cardiovascular physiology dr. poland room 3-007, sanger hall phone: 828-9557 e-mail:...
TRANSCRIPT
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CARDIOVASCULAR PHYSIOLOGY
Dr. Poland
Room 3-007, Sanger Hall
Phone: 828-9557
E-mail: [email protected]
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CARDIOVASCULAR SYSTEM
HEART(PUMP)
VESSELS(DISTRIBUTION SYSTEM)
RE
GU
LA
TIO
N
AUTOREGULATION
NEURAL
HORMONAL
RENAL-BODY FLUIDCONTROL SYSTEM
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PULMONARYCIRCULATION
1. LOW RESISTANCE2. LOW PRESSURE
(25/10 mmHg)
SYSTEMICCIRCULATION
1. HIGH RESISTANCE2. HIGH PRESSURE
(120/80 mmHg)
PARALLELSUBCIRCUITS
UNIDIRECTIONALFLOW
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VEINS
CAPACITYVESSELS
HEART
80 mmHg 120 mmHg
SYSTOLE
DIASTOLE
ARTERIES (LOW COMPLIANCE)
CAPILLARIES
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THE SYSTEMIC CIRCULATION
CAPACITY VESSELS
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NORMAL
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Na+
K+Na+
K+
-70 mV
RESTING
THRESHOLD
-0
Graduallyincreasing PNa
AUTOMATICITY
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PURKINJE FIBERS
BUNDLEBRANCHES
Sino-atrial(SA) node
Atrio-ventricular (AV) node
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INTERCALATED DISC (TIGHT JUNCTION)
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PACEMAKERS (in order of their inherent rhythm)
• Sino-atrial (SA) node
• Atrio-ventricular (AV) node
• Bundle of His
• Bundle branches
• Purkinje fibers
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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
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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
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SINGLE VENTRICULAR ACTION POTENTIAL
ECGP
Q S
T
R
1 mV
Repolarization of ventriclesDepolarization of ventricles
Depolarization of atria
ENDOCARDIAL FIBER
EPICARDIAL FIBER
ATRIALFIBER
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LARA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)
3 Bipolar Limb Leads:
I = RA vs. LA (+)
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LARA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)
3 Bipolar Limb Leads:
I = RA vs. LA (+)
II = RA vs. LL (+)
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LARA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)
3 Bipolar Limb Leads:
I = RA vs. LA (+)
II = RA vs. LL (+)
III = LA vs. LL (+)
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LARA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly & 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(+)
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LARA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly & 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(+)
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LARA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly & 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(+)
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V1 V2V3
V4
V5
V6
6 PRECORDIAL (CHEST) LEADS
Spine
Sternum
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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.
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LATE DIASTOLE
ATRIALSYSTOLE
ISOMETRIC VENTRICULARCONTRACTION
VENTRICULAR EJECTION
ISOMETRICVENTRICULARRELAXATION
THE CARDIAC CYCLE
DIASTOLE
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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)
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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
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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
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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
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CARDIAC OUTPUT = STROKE VOLUME x HEART RATE
Autoregulation (Frank-Starling “Law of the Heart”)
Contractility
SympatheticNervous System
ParasympatheticNervous System
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STRIATED MUSCLE
CARDIAC MUSCLE
SKELETAL MUSCLE
- Functional Syncytium- Automaticity
- Motor Units- Stimulated by Motor Nerves
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STRUCTURE OF A MYOCARDIAL CELL
Mitochondria Sarcolemma
T-tubule
SRFibrils
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SARCOLEMMA
10%Mitochondria
THICKMYOFILAMENT
THIN MYOFILAMENT
SRCa++
T-t
ub
ule
20%
80%
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REGULATAION OF CONTRACTILITY
• Recruitment of motor units
• Increase frequency of firing of motor nerves
• Calcium to trigger contraction
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INCREASING HEART RATE INCREASES CONTRACTILITY
NormalHeart Rate
Ca++ Ca++
FastHeart Rate Ca++ Ca++ Ca++ Ca++
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SERIES ELASTIC ELEMENTS
CONTRACTILE COMPONENT
(ACTIVE TENSION)
PARALLEL ELASTIC ELEMENTS
(PASSIVE TENSION)
TOTAL TENSION
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LENGTH-TENSION CURVE
TOTAL TENSION
ACTIVE TENSION
PASSIVE TENSION
OPTIMAL LENGTH (Lo)
RESTING LENGTHEQUILIBRIUM LENGTH
LENGTHLENGTH
TENSION
