CARDIOVASCULAR PHYSIOLOGY

1
CARDIOVASCULAR PHYSIOLOGY

• Dr. Poland
• Room 3-007, Sanger Hall
• Phone [phone]
• E-mail poland_at_hsc.vcu.edu

2
HEART (PUMP)
AUTOREGULATION
CARDIOVASCULAR SYSTEM
NEURAL
REGULATION
HORMONAL
VESSELS (DISTRIBUTION SYSTEM)
RENAL-BODY FLUID CONTROL SYSTEM
3
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
4
ARTERIES (LOW COMPLIANCE)
HEART
DIASTOLE
VEINS CAPACITY VESSELS
80 mmHg
120 mmHg
SYSTOLE
CAPILLARIES
5
THE SYSTEMIC CIRCULATION
CAPACITY VESSELS
6
NORMAL
7
AUTOMATICITY
Na
K
Gradually increasing PNa
K
Na
-0
-70 mV
THRESHOLD
RESTING
8
Atrio-ventricular (AV) node
Sino-atrial (SA) node
BUNDLE BRANCHES
PURKINJE FIBERS
9
INTERCALATED DISC (TIGHT JUNCTION)
10
PACEMAKERS (in order of their inherent rhythm)

• Sino-atrial (SA) node
• Atrio-ventricular (AV) node
• Bundle of His
• Bundle branches
• Purkinje fibers

11
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
12
ACTION POTENTIALS
VENTRICULULAR CELL
SAN
1
2
0
0
0
3
0
3
4
-50
-50
MEMBRANE POTENTIAL (mV)
4
-100
-100
13
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
14
ECG Recordings (QRS Vector pointing leftward,
inferiorly posteriorly)
3 Bipolar Limb Leads
RA
LA
I RA vs. LA ()
LL
15
ECG Recordings (QRS Vector pointing leftward,
inferiorly posteriorly)
3 Bipolar Limb Leads
RA
LA
I RA vs. LA ()
II RA vs. LL ()
LL
16
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
17
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()
18
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()
19
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()
20
6 PRECORDIAL (CHEST) LEADS
Spine
V6
V5
Sternum
V4
V3
V1
V2
21
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.
22
THE CARDIAC CYCLE
LATE DIASTOLE
DIASTOLE
ISOMETRIC VENTRICULAR RELAXATION
ATRIAL SYSTOLE
VENTRICULAR EJECTION
ISOMETRIC VENTRICULAR CONTRACTION
23
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
24
MEASUREMENT OF CARDIAC OUTPUT
THE FICK METHOD
VO2 (O2a - O2v) x Flow
Spirometry (250 ml/min)
VO2 O2a - O2v
Flow
Pulmonary Artery Blood (15 ml)
Arterial Blood (20 ml)
CARDIAC OUTPUT
PULMONARY BLOOD FLOW
VENOUS RETURN
PERIPHERAL BLOOD FLOW
25
VO2 O2a - O2v
.
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
26
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

27
Autoregulation (Frank-Starling Law of the
Heart)
CARDIAC OUTPUT STROKE VOLUME x HEART RATE
Contractility
Sympathetic Nervous System
Parasympathetic Nervous System
28
CARDIAC MUSCLE
- Functional Syncytium - Automaticity
STRIATED MUSCLE
SKELETAL MUSCLE
- Motor Units - Stimulated by Motor Nerves
29
STRUCTURE OF A MYOCARDIAL CELL
Sarcolemma
Mitochondria
T-tubule
SR
Fibrils
30
SARCOLEMMA
10
Mitochondria
20
80
T-tubule
Ca
SR
THICK MYOFILAMENT
THIN MYOFILAMENT
31
REGULATAION OF CONTRACTILITY

• Recruitment of motor units
• Increase frequency of firing of motor nerves
• Calcium to trigger contraction

