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Physiology Flashcards

1
Q

CO formulas (SV, HR, MAP, TPR)

A 
CO = SV x HR
MAP = CO x TPR (P = Q x R)
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2
Q

Pulse pressure formula

5 causes of increased pulse pressure
3 causes of decreased pulse pressure

A

pulse pressure = systolic pressure - diastolic pressure

Increases: hyperthyroidism, AR, aortic stiffening, OSA, exercise
Decreases: AS, post-MI shock, cardiac tamponade

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3
Q

What 3 factors change stroke volume?

A

CAP: contractility, afterload, preload

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4
Q

What 3 factors increase contractility? CND

A

catecholamines: increased Ca pump in SR, therefore increased [Ca]i

decreased [Na]e: decreased activity of Na/Ca exchanger (increased [Ca]i)

Digoxin: decreased Na/K pump –> incr. [Na]i –> decreased Na/Ca, incr. [Ca]i

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5
Q

What 4 factors increase myocardial oxygen demand?

A

increased with CARD: contractility, afterload, rate, diameter of ventricle

increased with wall tension (which = P x r / 2 x thickness)

increased afterload –> increased wall thickness to decrease wall tension and decrease O2 demand

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6
Q

What value approximates preload?

A
  • approximated by ventricular EDV

- depends on venous tone, circulating blood volume

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7
Q

What value approximates afterload?

A
  • approximated by MAP
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8
Q

Starling curve axes

A

stroke volume or CO vs. ventricular EDV

note: a left shift (increased CO for a given EDV) corresponds to an increase in contractility

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9
Q

Systemic resistance (R)

Give formulas and facts

A 
P = Q x R (R = P/Q)
Q = v x A

capillaries are highest cross-sectional area, lowest velocity

arterioles form the majority of TPR (organ removal = increased TPR, lead to decreased CO)

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10
Q

CO/preload interplay

inotropy, venous return, TPR

A

Inotropy: alters CO for a given preload
Venuos return: alters preload for a given CO
TPR: altered CO for a given preload

exercise: incr. inotropy, decr. TPR = increased CO
fluid retention: decr. inotropy, incr. preload = increased CO (to compensate for HF)

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11
Q

Contraction phase cycle

graph shows relationship between LV pressure vs. LV volume

A

1: isovolumetric contraction
2: systole
3: isovolumetric relaxation
4: diastole

increased contractility = decr. ESV (higher SV), left expansion
increased preload = incr. EDV (higher SV), right expansion
increased afterload = increased ESV (lower SV), narrowing from the left

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12
Q

Heart sounds

A

S1: mitral/tricuspid closure
S2: atrial/pulmonic closure
S3: increased flow velocity in early diastole (due to dilated ventricular chamber)
S4: heard in late diastole due to atrial kick

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13
Q

JVP waveforms

A 
a = atrial contraction
c = RV contraction
x = atrial relaxation
v = filling of right atrium
y = right atrium emptying into right ventricle
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14
Q

JVP characteristics on physical exam

A

multiphasic, non-palpable, occludable

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15
Q 
S2 splitting (normal, wide, fixed, paradoxical)
aortic vs. pulmonic valve closure
A

normal: incr. venous return w/ inspiration –> delayed PV closure
wide: pulm stenosis, RBBB –> delayed RV emptying
fixed: ASD –> const. incr. RV volume –> delayed PV closure

paradoxical: aortic stenosis, LBBB –> delayed aortic closure (pulmonic closes first! therefore paradoxical), gap closes on inspiration instead of widening

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16
Q

L sternal border auscultation

A

best for diastolic murmurs (eg. AR), or hypertrophic cardiomyopathy

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17
Q 
Effects of bedside maneuvers
Inspiration
Hand grip
Valsalva
Rapid squatting
A

Inspiration: incr. venous return, incr. intensity of R heart sounds
Hand grip: incr. afterload, incr. intensity of MR/VR/VSD
Valsalva (phase 2): decr. preload, incr. hypertrophic cardiomyopathy
Rapid squatting: incr. venous return, increased AS murmur, decr. hypertrophic cardiomyopathy

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18
Q 
Systolic heart murmurs
Aortic stenosis 
Mitral regurg
Mitral valve prolapse
VSD
A

AS: Crescendo-decrescendo (peripheral pulse is late and weak)
MR: holosystolic blowing
MVP: late systolic crescendo w/ click
VSD: holosystolic, harsh

