Cardiovascular Physiology

CARDIOVASCULAR PHYSIOLOGY

Dr. Poland

Room 3-007, Sanger Hall

Phone: 828-9557

E-mail: [email protected]

CARDIOVASCULAR SYSTEM

HEART(PUMP)

VESSELS(DISTRIBUTION SYSTEM)

RE

GU

LA

TIO

N

AUTOREGULATION

NEURAL

HORMONAL

RENAL-BODY FLUIDCONTROL SYSTEM

PULMONARYCIRCULATION

1. LOW RESISTANCE2. LOW PRESSURE

(25/10 mmHg)

SYSTEMICCIRCULATION

1. HIGH RESISTANCE2. HIGH PRESSURE

(120/80 mmHg)

PARALLELSUBCIRCUITS

UNIDIRECTIONALFLOW

VEINS

CAPACITYVESSELS

HEART

80 mmHg 120 mmHg

SYSTOLE

DIASTOLE

ARTERIES (LOW COMPLIANCE)

CAPILLARIES

THE SYSTEMIC CIRCULATION

CAPACITY VESSELS

NORMAL

Na+

K+Na+

K+

-70 mV

RESTING

THRESHOLD

-0

Graduallyincreasing PNa

AUTOMATICITY

PURKINJE FIBERS

BUNDLEBRANCHES

Sino-atrial(SA) node

Atrio-ventricular (AV) node

INTERCALATED DISC (TIGHT JUNCTION)

PACEMAKERS (in order of their inherent rhythm)

• Sino-atrial (SA) node

• Atrio-ventricular (AV) node

• Bundle of His

• Bundle branches

• Purkinje fibers

ME

MB

RA

NE

PO

TE

NT

IAL

(m

V)

-90

0

0

12

3

4

TIME

PHASE0 = Rapid Depolarization (inward Na+ current) 1 = Overshoot2 = Plateau (inward Ca++ current)

3 = Repolarization (outward K+ current)4 = Resting Potential

Mechanical Response

ME

MB

RA

NE

PO

TE

NT

IAL

(m

V)

0 0

-50 -50

-100 -100

SANVENTRICULULARCELL

ACTION POTENTIALS

0

12

3

4

4

0 3

SINGLE VENTRICULAR ACTION POTENTIAL

ECGP

Q S

T

R

1 mV

Repolarization of ventriclesDepolarization of ventricles

Depolarization of atria

ENDOCARDIAL FIBER

EPICARDIAL FIBER

ATRIALFIBER

LARA

LL

ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)

3 Bipolar Limb Leads:

I = RA vs. LA (+)

LARA

LL



I = RA vs. LA (+)

II = RA vs. LL (+)

LARA

LL



I = RA vs. LA (+)

II = RA vs. LL (+)

III = LA vs. LL (+)

LARA

LL



I = RA vs. LA (+)

II = RA vs. LL (+)

III = LA vs. LL (+)

3 Augmented Limb Leads:

aVR = (LA-LL) vs. RA(+)

LARA

LL



I = RA vs. LA (+)

II = RA vs. LL (+)

III = LA vs. LL (+)



aVL = (RA-LL) vs. LA(+)

LARA

LL



I = RA vs. LA (+)

II = RA vs. LL (+)

III = LA vs. LL (+)



aVL = (RA-LL) vs. LA(+)

aVF = (RA-LA) vs. LL(+)

V1 V2V3

V4

V5

V6

6 PRECORDIAL (CHEST) LEADS

Spine

Sternum

ECG Recordings: (QRS vector---leftward, inferiorly and posteriorly

3 Bipolar Limb Leads I = RA vs. LA(+) II = RA vs. LL(+) III = LA vs. LL(+)3 Augmented Limb Leads aVR = (LA-LL) vs. RA(+) aVL = (RA-LL) vs. LA(+) aVF = (RA-LA) vs. LL(+)

6 Precordial (Chest) Leads: Indifferent electrode (RA-LA-LL) vs.chest lead moved from position V1 through position V6.

LATE DIASTOLE

ATRIALSYSTOLE

ISOMETRIC VENTRICULARCONTRACTION

VENTRICULAR EJECTION

ISOMETRICVENTRICULARRELAXATION

THE CARDIAC CYCLE

DIASTOLE

ISOVOLUMETRIC RELAXATIONRAPID INFLOW

DIASTASISATRIAL SYSTOLE

EJECTION

ISOVOLUMETRICCONTRACTION

SYSTOLE DIASTOLE SYSTOLE

AORTICPRESSURE

ATRIALPRESSURE

VENTRICLEPRESSURE

ECG

PHONO-CARDIOGAM

VO

LU

ME

(m

l)P

RE

SS

UR

E (

mm

Hg)

