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CO2 Transport,[object Object],CO2 in blood – 4ml/dl,[object Object],Cl- shift*,[object Object]
CO2 Dissociation Curve,[object Object]
Regulation of Respiration,[object Object]
Regulation of Respiration,[object Object],Objective of ventilatory control:,[object Object],Establish automatic rhythm for respiration contraction,[object Object],Adjust this rhythm to accommodate varying,[object Object],Metabolic demands,[object Object],Mechanical conditions,[object Object],Non-ventilatory behaviours,[object Object],Arrangement of regulation,[object Object],Central control (CNS centres, central chemoreceptors),[object Object],Peripheral chemoreceptors,[object Object]
Resp upload3
Central Control of Breathing,[object Object],Medullary respiration centre,[object Object],Located in RF,[object Object],DRG,[object Object],Inspiration – RAMP signal,[object Object],Input – X (PCR, mechanoR in lungs), XI (PCR),[object Object],Output – Phrenic N. to diaphram,[object Object],VRG,[object Object],Inspiration & Expiration,[object Object],Not active during normal, quiet breathing,[object Object],Activated during exercise,[object Object],Apneustic centre,[object Object],Located in lower pons,[object Object],Stimulates inspiration during deep & prolonged inspiratory gasp,[object Object],Pneumotaxic centre,[object Object],Located in upper pons,[object Object],Inhibits inspiration – regulates inspiratory volume, RR,[object Object],Cerebral cortex,[object Object],Voluntary control of respiration,[object Object]
Hering Breuer Reflex,[object Object],Stretch R in bronchi and bronchioles,[object Object],Overstretching of lungs stimulates these R,[object Object],Signals sent to DRG – ,[object Object],Inhibition of RAMP occurs (pneumotaxic centre-like effect),[object Object],Hering Breuer reflex checks OVERINFLATION of lung,[object Object]
Central CRs,[object Object],Location:,[object Object],Ventral surface of medulla, ,[object Object],Near point of exit of CN IX & CN X ,[object Object],Only a short distance from the medullary inspiratory center,[object Object],Affects the centre directly,[object Object],Central CR sensitive to: ,[object Object],pH of CSF (decrease in pH – increases RR),[object Object],CO2 crosses BBB >> easier than H+,[object Object],(CO2 + H2O ----- H+ + HCO3),[object Object],Increase in CO2 & H+ ----- increases ventilation – decreases levels of CO2 & H+,[object Object],Role of CO2 in regulation of respiration is mainly acute (the H+ is adjusted within 1-2 days by kidneys!),[object Object],O2 DOES NOT affect CCR*,[object Object]
CO2 affects Ventilation*,**,[object Object]
Acid–Base Balance affects Ventilation,[object Object],Respiratory response in Metabolic Acidosis ,[object Object],E.g due to accumulation of acid ketone bodies DM,[object Object],Response: ,[object Object],Pronounced respiratory stimulation (Kussmaul breathing) 	,[object Object],The hyperventilation decreases alveolar PCO2 ("blows off CO2") ,[object Object],Thus produces a compensatory fall in blood [H+],[object Object],Respiratory response in Metabolic Alkalosis,[object Object],E.g: protracted vomiting with loss of HCl from body,[object Object],Response:,[object Object],Ventilation is depressed ,[object Object],Arterial PCO 2 rises, raising the [H+]toward normal,[object Object]
Acid–Base Balance affects Ventilation,[object Object],Respiratory Acidosis,[object Object],Can occur when Pco2 rises via:,[object Object],Direct inhibition of respiratory centres (sedatives, anesthetics),[object Object],Weakening of respiratory muscles (polio, MS, ALS),[object Object],Decreased CO2 exchange in pulmonary blood (COPD) ,[object Object],Renal adjustment of H+/HCO3- corrects for this,[object Object],Respiratory Alkalosis*,[object Object],Can occur when Pco2 decreases via:,[object Object],Hypoxemia causes hyperventilation (pneumonia, high altitude),[object Object],Direct ++ of resp. centers  (salicylate poisoning),[object Object],Psychogenic ,[object Object],Renal adjustment of H+/HCO3- corrects for this,[object Object]
Peripheral CRs,[object Object],Cells of PCR:,[object Object],Type I (glomus) cell,[object Object],Is +++ by:,[object Object],Decrease in Po2 (especially drop in Po2 between 60-30 mmHg),[object Object],Increase in Pco2 (generally not as imp as its effect on CCR; but its affect is 5 times more rapid on PCR than CCR – role in raising RR at exercise onset),[object Object],Decrease in pH,[object Object],Type- II cell,[object Object],Function: support,[object Object]