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19
Q

Diastolic heart murmurs

Describe sounds

A

AR: high-pitched blowing
MS: opening snap, rumbling late

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20
Q

Myocardial action potential

A

Phase 0: depol = opening of fast Na channels (influx)
Phase 1: inactivation of Na channels, opening of K channels (efflux)
Phase 2: opening of Ca channels (influx, L type), plateau
Phase 3: rapid repol, close of Ca channels, opening of slow K channels (efflux)
Phase 4: resting = K+ ep. pot., high K permeability

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21
Q

Cardiac vs. skeletal potentials

A
  1. ) Plateau in cardiac cells
  2. ) SR initiates in skeletal
  3. ) cardiac nodal cells spontaneously depolarize due to funny current
  4. ) cardiac myocardium are electrically coupled through gap junctions
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22
Q

Pacemaker cell potentials

A

Phase 0: upstroke, opening of Ca
Phase 3: Ca inactivate, then incr. K efflux
Phase 4: slow Na influx (funny current slowly depolarizes)

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23
Q

Funny current variables

A 
Ach/adenosine = decreased HR
catecholamines = increased HR
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24
Q

Congenital long QT syndrome

A

usually due to ion channel defects

sometimes seen with deafness

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25
Q

Brugada syndrome

A

Asian males, pseudo-RBBB, V1-V3 ST elevation
due to ion channel defect
tx: ICD

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26
Q

ANP vs. BNP

A

both: act via cGMP to vasodilate and decrease Na resorption by the kidney

ANP: increase with blood volume
BNP: increase with ventricular torsion

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27
Q

Aortic vs. carotid receptors

A

Aortic: located in arch, transmit through CN X
Carotid: located at bifurcation, transmit through CN IX

both to solitary nucleus in medulla

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28
Q

Baroreceptors stimulation

A

firing increases with stretch!

decreased stretch –> decr. firing –> incr. symp activation (BP, HP, etc.)

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29
Q

Carotid massage mechanism

A

Incr. pressure on carotid sinus = incr. stretch/incr. firing = incr. AV refractory period = decr. HR

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30
Q

Cushing reflex (incr. ICP, incr. BP, decr. HR)

A

incr. ICP –> cerebral ischemia –> incr. PCO2 –> symp reflex –> incr. BP –> incr. stretch –> decr. HR

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31
Q

Chemoreceptors (peripheral vs. central)

A

Peripheral: stimulated by decr. PO2, incr. PCO2, decr. blood pH

Central: pCO2, respond to levels in the brain interstitial fluid (CO2 flows better to bloodstream)

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32
Q

Insulin synthesis

A

Preproinsulin then…

RER: cleavage of signal peptide to proinsulin, folded and formation of disulfide bonds

Transport to Golgi

Immature granules: cleavage into insulin and C-peptide

Insulin packaged in mature granules for secretion

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33
Q

Insulin receptor

A
  • bind tyrosine kinase receptors
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34
Q

Insulin secretion

A

Glucose enters B-cell through GLUT2
Increased ATP/ADP ratio closes K channel (less K efflux)
Depolarization leads to Ca influx (acitvates phospholipase C, increased IP3 to further increase intra Ca)
High [Ca]i leads to granule release

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35
Q

Prolactin function and regulation

A
  • function: leads to milk production, decr. ovulation/spermatogenesis by decr. GnRH
  • hypothalamus secretes DA (inhibits prolactin) and TRH (stimulates prolactin)
  • prolactin inhibits GnRH, stimulates DA
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36
Q

GH function and secretion

A

linear growth, muscle mass and insulin resistance

Stimulated by GHRH during sleep and exercise

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37
Q

Appetite regulation

Ghrelin vs. Leptin

A

Ghrelin - stimulates hunger and GH release, produced by stomach

Leptin - satiety, produced by adipose, low in starvation, mutation = obesity

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38
Q

ADH synthesis and function

A

synthesized in supraoptic nucleus
V2 receptors: regulate serum osmolarity
V1 receptors: blood pressure

secretion regulated by osmoreceptors in the hypothalamus

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39
Q

17-OHase deficiency (decr. androstenedione)

A
  • blocks progenitors from cortisol/sex hormone production, only aldosterone is made
  • def = incr. aldosterone (incr. BP, K+ wasting), decr. sugar/sex hormones
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40
Q

21-hydroxylase deficiency (incr. 17-OH-P)

A

2nd step in aldosterone/cortisol synthesis

  • def = increased sex hormones, decr. salt/sugar hormones (decr. BP, high serum K+)
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41
Q