MEASUREMENT OF CARDIAC OUTPUT

THE FICK METHOD:

VO2 = ([O2]a - [O2]v) x Flow

Flow =VO2

[O2]a - [O2]v

Spirometry (250 ml/min)

Arterial Blood (20 ml%)Pulmonary Artery Blood (15 ml%)

CARDIAC OUTPUT

PERIPHERALBLOOD FLOW

VENOUS RETURN

PULMONARY BLOOD FLOW

CARDIAC OUTPUT (Q) =VO2

[O2]a - [O2]v

250 ml/min20 ml% - 15 ml%

=

= 5 L/min

.

Q = HR x SV.

SV =Q

HR

.

= 5 L/min70 beats/min

= 0.0714 L or 71.4 ml

CARDIAC INDEX = Qm2 body surface area

.

5 L/min1.6 m2=

= 3.1 L/min/m2

THE HEART AS A PUMP• REGULATION OF CARDIAC OUTPUT

– Heart Rate via sympathetic & parasympathetic nerves– Stroke Volume

• Frank-Starling “Law of the Heart”

• Changes in Contractility

• MYOCARDIAL CELLS (FIBERS)– Regulation of Contractility– Length-Tension and Volume-Pressure Curves– The Cardiac Function Curve

CARDIAC OUTPUT = STROKE VOLUME x HEART RATE

Autoregulation (Frank-Starling “Law of the Heart”)

Contractility

SympatheticNervous System

ParasympatheticNervous System

STRIATED MUSCLE

CARDIAC MUSCLE

SKELETAL MUSCLE

- Functional Syncytium- Automaticity

- Motor Units- Stimulated by Motor Nerves

STRUCTURE OF A MYOCARDIAL CELL

Mitochondria Sarcolemma

T-tubule

SRFibrils

SARCOLEMMA

10%Mitochondria

THICKMYOFILAMENT

THIN MYOFILAMENT

SRCa++

T-t

ub

ule

20%

80%

REGULATAION OF CONTRACTILITY

• Recruitment of motor units

• Increase frequency of firing of motor nerves

• Calcium to trigger contraction

INCREASING HEART RATE INCREASES CONTRACTILITY

NormalHeart Rate

Ca++ Ca++

FastHeart Rate Ca++ Ca++ Ca++ Ca++

SERIES ELASTIC ELEMENTS

CONTRACTILE COMPONENT

(ACTIVE TENSION)

PARALLEL ELASTIC ELEMENTS

(PASSIVE TENSION)

TOTAL TENSION

LENGTH-TENSION CURVE

TOTAL TENSION

ACTIVE TENSION

PASSIVE TENSION

OPTIMAL LENGTH (Lo)

RESTING LENGTHEQUILIBRIUM LENGTH

LENGTHLENGTH

TENSION

TENSION

SARCOMERE LENGTH ()

TE

NS

ION

MUSCLE LENGTH

PASSIVETENSION

ACTAIVE TENSION

TOTAL TENSION

CARDIAC MUSCLE

PR

ES

SU

RE

DIASTOLICPRESSURE CURVE

SYSTOLIC PRESSURE CURVE

HEART

End Diastolic VolumeEnd Systolic Volume

IsovolumetricPhase

Isotonic (Ejection) Phase

StrokeVolume

Pre-load

After-load

PR

ES

SU

RE



HEART


IsovolumetricPhase


StrokeVolume

Pre-load

After-load

INCREASED

CONTRACTILIT

Y

PR

ES

SU

RE



HEART


IsovolumetricPhase


StrokeVolume

Pre-load

After-load

DECREASED

CONTRACTILIT

Y

PR

ES

SU

RE



HEART


IsovolumetricPhase


StrokeVolume

Pre-load

After-load

INCREASED

FILLIN

G

CARDIAC FUNCTION CURVE

ST

RO

KE

VO

LU

ME

DIASTOLIC FILLING

Cardiac Output = Stroke Volume x Heart Rate

ConstantIf:

