The Respiratory System PDF - PHED 2217

The Respiratory System PHED 2217: Systematic Approach to Integrated Human Physiology Start of content after midterm Respiration: Pulmonary Ventilation Respiration (exchange of gases between atmosphere and body’s cells) involves four processes...

The Respiratory System PHED 2217: Systematic Approach to Integrated Human Physiology Start of content after midterm Respiration: Pulmonary Ventilation Respiration (exchange of gases between atmosphere and body’s cells) involves four processes Pulmonary ventilation: movement of gases between atmosphere and alveoli Pulmonary gas exchange: exchange of gases between alveoli and blood Gas transport: transport of gases in blood between lungs and systemic cells Tissue gas exchange: exchange of respiratory gases between the blood and the systemic cells Overview of Respiration Figure 23.18 Introduction to Pulmonary Ventilation Pulmonary ventilation (breathing): air movement between atmosphere and alveoli Consists of two cyclic phases Inspiration brings air into the lungs (inhalation) Expiration forces air out of the lungs (exhalation) Quiet breathing (eupnea), rhythmic breathing at rest Forced breathing, vigorous breathing accompanies exercise Autonomic nuclei in brainstem regulate breathing activity Skeletal muscles contract and relax changing thorax volume Volume changes result in changes in pressure gradient between lungs and atmosphere Air moves down its pressure gradient Air enters lung during inspiration; exits during expiration Mechanics of Breathing Skeletal muscles of breathing Muscles of quiet breathing Diaphragm and external intercostals contract for inspiration Diaphragm flattens when it contracts; external intercostals elevate ribs These muscles relax for expiration Muscles of forced inspiration Sternocleidomastoid, scalenes, pectoralis minor, and serratus posterior superior, contract for deep inspiration All are located superiorly in thorax Move rib cage superiorly, laterally, and anteriorly, increasing volume Erector spinae located along length of vertebral column Contracts to help lift rib cage Mechanics of Breathing Skeletal muscles of breathing (continued) Muscles of forced expiration Include internal intercostals, abdominal muscles, transversus thoracis, and serratus posterior inferior Contract during a hard expiration, for example, coughing Either pull the rib cage inferiorly, medially, posteriorly, or compress abdominal contents Collectively termed accessory muscles of breathing when paired with the muscles of forced inspiration Skeletal Muscles of Breathing Figure 23.19-top Mechanics of Breathing Volume changes in the thoracic cavity Thoracic volume changes vertically, laterally, and anterior-posteriorly Vertical changes result from diaphragm movement Flattens (by moving inferiorly) when contracted When relaxed, returns to original position, vertical dimensions decrease For relaxed breathing: only small movements required For forced expiration: abdominal muscle contraction causes larger movement of diaphragm superiorly  Figure 23.20 Mechanics of Breathing Volume changes in the thoracic cavity (continued) Lateral dimension changes Rib cage elevation widens thoracic cavity in inspiration Rib cage depression narrows thoracic cavity in expiration Changes due to activity (or relaxation) of all breathing muscles except diaphragm Anterior-posterior dimension changes Inferior part of sternum moves anteriorly in inspiration; posteriorly in expiration According to activity level of all breathing muscles except diaphragm Boyle’s Law Boyle’s gas law: Relationship of volume and pressure At constant temperature, pressure (P) of a gas decreases if volume (V) of the container increases, and vice versa P1 and V1 represent initial conditions and P2 and V2 the changed conditions P 1 V 1 = P 2V 2 Inverse relationship between gas pressure and volume Pressure Gradients An air pressure gradient exists when force per unit area is greater in one place than another If the two places are interconnected, air flows from high to low pressure until pressure is equal Access the text alternative for slide images. Mechanics of Breathing Volumes and pressures associated with breathing Atmospheric pressure: pressure of air in environment Changes with altitude Increased altitude = “thinner air” = lower pressure Sea level value is 760 mm Hg = 14.7 lbs per square inch = 1 atm Unchanged in process of breathing Alveolar volume: collective volume of alveoli Intrapulmonary pressure: pressure in alveoli Fluctuates with breathing May be higher, lower, or equal to atmospheric pressure Is equal to atmospheric pressure at end of inspiration and expiration Mechanics of Breathing Volumes and pressures associated with