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Physiology > Test 2 Combined- Pulm + Renal > Flashcards

Test 2 Combined- Pulm + Renal Flashcards

1
Q

8 major functions of the kidneys

A
  1. excretion of metabolic waste and foreign substances2. regulation of water and electrolytes3. regulation of extracellular fluid volume4. regulation of plasma osmolality5. regulation of RBC production6. regulation of vascular resistance 7. regulation of acid-base balance8. regulation of vitamin d production
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2
Q

path through kidneys

A

bownman’s capsule/renal corpuscle - proximal convoluted tubule- HENLE (straight proximal tubule- descending thin limb- ascending thin limb- ascending thick limb)- macula densa- distal convoluted tubule- cortical collecting duct- medullary collecting duct- papillary duct

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3
Q

parts of the JG apparatus

A

macula densa + extraglomerular mesangial cells (EGM)+ JG cells that produce renin/angiotensin II of afferent arterioles

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4
Q

3 layers of the filtration barrier for capillaries in the glomerulus

A
  1. endothelium of capillaries2. capillary basement membrane3. interdigitated podocytes
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5
Q

structure-function: glomerulus

A

(passive) ultrafiltration of low molecular weight substances & H20 from capillaries to bowman’s space

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6
Q

segments of proximal tubule

A

proximal convoluted tubule, proximal straight tubule

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7
Q

segments of henle’s loop

A

descending thin limbascending thin limbascending thick limb(includes macula densa)

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8
Q

segments of collecting duct

A

connecting tubulecortical collecting ductouter medullary collecting ductinner medullary collecting duct

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9
Q

structure-function: proximal tubule

A
  • high volume, low gradient re-absorption- has brush border to increase surface area- has lots of mitochondria to pump Na
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10
Q

3 basic processes of urine formation

A

1) ultrafilration- into bowman’s capsule2) reabsorption of water from ultrafiltrate into tissue3) secretion of solutes IN to tubular fluid to be excreted

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11
Q

structure-function: loop of henle

A
  • makes high interstitial osmolarity- poorly developed apical & basolateral surfaces
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12
Q

structure-function: distal tubule

A

low-volume, high gradient re-absoption- lots of mitochondria & extensive infoldings (well developed apical & basolateral surfaces)

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13
Q

structure-function: macula densa

A

contains the JGA, senses tubular flow

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14
Q

structure-function: collecting duct

A
  • concentration/dilution of final urine- has principal and intercalated cells
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15
Q

principal cells

A

moderately invaginated basolateral membrane, few mitochondria- reabsorb NaCl and secrete K+- acted on by aldosterone

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16
Q

intercalated cells

A
  • NO CILIUM- regulate acid-base- have high density of mitochondria- some secrete H+ (reabsorb HCO3-) and some secrete HCO3-
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17
Q

what are the two renal blood flow routes after the efferent arteriole?

A

1) peritubular capillaries- reabsorption of water & solutes from CORTEX= 90%2) vasa recta capillaries- reabsorption of water and solutes in the medulla= 10% (8% outer)

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18
Q

what is clearance and what are its units?

A

the volume of plasma completely cleared of any substance in 1 min; mL/min

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19
Q

what is the mass-balance relationship for the kidney?

A

PaRPFa= (PvRPFv)+(U*V)

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20
Q

two equations for excretion

A

Excretion= Filtration+ Secretion- Reabsorption OrExcretion= urine concentration* urine flow rate

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21
Q

what is the formula for clearance?

A

Cx= Ux * V/Pxor remember UV=PC

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22
Q

C < GFRC= GFRC > GFR

A

C < GFR- filtered & reabsorbedC= GFR- filteredC > GFR- filtered & secreted

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23
Q

what is inulin used to measure? what are some advantages/disadvantages?

A

-with inulin, GFR= clearance - tells you how well the kidneys are filtering - good b/c R=0, S=0; no hidden reserve, isn’t eaten or made, is measurable

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24
Q

what is creatinine used to measure? what are some advantages/disadvantages?

A
  • also used to measure GFR (GFR=clearance), but is a little off because there is some secretion - overestimates GFR - easy to measure in plasma, see constant relationship between GFR and plasma creatinine - remember creatinine increases in a muscular person
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25
Q

What is BUN used for?

A
  • BUN= plasma creatinine x 10, so also used to measure GFR BUT is less stable
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26
Q

what is PAH used to measure? what are some advantages/disadvantages?

A
  • the clearance rate is larger than the GFR normally (lots of secretion), but in people with low plasma, its almost all excreted - is used to measure renal plasma flow
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27
Q

what is eRPF?

A

effective renal plasma flow measured with PAH; assuming venous plasma concentration is 0 (which is isn’t, is actually about 10%, so RPF= 1.1xeRPF

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28
Q

how do you calculate RBF from RPF?

A

RBF= RPF/1-hct

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29
Q

what is the filtration fraction?

A

FF= GFR/RPF= Cinulin/CPAHnormally, 20%

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30
Q

volume relationship between renal liquid volumes

A

RBF > RPF> GFR> V

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31
Q

characteristics of glomerular capillaries

A
  • large filtration coefficient- low resistance- negatively charged - form ultrafiltrate - exclude plasma proteins
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32
Q

what is the equation for GFR?

A

GFR= Kf * (Pgc-Pbs-^gc+^bs)

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33
Q

what is Kf? greater in glomerular or systemic capillaries?

A

an intrinsic property of the glomerular capillary; Kf= permeability of gc * area of gc- greater in glomerular caps

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34
Q

how is GFR normally regulated?

A
  • changes in hydrostatic glomerular capillary pressure by changing afferent/efferent arteriolar resistant or pressure (amt of blood flow)
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35
Q

what is the equation for renal blood flow? what is the normal value?

A

RBF= (Prenal artery-Prenal vein)/ Rrenal vasculature ~ 4 mL blood/min *gm tissue~ 1200 mL blood/min

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36
Q

ranking of blood flow in different areas of the kidney

A

renal cortex (90%)outer medulla (8%)inner medulla (2%)

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37
Q

where is the greatest decrease in hydrostatic pressure? where does oncotic pressure increase and decrease?

A
  • across arterioles (efferent & afferent) b/c of high R- increases in glomerular capillaries & decreases in peritubular capillaries
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38
Q

what happens to GFR, Pgc, and RBF when you constrict the efferent arteriole?

