Download cardiovascular physiology

CARDIOVASCULAR
PHYSIOLOGY
Dr. Poland
Room 3-007, Sanger Hall
Phone: 828-9557
E-mail: [email protected]
HEART
(PUMP)
REGULATION
CARDIOVASCULAR
SYSTEM
VESSELS
(DISTRIBUTION SYSTEM)
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
ARTERIES (LOW COMPLIANCE)
HEART
DIASTOLE
VEINS
CAPACITY
VESSELS
80 mmHg
120 mmHg
SYSTOLE
CAPILLARIES
THE SYSTEMIC CIRCULATION
CAPACITY VESSELS
NORMAL
AUTOMATICITY
Na+
K+
Gradually
increasing PNa
Na+
+
K
-70 mV
THRESHOLD
RESTING
-0
Atrio-ventricular (AV) node
Sino-atrial
(SA) node
BUNDLE
BRANCHES
PURKINJE FIBERS
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
0
PHASE
0 = Rapid Depolarization
Mechanical Response
(inward Na+ current)
1
1 = Overshoot
2
2 = Plateau
(inward Ca++ current)
3 = Repolarization
+ current)
(outward
K
0
4 = Resting Potential
3
4
-90
TIME
MEMBRANE POTENTIAL (mV)
ACTION POTENTIALS
0
VENTRICULULAR
CELL
1
2
SAN
0
0
-50
0
3
-50
4
-100
-100
4
3
SINGLE VENTRICULAR ACTION POTENTIAL
ENDOCARDIAL FIBER
ATRIAL
FIBER
EPICARDIAL FIBER
R
1 mV
ECG
P
T
QS
Repolarization of ventricles
Depolarization of ventricles
Depolarization of atria
ECG Recordings (QRS Vector pointing leftward, inferiorly
& posteriorly)
3 Bipolar Limb Leads:
RA
LA
I = RA vs. LA (+)
LL
ECG Recordings (QRS Vector pointing leftward, inferiorly
& posteriorly)
3 Bipolar Limb Leads:
RA
LA
I = RA vs. LA (+)
II = RA vs. LL (+)
LL
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
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:
aVR = (LA-LL) vs. RA(+)
LL
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:
aVR = (LA-LL) vs. RA(+)
aVL = (RA-LL) vs. LA(+)
LL
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:
aVR = (LA-LL) vs. RA(+)
aVL = (RA-LL) vs. LA(+)
aVF = (RA-LA) vs. LL(+)
LL
6 PRECORDIAL (CHEST) LEADS
Spine
V6
V5
Sternum
V1
V2
V3
V4
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.
THE CARDIAC CYCLE
LATE DIASTOLE
DIASTOLE
ISOMETRIC
VENTRICULAR
RELAXATION
VENTRICULAR
EJECTION
ATRIAL
SYSTOLE
ISOMETRIC VENTRICULAR
CONTRACTION
EJECTION
PRESSURE (mmHg)
ISOVOLUMETRIC RELAXATION
RAPID INFLOW
ISOVOLUMETRIC
DIASTASIS
CONTRACTION
ATRIAL SYSTOLE
AORTIC
PRESSURE
ATRIAL
PRESSURE
VOLUME (ml)
VENTRICLE
PRESSURE
ECG
PHONOCARDIOGAM
SYSTOLE
DIASTOLE
SYSTOLE
MEASUREMENT OF CARDIAC OUTPUT
THE FICK METHOD:
VO2 = ([O2]a - [O2]v) x Flow
Spirometry (250 ml/min)
VO2
Flow =
[O2]a - [O2]v
Pulmonary Artery Blood (15 ml%)
Arterial Blood (20 ml%)
CARDIAC OUTPUT
PULMONARY BLOOD FLOW
VENOUS RETURN
PERIPHERAL
BLOOD FLOW
.
VO2
CARDIAC OUTPUT (Q) = [O ] - [O ]
2 a
2 v
=
250 ml/min
20 ml% - 15 ml%
= 5 L/min
.
Q = HR x SV
.
Q
SV =
HR
.
