Transcript cardiovascular

S1
Secretion
Reabsorption
Filtration
S2
Circulatory System Circulates
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Nutrients: glucose, amino acids, fatty acids, ketones, etc
Wastes:
Hormones: bound & free
Gases: CO2 and O2
Formed Elements: Cells and Cell Fragments
– Erythrocytes, Leukocytes, Thrombocytes = Platelets
Other roles of the Cardiovascular System
Thermoregulation
Blood Clotting
Reproduction (ex: penile erection)
S3
Blood volume ~ 5 liters
Figure 12.01
Serum = plasma – clotting factors
Entering and Exiting the blood
Components……
EPO and
“The Scoop on Tissie”
Discontinuous capillaries in
bone marrow, spleen, &
liver permit erythrocytes to
enter and exit blood.
Formed
elements
Hct = percentage
of blood volume
occupied by RBCs
Anemia
Blood doping & erythropoietin (hormone that
stimulates erythrocyte production in bone
marrow) to increase hematocrit
S4
Fig. 12.02
Arteries..away from heart
Veins..return to heart
Resting Cardiac Output = 5L/min
for each side!
When left heart
can’t pump all the
blood it receives
from pulmonary
circuit (due to high
aortic pressure
and/or damage to
left ventricle) blood
accumulates in
pulmonary circuit.
This is congestive
heart failure.
Symptom:
shortness of
breath.
Regional blood flow
determined by arteries
and arterioles.
S5
Figure 12.04
CO = 5L/min
for each circuit
Up to 35 L/min
in strenuous
exercise
S6
Pulmonary circuit
CO = 5 liters/min
Arterial Blood Pressure
Systemic Circuit
Exchange Vessels
What’s
missing?
CO = 5 liters/min
Recall Portal Systems!
Resistance Vessels
Microcirculation
Capacitance vessels
S7
Pulmonary circuit
Pressure gradients
makes fluids move.
Moving fluids flow,
but flow is limited by
resistance.
Resistance creates
pressure.
Systemic Circuit
Arterioles establish Mean Arterial Pressure
S8
Radius of arterioles
regulates Q to organs
F=Q=ΔP/R
Flow = Pressure gradient/Resistance
from Ohm’s Law (V=IR)
Double radius … 16x flow
R=
8Lη/πr4
Half radius….1/16th flow
Q= ΔP πr4
8Lη
Poiseulle’s equation
Smooth muscles
determine radius
S 14
Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance
MAP = CO x TPR
MAP = (HR x SV) x TPR
S1
Cardiac Output = Heart Rate X Stroke Volume
What regulates
heart rate?
What regulates
Stroke Volume?
CO = HR x SV
5L/min = 72 beat/min x 70 ml/beat
The Cardiac Cycle animation
Problems with valves:
Heart murmurs ≠ heart sounds
….Stenosis (narrowing) →Heart Murmurs (turbulent flow past a constriction)
Figure 12.07
note: origin of neonatal heat murmurs (foramen ovale)
….Prolapse (eversion) allows backflow (also generates murmurs)
S4
Tricuspid
Heart sounds
produced by
valve closings
Semilunar
Valves
Bicuspid
=Mitral
Animation
S3
Cardiac Myofiber
action potential
Plateau phase
Figure 12.13
Long refractory
period prevents
summation in
cardiac
myofibers
Cardiac
Myofiber
S4
Figure 12.11
S5
SA node cells
do not have stable
resting membrane
potential,
spontaneously
produce AP,
are Pacemaker cells
S5
Cardiac Pacemaker
action potential
Figure 12.14
Ectopic
Pacemaker
Pacemaker
Cells in
Conducting
System:
SA Node and
Bundle of His
Locations
other than
SA Node
These cells
set the
rhythm &
control
Heart Rate.
1QQ # 14: Answer one.
1. A) Which vessels are classified as exchange
vessels?
B) Why are they called exchange vessels?
2. A) What produces a heart sound?
B) What produces a heart murmur?
3. With all other factors held constant, how would
blood flow be affected by a doubling of the
pressure gradient?
4. A) Explain how a heart can continue to beat
even if the SA node is not functioning.
B) Would this heart rate be faster or slower
than the rate produced by the SA node?
S 15
Figure 12.22
Intrinsic Rate = 100 beat/min
2 effects of Parasymp:
hyperpolarization &
slower depolarization
S6
Figure 12.23
NE
Beta-adrenergic receptors
Effect of “Beta blockers”
EPI
ACh
mAChR
Effect of atropine
S7
What prevents the AP from being conducted from ventricles back to atria?