A

GFR and PGC increasebut constriction ALWAYS decreases renal blood flow

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39
Q

ways intrinsic autoregulation occurs to regulate GFR and RBF

A

1) smooth muscle myogenic theory2) tubuloglomerular feedback theory3) intrinsic vasodilators and vasoconstrictors

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40
Q

steps of tubuloglomerular feedback theory

A

1) increased GFR2) increased NaCl content in Henle’s loop (not re-absorbed)3) increased NaCl sensed by macula densa4) signal generated to increase the resistance in the afferent arteriole 5) GFR is decreased

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41
Q

what is the difference between renal shutdown and renal death?

A
  • renal shutdown- GFR=0, RBF= +, Urine production- none; happens when bp<70- renal death- RBF=0, happens when bp=0
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42
Q

ways extrinsic regulation occurs to regulate GFR and RBF

A

1) sympathetics2) blood borne & metabolic substances3) stress factors (hypoxia, hemorrage, RAAS)

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43
Q

major vasoconstrictors & vasodilators

A

vasoconstrictors- sympathetics, angiotensin II, endothelinvasodilators- prostaglandins (no change on GFR), NO, bradykinin, natriuretic peptides (no effect on RBF)

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44
Q

2 routes for the reabsorption of solute & water

A

1- paracellular- 1 step- around cells2- transcellular- 2 steps- through cells

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45
Q

3 types of membrane transport mechanisms

A
  • passive (simple, facilitated, osmosis)- 1* active- move up concentration gradient from hydrolysis of ATP- 2* active- required indirect energy source such as an ion gradient
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46
Q

what is the take away from Fick’s principle in the kidney?

A

if blood flow is restricted to the kidney, the kidney requires less oxygen

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47
Q

what are Tm and RPT? which is reached first and why?

A

Tm- transport maximumRPT- renal plasma threshold (mg/ml)- RPT reached first because of splay

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48
Q

what is actively occurring in glucose transport? how to calculated Tm for glucose?

A
  • normally filtered and ACTIVELY reabsorbed, if not get excretion- Tm= PaGFR-UV
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49
Q

what is actively occurring in PAH transport? how to calculated Tm for PAH?

A
  • normally excreted and ACTIVELY secreted, if not get filtration Tm= UV-PaGFR - filtered is always linear
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50
Q

what is diuresis and what are two examples of things that cause it?

A
  • urine flow rate > 1 mL/min- mannitol (filtered but not reabsorbed), glucose (when its not reabsorbed)
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51
Q

what percent of water/Na/Cl/K is reabsorbed in the proximal tubule? what percent of glucose/aa’s is reabsorbed in the proximal tubule?

A

67% & 100%

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52
Q

how is Na+ transported in the proximal tubule? what is the gradient driven by?

A
  • Na-H+ antiporter (H+ from H20+CO2 9n cells)- Na-organic substance symporter- later, have Na-2Cl-H+-anion paracellular antiporter
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53
Q

what are the major regulatory hormones for the proximal tubule?

A

angiotensin II, NE, E, Dop

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54
Q

how is Na+ transported in the loop of henle? what is the percent reabsorbed? which segment is impermeable?

A
  • Na/K/2Cl symporter- 25%- thin descending loop
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55
Q

how is Na+ transported in the distal tubule? what is the percent reabsorbed?

A
  • NaCl symporter early - Na+ channels late~5 %
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56
Q

how is Na+ transported in the collecting duct? what is the percent reabsorbed?

A
  • Na channels- ~3%
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57
Q

major regulatory hormones for the loop of henle and distal tubule?

A

Aldosterone, angiotensin II

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58
Q

major regulatory hormones for collecting duct?

A

aldosterne, ANP, BNP, urodilatin, uroguanylin, guanylin, angiotensin II

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59
Q

where is no water reabsorbed?

A
  • thin ascending & thick ascending limbs of Henle- distal tubule
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60
Q

which drugs increase NaCl and H20 reabsorption?

A

angiotensin II, aldosterone, sympathetic nerves

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61
Q

which drugs decreased NaCl and H20 reabsoption

A

ANP, BNP, urodilatin, uroguanylin, guanylin, dopamine

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62
Q

which drugs affect H20 reabsorption independent of NaCl?

A

ADH

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63
Q

what is the break down of where fluid resides?

A

ICF= 25 LECF= 14 L (ISF= 10.5, P= 3.5)

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64
Q

what makes up most of the composition of solutes? what is the relative concentration of proteins?

A
  • electrolytes (Na, K, Ca, Mg, Cl, HCO3)- ICFp>Pp>ISFp
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65
Q

what is a positive water balance?

A

intake > loss ; make hypoosmotic urine

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66
Q

how do you measure the body’s osmolarity?

A
  • by looking at the plasma osmolarity, specifically the concentration of Na (~290 mOSM/L)
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67
Q

what is another name for ADH? What makes up the preprohormone?

A
  • vasopressin- signal peptide, ADH, neurophysin, copeptin
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68
Q

relationship between ADH and urine excretion?

A
  • increased ADH decreases urine excretion
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69
Q

where is ADH made and stored?

A
  • made in endocrine cells of hypothalamus - stores in posterior pituitary
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70
Q

where are the two places with sensors that stimulate ADH release? what are they’re actions? which is more sensitive?

A
  • baroreceptors in carotid split & aortic arch (inhibits ADH release) - osmoreceptors in hypothalamus ** more sensitive (stimulate ADH release)
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71
Q

pathway baroreceptors use to affect ADH

A

CN 9 & 10 - medulla - PVN/SO hypothalamus - posterior pituitary- exocytosis in blood

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72
Q

what allows ADH system to respond rapidly?

A

ADH is rapidly degraded in the blood

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73
Q

what is the threshold for change in plasma osmolarity to secrete ADH? threshold for baroreceptors?

A
  • greater than 280 mosmsOR- decreased in bp by 10%
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74
Q

how does a decreased bp affect sensitivity to osmolarity?

A
  • becomes more sensitive to osmolarity, slope is increased
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75
Q

where does ADH target?

A

extracellular receptors in distal tubules & the collecting duct

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76
Q

what is the ADH pathway for increased H20 retention?

A
  • receptors - increase Gs- increase cAMP- increase PKA- insertion of aquaporin II into the membrane - increase in H20 permeability
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77
Q

where is urea permeable?

A

lower collecting duct

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78
Q

what are the 6 challenges to homeostasis?

A

hyper/hypo/iso osmoticexpansion & contraction

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79
Q

drink sea water

A

hyperosmotic expansion

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80
Q

blood transfusion

A

isosmotic expansion

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81
Q

saline transfusion

A

hyposmotic expansion

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82
Q

water deprivation, excessive sweating

A

hyperosmotic contraction

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83
Q

bleeding

A

isomotic contraction

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84
Q

concentrated urine

A

hyposmotic contraction

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85
Q

what is the equation for the anion gap?