11B-hydroxylase deficiency

A

3rd step in salt/sugar hormone synthesis

  • def = incr. 11-DOH-C (incr. BP, K+ wasting), decreased aldosterone/cortisol, increased sex hormones
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42
Q

Cortisol functions (BIG FIB)

A

increase in: Blood pressure (incr. alpha receptors = incr. sens. to Epi/NorEpi), Insulin resistance, Gluconeogenic

decrease in: Fibroblast activity, Inflammatory/Immune responses, Bone building

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43
Q

Albumin-bound Ca and pH

A

increased pH (more basic) = more neg. charge on albumin = more bound Ca –> hypocalcemia

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44
Q

Vit. D effects

A

increased absorption of Ca and PO4 from gut
increased bone resorption from Ca and PO4

regulation: stimulated by PTH, low Ca, low PO4

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45
Q

PTH effects (give target organs, molecular mediators, and stimulators)

A

leads to increased serum Ca, decreased serum PO4

  • kidney: incr. Vit. D, incr. Ca, decr. PO4 (so urine will have low Ca and high PO4)
  • bone: release of Ca and PO4 (osteoclasts by RANK-L)
  • increased MCSF and RANK-L
  • stimulated by low Ca, high PO4, low Mg
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46
Q

Calcitonin effects

A

opposes PTH

tones down Ca levels by decreasing bone resorption of Ca

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47
Q

Sex-hormone binding globulin (effects of incr./decr. levels)

A

increased SHBG –> decr. free testosterone –> gynecomastia

decreased SHBG –> incr. testosterone –> hirsutism

pregnancy and OCPs increase SHBG levels

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48
Q

Thyroid hormones (effect on metabolism, effects of T3)

A
  • control metabolic rate through Na/K ATPase activity (and thus O2 consumption)

T3: Brain maturation, Bone growth, B-adrenergic effects, Basal metabolism

TBG: decr. in hepatic failure, incr. in pregnancy

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49
Q

Iodine and thyroid hormones

A

T4 is converted to T3 by 5’-deiodinase (PTU blocks this also)

Thyroid peroxidase prepares idoine to be incorporated in T3 (PTU blocks this)

50
Q

Gastrin (G cells in antrum)

Effects and secretion

A

increased H+ secretion, mucosa, motility

stimulated by food in the stomach

abnormally increased in H. pylori, Z-E, PPI use

51
Q

Somatostatin (D cells in pancreas, mucosa)

A

decr. acid, decr. pancreatic/gall bladder secretions, decr. insulin/glucagon

Stimulated by acid

52
Q

Cholecystokinin/CCK (I cells in duodenum)

A

increased pancreatic secretions, delayed stomach emptying

acts on neural muscarinics

53
Q

Secretin (S cells in duodenum)

A

incr. HCO3, bile, decr. gastric acid

Allows for enzyme function in the duodenum

54
Q

GIP (K cells in duodenum)

A

exocrine: decr. H+
endocrine: incr. insulin

55
Q

motilin (small intestine)

A

incr. MMCs!

56
Q

VIP

A

incr. water/electrolyte secretion

stimulated by vagal nerve

57
Q

Parietal cell inputs and mechanisms for acid secretion

A

Ach, gastrin –> Gq –> IP3
histamine* –> Gs –> cAMP
Both increased H+/K+ ATPase

Prostaglandins, somatostatin –> Gi –> decr. cAMP

58
Q

Gastric acid regulation

A

Stimulated by histamine, Ach, gastrin

Inhibited by somatostatin, GIP, prostaglandins

59
Q

Pepsin (chief cells)

A

Protein digestion

vagal stimulation

pepsinogen –> pepsin in the presence of H+

60
Q

HCO3- (mucosal cells and Brunner glands)

A

Neutralize acid

Is secreted and then trapped in the mucus lining the epithelium

61
Q

Pancreatic secretions (give the 3 enzymes)

A

amylase - starch digestion
proteases are secreted as zymogens
trypsinogen - activates other proenzyes, requires activation by enterokinase and peptidase

62
Q

Carbohydrate absorption (give 3 glucose transporters)

A

Monosaccharides only through SGLT-1 (Na-dependent)
Fructose through GLUT-5
Transferred to bloodstream through GLUT-2

63
Q

D-xylose test

A

if intact mucosa, then absorbed and excreted in urine
if SIBO/Whipple’s, then decr. absorption and treated with Abx
if still not fixed, then structural deformity (eg. celiac)

