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Glossary of Respiratory Physiology week 2

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PVR eqn
PVR = (pulmonary artery P - pulmonary venous P) / Blood flow
Zone 1
- define
- compare pressures
apex

PA > Pa > Pv
Zone 2
- define
- compare pressures
middle

Pa > PA > Pv
Zone 3
- define
- compare pressures
base

Pa > Pv > PA
What two passive factors can change pulmonary blood flow?
(1) gravitational effects on Pa in the upright lung

(2) lung volume affects pulmonary vascular resistance (PVR), whereby high lung volumes "pull" the blood vessels open, decreasing their R and inc Q
What are some of the substances other than O2/NO that can alter PVR?
thromboxane A2 is produced in response to lung injuries and is a potent pulmonary vasoconstrictor

prostaglandin I2 is a vasodilator

Endothelins, released by pulmonary endothelial cells, are potent vasoconstrictors
what is the alveolar ventilation eqn used to predict?
alveolar PCO2
what is the alveolar gas eqn used to predict?
alveolar PO2
A difference between alveolar and arterial PO2 indicates what?
a gas exchange problem in the lungs
the body must maintain a normally alkaline pH in spite of the daily production of large amounts of two kinds of acid. What are they?
(1) Volatile Acid (CO2)

(2) Non-volatile of Fixed Acid (usually from amino acid and phospholipid metabolism)
Fixed Acids:
- sulfuric acid produced from?
produced from the catabolism of proteins having the sulfur-containing AAs cysteine, cystine, or methionine
Fixed Acids:
- phosphoric acid formed from?
formed from the catabolism of phospholipids
Fixed Acids:
- lactic acid produced when?
extreme exercise or shock
Fixed Acids:
- aceto-acetic acid and Beta-hydroxybutyric acid produced when?
produced in excess in uncontrolled diabetes mellitus
Henderson-Hasselbach eqn
pH = pK + log [A-]/[HA]
Strong acid
K?
pK?
dissociate?
Strong acid

High K
Low pK
Mostly H+, A-
Weak acid
K?
pK?
dissociate?
Weak acid

Low K
high pK
Mostly HA
in which two locations does buffering occur?
(1) ECF

(2) ICF
what is the most important extracellular buffer?
bicarbonate
what three factors contribute to the acid-base balance of the body and how fast do they work?
(1) Buffering -- ECF (sec-min), ICF (hours)

(2) Respiratory compensation (sec-min) -- changes in PCO2

(3) Renal Compensation / Correction (days) -- changes in HCO3-
the ability of a particular buffer to protect against pH changes depends on what two things?
(1) pK in relation to the body fluids pH

(2) concentration
most of the buffer capacity of proteins can be attributed to what?
the imidazole group of histidine
what is the most important non-bicarbonate buffer of whole blood?
Hemoglobin is by far the most important non-bicarbonate buffer of whole blood because of its high concentration inside the erythrocyte and its high buffer capacity (36 histidine residues).
How do H+ enter and leave the ICF in order to take advantage of the vast supply of ICF buffers?
(1) In respiratory disturbances CO2 readily crosses cell membranes

(2) in metabolic disturbances H+ can cross cell membranes in exchange for another cation, K+, or it can cross with an organic anion such as lactate, Beta-OH-butyrate, etc
is Hb a more effective buffer in its oxygenated or in its deoxygenated form?
deoxygenated
what are the four "simple" acid-base disturbances?
(1) metabolic acidosis

