Cardiovascular Physiology

Alan Sexton

Cardiac Muscle Properties

Automaticity Rhythmicity Conductivity Excitability Contractility

Definitions
Preloaded Muscle Afterloaded Muscle

ACTION POTENTIALS

NERNST EQUATION GOLDMAN FIELD EQUATION

Nernst Voltages
Vna +60 mV

Vk

-90 mV

Vcl

-70 mV

Ion Concentrations (mmol/l)

IN Na+ K+ ClProtein Other Cations+ Other Anions10 148 4 56 42 140 OUT 142 5 103 16 8 36

CHANNELS
FAST TYPE Max dV/dT TAW OF INACTIVATION Na+ 100-1000V/S 1-2 mSec SLOW Ca2+ 1-20V/S 50-200 mSec

CHANNELS
FAST THRESHOLD OF ACTIVATION ION OF INPORTANCE -60 TO -70mV Na+ SLOW -30 TO -40mV Ca2+

CHANNELS
FAST BLOCKERS TETRADOTOXIN SAXITOXIN LOCAL ANESTH SLOW MAGNESIUM VERAPAMIL

CHANNELS
FAST SITES SLOW

SA,AV NODES ATRIUM VENTRICLE ALL OTHER CARDIAC TISSUE HIS BUNDLE PURKINJE FIBRES

CHANNELS
GATES OPEN DUE TO STIMULI
VOLTAGE DEPENDENT LIGAND MECHANICAL STRETCH

CVP WAVE
A WAVE
ATRIAL CONTRACTION

C WAVE
BULGING TRICUSPID VALVE DURING ISOVOLUMETRIC CONTRACTION

V WAVE
VENTRICULAR FILLING

Cardiac Contraction

CARDIAC CONTRACTION
MEMBRANE DEPOLARISATION OF T SYSTEM CA++ RELEASED FROM CELLULAR STORES (SARCOPLASMIC RETIC) CA++ BINDS TO TROPONIN C STOPPING INHIBITORY EFFECT OF TROPOMYOSIN ON ACTINOMYOSIN ATPase.

CARDIAC CONTRACTION
Actinomyosin ATPase SUPPLIES ENERGY FOR BINDING OF ACTIN AND MYOSIN CROSS BRIDGES. X BRIDGE ATTACHMENT DRAWS THIN FILAMENTS INTO A BAND, REDUCING THE SARCOMERE LENGTH.

CARDIAC CONTRACTION
REPOLARISATION CAUSES PUMPING OF CA++ BACK TO S.R. LOST CA++ FROM TROPONIN BINDING SITES CAUSES INHIBITION OF ACTOMYOSIN ATPase BREAKING OF CROSS BRIDGES AND RELAXATION.

CONTRACTILITY
FACTORS RESPONSIBLE FOR CARDIAC PERFORMANCE WHEN LOADING FACTORS ARE KEPT CONSTANT. CONTRACTILITY DEFINES THE AMT OF WORK THE HEART DOES AT A GIVEN LOAD.

CONTRACTILITY
CONTRACTILITY IS NOT AN INCREASE IN THE FORCE OF CONTRACTION PER SE. STARLINGS LAW OF THE HEART STATES INCR PRELOAD LEADS TO INCR FORCE OF CONTRACTION.

CONTRACTILITY
INDEX OF CONTRACTION
PROPORTIONAL TO [CA2+]

dP/dT(max) isovolumetric contraction SYNONOMOUS WITH IONOTROPHY

PARAMETERS
MAX CO = 30-35 L/Min LVEDV = 140cc SV = 70cc EJECTION FRACTION
= SV/LVEDV = 50%

TERMINOLOGY
ELASTANCE = Stiffness
dP/dV

COMPLIANCE = Distensibility
dV/dP

? When to use elastance vs compliance

HEART ACTS AS A DEMAND PUMP

IF THERE IS NO CHANGE IN DEMAND FROM TISSUES FOR BLOOD, C.O. IS UNCHANGED INSPITE OF CHANGES TO HR AND SV. HR INCR 60 TO 120/Min = NO CHANGE IN CARDIAC OUTPUT.

