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CARDIOVASCULAR
PHYSIOLOGY
Dr. Poland
Room 3-007, Sanger Hall
Phone: 828-9557
E-mail: poland@hsc.vcu.edu
CARDIOVASCULAR
SYSTEM
HEART
(PUMP)
VESSELS
(DISTRIBUTION SYSTEM)
REGULATION
AUTOREGULATION
NEURAL
HORMONAL
RENAL-BODY FLUID
CONTROL SYSTEM
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
VEINS
CAPACITY
VESSELS
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
Gradually
increasing PNa
AUTOMATICITY
PURKINJE FIBERS
BUNDLE
BRANCHES
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
-90
0
0
1
2
3
4
TIME
PHASE
0 = Rapid Depolarization
(inward Na+ current)
1 = Overshoot
2 = Plateau
(inward Ca++ current)
3 = Repolarization
(outward K+ current)
4 = Resting Potential
Mechanical Response
MEMBRANE
POTENTIAL
(mV)
0 0
-50 -50
-100 -100
SAN
VENTRICULULAR
CELL
ACTION POTENTIALS
0
1
2
3
4
4
0 3
SINGLE VENTRICULAR ACTION POTENTIAL
ECG
P
Q S
T
R
1 mV
Repolarization of ventricles
Depolarization of ventricles
Depolarization of atria
ENDOCARDIAL FIBER
EPICARDIAL FIBER
ATRIAL
FIBER
LA
RA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly
& posteriorly)
3 Bipolar Limb Leads:
I = RA vs. LA (+)
LA
RA
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly
& posteriorly)
3 Bipolar Limb Leads:
I = RA vs. LA (+)
II = RA vs. LL (+)
LA
RA
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 (+)
LA
RA
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(+)
LA
RA
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(+)
LA
RA
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 V2
V3
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
ATRIAL
SYSTOLE
ISOMETRIC VENTRICULAR
CONTRACTION
VENTRICULAR
EJECTION
ISOMETRIC
VENTRICULAR
RELAXATION
THE CARDIAC CYCLE
DIASTOLE
ISOVOLUMETRIC RELAXATION
RAPID INFLOW
DIASTASIS
ATRIAL SYSTOLE
EJECTION
ISOVOLUMETRIC
CONTRACTION
SYSTOLE DIASTOLE SYSTOLE
AORTIC
PRESSURE
ATRIAL
PRESSURE
VENTRICLE
PRESSURE
ECG
PHONO-
CARDIOGAM
VOLUME
(ml)
PRESSURE
(mmHg)
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
PERIPHERAL
BLOOD FLOW
VENOUS RETURN
PULMONARY BLOOD FLOW
CARDIAC OUTPUT (Q) =
VO2
[O2]a - [O2]v
250 ml/min
20 ml% - 15 ml%
=
= 5 L/min
.
Q = HR x SV
.
SV =
Q
HR
.
=
5 L/min
70 beats/min
= 0.0714 L or 71.4 ml
CARDIAC INDEX =
Q
m2 body surface
area
.
5 L/min
1.6 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
Sympathetic
Nervous System
Parasympathetic
Nervous 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
SR
Fibrils
SARCOLEMMA
10%
Mitochondria
THICK
MYOFILAMENT
THIN MYOFILAMENT
SR
Ca++
T-tubule
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
Normal
Heart Rate
Ca++ Ca++
Fast
Heart 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 LENGTH
EQUILIBRIUM LENGTH
LENGTH
LENGTH
TENSION
TENSION
SARCOMERE LENGTH ()
TENSION
MUSCLE LENGTH
PASSIVE
TENSION
ACTAIVE TENSION
TOTAL TENSION
CARDIAC MUSCLE
PRESSURE
DIASTOLIC
PRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic Volume
End Systolic Volume
Isovolumetric
Phase
Isotonic (Ejection) Phase
Stroke
Volume
Pre-load
After-load
PRESSURE
DIASTOLIC
PRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic Volume
End Systolic Volume
Isovolumetric
Phase
Isotonic (Ejection) Phase
Stroke
Volume
Pre-load
After-load
PRESSURE
DIASTOLIC
PRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic Volume
End Systolic Volume
Isovolumetric
Phase
Isotonic (Ejection) Phase
Stroke
Volume
Pre-load
After-load
PRESSURE
DIASTOLIC
PRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic Volume
End Systolic Volume
Isovolumetric
Phase
Isotonic (Ejection) Phase
Stroke
Volume
Pre-load
After-load
CARDIAC FUNCTION CURVE
STROKE
VOLUME
DIASTOLIC FILLING
Cardiac Output = Stroke Volume x Heart Rate
Constant
If:
Then:  CO reflects SV
Right Atrial Pressure (RAP) reflects Diastolic Filling
CARDIAC FUNCTION CURVE
CARDIAC
OUTPUT
(L/min)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
Volume
Pressure
THE FRANK- STARLING “LAW OF THE HEART”
CARDIAC FUNCTION CURVE
CARDIAC
OUTPUT
(L/min)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
CARDIAC FUNCTION CURVE
CARDIAC
OUTPUT
(L/min)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
CARDIAC FUNCTION CURVE
CARDIAC
OUTPUT
(L/min)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
CARDIAC FUNCTION CURVE
CARDIAC
OUTPUT
(L/min)
RAP mmHg
15-
10-
5-
-4 0 +4 +8
THE FRANK- STARLING “LAW OF THE HEART”
P1 P2
P1 > P2
FLOW
FLOW = P
R
P = FLOW x R
R =
mm Hg
L/min
or
ml/sec
mm Hg
ml/sec
Peripheral Resistance Units (PRU)
P
FLOW
LAMINAR or STREAMLINE
FLOW
P2
P1
P1 > P2
-Cone Shaped Velocity Profile
-Not Audible with a Stethoscope
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
RT = RA + RC + RV
RESISTANCES IN PARALLEL
R1
R2
R3
PA
PV
FlowT = Flow1 + Flow2 + Flow3
P
RT
P
R1
P
R2
P
R3
= + +
1
RT
1
R1
1
R2
1
R3
= + +
1
R1
1
R2
1
R3
RT
1
+ +
=
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 /8l
Q = vr2
Poiseuille's Law
Pr4
8l
Q =
P
R
Flow =
R = 8l/r4
TOTAL PERIPHERAL RESISTANCE
TPR = Aortic Pressure - RAP
FLOW
TPR =
100 - 0 mmHg
83.3 ml/sec (5 L/min)
= 1.2 PRU’s
SYSTEMIC CIRCULATION:
PULMONARY CIRCULATION:
Pul. R. =Pul. Art. P. - LAP
FLOW
Pul. R. = 15 - 5 mmHg
83.3 ml/sec
= 0.12 PRU’s
VASCULAR COMPLIANCE
C =
V
P
PRESSURE
(mmHg)
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 ml
100 mmHg
300 ml
5 mmHg
Sym
Sym
MEAN CIRCULATORY PRESSURE
PRESSURE
(mmHg)
7-
1 2 3 4 5 6
Unstressed
Volume
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
Precapillary
Sphincters
Capillaries
Venule
?
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
DIFFUSION BETWEEN BLOOD & INTERSTITIAL FLUID
Plasma Proteins
BLOOD
O2 CO2 Glucose
INTERSTITIAL
FLUID
CELL
active transport
FLUID BALANCE
40-
30-
20-
10-
0-
PRESSURE
(mmHg)
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 mmHg
Inward 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-
PRESSURE
(mmHg)
Filtration vs. Reabsorption
Filtration Reabsorption
Via
lymphatics
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 protect
capillaries
VENOUS PUMP keeps PV < 25 mm Hg
Veins Arteries
190 mm Hg
100 mm Hg
0
ARTERIES
VEINS
(RAP)
7 mmHg
7 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-
PBF
or
VENOUS
RETURN
(L/min)
-4 0 +4 +8
RAP (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
PRESSURE
(mmHg)
7-
1 2 3 4 5 6
Unstressed
Volume
Stressed Volume
BLOOD VOLUME (L)
 VOLUME
 MCP
 VOLUME
 MCP
Normal
Hemorrhage
Infusion
MEAN CIRCULATORY PRESSURE
PRESSURE
(mmHg)
7-
1 2 3 4 5 6
Unstressed
Volume
Stressed Volume
BLOOD VOLUME (L)
Normal
VENOCONSTRICTION
MEAN CIRCULATORY PRESSURE
PRESSURE
(mmHg)
7-
1 2 3 4 5 6
Unstressed
Volume
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-
PBF
or
VENOUS
RETURN
(L/min)
-4 0 +4 +8
RAP (mmHg)
 MCP
 MCP
 Blood Volume
or
Venoconstriction
 Blood Volume
or
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-
PBF
or
VENOUS
RETURN
(L/min)
-4 0 +4 +8
RAP (mmHg)
 TPR
 TPR
Vasoconstriction