A

[Na]- ([Cl]+[HCO3-])= ~15 meq/L

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86
Q

if the anion gap is not greater than 15 meq, but there is a pH problem, where should you look?

A

renal or GI system

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87
Q

what is the anion gap for vomiting? for diabetes?

A

vomiting= GI= 15diabetes= pancreas= 35

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88
Q

which diuretics are K+ wasting? which is the strongest?

A
  • mannitol, diamox, lasix, hydrochlorothiazide (MDLH spare K)- lasix is the strongest
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89
Q

which diuretics are K+ sparing? where do they typically act?

A

spironolactone, amiloride, triamterene - act on distal tubule & collecting duct

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90
Q

what does mannitol do?

A

holds H20 in proximal tubule (where majority of H20 is reabsorbed)

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91
Q

what does acetazolamide do?

A

inhibits carbonic anhydrase in the proximal tubule; no formation of CO2 & H20 which diffuse back into cell and provide H+ for antiport with Na; see more bicarb in both proximal & distal tubule b/c can’t combine with protons

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92
Q

what does lasix do?

A

inhibits Na/Ca/Mg reapsorption in thick ascending limb

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93
Q

what does hydrochlorothiazide do?

A

inhibits Na/Cl transport in distal tubule by competing with Cl site on transporters

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94
Q

what does spironolactone do?

A

compete with aldosterone in distal tubule & collecting duct

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95
Q

what does amiloride do?

A

blocks Na channels on luminal side of the collecting duct

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96
Q

what does triamterne do?

A

blocks epithelial Na channels in collecting duct

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97
Q

what is hyperkalemia defined as in the clinical setting?

A

when potassium intake exceeds output ; when you have an ECF composition of 5mEq/L (4mEq/L is normal)

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98
Q

what is hypokalemia defined as in the clinical setting?

A

<3.5 mEq/L (4mEq/L is normal)

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99
Q

where are alveolar (A) PO2 & PCO2 set? where are arterial (a) PO2 & PCO2 set before they enter the alveoi?

A

PAO2= 100 mmHgPACO2= 40 mmHgPaO2= 40 mmHgPaCO2= 46 mmHg

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100
Q

what happens in shunt alveoli? what happens in dead space alveoli?

A

shunt- ventilated but not perfused (PaO2= 40, PaCO2= 45); V/Q= 0dead space- perfused by not ventilated- PaO2= 150, PaCo2= 0); V/Q= infinity

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101
Q

what happens to the V/Q ratio in the bottom of the lung?

A
  • have more blood flow than ventilation; V/Q ratio is very low
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102
Q

what does a high V/Q ratio represent?

A
  • high alveolar ventilation; low alveolar perfusion- like dead space alveolus - ventilation exceeds perfusion
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103
Q

what happens to the V/Q ratio at the top of the lungs?

A
  • have more ventilation than blood flow (but still less ventilation than the bottom of the lung) - however, the relative ratio causes a high V/Q ratio- get over-ventilation & dead space (alveolar PaO2 is higher and CO2 lower)
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104
Q

The majority of oxygenated blood leaving the lung comes from the _____, this causes the arterial PO2 to be ______ than atmospheric pressure

A

base, lower

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105
Q

what is the AaDO2 and what is normal?

A
  • alveolar-arterial PO2 difference; - - normal is less than 15
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106
Q

what are the two reasons for AaDO2?

A

1) V-Q inequality2) Anatomic shunt- veins that go directly into LV

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107
Q

how do you calculate AaDO2?

A

alveolar PO2 (gas equation= 100 mmHg) - arterial PO2 (blood draw)

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108
Q

what is hypoxemia?

A

when arterial blood oxygen (PaO2) is below 80 mmHg

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109
Q

what are the four causes of hypoxemia?

A
  1. hypoventilation2. diffusion limitation3. shut (anatomic or physiologic)4. V/Q mismatch
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110
Q

what 2 things happen during hypoventilation? What happens to AaDO2? What is the arterial PO2 response to 100% oxygen? what is hypoventilation caused by?

A
  1. alveolar PO2 decreases2. alveolar CO2 increases-AaDO2 is normal (gas exchange is normal)-arterial PO2 increases with 100% O2- caused by drugs that depress central drive to breathe
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111
Q

With diffusion limitation, what happens to AaDO2? What is the arterial PO2 response to 100% oxygen? what is diffusion limitation caused by?

A
  • AaDO2 increases (have more alveolar, less arterial) - arterial PO2 increases with 100% O2- caused by lung edema, fibrosis, capillary block
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112
Q

With an anatomic/physiological shunt, what happens to AaDO2? What is the arterial PO2 response to 100% oxygen? what happens to arterial PCO2?

A
  • AaDO2 increases (have more alveolar, less arterial) - additional O2 will not increase arterial PO2 b/c shunted blood isn’t exposed to enriched O2 (a physiological shunt will decrease O2 on 100% O2) - PCO2 does not change b/c chemoreceptors which increase ventilation
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113
Q

what is the main cause of hypoxemia in patients with respiratory disorders?

A

V/Q inequality with LOW V/Q ratio

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114
Q

In V/Q inequality, what happens to AaDO2? Does 100% O2 help?

A
  • AaDO2 is increased (high alveolar, low arterial) - 100% O2 helps
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115
Q

2 ways O2 is transported in blood, and which does blood gas analysis measure?

A
  1. dissolved (= blood gas, PaO2)2. bound to hemoglobin
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116
Q

what is Henry’s law?

A

the concentration of a solute gas in a solution is directly proportional to the partial pressure of that gas above the solution (C=khP)

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117
Q

dissolved PaO2 measured as mL/min

A

3mL O2 dissolves/ 1L blood X 5 L/min= 15 mL O2/min

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118
Q

At partial pressures < 60 mmHg: small changes in pressure lead to _______

A

release of large amounts of O2

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119
Q

what is the normal P50 for O2? what happens if it’s higher?

A

27 mmHg- if higher, have right shift of the curve, less affinity for O2, and lower saturation

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120
Q

what is the Bohr effect?

A

decreased P50= increased affinity and a left shift is caused by- decreased temp- decreased PCO2- decreased DPG- increased pH

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121
Q

what is CO’s affinity for hemoglobin like?

A
  • affinity of CO for Hb is 200 times greater; all binding sites are occupied at 1 mmHg CO- affinity for O2 is also enhanced and unloading prevented
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122
Q

what is SO2? what is is normally and what is the PaO2 at 90%?