VR=CO
DUE TO
HETEROMETRIC AUTOREGULATION
STARLINGS LAW OF THE HEART

HOMEOMETRIC AUTOREGULATION
TREPP EFFECT (BOWDITCH) ANREP EFFECT

FACTORS AFFECTING EDV

VENTRICULAR COMPLIANCE FACTORS AFFECTING VENOUS RETURN

Cardiac Asynchrony
Rt Atrial Systole before left. Left Ventric Systole before right. Rt Ventric ejects before left. In expiration
Aortic & Pulm valve close together.

In inspiration
Aortic valve closes before pulm.

HETEROMETRIC AUTOREGULATION
FRANK STARLING MECHANISM LENGTH TENSION RELATIONSHIP

Isovolumetric Contraction
In intact hearts, the equivalent of the lengthtension relationship is the pressure-volume relationship measured in isovolumetric contraction. The pressure developed is determined by LaPlaces Law.

Isovolumetric Contraction

Isovolumetric Contraction
The radius and not ventricular volume determines Pressure. Increasing ventricular EDV by 50% will increase radius by 14%. The sarcomere length will be reflected in a change in circumference. Because the Tension-length curve is steep, this small change in sarcomere length can result in a large change in tension.

Isovolumetric Contraction

HOMEOMETRIC AUTOREGULATION
INCR CONTRACTILITY DUE TO
HR (BOWDITCH EFFECT)

AORTIC PRESSURE (ANREP EFFECT)

PHASES OF SYSTOLE
ISOVOLUMETRIC CONTRACTION
VALVES CLOSED

ISOTONIC CONTRACTION
RAPID/SLOWER EJECTION PHASES

PROTODIASTOLE
NO EJECTION, CLOSING AORTIC VALVE

PHASES OF DIASTOLE
ISOVOLUMETRIC RELAXATION
VALVES CLOSED

FILLING PHASES
RAPID 60% SLOWER 10%

ATRIAL SYSTOLE
30%

WIGGERS DIAGRAM
AGE DIFFERENCES
dP/dT in isovol contn is decr in elderly decr HR with incr vagal tone in elderly peak pressure is higher in ventricle and aorta in elderly pressure wave velocity is higher in elderly

CARDIAC VS SKELETAL MUSCLE

CARDIAC SKELETAL RESTING TENSION TETANY GENERATION T TUBULAR SYSTEM ++++ NO +++ NIL EASY TO GENERATE +

CARDIAC VS SKELETAL MUSCLE

CARDIAC SKELETAL SARCOPLASMIC RETICULUM MITOCHONDRIA COLLAGEN + ++++ +++ ++++ ++ +

CARDIAC VS SKELETAL MUSCLE

CARDIAC FIBRE ARRANGEMENT CAPILLARY DENSITY ORGAN RESISTANCE COMPLEX 2000 PER MM3 0.2 PRU SKELETAL SIMPLE 300 PER MM3 16-24 PRU

CARDIAC VS SKELETAL MUSCLE

CARDIAC FIBRE BRANCHING TRANSITION TIME FROM RELAXED TO FULL TENSION MUCH SKELETAL NIL

SLOW

FAST

SMOOTH MUSCLE CONTRACTION

CONTRACTION LINKED TO CA2+ ENTERING CELL DUE TO
NERVE STIMULATION HORMONAL STIMULATION FIBRE STRETCH CHEMICAL CHANGES IN CELL

SMOOTH MUSCLE CONTRACTION

4 CA2+ BINDS INTRACELLULARLY WITH 1 CALMODULIN. CA- CALMODULIN COMPLEX BINDS WITH AND ACTIVATES MYOSIN KINASE, A PHOSPHORYLATING ENZYME. PHOSPHORYLATION OF MYOSIN HEAD CAUSES CONTRACTION.

SMOOTH MUSCLE CONTRACTION

Onset and duration of contraction is determined by the [myosin kinase]

SMOOTH MUSCLE CONTRACTION

SMOOTH MUSCLE HAS THE ABILITY TO MAINTAIN FORCE OF CONTRACTION IN SPITE OF ANY STRETCH OR SHORTENING.

SMOOTH MUSCLE RELAXATION

RELAXATION OCCURS WITH REVERSAL OF THE CONTRACTILE PROCESSES EXCEPT THAT THE ENZYME MYOSIN PHOSPHATASE IS NEEDED TO SPLIT PHOSPHATE FROM THE MYOSIN HEAD. SPEED OF RELAXATION IS PROPORTIONAL TO [MYOSIN PHOSPHATASE]

CVS REGULATORY MECHANISMS

WHY REGULATE C.O. ?
Differing metabolic rate of organs Differing temperatures Differing I.V.V.

