Transcript Slide 1

Chapter 19: Physiology of the
Cardiovascular System
INTRODUCTION
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MAJOR FUNCTION OF THE CV SYSTEM – DEPENDS ON
CONTINOUS AND CONTROLLED FLOW OF BLOOD
THROUGH CAPILLARIES
– Major Function of the CV System = Transportation
– Transportation depends on flow of blood through
capillaries
- Blood flow through capillaries must be:
– Continuous  To meet cell’s needs
– Controlled (changed)  To meet the changing
needs of cells
– How is this accomplished?
• Homoeostatic control mechanisms
(hemodynamics)
• Hemodynamics: collection of mechanisms that
influence the dynamic (active and changing)
circulation of blood
Conduction System of the Heart
• Conduction system of the heart (Figure
19-2)
– System responsible for conducting
nerve impulses over the heart
– The action potentials (impulses) of
the heart that trigger contractions
must be coordinated carefully.
– Composed of four major structures
(all modified cardiac muscle)
• Sinoatrial (SA) node
• Atrioventricular (AV) node
• AV bundle (bundle of His)
• Subendocardial branches
(Purkinje fibers)
Conduction System of the Heart (cont.)
• SINOATRIAL (SA) NODE
– Location: in the right atrium near the
opening of the superior vena cava
– “Pacemaker of the Heart”
» Nerve impulses start here
» Discharges a set # of nerve
impulses per minute
• ATRIOVENTRICULAR (AV) NODE
– Location: in the right atrium along the
interatrial septum
• ATRIOVENTRICULAR (AV) BUNDLE (BUNDLE
OF HIS)
– Location: originates in the AV node,
spreads down the interventricular
septum in 2 branches - L & R
• PURKINGE FIBERS
– Location: extensions of the AV Bundle
into the walls of the ventricles
Sequence of Cardiac Stimulation
• Specific sequence:
– SA node discharges a nerve impulse 
travels to LA and to AV node  atria
contract
– Nerve impulse travels from AV node to AV
bundle (L&R branches) to purkinge fibers 
ventricles contract
– Result: 1 complete cardiac cycle (pumping
cycle), Assoc. with 1 heartbeat
– Process repeats
• Interatrial bundle of conducting fibers
facilitates rapid conduction to left atrium
• As signal enters AV node through internodal
bundles of conducting fibers, conduction slows,
permitting contraction of both atrial chambers
before impulse reaches the ventricles
Electrocardiogram (ECG)
– Measures heart’s electrical activity (graphic record)
– Provides a record of the electrical events that precede the
contractions of the heart
– Electrodes of an electrocardiograph are attached to the
subject
– Changes in voltage are recorded that represent changes in
the heart’s electrical activity (Figure 19-4)
– EKG waves
• Normal waves
– P wave: depolarization of the atria
– QRS complex: depolarization of the ventricles,
repolarization of the atria
– T wave: repolarization of the ventricles
– Measurement of the intervals between P, QRS,
and T waves can provide information about the
rate of conduction of an action potential through
the heart
– Clinical significance
• EKG can show problems related to the spread of nerve
impulses over the conduction system
Cardiac Cycle
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Cardiac cycle: a complete heartbeat
consisting of contraction (systole) and
relaxation (diastole) of both atria and both
ventricles (5 steps)
The cycle is often divided into time intervals
– Step 1: Atrial systole
• Contraction of atria completes
emptying of blood out of the atria
into the ventricles
• AV valves are open; semiluminar (SL)
valves are closed
• Ventricles are relaxed and fill with
blood
• This cycle begins with the P wave of
the ECG
Important Events of the Cardiac Cycle
– Step 2: Isovolumetric ventricular contraction
• Occurs between the start of ventricular systole and
the opening of the SL valves
• Ventricular volume remains constant as the
pressure increases rapidly
• Onset of ventricular systole coincides with the R
wave of the ECG and the appearance of the first
heart sound
– Step 3: Ejection
• SL valves open and blood is ejected from the heart
when the pressure gradient in the ventricles
exceeds the pressure in the pulmonary artery and
aorta
• Rapid ejection: initial short phase characterized by
a marked increase in ventricular and aortic
pressure and in aortic blood flow
• Reduced ejection: characterized by a less-abrupt
decrease in ventricular volume; coincides with the
T wave of the ECG
Important Events of the Cardiac Cycle (cont.)
