High Yield Relationships—Slide # 1

Q =PR CO = HR X SV C =

PV

CSV

PP =R ∝

Lr4

T ∝ Pr (LaPlace)

Pulse pressure (PP) = systolic - diastolic

P ∝ R

MAP = 1/3 PP + diastolic pressure

Velocity = Q/CSAP = height X density X gravity

Uptake of O2

A – V O2 difference Flow =

MAP = CO X TPR

Reynold’s # = (velocity) (diameter) (density) / viscosity

EF = SV/EDV X 100

Cardiac Index = CO/ body surface area (BSA)

MAP = CO X TPR

4 factors determine

1. HR ( CO exercise; CO with tachyarrhythmias)

2. Contractility (direct)

3. Afterload (inverse)

4. Preload (direct)

Directly related to venous return

• Blood volume (direct)

• Venous compliance (inverse)

Tone of arterioles

• Sympathetic (alpha)

• AII

• AVP

• Epi (alpha/beta-2)

• Metabolism

• NO

• Pharm integration

Whole Body CV Regulation—Slide # 2

Anti-hypertensive drugs

Short/Long Term MAP Reg—Slide # 3

Mean Arterial Pressure

Inhibits Stimulates

Baroreceptor activity

Sympathetic activity

Contractility

TPRCardiac output

Heart rate

Veno-

constriction

Stroke volumePreload

M2

Parasympathetic activity

Urine volume

Blood volume

Renin

A II

VR

VRF-S

Aldo

Shock

Autonomic drugs

100 150

40

80

120

50

Pres

sure

(mm

Hg)

Volume (ml)

Passive tension

PV Loops: Systolic/Diastolic Dysfunction Systolic dysfunction:

decreased contractility results in elevated volumes

Diastolic dysfunction: decreased compliance

causes increased pressure

Slide #4

Pg 143

IPP—Pulmonary Blood Flow—Slide # 5Inspiration

PTM = 0 – -5 = 5

Becomes more

negative

RA in chest expands pressure so Q (VR)

Increased output delays closing of pulmonic valve

(physiologic splitting of S2)

PTM for pulmonary

vessels; their volume increases

Increases pulmonary vascular resistance

Flow to LH

MAP = CO X TPR

Inspiration decreases vagal outflow to the heart, thus HR increases (respiratory sinus arrhythmia)

Veins here are unaffected

Differential for Causes of Hypoxemia—Slide # 6

Low PaO2(hypoxemia)

A – a gradient

FIO2 corrects

PaCO2 likely elevated

Normal

Cause is PAO2

Elevated

Increase FIO2

Doesn’t correct PaO2

Cause is right-to-left shunts

Corrects PaO2

VA/Q mismatch

Diffusion impairment

PAO2: calculate using alveolar air equation or

use end-tidal PO2

Relationships/Equations for Renal—Slide # 7

GFR RPF

FF =

FF impacts Pc!!!Filtered load = GFR X PX

Rate of excretion = UX X V

Transport = excretion – filtered load

Renal clearance =

UX X V

PX

UPAH X V CPAH =

PPAH

ERPF =

Renal blood flow =1- HctERPF

Factors Affecting GFR and FF—Slide # 8

Glomerular cap

pressure

Peritubular cap

pressure

Nephron plasma

flow

GFR FF

Constrict efferent

Dilate efferent

Constrict afferent

Dilate afferent

50

100

0[H]

% R

espo

nse

E + S (ES) E + P H + R (HR) response stimulus response

50

100

0[S]

Velo

city

(% o

f max

)

Michaelis-Menten

Km

Vmax: determined by [E] & [S]

Properties of Receptors—Slide # 9

[H] is limiting

[S] is limiting

[R] is one factor

50

100

0Log [A]

% R

espo

nse

50

100

0[H]

% R

espo

nse

Properties of Receptors—Slide # 10

H + R (HR) response stimulus response

A + R (AR) response stimulus response

EC50

[H] is limiting

[H] is limiting

[R] is one factor

Overview of AVP Pathophysiology—Slide # 11

Low

Dehydration(2O)

High

Primary Poly-dipsia (2O)

SIADH(1O)

Plasma AVP

POSM

UOSM<< 1

POSM

UOSM>> 1

LowHigh

LowHigh

Plasma osmolality

*Nephro DI (1O)

Plasma AVP

POSM

UOSM<< 1

POSM

UOSM>> 1

Neuro DI* (1O)

Note: AVP=ADH

Metabolism—Cortisol—Slide # 12

Glucose

G6-phos

Glucose 6-P

GlucokinaseGly

phos

GlycogenGly

synthase

PEPCK

Fructose 1,6-bisphosphatase

PDH (thiamine)

Acetyl CoAPyruvate carboxylase

(biotin)

OAA

Lactate

LDH

Acetyl CoA carboxylase

Malonyl CoA

TCA Ketones

FAFA

synthase

Pyruvate kinase

PFK-1 (via PFK-2)

Pyruvate

AA (alanine)

Cortisol

Cortisol

Glucose

G6-phos

Glucose 6-P

GlucokinaseGly

phos

GlycogenGly

synthase

PEPCK

Fructose 1,6-bisphosphatase

PDH (thiamine)

Acetyl CoAPyruvatecarboxylase

(biotin)

OAAAcetyl CoA carboxylase

Malonyl CoA

TCA Ketones

FAFA

synthase

Pyruvate kinase

PFK-1 (via PFK-2)

Pyruvate

AA (alanine)

Insulin stimulatesGlucagon stimulates

Insulin—Glucagon—Slide # 13

Urea

Bone Remodeling—Slide # 14

RANK-L promotes resorption

OPG reduces resorption

High glucocorticoids: RANK-L; OPG

Sexual Differentiation—Slide # 15

Wolffian ducts

Müllerian ducts

Wolffian ducts

Müllerian ducts

Fallopian tubes,

uterus, inner vagina

Epididymis, vas

deferens, seminal vesicles

Epididymis, vas

deferens, seminal vesicles

T = TestosteroneSRY = sex determining

region of Y

MIH = Müllerian inhibiting hormone

Ovaries

Fallopian tubes, uterus,

inner vagina

XY has SRY

XX—no SRY Testes

TMIH

Regress Regress

Undifferentiated gonad

Sexual Differentiation—Slide # 16

Ovaries Testes

Undifferentiated organs

DHT

Clitoris, outer vagina, labia

Penis, scrotum, &

prostate

No DHT

Testosterone dihydrotestosterone (DHT)5 alpha-reductase

Menopause—Slide # 17

Test/A

17-Estradiol

CholesCholes

Adipose tissue

Adrenal cortexBlood

A

DHEA

FSH/LHACTH

aromataseEstrone

aromatase

Ovary

DHEA A

Tumor Growth

Anastrozole

Letrozole Tamoxifen

Raloxifene

Polycystic Ovarian Syndrome—Slide # 18PCOS

Hirsutism; irregular menstrual bleeding; chronic anovulation; obesity; insulin resistance; infertility

Thecalhormone

production

Adipose estrone

LH FSH

Pituitary

Follicle maturationaromatase Estradiol

anovulation

Androgens

Adrenal

AdiposeOvaries

Androgens

Oral contraceptives to LH

Thiazolidinediones; Metformin

insulin

SHBG

Clomiphene: FSH

Dexamethasone