breathing (cont’d.) Intrapleural pressure: pressure in pleural cavity Fluctuates with breathing Is lower than intrapulmonary pressure (keeps lungs inflated) About 4 mm Hg lower than intrapulmonary pressure between breaths Volume changes create pressure changes and air flows down its pressure gradient During inspiration: thoracic volume increases, thoracic pressure decreases, so air flows in During expiration: thoracic volume decreases, thoracic pressure increases, so air flows out Volumes and Pressures with Breathing Figure 23.21b Mechanics of Breathing Quiet Inspiration Diaphragm and external intercostals contract increasing thoracic volume Diaphragm movement accounts for 2/3 of volume change; external intercostal movement accounts for 1/3 Intrapleural volume increases, so intrapleural pressure decreases Lungs pulled by pleurae, so lung volume increases and intrapulmonary pressure decreases Because intrapulmonary pressure is less than atmospheric pressure, air flows in until these pressures are equal Typically 0.5 L flows in as tidal volume Mechanics of Breathing Quiet Expiration Diaphragm and external intercostals relax decreasing thoracic volume Pleural cavity volume decreases, so intrapleural pressure increases Elastic recoil pulls lungs inward, so alveolar volume decreases and intrapulmonary pressure increases Since intrapulmonary pressure is greater than atmospheric pressure, air flows out until these pressures are equal About 0.5 L of air leaves the lung Mechanics of Quiet Breathing Figure 23.22 Mechanics of Breathing Forced breathing Involves steps similar to quiet breathing Requires contraction of additional muscles Causes greater changes in thoracic cavity volume and intrapulmonary pressure More air moves into and out of lungs Significant chest volume changes are apparent Nervous Control of Breathing Autonomic nuclei within the brain coordinate breathing Respiratory center of the brainstem Medullary respiratory center contains two groups Ventral respiratory group (VRG) in anterior medulla Dorsal respiratory group (DRG) in posterior medulla Pontine respiratory center in pons also known as pneumotaxic center Brainstem neurons influence respiratory muscles VRG neurons synapse with lower motor neurons of skeletal muscles in spinal cord Lower motor neuron axons project to respiratory muscles Axons innervating diaphragm travel in phrenic nerves Axons innervating intercostal muscles travel in intercostal nerves Nervous Control of Breathing Chemoreceptors monitor changes in concentrations of H+, PCO2 and PO2 Central chemoreceptors in medulla monitor pH of CSF Central NS CSF pH changes are caused by changes in blood PCO2 CO2 diffuses from blood to CSF where carbonic anhydrase is Carbonic anhydrase builds carbonic acid from CO2 and water Peripheral chemoreceptors are in aortic and carotid bodies Stimulated by changes in H+ or respiratory gases in blood Respond to H+ produced independently of CO2 For example, H+ from ketoacidosis (from fatty acid metabolism) Carotid chemoreceptors send signals to respiratory center via glossopharyngeal nerve Aortic chemoreceptors send signals to respiratory center via vagus nerve Nervous Control of Breathing Other receptors also influence respiration Irritant receptors in air passageways stimulated by particulate matter Baroreceptors in pleurae and bronchioles respond to stretch Proprioceptors of muscles and joints are stimulated by body movements Respiratory Center Figure 23.23 Nervous Control of Breathing Physiology of quiet breathing Inspiration begins when VRG inspiratory neurons fire spontaneously Signals are sent from VRG to nerve pathways exciting skeletal muscles for about 2 seconds Diaphragm and external intercostals contract causing air to flow in Quiet expiration occurs when VRG is inhibited Signals from inspiratory neurons are relayed to VRG expiratory neurons Expiratory neurons send inhibitory signals back (negative feedback) Signals no longer sent to inspiratory muscles (for about 3 sec) Diaphragm and external intercostals relax causing air to flow out Nervous Control of Breathing Physiology of quiet breathing (continued) Respiration rate for normal, quiet breathing is eupnea Average of 12 to 15 breaths per minute Pontine respiratory center facilitates smooth transitions between inspiration and expiration Sends signals to medullary respiratory center Damage to pons causes erratic breathing Nervous Control of Breathing Reflexes that alter breathing rate and depth Chemoreceptors alter breathing by sending signals to DRG, which are then relayed to VRG VRG triggers changes in rhythm and force of breathing Rate changes by altering amount of time in inspiration and expiration Depth changes by stimulation of accessory muscles