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Each Hb molecule is composed of 4 polypeptide chains, each with a iron-containing heme group Oxyhemoglobin (HbO2): hemoglobin-O2 combination Reduced hemoglobin (deoxyhemoglobin) (HHb): hemoglobin that has released O2 As O2 binds, Hb changes shape, increasing its affinity for O2 increases As O2 is released, Hb shape change causes a decrease in affinity for O2 Fully saturated (100%): all four heme groups carry O2 Partially saturated: when only one to three hemes carry O2 Influence of PO2 on hemoglobin saturation PO2 heavily influences binding and release of O2 with hemoglobin Percent of Hb saturation can be plotted against PO2 concentrations Resulting graph is not linear, but an S-shaped curve Referred to as an oxygen-hemoglobin dissociation curve In arterial blood: PO2 is 100 mm Hg and contains 20 ml of oxygen per 100 ml blood (20 volume %) Venous reserve: oxygen remaining in venous blood that can still be used Influence of other factors on hemoglobin saturation Increases in temperature, H+, PCO2, and BPG can modify structure of hemoglobin Results in a decrease for Hb’s affinity for O2 Occurs in systemic capillaries Enhances O2 unloading, causing a shift inO2-hemoglobin dissociation curve to right Decreases in these factors shift curve to left Decreases oxygen unloading from blood BPG is produced by RBCs during glycolysis; BPG levels rise when oxygen levels are low As cells metabolize glucose, they use O2, causing: Increases in PCO2 and H+ in capillary blood Declining blood pH (acidosis) and increasing Pco2 cause Hb-O2 bond to weaken Referred to as Bohr effect O2 unloading occurs where needed most Heat production in active tissue directly and indirectly decreases Hb affinity for O2 Allows increased O2 unloading to active tissues CARBON DIOXIDE TRANSPORT CO2 is transported in blood in three forms: 7 to 10% is dissolved in plasma as PCO2 20% of CO2 is bound to the globin part of hemoglobin Referred to as carbaminohemoglobin 70% is transported as bicarbonate ions (HCO3–) in plasma Formation of bicarbonate involves CO2 combining with water to form carbonic acid (H2CO3), which quickly dissociates into bicarbonate and H+ Occurs primarily in RBCs, where enzyme carbonic anhydrase reversibly and rapidly catalyzes this reaction In systemic capillaries, after HCO3– is created, it quickly diffuses from RBCs into plasma Outrush of HCO3– from RBCs is balanced as Cl– moves into RBCs from plasma Referred to as chloride shift In pulmonary capillaries, the processes occur in reverse HCO3– moves into RBCs while Cl moves out of RBCs back into plasma HCO3– binds with H+ to form H2CO3 H2CO3 is split by carbonic anhydrase into CO2 and water CO2 diffuses into alveoli Haldane effect Amount of CO2 transported is affected by PO2 The lower the PO2 and hemoglobin O2 saturation, the more CO2 can be carried in blood Reduced hemoglobin buffers H+ and forms carbaminohemoglobin more easily Process encourages CO2 exchange at tissues and at lungs At tissues, as more CO2 enters blood, more oxygen dissociates from hemoglobin (Bohr effect) As HbO2 releases O2, it more readily forms bonds with CO2 to form carbaminohemoglobin Influence of CO2 on blood pH Carbonic acid–bicarbonate buffer system: helps blood resist changes in pH If H+ concentration in blood rises, excess H+ is removed by combining with HCO3– to form H2CO3, which dissociates into CO2 and H2O If H+ concentration begins to drop, H2CO3 dissociates, releasing H+ HCO3– is considered the alkaline reserve of carbonic acid-bicarbonate buffer system Changes in respiratory rate and depth affect blood pH Respiratory rhythms are regulated by higher brain centers, chemoreceptors, and other reflexes Neural controls involve neurons in reticular formation of medulla and pons Medullary respiratory centers Clustered neurons in two areas of medulla are most important: Ventral respiratory group Dorsal respiratory group Ventral respiratory group (VRG) Rhythm-generating and integrative center Consists of network of neurons in brain stem that extends from spinal cord to pons-medulla junction Sets eupnea: normal respiratory rate and rhythm (12–15 breaths/minute) Its inspiratory neurons excite inspiratory muscles via phrenic (diaphragm) and intercostal nerves (external intercostals) Expiratory neurons inhibit inspiratory neurons Dorsal respiratory group (DRG) Network of neurons located near root of cranial nerve IX Group integrates input from peripheral stretch and chemoreceptors, then sends information to VRG neurons Much is not known about this group of neurons Pontine respiratory centers Neurons in this center influence and modify activity of VRG Act to smooth out transition between inspiration and expiration and