Fibrous connective tissue between atria and ventricles prevents the
conduction of action potential. Only route is via AV node, bundle of His,
bundle branches, Purkinje fibers, and to ventriclular myofibers.
S8
“Sis-toe-lee”
1st Heart Sound =
Closure of
Atrioventricular
(AV) valves at
beginning of
Ventricular
Systole
“die-ass-toe-lee”
2nd Heart Sound =
Closure of Semilunar
valves at beginning
of Ventricular
Diastole
S9
Figure 12.20
Systolic
Diastolic
Atrial Fibrillation
Stroke Volume
Ejection Fraction = SV/EDV
Ventricular
Fibrillation &
Defibrillation
Animation
S 10
Events are same for Cardiac Cycle for Right Side
of Heart; only difference is lower systolic pressures
in right atrium and right ventricle.
S1
So far, we’ve dealt with the factors that
control Cardiac Output by changing
heart rate.
3
CO = HR x SV
2
+ sympathetic
- parasympathetic
1
5L/min = 72 beat/min x 70 ml/beat
35L/min = ? beat/min x ? ml/beat
S2
Figure 12.20
Stroke Volume
Animation
S3
Frank-Starling Law of the Heart
Does not depend on hormones or nerves
Assures that the heart adjusts its output based on VENOUS RETURN
Ventricular Function Curve
Ways to enhance
Venous Return:
1) muscle contractions
2) “respiratory pump”
3) venoconstriction
FS LoH = SV is proportional to EDV
↑VR→ ↑EDV → ↑SV
S4
Length-tension “curve” for Cardiac muscle
Fig. 09.21
High EDV
Low EDV
Overinflation of
ventricles leads to less
effective pumping
S5
Overinflation of
ventricles results in
reduction in stroke
volume
Treatments?
…..diuretics
S6
NE from Symp
postganglionics
& EPI from
Adrenal medulla
Contractility
Increase Ejection Fraction
Note: cardiac myofibers
NOT innervated by
parasympathetic division
S7
3 Effects of
Sympathetic
Stimulation
1: Increase rate of contraction
2: Increase peak tension
3: Decrease twitch duration
Why should the
contraction be shorter?
Afterload is analogous to trying to pump more air into a tire that is already fully inflated
(heart contracting to overcome diastolic pressure.)
S9
High blood pressure increases the workload of the heart….. Cardiac
hypertrophy….increase chance of irregular conduction of AP through heart
Hypertrophic cardiomyopathy
S8
Summary: Control of Stroke Volume
FS LoH
• End diastolic volume (preload)
• Contractility (strength of ventricular
contraction due to adrenergic stimulation)
• Pressure in arteries that must be
overcome = Afterload
S 11
Factors that control Cardiac Output by
changing heart rate and stroke volume.
Afterload (MAP)
CO = HR x SV
EDV (FSLoH)
+ sympathetic
- parasympathetic
contractility
5L/min = 72 beat/min x 70 ml/beat
35L/min = ? beat/min x ? ml/beat
Summary of Factors that Regulate Cardiac Output
S 12
Fig. 12.28
Even persons with heart
transplants can adjust CO
in the absence of
innervation of heart.
S 13
Heart is pump that generates
pressure gradient.
Blood flows through vessels,
which have resistance.
Arterioles have greatest
resistance and create
“backpressure” in the arteries
and aorta.
Mean Arterial Pressure = diastolic +1/3(systolic – diastolic)
= 70 + 1/3(120-70)
= 70 + 17
= 87 mm Hg
S 11
Factors that control Cardiac Output by
changing heart rate and stroke volume.
Afterload (MAP)
CO = HR x SV
EDV (FSLoH)
+ sympathetic
- parasympathetic
contractility
5L/min = 72 beat/min x 70 ml/beat
35L/min = ? beat/min x ? ml/beat
S1
Properties of Blood Vessels
All vessels and heart chambers lined with ENDOTHELIAL cells (simple squamous)
• Arteries
• Arterioles Variable Resistance vessels
• Capillaries
Exchange
• Venules
Capacitance vessels, high
• Veins
compliance, low pressure,
Elastic, low compliance, large
diameter, low resistance vessels
Wall = simple squamous endothelium
No smooth muscle; cannot change diameter
valves for unidirectional flow
S2
Aorta
Brachial or
Femoral artery
Fig. 12.29
Damage to artery vs vein
Pusatile flow
S3
Fig. 12.39b
Analogy: river width and flow
S4
Fig. 12.30
Stretching elastic connective tissue
Elastic recoil of
stretched arterial walls
during ventricular
systole maintains
arterial pressure during
diastole as blood drains
into arterioles.