Ventilation increases in response to Central chemoreceptors detecting increase in H+ concentration of CSF Peripheral chemoreceptors detecting increase in blood H+ or PCO2 Increased ventilation expels more CO2 returning conditions to normal Ventilation decreases if chemoreceptors detect decreases in H+ or PCO2 Nervous Control of Breathing Reflexes that alter breathing rate and depth (cont’d.) Blood PCO2 is most important stimulus affecting breathing Raising blood PCO2 by 5 mm Hg causes doubling of breathing rate CO2 fluctuations influence sensitive central chemoreceptors CO2 combines with water to form carbonic acid in CSF CSF lacks protein buffers and so its pH change triggers reflexes Blood PO2 is not a sensitive regulator of breathing Arterial oxygen must decrease from 95 to 60 mm Hg to have major effect independent of PCO2 When PO2 drops it causes peripheral chemoreceptors to be more sensitive to blood PCO2 Nervous Control of Breathing Reflexes that alter breathing rate and depth (cont’d.) Altering breathing through other receptors Joint and muscle proprioceptors are stimulated by body movement Signal respiratory center to increase breathing depth Baroreceptors within visceral pleura and bronchiole smooth muscle Send signals to respiratory center when overstretched Initiate inhalation reflex (Hering-Breuer reflex) to shut off inspiration and protect against overinflation Irritant receptors initiate sneeze reflex and cough reflex Exaggerated intake of breath followed by closure of larynx Contraction of abdominal muscles Abrupt opening of vocal cords and explosive blast of exhaled air Nervous Control of Breathing Reflexes that alter breathing rate and depth (cont’d.) Action of higher brain centers Hypothalamus increases breathing rate if body is warm Works through respiratory center Limbic system alters breathing rate in response to emotions Works through respiratory center Frontal lobe of cerebral cortex controls voluntary changes in breathing patterns Bypasses respiratory center stimulating lower motor neurons directly Nervous Control of Breathing Nervous control of respiratory system structures and breathing structures Respiratory system includes smooth muscles and glands Innervated by axons of lower motor neurons of autonomic nervous system Controlled by autonomic brainstem nuclei Breathing muscles are skeletal muscles Innervated by lower motor neurons of somatic nervous system Controlled by brainstem autonomic nuclei, cerebral cortex, and somatic nervous system Thus, there are both reflexive and conscious controls of breathing Minute Ventilation and Alveolar Ventilation Minute ventilation Process of moving air into and out of the lungs Amount of air moved between atmosphere and alveoli in 1 minute Tidal volume = amount of air per breath Respiration rate = number of breaths per minute Tidal volume × Respiration rate = Minute ventilation 500 mL × 12 breaths/min = 6 L/ minute (typical amount) Minute Ventilation and Alveolar Ventilation Anatomic dead space: conducting zone space No exchange of respiratory gases About 150 mL Alveolar ventilation Amount of air reaching alveoli per minute (Tidal volume − anatomic dead space) × Respiration rate = Alveolar ventilation (500 mL − 150 mL) × 12 = 4.2 L/min Deep breathing maximizes alveolar ventilation  Relationships Among Tidal Volume, Breathing Rate, and Both Total and Alveolar Minute Ventilation Dead Space Alveolar Tidal Total Minute Breathing Rate Minute Minute Condition Volume x = Ventilation - = (Breaths/min) Ventilation Ventilation (mL) (mL/min) (mL/min) (mL/min) Normal 500 12 6000 (150 mL x 12) 4200 Breathing Shallow 150 40 6000 (150 mL x 40) 0 Breathing Deep Breathing 1000 6 6000 (150 mL x 6) 5100 Deep breathing 1000 6 6000 150 ml x 6 5100 33 Minute Ventilation and Alveolar Ventilation Physiologic dead space Normal anatomic dead space + any loss of alveoli Some disorders decrease number of alveoli participating in gas exchange Due to damage to alveoli or changes in respiratory membrane (for example, pneumonia) Anatomic dead space = physiologic dead space in healthy individual where loss of alveoli is minimal Measuring Respiratory Function Spirometer measures respiratory volume Can be used to assess respiratory health Standard values are available (for example, for people of different ages) Four volumes measured by spirometry Tidal volume: amount of air inhaled or exhaled per breath during quiet breathing Inspiratory reserve volume (IRV): amount of air that can be forcibly inhaled beyond the tidal volume Measure of compliance Expiratory reserve volume (ERV): amount that can be forcibly exhaled beyond tidal volume Measure of elasticity Residual volume: amount of air left in the lungs after the most forceful