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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