Atherosclerosis
Recoil of elastic connective tissue
Point of Confusion: Smooth muscles in arterial walls
DO NOT rhythmically contract, do not pump!
S5
Arteries and Arterial Pressure
Mean Arterial Pressure
Arterioles have two main
functions:
1) regulate flow to tissues
and organs and
2) responsible for Total
Peripheral Resistance
which influences Blood
Pressure.
MAP = CO x TPR
Poiseulle’s Equation
Arteriole
S6
Fig. 12.50
Heart
Arteries
Mean
Arterial
Pressure
Totol Peripheral Resistance
CNS
Skin
Sk. Muscle
Gut
Arterioles
Kidneys
Cardiac
Output
S7
Receptors for other ligands
Alpha receptors
more common
except in skeletal
muscle arterioles
which have more
B2 receptors
S8
Fig. 12.36
Metabolic vasodilators
No parasympathetic
innervation of arterioles!
Importance of sympathetic
“tone.”
Metabolic autoregulation, flow autoregulation, myogenic autoregulation
S4
Figure 12.02
Arteries = 10% of Blood Volume
Veins = 60% of Blood Volume
Arterioles = Resistance vessels
Capillaries = 5% of Blood Volume
S5
Capillaries:
Continuous, discontinuous, and fenestrated capillaries:
Ex: brain
liver
endocrine glands
Figure 12.38
Generate
vasodilators
and
vasoconstrictors
Arterioles:
1) Extrinsic control by hormones and nerves
2) Intrinsic (local) control by
…..a) metabolic autoregulation,
…..b) flow autoregulation, and
…..c) myogenic autoregulation.
1QQ # 15 Answer one.
1. Describe metabolic autoregulation and
list four substances that are classified as
metabolic vasodilators.
2. What is the main difference between flow
autoregulation and metabolic
autoregulation?
3. Explain why the pressure in a major
artery doesn’t fall to 0 during ventricular
diastole.
S6
Capillary exchange by: Diffusion, vesicle
transport, bulk flow, mediated transport
S7
Fig. 12.40
Diffusion is
the most
important
mode of
exchange of
nutrients
S8
Figure 12.41
Colloids
Crystalloids
= colloids (impermeable proteins)
Bulk Flow
S9
Cell Membrane: selectively permeable
Capillaries: highly permeable except to proteins
S 10
Bulk Flow through aqueous channels and intracellular clefts
Figure 12.42
Regulated
by arterioles
Starling Forces
Net filtration = 4L/day
Main difference in the Pulmonary circuit?
S 11
Fig. 12.43
Pc
Pc
Pc
S 12
Who Cares?
Aunt Esther
Cancer of the liver;
Failure of hepatocytes to
produce plasma colloids
S 13
Figure 12.41
Colloids
Crystalloids
Bulk Flow
S1
Figure 12.47
Fate of 4 L/d excess filtrate
Mode of propulsion?
Liver &
Bone Marrow
& Spleen
S2
Veins are
Capacitance vessels
(high compliance)
with valves for
unidirectional flow
Figure 12.44
Arteries are
low compliance,
so any increase in
volume increases
pressure.
S3
MAP = CO x TPR
Fig. 12.53
Negative feedback control:
stimulus,
receptors,
afferent pathway(s),
integrator,
efferent pathway(s),
effector(s)
response(s)
+ other baroreceptors
S4
Fig. 12.54
What happens to the set point for MAP during exercise?
S2
Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance
MAP = CO x TPR
MAP = (HR x SV) x TPR
S6
Test 3 Hemorrhage Diagram
On one page, create a well-organized diagram for the following.
Beginning with a loss of about 1 liter of blood from a vein,
diagram the early events associated with hemorrhage and the
negative feedback responses to hemorrhage in a well-organized
diagram. Write legibly! Completeness, accuracy, and detail,
together with the proper sequence earn maximal points.
The following abbreviations can be used: ACE, AI, AII, Aldo
(aldosterone), JGA, mAChR, Hct, Q, SV, EF (ejection fraction), RBC,
HR, EDV, ACh, ANH, ADH, CO, TPR, EPO, VR, MAP, EPI, NE, SAN
(SA Node), aAdR , bAdR, Symp (sympathetic), Parasymp
(parasympathetic), PV (plasma volume), r (radius), Pc, fAP (frequency
of action potentials.) Any other abbreviations must be defined. "If in
doubt, write it out!" Use single headed arrows (→) to indicate
sequential relationships and doubled-stemmed arrows to indicate
increases or decreases.