Then: CO reflects SV

Right Atrial Pressure (RAP) reflects Diastolic Filling


CA

RD

IAC

OU

TP

UT

(L

/min

)

RAP mmHg

15-

10-

5-

-4 0 +4 +8

Volume

Pre

ssur

e

THE FRANK- STARLING “LAW OF THE HEART”


CA

RD

IAC

OU

TP

UT

(L

/min

)

RAP mmHg

15-

10-

5-

-4 0 +4 +8


IncreasedContractility


CA

RD

IAC

OU

TP

UT

(L

/min

)

RAP mmHg

15-

10-

5-

-4 0 +4 +8


DecreasedContractility


CA

RD

IAC

OU

TP

UT

(L

/min

)

RAP mmHg

15-

10-

5-

-4 0 +4 +8


IncreasedHeart Rate


CA

RD

IAC

OU

TP

UT

(L

/min

)

RAP mmHg

15-

10-

5-

-4 0 +4 +8


DecreasedHeart Rate

P1 P2

P1 > P2

FLOW

FLOW = PR

P = FLOW x R

R =

mm Hg

L/minor

ml/secmm Hgml/sec

Peripheral Resistance Units (PRU)

PFLOW

LAMINAR or STREAMLINE FLOW

P2P1

P1 > P2

-Cone Shaped Velocity Profile-Not Audible with a Stethoscope

MEASURING BLOOD PRESSURETURBULENT FLOW

1. Cuff pressure > systolic blood pressure--No sound.2. The first sound is heard at peak systolic pressure.3. Sounds are heard while cuff pressure < blood pressure.4. Sound disappears when cuff pressure < diastolic pressure.

RESISTANCES IN SERIESRT = RA + RC + RV

RESISTANCES IN PARALLEL

R1

R2

R3

PAPV

FlowT = Flow1 + Flow2 + Flow3

PRT

PR1

PR2

PR3

= + +

1 RT

1 R1

1 R2

1 R3

= + +

1 R1

1 R2

1 R3

RT1

+ +=

If: R1 = 2; R2 = 4; R3 = 6 PRU’s

Then a series arrangement gives:

RT = R1 + R2 + R3

RT = 12 PRU’s

But a parallel arrangement gives:

RT = =1.94 PRU’s

1

1 R1

1 R2

1 R3

+ +

v = Pr2 /8l

Q = vr2

Poiseuille's Law

Pr4

8lQ =

PRFlow =

R = 8l/r4

TOTAL PERIPHERAL RESISTANCE

TPR = Aortic Pressure - RAPFLOW

TPR = 100 - 0 mmHg 83.3 ml/sec (5 L/min)

= 1.2 PRU’s

SYSTEMIC CIRCULATION:

PULMONARY CIRCULATION:

Pul. R. =Pul. Art. P. - LAPFLOW

Pul. R. = 15 - 5 mmHg83.3 ml/sec

= 0.12 PRU’s

VASCULAR COMPLIANCEC =

VP

PR

ES

SU

RE

(m

mH

g)

VOLUME (L)

1 2 3 4

Arteries

Veins

100- Sym

Sym

Cv = 24 x Ca

Ca = =2.5 ml/mmHg

Cv = = 60 ml/mmHg

250 ml100 mmHg

300 ml5 mmHg

Sym

Sym

MEAN CIRCULATORY PRESSURE

PR

ES

SU

RE

(m

mH

g)

7-

1 2 3 4 5 6

UnstressedVolume

Stressed Volume

VOLUME (L)

MCP = 7 mmHg

CAPILLARIES

• Pressure inside is 35 to 15 mmHg

• 5% of the blood is in capillaries

• exchange of gases, nutrients, and wastes

• flow is slow and continuous

Metarteriole

Arteriole

PrecapillarySphincters

Capillaries

Venule

?

