The Chemoreflex Control of Breathing and Its Measurement
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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. -
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. -
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. -
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). -
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 -
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). -
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. -
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. -
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. -
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 -
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. -
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.