| Question |
Answer |
| Role of Cerebral Cortex in regulation of ventilation |
Think CC=CC. Conscious Control of ventilation. Speech and singing |
| Mechanism of rythmic ventilation |
Dorsal Resp. Group (DRG), like the SA node of breathing |
| Identify the types of medullary respiratory neurons |
DRG, VRG. DRG= maintain normal breathing, VRG= during exercise or diseaseto activate the accessory muscles |
| Where is the apneustic center? |
Caudal pons(LOWER), boost inspiratory effort = "GASP" |
| Where is the pneumotaxic center? |
Cephalic pons(UPPER/HEAD), responsible for "Panting" , increased rate and tidal V |
| Where are the peripheral chemoreceptors? |
Aortic Arch and Carotid Sinus |
| Which nerve innervates the Carotid peripheral chemoreceptors? |
Glossophryngeal |
| Which nerve innervates the Aortic bodies? |
Vagus |
| Chemical stimulus of the peripheral chemoreceptors? |
LOW PO2 <60mmHg, LOW pH |
| Location of chemical chemorecptors? |
Ventiolateral= Front and sides, immersed in CSF |
| Stimulation of chemical chemorecptors? |
HIGH CO2, LOW pH |
| What is the normal ventilatory response to CO2? |
CO2 is the strongest stimuli to ventilation |
| Factors which affect vent response to CO2? |
Drugs depress the medullary center, Narcotics like heroin, Morphine, and Barbituates, Pent, and Sero. Also airway obstruction(COPD, athsma) |
| What is the vent response to hypoxemia? |
Ve increases, rate increases when PO2<60mmHg |
| Changes in vent response to hypoxia during hypercapnia? |
Hypercapnia augments hypoxic response |
| Changes in vent response to hypoxia during hypocapnia? |
Hypocapnia diminishes hypoxic drive |
| What is the vent response to acute reduction in pH? |
Ve increases, stimulates peripheral chemoreceptors |
| Significance of blood brain barrier and CPF |
Gases diffuse easily across and Ions need active transport/slow. CSF pH= 7.32=little buffer capability |
| Chronic Resp. Acidoiss |
HCO3 increases in CSF and central chemmorectors are made non-responsive, then the LOW PO2stimulate the peripheral chemorecptors creating a hypoxic drive |
| Ketoacidosis causes |
stimulation of both CC and PC causing Kussmaul's brething patern(Big R, Big Vt), and PaCO2 drops into the 20s |
| Apneustic Breathing |
Gasping= sustained inspiratory maneuver from BRAINSTEM injuries |
| BIOT's Breathing |
10-20 seconds ofapnea followed by 3-5 identical volume breaths. NEURO pts/INCREASE ICP |
| Cheyne-Stokes Respiration |
"Crescendo-Decrescendo" pattern, HEART failure or servre brain damage |
| Kussmaul's Breathing |
From KETOACIDOSIS, rapid, deep breathing |
| Proprioceptors |
sensory end organs in muscles, tendons, ligaments that are stimulated by increased movement associated with changing resp mechanics of lung and chest wall |
| What triggers the proprioceptors? |
Decreased lung compliance(edema, fibrosis, consolidation), Decreased chest wall compliance(acities, obesity), Increased airway resistance(secretions and broncospasm), exercise |
| Physiologial role of chest wall proprioceptors? |
Control feeling of dypsnea when chronic conditions are present from exercise or disease |
| 3 Pulmonary Vagal sensory reflexes |
Pulmonary stretch receptors(Hering-Bruerer), Irritant, and Juxtapulmonary(J) receptors |
| Where are the pulmonary stretch receptors? |
Located in smooth muscles of conducting airways |
| What stimulates pulmonary stretch receptors? |
Increased lung V, decrease intrapleural P |
| What are the physiological response to stimulation of PSR? |
inhibit inspiration(to protect from hyperinflation), Bronchodilation, increased HR |
| Paradoxical Reflex of the Head in newborns when PSR stim. |
GASP, with subtle breath stack to create FRC |
| Where are the Irritant recptors? |
between the epithelium cells in the conducting airway |
| What stimulates the Irritant recptors? |
Dust, smoke, chemicals, or mechanical from foreign bodies |
| What are the pyhsiological responses to stim of Irritant receptors? |
Cough, broncoconstrition, hypernea, Laryngeal constriction=GRUNT on Exp. |
| Where are the "J" receptors located? |
within the pulmonary interstitium |
| What stimulates the "J" receptors? |
edema, emboli |
| What are the physiological responses to stim of "J" receptors? |
Rapid shallow breathing, GRUNT, tachypnea, hyponea |
| 3 major fetal circulation shunts |
Ductus Venosus, Foramen Ovale, Ductus Arteriosis |
| Ductus Venosus |
communicates the umbilical vein with the IVC |
| Foramen Ovale |
communicates the Right and Left Atria via one way valve, closes when cord is clamped and Right atrial P drops as IVC blood flow drops |
| Ductus Arteriosis |
communicates the pulmonary artery with the descending aorta, closes as PVR drops and levels of PGE1 drops and PaO2 increases >60mmHg |
| What are cardiopulm. adaptive changes in high alt. dwellers? |
increased lung size, polycythemia due to hypoxemia=erythropoetin from kidneys to stim bone marrow to make more RBC |
| Normal pulmonary adaptive changes during exercise |
increased Ve, increased aveolar ventilation(up to 65% MBC), increased diffusion x3 |
| Normal cardiovascular adaptive changes during exercise |
increased O2 comsuption, increased ER, decreased SvO2 as more go to tissues, increased C(a-v)O2, increased HR x 200%, CO reaches 90% max |
| Benefits to cardiopulmonary training |
increased SV, lower rest HR, increased muscle strength, decreased myocardial and respiratory O2 cost |
| What altered resistive and elastic forces increase WOB? |
Increased resistance, decreased compliance, decreased conductance, decreased elastance |
| normal value of WOB |
0.5 joules/L |
| Define and state normal value for oxygen cost of breathing |
O2 consupmtion of resp. muscles <5% of total O2 consumption(12ml/min)out of 250 |
| Increased O2 cost of breathing is from ? |
increased resistance, decreased compliance, decreasedconductance, decreased elastance, empysema is too elastic but uses 120ml/min O2 consumption=almost 1/2 |
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