Resp1- Resp Phys 2

resting tidal volume (V_T)

dead space (V_D); conducting zone; respiratory zone (V_A); gas exchange

inspiratory reserve volume (IRV)

increases; decreases; the difference b/w the max and min V_L.

functional residual capacity (FRC)

the balance b/w elastic recoil forces of the chest wall and lung (chest wants to expand, lungs want to contract/get smaller).

expiratory reserve volume (ERV)

residual volume (RV)

RV= FRC - ERV

• FRC= functional residual capacity
• ERV= expiratory reserve volume

strength of respiratory muscles, lung compliance, stiffness of chest wall, airway patency

less; higher

vital capacity (VC)

VC= V_T + IRV + ERV

• IRV= inspiratory reserve volume
• ERV= expiratory reserve volume

total lung capacity (TLC)

TLC = IRV + V_T + ERV + RV

• IRV= inspiratory reserve volume
• ERV= expiratory reserve volume
• RV= residual volume

anatomic dead space (V_D)

alveolar dead space

almost zero- alveolar dead space in abnormal and can indicate a blocked bronchiole, fluid in alveoli, etc.

ventialtion- perfusion matching (rate of V_A ÷ rate of Q)

anatomic + alveolar dead space; therefore, should equal anatomic dead space in a normal animal

volume of lung that is not producing CO2.

ventilation

respiratory rate (f- breaths/min) and tidal volume (V_T- mL/breath).

minute ventilation (V^._M)

f x V_T

with V_T= V_A + V_D (must take dead space into account); therefore...

• (f x V^._A) + (f x V^._D)
• V^._A + V^._D

alveolar ventilation rate (V^._A)

inspired air contains essentially no CO2; all CO2 in expired air must come from pulmonary capillary blood in functional alveoli; thus, V^._A can be calculated from expired CO2.

with rapid shallow breathing (increased minute ventilation), all air is going into dead space them immediately being exhaled (low alveolar ventilation); with slow deep breathing (decreased minute ventilation), air makes it down to respiratory zone to have a physiologic effect (increased alveolar ventilation)

you're filling dead space (the tube) when mechanically ventilating; therefore, alveolar ventilation requires MUCH higher volumes of air

depth of respiration; respiration rate (f)

dead space volume is fixed and must be ventilated on every breath; if V_T decreases, dead space is still ventilated but alveoli get decreased air.

increased

decreased

skeletal; spontaneous contraction

excitation of diaphragm and intercostal mm.; motor nerves

• bursts of action potential to diaphragm and inspiratory intercostal muscles.
• action potentials cease.

not necessary; a passive process

discharge in synchrony;cease firing

apneustic center (terminate inspiration), pneumotaxic center (modifies apneustic), central chemoreceptors, baroreceptors

peripheral chemoreceptors, thoracic stretch receptors, J receptors

composition of arterial blood (peripheral chemoreceptors) and CSF (central chemoreceptors), spatial orientation of chest and lungs, ventilatory effort

high arterial partial presure of CO2 (P_{a CO2})

• peripheral- arterial walls
• central- ventral surface of the 4th ventricle

increase in brain extracellular fluid, mainly due to an increase in arterial partial pressure of CO2 (P_{a CO2}).

increased tidal volume (V_T).

NO

carotid bodies (at bifurcation of common carotid arteries- glossopharyngeal n.), aortic bodies (in aortic arch- vagus n.)

decrease in arterial partial pressure of oxygen (contrast to central), increase in arterial [H+] due to increased arterial partial pressure of CO2 (ie. decreased arterial pH)

increase respiration rate (f), increased tidal volume (V_T)

P_{a O2} remains normal; anemia (reduced Hgb so less total O2 carried by blood but the same amount of O2 dissolved in plasma), CO poisoning (competes with O2 for binding to Hgb but does not affect conc of O2 dissolved in plasma)

P_{A CO2}; P_{a CO2}

body pH must be kept in a very tight range to maintain integrity of enzymes/proteins/etc; therefore, slight increases in CO2, causing arterial pH to drop, elicits an increase in alveolar ventilation rate.

40 mmHg

increased [H+] (formation of carbonic acid, which dissociates to H+ and bicarb)--> increased arterial acid sensed by peripheral chemoreceptors--> stimulation of medullary inspiratory neurons

direct suppression of activity of medullary inspiratory neurons.

excessive production of organic acids (metabolic acidosis) or excessive loss of [H+] (metabolic alkalosis) [both are independent of arterial CO2...respiratory system tries to compensate]

peripheral chemoreceptors;  alveolar ventilation rate; P_{a CO2}

metabolic acidosis

hyperventilation; reduce P_{a CO2} and lower arterial [H+] towards normal.

metabolic alkalosis

hypoventilation; elevate P_{a CO2} and help restore arterial [H+] towards normal.

reflex inputs from mechanoreceptors in joints/muscles, increased body temperature, inputs to respiratory neurons form cortical centers, increased plasma [epinephrine], increased plasma [K+], conditioned response (mental preparation for an athletic event)

skeletal muscles of thoracic wall and diaphragm (more in intercostal mm.)

airway smooth muscles, afferent to medulla

large lung inflation volumes (very large tidal volume over an extended period of time); vagal inhibition of medullary inspiratory neurons.

inhibit inspiratory neurons, promote tachycardia and bronchodilation

direct inhibition of inspiratory center due to a large, prolonged inflation volume--> prevents activation of inspiratory center by apneustic center.

• cough reflex- triggers deep inspiration followed by violent expiration
• sneeze reflex- triggers forcible contraction of diaphragm and chest wall
• apneustic reflex- immediate cessation of respiration following inhalation of noxious gas

larynx, trachea, bronchi

nose and pharynx

cold air, odors, physical and chemical irritants

increased mucus secretion, apnea (brief period when you don't breath right after a sneeze), reduced cardiac output.

vocal cords; mechanical stimulation

laryngeal receptors are stimulated by the ET tube, causing a cough reflex

alveolar walls; increased interstitial pressure (maybe due to microemboli, pulmonary edema)

tachypnea (primarily ventilating dead space), dyspnea, dry cough, uncomfortable sensation of pressure in chest, hypotension

dyspnea

descending pathways from cerebral cortex to motor neurons of respiratory muscles.

voluntary control of breathing is possible, but it cannot override the physiologic stimulus of elevated P_{a CO2} or [H+]

P_{a CO2}; P_{a O2}; low P_{a CO2} reduces respiratory drive.

expiration against closed glottis to raise intrathoracic pressure, which is transmitted to the abdomen to help with defecation and parturition.

inadequate dilation of upper airway on inspiration

alveolar ventilation rate

paradoxical breathing

regularly increasing then decreasing tidal volume follow by periods of apnea

[low bloodflow states] heart failure, hemorrhagic shock

grossly irregular breathing pattern

medullary lesions

rapid deep breaths

metabolic acidosis (ketoacidosis)- compensation by converting H+ to CO2, which is exhaled

diaphragm

laryngeal and genioglossal muscles

the work done by the respiratory muscles

elastic properties of the lungs/chest wall (compliance), flow resistive properties of airways/parenchyma (resistance)

transpulmonary pressure (P_TP); lung compliance (C_L)

compliance

V_L; P_TP

static compliance (C_STAT)

dynamic compliance (C_DYN)

less than or equal to