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CARDIOVASCULAR

PHYSIOLOGY
Dr. Poland
Room 3-007, Sanger Hall
Phone: 828-9557
E-mail: poland@hsc.vcu.edu
HEART
(PUMP)
AUTOREGULATION

REGULATION
CARDIOVASCULAR
SYSTEM NEURAL

HORMONAL
VESSELS
(DISTRIBUTION SYSTEM) 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
80 mmHg 120 mmHg
CAPACITY
VESSELS

SYSTOLE

CAPILLARIES
THE SYSTEMIC CIRCULATION
CAPACITY VESSELS
NORMAL
AUTOMATICITY
Na +
K+
Gradually
increasing PNa
Na+
K+
-70 mV -0

THRESHOLD
RESTING
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
PHASE
Mechanical Response 0 = Rapid Depolarization
(inward Na+ current)
MEMBRANE POTENTIAL (mV)

1 1 = Overshoot
0 2
2 = Plateau
(inward Ca++ current)
3 = Repolarization
0 (outward K+ current)
4 = Resting Potential
3

-90 4

TIME
ACTION POTENTIALS

VENTRICULULAR
MEMBRANE POTENTIAL (mV)

SAN
CELL
1
0 2
0
0 3
0 3 4
-50 -50

4
-100 -100
SINGLE VENTRICULAR ACTION POTENTIAL

ATRIAL ENDOCARDIAL FIBER


FIBER
EPICARDIAL FIBER

1 mV

ECG T
P
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:


LL
aVR = (LA-LL) vs. RA(+)
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(+)
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(+)


6 PRECORDIAL (CHEST) LEADS

Spine

V6
V5
Sternum V4
V1 V2 V3
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 ATRIAL
RELAXATION SYSTOLE

VENTRICULAR
EJECTION ISOMETRIC VENTRICULAR
CONTRACTION
EJECTION
ISOVOLUMETRIC RELAXATION
RAPID INFLOW
ISOVOLUMETRIC DIASTASIS
CONTRACTION ATRIAL SYSTOLE
PRESSURE (mmHg)

AORTIC
PRESSURE

ATRIAL
PRESSURE
VENTRICLE
PRESSURE
VOLUME (ml)

ECG

PHONO-
CARDIOGAM
SYSTOLE DIASTOLE SYSTOLE
MEASUREMENT OF CARDIAC OUTPUT

THE FICK METHOD:

VO2 = ([O2]a - [O2]v) x Flow

VO2 Spirometry (250 ml/min)


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) =
[O2]a - [O2]v

= 250 ml/min
20 ml% - 15 ml%
= 5 L/min
.
Q = HR x SV .
.
Q CARDIAC INDEX = Q 2
SV = m body surface
HR
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
SARCOLEMMA

20% Mitochondria
T-tubule 10%
80%
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 Ca++ Ca++


Heart Rate

Fast
Heart Rate Ca++ Ca++ Ca++ Ca++
SERIES ELASTIC
ELEMENTS
CONTRACTILE
PARALLEL ELASTIC COMPONENT
ELEMENTS
(ACTIVE TENSION)
(PASSIVE TENSION)

TOTAL
TENSION
LENGTH-TENSION CURVE

TOTAL TENSION

ACTIVE
TENSION TENSION

PASSIVE TENSION
OPTIMAL LENGTH (Lo)
EQUILIBRIUM LENGTH RESTING LENGTH
LENGTH
LENGTH
TENSION

SARCOMERE LENGTH ()


CARDIAC MUSCLE

TOTAL TENSION

ACTAIVE TENSION
TENSION

PASSIVE
TENSION
MUSCLE LENGTH
HEART
SYSTOLIC PRESSURE CURVE

Isotonic (Ejection) Phase


After-load
PRESSURE

Isovolumetric
Phase
Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume


D
E ITY HEART
S
A IL
E
R CT SYSTOLIC PRESSURE CURVE
C
IN RA
NT
CO
Isotonic (Ejection) Phase
After-load
PRESSURE

Isovolumetric
Phase
Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume


ED Y HEART
AS IT
RE TIL SYSTOLIC PRESSURE CURVE
EC AC
D TR
O N
C
Isotonic (Ejection) Phase
After-load
PRESSURE