(2) metabolic alkalosis

(3) respiratory acidosis

(4) respiratory alkalosis
metabolic acidosis
caused by excess fixed acid, either due to ingestion of acid, overproduction of acid (e.g. diabetic ketoacidosis), or loss of HCO3- (diarrhea)
metabolic alkalosis
caused by loss of fixed H+ (e.g. vomiting)
respiratory acidosis
caused by hypoventilation leading to retention of CO2, increased PCO2, and decreased pH (H-H eqn); buffering takes place almost exclusively in the ICF
respiratory alkalosis
caused by hyperventilation leading to loss of excess CO2, decreased PCO2, and inc pH (H-H eqn); buffering is exclusively in the ICF
V/Q ratio
expresses the matching of ventilation (V in L/min) to perfusion or blood flow (Q in L/min)
what is the average normal value of V/Q for the entire lung?
0.8
how does V/Q vary with lung position?
The variations in blood flow are greater than the variations for ventilation, such that the apex has a higher V/Q and base has a lower V/Q
V/Q matching
ventilation and perfusion are "matched up", that ventilated alveoli are close to perfused capillaries, which provides for ideal gas exchange
dead space
the volume of the airways and the lungs that does not participate in gas exchange
anatomic dead space
the volume of the conducting airways
physiologic dead space
includes the anatomic dead space plus fxnal dead space in alveoli (alveoli that are ventilated but not perfused)
shunts
occur when a portion of the pulmonary blood flow bypasses the alveoli
physiologic shunt
normally, a small portion (2%) of the pulmonary blood flow bypasses the alveoli
right-to-left cardiac shunt
defects in the intraventricular septum can result in as much as 50% oif the CO being routed from the right ventricle to the left ventricle, bypassing the lungs; always hypoxemia
left-to-right cardiac shunt
more common; blood is shunted from left heart to right heart, recycled to the lungs
intrapulmonary shunts
blood shunted within the lungs, such that a portion of the pulmonary blood flow perfuses lung regions that are not ventilated; there can be no gas exchange and there is always hypoxemia
what happens to the A-a when there is a shunt?
the A-a gradient is inc when there is a shunt
hypoxemia
dec in arterial PO2
T/F V/Q defect always causes hypoxemia
T
hypoxia
decreased O2 delivery to the tissues
5 causes of hypoxia
(1) anemia
(2) dec CO
(3) hypoxemia
(4) CO poisoning (dec O2-binding capacity of Hb)
(5) CN poisoning (uncoupler of oxidative phosphorylation)
describe the three-fold role of the kidneys in normal acid-base balance
(1) reabsorption of HCO3-
- no net secretion of H+

(2) secretion of titratable H+
- net secretion of H+ and synth of new HCO3-

(3) secretion of H+ as NH4+
- net secretion of H+ and synth of new HCO3-
- potential supply of NH3 is huge therefore so is the potential for H+ secretion
what effect does plasma [Cl-] have on reabsorption of filtered HCO3-?
reciprocal relationship between plasma Cl- and plasma HCO3-

e.g. if plasma Cl- goes up, plasma HCO3- goes down, the filtered load of HCO3- goes down, and the amount of HCO3- reabsorbed goes down
what effect does ECF vol expansion have on reabsorption of filtered HCO3-?
dec HCO3- reabs

- dec peritubular capillary osmotic pressure
- inc peritubular capillary hydrostatic pressure
- dec reabsorp
what effect does ECF vol contraction have on reabsorption of filtered HCO3-?
inc HCO3- reabs

- inc peritubular capillary osmotic pressure
- dec peritubular capillary hydrostatic pressure
- inc reabsorp
what effect does A-II have on reabsorption of filtered HCO3-?
inc A-II --> stimulates Na+-H+ exchange --> inc reabsorp of HCO3-
what effect does arterial pCO2 have on reabsorption of HCO3-?
inc pCO2 --> inc reabsorp
three steps of excretion of H+ as NH4+
(1) in proximal tubule cells NH3 synth from glutamine, converted to NH4+, secreted; HCO3- reabsorb

(2) some NH4+ excreted, rest substitutes for K+ in Na+-K+-2Cl- cotransporter of thick asc limb, added to solutes of the medullary interstitium

(3) in intercalated cells of collecting duct NH3 diffuses from medullary interstitium into lumen --> NH4+ --> excreted
show centers / groups / receptors that regulate breathing

get it?
apneustic center
lower pons, activates the dorsal respiratory group
ventral respiratory group
medulla, only active during exercise as it is the expiratory center of the medulla
central chemoreceptors: steps in detecting an inc in PCO2
(1) CO2 in blood crosses blood-brain barrier and enters the CSF --> H2O + CO2 --> H2CO3 --> H+

(2) dec pH

(3) central chemoreceptors detect inc H+ in CSF and direct dorsal respiratory group to inc the breathing rate
mechanoreceptors
located in the muscles and joints that detect motion of the limbs; early inc in breathing rate
irritant receptors
to noxious chemicals and particles, located in the linings of the airways, cause constriction of bronchial smooth muscle and an inc in breathing rate
J receptors
located in alveolar walls, congestion of pulmonary capillaries with blood, such as left heart failure (blood backs up into pulmonary capillaries) causes rapid shallow breathing
what happens to V/Q ratio in the lungs, the amount of physiologic dead space, and the arterial PO2 and PCO2 during exercise?
V/Q ratio becomes more even across lungs

less physiologic dead space

arterial PO2 and PCO2 do NOT change
in exercise what happens to the Hb-O2 dissociation curve?
it shifts to the right
what four things are the result of high altitude hypoxemia?
(1) hyperventilation

(2) inc synth of 2,3 DPG

(3) inc synth of erythropoeitin

(4) hypoxic vasoconstriction (inc pulmonary resistance)

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