64
Q

Peyer patches

A

M-cells: APCs

B-cells transform to IgA-secreting plasma cells in the lamina propia

65
Q

Bile production (give rate limiting step and three functions)

A

rate-limiting step: cholesterol 7-a-hydroxylase

functions: digestion, cholesterol excretion, anti-microbials

66
Q

Bilirubin

A

macs: heme –> unconj. bilirubin (bound to albumin in blood)
liver: unconj. bili + albumin –> conj. bili
gut: conj. bili –> urobilinogen (20% reabsorbed, 10% of which is secreted in urine and 90% of which is sent back to liver in enterohepatic circulation)

liver enzyme: UDP-gluconyltransferase

67
Q

Anticoagulants
Give the Xa inhibitors
Give the IIa (thrombin) inhibitors

A

Xa inhibs: LMWH*, heparin, rivaroxaban, fondaparinux

IIa inhibs: heparin*, LMWH, argatroban

68
Q

Hemophilias

Give type and factor affected

A

All have lack of functional clotting factors

A: decr. 8
B: decr. 9
C: decr. 11

69
Q

Describe the clotting pathways

A

Intrinsic: [12 –> 11 –> 9] –> 10 –> 2 (thrombin) –> 1 (fibrin)
Extrinsic: [7 –> 10]

Note: 8 (9 –>10) and 5 (10 –> 2) both require Ca and phospholipid

70
Q

Platelet plug formation (give 5 steps and notable factors)

A

Injury: transient vasoconstriction
Exposure: vWF (WP bodies, alpha granules) binds exposed collagen
Adhesion: plts adhere by GpIb, release ADP, Ca, TxA2
Activation: ADP in plt –> GpIIb/IIIa
Aggregation: fibrinogen binds GpIIb/IIIa, links plts

71
Q

Give thrombotic (platelet) anticoagulants

A 
Aspirin = decr. COX-1 --> decr. TxA2
Clopidogrel = decr. GpIIb/IIIa
72
Q

Ristocetin assay

A

normally ristocetin activates vWF to bind Gp1b

failure of agglutination during assay = vWF disease or Bernard-Soulier (decr. plt adhesion)

73
Q

Describe 3 platelet defects

A

Glanzmann - decr. GpIIb/IIIa (decr. activation)
vWF disease
Bernard-Soulier - decr. GpIb (decr. adhesion)

74
Q

Glomerular filtration (give 3 components of the barrier)

A
  1. ) fenestrated endothelium (size barrier)
  2. ) BM w/ heparan (neg. charge)
  3. ) podocyte foot processes
75
Q

Clearance formula

A

Cx = (Ux times V) / Px
in words, clearance is equal to urine conc. times urine flow rate all over plasma conc.

If Cx > GFR, then net secretion
If Cx < GFR, then net reabsorption

76
Q

GFR

A

GFR = Cinulin (inulin has no net secretion or reabsorption)

Also, GFR = Kf[(Pgc - Pbc) - (πgc - πbc)]

Normal = 100 mL/min

Creatinine overestimates due to slight secretion (clearance is abnormally elevated)

77
Q

Effective renal plasma flow

A

eRPF = Cpah (PAH is freely filtered and secreted)

RBF = RPF/(1 - Hct)

  • note: underestimated by 10%
78
Q

Filtration fraction formula

A

FF = GFR /RPF (normal = 20%)
in words, the proportion of fluid entering kidney that then enters the tubules
This has to be manipulated in situations where the blood flow to the kidney itself is variable

79
Q

Afferent/efferent arteriole physiology

A

Afferent dilation (prostaglandins): increased GFR/RPF, no effect on FF

Afferent constriction (symp NS): decreased GFR

Efferent constriction (Ang. II): decr. RPF, incr. GFR, incr. FF)

80
Q

Glucose in the kidney

A

mainly reabsorbed in PCT by Na/glucose co-transporter

> 200 = glucosuria, >375 = saturation of transporters

81
Q

Hartnup disease (amino acid transport)

A

Decreased AA transporters in the PCT –> neutral aminoaciduria

Leads to decr. tryptophan –> decr. niacin –> PELLAGRA

Tx: high-protein diet

82
Q

Proximal tubule

give function and two compounds that act here

A

reabsorb glucose/AA/HCO3/Na/Cl/PO4/K/H20
- secretes NH4+ to maintain luminal charge

Ang II: incr. Na/H exchange, incr. Na/H2O/HCO3 absorption
Acetazolomide: decr. carbonic anhydrase –> decr. HCO3 reabsorption

83
Q

Thin descending loop of Henle function

A

Water reabsorption according to medullary gradient

  • aka concentrating segment
  • NO SODIUM TRANSPORT
84
Q

Thick ascending loop function

A
  • Na/K/Cl reabsorption
  • also, induced paracellular reabsorption of Ca/Mg

NO H2O transport!