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TENSION
SARCOMERE LENGTH ()
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TE
NS
ION
MUSCLE LENGTH
PASSIVETENSION
ACTAIVE TENSION
TOTAL TENSION
CARDIAC MUSCLE
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PR
ES
SU
RE
DIASTOLICPRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic VolumeEnd Systolic Volume
IsovolumetricPhase
Isotonic (Ejection) Phase
StrokeVolume
Pre-load
After-load
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PR
ES
SU
RE
DIASTOLICPRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic VolumeEnd Systolic Volume
IsovolumetricPhase
Isotonic (Ejection) Phase
StrokeVolume
Pre-load
After-load
INCREASED
CONTRACTILIT
Y
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PR
ES
SU
RE
DIASTOLICPRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic VolumeEnd Systolic Volume
IsovolumetricPhase
Isotonic (Ejection) Phase
StrokeVolume
Pre-load
After-load
DECREASED
CONTRACTILIT
Y
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PR
ES
SU
RE
DIASTOLICPRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic VolumeEnd Systolic Volume
IsovolumetricPhase
Isotonic (Ejection) Phase
StrokeVolume
Pre-load
After-load
INCREASED
FILLIN
G
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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
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CARDIAC FUNCTION CURVE
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”
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CARDIAC FUNCTION CURVE
CA
RD
IAC
OU
TP
UT
(L
/min
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
IncreasedContractility
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CARDIAC FUNCTION CURVE
CA
RD
IAC
OU
TP
UT
(L
/min
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
DecreasedContractility
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CARDIAC FUNCTION CURVE
CA
RD
IAC
OU
TP
UT
(L
/min
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
IncreasedHeart Rate
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CARDIAC FUNCTION CURVE
CA
RD
IAC
OU
TP
UT
(L
/min
)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
DecreasedHeart Rate
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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
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LAMINAR or STREAMLINE FLOW
P2P1
P1 > P2
-Cone Shaped Velocity Profile-Not Audible with a Stethoscope
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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.
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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
+ +=
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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
+ +
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v = Pr2 /8l
Q = vr2
Poiseuille's Law
Pr4
8lQ =
PRFlow =
R = 8l/r4
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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
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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
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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
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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
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Metarteriole
Arteriole
PrecapillarySphincters
Capillaries
Venule
?
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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
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DIFFUSION BETWEEN BLOOD & INTERSTITIAL FLUID
Plasma ProteinsBLOOD
O2 CO2 GlucoseINTERSTITIAL
FLUID
CELL
active transport
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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)
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CAPILLARY FLUID SHIFT
Pout > c Pout < c
Pc Pc
FAVORS FILTRATION FAVORS REABSORPTION
PULMONARY CIRCULATION
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FLUID BALANCE
40-
30-
20-
10-
0-
PR
ES
SU
RE
(m
mH
g)Filtration vs. Reabsorption
Filtration Reabsorption
Vialymphatics
RADIAL FLOW
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Anchoring Filaments
“PUMP” Compression Smooth muscle contraction
2 - 4 L/day ( 125 ml/hr)
LYMPHATIC CAPILLARY
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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
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ARTERIESVEINS (RAP)
7 mmHg7 mmHg
RAP
Art. BP
Peripheral Blood Flow
HEART
CO = PBF
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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
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THE VASCULAR FUNCTION CURVE
10-
5-
0-
PBFor
VENOUSRETURN(L/min)
-4 0 +4 +8RAP (mmHg)
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WAYS TO ALTER THE VASCULAR FUNCTION CURVE
• CHANGE THE MEAN CIRCULATORY PRESSURE
• CHANGE BLOOD VOLUME
• CHANGE VENOUS CAPACITY
• CHANGE TOTAL PERIPHERAL RESISTANCE
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MEAN CIRCULATORY PRESSURE
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
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MEAN CIRCULATORY PRESSURE
PR
ES
SU
RE
(m
mH
g)
7-