VASOMOTION = Intermittent flow due to constriction-relaxation cycles of precapillary shpinctersor arteriolar smooth muscle (5 - 10/min)

AUTOREGULATION OF VASOMOTION:

1. Oxygen Demand Theory (Nutrient Demand Theory)O2 is needed to support contraction (closure)

2. Vasodilator TheoryVasodilator substances produced (via O2)e.g. Adenosine Heart CO2 Brain Lactate, H+, K+ Skeletal Muscle

3. Myogenic Activity

DIFFUSION BETWEEN BLOOD & INTERSTITIAL FLUID

Plasma ProteinsBLOOD

O2 CO2 GlucoseINTERSTITIAL

FLUID

CELL

active transport

FLUID BALANCE

40-

30-

20-

10-

0-

PR

ES

SU

RE

(m

mH

g)Filtration vs. Reabsorption

Outward Forces:1. Capillary blood pressure (Pc = 35 to 15 mmHg)2. Interstitial fluid pressure (PIF = 0 mmHg)3. Interstitial fluid colloidal osmotic pressure (IF = 3 mmHg)

TOTAL = 38 to 18 mmHgInward Force:1. Plasma colloidal osmotic pressure (C = 28 mmHg)

CAPILLARY FLUID SHIFT

Pout > c Pout < c

Pc Pc

FAVORS FILTRATION FAVORS REABSORPTION

PULMONARY CIRCULATION

FLUID BALANCE

40-

30-

20-

10-

0-

PR

ES

SU

RE

(m

mH

g)Filtration vs. Reabsorption

Filtration Reabsorption

Vialymphatics

RADIAL FLOW

Anchoring Filaments

“PUMP” Compression Smooth muscle contraction

2 - 4 L/day ( 125 ml/hr)

LYMPHATIC CAPILLARY

Effects of gravity on arterial and venous pressures.Each cm of distance produces a 0.77 mmHg change.

Sphincters protectcapillaries

VENOUS PUMP keeps PV < 25 mm Hg

Veins Arteries

190 mm Hg

100 mm Hg0

ARTERIESVEINS (RAP)

7 mmHg7 mmHg

RAP

Art. BP

Peripheral Blood Flow

HEART

CO = PBF

Cv = 24 x Ca P RAP Pv Pa P= Pa - Pv TPR PBF=TPR(mmHg) (mmHg) (mmHg) (mmHg) (PRU’s) (ml/sec)

7 7 7 0 1.2 0 6 31 25 1.2 20.8 5 55 50 1.2 41.7 4 79 75 1.2 62.5 0 3 103 100 1.2 83.3 (5 L/min)

RELATIONSHIP BETWEEN RAP and PBF

THE VASCULAR FUNCTION CURVE

10-

5-

0-

PBFor

VENOUSRETURN(L/min)

-4 0 +4 +8RAP (mmHg)

WAYS TO ALTER THE VASCULAR FUNCTION CURVE

• CHANGE THE MEAN CIRCULATORY PRESSURE

• CHANGE BLOOD VOLUME

• CHANGE VENOUS CAPACITY

• CHANGE TOTAL PERIPHERAL RESISTANCE


PR

ES

SU

RE

(m

mH

g)

7-

1 2 3 4 5 6

UnstressedVolume

Stressed Volume

BLOOD VOLUME (L)

VOLUME MCP

VOLUME MCP

Normal

Hemorrhage

Infusion


PR

ES

SU

RE

(m

mH

g)

7-

1 2 3 4 5 6

UnstressedVolume

Stressed Volume

BLOOD VOLUME (L)

Normal

VENOCONSTRICTION


PR

ES

SU

RE

(m

mH

g)

7-

1 2 3 4 5 6

UnstressedVolume

Stressed Volume

BLOOD VOLUME (L)

Normal

VENODILATION


7 7 7 0 1.2 0 6 31 25 1.2 20.8 5 55 50 1.2 41.7 4 79 75 1.2 62.5 0 3 103 100 1.2 83.3 (5 L/min)

8 8 8 0 1.2 0 7 32 25 1.2 20.8 6 56 50 1.2 41.7 5 80 75 1.2 62.5 4 104 100 1.2 83.3 (5 L/min) 0 3 128 125 1.2 104.2 (6.25 L

min


MCP


10-

5-

0-

PBFor

VENOUSRETURN(L/min)

-4 0 +4 +8RAP (mmHg)

MCP

MCP

Blood Volumeor

Venoconstriction

Blood Volumeor

Venodilation


7 7 7 0 1.2 0 6 31 25 1.2 20.8 5 55 50 1.2 41.7 4 79 75 1.2 62.5 0 3 103 100 1.2 83.3 (5 L/min)

7 7 7 0 2.0 0 6 31 25 2.0 12.5 5 55 50 2.0 25.0 4 79 75 2.0 37.5 0 3 103 100 2.0 50.0 (3 L/min)


