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CARDIOVASCULAR PHYSIOLOGY. Dr. Poland Room 3-007, Sanger Hall Phone: 828-9557 E-mail: [email protected] HEART (PUMP). AUTOREGULATION. CARDIOVASCULAR SYSTEM. NEURAL. REGULATION. HORMONAL. VESSELS (DISTRIBUTION SYSTEM). RENAL-BODY FLUID CONTROL SYSTEM. PULMONARY CIRCULATION.

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cardiovascular physiology

CARDIOVASCULAR PHYSIOLOGY

Dr. Poland

Room 3-007, Sanger Hall

Phone: 828-9557

E-mail: [email protected]

slide2
HEART

(PUMP)

AUTOREGULATION

CARDIOVASCULAR SYSTEM

NEURAL

REGULATION

HORMONAL

VESSELS

(DISTRIBUTION SYSTEM)

RENAL-BODY FLUID

CONTROL SYSTEM

slide3
PULMONARY

CIRCULATION

1. LOW RESISTANCE

2. LOW PRESSURE

(25/10 mmHg)

SYSTEMIC

CIRCULATION

1. HIGH RESISTANCE

2. HIGH PRESSURE

(120/80 mmHg)

PARALLEL

SUBCIRCUITS

UNIDIRECTIONAL

FLOW

slide4
ARTERIES (LOW COMPLIANCE)

HEART

DIASTOLE

VEINS

CAPACITY

VESSELS

80 mmHg

120 mmHg

SYSTOLE

CAPILLARIES

slide5
THE SYSTEMIC CIRCULATION

CAPACITY VESSELS

slide7
AUTOMATICITY

Na+

K+

Gradually

increasing PNa

K+

Na+

-0

-70 mV

THRESHOLD

RESTING

slide8
Atrio-ventricular (AV) node

Sino-atrial

(SA) node

BUNDLE

BRANCHES

PURKINJE FIBERS

pacemakers in order of their inherent rhythm
PACEMAKERS (in order of their inherent rhythm)
  • Sino-atrial (SA) node
  • Atrio-ventricular (AV) node
  • Bundle of His
  • Bundle branches
  • Purkinje fibers
slide11
PHASE

Mechanical Response

0 = Rapid Depolarization

(inward Na+ current)

1

1 = Overshoot

2

0

2 = Plateau

(inward Ca++ current)

3 = Repolarization

(outward K+ current)

0

MEMBRANE POTENTIAL (mV)

4 = Resting Potential

3

4

-90

TIME

slide12
ACTION POTENTIALS

VENTRICULULAR

CELL

SAN

1

2

0

0

0

3

0

3

4

-50

-50

MEMBRANE POTENTIAL (mV)

4

-100

-100

slide13
SINGLE VENTRICULAR ACTION POTENTIAL

ENDOCARDIAL FIBER

ATRIAL

FIBER

EPICARDIAL FIBER

R

1 mV

ECG

T

P

Repolarization of ventricles

Q S

Depolarization of ventricles

Depolarization of atria

slide14
ECG Recordings (QRS Vector pointing leftward, inferiorly

& posteriorly)

3 Bipolar Limb Leads:

RA

LA

I = RA vs. LA (+)

LL

slide15
ECG Recordings (QRS Vector pointing leftward, inferiorly

& posteriorly)

3 Bipolar Limb Leads:

RA

LA

I = RA vs. LA (+)

II = RA vs. LL (+)

LL

slide16
ECG Recordings (QRS Vector pointing leftward, inferiorly

& posteriorly)

3 Bipolar Limb Leads:

RA

LA

I = RA vs. LA (+)

II = RA vs. LL (+)

III = LA vs. LL (+)

LL

slide17
ECG Recordings (QRS Vector pointing leftward, inferiorly

& posteriorly)

3 Bipolar Limb Leads:

RA

LA

I = RA vs. LA (+)

II = RA vs. LL (+)

III = LA vs. LL (+)

3 Augmented Limb Leads:

LL

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

slide18
ECG Recordings (QRS Vector pointing leftward, inferiorly

& posteriorly)

3 Bipolar Limb Leads:

RA

LA

I = RA vs. LA (+)

