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Lecture 11

PHGY 210- Lecture 11- Dr. Lauzon.docx

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Department
Physiology
Course
PHGY 210
Professor
Ann Wechsler
Semester
Winter

Description
Lecture 11- Wednesday, January 27 , 2010 th -frc does not mean that the lung is empty. There is still 1.2 L of air in the lungs at frc. H. Respiratory Failure Respiratory failure occurs when the respiratory system is unable to do its job properly, due to failure of: 1)the gas exchanging capabilities of the lungs; 2)the neural control of ventilation (i.e. the drive to breathe); 3)the neuromuscular breathing apparatus (i.e. the respiratory muscles and their innervation). I. Arterial Hypoxia (Hypoxemia) Blood hypoxia refers to deficient blood oxygenation, i.e. low PaO2 and low % Hb saturation. In hypoxic conditions, if PaO2 decreases below 60 mm Hg, O2 content in arterial and venous blood becomes lower than the normal values at sea level. There are 5 general causes of hypoxia: 1) Inhahlation of low PO2 (e.g. at high altitude). 2) Hypoventilation: PaO2 decreases and PaCO2 increases. It means that alveolar ventilation in relation to the metabolic CO2 production is reduced. Hypoventilation occurs due to: diseases affecting the central nervous system, neuromuscular diseases, barbiturates, other drugs and narcotics. 3) Ventilation/perfusion imbalance in the lungs: this occurs when the amount of fresh gas reaching an alveolar region per breath is either too little or too much for the blood flow through the capillaries of that region. 4) Shunts of blood across the lungs: venous blood bypasses the gas exchanging region of the lungs and returns to systemic circulation, deoxygenated. 5) O2 diffusion impairment (e.g. thickening of the alveolar-capillary membrane, or pulmonary edema). VI Control of Breathing A. Voluntary vs Automatic Breathing When we think of respiration, we think of an automatic, involuntary activity that brings enough air into the pulmonary alveoli to maintain the O2 and CO2 tensions of alveolar gas or arterial blood at optimal levels in different conditions, e.g. sleep, rest, or exercise. The central nervous system controls gas exchange by integrating all the information coming from the periphery which in turn, gives an adequate depth and frequency of breathing (minute ventilation). In fact, breathing is under both voluntary (e.g. voluntary hyperventilation) and involuntary (e.g. while asleep) control. Anatomically, there are separate neurological structures for automatic and voluntary control, although the two systems interact. The cerebral hemispheres (Figure 29 a) control voluntary breathing that can be effective even when automatic control no longer functions while the brainstem (Figure 29 a) controls involuntary breathing. Breaking Point: If you stop ventilation voluntarily, you will find that in spite of your efforts to prevent it, breathing will eventually start again. This occurs because the arterial PCO2 has reached about 50 mm Hg and arterial PO2 has reached about 70 mm Hg, at which point voluntary control is over-ridden. This is called the breaking point. The over- riding of the voluntary control by the automatic control depends upon the information from the receptors sensitive to CO2 and O2 levels (in arterial blood and/or cerebro-spinal fluid). see picture in slides B. Structures Involved in the Control of Breathing The neuronal structures involved in involuntary control of breathing are located in the brain stem (pons and medulla). Like in other physiological systems, there are 3 basic elements in the respiratory control system (figure 29b): 1) sensors: these gather information about lung volume (pulmonary receptors) and O2 and CO2 content (chemoreceptors). 2) controllers: information from the sensors is sent to the controller, in the pons and medulla, via afferent neural fibers. Once it has reached the pons and medulla, the peripheral information and inputs from the higher structures of the central nervous system are integrated. 3) effectors: as a result of the integration, neuronal impulses are generated and sent via spinal motoneurons to the effectors, i.e. the respiratory muscles. This results in ventilation being adjusted to the person's metabolic needs. Since the main function of the lungs is to exchange O2 and CO2 between alveolar gas and blood, whenever the demand for O2 and the production of CO2 increase (as during exercise), ventilation must increase too, to satisfy this requirement. see picture in slides C. Respiratory Neurons Pattern of breathing Medulla: There are pacemaker cells in the medulla. They are mainly located into 2 groups of cells: ventral respiratory group (contains the pre-Botzinger complex) that generate the basic rhythm, and dorsal respiratory group that receives several sensory inputs. All these cells connect to inspiratory motor neurons. The ventral and dorsal groups also connect to each other.  Respiratory neurons in the medulla generate the basic respiratory rhythmicity. (^more even) Pons (upper): Cells located in the rostral (upper) pons (called the pneumotaxic center) modify the inspiratory activity of the centers in the medulla. These cells “turn-off” inspiration leading to smaller tidal volume. This also leads to an increase in breathing frequency to maintain adequate alveolar ventilation.  Cutting the pneumotaxic centers causes breathing to become deep and slow (this is the same effect as cutting the vagus nerves which bring afferent information). (^more even) Pons (lower): Cells located in the lower pons (called the apneustic center) send excitatory impulses to the respiratory groups of the medulla, thus promoting inspiration. Removing influence of both the upper pons and the vagus nerves causes apneuses (tonic inspiratory activity interrupted by short expirations). This type of breathing is seen in some severe types of brain injury. (^uneven) D. Chemoreceptors PO2, PCO2, and pH in arterial blood are detected by chemoreceptors. If these pressures or pH are changed, ventilation will also change in attempt to return the gas pressures to their normal values. Information from the chemoreceptors is carried to the respiratory neurons. In turn, the activity of respiratory neurons will increase if PaO2 is too low (less than 60 mm Hg) or PaCO2 is higher than 40 mm Hg. The activity of the respiratory neurons will decrease if PaO2 is higher than 100 mm Hg or PaCO2 is lower than 40 mm Hg. There are 2 types of chemoreceptors: central and p
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