Isovolumetric
Phase

Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume


HEART

G D
I N SE
LL A
SYSTOLIC PRESSURE CURVE
FI RE
C
IN

Isotonic (Ejection) Phase


After-load
PRESSURE

Isovolumetric
Phase
Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume


CARDIAC FUNCTION CURVE

Cardiac Output = Stroke Volume x Heart Rate


STROKE VOLUME
If: Constant

Then:  CO reflects SV

DIASTOLIC FILLING
Right Atrial Pressure (RAP) reflects Diastolic Filling
CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”

CARDIAC OUTPUT (L/min) 15-

10-

Pressure
5-

Volume

-4 0 +4 +8
RAP mmHg
CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”

CARDIAC OUTPUT (L/min) 15- Inc


Co rease
ntr d
a ct
i lit
10- y

5-

-4 0 +4 +8
RAP mmHg
CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”

CARDIAC OUTPUT (L/min) 15- De


c
Co reas
ntr ed
a ct
i lit
10- y

5-

-4 0 +4 +8
RAP mmHg
CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”

CARDIAC OUTPUT (L/min) 15- Inc


He rease
art d
Ra
te
10-

5-

-4 0 +4 +8
RAP mmHg
CARDIAC FUNCTION CURVE
THE FRANK- STARLING “LAW OF THE HEART”

CARDIAC OUTPUT (L/min) 15- De


He creas
art ed
Ra
te
10-

5-

-4 0 +4 +8
RAP mmHg
P1 > P2
P1 FLOW P2

mm Hg
P = FLOW x R

FLOW = P
R
R= P
FLOW

L/min
or mm Hg
ml/sec 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. 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
FlowT = Flow1 + Flow2 + Flow3

P P
= + P + P R1
RT R1 R2 R3
PV PA
1 = 1 + 1 + 1 R2
RT R1 R2 R3
R3
RT = 1
1 + 1 + 1
R1 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 + 1 =1.94 PRU’s
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
100 - 0 mmHg = 1.2 PRU’s
TPR =
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
VASCULAR COMPLIANCE
V
C=
P
Arteries
Ca = 250
100
ml
mmHg =2.5 ml/mmHg
100- Sym
PRESSURE (mmHg)

Cv = 300 ml = 60 ml/mmHg
5 mmHg
Sym
Cv = 24 x Ca

Veins
Sym
Sym
1 2 3 4
VOLUME (L)
MEAN CIRCULATORY PRESSURE

Unstressed
PRESSURE (mmHg)
Volume
Stressed Volume

7-

MCP = 7 mmHg

1 2 3 4 5 6
VOLUME (L)
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
Capillaries
Sphincters ?
Metarteriole

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

INTERSTITIAL
FLUID O2 CO2 Glucose
active transport
CELL
FLUID BALANCE
Filtration vs. Reabsorption
40- Outward Forces:
1. Capillary blood pressure
(Pc = 35 to 15 mmHg)
PRESSURE (mmHg)

30-
2. Interstitial fluid pressure
(PIF = 0 mmHg)
20- 3. Interstitial fluid colloidal
osmotic pressure
(IF = 3 mmHg)
10- TOTAL = 38 to 18 mmHg
Inward Force:
1. Plasma colloidal osmotic
pressure (C = 28 mmHg)
0-
CAPILLARY FLUID SHIFT
Pout > c Pout < c

Pc Pc

FAVORS FILTRATION FAVORS REABSORPTION


PULMONARY CIRCULATION
FLUID BALANCE
Filtration vs. Reabsorption
40-
PRESSURE (mmHg)

30-
Via
lymphatics
20-
Filtration Reabsorption

10-
RADIAL 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 CO = PBF ARTERIES
(RAP)  RAP

7 mmHg  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 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)
THE VASCULAR FUNCTION CURVE

10-
PBF
or
VENOUS
RETURN 5-
(L/min)

0-
-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

Unstressed Stressed Volume


PRESSURE (mmHg)
Volume
Infusion  VOLUME
7- Normal  MCP

Hemorrhage  VOLUME
 MCP

1 2 3 4 5 6
BLOOD VOLUME (L)
MEAN CIRCULATORY PRESSURE
VENOCONSTRICTION
Unstressed Stressed Volume
PRESSURE (mmHg)
Volume

7- Normal

1 2 3 4 5 6
BLOOD VOLUME (L)
MEAN CIRCULATORY PRESSURE
VENODILATION
Unstressed Stressed Volume
PRESSURE (mmHg)
Volume

7- Normal

1 2 3 4 5 6
BLOOD VOLUME (L)
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 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)

 MCP 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
THE VASCULAR FUNCTION CURVE