II = RA vs. LL (+)

III = LA vs. LL (+)

3 Augmented Limb Leads:

LL

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

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

slide19
ECG Recordings (QRS Vector pointing leftward, inferiorly

& posteriorly)

3 Bipolar Limb Leads:

RA

LA

I = RA vs. LA (+)

II = RA vs. LL (+)

III = LA vs. LL (+)

3 Augmented Limb Leads:

LL

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

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

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

slide20
6 PRECORDIAL (CHEST) LEADS

Spine

V6

V5

Sternum

V4

V3

V1

V2

slide21
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.

slide22
THE CARDIAC CYCLE

LATE DIASTOLE

DIASTOLE

ISOMETRIC

VENTRICULAR

RELAXATION

ATRIAL

SYSTOLE

VENTRICULAR

EJECTION

ISOMETRIC VENTRICULAR

CONTRACTION

slide23
EJECTION

ISOVOLUMETRIC

CONTRACTION

ISOVOLUMETRIC RELAXATION

RAPID INFLOW

DIASTASIS

ATRIAL SYSTOLE

AORTIC

PRESSURE

PRESSURE (mmHg)

ATRIAL

PRESSURE

VENTRICLE

PRESSURE

VOLUME (ml)

ECG

PHONO-

CARDIOGAM

SYSTOLE DIASTOLE SYSTOLE

slide24
MEASUREMENT OF CARDIAC OUTPUT

THE FICK METHOD:

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

Spirometry (250 ml/min)

VO2

[O2]a - [O2]v

Flow =

Pulmonary Artery Blood (15 ml%)

Arterial Blood (20 ml%)

CARDIAC OUTPUT

PULMONARY BLOOD FLOW

VENOUS RETURN

PERIPHERAL

BLOOD FLOW

slide25
.

VO2

[O2]a - [O2]v

CARDIAC OUTPUT (Q) =

250 ml/min

20 ml% - 15 ml%

=

= 5 L/min

.

Q = HR x SV

.

.

Q

m2 body surface

area

Q

HR

CARDIAC INDEX =

SV =

5 L/min

70 beats/min

=

5 L/min

1.6 m2

=

= 0.0714 L or 71.4 ml

= 3.1 L/min/m2

the heart as a pump
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
slide27
Autoregulation

(Frank-Starling “Law of the Heart”)

CARDIAC OUTPUT = STROKE VOLUME x HEART RATE

Contractility

Sympathetic

Nervous System

Parasympathetic

Nervous System

slide28
CARDIAC MUSCLE

- Functional Syncytium

- Automaticity

STRIATED MUSCLE

SKELETAL MUSCLE

- Motor Units

- Stimulated by Motor Nerves

slide29
STRUCTURE OF A MYOCARDIAL CELL

Sarcolemma

Mitochondria

T-tubule

SR

Fibrils

slide30
SARCOLEMMA

10%

Mitochondria

20%

80%

T-tubule

Ca++

SR

THICK

MYOFILAMENT

THIN MYOFILAMENT

regulataion of contractility
REGULATAION OF CONTRACTILITY
  • Recruitment of motor units
  • Increase frequency of firing of motor nerves
  • Calcium to trigger contraction
increasing heart rate increases contractility
INCREASING HEART RATE INCREASES CONTRACTILITY

Ca++

Ca++

Normal

Heart Rate

Fast

Heart Rate

Ca++

Ca++

Ca++

Ca++

slide33
SERIES ELASTIC ELEMENTS

CONTRACTILE COMPONENT

(ACTIVE TENSION)

PARALLEL ELASTIC ELEMENTS

(PASSIVE TENSION)

TOTAL TENSION

slide34
LENGTH-TENSION CURVE

TOTAL TENSION

ACTIVE TENSION

TENSION

PASSIVE TENSION

OPTIMAL LENGTH (Lo)

