amplitude • Rhythm generator for breathing rate Control of Respiration Bioengineering 6000 CV Physiology Peripheral Chemosensors • Carotid and Aortic bodies • Sensitive to PO2, PsCO2, and pH (CO2 sensitivity may originate in pH) • Responses are coupled • Adapt to CO2 levels • All O2 sensing is here! • Carotid body sensors more sensitive than aortic bodies Control of Respiration Bioengineering 6000 CV Physiology O2 Sensor Details • Glomus cells • K-channel with O2 sensor • O2 opens channel and hyperpolarizes cell • Drop in O2 causes reduction in K current and a depolarization • Resulting Ca2+ influx triggers release of dopamine • Dopamine initiates action potentials in sensory nerve Control of Respiration Bioengineering 6000 CV Physiology Central CO2/pH Chemoreceptors • Sensitive to pH in CSF • CSF poorly buffered • H+ passes poorly through BBB but CO2 passes easily • Blood pH transmitted via CO2 to CSF • Adapt to elevated CO2 levels (reduced pH) by transfer of - - HCO3
    [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]
  • Arterial Blood Gases: Their Meaning and Interpretation*
    Arterial Blood Gases: Their Meaning and Interpretation* WALTER J. O'DONOHUE, JR., M.D. Assistant Professor of Medicine, Director of Inhalation Therapy, Department of Internal Medicine, Medical College of Virginia, Health Sciences Division of Virginia Commonwealth University, Richmond, Virginia The measurement of arterial blood gases is cause the glass plunger moves more freely and essential in the management of respiratory failure allows easy detection of arterial pulsation. After and in the diagnostic assessment of the nature and the puncture, the artery should be compressed by severity of pulmonary disease. Adequate therapy hand for no less than five minutes. If the blood for patients with acute respiratory insufficiency gas analysis is not done immediately, the capped is often impossible without the information ob­ syringe should be placed in an iced container. tained from arterial blood gases. These studies must Equipment for blood gas analysis is readily avail­ be readily available around the clock, including able and relatively easy to operate. The cost of nights, weekends, and holidays and should not have basic equipment is approximately $3,000. An to depend upon a technician called in from home. arterial blood sample of 3-5 cc is sufficient for a A ready knowledge of arterial blood gases in acute complete study. Micromethods are also available respiratory failure is just as important to good for "arterialized" capillary blood obtained by punc­ medical care as knowing the urine sugar and ace­ ture of a hyperemic ear or fingertip. Only ar­ tone in diabetic ketoacidosis or the blood count terial blood is of consistent value in detecting the in an acute infection.
    [Show full text]