1 2 3 4 5 6
UnstressedVolume
Stressed Volume
BLOOD VOLUME (L)
Normal
VENOCONSTRICTION
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MEAN CIRCULATORY PRESSURE
PR
ES
SU
RE
(m
mH
g)
7-
1 2 3 4 5 6
UnstressedVolume
Stressed Volume
BLOOD VOLUME (L)
Normal
VENODILATION
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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
RELATIONSHIP BETWEEN RAP and PBF
MCP
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THE VASCULAR FUNCTION CURVE
10-
5-
0-
PBFor
VENOUSRETURN(L/min)
-4 0 +4 +8RAP (mmHg)
MCP
MCP
Blood Volumeor
Venoconstriction
Blood Volumeor
Venodilation
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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)
RELATIONSHIP BETWEEN RAP and PBF
TPR
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THE VASCULAR FUNCTION CURVE
10-
5-
0-
PBFor
VENOUSRETURN(L/min)
-4 0 +4 +8RAP (mmHg)
TPR
TPR
Vasoconstriction
Vasodilation
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CARDIAC & VASCULAR FUNCTION CURVES
RAP mmHg
15-
10-
5-
-4 0 +4 +8
CARDIACOUTPUT
or
PERIPHERALBLOOD FLOW[Venous Return]
(L/min)
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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
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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
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BP (Kidney) Renin
Angiotensinogen (renin substrate)
Angiotensin
Aldosterone
Kidney
sodium & water retention
Vasoconstriction
Venoconstriction
RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM
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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
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HypothalamicOsmoreceptors
BP via Posterior Pituitary Vasopressin (ADH)(Atrial Receptors)
Vasoconstriction WaterVenoconstriction Retention
VASOPRESSIN(ANTIDIURETIC HORMONE)
XX
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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
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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
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HEMORRHAGEP
ress
ure
7-
1 2 3 4 5Blood Volume (L)
MCP
-4 0 +4 +8RAP (mmHg)
COor
PBF(L/min)
COBP
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CARDIAC & VASCULAR FUNCTION CURVES
RAP mmHg
15-
10-
5-
-4 0 +4 +8
CARDIACOUTPUT
or
PERIPHERALBLOOD FLOW[Venous Return]
(L/min)
Response to Hemorrhage HR & ContractilityVenoconstriction ( MCP)Vasoconstriction ( TPR)
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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
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SYNCOPE (FAINTING)
Postural syncope(Blood pooling in the extremities)
Vasovagal syncope
Carotid sinus syncope
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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)
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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
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CARDIAC & VASCULAR FUNCTION CURVES
RAP mmHg
15-
10-
5-
-4 0 +4 +8
CARDIACOUTPUT
or
PERIPHERALBLOOD FLOW[Venous Return]
(L/min)
Response to Syncope (Fainting HR & ContractilityVenoconstriction ( MCP)Vasoconstriction ( TPR)
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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
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CARDIAC & VASCULAR FUNCTION CURVES
RAP mmHg
15-
10-
5-
-4 0 +4 +8
CARDIACOUTPUT
or
PERIPHERALBLOOD FLOW[Venous Return]
(L/min)
Cardiac Failure
Adjustments to Failure
SYMPTOMS:Systemic EdemaPulmonary CongestionEnlarged Heart
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PR
ES
SU
RE
DIASTOLICPRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic VolumeEnd Systolic Volume
IsovolumetricPhase
Isotonic (Ejection) Phase
StrokeVolume
Pre-load
After-load
CARDIAC
FAILURE
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TEMPERATURE REGUALTION
• Body Temperature
• Heat Production
• Heat Loss
• Temperature Regulation– Heat Exhaustion– Heat Stroke– Hypothermia
• Fever
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COLDWARM
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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?
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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)
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HEAT LOSS
COOL HOTRADIATIONCONDUCTION 70% CONVECTION
VAPORIZATION 30% Insensible Water Loss * *Sweating *
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SKIN HYPOTHALAMUS
SweatingVasodilation
VasoconstrictionShivering
W
W
W
Set
point
C
WarmReceptors
ColdReceptors
Preoptic Area
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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.
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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!
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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
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Actual CoreTemperature
Onset ofFever
FeverBreaks
ReferenceTemperatureor Set Point
ShiveringVasoconstriction
SweatingVasodilation