CVS REGULATORY MECHANISMS

HOW TO REGULATE C.O. ?
Neural, humoral and local mechanisms. Mechanisms alter SV, vessel calibre and venous capacitance.

Factors which Increase H.R.

Bainbridge Reflex Pain Noradrenalin Decreased Baroreceptor Activity Inspiration Hypoxia Thyroxin

Baroreceptor Reflex

Baroreceptor Reflex

Factors which Decrease H.R.

Incr Baroreceptor Activity Expiration Fear Incr ICP (Cushings reflex) Vagal Stimuli Grief

Factors which Increase C.O.

An iety Eating E citement E erci e

Increa ed temperature Pregnancy Adrenalin Hi tamine

Factors which Decrease C.O.

Sitting/standing up Rapid Arrhythmias Heart Disease

Cardiovascular Physiology
Factors which increase HR tend to increase BP

EXCEPT
Bainbridge Reflex Cushings Reflex

FACTORS AFFECTING MYOCARDIAL O USE

2

Ventricular Wall Tension Contractility Heart Rate Basal O2 Consumption External Work performed Energy for electrical activation

VO

= 9ccO2/100G/MIN

FACTORS AFFECTING MYOCARDIAL O DELIVERY

2

[02] IN BLOOD CORONARY BLOOD FLOW

PERFUSION PRESSURE CALIBRE OF VESSELS DURATION OF FLOW

[O2] IN BLOOD
HAEMOGLOBIN LEVEL g/L SATURATION [O2] IN HAEMOGLOBIN =1.34 cc/g [O2] IN SERUM
PAO2 O2 SOLUBILITY IN SERUM =0.003cc/100cc serum/mmHg

CARDIAC OUTPUT
Measurement
Quantitate HR x SV (BP)/SVR

FICK PRINCIPLE

STEWART HAMILTON PRINCIPLE

CO = VO2/[A-V]O2

[ DYE MASS ] CO = ---------------------INTEGRAL C.dt

Cardiac Output

Cardiac Output

Cardiac Output

Cardiac Output

Cardiac Output

Intravascular Volume
Measurement
RISA Tagged RBCs

=0.08% Body Weight

Intravascular Volume
Heart Lungs Veins Arteries Capillaries 12% 18% 54% 11% 5%

COMPARTMENT EXPANSION PER LITRE OF ADMINISTERED FLUID

FLUID NORMAL SALINE 5% DEXTROSE IVV 250cc 83cc INTERSTITIUM 750cc 250cc 500cc ICV 0cc 667cc 333cc

N/2 + 167cc DEXTROSE

COMPARTMENT EXPANSION PER LITRE OF ADMINISTERED FLUID

FLUID COLLOID 3% SALINE IVV 1000cc 600cc INTERSTITIUM 0cc 1900cc ICV 0cc -1500cc

Intravascular Volume Depletion

Death if :
I.V.V. decr BY 10% WITHOUT BARORECEPTORS I.V.V. decr BY 40% WITH BARORECEPTORS Hb LEVEL < 20 g/L {I.V.V. IS MORE IMPORTANT THAN Hb}

CVS Response to 1 Litre loss of IVV

Vaso/Venoconstriction Incr HR Decr RBF Decr urine output Interstitial fluid transfer
MAX 1LITRE/HR

Starlings Forces

CVS Response to 1 Litre loss of IVV

Delayed Response
Incr plasma proteins in 2-3 days Incr erythropoietin with normal Hb in 4-8 weeks

DECREASED IVV
SENSORS
DECR [Na] DISTAL TUBULE DECR PRESSURE IN AFFERENT ARTERIOLS

RESPONSES
INCR SYMP N.S. RENIN RELEASE

CVS Response to 1L blood to normovolaemic person

Incr Incr Incr Incr IVV by 20% Mean BP by 15mmHg CVP by 7mmHg C.O. to 10-15L/Min

CVS Response to 1L blood given to normovolaemic patient

Incr Venous Pooling Capillary loss of fluid to ISF Baroreceptor Response

RAPID INFUSION 1L N/S

INCR IVV 250cc = 5%
NO OSMORECEPTOR STIM NO VOLUME RECEPTOR STIM (<8%)
NO ADH RELEASE

GLOMERULOTUBULAR IMBALANCE
DECR ONCOTIC PRESSURE INCR GFR, URINE FLOW

RENAL BODY FLUIDS MECHANISM

INCR BP, GFR, URINE FLOW

IVV OVERLOAD
INCREASED
IVV CVP WEDGE BLOOD PRESSURE

IVV OVERLOAD
RESPONSES
ATRIAL MONOCYTES SECRETE ANP
INCR Na, WATER LOSS INHIBIT RENIN, ALDOSTERONE, ADH

STIMULATE LOW PRESS RECEPTORS

INHIBIT ADH INCR HR, VASO/VENODILATION.