expiration Measuring Respiratory Function Four capacities calculated from respiratory volumes Inspiratory capacity (IC) Tidal volume + inspiratory reserve volume Functional residual capacity (FRC) Expiratory reserve volume + residual volume Volume left in the lungs after a quiet expiration Vital capacity Tidal volume + inspiratory and expiratory reserve volumes Total amount of air a person can exchange through forced breathing Total lung capacity (TLC) Sum of all volumes, including residual volume Maximum volume of air that the lungs can hold Measuring Respiratory Function Additional respiratory measurements—rates of air movement Forced expiratory volume (FEV) Percent of vital capacity that can be expelled in a set period of time FEV1 = percentage expelled in one second 75 to 85% of vital capacity in a healthy person Less in emphysema patients and others with poor expiration Helps distinguish: Chronic obstructive disorder (COPD), such as emphysema, where it is difficult to expire Chronic restrictive pulmonary disease (CRPD), such as pulmonary fibrosis, where it is difficult to inspire Measuring Respiratory Function Additional respiratory measurements—rates of air movement (continued) Maximum voluntary ventilation (MVV) Greatest amount of air that can be taken in and then expelled from the lungs in 1 minute Breathing as quickly and as deeply as possible Can be as high as 30 L/min (compared to 6 L/min at rest) All respiratory disorders impair this End here Respiratory Volumes and Capacities Figure 23.25 Overview of Respiration Lec acc ended here Figure 23.18 Chemical Principles of Gas Exchange Start cards here Partial pressure and Dalton’s law Partial pressure: pressure exerted by each gas within a mixture of gases, measured in mm Hg Written with P followed by gas symbol (that is, PO2 ) Each gas moves independently down its partial pressure gradient during gas exchange Atmospheric pressure = 760 mm Hg at sea level Total pressure all gases collectively exert in the environment Includes N2, O2, CO2, H2O, and other minor gases Chemical Principles of Gas Exchange Partial pressure and Dalton’s law (continued) Total pressure × % of gas = Partial pressure of that gas Nitrogen is 78.6% of the gas in air 760 mm HG × 78.6% = 597 mm Hg = partial pressure of nitrogen Partial pressures added together equal the total atmospheric pressure Dalton’s law The total pressure in a mixture of gases is equal to the sum of the individual partial pressures Partial Pressure Oxygen and carbon dioxide must know. Must know 760 mmGH and oxygen 20.9% and CO2 in air 0.04% Chemical Principles of Gas Exchange Relevant partial pressures in the body Reasons partial pressures in alveoli differ from atmospheric partial pressures Air from environment mixes with air remaining in anatomic dead space Oxygen diffuses out of alveoli into the blood; carbon dioxide diffuses from blood into alveoli More water vapor is present in alveoli than in atmosphere Within alveoli, the… percentage and partial pressure of O2 are lower than in atmosphere percentage and partial pressure of CO2 are higher than in atmosphere partial pressures of respiratory gases normally stay constant Chemical Principles of Gas Exchange Relevant partial pressures in the body (continued) In systemic cells, partial pressures of gases reflect cellular respiration (use of O2, production of CO2) The percentage of O2 lower and CO2 higher than in alveoli Under resting, normal conditions the partial pressures remain constant In circulating blood, gas partial pressures are not constant O2 enters blood in pulmonary capillaries; CO2 leaves O2 leaves blood in systemic capillaries; CO2 enters Partial Pressures and Gas Solubility Figure 23.27 Chemical Principles of Gas Exchange Partial pressure gradients Gradient exists when partial pressure for a gas is higher in one region of the respiratory system than another Gas moves from region of higher partial pressure to region of lower partial pressure until pressures become equal Both types of gas exchange depend on gradients Alveolar gas exchange: between blood in pulmonary capillaries and alveoli Systemic gas exchange: between blood in systemic capillaries and systemic cells Chemical Principles of Gas Exchange Gas solubility and Henry’s law Henry’s law: at a given temperature, the solubility of a gas in liquid is dependent upon the Partial pressure of the gas in the air Solubility coefficient of the gas in the liquid Partial pressure: driving force moving gas into liquid Determined by total pressure and percentage of gas in the mixture for example, CO2 is forced into soft drinks under high pressure Solubility coefficient: volume of gas that dissolves in a specified volume of liquid at a given temperature and