TPR


10-

5-

0-

PBFor

VENOUSRETURN(L/min)

-4 0 +4 +8RAP (mmHg)

TPR

TPR

Vasoconstriction

Vasodilation

CARDIAC & VASCULAR FUNCTION CURVES

RAP mmHg

15-

10-

5-

-4 0 +4 +8

CARDIACOUTPUT

or

PERIPHERALBLOOD FLOW[Venous Return]

(L/min)

CHANGES IN CARDIOVASCULAR

PERFORMANCE

BY ALTERING THE CARDIAC FUNCTION CURVE- CHANGING CONTRACTILITY- CHANGING HEART RATE

BY ALTERING THE VASCULAR FUNCTION CURVE- CHANGING MEAN CIRCULATORY PRESSURE

Blood VolumeVenous Capacity

- CHANGING TOTAL PERIPHERAL RESISTANCE

MOTOR CORTEXHYPOTHALAMUS

VASOMOTOR CENTERPRESSOR AREA

DEPRESSOR AREACARDIOINHIBITORY AREA

Vagus

HEARTArterioles

VeinsAdrenalMedulla

BaroreceptorsCarotid SinusAortic Arch

ChemoreceptorsCarotid BodiesAortic Bodies

Bainbridge Reflex ( Heart Rate)Atrial Receptors Volume Reflex ( Urinary OUTPUT)

a. Vascular Sympathetic Toneb. ADH Secretionc. Aldosterone Secretion

Chemosensitive Area

GlossopharyngealNerve

SympatheticNervousSystem

BP (Kidney) Renin

Angiotensinogen (renin substrate)

Angiotensin

Aldosterone

Kidney

sodium & water retention

Vasoconstriction

Venoconstriction

RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM

HORMONAL REGULATION

• Epinephrine & Norepinephrine– From the adrenal medulla

• Renin-angiotensin-aldosterone– Renin from the kidney– Angiotensin, a plasma protein– Aldosterone from the adrenal cortex

• Vasopressin (Antidiuretic Hormone-ADH)– ADH from the posterior pituitary

HypothalamicOsmoreceptors

BP via Posterior Pituitary Vasopressin (ADH)(Atrial Receptors)

Vasoconstriction WaterVenoconstriction Retention

VASOPRESSIN(ANTIDIURETIC HORMONE)

XX

RENAL--BODY FLUID CONTROL MECHANISM

8-

7-

6-

5-

4-

3-

2-

1-

-8

-7

-6

-5

-4

-3

-2

-1

UninaryOutput

(x normal)

FluidIntake

(x normal)

50 100 150

Normal

ARTERIAL BLOOD PRESSURE (mmHg)

P alone

All Mechanisms

3 x Normal

HYPERTENSION (140/90 mmHg)Secondary Hypertension (10%) [e.g., Pheochromocytoma]Essential Hypertension (90%)

- Normal cardiac output- Cardiac hypertrophy [left ventricle]- “Resetting” of the baroreceptors- Thickening of vascular walls

ARTERIAL PRESSURE-URINARY OUTPUT THEORYHypertension causes thickening of vascular walls

NEUROGENIC THEORYThickening of vascular walls causes hypertension

TREATMENT: Reduce stressSympathetic blockers Low sodium dietDiuretics

HEMORRHAGEP

ress

ure

7-

1 2 3 4 5Blood Volume (L)

MCP

-4 0 +4 +8RAP (mmHg)

COor

PBF(L/min)

COBP


RAP mmHg

15-

10-

5-

-4 0 +4 +8

CARDIACOUTPUT

or


(L/min)

Response to Hemorrhage HR & ContractilityVenoconstriction ( MCP)Vasoconstriction ( TPR)

RESPONSE TO HEMORRHAGE Sympathetic tone via baroreceptor reflex

Heart rate and contractility– Venoconstriction ( MCP)– Vasoconstriction ( arterial BP & direct blood to

vital organs)

• Restore Blood Volume– Capillary fluid shift ( BP favors reabsorption) Urinary output ( Arterial BP, ADH, Renin-

Angiotensin-Aldosterone)

• Restore plasma proteins & hematocrit

SYNCOPE (FAINTING)

Postural syncope(Blood pooling in the extremities)

Vasovagal syncope

Carotid sinus syncope

SYNCOPE (FAINTING)Blood pooling in the extremities

PR

ES

SU

RE

(m

mH

g)