A

oxygen saturation- the amount of O2 combined with hemoglobin/capacityOR O2 binding sites occupied normal- 97.5hyoxemia (80mm Hg PO2)- 94.590%= 60 mmHg= danger

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123
Q

what is the concentration of O2 when SO2= 100%?

A

1 g hb= 1.34 mL O215 g hb= 20.1 mL O2/ 100 mL blood

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124
Q

what is the SO2 in tissue? how much O2 is extracted from the blood?

A

SO2= 75% (15.1 mL O2/100) = 19.5-15.1= 4.4 mLO2/100 mL blood (or 220mL O2/min)

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125
Q

how is CO2 transported in the blood?

A
  1. dissolved (10%)2. ** as bicarb (HCO3-) (60-70%)3. as carbamino compounds with proteins (carbaminohemoglobin) (20-30%)
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126
Q

dissolved Co2 per 1 mmHg of PCO2

A

0.067 mL Co2/100mL of blood (20x more than O2)

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127
Q

equation for bicarbonate

A

Co2+H20 H2CO3 H+ + HCO3-

128
Q

what is the haldane effect?

A
  • free Hb can bind more CO2 than HbO2- SO lower O2 saturation, larger CO2 concentration
129
Q

what’s the chloride shift caused by?

A

an increase in H+ or HCO3- causes HCO3- to diffuse out and Cl- to move in to maintain electrical neutrality

130
Q

what happens when you get a decrease in pH?

A

H+ shifts equation left, increase CO2, causes right shift of O2 dissociation curve (higher P50), facilitates offloading, Hb carries more CO2

131
Q

what are the 4 major types of tissue hypoxia?

A
  1. hypoxic hypoxia (cyanosis from decreased PaO2)2. circulatory hypoxia (reduced blood flow to tissues)3. anemic hypoxia (blood can’t carry O2)4. histotoxic hypoxia (cell can use O2 due to poison)
132
Q

T/F- CO2 dissociation curve is directly proportional to PCO2

A

T

133
Q

what is tissue hypoxia?

A

insufficient O2 is available to maintain adequate aerobic metabolism

134
Q

2 factors determining O2 delivery to the tissues?

A

O2 contentblood flow

135
Q

where are the respiratory centers responsible for generating and controlling the rhythmic pattern located?

A

generating- medulla (automatic) controlling- pons

136
Q

major sites of respiratory control for autonomic respiration

A
  1. control center- brainstem2. central chemoreceptors3. peripheral chemoreceptors4. pulmonary mechanoreceptors/sensory nerves
137
Q

major sites of respiratory control for voluntary respiration

A
  1. motor cortex (hyper/hypoventilation) 2. output to CST
138
Q

two groups of cells in the medulla that generate breathing pattern

A

dorsal respiratory group- inspirationventral respiratory group- expiration (and a little inspiration)

139
Q

two groups of cells in the pontine respiratory group

A
  • apneustic center- lower pons- excitatory effect on DRG (stimulates inspiration) - pneumotaxic center- higher pons- inhibits DRG (inhibits inspiration)- associated with fine control of the frequency of breathing
140
Q

where are the central chemoreceptors located? what are they sensitive to?

A
  • ventrolateral surface of the medulla oblongata; - sensitive to changes in pH in CSF (PCO2)- responsible for most of min-by-min control (60-70% of response)- H+ can cross BBB at low pH
141
Q

2 sites of peripheral chemoreceptors? what do they respond to?

A
  • carotid body* (CN9) & aortic arch (vagus)- respond to decreases in PO2**, decreases in pH (carotid only), increases is PCO2- carotid body has robust firing when PaO2 < 70 mmHg; not important during normal conditions; has fast response- CB responds to arterial PO2
142
Q

what is the Hering-Breur inflation and deflation reflex? what receptors does it involve?

A
  • inflation of the lung inhibits inspiratory muscle activity (CN10) - deflation initiates inspiratory activity - pulmonary stretch receptors
143
Q

what are irritant receptors?

A
  • rapidly adapting stretch receptors- respond to irritants- smoke, dust, cold air- cause bronchoconstriction - asthma?
144
Q

what are J receptors and bronchial C fibers?

A
  • juxtacapillary receptors- endings are in capillary walls- inject something into pulmonary circulation, get rapid response- cause rapid shallow breathing (e.g. pulmonary edema) - bronchial C- supplied by bronchial circulation
145
Q

other receptors

A
  • nose/upper airway receptors- joint/muscle pain- pain/temperature- arterial baroreceptors
146
Q

what happens to the ventilatory response to CO2 (slope of response curve) when you lower PaO2? what are some things that lower the ventilatory response?

A
  • ventilation at a given PaCO2 is higher- ventilatory response to CO2 become steeper than 2-3 mL/min- lowered by sleep, aging, drugs, COPD (increased work of breathing)
147
Q

what happens to ventilation at a fixed high PCO2 when O2 is decreased? what is this called? when does it become important?

A
  • as PO2 drops, ventilation increases rapidly - (occurs when PaO2 is below 100 mmHg, versus 50-70 mmHg normally)- called hypoxic stimulation; is important in patients with chronic CO2 retention
148
Q

what happens to PaO2, PCO2, and pH during moderate exercise? severe exercise?

A

moderate exercise- gases don’t change but ventilation is still increasedsevere exercise- cross anaerobic threshold, lactic acid released, pH decreased, ventilation increases

149
Q

what is the difference between obstructive sleep apnea and central sleep apnea?

A
  • with both, see depressed airflow for a period of time- with central sleep apnea, also see decreases in pleural pressure, signifying that the diaphragm is not receiving signals to contract
150
Q

what does Kussmaul breathing look like and what is it a sign of?

A
  • deep breathing with reduced frequency- typical in metabolic acidosis
151
Q

what does apneustic respiration look like?

A
  • sustained periods of inspiration followed by brief expiration - losing input from vagal nerve/pneumotaxic center (inhibits DRG (inhibits inspiration)- associated with fine control of the frequency of breathing)
152
Q

what are two examples of end of the line, shakey breathing? what are they mostly due to?

A

cheyne-stokes (rapid bouts of hyperventilation), biots (slow bouts of hyperventilation)- brain injury, neuronal damage

153
Q

what happens to barometric pressure and inspired PO2 with higher altitude?

A

both decrease - low PO2 is the most important problem at high altitude

154
Q

how does acclimatization occur when climbing mt everest?

