cardiovascular physiology. cardiovascular physiology lectures

CARDIOVASCULAR CARDIOVASCULAR PHYSIOLOGYPHYSIOLOGY

CARDIOVASCULAR PHYSIOLOGYCARDIOVASCULAR PHYSIOLOGYLECTURESLECTURES

INTRODUCTION TO INTRODUCTION TO CARDIOVASCULAR CARDIOVASCULAR

PHYSIOLOGYPHYSIOLOGY

GENERAL ASPECTS OF THE GENERAL ASPECTS OF THE CARDIOVASCULAR SYSTEMCARDIOVASCULAR SYSTEM

MAIN FUNCTIONS OF THE MAIN FUNCTIONS OF THE CIRCULATORY SYSTEMCIRCULATORY SYSTEM

Transport and distribute essential Transport and distribute essential substances to the tissues.substances to the tissues.

Remove metabolic byproducts.Remove metabolic byproducts.Adjustment of oxygen and nutrient Adjustment of oxygen and nutrient

supply in different physiologic states.supply in different physiologic states.Regulation of body temperature.Regulation of body temperature.Humoral communication.Humoral communication.

PUMP

DISTRIBUTING

TUBULESTHINVESSELS

COLLECTINGTUBULES

THE MAIN CIRCUIT

Pressure Profile of the Circulatory Pressure Profile of the Circulatory SystemSystem

ELASTIC TISSUE

MUSCLE

Distribution of Blood in the Distribution of Blood in the Circulatory SystemCirculatory System

Organization in the Circulatory SystemOrganization in the Circulatory System

SERIES AND

PARALLEL CIRCUITS

CARDIAC CARDIAC ELECTROPHYSIOLOGYELECTROPHYSIOLOGY

GENESIS OF THE MEMBRANE POTENTIAL GENESIS OF THE MEMBRANE POTENTIAL AND EQUATIONS TOAND EQUATIONS TO REMEMBER!!REMEMBER!!

EK = -60 LOG ([Ki]/[Ko]) = -94mv

ENa = -60 LOG ([Nai]/[Nao]) = +70mv

Em = RT/F ln

PK (K+)o + PNa(Na+)o + PCl(Cl-)i

PK (K+)I + PNa(Na+)i + PCl(Cl-)o

THE RESTING MEMBRANE POTENTIAL THE RESTING MEMBRANE POTENTIAL OF THE CARDIAC CELLOF THE CARDIAC CELL

If membrane permeableonly to K+

If membrane permeableTo both Na+ and K+

If membrane permeableTo Na+, K+ plus withA Na+/K+ Pump

WHY NOT Na+ 0R Ca++ FOR THE CARDIAC CELLMEMBRANE POTENTIAL ?

Na+

EXTRACELL.