CARDIAC INDEX = Q 2
m body surface
area
= 5 L/min
5 L/min
70 beats/min
=
1.6 m2
= 0.0714 L or 71.4 ml
= 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
Autoregulation
(Frank-Starling “Law of the Heart”)
CARDIAC OUTPUT = STROKE VOLUME x HEART RATE
Contractility
Sympathetic
Nervous System
Parasympathetic
Nervous System
CARDIAC MUSCLE
- Functional Syncytium
- Automaticity
STRIATED MUSCLE
SKELETAL MUSCLE
- Motor Units
- Stimulated by Motor Nerves
STRUCTURE OF A MYOCARDIAL CELL
Mitochondria
Sarcolemma
T-tubule
SR
Fibrils
T-tubule
SARCOLEMMA
20%
80%
Mitochondria
10%
Ca++
SR
THICK
MYOFILAMENT
THIN MYOFILAMENT
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
Fast
Heart Rate
Ca++
Ca++
Ca++
Ca++
Ca++
Ca++
SERIES ELASTIC
ELEMENTS
CONTRACTILE
COMPONENT
PARALLEL ELASTIC
ELEMENTS
(ACTIVE TENSION)
(PASSIVE TENSION)
TOTAL
TENSION
LENGTH-TENSION CURVE
TOTAL TENSION
ACTIVE
TENSION
TENSION
EQUILIBRIUM LENGTH
LENGTH
LENGTH
PASSIVE TENSION
OPTIMAL LENGTH (Lo)
RESTING LENGTH
TENSION
SARCOMERE LENGTH ()
CARDIAC MUSCLE
TOTAL TENSION
TENSION
ACTAIVE TENSION
PASSIVE
TENSION
MUSCLE LENGTH
HEART
SYSTOLIC PRESSURE CURVE
Isotonic (Ejection) Phase
PRESSURE
After-load
Isovolumetric
Phase
Stroke
Volume
Pre-load
End Systolic Volume
DIASTOLIC
PRESSURE CURVE
End Diastolic Volume
HEART
SYSTOLIC PRESSURE CURVE
Isotonic (Ejection) Phase
PRESSURE
After-load
Isovolumetric
Phase
Stroke
Volume
Pre-load
End Systolic Volume
DIASTOLIC
PRESSURE CURVE
End Diastolic Volume
HEART
SYSTOLIC PRESSURE CURVE
Isotonic (Ejection) Phase
PRESSURE
After-load
Isovolumetric
Phase
Stroke
Volume
Pre-load
End Systolic Volume
DIASTOLIC
PRESSURE CURVE
End Diastolic Volume
HEART
SYSTOLIC PRESSURE CURVE
Isotonic (Ejection) Phase
PRESSURE
After-load
Isovolumetric
Phase
Stroke
Volume
Pre-load
End Systolic Volume
DIASTOLIC
PRESSURE CURVE
End Diastolic Volume
CARDIAC FUNCTION CURVE
STROKE VOLUME
Cardiac Output = Stroke Volume x Heart Rate
If: Constant
Then:  CO reflects SV
DIASTOLIC FILLING
Right Atrial Pressure (RAP) reflects Diastolic Filling
CARDIAC FUNCTION CURVE
15-
10-
Pressure
CARDIAC OUTPUT (L/min)
THE FRANK- STARLING “LAW OF THE HEART”
5-
Volume
-4
0
+4
RAP mmHg
+8
CARDIAC FUNCTION CURVE
CARDIAC OUTPUT (L/min)
THE FRANK- STARLING “LAW OF THE HEART”
15-
10-
5-
-4
0
+4
RAP mmHg
+8
CARDIAC FUNCTION CURVE
CARDIAC OUTPUT (L/min)
THE FRANK- STARLING “LAW OF THE HEART”
15-
10-
5-
-4
0
+4
RAP mmHg
+8
CARDIAC FUNCTION CURVE
CARDIAC OUTPUT (L/min)
THE FRANK- STARLING “LAW OF THE HEART”
15-
10-
5-
-4
0
+4
RAP mmHg
+8
CARDIAC FUNCTION CURVE
CARDIAC OUTPUT (L/min)
THE FRANK- STARLING “LAW OF THE HEART”
15-
10-
5-
-4
0
+4
RAP mmHg
+8
P1 > P2
P1
mm Hg
FLOW
P2
P = FLOW x R
FLOW = P
R
R=
L/min
or
ml/sec
P
FLOW
mm Hg
ml/sec
Peripheral Resistance Units (PRU)
LAMINAR or STREAMLINE
FLOW
P1
P2
P1 > P2
-Cone Shaped Velocity Profile
-Not Audible with a Stethoscope
MEASURING BLOOD PRESSURE
TURBULENT FLOW
1.