A
  • hyperventilation, reducing the PaCO2 via hypoxic stimulation of peripheral chemoreceptors
155
Q

what allows the PO2 of mixed venous blood at higher altitudes to be only 7mmHg lower?

A
  • polycythemia- increase in red blood cell concentration over time- erythropoietin from kidney increases Hb/O2 carrying capacity
156
Q

parts of the physiological response to high altitude

A
  • hyperventilation- polycythemia- shift of binding curve due to changes in 2,3 DPG- maximal breathing capacity increases with less dense air- alveolar hypoxia results in pulmonary vasoconstriction, right heart hypertrophy and pulmonary edema
157
Q

what is the diving response?

A
  • peripheral vasoconstriction due to sympathetic activity induced by apnea and enhanced by cold water on face - results in initial hypertension (sympathetics)- then vagally induced bradycardia * lower HR gives a higher O2 saturation
158
Q

when does hypoxic loss of conciousness occur?

A

PO2: 20-25 mmHg

159
Q

3 preventable pathophysiological mechanisms that lead to death in divers

A

1) hyperventilation- reduces CO2 drive to breath, hypoxic signal is voluntarily overridden 2) ascent blackout- PO2 in lungs decreases as you ascend, exacerbated b/c less O2 left3) carbohydrate depletion- less CO2 production reduces hypoxic drive to breathe

160
Q

what happens to the lungs as you descend?

A
  • when mechanical compression of the wall has occurred, maintenance of pressure equilibrium is achieved by redistribution of blood volume from extra-throacic to intra-thoracic - leads to edema and capillary rupture
161
Q

when does decompression sickness occur?

A
  • decreased breathing over-saturates tissues with nitrogen- decreased pressure causes it to leak out too quickly- N2 can form bubbles which cause pain in joints
162
Q

what is inert gas narcosis?

A
  • increased N2 causes euphoria/loss of coordination, coma
163
Q

what are the effects of high O2 for prolonged periods of time?

A
  • in CNS- vomiting/dizzy/vision/hearing impairment (confusion/seizures/coma @ 4ATM)- in Lung- lower tolerance- high O2 can cause damage of endothelial cells/pulmonary capillaries/ substernal pain, impaired gas exchange, etc.
164
Q

what can hyperbaric O2 therapy be used for?

A
  • CO poisoning- anemic crisis- gas gangrene- impaired bone/wound healing
165
Q

4 functions of the respiratory system

A

1) O2 in, CO2 out2) barrier function3) metabolic function (angiotensin)4) host-defense/immune function

166
Q

what makes up the upper airway? lower?

A
  • nose, pharynx, glottis, vocal cords- trachea, bronchial tree, alveoli
167
Q

what is the function of the upper airway?

A
  • to condition air (warm it to body temp) and humidify it - also provides ~50% of total resistance
168
Q

at what level of the lung can a piece be removed? what is this called?

A
  • a bronchopulmonary segment= region supplied by 1 segmental bronchi - is the anatomic unit of the lung
169
Q

whats the difference between a pneumothroax and a pleural effusion?

A

pneumothorax- air between visceral (close) and parietal pleurapleural effusion- fluid

170
Q

what is the physiological unit?

A
  • respiratory unit= respiratory bronchioles, alveolar ducts, and the alveoli - 5 mm tall, but make up a lot of surface area (2.5-3 L) or SA of 50-100m^2
171
Q

what are conducting airways? what does this form? what is it’s volume?

A
  • bronchi that contain cartilage + non-respiratory (w/o alveoli) bronchioles - makes anatomic dead space- 150 mL - goes up to 16th branch point
172
Q

what are type 1 and type 2 epithelial cells?

A
  • type 1= very long, 98% surface area, site for gas exchange- type 2= produce surfactant - exist in a 1:1 ratio in adults- neonates don’t have type 2
173
Q

laplace relationship for lungs

A

inward pressure= 2*surface tension/ radius

174
Q

what does surfactant do? is there more in smaller or larger alveoli?

A
  • decreases surface tension; more in smaller alveoli
175
Q

what allows for the stability of alveoli

A
  1. surfactant2. interdependence- alveoli mechanically linked together
176
Q

what allows for the interdependence of alveoli?

A
  • collateral ventilation provided by: pores of kohn- adjacent alveolichannels of lambert- terminal airways- alveolichannels of martin- interbronchial
177
Q

where do bronchial veins come from and where do they go?

A
  • from bronchiole arteries leading to terminal bronchioles - 1/3 blood goes back to heart, 2/3 drains into pulmonary circulation (admixture)
178
Q

3 ways inhaled materials are deposited

A

impaction (large in pharynx)sedementation (medium in small airways)diffusion (small in alveoli)

179
Q

what is the mucociliary clearance system?

A
  • removes inhaled particles, consists of: * mucus layer* pericillary fluid* cilia- beat in coordinated fashion, propel stuff up
180
Q

pathway of lungs

A

trachea2 main stem bronchilobular bronchi (6 total)segmental bronchi (bronchopulmonary segment)bronchioles - non-respiratory bronchioles - respiratory alveolar ducts

181
Q

3 ways particles are cleared

A
  • they’re swallowed- mucociliary system- alveolar macrophages eat them
182
Q

2 circulation pathways of lung

A
  • bronchial- lungs can survive without- pulmonary- largest vascular bed in body
183
Q

where do you lose cilia? where do you lose smooth muscle? where do you lose cartilage & mucus glands?

A
  • alveolar ducts- alveolar sacs- bronchioles
184
Q

what is Boyle’s law?

A

at a fixed temperature, the volume of gas is inversely proportional to the pressure exerted by the gas

185
Q

muscles of active expiration

A
  • internal intercostals- flattens ribs and sternum further - abdominal muscles- causes diaphragm to be pushed further upwards
186
Q

muscles of inspiration

A
  • external intercostals- ribs go up and out (lateral & anteroposterior) - diaphragm- 75% increase in thorax volume- muscle flattens and goes down (vertical)
187
Q

accessory muscles of inspiration

A
  • SCN- scalenus - contraction used for forceful inspiration; lift sternum and ribs 1 & 2
188
Q

what is the diaphragm stimulated by?

A

phrenic nerve (C3-C5)

189
Q

volumes- tidal, IRV, ERV, Residual

A

Vt- 500 mL (quiet breathing)IRV- 3,000 mL (volume inhaled past tidal)ERV- 1,200 mL (volume exhaled past tidal)RV- 1,200 mL (what’s left)

190
Q

inspiratory capacity

A

IC= IRV+ Vt= 3.5 L

191
Q

functional residual capacity

A

FRC= ERV+ RV= 2.4 L

192
Q

Vital capacity

A

VC= IRV+ Vt+ ERV= 4.6 L

193
Q

Total lung capacity

A

TLC= IRV + Vt+ ERV+ RV= 5.8 L

194
Q

which volumes and capacities cannot be measured with a spirometer?