pressure A constant that depends upon interactions between molecules of the gas and liquid Chemical Principles of Gas Exchange Gas solubility and Henry’s law (continued) Gases vary in their solubility in water Carbon dioxide about 24 times as soluble as oxygen CO2 moves more readily than 02 does Nitrogen about half as soluble as oxygen Does not rlly move It does not normally dissolve in blood in significant amounts Gases with low solubility require larger pressure gradients to “push” the gas into the liquid Overview of Gas Exchange Pulmonary Gas Exchange Movement of O2 PO2 in alveoli is 104 mm Hg PO2 of blood entering pulmonary capillaries is 40 mm Hg Oxygen diffuses across respiratory membrane from alveoli into the capillaries Moves down its partial pressure gradient Continues until blood PO2 is equal to that of alveoli Levels in alveoli remain constant as fresh air continuously enters Pulmonary Gas Exchange Movement of CO2 PCO2 in alveoli is 40 mm Hg PCO2 in blood of pulmonary capillaries is 45 mm Hg Carbon dioxide diffuses from blood to alveoli Moves down its partial pressure gradient Continues until blood levels equal alveoli levels Levels in alveoli remain constant Pulmonary Gas Exchange Pulmonary Gas Exchange Efficiency of gas exchange at respiratory membrane Anatomical features of membrane contributing to efficiency Large surface area (70 square meters) Minimal thickness (0.5 micrometers) Physiologic adjustments: ventilation-perfusion coupling Ability of bronchioles to regulate airflow and arterioles to regulate blood flow Ventilation changes by bronchodilation or bronchoconstriction for example, dilation in response to increased PCO2 in air in bronchiole Perfusion changes by pulmonary arteriole dilation or constriction for example, dilation in response to either decreased PCO2 or increased PO2 in blood Ventilation-Perfusion Coupling Tissue Gas Exchange Oxygen diffuses out of systemic capillaries to enter systemic cells Partial pressure gradient drives the process PO2 in systemic cells 40 mm Hg PO2 in systemic capillaries is 95 mm Hg Continues until blood PO2 is 40 mm Hg Systemic cell PO2 stays fairly constant Oxygen delivered at same rate it is used unless engaging in strenuous activity Tissue Gas Exchange Movement of CO2 Diffuses from systemic cells to blood Partial pressure gradient driving process PCO2 in systemic cells 45mm Hg PCO2 in systemic capillaries 40 mm Hg Diffusion continuing until blood PCO2 is 45 mm Hg Tissue Gas Exchange Oxygen Transport Blood’s ability to transport oxygen depends on Solubility coefficient of oxygen This is very low, and so very little oxygen dissolves in plasma Presence of hemoglobin The iron of hemoglobin attaches oxygen About 98% of O2 in blood is bound to hemoglobin HbO2 is oxyhemoglobin (with oxygen bound) HHb is deoxyhemoglobin (without bound oxygen) Carbon Dioxide Transport Carbon dioxide has three means of transport As CO2 dissolved in plasma (7%) As CO2 attached to amine group of globin portion of hemoglobin (23%) HbCO2 is carbaminohemoglobin As bicarbonate dissolved in plasma (70%) CO2 diffuses into erythrocytes, carbonic anhydrase catalyzes reaction with water to form bicarbonate and hydrogen ion Chloride shift: bicarbonate diffuses into plasma, chloride into erythrocyte CO2 is regenerated when blood moves through pulmonary capillaries and the process is reversed  Very important; must know Conversion of Carbon Dioxide to Bicarbonate Figure 23.31 Hemoglobin as a Transport Molecule Hemoglobin transports Oxygen attached to iron Carbon dioxide bound to the globin Hydrogen ions bound to the globin Binding of one substance causes a change in shape of the hemoglobin molecule Influences the ability of hemoglobin to bind or release the other two substances Hemoglobin as a Transport Molecule Hemoglobin and Binding of Oxygen Each hemoglobin can bind up to four O2 molecules One on each iron atom in the hemoglobin molecule Percent O2 saturation of hemoglobin is crucial It is the amount of oxygen bound to available hemoglobin Saturation increases as PO2 increases Cooperative binding effect: each O2 that binds causes a change in hemoglobin making it easier for next O2 to bind Graphed in the oxygen-hemoglobin saturation curve S-shaped, nonlinear relationship As we breathe O2 at high altitude it does not a ect performance or at sea level. Only consume supplemental oxygen at super high altitudes since hemoglobin cannot carry O2 to systemic cells Oxyhemoglobin association curve Lec ended here Maybe draw on exam Hemoglobin as a Transport Molecule Start cue cards here Hemoglobin and binding of oxygen (continued) Large changes in saturation occur with small increases of PO2 at lower partial pressures (that is, curve is initially steep) At