PURE WATER LOSS

DECR TBW AND INCR OSMOLALITY SENSED BY OSMORECEPTORS, LEADING TO INCR ADH (THIRST, INCR WATER REABSORPTION IN KIDNEY) PROCESS OF WATER RETURNING TO BODY CONTINUES UNTIL OSMOLARITY IS NORMAL.

THRESHOLDS
ADH SECn = 1% CHANGE IN OSMOL ADH SECn = 10% CHANGE IN IVV AS SENSED BY LOW PRESSURE VOLUME RECEPTORS

REGIONAL BLOOD FLOW

AUTOREGULATION
SITES
KIDNEY, MESENTRY, BRAIN, LIVER SKELETAL MUSCLE, MYOCARDIUM

THEORIES
MYOGENIC METABOLIC

REGIONAL BLOOD FLOW

NEUROGENIC REGULATION
ALL BLOOD VESSELS HAVE SYMP INNERVATION EXCEPT CAPILLARIES AND VENULES.

CHOLINERGIC SYMP VASODILATOR FIBRES IN

SK MUSCLE, LUNGS, KIDNEY, UTERUS

REGIONAL BLOOD FLOW

% CARDIAC OUTPUT 15 5 25 25 % BODY WEIGHT 2 0.5 0.5 2

BRAIN HEART KIDNEY LIVER

REGIONAL BLOOD FLOW

% CARDIAC OUTPUT 5 15 5 5 % BODY WEIGHT 22 42 15 16

SKIN SK MUSCLE BONE OTHER

REGIONAL BLOOD FLOW

ORGANS EXTRAVASC COMPRES AUTOREGULAT MAJOR AUTONOMIC STIM SYMP WEAK NO P/SYM AV SYMP ART SYMP BETA ADR NOTES RECEPT ALPHA BETA COLLATS 27cc/min TEMP REGULN INCR X20 EXERCISE COLLATS MONROE KELLY

HEART

YES

SKIN SK. MUSCLE BRAIN

AV=NIL ART=MIN

YES

INCR CHOL/SYM WITH INCR EXERCISE BASAL MAJOR WEAK SYM/PSYM

REGIONAL BLOOD FLOW

ORGANS EXTRAVASC COMPRES AUTOREGULAT AUTONOMIC STIM WEAK SYMP SYMP SIGNFIC SYMP SIGNFIC NIL ALPHA BETA ADR RECEPT NOTES

LUNG RENAL SPLANC

YES NIL ALVEOLI X MAJOR

HYPOXIC VASOCONSTN

NO COLLATS VASODILAT WITH INGESTION

YES SPLEEN X

MINOR

LIVER

PORT=NO HEPATIC= MINOR

REGIONAL BLOOD FLOW

PHYSICAL FACTORS AFFECTING FLOW INCLUDE
MEAN BLOOD PRESSURE BLOOD VISCOSITY REGIONAL VESSEL CALIBRE

REGULATION OF PERIPHERAL VASCULATURE

NEURAL REGULATORY MECHANISMS CIRCULATING VASOCONSTRICTORS CIRCULATING VASODILATORS ENDOTHELIAL EFFECTS

REGULATION OF PERIPHERAL VASCULATURE

CIRCULATING VASOCONSTRICTORS
ADH NAD ADR ANGIOTENSIN

REGULATION OF PERIPHERAL VASCULATURE

CIRCULATING VASODILATORS
ATRIAL NATURETIC PROTEIN 28AA VIP BRADYKININ 9AA KALIDIN 10AA

REGULATION OF PERIPHERAL VASCULATURE

ENDOTHELIAL EFFECTS
VASOCONSTRICTOR
ENDOTHELIN

VASODILATOR
EDRF (NITRIC OXIDE)
BRADYKININ, VIP, SUBST P, ACh, PLATELET BYPRODUCTS

VIA HISTAMINE RECEPTORS

2

HISTAMINE, ANP, ADENOSINE

ADRENERGIC RECEPTORS
Alpha
SMOOTH MUSCLE CONTRACTION INTESTINAL SPHINCTERS, MYDRIASIS, ERECTOR PILI, BILIARY TRACT, UTERUS VAS DEFERENS, VASOCONSTRICTION EXCEPT IN HEART/BRAIN/SK MUSCLE. INHIBITION OF INSULIN RELEASE