2.
3.
4.
Cuff pressure > systolic blood pressure--No sound.
The first sound is heard at peak systolic pressure.
Sounds are heard while cuff pressure < blood pressure.
Sound disappears when cuff pressure < diastolic pressure.
RESISTANCES IN SERIES
RT = RA + RC + RV
RESISTANCES IN PARALLEL
FlowT = Flow1 + Flow2 + Flow3
P = P + P + P
RT
R1
R2 R3
1 = 1 + 1 + 1
RT R1 R2
R3
RT =
1
1 + 1 + 1
R1 R2 R3
R1
PV
PA
R2
R3
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:
1
RT = 1
=1.94 PRU’s
1
1
+
+
R1
R2 R3
Poiseuille's Law
v = Pr2 /8l
P
Flow = R
Q = vr2
Pr4
Q = 8l
R = 8l/r4
TOTAL PERIPHERAL RESISTANCE
SYSTEMIC CIRCULATION:
TPR = Aortic Pressure - RAP
FLOW
TPR =
100 - 0 mmHg
= 1.2 PRU’s
83.3 ml/sec (5 L/min)
PULMONARY CIRCULATION:
Pul. R. = Pul. Art. P. - LAP
FLOW
Pul. R. = 15 - 5 mmHg = 0.12 PRU’s
83.3 ml/sec
PRESSURE (mmHg)
VASCULAR COMPLIANCE
V
C=
P
Arteries
ml
Ca = 250
=2.5 ml/mmHg
100
mmHg
100Sym
ml = 60 ml/mmHg
Cv = 300
5 mmHg
Sym
Cv = 24 x Ca
Veins
Sym
1
2
Sym
4
3
VOLUME (L)
PRESSURE (mmHg)
MEAN CIRCULATORY PRESSURE
Unstressed
Volume
Stressed Volume
7MCP = 7 mmHg
1
2
3
4
VOLUME (L)
5
6
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
Arteriole
Precapillary
Sphincters
Capillaries
Metarteriole
Venule
?
VASOMOTION = Intermittent flow due to constrictionrelaxation 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
INTERSTITIAL
FLUID
CELL
O2
CO2 Glucose
active transport
PRESSURE (mmHg)
FLUID BALANCE
Filtration vs. Reabsorption
40Outward Forces:
1. Capillary blood pressure
(Pc = 35 to 15 mmHg)
302. Interstitial fluid pressure
(PIF = 0 mmHg)
3. Interstitial fluid colloidal
20osmotic pressure
(IF = 3 mmHg)
10-
0-
TOTAL = 38 to 18 mmHg
Inward Force:
1. Plasma colloidal osmotic
pressure (C = 28 mmHg)
CAPILLARY FLUID SHIFT
Pout > c
Pc
FAVORS FILTRATION
Pout < c
Pc
FAVORS REABSORPTION
PULMONARY CIRCULATION
FLUID BALANCE
PRESSURE (mmHg)
Filtration vs. Reabsorption
40-
30Via
lymphatics
20Filtration
Reabsorption
10RADIAL FLOW
0-
LYMPHATIC CAPILLARY
2 - 4 L/day ( 125 ml/hr)
“PUMP”
Compression
Smooth muscle contraction
Anchoring Filaments
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
HEART
 Art. BP
VEINS
(RAP)
CO = PBF
 RAP
7 mmHg 
ARTERIES
7 mmHg
Peripheral Blood Flow
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
0
7
6
5
4
3
7
31
55
79
103
0
25
50
75
100
1.2
1.2
1.2
1.2
1.2
0
20.8
41.7
62.5
83.3 (5 L/min)
THE VASCULAR FUNCTION CURVE
10PBF
or
VENOUS
RETURN 5(L/min)
0-
-4
0
+4
RAP (mmHg)
+8
WAYS TO ALTER THE
VASCULAR FUNCTION CURVE
• CHANGE THE MEAN
CIRCULATORY PRESSURE
• CHANGE BLOOD VOLUME
• CHANGE VENOUS CAPACITY
• CHANGE TOTAL PERIPHERAL