vice versa Transmit impulses to VRG that modify and fine-tune breathing rhythms during vocalization, sleep, exercise Lesions in this area of brain lead to apneustic breathing, where patient takes prolonged inspirations Factors Influencing Breathing Rate and Depth Respiratory centers are affected by: Chemical factors Influence of higher brain centers Pulmonary irritant reflexes Inflation reflex Chemical factors Most important of all factors affecting depth and rate of inspiration Changing levels of PCO2, PO2, and pH are most important Levels of these chemicals are sensed by: Central chemoreceptors: located throughout brain stem Peripheral chemoreceptors: found in aortic arch and carotid arteries Influence of PCO2 Most potent and most closely controlled If blood PCO2 levels rise (hypercapnia), CO2 accumulates in brain and joins with water to become carbonic acid Carbonic acid dissociates, releasing H+, causing a drop in pH (increased acidity) Increased H+ stimulates central chemoreceptors of brain stem, which synapse with respiratory regulatory centers Respiratory centers increase depth and rate of breathing, which act to lower blood PCO2, and pH rises to normal levels If blood PCO2 levels decrease, respiration becomes slow and shallow Apnea: breathing cessation that may occur when PCO2 levels drop abnormally low Swimmers sometimes voluntarily hyperventilate to enable them to hold their breath longer Hyperventilation: increased depth and rate of breathing that exceeds body’s need to remove CO2 May be caused by anxiety attacks Leads to decreased blood CO2 levels (hypocapnia) Causes cerebral vasoconstriction and cerebral ischemia, resulting in dizziness, fainting Early symptoms include tingling and involuntary muscle spasms in hands and face Treatment: breathing into paper bag increases CO2 levels being inspired pH can modify respiratory rate and rhythm even if CO2 and O2 levels are normal Mediated by peripheral chemoreceptors Decreased pH may reflect CO2 retention, accumulation of lactic acid, or excess ketone bodies Respiratory system controls attempt to raise pH by increasing respiratory rate and depth Rising CO2 levels are most powerful respiratory stimulant Normally, blood PO2 affects breathing only indirectly by influencing peripheral chemoreceptor sensitivity to changes in PCO2 When arterial PO2 falls below 60 mm Hg, it becomes major stimulus for respiration (via peripheral chemoreceptors) Changes in arterial pH resulting from CO2 retention or metabolic factors act indirectly through peripheral chemoreceptors Influence of higher brain centers Hypothalamic controls: act through limbic system to modify rate and depth of respiration Example: breath holding that occurs in anger or gasping with pain Change in body temperature changes rate Cortical controls: direct signals from cerebral motor cortex that bypass medullary controls Example: voluntary breath holding at least until brain stem reinstates breathing when blood CO2 becomes critical Pulmonary irritant reflexes Receptors in bronchioles respond to irritants such as dust, accumulated mucus, or noxious fumes Receptors communicate with respiratory centers via vagal nerve afferents Promote reflexive constriction of air passages Same irritant triggers a cough in trachea or bronchi or a sneeze in nasal cavity Inflation reflex Hering-Breuer reflex (inflation reflex) Stretch receptors in pleurae and airways are stimulated by lung inflation Send inhibitory signals to medullary respiratory centers to end inhalation and allow expiration May act as protective response more than as a normal regulatory mechanism Exercise Hyperpnea: increased ventilation in response to metabolic needs Ventilation increases abruptly, increases gradually, then reaches steady state; when exercise stops, there is a small, abrupt decline in ventilation, followed by a gradual decrease PCO2, PO2, and pH remain surprisingly constant during exercise Abrupt increase in ventilation that occurs as exercise begins involves three neural factors: 1Psychological stimuli: anticipation of exercise 2Simultaneous cortical motor activation of skeletal muscles and respiratory centers 3Excitatory impulses to respiratory centers from proprioceptors in moving muscles, tendons, joints Ventilation declines suddenly as exercise ends is because the three neural factors are shut off Exercise leads to anaerobic respiration and the formation of lactic acid Lack of oxygen in muscles is not from poor respiratory function, but rather from insufficient cardiac output or skeletal muscle inability to increase oxygen uptake Acclimatization: respiratory & hematopoietic adjustments are made with long-term moves to high altitude Chemoreceptors become more responsive to PCO2 when PO2 declines