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Respiratory Physiology Review Notes

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Respiratory Physiology Review
Anatomy Review:
-2 bronchi, 3 right and left bronchioles terminal bronchioles (do not participate in gas
exchange) ,no cartilage, rely on elastic recoil of lungs to stay open.
Pressures:
-opposing pressures in pulmonary capillaries
-hydrostatic pressure = pushing pressure generated by the pumping of the heart (forcing
everything through)
-oncotic pressure = pulling pressure, generated by plasma proteins (fluid leaks out- into 3
rd
spacing
Ventilation/ Perfusion:
-usually 1:1 ratio 4-5L/min of blood perfuses the lungs, 4-5L/min gas reaches alveoli
-imbalance = problems!
-Apex vent > perfusion
- Base perfusion
-Ventilation of alveoli brings o2 into lung, removes CO2
-perfusion of pulmonary capillaries blood being sent to the lungs
V/Q mismatch; Shunt
Shunt inadequate ventilation (more perfusion than ventilation more trains than
passengers)
2-5% is normal
Anatomic Ventricular-septal defects
Intrapulmonary: blood returns to the heart WITHOUT having gas exchange
ex: Pneumonia, Atelectasis- interfere w proper ventilation (blood flor IS circulating, but not
being oxygenated)
Shunt vs. Dead Space
-Dead-space= poor perfusion! There IS ventilation
Anatomic airway not participating in gas exchange (blood is NOT circulating- oxygen is there,
but not attaching to anything.
Alveolar pathological = PE, hypotension, positive pressure ventilation, CPAP, BiPAP

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Ventilation:
Compliance lungs ability to yield to intra-alveolar pressure during inspiration
-alveoli are more compliant at the bases (smaller in diameter) than apex alveoli
at bases inflate more
- Decrease= pulm fibrosis, alveolar edema (restricting expansion!)
-Increase = COPD= elastic fibers are destroyed (expand, no recoil!)
Airflow Resistance problems from a change in airway radius/pattern of airflow
-ETT secretions in airway, condensation in tubing(from humidifier!)
-a DECREASE in airway size = INCREASE in airway resistance ; 1:1 ratio- longer tubing/more
resistance
-Elastic resistance: lungs natural tendency to contract
-2 forces counter elasticity Chest rigity combined w pleural fluid tensions(neg pressure)
secretion of surfactant; secreted by type II pneumocytes
-Non- Elastic resistance: results from the force exerted on the thorax by the diaphragm and the
abdominal contents which inhibit downward expansion
-usually not a problem
-problematic in; obesity, abd. Distension, ascites, late term pregnancy
Chemoreceptor control: (CO2, O2, pH)
-Monitor body’s ventilatory status, signals the resp center to adjust the rate and rhythm
-Central; In anterior medulla, sensitive to pH and PaCO2 changes// changes RR and TV in
response (get rid of the CO2)
-Peripheral; in aortic and carotid bodies- monitor pH changes
Neurological Control:
-Medulla; primary resp control center
-regulates rate and depth in response to pH and paCO2
-Pons; regulates rhythm
-Cerebral Cortex; conscious control from motor areas
Acid Base Balance:
Review normals;
-pH; 7.35-7.45
-PaO2; 80-100 (pressure pushing O2 into the blood stream)
-SaO2: >95%
-PaCO2: 35-45 (in normal person, >70 can equal death)
-resp system compensation
-HCO3: 22-26
-renal system compensation

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Respiratory Physiology Review Anatomy Review: -2 bronchi, 3 right and left → bronchioles → terminal bronchioles (do not participate in gas exchange) ,no cartilage, rely on elastic recoil of lungs to stay open. Pressures: -opposing pressures in pulmonary capillaries -hydrostatic pressure = pushing pressure generated by the pumping of the heart (forcing everything through) -oncotic pressure = pulling pressure, generated by plasma proteins (fluid leaks out- into 3rd spacing Ventilation/ Perfusion: -usually 1:1 ratio → 4-5L/min of blood perfuses the lungs, 4-5L/min gas reaches alveoli -imbalance = problems! -Apex → vent > perfusion - Base → perfusion -Ventilation of alveoli → brings o2 into lung, removes CO2 -perfusion of pulmonary capillaries → blood being sent to the lungs V/Q mismatch; Shunt Shunt→ inadequate ventilation (more perfusion than ventilation – more trains than passengers) 2-5% is normal Anatomic → Ventricular-septal defects Intrapulmonary: blood returns to the heart WITHOUT having gas exchange ex: Pneumonia, Atelectasis- interfere w proper ventilation (blood flor IS circulating, but not being oxygenated) Shunt vs. Dead Space -Dead-space= poor perfusi ...
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