A

RV, FRC, TLC

195
Q

two ways to measure RV

A

1) helium dilution- requires ventilated tissue2) body plethysmography

196
Q

what determines the volume of air in the lungs? what is the equation for specific compliance?

A
  • compliance = change in volume/ change in pressure = 0.2 L/cm H2O - specific compliance= lung compliance/lung volume
197
Q

what is hysteresis?

A

the dissipation of energy between inflating & deflating the lungs

198
Q

what is the compliance like in emphysema?

A
  • lose elastin- high compliance- lung easier to inflate- low pressure at high volumes
199
Q

what is the compliance like in fibrosis?

A

decrease compliance b/c of fibrotic tissue; higher pressure at lower volumes

200
Q

what determines the volume of air in the lungs?

A

lung (elastic pulling it together): chest-wall (muscles pulling out) interactions

201
Q

atmosphereintra-alveolarintra-pleural pressures

A

760 mmHg760 mmHg756 mmHg

202
Q

how do you calculate trans-lung pressure (Pl)?

A

Pl= Pa-Ppl= 760-756= 4 mmHg- pressure of lung wall on pleural cavity

203
Q

how do you calculate transmural pressure (Pw)?

A

Pw= Ppl-Pb = 756-760 = -4 mmHg- Pb= pressure on chest wall from air outside- Pw= difference between pleural cavity and thoracic wall

204
Q

how do you calculate pressure across the respiratory system?

A

Prs= Pl + Pw= 0

205
Q

T/F Intrapleural pressure is always below atmospheric pressure

A

T

206
Q

At points with no air flow, volume is ____ and pleural pressure is _______, alveolar pressure is ____

A

max, minimum (the most negative), 0

207
Q

3 patterns of gas flow

A

laminar, transitional, turbulent

208
Q

what two things is air flow determined by?

A

pattern of gas flowresistant to air flow by airways

209
Q

where does laminar flow begin? where is true laminar flow present?

A

smaller airways of the conducting zone; in small bronchioles

210
Q

where is the highest resistance found? why?

A
  • generation 4- medium sized bronchi that are short and branch frequently - air flow is turbulent- remember air flow at any 1 generation is really parallel
211
Q

3 inspiratory airflow profiles

A

0-9: tubulent, high resistance 10-16: laminar flow, some resistance17-23: diffusive, respiratory zone, no resistance, independent of respiratory cycle

212
Q

2 things that decrease air way resistance, 4 things that increase it

A
  • decreased by increased lung volume (inhalation), sympathetics - increased by vagal stimulation, mucus, edema, contraction of smooth muscle
213
Q

what is the main measure of airway resistance?

A

FEV1- the forced expiratory volume in 1 second (smaller= higher resistance to expiration)

214
Q

what is the most important pulmonary function test measurement?

A

FEV1/FVC- greater than 75% are normal, less than 75% are obstructive

215
Q

what happens as lung volume increases?

A
  • force of inspiratory muscles decreases- lung recoil pressure increases- airway resistance decreases- PIFR (peak inspiratory flow rate) is between TLC and RV
216
Q

where does PEFR occur and what happens to it as it approaches resting volume?

A

first 20% of cycle; get expiratory flow limitation

217
Q

what is the effort independent region of flow-volume curve? what is dynamic compression determined by?

A

no matter how strongly you try and exhale, the flow rate always converges the closer to get to the reserve volume; determined by alveolar- pleural pressure

218
Q

when is airflow effort dependent?

A

at higher lung volumes (early expiration)

219
Q

what is flow limitation caused by?

A

the compression of airways when pressure outside is greater than the pressure inside airway

220
Q

what is the equal pressure point?

A

where pressure in the airway is equal to pleural pressure in a region without cartilage

221
Q

which breathing parameter is reduced with obstructive lung disease (asthma, COPD)? Whic is reduced in restricted lung disease (fibrosis)?

A

FEV1- obstructiveFVC- restrictive

222
Q

which receptor does albuterol act on? which parameter does it increase?

A

beta-2 agonist; increases FEV1 and FVC

223
Q

what are the two main components of respiratory work (O2 consumption)?

A
  • elastic work (overcomes elastic recoil) - resistance work (overcomes airflow resistance)
224
Q

what is elastic work proportional to? flow-resistive work?

A

elastic work- tidal volumeflow-resistive work- frequency of breathing

225
Q

what is the compensation for the increase in work cause by fibrosis? COPD?

A

fibrosis- breathe shallow & rapidlyCOPD- breathe slower & deeper

226
Q

what is the ideal gas law?

A

PV=nRT

227
Q

what do Dalton & Amagat’s laws state?

A

Dalton- sum of partial pressures= total pressureAmagat- sum of partial volumes= total volume

228
Q

what are the partial pressures of O2, N2, and water vapor in humidified air before gas reaches the alveolus?

A

PO2= 7600.21= 160 mmHgPN2= 7600.79= 600 mmHgPH2O= 47 mmHg- dilutes other gases!

229
Q

how do you calculate the partial pressure of tracheal O2?

A

(Patm-Ph2O) X Flow of O2= 150 mmHg(760-47)*0.21

230
Q

what is the alveolar gas equation?

A

Pao2= Pio2- (Paco2/R)where Pio2= (Patm-Pwater)xFiO2

231
Q

what is the ideal alveolar oxygen amount?

A

102 mmHg

232
Q

what is the respiratory quotient?

A

R= excreted CO2/ O2 taken up

233
Q

what is the fraction of alveolar CO2 determined by?

A

metabolism & rate of ventilation- inversely proportional to ventilation* a 50% reduction in ventilation will double Pco2- directly proportional to production

234
Q

equation for the partial pressure of CO2

A

PCO2= VCO2(production) X (Patm-Ph2o)/alveolar ventilation

235
Q

where is inspired air shunted to? why?

A

lung base- base of lung has more alveoli - the base is more compliant, can hold more reserve

236
Q

what is a time constant? what does a long time constant mean?

A

the rate at which the alveoli fills t= resistance x compliance - longer= slow filling & emptying

237
Q

what happens to the time constant when you increase resistance?

A
  • alveoli fills more slowly & becomes under-ventilated
238
Q

what happens to the time constant when you decrease compliance?