RESISTANCE
PRESSURE (mmHg)
MEAN CIRCULATORY PRESSURE
7-
Unstressed
Volume
Infusion
Normal
Stressed Volume
Hemorrhage
1
2
3
4
5
BLOOD VOLUME (L)
 VOLUME
 MCP
 VOLUME
 MCP
6
MEAN CIRCULATORY PRESSURE
PRESSURE (mmHg)
VENOCONSTRICTION
Unstressed
Volume
7-
Stressed Volume
Normal
1
2
3
4
5
BLOOD VOLUME (L)
6
MEAN CIRCULATORY PRESSURE
PRESSURE (mmHg)
VENODILATION
Unstressed
Volume
7-
Stressed Volume
Normal
1
2
3
4
5
BLOOD VOLUME (L)
6
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
0
 MCP 8
0
7
6
5
4
3
7
31
55
79
103
0
25
50
75
100
1.2
1.2
1.2
1.2
1.2
0
20.8
41.7
62.5
83.3 (5 L/min)
8
7
6
5
4
3
8
32
56
80
104
128
0
25
50
75
100
125
1.2
1.2
1.2
1.2
1.2
1.2
0
20.8
41.7
62.5
83.3 (5 L/min)
104.2 (6.25 L
min
THE VASCULAR FUNCTION CURVE
10PBF
or
VENOUS
RETURN 5(L/min)
 Blood Volume
or
Venodilation
0-
 MCP
 Blood Volume
or
Venoconstriction
 MCP
-4
0
+4
RAP (mmHg)
+8
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
0
 TPR 7
0
7
6
5
4
3
7
31
55
79
103
0
25
50
75
100
1.2
1.2
1.2
1.2
1.2
0
20.8
41.7
62.5
83.3 (5 L/min)
7
6
5
4
3
7
31
55
79
103
0
25
50
75
100
2.0
2.0
2.0
2.0
2.0
0
12.5
25.0
37.5
50.0 (3 L/min)
THE VASCULAR FUNCTION CURVE
Vasodilation
10PBF
or
VENOUS
RETURN 5(L/min)
Vasoconstriction 0-
 TPR
 TPR
-4
0
+4
RAP (mmHg)
+8
CARDIAC & VASCULAR
FUNCTION CURVES
CARDIAC 15OUTPUT
or
10-
PERIPHERAL
BLOOD FLOW
[Venous Return] 5-
(L/min)
-4
0
+4
RAP mmHg
+8
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
Chemosensitive Area
Glossopharyngeal
Nerve
Sympathetic
Nervous
System
VASOMOTOR CENTER
PRESSOR AREA
DEPRESSOR AREA
CARDIOINHIBITORY AREA
Baroreceptors
Carotid Sinus
Aortic Arch
Chemoreceptors
Carotid Bodies
Aortic Bodies
Atrial Receptors
Vagus
HEART
Arterioles
Veins
Adrenal
Medulla
Bainbridge Reflex ( Heart Rate)
Volume Reflex ( Urinary OUTPUT)
a.  Vascular Sympathetic Tone
b.  ADH Secretion
c.  Aldosterone Secretion
RENIN-ANGIOTENSIN-ALDOSTERONE MECHANISM
Angiotensinogen (renin substrate)
 BP
(Kidney)
Renin
Angiotensin
Vasoconstriction
Venoconstriction
Aldosterone
Kidney
 sodium & water retention
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
VASOPRESSIN
(ANTIDIURETIC HORMONE)
Hypothalamic
Osmoreceptors
 BP via Posterior Pituitary
 Vasopressin (ADH)
X
(Atrial Receptors)
X
Vasoconstriction
 Water
Venoconstriction
Retention
RENAL--BODY FLUID
CONTROL MECHANISM
8- All Mechanisms
76Fluid 5Intake
4(x normal)
3- 3 x Normal
21- Normal
-8
-7
-6
Uninary
-5
Output
-4 (x normal)
-3
P alone -2
-1
50
100
150
ARTERIAL BLOOD PRESSURE (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
Pressure
7MCP
CO
or
PBF
1 2 3 4 5 (L/min)
Blood Volume (L)