10-  Blood Volume


PBF or
or  MCP Venoconstriction
VENOUS
RETURN 5-
(L/min)
 MCP
 Blood Volume 0-
or -4 0 +4 +8
Venodilation RAP (mmHg)
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 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)

 TPR 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)
THE VASCULAR FUNCTION CURVE

Vasodilation
10-
PBF  TPR
or
VENOUS
RETURN 5-
(L/min)
 TPR
Vasoconstriction 0-
-4 0 +4 +8
RAP (mmHg)
CARDIAC & VASCULAR
FUNCTION CURVES
15-
CARDIAC
OUTPUT

or 10-

PERIPHERAL
BLOOD FLOW
[Venous Return] 5-

(L/min)

-4 0 +4 +8
RAP mmHg
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 Sympathetic
Chemosensitive Area Nervous
System
VASOMOTOR CENTER
PRESSOR AREA
Glossopharyngeal DEPRESSOR AREA
Nerve
CARDIOINHIBITORY AREA

Baroreceptors Vagus
Carotid Sinus HEART
Aortic Arch
Arterioles
Chemoreceptors Veins
Adrenal
Carotid Bodies
Aortic Bodies Medulla
Bainbridge Reflex ( Heart Rate)
Atrial Receptors 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 Aldosterone
Venoconstriction 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)


(Atrial Receptors) X
X
Vasoconstriction  Water
Venoconstriction Retention
RENAL--BODY FLUID
CONTROL MECHANISM
8- All Mechanisms -8
7- -7
6- -6
Fluid Uninary
5- -5 Output
Intake
(x normal) 4- 3 x Normal -4 (x normal)
3- -3
2- P alone -2
1- Normal -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
7-
MCP CO
Pressure

or CO
PBF BP
1 2 3 4 5 (L/min)
Blood Volume (L)

-4 0 +4 +8
RAP (mmHg)
CARDIAC & VASCULAR
FUNCTION CURVES
15-
CARDIAC
OUTPUT

or 10-
Response to Hemorrhage
PERIPHERAL  HR & Contractility
BLOOD FLOW Venoconstriction ( MCP)
[Venous Return] 5- Vasoconstriction ( TPR)

(L/min)

-4 0 +4 +8
RAP mmHg
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
Unstressed Stressed Volume
PRESSURE (mmHg)

Volume
7- Normal
 Unstressed Vol.
Syncope (Fainting)  Stressed Vol.
 MCP

1 2 3 4 5 6
BLOOD VOLUME (L)
SYNCOPE (FAINTING)
Blood pooling in the extremities
7-
MCP CO
Pressure

or CO
PBF BP
1 2 3 4 5 (L/min)
Blood Volume (L)

-4 0 +4 +8
RAP (mmHg)
CARDIAC & VASCULAR
FUNCTION CURVES
15-
CARDIAC
OUTPUT

or 10-
Response to Syncope (Fainting
PERIPHERAL  HR & Contractility
BLOOD FLOW Venoconstriction ( MCP)
[Venous Return] 5- Vasoconstriction ( TPR)

(L/min)

-4 0 +4 +8
RAP mmHg
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
15-
CARDIAC
OUTPUT SYMPTOMS:
Systemic Edema
or Pulmonary
10- Congestion
Enlarged Heart
PERIPHERAL
BLOOD FLOW Adjustments to Failure
[Venous Return] 5- Cardiac Failure
(L/min)

-4 0 +4 +8
RAP mmHg
HEART
I AC
RD RE SYSTOLIC PRESSURE CURVE
CA ILU
FA

Isotonic (Ejection) Phase


After-load
PRESSURE

Isovolumetric
Phase

Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume


TEMPERATURE REGUALTION
• Body Temperature
• Heat Production
• Heat Loss
• Temperature Regulation
– Heat Exhaustion
– Heat Stroke
– Hypothermia
• Fever
WARM COLD
Temperature Upper limit of survival?
regulation
seriously Heat stroke
impaired Brain lesions
Fever therapy
Temperature Febrile disease
regulation and
efficient in Hard exercise
febrile disease Usual range of normal
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

Preoptic Area

W Sweating
Set Vasodilation
Warm W
Receptors
point Vasoconstriction
W C Shivering
Cold
Receptors
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 = endogenous pyrogen
proteins, dust

Arachidonic Acid

Prostaglandins Aspirin

RAISES THE “SET POINT”


Shivering Sweating
Vasoconstriction Vasodilation

Reference
Temperature Actual Core
or Set Point
Temperature

Onset of Fever
Fever Breaks

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