INTRA-CELL. Em

145Mm 15Mm 70mv

Ca++ 3Mm 10-7 M 132mv

K+ 5Mm 145Mm -100mv

ACTION POTENTIALS FROM DIFFERENT ACTION POTENTIALS FROM DIFFERENT AREAS OF THE HEARTAREAS OF THE HEART

mv

0

-80mv

mv

0

-80mv

mv

0

-80mv

ATRIUM VENTRICLE

SA NODE

time

ELECTROPHYSIOLOGY OF THE FAST ELECTROPHYSIOLOGY OF THE FAST RESPONSE FIBERRESPONSE FIBER

PHASE 0 OF THE FAST FIBER ACTION PHASE 0 OF THE FAST FIBER ACTION POTENTIALPOTENTIAL

hm

Na+

-90mv

A

Na+

mmh

-65mvB

mh

Na+

0mvC m

h

Na+

D+20mv

Na+

mh+30mv

E

ChemicalGradient

ElectricalGradient

KK++ CURRENTS AND REPOLARIZATION CURRENTS AND REPOLARIZATION

PHASE 1-TRANSIENT OUTWARD PHASE 1-TRANSIENT OUTWARD CURRENT (TOC) ICURRENT (TOC) Itoto

PHASE 1-3-DELAYED RECTIFIER PHASE 1-3-DELAYED RECTIFIER CURRENT ICURRENT IKK

PHASE 1-4-INWARDLY RECTIFIED PHASE 1-4-INWARDLY RECTIFIED CURRENT ICURRENT IKlKl

THE PLATEAU PHASE AND CALCIUM THE PLATEAU PHASE AND CALCIUM IONSIONS

L Ca++ CHANNELSL Ca++ CHANNELS

T Ca++ CHANNELST Ca++ CHANNELS

OPEN

+10MV

-20MV

CLINICAL VALUE

Ca++ BLOCKERS

NO (physiological)

EFFECTS OF Ca++ CHANNEL BLOCKERS EFFECTS OF Ca++ CHANNEL BLOCKERS AND THE CARDIAC CELL ACTION POTENTIALAND THE CARDIAC CELL ACTION POTENTIAL

DILTIAZEM

10 uMol/L30 uMol/L10

30

10

FO

RC

EA

CT

ION

PO

TE

NT

IAL

TIME

CONTROL

CONTROL

30

Clinical CorrelationClinical CorrelationEarly After-DepolarizationsEarly After-Depolarizations

Early After-Depolarization

0mV

-60mV

-90mV

Torsades de Pointes

OVERVIEW OF SPECIFIC EVENTS IN THE OVERVIEW OF SPECIFIC EVENTS IN THE VENTRICULAR CELL ACTION POTENTIALVENTRICULAR CELL ACTION POTENTIAL

Overview of Important Channels in Cardiac Overview of Important Channels in Cardiac ElectrophysiologyElectrophysiology

Sodium Channels

     Fast Na+ Phase 0 depolarization of non-pacemaker cardiac action potentials

     Slow Na+ "Funny" pacemaker current (If) in cardiac nodal tissue

Potassium Channels

     Inward rectifier (Iir or IK1)

Maintains phase 4 negative potential in cardiac cells

     Transient outward (Ito)

Contributes to phase 1 of non-pacemaker cardiac action potentials

     Delayed rectifier (IKr)

Phase 3 repolarization of cardiac action potentials

More Channels!More Channels!

Calcium Channels

     L-type (ICa-L)

Slow inward, long-lasting current; phase 2 non-pacemaker cardiac action potentials and phases 4 and 0 of SA and AV nodal cells; important in vascular smooth muscle contraction

     T-type (ICa-T)

Transient current that contributes to phase 4 pacemaker currents in SA and AV nodal cells

ELECTROPHYSIOLOGY OF THE ELECTROPHYSIOLOGY OF THE SLOW RESPONSE FIBERSLOW RESPONSE FIBER

RECALL: INWARD Ca++ CURRENT CAUSES DEPOLARIZATION

0

-80

-400

2

34

ERP RRP

time (msec)

mvs

CONDUCTION OF THE ACTION CONDUCTION OF THE ACTION POTENTIAL IN CARDIAC FIBERSPOTENTIAL IN CARDIAC FIBERS

---

----- - ----- --+ +

+ + + + + + ++ + + ++ +

FIBER A FIBER B

DEPOLARIZEDZONE

POLARIZED ZONE

LOCAL CURRENTS

CONDUCTION OF THE ACTION CONDUCTION OF THE ACTION POTENTIALPOTENTIAL

FAST RESPONSE: Depends on FAST RESPONSE: Depends on Amplitude,Rate of Change,level of Amplitude,Rate of Change,level of Em.Em.

SLOW RESPONSE: Slower SLOW RESPONSE: Slower conduction.More apt to conduction conduction.More apt to conduction blocks.blocks.

WHAT ABOUT MYOCARDIAL WHAT ABOUT MYOCARDIAL INFARCTS AND CONDUCTION?INFARCTS AND CONDUCTION?