7-

1 2 3 4 5 6

Unstressed

Volume

Stressed Volume

BLOOD VOLUME (L)

Unstressed Vol. Stressed Vol. MCP

Normal

Syncope (Fainting)

Pre

ssu

re

7-

1 2 3 4 5Blood Volume (L)

MCP

-4 0 +4 +8RAP (mmHg)

COor

PBF(L/min)

COBP

SYNCOPE (FAINTING)Blood pooling in the extremities


RAP mmHg

15-

10-

5-

-4 0 +4 +8

CARDIACOUTPUT

or


(L/min)

Response to Syncope (Fainting HR & ContractilityVenoconstriction ( MCP)Vasoconstriction ( TPR)

CARDIAC FAILURECAUSES: Impairment of electrical activity

Muscle damageValvular defectsCardiomyopathiesResult of drugs or toxins

PROBLEM: Maintaining circulation with a weak pump( Cardiac output & cardiac reserve; RAP)

SOLUTIONS: Sympathetic tone via baroreceptor reflex - Heart rate and contractility

-Venoconstriction ( MCP)-Vasoconstriction ( Arterial BP)

Fluid retention ( MCP)-Capillary fluid shift-ADH-Renin-angiotensin-aldosterone


RAP mmHg

15-

10-

5-

-4 0 +4 +8

CARDIACOUTPUT

or


(L/min)

Cardiac Failure

Adjustments to Failure

SYMPTOMS:Systemic EdemaPulmonary CongestionEnlarged Heart

PR

ES

SU

RE



HEART


IsovolumetricPhase


StrokeVolume

Pre-load

After-load

CARDIAC

FAILURE

TEMPERATURE REGUALTION

• Body Temperature

• Heat Production

• Heat Loss

• Temperature Regulation– Heat Exhaustion– Heat Stroke– Hypothermia

• Fever

COLDWARM

Upper limit of survival?Heat strokeBrain lesionsFever therapyFebrile disease andHard exerciseUsual range of normal

Temperatureregulationseriouslyimpaired

Temperatureregulationefficient in

febrile diseasehealth and work

Temperatureregulationimpaired

Temperatureregulation

lost Lower limitof survival?

HEAT PRODUCTION

BASAL METABOLIC RATE- Catecholamines-Hyperthyroidism

FOOD INTAKE (Specific Dynamic Action)-lasts up to 6 hours after a meal

PHYSICAL ACTIVITY-Exercise (20 x BMR)-Shivering (5 x BMR)

HEAT LOSS

COOL HOTRADIATIONCONDUCTION 70% CONVECTION

VAPORIZATION 30% Insensible Water Loss * *Sweating *

SKIN HYPOTHALAMUS

SweatingVasodilation

VasoconstrictionShivering

W

W

W

Set

point

C

WarmReceptors

ColdReceptors

Preoptic Area

Interaction Between Peripheral & Central Sensors

Cooling the skin raises the set point above which sweating begins.Warm skin--sweating occurs above 36.7CCold skin--sweating occurs above 37.4 C

The body is reluctant to give off heat (sweat) in a cold environment.

Warming the skin lowers the set point below which shivering begins.Cold skin: shivering occurs at 37.1CWarm skin: shivering occurs at 36.5C

The body is reluctant to produce heat (shiver) in a warm environment.

LIMITS TOTEMPERATURE REGULATION

Heat Exhaustion: Inadequate water/salt replacementBody temperature may be normalSymptoms: cerebral dysfunction

nauseafatique

Vasodilaton causing fatigue or fainting

Heat Stroke: Temperature regulation lostSymptoms: high body temperature

NO sweatingdizziness or

loss of consciousnessBody temperature MUST be lowered!

FEVER = an abnormally high body temperaturePYROGEN = a fever producing substance

PYROGEN WBC bacterial toxins, leukocytes,viruses, pollen, + monocytes = endogenous pyrogenproteins, dust

Arachidonic Acid

Prostaglandins Aspirin

RAISES THE “SET POINT”

FEVER

Actual CoreTemperature

Onset ofFever

FeverBreaks

ReferenceTemperatureor Set Point

ShiveringVasoconstriction

SweatingVasodilation

Cardiovascular Physiology

Health & Medicine

Transcript of Cardiovascular Physiology