ADRENERGIC RECEPTORS
beta1
HEART
CHRONOTROPHIC IONOTROPHIC

ADIPOCYTES
INCREASES LIPOLYSIS

ADRENERGIC RECEPTORS
beta2
RELAXATION
VASODILATOR
BRONCHUS, UTERUS, INTESTINE

METABOLIC
GLYCOGENOLYSIS INSULIN RELEASE

TREMOR
SKELETAL MUSCLE

 CIRCULATING CATECHOLAMINES
INCR NAD > INCR ADR
PHYSICAL EXERCISE POSTURAL CHANGE

INCR ADR > INCR NAD

HYPOGLYCAEMIA CAFFEINE PSYCHOLOGICAL STRESS

Blood Pressure
Defn: PRESSURE IN VARIOUS VASCULAR CHAMBERS. Measurement Methods
Direct: Strain gauge resistors Indirect:
Auscultation Palpation Oscillotonometry Doppler

VENOUS RETURN & THE VASCULAR FUNCTION CURVE

Factors Affecting Venous Return

Cardiac Muscle Pump (vis a tergo) Skeletal Muscle Pump Thoracic Pump Intrapericardial Pressure Venous Tone Atrial Kick Posture Blood Volume

EXERCISE & CVS

Exercise
At Rest VO2 cc Lactate mg/100cc RR TV Min Vent (L) 250 12 350 4.5 Average 2500 4-8 30 2000 50 Maximum 5000 16-19 60 2200 120

Exercise
At Rest HR SV CO 70 60 4 Average 120 90 10 160 +0.5 Maximum 200 150 35 180 +2

Systolic BP 120 Temp Co -

Temperature Regulation
Inputs

SKIN HYPOTHALAMUS SPINAL CORD DEEP ABDOMINAL, THORACIC STRUCTURES OTHER PARTS OF BRAIN

TEMPERATURE REGULATION
HOT/COLD RECEPTORS TRANSMIT VIA Adelta AND C FIBRES TO THE HYPOTHALAMUS. THE RESPONSE TO WARMTH IS
SWEATING, VASODILATION, BEHAVIOUR CHANGE.

THE RESPONSE TO COLD IS

SHIVERING, THERMOGENESIS, VASOCONSTRICTION, BEHAVIOUR CHANGE

CVS Response to Standing

Incr Incr Incr Incr Vasoconstriction Venoconstriction Heart Rate Contractility

VALSALVA MANEOUVRE

VALSALVA MANEOUVRE
DESCRIBED 1704 1851 IMPERCEPTIBLE PULSE 4 PHASES
INCR MEAN BP DECR BP, INCR HR RELEASE OF STRAIN
DECR VR TO LEFT HEART, CO, BP

VR TO LEFT HEART NORMAL

OVERSHOOT OF BP WITH VASOCONSTn

PHYSIOLOGY OF EXTERNAL CARDIAC COMPRESSION

MEASUREMENT OF CEREBRAL BLOOD FLOW

KETTY SCHMIDT TECHNIQUE

CEREBRAL AUTOREGULATION
ABILITY OF THE BRAIN TO BALANCE BLOOD FLOW WITH METABOLIC RATE IN SPITE OF FLUCTUATIONS IN PERFUSION PRESURE

CEREBRAL AUTOREGULATION
FAILS IF
PERFUSION PRESSURE > 160mmHg PERFUSION PRESSURE < 60mmHg HEAD INJURY OCCURS PROLONGED ELEVATION OF ICP>30mmHg

Cerebral Compliance Curve

MONROE KELLIE DOCTRINE

HEPATIC BLOOD FLOW

TOTAL 1500cc / MIN HEPATIC ARTERY 300-500cc/MIN MEAN BP 90mmHg (40% OXYGEN SUPPLY) PORTAL VEIN 1000-1200cc/MIN MEAN BP 10mmHg (60% OXYGEN SUPPLY)