EFFECTS OF HIGH K+ ON CONDUCTION EFFECTS OF HIGH K+ ON CONDUCTION AND AP OF FAST FIBERSAND AP OF FAST FIBERS

WHAT HAS VARIED? LOOK AT: Em,AP SLOPE-AMPLITUDE

0MV

0MV

K+=3mM K+=7mM K+=14mM

K+=16mM

K+=3mM

Em

AP

-AM

P

HIGH K+ AND m/h Na+ GATESHIGH K+ AND m/h Na+ GATES

HIGH K+LOWEREm

CLOSED h GATES(SOME)

LOWER Na+ ENTRYLOWER APAMPLITUDE

EXCITABILITY OF FAST AND SLOW EXCITABILITY OF FAST AND SLOW FIBERSFIBERS

FAST m/h GATES COMPLETE RESET AFTERPHASE 3CONSTANT AND COMPLETE RESPONSE IN PHASE 4

SLOW LONG RELATIVE REFRACTORYPERIOD.POST-REPOLARIZATION REFRACTORINESS

AFTER THE EFFECTIVE OR ABSOLUTE AFTER THE EFFECTIVE OR ABSOLUTE REFRACTORY PERIOD (FAST FIBER)REFRACTORY PERIOD (FAST FIBER)

TIME

MV

-80

0

RRP

ARP

POST-REPOLARIZATION POST-REPOLARIZATION REFRACTORINESS (SLOW FIBER)REFRACTORINESS (SLOW FIBER)

A

B

C

MV

TIME

-60

0

200 MSEC

POSTREPO

AUTOMATICITY RHYTMICITY

SA NODE

AV NODE

IDIOVENTRICULAR-PACEMAKERS

ectopicfoci

THE SA NODE PACEMAKER POTENTIALTHE SA NODE PACEMAKER POTENTIAL

CHARACTERISTICS OF THE CHARACTERISTICS OF THE PACEMAKER POTENTIALPACEMAKER POTENTIAL

RECALL: PHASE 4-PACEMAKER POTENTIAL(PP) OBSERVED HERE. FREQUENCY DEPENDS ON: THRESHOLD,RESTING POTENTIALS AND SLOPE OF THE PP

CAUSES OF THE PACEMAKER CAUSES OF THE PACEMAKER POTENTIALPOTENTIAL

OUT

IN

Na+

if

Ca++

iCaK+

iK

THE PACEMAKER POTENTIAL THE PACEMAKER POTENTIAL CURRENTS AFTER DEPOLARIZATIONCURRENTS AFTER DEPOLARIZATION

if iCa

iKWHICH CURRENT WILL BE MORE AFFECTED BYADRENERGIC STIMULATION? WHICH BY CHOLINERGICSTIMULATION?

LOOKING AT THE PACEMAKER LOOKING AT THE PACEMAKER CURRENTSCURRENTS

voltage

ionic currentsiCa

iK

if

EFFECTS OF Ca++ CHANNEL BLOCKERS EFFECTS OF Ca++ CHANNEL BLOCKERS ON THE PACEMAKER POTENTIALON THE PACEMAKER POTENTIAL

CONTROL NIFEDIPINE

(5.6 X 10-7 M)0

-60

MV

TIME

OVERDRIVE SUPRESSION AND OVERDRIVE SUPRESSION AND AUTOMATICITY OF PACEMAKER CELLSAUTOMATICITY OF PACEMAKER CELLS

Na+/K+ ATPase ENHANCEMENT Na+/K+ ATPase ENHANCEMENT BY HIGH FREQUENCY.BY HIGH FREQUENCY.

CONSEQUENT CONSEQUENT HYPERPOLARIZATION.HYPERPOLARIZATION.

SUPRESSION OF AUTOMATICITY.SUPRESSION OF AUTOMATICITY.RECOVERY TIME REQUIRED.RECOVERY TIME REQUIRED.ECTOPIC FOCI/SICK SINUS ECTOPIC FOCI/SICK SINUS

SYNDROME.SYNDROME.