A
  • alveoli fills faster than the normal unit but only receives half the ventilation
239
Q

what are the 4 features of the N2 curve obtained from the nitrogen washout test

A

1) %N2 starts at 0 for some volume as the dead spaces empty2) rapid upswing in % N2 as alveolar regions empty3) alveolar plateau where there is equal emptying of all lung zones4) there is a second upswing due to slowly emptying alveoli

240
Q

what can the nitrogen washout test measure?

A

anatomical dead space- volume in the middle of the first upward inflection

241
Q

what is the equation for ventilation?

A

v= frequency x tidal volume

242
Q

what is physiological dead space and how can it be calculated?

A
  • total volume that does not participate in gas exchange- anatomical dead space + alveoli that are ventilated but not perfused - measure fraction of expired CO2 and compare it to PaCO2 in blood
243
Q

The larger the tidal volume, the ____ the dead space ventilation; To increase alveolar ventilation, a _______ in tidal volume is more effective than a ______ in the frequency of breathing

A

smaller

244
Q

What is Fick’s law?

A
  • transfer of gas is proportional to the area that it has to go through, a constant, and the difference in partial pressure- the transfer of gas is also indirectly proportional to thickness
245
Q

What is Graham’s law?

A
  • the rate of diffusion is direction proportional to the solubility coefficient of the gas- inversely proportional to the sqrt of the molecular weight
246
Q

if there is no difference between the partial pressure for a gas in alveoli and end capillary blood, what is flow limited by? what is an example?

A
  • perfusion limited, NO
247
Q

perfusion vs diffusion

A

perfusion- process of delivering bloodvsdiffusion- movement of a substance

248
Q

properties of pulmonary arteries

A
  • carry deoxy blood- thin wall, minimal smooth muscle- 7X more compliant- easily distensible - low pressure *** exposed to alveolar pressure
249
Q

3 ways to challenge diffusion of O2

A

1) thicken walls (fibrosis)2) exercise (decrease time of blood in caps)3) drop alveolar PO2 in high altitude, gradient drops

250
Q

pulmonary vascular resistance changes with changes in vascular pressure how? and by which mechanisms?

A
  • decreases1) recruits more capillaries2) capillaries distend to accommodate more blood
251
Q

what is pulmonary vascular resistance?

A

change in pressure between pulmonary artery (14) and left atrium (8) / blood flow ( 6 L/min)- comes out to 1mmHg/L/min (LOW!!!!)

252
Q

what is PVR regulated by?

A
  • gravity- lung volume changing alveolar pressure & extra-alveolar pressure - A-V pressure gradient
253
Q

alveolar resistance ___ as you approach total lung capacity, while extra-alveolar resistance ______

A

alveolar- increases (squishing vessels in alveoli)extra-alveolar- decreases (expanding)

254
Q

when is PVR the least?

A

at the functional residual capacity (stable resting point)

255
Q

two reasons for blood flow to be higher in the base than the apex

A

1) more lung tissue at the base due to shape of lung2) gravity pulls blood down easier

256
Q

names of 3 zones of the lung

A

zone 1- no-flow zonezone 2- waterfall zonezone 3- normal zone

257
Q

what is hypoxic vasoconstriction and what does it depend on?

A
  • if blood is exposed to low PO2 in the alveoli, the vessels constrict- depends on the ALVEOLAR concentration of O2, not the blood - shifts blood from poorly ventilated areas to well ventilated areas; is important at birth
258
Q

what is fluid movement across capillary governed by? how does edema develop?

A
  • starling forces- hydrostatic & oncotic pressures- when drainage rate exceeds maximum lymphatic flow
259
Q

excessive filtration from pulmonary capillaries leads to ____, while excessive filtration from systemic capillaries leads to ____

A
  • engorgement of alveolar walls & alveolar flooding- engorgement of pleural space & pleural effusions (decreased lung volume)
260
Q

what is the difference between obstructive and restrictive lung diseases?

A

obstructive- can’t exhalerestrictive- can’t fully expand

261
Q

difference between osmolarity and osmolality?

A

R= osmol/LL= osmol/kg

262
Q

what is antidiuresis?

A

normal land-dweller state: when you have high ADH in the blood, urine excretion is low, high reabsorption of urea

263
Q

what contributes to the hyperosmotic gradient from cortex to medulla?

A

urea- 50%- 600 osmolNa- 25%- 300 osmolCl- 25%- 300 osmol

264
Q

3 mechanisms that generate hyperosmotic gradient from from cotex to medulla?

A
  1. countercurrent multiplier- permeability differences for Na and H202. urea cycle- leaking out in collecting duct & only participating in right loop3. countercurrent exchanger- slow vasa recta flow (permeable to everything) allows time for Na to move in and H20 to move out
265
Q

5 requirements for hyperosmolarity

A

1) long loops of Henle2) blood & urine flowing in opposite direction3) active salt pumping (in basolateral membrane of cells near TAL/DT/CD)4) differential permeabilities5) destruction takes days to re-establish

266
Q

equation for osmolar clearance (Cosm)

A

Cosm= V * Uosm/Posm

267
Q

what is Ch20? what is -Ch20 also called? what is the equation for Ch20?

A

Ch20= the amount of pure water kidney adds to urine-Ch20= TcH20Ch20= V-Cosm

268
Q

do alterations in Na change the volume or Na concentration of the ECF?

A

only the volume!!

269
Q

what is the ECV?

A

effective circulating volume- the portion of the ECF that is effectively perfusing the tissues (normally direction proportional to ECF)

270
Q

what are the 4 ways of regulating renal salt excretion via afferent sensors?

A

a- venous (increased atrial stretch, increased ANP, natriuresis)b- arterial (increased barros, decreased symp, decreased ADH)c- hepatic sensors (increased liver p, decreased symp)d- CNS sensors (increased Na in CSF, decreased symp)

271
Q

what is natriuresis?

A

increased sodium secretion in urine, followed by water

272
Q

what is the sympathetic pathway

A

increased sympathetics decreases GFR by constricting afferent arteriole, which increases renin (RAAS) and increases Na reabsorption

273
Q

what are the affects of angiotensin II and aldosterone?

A

angiotensin II- Na is reabsorbed proximally, causes secretion of ADHaldosterone- increases NA reabsorption in TAL, DT, CD

274
Q

how do ANP, BNP, and urodilatin work?

A

decrease aldosterone, decrease renin (decreases Na reabsorption), (decrease sympathetics- increase GFR- increase Na in tube- increase Na excretion)

275
Q

what are the 3 things that stimulate renin secretion?