HEPATIC BLOOD FLOW

OXYGEN CONSUMPTION
50cc / MIN 20% OF TOTAL BODY USAGE SAME AS BRAIN USAGE

HEPATIC BLOOD FLOW

MEASUREMENT
CLEARANCE OF INDOCYANINE GREEN NO ENTEROHEPATIC CIRCULATION ESTABLISH CONSTANT INFUSION HBF= INFUSION RATE/{[HA]-[HV]} FICK PRINCIPAL

RENAL TERMINOLOGY
GLOMERULOTUBULAR BALANCE FILTRATION FRACTION RENAL CLEARANCE COUNTER CURRENT MECHANISM OSMOLAR CLEARANCE FREE WATER CLEARANCE

GLOMERULOTUBULAR BALANCE
ONCOTIC PRESSURE MEDIATION OF INAPPROPRIATE FLUCTUATIONS IN GFR THUS MAINTAINING A CONSTANT FILTRATION FRACTION.

TUBULOGLOMERULAR BALANCE
ANGIOTENSIN MEDIATED FLUCTUATION IN ARTERIOLAR CALIBRE TO AMELIORATE FLUCTUATIONS IN DT [WATER,NA], RESULTING IN GFR/FILTRATION FRACTION CHANGE. THEREFORE, TUBULAR REGULATION OF GFR IN THE PRESENCE OF CHANGES TO MAP.

RENAL BLOOD FLOW

25% C.O. 3cc/gm/min A-V diff 1-2vol% VO2 25% BASAL METABOLISM 75% Na + transport pump

RENAL BLOOD FLOW

DISTRIBUTION
CORTICAL FLOW CORTICO-MEDULLARY VASA RECTI AV SHUNTS 85% 10% 2% 3%

Symp Stimulation causes redistribution to juxtamedullary nephrons

RENAL BLOOD FLOW

Anatomy
RENAL ARTERY INTERLOBAR ARTERY ARCUATE ARTERY INTERLOBULAR ARTERY AFFERENT ARTERIOLE GLOMERULUS EFFERENT ARTERIOLE
VASA RECTI (JUXTAMEDULLARY) CORTICAL PERITUBULAR CAPILLARIES

RENAL BLOOD FLOW

SYMPATHETIC STIMULATION
REDISTRIBUTION OF FLOW CORTICAL TO MEDULLARY. IF INTENSE, DECR RBF, GFR

DOPAMINERGIC RECEPTORS
DILATATION

ANGIOTENSIN II
VASOCONSTRICTION

RENAL BLOOD FLOW

BRADYKININ
DILATATION

Pg E2
DILATATION

Autoregulation

RENAL BLOOD FLOW

MEASUREMENT
RBF = RPF (1 - PCV) -1 RPF = ( UX V ) / (RA X - RV X) PAH IS USED SINCE RV PAH = O

CORTICAL NEPHRONS
85 % OF NEPHRONS OUTER 2/3 OF KIDNEY SHORT LOOP ( NOT IN MEDULLA) SALT-LOSING FUNCTION

JUXTAMEDULLARY NEPHRONS
15 % OF GLOMERULI CORTICOMEDULLARY JUNCTION LONG LOOPS OF HENLE IN MEDULLA VASA RECTI CLOSE TO LOOPS FUNCTIONALLY HIGH GFR SALT/WATER RETAINING FEATURES

RENAL BLOOD FLOW

ITE DRO TATI RE RE ON OTI RE RE mm g

RENAL ARTER

mm g 90 ~ 60

25 25 30

AFFERENT ARTERIOLE LO ER LAR A ILLARIE

RENAL BLOOD FLOW

ITE DRO TATI RE RE ON OTI RE RE mm g

BOW AN A E EFFERENT ARTERIOLE ORTI AL INTER TITI

mm g 10 ~ 15

~ 35 ~

RENAL BLOOD FLOW

SITE

HYDROSTATIC ONCOTIC PRESSURE PRESSURE mmHg mmHg

PERITUBULAR CAPILLARIES

30

GFR
= FC {(PGC - PGB) - (PiGC - PiGB)}
FC = FILTRATION COEFFICIENT = 8-16 cc/min/m2 capillary area P = HYDROSTATIC PRESSURE Pi = ONCOTIC PRESSURE GC = GLOMERULAR CAPILLARY GB = GLOMERULAR BOWMANS SPACE