THE CONDUCTION SYSTEM OF THE THE CONDUCTION SYSTEM OF THE HEARTHEART

ATRIAL AND ATRIOVENTRICULAR ATRIAL AND ATRIOVENTRICULAR CONDUCTIONCONDUCTION

RA LA

RV LV

SANBACHMANS PATH

INTERNODAL PATHS AN REGION

N REGION

NH REGION

BH

LEFT BUNDLEBRANCH

RIGHT BUNDLE BRANCH

AV NODE

NODAL DELAYNODAL DELAY

REGION OFDELAY

AV NODE

NA REGIONFAST CONDUCTION

N REGION SLOW CONDUCTION

NH REGIONFAST CONDUCTION

LONGER PATH

SHORTER PATH

REFLECTED IN THE P-QRS INTERVALOF THE ECG

UNI AND BIDIRECTIONAL BLOCKUNI AND BIDIRECTIONAL BLOCKCLINICAL IMPLICATIONSCLINICAL IMPLICATIONS

NORMALANTEGRADEBLOCK

BI

REENTRYUNIDIRECTIONALBLOCK

A B

C D

Clinical CorrelationClinical CorrelationRe-entry TachycardiasRe-entry Tachycardias

Paroxysmal Supraventricular TachycardiaParoxysmal Supraventricular Tachycardia

Normal Conduction

Slow Pathway

Fast Pathway

Ischemic Tissue

Fast Pathway

Slow Pathway

Re-Entry Circuit

AV NODE AND AV BLOCKSAV NODE AND AV BLOCKS

FOCUS ON N REGION

NORMAL ECG

1ST DEGREE

PROLONGUED AVCONDUCTION TIME

2ND DEGREE

1/2 ATRIAL IMPULSES CONDUCTED TO VENTRICLES

3RD DEGREE

VAGAL MEDIATIONIN N REGION/COMPLETEBLOCK

CONDUCTION IN THE VENTRICLESCONDUCTION IN THE VENTRICLES

PURKINJE FIBERS WITH LONG PURKINJE FIBERS WITH LONG REFRACTORY PERIODS.REFRACTORY PERIODS.

PROTECTION AGAINST PREMATURE PROTECTION AGAINST PREMATURE ATRIAL DEPOLARIZATIONS AT SLOW ATRIAL DEPOLARIZATIONS AT SLOW HEART RATES.HEART RATES.

AV NODE PROTECS AT HIGH HEART AV NODE PROTECS AT HIGH HEART RATES.RATES.

QUICK QUIZQUICK QUIZWhich of the following is not true about the effect ofacetylcholine (Ach) in the electrophysiology of the cardiac pacemaker cell:A. Ach lowers the magnitude of the minimum repolarization potential.B. Ach lowers the slope of the pacemaker potential.C. Ach decreases the SA node frequency.D.Ach increases the ik current of the pacemaker cell.E. Ach decreases the iCa++ current of the pacemaker cell.

The main reason why the AV node filters out high stimulation frequencies from the SA node is:A. The long pathway that the stimulus must traverse in the AV node.B. Post Repolarization Refractoriness of AV nodal cells.C. The AV nodal cell is always hyperpolarizedD. Ca++ is the main ion in Phase 0 of the AV nodal cell.E. I need to review this section very fast.

CARDIAC CARDIAC MECHANICSMECHANICS

MAIN THEMESMAIN THEMES

THE HEART AS A PUMPTHE HEART AS A PUMP

THE CARDIAC CYCLETHE CARDIAC CYCLE

CARDIAC OUTPUTCARDIAC OUTPUT

LENGHT/ TENSION AND THE FRANK-LENGHT/ TENSION AND THE FRANK-STARLING RELATIONSTARLING RELATION

LE

FT

VE

NT

RIC

UL

AR

PR

ES

SU

RE

INITIAL MYOCARDIAL FIBER LENGHTLEFT VENTRICULAR END-DIASTOLIC VOLUME

PRELOAD AND AFTERLOAD IN THE PRELOAD AND AFTERLOAD IN THE HEARTHEART

INCREASE IN FILLING INCREASE IN FILLING PRESSURE=INCREASED PRELOADPRESSURE=INCREASED PRELOAD

PRELOAD REFERS TO END PRELOAD REFERS TO END DIASTOLIC VOLUME.DIASTOLIC VOLUME.