– Step 4: Isovolumetric ventricular relaxation
• Ventricular diastole begins with this phase
• Occurs between closure of the SL valves and
opening of the AV valves
• A dramatic fall in intraventricular pressure but no
change in volume
• The second heart sound is heard during this period
– Step 5: Passive ventricular filling
• Returning venous blood increases intra-atrial
pressure until the AV valves are forced open and
blood rushes into the relaxing ventricles
• Influx lasts approximately 0.1 second and results in
a dramatic increase in ventricular volume
• Diastasis: later, longer period of slow ventricular
filling at the end of ventricular diastole lasting
approximately 0.2 second; characterized by a
gradual increase in ventricular pressure and volume
Heart Sounds
• During each cardiac cycle the heart
makes sounds.
– Systolic sound (“contraction sound”)
•
First sound, believed to be caused primarily by the
contraction of the ventricles and vibrations of the closing
AV valves (step 2 of the cardiac cycle)
• Heart sound - “lubb-dupp”
– Diastolic sound (“relaxation sound”)
• short, sharp sound; thought to be caused
by vibrations of the closing of SL valves
• Step 4 of cardiac cycle
• Heart sound – “dupp”
– Heart sounds have clinical significance
because they provide information
about the functioning of the valves of
the heart
– Heart murmur
• Abnormal heart sound - “swishing”
PRIMARY PRINCIPLE OF CIRCULATION
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Blood flows because of a pressure
gradient
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high pressure (aorta: 100 mm Hg)  low
pressure (venae cavae: 0 mm Hg)
Pumping action causes fluctuation in aortic blood
pressure (systolic 120 mm Hg: diastolic 80 mm
Hg)
Blood circulates from the left ventricle to
the right atrium of the heart because of
blood pressure gradient
Measurement of blood flow is based on
Newton’s first and second law of motion
P1-P2 is the symbol used to represent a
pressure gradient, with P1 representing
the higher pressure and P2 the lower
pressure
Perfusion pressure: pressure gradient
needed to maintain blood flow through a
local tissue
Arterial Blood Pressure
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High blood pressure must be maintained in the
arteries to keep blood flowing in the CV system
Primary determinant of arterial blood pressure is
the volume of blood in the arteries
A direct relation exists between arterial blood
volume and arterial pressure (Figure 19-10)
Cardiac output: volume of blood pumped out of a
ventricle of the heart per unit of time (ml/min or
L/min)
– General principles and definitions
• Cardiac output (CO): determined by
stroke volume and heart rate
• Stroke volume (SV): volume pumped per
heartbeat
• CO (volume/min) = SV (volume/beat) 
HR (beats/min)
• In practice, CO is computed by Fick’s
formula
• Heart rate and SV determine CO, so
anything that changes either also tends
to change CO, arterial blood volume, and
blood pressure in the same direction
Arterial Blood Pressure
• Relationship between arterial blood volume
and blood pressure.
Factors That Affect Stroke Volume
• Starling’s law of the heart (Frank-Starling
mechanism)
• Mechanical factor that affects stroke
volume
– The longer, or more stretched, the heart fibers
at the beginning of contraction, the stronger the
contraction (i.e. the more blood returned to the
heart, the stronger the contraction)
– The amount of blood in the heart at the end of
diastole determines the amount of stretch
placed on the heart fibers
– Exceptions: Too much stretching of cardiac
muscle fibers has the opposite effect (i.e. makes
the contraction less strong)
• The myocardium contracts with enough
strength to match its pumping load (within
certain limits) with each stroke, unlike
mechanical pumps
Factors that Affect
Stroke Volume
• Contractility (strength of contraction) can
also be influenced by chemical factors
(Figure 19-13)
• Neural factors
– Norepinephrine
• Endocrine factors
– Epinephrine
• Mechanical factors
– Triggered by stress, exercise
Factors that Affect Heart Rate
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SA node normally initiates each heartbeat BUT the rate
of the heartbeat can be altered
HOW?