EQUILIBRIUM LENGTH

RESTING LENGTH

LENGTH

LENGTH

slide35
TENSION

SARCOMERE LENGTH ()

slide36
CARDIAC MUSCLE

TOTAL TENSION

ACTAIVE TENSION

TENSION

PASSIVE

TENSION

MUSCLE LENGTH

slide37
HEART

SYSTOLIC PRESSURE CURVE

Isotonic (Ejection) Phase

After-load

Isovolumetric

Phase

PRESSURE

Stroke

Volume

DIASTOLIC

PRESSURE CURVE

Pre-load

End Systolic Volume

End Diastolic Volume

slide38
HEART

INCREASED

CONTRACTILITY

SYSTOLIC PRESSURE CURVE

Isotonic (Ejection) Phase

After-load

Isovolumetric

Phase

PRESSURE

Stroke

Volume

DIASTOLIC

PRESSURE CURVE

Pre-load

End Systolic Volume

End Diastolic Volume

slide39
HEART

DECREASED

CONTRACTILITY

SYSTOLIC PRESSURE CURVE

Isotonic (Ejection) Phase

After-load

Isovolumetric

Phase

PRESSURE

Stroke

Volume

DIASTOLIC

PRESSURE CURVE

Pre-load

End Systolic Volume

End Diastolic Volume

slide40
HEART

INCREASED

FILLING

SYSTOLIC PRESSURE CURVE

Isotonic (Ejection) Phase

After-load

Isovolumetric

Phase

PRESSURE

Stroke

Volume

DIASTOLIC

PRESSURE CURVE

Pre-load

End Systolic Volume

End Diastolic Volume

cardiac function curve
CARDIAC FUNCTION CURVE

Cardiac Output = Stroke Volume x Heart Rate

Constant

If:

STROKE VOLUME

Then:

 CO reflects SV

DIASTOLIC FILLING

Right Atrial Pressure (RAP) reflects Diastolic Filling

cardiac function curve1
CARDIAC FUNCTION CURVE

THE FRANK- STARLING “LAW OF THE HEART”

15-

10-

CARDIAC OUTPUT (L/min)

Pressure

5-

Volume

-4

0

+4

+8

RAP mmHg

cardiac function curve2
CARDIAC FUNCTION CURVE

THE FRANK- STARLING “LAW OF THE HEART”

15-

Increased

Contractility

10-

CARDIAC OUTPUT (L/min)

5-

-4

0

+4

+8

RAP mmHg

cardiac function curve3
CARDIAC FUNCTION CURVE

THE FRANK- STARLING “LAW OF THE HEART”

15-

Decreased

Contractility

10-

CARDIAC OUTPUT (L/min)

5-

-4

0

+4

+8

RAP mmHg

cardiac function curve4
CARDIAC FUNCTION CURVE

THE FRANK- STARLING “LAW OF THE HEART”

15-

Increased

Heart Rate

10-

CARDIAC OUTPUT (L/min)

5-

-4

0

+4

+8

RAP mmHg

cardiac function curve5
CARDIAC FUNCTION CURVE

THE FRANK- STARLING “LAW OF THE HEART”

15-

Decreased

Heart Rate

10-

CARDIAC OUTPUT (L/min)

5-

-4

0

+4

+8

RAP mmHg

slide47
P1 > P2

P1

FLOW

P2

mm Hg

P = FLOW x R

P

R

FLOW =

P

FLOW

R =

L/min

or

ml/sec

mm Hg

ml/sec

Peripheral Resistance Units (PRU)

laminar or streamline flow
LAMINAR or STREAMLINE FLOW

P1

P2

P1 > P2

-Cone Shaped Velocity Profile

-Not Audible with a Stethoscope

slide49
MEASURING BLOOD PRESSURE

TURBULENT 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 series
RESISTANCES IN SERIES

RT = RA + RC + RV

RESISTANCES IN PARALLEL

FlowT = Flow1 + Flow2 + Flow3

P

RT

P

R1

P

R2

P

R3

=

+

+

R1

PV

PA

1

RT

1

R1

1

R2

1

R3

R2

=

+

+

R3

1

RT

=

1

R1

1

R2

1

R3

+

+

slide51
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

+

+

slide52
Poiseuille's Law

v = Pr2 /8l

P

R

Flow =

Q = vr2

Pr4

8l

Q =

R = 8l/r4

total peripheral resistance
TOTAL PERIPHERAL RESISTANCE

SYSTEMIC CIRCULATION:

Aortic Pressure - RAP

FLOW

TPR =

100 - 0 mmHg

83.3 ml/sec (5 L/min)

= 1.2 PRU’s

TPR =

PULMONARY CIRCULATION:

Pul. Art. P. - LAP

FLOW

Pul. R. =

15 - 5 mmHg

83.3 ml/sec

Pul. R. =

= 0.12 PRU’s

vascular compliance
VASCULAR COMPLIANCE

V

P

C =

Arteries

250 ml

100 mmHg

Ca = =2.5 ml/mmHg

100-

Sym

300 ml

5 mmHg

Cv = = 60 ml/mmHg

Sym

Cv = 24 x Ca

PRESSURE (mmHg)

Veins

Sym

Sym

1

4

2

3

VOLUME (L)

mean circulatory pressure
MEAN CIRCULATORY PRESSURE

Unstressed

Volume

Stressed Volume

7-

PRESSURE (mmHg)

MCP = 7 mmHg

1 2 3 4 5 6

VOLUME (L)

capillaries
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
slide57
Arteriole

?

Precapillary

Sphincters

Capillaries

Metarteriole

Venule

slide58
VASOMOTION = Intermittent flow due to constriction-

relaxation cycles of precapillary shpincters

or 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 Theory

Vasodilator substances produced (via  O2)

e.g. Adenosine  Heart

CO2  Brain

Lactate, H+, K+  Skeletal Muscle

3. Myogenic Activity

slide59
DIFFUSION BETWEEN BLOOD & INTERSTITIAL FLUID

Plasma Proteins

BLOOD

INTERSTITIAL

FLUID

O2

CO2

Glucose

active transport

CELL

slide60
FLUID BALANCE

Filtration vs. Reabsorption

40-

30-

20-

10-

0-

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 mmHg

PRESSURE (mmHg)

Inward Force:

1. Plasma colloidal osmotic

pressure (C = 28 mmHg)

capillary fluid shift
CAPILLARY FLUID SHIFT

Pout > c Pout < c

Pc

Pc

FAVORS FILTRATION

FAVORS REABSORPTION

PULMONARY CIRCULATION

slide62
FLUID BALANCE

Filtration vs. Reabsorption

40-

30-

20-

10-

0-

Via

lymphatics

PRESSURE (mmHg)

Filtration Reabsorption

RADIAL FLOW

slide63
LYMPHATIC CAPILLARY

2 - 4 L/day ( 125 ml/hr)

“PUMP”

Compression

Smooth muscle contraction

Anchoring Filaments

slide64
Effects of gravity on arterial and venous pressures.

Each cm of distance produces a 0.77 mmHg change.

Veins Arteries

0

100 mm Hg

190 mm Hg

Sphincters protect

capillaries

VENOUS PUMP keeps PV < 25 mm Hg

slide65
HEART

 Art. BP

CO = PBF

VEINS

(RAP)

ARTERIES

 RAP

7 mmHg 

7 mmHg

Peripheral Blood Flow

slide66
RELATIONSHIP BETWEEN RAP and 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)

slide67
THE VASCULAR FUNCTION CURVE

10-

5-

0-

PBF

or

VENOUS

RETURN

(L/min)

-4 0 +4 +8

RAP (mmHg)

ways to alter the vascular function curve
WAYS TO ALTER THE VASCULAR FUNCTION CURVE
  • CHANGE THE MEAN CIRCULATORY PRESSURE
      • CHANGE BLOOD VOLUME
      • CHANGE VENOUS CAPACITY
  • CHANGE TOTAL PERIPHERAL RESISTANCE
mean circulatory pressure1
MEAN CIRCULATORY PRESSURE

Unstressed

Volume

Stressed Volume

Infusion

 VOLUME

 MCP

Normal

7-

PRESSURE (mmHg)

 VOLUME

 MCP

Hemorrhage

1 2 3 4 5 6

BLOOD VOLUME (L)

mean circulatory pressure2
MEAN CIRCULATORY PRESSURE

VENOCONSTRICTION

Unstressed

Volume

Stressed Volume

Normal

7-

PRESSURE (mmHg)