Vasodilation
CARDIAC & VASCULAR
FUNCTION CURVES
RAP mmHg
15-
10-
5-
-4 0 +4 +8
CARDIAC
OUTPUT
or
PERIPHERAL
BLOOD 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 Volume
Venous Capacity
- CHANGING TOTAL PERIPHERAL RESISTANCE
MOTOR CORTEX
HYPOTHALAMUS
VASOMOTOR CENTER
PRESSOR AREA
DEPRESSOR AREA
CARDIOINHIBITORY AREA
Vagus
HEART
Arterioles
Veins
Adrenal
Medulla
Baroreceptors
Carotid Sinus
Aortic Arch
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
Chemosensitive Area
Glossopharyngeal
Nerve
Sympathetic
Nervous
System
 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
Hypothalamic
Osmoreceptors
 BP via Posterior Pituitary  Vasopressin (ADH)
(Atrial Receptors)
Vasoconstriction  Water
Venoconstriction Retention
VASOPRESSIN
(ANTIDIURETIC HORMONE)
X
X
RENAL--BODY FLUID
CONTROL MECHANISM
8-
7-
6-
5-
4-
3-
2-
1-
-8
-7
-6
-5
-4
-3
-2
-1
Uninary
Output
(x normal)
Fluid
Intake
(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 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
Pressure
7-
1 2 3 4 5
Blood Volume (L)
MCP
-4 0 +4 +8
RAP (mmHg)
CO
or
PBF
(L/min)
CO
BP
CARDIAC & VASCULAR
FUNCTION CURVES
RAP mmHg
15-
10-
5-
-4 0 +4 +8
CARDIAC
OUTPUT
or
PERIPHERAL
BLOOD FLOW
[Venous Return]
(L/min)
Response to Hemorrhage
 HR & Contractility
Venoconstriction ( 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
PRESSURE
(mmHg)
7-
1 2 3 4 5 6
Unstressed
Volume
Stressed Volume
BLOOD VOLUME (L)
 Unstressed Vol.
 Stressed Vol.
 MCP
Normal
Syncope (Fainting)
Pressure
7-
1 2 3 4 5
Blood Volume (L)
MCP
-4 0 +4 +8
RAP (mmHg)
CO
or
PBF
(L/min)
CO
BP
SYNCOPE (FAINTING)
Blood pooling in the extremities
CARDIAC & VASCULAR
FUNCTION CURVES
RAP mmHg
15-
10-
5-
-4 0 +4 +8
CARDIAC
OUTPUT
or
PERIPHERAL
BLOOD FLOW
[Venous Return]
(L/min)
Response to Syncope (Fainting
 HR & Contractility
Venoconstriction ( MCP)
Vasoconstriction ( TPR)
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 CURVES
RAP mmHg
15-
10-
5-
-4 0 +4 +8
CARDIAC
OUTPUT
or
PERIPHERAL
BLOOD FLOW
[Venous Return]
(L/min)
Cardiac Failure
Adjustments to Failure
SYMPTOMS:
Systemic Edema
Pulmonary
Congestion
Enlarged Heart
PRESSURE
DIASTOLIC
PRESSURE CURVE
SYSTOLIC PRESSURE CURVE
HEART
End Diastolic Volume
End Systolic Volume
Isovolumetric
Phase
Isotonic (Ejection) Phase
Stroke
Volume
Pre-load
After-load
TEMPERATURE REGUALTION
• Body Temperature
• Heat Production
• Heat Loss
• Temperature Regulation
– Heat Exhaustion
– Heat Stroke
– Hypothermia
• Fever
COLD
WARM
Upper limit of survival?
Heat stroke
Brain lesions
Fever therapy
Febrile disease
and
Hard exercise
Usual range of normal
Temperature
regulation
seriously
impaired
Temperature
regulation
efficient in
febrile disease
health and work
Temperature
regulation
impaired
Temperature
regulation
lost Lower limit
of 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 HOT
RADIATION
CONDUCTION 70% 
CONVECTION
VAPORIZATION 30% 
Insensible Water Loss * *
Sweating *
SKIN HYPOTHALAMUS
Sweating
Vasodilation
Vasoconstriction
Shivering
W
W
W
Set
point
C
Warm
Receptors
Cold
Receptors
Preoptic Area
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
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 = 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”
FEVER
Actual Core
Temperature
Onset of
Fever
Fever
Breaks
Reference
Temperature
or Set Point
Shivering
Vasoconstriction
Sweating
Vasodilation

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PHIS502CVf(1).ppt