-4
CO
BP
0
+4
+8
RAP (mmHg)
CARDIAC & VASCULAR
FUNCTION CURVES
CARDIAC 15OUTPUT
or
10-
Response to Hemorrhage
 HR & Contractility
Venoconstriction ( MCP)
Vasoconstriction ( TPR)
PERIPHERAL
BLOOD FLOW
[Venous Return] 5-
(L/min)
-4
0
+4
RAP mmHg
+8
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, ReninAngiotensin-Aldosterone)
• Restore plasma proteins & hematocrit
SYNCOPE (FAINTING)
Postural syncope
(Blood pooling in the extremities)
Vasovagal syncope
Carotid sinus syncope
PRESSURE (mmHg)
SYNCOPE (FAINTING)
Blood pooling in the extremities
Unstressed
Stressed Volume
Volume
7-
Normal
Syncope (Fainting)
1
2
3
4
5
BLOOD VOLUME (L)
 Unstressed Vol.
 Stressed Vol.
 MCP
6
SYNCOPE (FAINTING)
Blood pooling in the extremities
Pressure
7MCP
CO
or
PBF
1 2 3 4 5 (L/min)
Blood Volume (L)
-4
CO
BP
0
+4
+8
RAP (mmHg)
CARDIAC & VASCULAR
FUNCTION CURVES
CARDIAC 15OUTPUT
or
10Response to Syncope (Fainting
 HR & Contractility
Venoconstriction ( MCP)
Vasoconstriction ( TPR)
PERIPHERAL
BLOOD FLOW
[Venous Return] 5-
(L/min)
-4
0
+4
RAP mmHg
+8
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
CARDIAC 15OUTPUT
or
SYMPTOMS:
Systemic Edema
Pulmonary
Congestion
Enlarged Heart
10-
PERIPHERAL
BLOOD FLOW
[Venous Return] 5-
Adjustments to Failure
Cardiac Failure
(L/min)
-4
0
+4
RAP mmHg
+8
HEART
SYSTOLIC PRESSURE CURVE
Isotonic (Ejection) Phase
PRESSURE
After-load
Isovolumetric
Phase
Stroke
Volume
Pre-load
End Systolic Volume
DIASTOLIC
PRESSURE CURVE
End Diastolic Volume
TEMPERATURE REGUALTION
•
•
•
•
Body Temperature
Heat Production
Heat Loss
Temperature Regulation
– Heat Exhaustion
– Heat Stroke
– Hypothermia
• Fever
WARM
COLD
Temperature
regulation
seriously
impaired
Temperature
regulation
efficient in
febrile disease
health and work
Upper limit of survival?
Heat stroke
Brain lesions
Fever therapy
Febrile disease
and
Hard exercise
Usual range of normal
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
RADIATION
CONDUCTION
CONVECTION
VAPORIZATION
Insensible Water Loss
Sweating
HOT
70%

30%
*

*
*
SKIN
HYPOTHALAMUS
Preoptic Area
W
Warm
Receptors
Set
W
point
W
Cold
Receptors
Sweating
Vasodilation
C
Vasoconstriction
Shivering
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
FEVER = an abnormally high body temperature
PYROGEN = a fever producing substance
PYROGEN
WBC
bacterial toxins,
leukocytes,
viruses, pollen, + monocytes
proteins, dust
= endogenous pyrogen
Arachidonic Acid
Prostaglandins
Aspirin
RAISES THE “SET POINT”
Shivering
Vasoconstriction
Reference
Temperature
or Set Point
Onset of
Fever
Sweating
Vasodilation
Actual Core
Temperature
Fever
Breaks