1 2 3 4 5 6

BLOOD VOLUME (L)

mean circulatory pressure3
MEAN CIRCULATORY PRESSURE

VENODILATION

Unstressed

Volume

Stressed Volume

Normal

7-

PRESSURE (mmHg)

1 2 3 4 5 6

BLOOD VOLUME (L)

slide72
RELATIONSHIP BETWEEN RAP and 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)

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

slide73
THE VASCULAR FUNCTION CURVE

10-

5-

0-

 Blood Volume

or

Venoconstriction

PBF

or

VENOUS

RETURN

(L/min)

 MCP

 MCP

 Blood Volume

or

Venodilation

-4 0 +4 +8

RAP (mmHg)

slide74
RELATIONSHIP BETWEEN RAP and 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)

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

slide75
THE VASCULAR FUNCTION CURVE

Vasodilation

10-

5-

0-

PBF

or

VENOUS

RETURN

(L/min)

 TPR

 TPR

Vasoconstriction

-4 0 +4 +8

RAP (mmHg)

cardiac vascular function curves
CARDIAC & VASCULAR FUNCTION CURVES

15-

CARDIAC

OUTPUT

or

PERIPHERAL

BLOOD FLOW

[Venous Return]

(L/min)

10-

5-

-4

0

+4

+8

RAP mmHg

changes in cardiovascular performance
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 Volume

Venous Capacity

- CHANGING TOTAL PERIPHERAL RESISTANCE

slide78
MOTOR CORTEX

HYPOTHALAMUS

Sympathetic

Nervous

System

Chemosensitive Area

VASOMOTOR CENTER

PRESSOR AREA

DEPRESSOR AREA

CARDIOINHIBITORY AREA

Glossopharyngeal

Nerve

Vagus

Baroreceptors

Carotid Sinus

Aortic Arch

HEART

Arterioles

Veins

Adrenal

Medulla

Chemoreceptors

Carotid Bodies

Aortic Bodies

Bainbridge Reflex ( Heart Rate)

Atrial Receptors Volume Reflex ( Urinary OUTPUT)

a.  Vascular Sympathetic Tone

b.  ADH Secretion

c.  Aldosterone Secretion

slide79
RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM

Angiotensinogen (renin substrate)

Angiotensin

Aldosterone

Kidney

sodium & water retention

 BP (Kidney)

Renin

Vasoconstriction

Venoconstriction

hormonal regulation
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
slide81
VASOPRESSIN

(ANTIDIURETIC HORMONE)

Hypothalamic

Osmoreceptors

 BP via Posterior Pituitary  Vasopressin (ADH)

(Atrial Receptors)

Vasoconstriction  Water

Venoconstriction Retention

X

X

renal body fluid control mechanism
RENAL--BODY FLUID CONTROL MECHANISM

-8

-7

-6

-5

-4

-3

-2

-1

8-

7-

6-

5-

4-

3-

2-

1-

All Mechanisms

Uninary

Output

(x normal)

Fluid

Intake

(x normal)

3 x Normal

P alone

Normal

50 100 150

ARTERIAL BLOOD PRESSURE (mmHg)

hypertension 140 90 mmhg
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 THEORY

Hypertension causes thickening of vascular walls

NEUROGENIC THEORY

Thickening of vascular walls causes hypertension

TREATMENT: Reduce stress

Sympathetic blockers

Low sodium diet

Diuretics

hemorrhage
HEMORRHAGE

7-

MCP

CO

or

PBF

(L/min)

CO

BP

Pressure

1 2 3 4 5

Blood Volume (L)

-4 0 +4 +8

RAP (mmHg)

cardiac vascular function curves1
CARDIAC & VASCULAR FUNCTION CURVES

15-

CARDIAC

OUTPUT

or

PERIPHERAL

BLOOD FLOW

[Venous Return]

(L/min)

10-

Response to Hemorrhage

 HR & Contractility

Venoconstriction ( MCP)

Vasoconstriction ( TPR)

5-

-4

0

+4

+8

RAP mmHg

response to hemorrhage
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
slide87
SYNCOPE (FAINTING)Postural syncope(Blood pooling in the extremities) Vasovagal syncopeCarotid sinus syncope
syncope fainting blood pooling in the extremities
SYNCOPE (FAINTING)Blood pooling in the extremities

Unstressed

Volume

Stressed Volume

Normal

7-

 Unstressed Vol.