PO2 higher than 60 mm Hg only small changes in saturation occur About 90% saturation at 60 mm Hg Hemoglobin saturation is about 98% at pulmonary capillaries as PO2 is 104 mm Hg Saturation can only reach 100% at pressures above 1 atm (for example, in hyperbaric oxygen chambers) Hemoglobin as a Transport Molecule Hemoglobin and binding of oxygen (continued) Can use graph to determine saturation at a given PO2 At 5000 ft, alveolar PO2 is 81 mm Hg Corresponds to a hemoglobin saturation of 95% At 17,000 ft, alveolar PO2 is 40 mm Hg Corresponds to a hemoglobin saturation of 75% Altitude sickness Adverse physiologic effects from a decrease in alveolar PO2 and low oxygen saturation Includes symptoms of headache, nausea, pulmonary edema, and cerebral edema Hemoglobin as a Transport Molecule Hemoglobin and binding of oxygen (continued) Some (not all) oxygen released from hemoglobin at systemic capillaries 98% saturation as it leaves the lungs (at sea level) About 75% saturation after passing systemic cells at rest Only 20 to 25% of transported oxygen is released Oxygen reserve: O2 remaining bound to hemoglobin after passing through systemic circulation Provides a means for additional oxygen to be delivered under increased metabolic demands (for example, exercise) Vigorous exercise produces a significant drop in saturation Blood leaving capillaries in active muscles only about 35% saturated Hemoglobin as a Transport Molecule Hemoglobin’s binding and release of oxygen CO2 binding to hemoglobin Binding causes release of more oxygen from hemoglobin H+ binding to hemoglobin Hydrogen ion binds to hemoglobin and causes a conformational change This causes decreased affinity for O2 and oxygen release Called the Bohr effect Hemoglobin as a Transport Molecule Hemoglobin’s binding and release of oxygen (continued) Temperature Elevated temperature diminishes hemoglobin’s hold on oxygen Presence of 2,3-BPG: a molecule in erythrocytes Molecule binds hemoglobin, causing release of additional oxygen Certain hormones stimulate erythrocytes to produce 2, 3-BPG Thyroid, epinephrine, growth hormone, and testosterone Hemoglobin as a Transport Molecule Influence on the oxygen-hemoglobin saturation curve Some variables decrease oxygen affinity for hemoglobin Causes a shift right for example, increased temperature, increase in hydrogen ion Other variables increase oxygen affinity to hemoglobin Causes a shift left for example, decreased temperature, decrease in hydrogen ion Draw, explain signi cance, and why Bohr e ect is important for O2 in exercise Effects of Hyperventilation and Hypoventilation on Cardiovascular Function Hyperventilation: breathing rate or depth above body’s demand Caused by anxiety, ascending to high altitude, or voluntarily PO2 rises and PCO2 fall in the air of alveoli Additional oxygen does not enter blood because hemoglobin is already 98% saturated There is greater loss of CO2 from blood, called hypocapnia Effects of Hyperventilation and Hypoventilation on Cardiovascular Function Hyperventilation (continued) Low blood CO2 causes vasoconstriction Brain vessel constriction can decrease oxygen delivery to the brain May decrease blood hydrogen ion concentration If buffers cannot compensate, result is respiratory alkalosis Hyperventilation may cause Feeling faint or dizzy, numbness, tingling, cramps, and tetany If prolonged, disorientation, loss of consciousness, coma, possible death Effects of Hyperventilation and Hypoventilation on Cardiovascular Function Hypoventilation: breathing too slow (bradypnea) or too shallow (hypopnea) Causes include: airway obstruction, pneumonia, brainstem injury, other respiratory conditions O2 levels down, CO2 levels up in alveoli Blood PO2 decreases (hypoxemia); and can lead to low oxygen in tissues (hypoxia) Blood PCO2 increases (hypercapnia) Effects of Hyperventilation and Hypoventilation on Cardiovascular Function Hypoventilation (continued) May result in inadequate oxygen delivery May result in increased hydrogen ion concentration due to high blood PCO2 Might result in respiratory acidosis May cause Lethargy, sleepiness, headache, polycythemia, cyanotic tissues If prolonged, convulsions, loss of consciousness, death Breathing and Exercise While exercising, breathing type = hyperpnea to meet increased tissue needs Breathing depth increases while rate remains the same Blood PO2 and Blood PCO2 remain relatively constant Increased cellular respiration compensated for by deeper breathing, increased cardiac output, greater blood flow The respiratory center is stimulated from one or more causes Proprioceptive sensory signals in response to movement Motor output from cerebral cortex relayed to respiratory center Conscious anticipation of exercise