AFTERLOAD IS THE AORTIC AFTERLOAD IS THE AORTIC PRESSURE DURING THE EJECTION PRESSURE DURING THE EJECTION PERIOD/AORTIC VALVE OPENINGPERIOD/AORTIC VALVE OPENING..

LAPLACES’S LAW & WALL STRESS, LAPLACES’S LAW & WALL STRESS, WS = P X R / 2(wall thickness)WS = P X R / 2(wall thickness)

LEFT VENTRICULAR PRESSURE AND LEFT VENTRICULAR PRESSURE AND AFTERLOAD AT CONSTANT PRELOADSAFTERLOAD AT CONSTANT PRELOADS

LE

FT

VE

NT

RIC

UL

AR

PR

ES

SU

RE

AFTERLOAD (aortic pressure)

NOTE: WHAT HAPPENS IN THE NORMAL HEART VS ONE IN THE LAST PHASES OF CARDIAC FAILURE?

PEAKISOMETRICFORCE

EFFECT OF INCREASEDPRELOAD

CONTRACTILITY:THE VENTRICULAR CONTRACTILITY:THE VENTRICULAR FUNCTION CURVEFUNCTION CURVE

CHANGES INCONTRACTILITY

EFFECT?

dP/dt AS A VALUABLE INDEX OF dP/dt AS A VALUABLE INDEX OF CONTRACTILITYCONTRACTILITY

LE

FT

VE

NT

RIC

UL

AR

P

RE

SS

UR

E (

mm

Hg) 120

40

TIME (s).2 .6

A

B

C

MAX dP/dt

CARDIAC CYCLECARDIAC CYCLE

Atr

ial S

ysto

le

Mitral Closes

Isov

olum

ic c

ontr

act.

Aortic opens

S1

Rap

id E

ject

ion

Red

uced

Eje

ctio

n

Isov

olum

ic R

elax

.

Aorticcloses

Rap

id V

entr

icul

arF

illi

ng

Mitralopens

S2

Red

uced

Ven

tric

ular

F

illi

ng Atr

ial S

ysto

le

QUICK QUIZQUICK QUIZHow to find out that you know the Cardiac Cycle.How to find out that you know the Cardiac Cycle.

150

50

LE

FT

VE

NT

RIC

UL

AR

VO

LU

ME

(M

L)

TIME (SEC)

Atrialsystole

Mitral closes

Aortic opens

Aortic closes Mitral

opens

Clinical CorrelationClinical CorrelationDiagnosis of Aortic Stenosis by Pressure GraphsDiagnosis of Aortic Stenosis by Pressure Graphs

Normal

Aorta

Ventricle

Aorta

Ventricle

Aortic Stenosis

LEFT VENTRICULAR LEFT VENTRICULAR PRESSURE/VOLUME P/V LOOPPRESSURE/VOLUME P/V LOOP

LE

FT

VE

NT

RIC

UL

AR

PR

ES

SU

RE

(m

mH

g)

LEFT VENTRICULAR VOLUME (ml)

A BC

D

EF

100 150500

120

40

80

END OF DIASTOLE

END OF SYSTOLE

EFFECT OF PRELOAD ON EFFECT OF PRELOAD ON THE VENTRICULAR P/V LOOPTHE VENTRICULAR P/V LOOP

VOLUME (ml)

LE

FT

VE

NT

RIC

UL

AR

PR

ES

SU

RE

(m

mH

g) ESV

1 2 3

EDVs

EFFECT OF AFTERLOAD IN EFFECT OF AFTERLOAD IN THE LEFT VENTRICULAR P/V THE LEFT VENTRICULAR P/V

LOOPLOOP

VOLUME (ml)