85
Q

Distal Convoluted Tubule

A

reabsorb Na/Cl
- site of the MOST DILUTE URINE

  • PTH: increased Na/Ca reabsorption on basal/blood side
86
Q

Collecting tubule

Give details of aldosterone/ADH effects

A
  • reabsorb Na, secrete K

Aldosterone: nuclear receptor, increased mRNA to increased Na/K pump and ENaC on principal cell. Loss of lumen positivity leads to K wasting

ADH: through V2 receptors, leads to increased aquaporins on apical side

87
Q

Fanconi anemia effects and causes

A

Generalized reabsorptive defects

Increased excretion of everything –> metabolic acidosis (Type 2/proximal RTA)

Causes: Wilson’s, ischemia, multiple myeloma

88
Q

Bartter syndrome defect and effects

A

defect in Na/K/2Cl transporter in ascending limb

leads to hypokalemia, metabolic alkalosis, and hypercalciuria

89
Q

Gitelman syndrome defect and effects

A

defect in Na/Cl transporter in DCT

less severe than Bartter

90
Q

Liddle syndrome defect and effects

A

gain of function mutation in ENaC

  • leads to hypertension, hypokalemia
    tx: amiloride (ENaC inhibitor)
91
Q

Apparent mineralocorticoid excess

A

11 B-OH dH leads to failure of cortisol –> cortisone

incr. cortisol –> activation of MC receptors

leads to HTN, K wasting

  • acquired from licorice
92
Q

RAAS sensors

A
  1. ) JG cells (respond to low BP) secrete renin
  2. ) macula densa (respond to low distal Na delivery) release adenosine
  3. ) B1 receptors (respond to incr. symp drive)
93
Q

RAAS function

A

increased renin cleaves angiotensinogen to AT-1

ACE (from pulmonary endothelium) cleaves AT-1 to AT-2 (also breaks down bradykinin)

94
Q

Effects of angiotensin-2 (six total)

A

Vasoconstriction: AT1 receptor of vascular smooth muscle

Efferent arteriole constriction: increased FF/GFR to preserve renal function

Aldosterone: principal cells (incr. ENaC, basal Na/K pump), alpha-intercalated (H+ ATPases)

ADH: increased aquaporins

PCT: incr. Na/H activity (incr. Na/HCO3, H2O reabsorption)

hypothalamus: stimulates thirst

95
Q

Atrial natriuretic peptide

A
  • acts on afferent arteriole to increase GFR

- also decreases Na reabsorption in the DCT

96
Q

Renal tubular acidoses

give name, location, electroytes involved

A

Type I distal: alpha-intercalated, no new HCO3, decr. H secretion, assoc. with hypokalemia

Type II proximal: decr. PCT HCO3 reabsorption, hypokalemia

Type IV hyperkalemic: hypo-aldosterone leads to excess K, decreased NH4 secretion
- can be either an absolute reduction in aldosterone or aldosterone resistance

97
Q

Estrogen sources and hormone secreted

A

Ovary: estradiol
Adipose: estrone
Placenta: estriol

Estradiol > estrone > estriol

98
Q

Estrogen receptor

A

Expressed in cytoplasm

Translocates to nucleus when bound by estrogen

99
Q

Estrogen functions

A

Development, increased estrogen/LH/progesterone receptors

increased SHBG, incr. HDL, decr. LDL

Incr. endometrial proliferation

100
Q

Progesterone sources

A

Corpus luteum, placenta, adrenal cortex, testes

101
Q

Progesterone function

A

stimulate endometrial glands and spiral arteries

Production of thick cervical mucus

incr. body temp, decr. endometrial proliferation

102
Q

Oogenesis

A

primary oocytes: 2N, 4C, frozen in prophase I until ovulation (46 sister chromatids)
secondary oocytes: 1N, 2C, frozen in metaphase II until fertilization (23 sister chromatids)

103
Q

Fertilization

A

Sperm entering oocyte triggers cortical reaction (prevention of another sperm from entering, continuation of second division, leading to extrusion of polar body)