32
INCREASING HEART RATE INCREASES CONTRACTILITY
Ca
Ca
Normal Heart Rate
Fast Heart Rate
Ca
Ca
Ca
Ca
33
SERIES ELASTIC ELEMENTS
CONTRACTILE COMPONENT (ACTIVE TENSION)
PARALLEL ELASTIC ELEMENTS (PASSIVE TENSION)
TOTAL TENSION
34
LENGTH-TENSION CURVE
TOTAL TENSION
ACTIVE TENSION
TENSION
PASSIVE TENSION
OPTIMAL LENGTH (Lo)
RESTING LENGTH
EQUILIBRIUM LENGTH
LENGTH
LENGTH
35
TENSION
SARCOMERE LENGTH (?)
36
CARDIAC MUSCLE
TOTAL TENSION
ACTAIVE TENSION
TENSION
PASSIVE TENSION
MUSCLE LENGTH
37
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
38
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
39
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
40
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
41
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
42
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
43
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
44
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
45
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
46
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
47
P1 gt P2
P1
P2
FLOW
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)
48
LAMINAR or STREAMLINE FLOW
P2
P1
P1 gt P2
-Cone Shaped Velocity Profile -Not Audible with a
Stethoscope
49
MEASURING BLOOD PRESSURE TURBULENT FLOW
1. Cuff pressure gt systolic blood pressure--No
sound. 2. The first sound is heard at peak
systolic pressure. 3. Sounds are heard while
cuff pressure lt blood pressure. 4. Sound
disappears when cuff pressure lt diastolic
pressure.
50
RESISTANCES IN SERIES
RT RA RC RV
RESISTANCES IN PARALLEL
FlowT Flow1 Flow2 Flow3
?P RT
?P R1
?P R2
?P R3



R1
PA
PV
1 RT
1 R1
1 R2
1 R3
R2



R3
1
RT

1 R1
1 R2
1 R3


51
If R1 2 R2 4 R3 6 PRUs Then a series
arrangement gives RT R1 R2 R3 RT 12
PRUs But a parallel arrangement gives RT
1.94 PRUs
1
1 R1
1 R2
1 R3


52
Poiseuille's Law
v ?Pr2 /8?l
?P R
Flow
Q v?r2
?P?r4 8?l
Q
R 8?l/?r4
53
TOTAL PERIPHERAL RESISTANCE
SYSTEMIC CIRCULATION
Aortic Pressure - RAP FLOW
TPR
100 - 0 mmHg 83.3 ml/sec (5 L/min)
1.2 PRUs
TPR
PULMONARY CIRCULATION
Pul. Art. P. - LAP FLOW
Pul. R.
15 - 5 mmHg 83.3 ml/sec
Pul. R.
0.12 PRUs
54
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)
55
MEAN CIRCULATORY PRESSURE
Unstressed Volume
Stressed Volume
7-
PRESSURE (mmHg)
MCP 7 mmHg
1 2 3 4 5
6
VOLUME (L)
56
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

57
Arteriole
?
Precapillary Sphincters
Capillaries
Metarteriole
Venule
58
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
59
DIFFUSION BETWEEN BLOOD INTERSTITIAL FLUID
Plasma Proteins
BLOOD
INTERSTITIAL FLUID
O2
CO2
Glucose
active transport
CELL
60
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)
61
CAPILLARY FLUID SHIFT
Pout gt ?c Pout lt ?c
?Pc
?Pc
FAVORS FILTRATION
FAVORS REABSORPTION
PULMONARY CIRCULATION
62
FLUID BALANCE
Filtration vs. Reabsorption
40- 30- 20- 10- 0-
Via lymphatics
PRESSURE (mmHg)
Filtration Reabsorption
RADIAL FLOW
63
LYMPHATIC CAPILLARY
2 - 4 L/day (? 125 ml/hr)
PUMP Compression Smooth muscle contraction
Anchoring Filaments
64
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 lt 25 mm Hg
65
HEART
? Art. BP
CO PBF
VEINS (RAP)
ARTERIES
? RAP
?7 mmHg
7 mmHg ?
Peripheral Blood Flow
66
RELATIONSHIP BETWEEN RAP and PBF
Cv 24 x Ca ?P
RAP Pv Pa ?P Pa - Pv
TPR PBFTPR (mmHg) (mmHg) (mmHg) (mmHg)
(PRUs) (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)
67
THE VASCULAR FUNCTION CURVE
10- 5- 0-
PBF or VENOUS RETURN (L/min)
-4 0 4
8
RAP (mmHg)
68
WAYS TO ALTER THE VASCULAR FUNCTION CURVE