LE

FT

VE

NT

RIC

UL

AR

PR

ES

SU

RE

(m

mH

g)

12

3

EDV

ESPVR

ESV

ESVESV

EFFECT OF CONTRACTILITY ON EFFECT OF CONTRACTILITY ON THE LV P/V LOOPTHE LV P/V LOOP

VOLUME (ml)

LE

FT

VE

NT

RIC

UL

AR

PR

ES

SU

RE

(m

mH

g)

12

ESPVR 2

ESPVR 1

QUICK QUIZQUICK QUIZ

PRELOAD AFTERLOAD CONTRACTILITY

CARDIAC OUTPUT AND THE FICK CARDIAC OUTPUT AND THE FICK PRINCIPLEPRINCIPLE

BODY O2 CONSUMPTION

250mlO2/min

PaO2

0.15mlO2/ml blood

PvO2

0.20mlO2/ml blood

PULMONARYARTERY

PULMONARYVEIN

CARDIAC OUTPUT=O2 CONSUMPTION (ml/min)

PvO2- PaO2

Pulmonary capillaries

Lungs

HEMODYNAMICSHEMODYNAMICS

VELOCITY,FLOW,PRESSUREVELOCITY,FLOW,PRESSURELAMINAR FLOWLAMINAR FLOWPOISEUILLE’S LAWPOISEUILLE’S LAWRESISTANCE(SERIES-PARALLEL)RESISTANCE(SERIES-PARALLEL)TURBULENT FLOW AND TURBULENT FLOW AND

REYNOLD’S NUMBERREYNOLD’S NUMBER

CHAPTER 5 B&L

REQUIRED CONCEPTSREQUIRED CONCEPTS

VELOCITY = DISTANCE / TIME V = D / T

FLOW = VOLUME / TIME Q = VL / T

VELOCITY -FLOW- AREA

V = Q / A

CROSS SECTIONAL AREA AND CROSS SECTIONAL AREA AND VELOCITYVELOCITY

Q=10ml/s

A= 2cm2 10cm2 1cm2

V= 5cm/s 1cm/s 10cm/s

V = Q / A

a b c

HYDROSTATIC PRESSUREHYDROSTATIC PRESSURE

136cm

0

0100

200

P = p x g x h

P = Pressure mmHgp = densityg = gravityh = height

0100

200

0

100mmHg

0100

200

0100

200

136cm

ENERGY OF A STATIC VS A DYNAMIC ENERGY OF A STATIC VS A DYNAMIC FLUIDFLUID

TOTAL ENERGY= POTENTIAL E. + KINETIC E. TE = PE + KE

FLUID AT REST (HYDROSTATIC )

FLUID IN MOTION (HYDROSTATIC + HYDRODYNAMIC)

VELOCITY AND PRESSUREVELOCITY AND PRESSURE

0

0100

200

POISEUILLE’S LAWPOISEUILLE’S LAW GOVERNING FLUID GOVERNING FLUID FLOW(Q) THROUGH CYLINDRIC TUBESFLOW(Q) THROUGH CYLINDRIC TUBES

(FLOW)Q(FLOW)Q = (Pi - Po) r

DIFFERENCEIN PRESSURE RADIUS

8nL

VISCOSITY

4

LENGHT

RESISTANCE TO FLOW IN THE RESISTANCE TO FLOW IN THE CARDIOVASCULAR SYSTEMCARDIOVASCULAR SYSTEM

BASIC CONCEPTS

Rt = R1 + R2 + R3…. SERIES RESISTANCE

1/Rt = 1/R1 + 1/R2 + 1/R3… PARALLEL RES.

WHAT REALLY HAPPENS IN THE CVS?