A

1) perfusion pressure sensed by baroreceptors in afferent arteriole2) sympathetic nerves that innervate afferent arterioles 2) tubuloglomerular feedback senses decreased NaCl in macula densa

276
Q

when is ANP released from atria?

A

1) increase in extracellular fluid volume2) increase in arterial pressure (increase in LV pressure)3) increase in venous pressure (increase in right atrial pressure)

277
Q

what does reabsorption depend on in 3 parts of kidney?

A

1- proximal- filtered load2- TAL- Na delivery rate3- DT/CD- Na load remaining

278
Q

during euvolemia, you have a _______; what percent of Na is filered?

A

net zero Na balance -99% is filtered

279
Q

what happens to GFR during volume expansion?

A

GFR increases, decrease reabsorption in proximal tubule and collecting duct- see decrease sympathetics, increased urodilatin, increased ANP and BNP

280
Q

what happens during edema? how can it be fixed?

A
  • see decrease in ECV and plasma volumes- fixed by giving diuretics to decrease Pc and increase PIc
281
Q

what are 3 things that cause K+ release from the cell?

A

1) epinephrine acting on alpha receptors2) cell lysis (burns, surgery)3) hyperosmolarity

282
Q

what are 5 things that cause K+ uptake by the cell?

A

1) epinephrine activating B2 receptors, especially during exercise2) increased extracellular K+ stimulating the Na/K ATPase3) insulin (especially following a meal)4) aldosterone 5) hyposmolarity

283
Q

what percent of K+ in kidneys is reabsorbed? what percent is excreted?

A

85-95% is reabsorbed (decreases with more in diet)15-80% is excreted (increased with more in diet)

284
Q

what 3 factors regulate K+ secretion in the DT & collecting duct

A

1) Na-K atp pump2) cell-lumen -40 electrochemical gradient 3) K+ permeability of apical membrane

285
Q

5 factors altering K+ secretion

A

1) hormones (aldosterone, GCs ADH)2) tubular fluid flow 3) dietary intake 4) metabolic acidosis 5) diuretics

286
Q

3 hormones that control distribution of Ca2+ between bone and ECF

A

1) parathyroid hormone2) calcitriol3) calcitonin

287
Q

what does parathyroid hormone do?

A
  • released with low Ca2+ - increase Ca & Pi in plasma by increasing kidney reabsorption, decreases Ca excretion, increases Pi excretion - stimulates bone resorption- stimulates calcitrol
288
Q

what does calcitriol do?

A
  • made in proximal tubule of kidney - stimulates the reabsoption of Ca2+ and Pi by the kidney- inhibits the excretion of Ca2+ and Pi- - stimulates bone resorption
289
Q

what does calcitonin do?

A
  • protects against high Ca2+- stimulates bone formation (decreases plasma concentration of Ca2+) & the excretion of Ca2- has same effect on Ca2+ and Pi
290
Q

when do you see the spillover effect for phosphate?

A

when you have excess plasma Pi- plasma concentration at rest is super close to RPT, so any extra is filtered/excreted

291
Q

glomerulotubular balance vs. tubuloglomerular feedback

A

GT balance- 67% of what’s put in is reabsorbedvsTG feedback- Na sensed by macula densa controls afferent arteriole and GFR

292
Q

what is a non-volatile acid? what is a volatile acid?

A
  • not derived from CO2 (H2CO3 is the ONLY volatile acid- can be excreted as gas by lungs)
293
Q

what is a titratable acid and what is an example?

A
  • any acid that will lose a proton at physologic pH (e.g. H2PO4-)- HPO4- combines with H+ in tubule
294
Q

where is the majority of bicarb reabsorbed? how?

A

proximal tubule as H20 + CO2 when H+ is secreted

295
Q

which buffer is able to adjust it’s quantity based on acidosis?

A
  • ammonium- NH4
296
Q

what happens in the distal tubule?

A

have no CA & most of bicarb has been reabsorbed so mostly have secretion of H+ via H+ K ATPase and H+ ATPase inserted with ISF is acidified

297
Q

what is the difference between type 1 and type 2 RTA?

A

type 1- distal nephron doesn’t secrete H+, H+ goes back into bloodtype 2- proximal tubule creates acidosis because low CA inhibits H+ recycling, HCO3- isn’t reabsorbed

298
Q

how is bicarb regulated near RPT?

A

have HCO3-/Cl- antiporter in collecting duct

299
Q

7 factors that regulate HCO3 reabsorption

A

1 GFR2 Na balance3 systemic acid-base balance4 aldosterone5 arterial K+6 arterial Cl- 7 ECV

300
Q

3 forms of protons in urine

A

1 free hydrogen ions2 titratable acids with HPO4- 3 diffusion trapped with NH4+

301
Q

2 ways in which NH4 is secreted into collecting duct

A

1 non-ionic diffusion and trapping- NH3 follows H+ getting pumped into lumen2 NH4- H+ antiporters in basolateral & apical membranes

302
Q

how does hypokalemia influence pH?

A
  • low K+ stimulates H+ secretion into tubule- have H+/K+ antiporter on basolateral membrane, if K+ isn’t coming into cell, H+ won’t be put back into blood, will be extruded into tube instead
303
Q

3 major systems that maintain plasma H+? which is fastest?)

A

1) chemical buffering2) renal system (slow)3) respiratory system (fast)

304
Q

what is the henderson-hasselbach equation adjusted for renal?

A

pH= pKa + log (kidney- bicarb)/(lung- PCO2*0.03)

305
Q

where is phosphate a weak buffer, and where is it stronger?

A

weak- blood stronger- kidney

306
Q

what is the assumed pKa of blood?

A

6.1

307
Q

what is the difference between an open and closed buffer system?

A
  • open- can easily get rid of acids (Co2 expiration, H+ excretion)- closed- total concentration is fixed, just juggle between associated and dissociated forms (Hb, phosphate)
308
Q

what happens to open system buffering power as pH decreases?

A

it increases exponentially, because pCO2 rises and that facilitates removal (closed system peaks where pH= pKa)

309
Q

what is the isohydric principle?

A

when a solution contains more than 1 buffer, all buffer pairs are at equilibrium with the same proton concentration

310
Q

normal pH

A

7.35-7.45

311
Q

normal PaCO2

A

35-45

312
Q

normal bicarb

A

22-28 mM

313
Q

normal H+

A

35-45 nM

314
Q

what is the compensation for metabolic acidosis?

A
  • dec pH- dec Co2COMP: decrease CO2 more
315
Q

what is the compensation for respiratory alkalosis?

A
  • inc pH- dec Co2COMP: decrease HCO3

Physiology (22 decks)

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