• CHANGE THE MEAN CIRCULATORY PRESSURE
• CHANGE BLOOD VOLUME
• CHANGE VENOUS CAPACITY
• CHANGE TOTAL PERIPHERAL RESISTANCE

69
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)
70
MEAN CIRCULATORY PRESSURE
VENOCONSTRICTION
Unstressed Volume
Stressed Volume
Normal
7-
PRESSURE (mmHg)
1 2 3 4 5
6
BLOOD VOLUME (L)
71
MEAN CIRCULATORY PRESSURE
VENODILATION
Unstressed Volume
Stressed Volume
Normal
7-
PRESSURE (mmHg)
1 2 3 4 5
6
BLOOD VOLUME (L)
72
RELATIONSHIP BETWEEN RAP and PBF
Cv 24 x Ca ?P
RAP Pv Pa ?P Pa - Pv
TPR PBFTPR (mmHg) (mmHg) (mmHg) (mmHg)
(PRUs) (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
73
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)
74
RELATIONSHIP BETWEEN RAP and PBF
Cv 24 x Ca ?P
RAP Pv Pa ?P Pa - Pv
TPR PBFTPR (mmHg) (mmHg) (mmHg) (mmHg)
(PRUs) (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
75
THE VASCULAR FUNCTION CURVE
Vasodilation
10- 5- 0-
PBF or VENOUS RETURN (L/min)
? TPR
? TPR
Vasoconstriction
-4 0 4
8
RAP (mmHg)
76
CARDIAC VASCULAR FUNCTION CURVES
15-
CARDIAC OUTPUT or PERIPHERAL BLOOD
FLOW Venous Return (L/min)
10-
5-
-4
0
4
8
RAP mmHg
77
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
78
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
79
RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM
Angiotensinogen (renin substrate) Angiotensin
Aldosterone Kidney ? sodium water
retention
? BP (Kidney) Renin
Vasoconstriction Venoconstriction
80
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

81
VASOPRESSIN (ANTIDIURETIC HORMONE)
Hypothalamic Osmoreceptors ? BP via Posterior
Pituitary ? Vasopressin (ADH) (Atrial
Receptors) Vasoconstriction ?
Water Venoconstriction Retention
X
X
82
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)
83
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 Red
uce stress Sympathetic blockers Low sodium
diet Diuretics
84
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)
85
CARDIAC VASCULAR FUNCTION CURVES
15-
CARDIAC OUTPUT or PERIPHERAL BLOOD
FLOW Venous Return (L/min)
10-
Response to Hemorrhage ? HR Contractility Venoc
onstriction (? MCP) Vasoconstriction (? TPR)
5-
-4
0
4
8
RAP mmHg
86
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

87
SYNCOPE (FAINTING)Postural syncope(Blood
pooling in the extremities) Vasovagal
syncopeCarotid sinus syncope
88
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)
89
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)
90
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
91
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
92
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
93
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
94
TEMPERATURE REGUALTION

• Body Temperature
• Heat Production
• Heat Loss
• Temperature Regulation
• Heat Exhaustion
• Heat Stroke
• Hypothermia
• Fever

95
COLD
WARM
96
Temperature regulation seriously impaired Tempera
ture regulation efficient in febrile
disease health and work Temperature regulation im
paired 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?
97
HEAT PRODUCTION
BASAL METABOLIC RATE - Catecholamines -Hyperth
yroidism FOOD INTAKE (Specific Dynamic
Action) -lasts up to 6 hours after a
meal PHYSICAL ACTIVITY -Exercise (20 x
BMR) -Shivering (5 x BMR)
98
HEAT LOSS
COOL HOT RADIATION CONDUCTION 70
? CONVECTION VAPORIZATION 30
? Insensible Water Loss
Sweating
99
SKIN HYPOTHALAMUS
Preoptic Area
Sweating Vasodilation
W
Set point
Warm Receptors Cold Receptors
W
Vasoconstriction Shivering
W
C
100
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.
101
LIMITS TOTEMPERATURE REGULATION
Heat Exhaustion Inadequate water/salt
replacement Body temperature may be
normal Symptoms cerebral dysfunction naus
ea 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!
102
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 Asp
irin RAISES THE SET POINT
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Shivering Vasoconstriction
Sweating Vasodilation
Reference Temperature or Set Point
Actual Core Temperature
Fever Breaks
Onset of Fever