ARTERY

ARTERIOLES

CAPILLARIES

LOWER R HIGHER R LOWER R

SERIES PARALLELR1 R2 R3

R1

R3R2

LAMINAR VS TURBULENT FLOWLAMINAR VS TURBULENT FLOWTHE REYNOLD’S NUMBERTHE REYNOLD’S NUMBER

LAMINARFLOW

TURBULENTFLOW

Nr = pDv / n

p = densityD = diameterv = velocityn = viscosity

laminar = 2000 or less

QUICK QUIZZQUICK QUIZZ

1. Which of the following vessels will produce a dramatic decrease in blood flow through the tissues by a change in radius?

A. AortaB. VenulesC. ArteriolesD. Capillaries

3. After a bout with hemorrhagic Dengue you would expectto find a heart murmur at a lower level than before the disease.A. True B. False

PV Loop RefresherPV Loop Refresher

A

B A

B

What happens from A to B?

ARTERIAL SYSTEMARTERIAL SYSTEM

COMPLIANCECOMPLIANCEMEAN ARTERIAL PRESSUREMEAN ARTERIAL PRESSUREPULSE PRESSUREPULSE PRESSUREPRESSURE MEASUREMENTPRESSURE MEASUREMENT

THE CONCEPT OF THE HYDRAULIC THE CONCEPT OF THE HYDRAULIC FILTERFILTER

SYSTOLE DIASTOLE

COMPLIANT

RIGID

EFFECTS OF PUMPING THROUGH A EFFECTS OF PUMPING THROUGH A RIGID VS A COMPLIANT DUCTRIGID VS A COMPLIANT DUCT

O2

CO

NS

UM

PT

ION

(m

lO2/

100g

/bea

t)

0.1

0

STROKE VOLUME (ml)5 15

NATIVE AORTA

PLASTIC TUBING

STATIC P-V RELATIONSHIP IN THE STATIC P-V RELATIONSHIP IN THE AORTAAORTA

% I

NC

RE

AS

E I

N V

OL

UM

E

PRESSURE (mmHg)

ELASTIC MODULUS OR ELASTANCEELASTIC MODULUS OR ELASTANCE

Ep = P / Da/Db

Ep= ELASTIC MODULUS Da= MAX. CHANGE IN AORTIC DIAMETER. Db= MEAN AORTIC DIAM.

ELASTANCE COMPLIANCE

P V PV

EP IS INVERSELY PROPORTIONAL TO C

MEAN ARTERIAL PRESSURE (MAP)

CARDIAC OUTPUT PERIPHERAL RESISTANCE

REMEMBER OHMS LAW?

INSTANTANEOUSINCREASE

STEADY STATEINCREASE

EFFECT OF COMPLIANCE ON MAPEFFECT OF COMPLIANCE ON MAP

Pa = Qh - Qr / Ca

Qh- inflow (CO)Qr- outflowCa- CompliancePa- MAP

AR

TE

RIA

L P

RE

SS

UR

E (

mm

Hg)

TIME

SMALL Ca

LARGE Ca

INCREASE CARDIAC OUTPUT

PULSE PRESSURE

STROKE VOLUME COMPLIANCE

V4

VB

V3

V2

VA

V1

P1 PA P2 PP33 PB P4

VOLUME

PRESSURE

PULSE PRESSUREEFFECTS OF:

COMPLIANCE TOTAL PERIPHERAL RESISTANCE

TPR

A B

VASCULAR FUNCTION CURVE

HOW CARDIAC OUTPUT REGULATESCENTRAL VENOUS PRESSURE

CARDIAC FUNCTION CURVE

HOW CENTRAL VENOUS PRESSURE (PRELOAD)REGULATES CARDIAC OUTPUT

COUPLING OF THE HEART AND BLOOD VESSELS

CHAPTER 9 B&L

VASCULAR FUNCTION CURVEHOW CHANGES IN CARDIAC OUTPUT INDUCECHANGES IN CENTRAL VENOUS PRESSURE?

