cardiovascular physiology
DESCRIPTION
TRANSCRIPT
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
ECG Recordings (QRS Vector pointing leftward, inferiorly & posteriorly)
3 Bipolar Limb Leads:
I = RA vs. LA (+)
II = RA vs. LL (+)
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 (+)
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(+)
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(+)
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(+)
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
DIASTOLICPRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic VolumeEnd Systolic Volume
IsovolumetricPhase
Isotonic (Ejection) Phase
StrokeVolume
Pre-load
After-load
INCREASED
CONTRACTILIT
Y
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
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
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
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”
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
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
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
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
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
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
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
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
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
THE VASCULAR FUNCTION CURVE
10-
5-
0-
PBFor
VENOUSRETURN(L/min)
-4 0 +4 +8RAP (mmHg)
MCP
MCP
Blood Volumeor
Venoconstriction
Blood Volumeor
Venodilation
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
THE VASCULAR FUNCTION CURVE
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
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)
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
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)
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
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
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
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