 Stressed Vol.

 MCP

PRESSURE (mmHg)

Syncope (Fainting)

1 2 3 4 5 6

BLOOD VOLUME (L)

syncope fainting blood pooling in the extremities1
SYNCOPE (FAINTING)Blood pooling in the extremities

7-

MCP

CO

or

PBF

(L/min)

CO

BP

Pressure

1 2 3 4 5

Blood Volume (L)

-4 0 +4 +8

RAP (mmHg)

cardiac vascular function curves2
CARDIAC & VASCULAR FUNCTION CURVES

15-

CARDIAC

OUTPUT

or

PERIPHERAL

BLOOD FLOW

[Venous Return]

(L/min)

10-

Response to Syncope (Fainting

 HR & Contractility

Venoconstriction ( MCP)

Vasoconstriction ( TPR)

5-

-4

0

+4

+8

RAP mmHg

cardiac failure
CARDIAC FAILURE
  • CAUSES: Impairment of electrical activity
  • Muscle damage
  • Valvular defects
  • Cardiomyopathies
  • Result 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
cardiac vascular function curves3
CARDIAC & VASCULAR FUNCTION CURVES

15-

CARDIAC

OUTPUT

or

PERIPHERAL

BLOOD FLOW

[Venous Return]

(L/min)

SYMPTOMS:

Systemic Edema

Pulmonary

Congestion

Enlarged Heart

10-

Adjustments to Failure

5-

Cardiac Failure

-4

0

+4

+8

RAP mmHg

slide93
HEART

CARDIAC

FAILURE

SYSTOLIC PRESSURE CURVE

Isotonic (Ejection) Phase

After-load

Isovolumetric

Phase

PRESSURE

Stroke

Volume

DIASTOLIC

PRESSURE CURVE

Pre-load

End Systolic Volume

End Diastolic Volume

temperature regualtion
TEMPERATURE REGUALTION
  • Body Temperature
  • Heat Production
  • Heat Loss
  • Temperature Regulation
    • Heat Exhaustion
    • Heat Stroke
    • Hypothermia
  • Fever
slide95
COLD

WARM

slide96
Temperature

regulation

seriously

impaired

Temperature

regulation

efficient in

febrile disease

health and work

Temperature

regulation

impaired

Temperature

regulation

lost

Upper limit of survival?

Heat stroke

Brain lesions

Fever therapy

Febrile disease

and

Hard exercise

Usual range of normal

Lower limit

of survival?

heat production
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
HEAT LOSS

COOLHOT

RADIATION

CONDUCTION 70% 

CONVECTION

VAPORIZATION 30% 

Insensible Water Loss * *

Sweating *

slide99
SKINHYPOTHALAMUS

Preoptic Area

Sweating

Vasodilation

W

Set

point

Warm

Receptors

Cold

Receptors

W

Vasoconstriction

Shivering

W

C

interaction between peripheral central sensors
Interaction Between Peripheral & Central Sensors

Cooling the skin raises the set point above which sweating begins.

Warm skin--sweating occurs above 36.7C

Cold 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 37.1C

Warm skin: shivering occurs at 36.5C

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

limits to temperature regulation
LIMITS TOTEMPERATURE REGULATION

Heat Exhaustion: Inadequate water/salt replacement

Body temperature may be normal

Symptoms: cerebral dysfunction

nausea

fatique

Vasodilaton causing fatigue or fainting

Heat Stroke: Temperature regulation lost

Symptoms: high body temperature

NO sweating

dizziness or

loss of consciousness

Body temperature MUST be lowered!

fever
FEVER

FEVER = an abnormally high body temperature

PYROGEN = a fever producing substance

PYROGEN WBC

bacterial toxins, leukocytes,

viruses, pollen, + monocytes = endogenous pyrogen

proteins, dust

Arachidonic Acid

Prostaglandins Aspirin

RAISES THE “SET POINT”

slide103
Shivering

Vasoconstriction

Sweating

Vasodilation

Reference

Temperature

or Set Point

Actual Core

Temperature

Fever

Breaks

Onset of

Fever

ad