CE

NT

RA

L V

EN

OU

R P

RE

SS

UR

E (

mm

Hg)

-1

8

CARDIAC OUTPUT (L/min)

0 8

VASCULAR FUNCTIONCURVE

Pmc

B

A

HOW BLOOD VOLUME AND VENOMOTOR TONE CHANGE THE VASCULAR FUNCTIONCURVE?

CE

NT

RA

L V

EN

OU

R P

RE

SS

UR

E (

mm

Hg)

-10 8

VASCULAR FUNCTIONCURVE

CARDIAC OUTPUT (L/min)

TRANSFUSION

NORMAL

HEMORRHAGE

8

TOTAL PERIPHERAL RESISTANCEAND THE VASCULAR FUNCTION CURVE.

CE

NT

RA

L V

EN

OU

R P

RE

SS

UR

E (

mm

Hg)

-1

8

0 8

VASCULAR FUNCTIONCURVE

CARDIAC OUTPUT (L/min)

NORMAL

VASODILATION

VA

SOCO

NSTRICTIO

N

THE CARDIAC FUNCTION CURVE

CENTRAL VENOUS PRESSURE (mmHg)

CA

RD

IAC

OU

TP

UT

(L

/min

)

EFFECTS OF SYMPATHETIC STIMULATIONON THE CARDIAC FUNCTION CURVE

CA

RD

IAC

OU

TP

UT

(L

/min

)

CENTRAL VENOUS PRESSURE (mmHg)

HOW BLOOD VOLUME AND PERIPHERALRESISTANCE CHANGE THE CARDIAC FUNCTION CURVE?

CA

RD

IAC

OU

TP

UT

(L

/min

)

CENTRAL VENOUS PRESSURE (mmHg)

VOLUME RESISTANCE

THE CARDIAC FUNCTION CURVE IN HEART FAILURE

CENTRAL VENOUS PRESSURE (mmHg)

CA

RD

IAC

OU

TP

UT

(L

/min

)

HEART - BLOOD VESSELSHEART - BLOOD VESSELSCOUPLINGCOUPLING

PUMP ARTERIESVEINS

Qh 5L/min

Qr5L/min

PERIPHERAL R= Pa - Pv / Qr

R = 20mmHg/L/min

MPA=102mmHgCPV=2mmHg=Pv

COMPLIANCESCv = 19CaCv>>>>Ca

MORMAL FUNCTION

Pa

CARDIAC ARREST!CARDIAC ARREST!INMEDIATE EFFECTINMEDIATE EFFECT

PUMP ARTERIESVEINS

Qh 0L/min

Qr5L/min

CPV=2mmHg=Pv

Pa

FLOW STOPS HERE

FLOW CONTINUES HRETRANSFER ART-->VEINS

R = 20mmHg/L/minQr= Pa - Pv/20

Qr CONTINUES AS LONG ASA PRESSURE GRADIENT IS SUSTAINED

CARDIAC ARRESTCARDIAC ARRESTSTEADY STATESTEADY STATE

PUMP ARTERIESVEINS

Qh 0L/min

Qr0L/min

Pv = 7mmHg = MEAN CIRCULATORY PRESSURE OR Pmc

Pa = 7mmHg

FLOW STOPPED

FLOW STOPPED

Qr = 0 ( NO Pa - Pv DIFFERENCE)

95mmHg

5mmHg

WE START PUMPING!WE START PUMPING!INMEDIATE EFFECTINMEDIATE EFFECT

PUMP ARTERIESVEINS

Qh 1L/min

Qr0L/min

Pv = 7mmHg

Pa = 7mmHg

FLOW STARTS

NO FLOW HERE YET

SOME VENOUS BLOOD

FLOW RETURNS AT Qr AT THE NEW FLOW RETURNS AT Qr AT THE NEW QhQh

PUMP ARTERIESVEINS

Qh 1L/min

Qr1L/min

Pv = 6mmHg

Pa = 26mmHg

FLOW STARTS

R = 20mmHg

Qr = Pa - Pv / 20 = 1L/min