104
Q

Ovulation

A

increased estrogen past the inhibitory threshold leads to an LH surge, which induces ovulation (follicle rupture) and progesterone-induced rise in temperature

Fertilization must happen within 1 day, in the ampulla

105
Q

Lactation (describe roles of prolactin and oxytocin)

A

Prolactin - induces milk production, decreases reproductive potential

Oxytocin - assists in milk letdown, promotes uterine contractions

106
Q

hCG (give source and function)

A

source: syncytiotrophoblasts
function: maintian corpus luteum for first 8-10 weeks

incr. in twins, Down’s, moles
decr. in ectopic, Edward/Patau

107
Q

Spermatogenesis

A

full cycle takes 2 months

spermatogonium: 2N, 2C (46 chromosomes), then become… (after leaving blood-testis barrier)

primary spermatocyte: 2N, 4C (46 sister chromatids)
secondary spermatocyte: 1N, 2C (23 sister chromatids)

Spermatid: 1N, 1C, then undergoes maturation (loss of cytoplasmic contents and gain of acrosomal cap) to become spermatozoon

108
Q

Androgens (potency, function, conversion enzymes)

A

DHT > testosterone > androstenedione

testosterone: differentiation, growth spurt, voice, libido
DHT: penis, scrotum, prostate (then, balding, sebaceous glands)

5a-reductase: testosterone –> DHT
aromatase: convert androgens to estrogen in adipose tissue (estrogen helps close epiphyseal plates)

109
Q

Lung volumes

Describe IC, ERV, VC

A

FRC is the base line (RV + ERV), and a normal breath in is the TV
Maximal inspiration from FRC = TV + IRV = IC
Maximal expiration from FRC = ERV

Maximal inspiration/expiration overall: ERV + TV + IRV = VC (vital capacity)

110
Q

Physiologic dead space

give formula as well

A

Volume of air that does not participate in gas exchange

= tidal volume times (arterial CO2 - expired CO2)/arterial CO2

111
Q

Hemoglobin

taut (low affinity) vs. relaxed (high affinity)

A

Taut in tissues! Therefore allows O2 unloading
- more taut = R shift (incr. H+, 2-3BPG, temp)

Relaxed in respiration! Therefore allows O2 binding

112
Q

Methemoglobin

A

Oxidized Hb, increased affinity for CN

Causes by nitrites/thiosulfate, which is used to treat CN poisioning

113
Q

Carboxyhemoglobin

A

Hb bound to CO, decr. O2 capacity, decr. O2 unloading

114
Q

Hb dissociation curve (describe shape, shifts)

A

Hb: positive cooperativity (incr. O2 binding = incr. affinity) leads to higher binding potential

R shift = lower saturation for a given pO2, caused by incr. H+, temp, 2/3BPG

115
Q

Oxygen content of the blood

A

Dissolved O2 + (Hb times 1.34 mLO2/gHb times %sat)

Note! O2 delivery = O2 content times CO

116
Q

Pulmonary circulation

A

normally, low resistance with incr. compliance

Note, opposite reactivity from systemic circulation; low PaO2 (hypoxemia) –> vasoconstriction

117
Q

Gas diffusion

A

In normal resting human: O2 and CO2 are perfusion-limited (PaO2 depends on flow rate)

In emphysema and fibrosis, O2 is diffusion-limited, and therefore doesn’t PaO2 does not equal PAO2 by the time blood leaves the capillary

118
Q

Pulmonary vascular resistance

A

PVR = pressure in pulm. artery minus pressure in left atrium all divided by cardiac output (recall, R = deltaP/Q)

119
Q

Alveolar gas equation

A

PAO2 = PIO2 - PaCO2/RQ = 150 - PaCO2/0.8

normal A-a gradient = 10-15 mmHg
incr. A-a gradient = V/Q mismatch, shunt, diffusion impairment

120
Q

Hypoxemia

A

normal A-a: high altitude, hypoventilation

increased A-a: V/Q mismatch, shunting, diffusion impairment

121
Q

CO2 transport (Haldane effect, Bohr effect)

A

90% as HCO3-, 5% as HbCO2, 5% dissolved

When O2 binds to Hb in the lungs, H+ is let go and forms CO2, allowing for unloading and expiration

In peripheral tissue, incr. H+ from metabolism leads to incr. O2 unloading

122
Q

High altitude effects

A

incr. ventilation, decr. PaCO2, incr. EPO, incr. 2,3BPG (shift of curve to right)

also, incr. renal excretion of HCO3

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