FACTORS AFFECTING GFR

FC
DISEASE AND STATE OF MEMBRANE AREA OF MEMBRANE

PRESSURE CHANCE
ARTERIAL PRESSURE CHANGE IN ARTERIOLE RESISTANCE

Pi
[PLASMA PROTEINS] RENAL PLASMA FLOW RATE

FLUID UPTAKE IN PERITUBULAR CAPILLARIES

180 LITRES PER DAY PROXIMAL CAPILLARY TUBULE UPTAKE IS PROPORTIONAL TO
LOW HYDROSTATIC PRESSURE IN PERITUBULAR CAPILLARIES (PTC) HIGH ONCOTIC PRESSURE IN PTC NaCl/Water FILTERED

FLUID UPTAKE IN PERITUBULAR CAPILLARIES

DISTAL CAPILLARY UPTAKE IS DETERMINED BY ADH LEVELS, DETERMINING WATER CONDUCTANCE IN THE DCT AND CD.

TRANSPORT MECHANISMS
CATIONS
ACTIVE MECHANISMS

ANIONS
PASSIVE MECHANISMS

WATER MAX 99% of FILTERED VOL REABSORBED WITH ADH. MIN 88%

TRANSPORT MECHANISMS
50% UREA REABSORBED NH3 PRODUCED IN PT, DT HCO3- REABSORBED IN PROPORTION TO H+ SECn

TRANSPORT MECHANISMS
ACTIVE REABSORPTION
Ca2+, Mg, Na+(8% DUE TO ALDOST)

PASSIVE REABSORPTION
Cl, HCO3,WATER (ADH DEPENDANE) ACTIVE SECRETION H+, K+, NH3

TRANSPORT MECHANISMS

WATER REABSORPTION
PT 75% LOOP OF HENLE 5% DT 15% ADH DEPENDANT CD 5% ADH DEPENDANT

TRANSPORT MECHANISMS

NACL REABSORPTION
PT 70% LOOP OF HENLE 22% DT 5% ALDOSTERONE DEPENDANT CD 3% ALDOSTERONE DEPENDANT

ELECTROLYTE CONCENTRATIONS
BOWMANS SPACE
[NA+] = 130mm/L WATER FLOW = 116cc/Min

PROXIMAL TUBULE
70% NA+ REABSORBED 75% WATER REABSORBED

ELECTROLYTE CONCENTRATIONS
LOOP OF HENLE
22% NA+ REABSORBED 5% WATER REABSORBED DESCENDING LIMB
HIGH GH2O LOW GNACL LOW GUREA

ASCENDING LIMB
NO GH2O HIGH GNACL NO GUREA

ELECTROLYTE CONCENTRATIONS DT,CD

GH2O ADH DEPENDANT NO GNACL CORTICAL SECMENT OF CD
NO GUREA

MEDULLARY SEGMENT OF CD
HIGH GUREA

ULTRAFILTRATE [] VS PLASMA
PA REAT I ULI UREA E D F L P F PT E LE 15 20 4 4 1.5 5 5 15 DT 50 10 10 35 D 585 140 125 50

ULTRAFILTRATE [] VS PLASMA
CLK+ Na+ HCO3 END OF LOOP OF PT HENLE 1 0.4 1 1 0.2 0.3 0.3 0.15 DT .075 1 0.5 0.1 CD 1 10 1 0.1

MAJOR DETERMINANT OF [Na+] ?

ADH ALDOSTERONE

MAJOR DETERMINANT OF [Na] ?

ALDOSTERONE
Na REABSORPTION D.T. ACTS ON 3% FILTERED NA+ TAKES 3-4DAYS TO AFFECT NA+ CONCENTRATION

MAJOR DETERMINANT OF [Na] ?

ADH
ACTS ON D.T. AFFECTING WATER CONDUCTANCE. 20% OF FILTERED WATER REACHES D.T. TAKES 3-4 HRS TO AFFECT NA+ CONCENTRATION

MAJOR DETERMINANT OF [Na] ?

ADH HAS GREATER INFLUENCE ON [NA] THAN ALDOSTERONE BECAUSE ADH REGULATES WATER MUCH FASTER.

MAJOR DETERMINANT OF [Na] ?

TOTAL BODY Na IS PROPORTIONAL TO ECV AND IS REGULATED BY ALDOSTERONE.