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
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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
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(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
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(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)