Peripheral CRs,[object Object],Blood flow  to each carotid body is VERY high!!* ,[object Object],Hence O2 needs are met largely by dissolved O2 alone ,[object Object],Therefore, the receptors are NOT +++ in conditions such as anemia or CO poisoning** ,[object Object],Powerful stimulation is also produced by cyanide, which prevents O2 utilization at the tissue level ,[object Object],Infusion of K+ increases discharge rate in CR afferents,[object Object],Plasma K+ level is increased during exercise, the increase may contribute to exercise-induced hyperpnea.,[object Object]
Po2, Pco2, H+Scenarios In Respiration Control ,[object Object],Changing Po2 (Pco2 & H+ = constant),[object Object],Po2 below 100 mmHg profoundly influences respiration control,[object Object],Changing Po2 (Pco2 & H+ = fluctuating),[object Object],Decreasing Po2increases RR,[object Object],Increasing RR – increased CO2 blow-off – decreasing Pco2 – which inhibits RR,[object Object],Acclimatization:,[object Object],Decreased sensitivities of CNS resp. centres to CO2,[object Object]
Respiratory Response to Exercise,[object Object]
Respiratory Response to High Altitude,[object Object]

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Editor's Notes

  1. *hematocrit of venous blood is normally 3% greater than that of the arterial blood. In the lungs, the Cl– moves out of the cells and they shrink
  2. Apneustic Center : Apneusis is an abnormal breathing pattern with prolonged inspiratory gasps, followed by brief expiratory movement. Stimulation of the apneustic center in the lower pons produces this breathing pattern in experimental subjects. Stimulation of these neurons apparently excites the inspiratory center in the medulla, prolonging the period of action potentials in the phrenic nerve, and thereby prolonging the contraction of the diaphragm. Pneumotaxic Center : The pneumotaxic center turns off inspiration, limiting the burst of action potentials in the phrenic nerve. In effect, the pneumotaxic center, located in the upper pons, limits the size of the tidal volume, and secondarily, it regulates the respiratory rate. A normal breathing rhythm persists in the absence of this center.
  3. *(as its levels are maintained even with fluctuating Palvo2 while CO2 levels fluctuate appropriately)
  4. *Responses of normal subjects to inhaling O2 and approximately 2, 4, and 6% CO2. The relatively linear increase in respiratory minute volume in response to increased CO2 is due to an increase in both the depth and rate of respiration.**Of course, this linearity has an upper limit. When the PCO 2 of the inspired gas is close to the alveolar PCO 2, elimination of CO2 becomes difficult. When the CO2 content of the inspired gas is more than 7%, the alveolar and arterial PCO 2 begin to rise abruptly in spite of hyperventilation. The resultant accumulation of CO2 in the body (hypercapnia) depresses the central nervous system, including the respiratory center, and produces headache, confusion, and eventually coma (CO2narcosis).
  5. *mediated via peripheral CR
  6. Ventilatory Response to Oxygen LackWhen the O2 content of the inspired air is decreased, respiratory minute volume is increased. The stimulation is slight when the PO2 of the inspired air is more than 60 mm Hg, and marked stimulation of respiration occurs only at lower PO2 values (Figure 37–9). However, any decline in arterial PO2 below 100 mm Hg produces increased discharge in the nerves from the carotid and aortic chemoreceptors. There are two reasons why this increase in impulse traffic does not increase ventilation to any extent in normal individuals until the PO2 is less than 60 mm Hg. Because Hb is a weaker acid than HbO2, there is a slight decrease in the H+ concentration of arterial blood when the arterial PO2 falls and hemoglobin becomes less saturated with O2. The fall in H+ concentration tends to inhibit respiration. In addition, any increase in ventilation that does occur lowers the alveolar PCO2, and this also tends to inhibit respiration. Therefore, the stimulatory effects of hypoxia on ventilation are not clearly manifest until they become strong enough to override the counterbalancing inhibitory effects of a decline in arterial H+ concentration and PCO2.
  7. *in each 2-mg carotid body is about 0.04 mL/min, or 2000 mL/100 g of tissue/min compared with a blood flow 54 mL or 420 mL per 100 g/min in the brain and kidneys, respectively. **in which the amount of dissolved O2 in the blood reaching the receptors is generally normal, even though the combined O2 in the blood is markedly decreased.