– 1. Cardiac pressor reflexes (pressoreflexes)
• Receptors sensitive to changes in pressure
(baroreflexes)
• Ex. aortic baroreceptors and carotid
baroreceptors
– located in the aorta and carotid sinus
– Send afferent nerve fibers to cardiac
control centers in medulla oblongata
– Work with integrators in the cardiac
control centers through negative feedback
loop called pressoreflexes or baroreflexes
to oppose changes in pressure by
adjusting heart rate
Factors that Affect Heart Rate (cont.)
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2. Carotid sinus reflex (negative feedback loop)
– Sensory fibers from carotid sinus baroreceptors
run through the carotid sinus nerve and the
glossopharyngeal nerve to the cardiac control
center
– Parasympathetic impulses leave the cardiac
control center, travel through the vagus nerve to
reach the SA node
– Acetylcholine released from vagus fibers
decreases the rate of SA firing and heart rate
– Vagal inhibition – “break” of the heart
– Aortic reflex (negative feedback loop)
– Sensory fibers extend from baroreceptors located
in the wall of the arch of the aorta through the
aortic nerve and through the vagus nerve to
terminate in the cardiac control center
– END RESULT = Decreased heart rate
Other Reflexes that Influence Heart Rate
↑ Heart Rate
↓ Heart Rate
Anxiety, fear, and anger
Grief
Exercise
Decreased blood temperature
Increased blood temperature
Stimulation of skin cold
receptors
Stimulation of skin heat
receptors
Norepinephrine (released from
sympathetic response)
Peripheral Resistance
• Helps determine aterial blood pressure
• Definition - resistance to blood flow imposed
by the force of friction between blood and the
walls of its vessels
• Factors that influence peripheral resistance:
• 1. Blood viscosity: the thickness of
blood as a fluid
– High plasma protein
concentration can slightly
increase blood viscosity
– High hematocrit can increase
blood viscosity
– Anemia, hemorrhage, or other
abnormal conditions may also
affect blood viscosity
– Means blood meets friction as it
flows
Factors that Affect Peripheral Resistance
• 2. Diameter of arterioles (Figure 1917)
– Vasomotor control mechanism:
muscles in walls of arteriole may
constrict (vasoconstriction) or
dilate (vasodilation), thus
changing diameter of arteriole
– Controls amount of blood that
runs from arteries to arterioles
– Small changes in blood vessel
diameter cause large changes in
resistance
– Means blood meets resistance in
arteries as it flows (ideal control
system)
Parts of the Vasomotor Control Mechanism
1. Vasomotor center or “vasoconstrictor
center” – area in the medulla
– When stimulated initiates an
impulse outflow by sympathetic
fibers that ends in the smooth
muscle surrounding resistant
vessels, arterioles, venules, and
veins of the blood “reserviors”
causing their constriction
2. Vasomotor pressoreflexes
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Initiated by change in aterial blood pressure
The change stimulates aortic and carotid
baroreceptors
Results in arterioles and venules of the blood
reservoirs dilating
Decrease in arterial blood pressure results in
stimulation of vasoconstrictor centers, causing
vascular smooth muscle to constrict
Parts of the Vasomotor Control Mechanism (cont.)
3. Vasomotor chemoreflexes
- chemoreceptors located in aortic and carotid bodies are
sensitive to hypercapnia, hypoxia, and decreased arterial blood
pH
4. Medullary ischemic reflex
- acts during emergency situation when blood flow to the
medulla is decreased; causes marked arteriole and venous
constriction
5. Higher brain centers
- impulses from centers in cerebral cortex and hypothalamus
transmitted to vasomotor centers in medulla to help control
vasoconstriction and dilation
VENOUS RETURN TO THE HEART
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Venous return: amount of blood returned to the heart
by the veins (venous blood = deoxygenated blood)
Affected by several factors
– Stress-relaxation effect: occurs when a change in
blood pressure causes a change in vessel diameter
(because of elasticity) and thus adapts to the new
pressure to keep blood flowing (works only within
certain limits)
– Gravity: the pull of gravity on venous blood
• While sitting or standing tends to cause a decrease in venous
return (orthostatic effect)
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Venous pumps – help to overcome the influence of
gravity to maintain the pressure gradient of blood
– Pump unoxygenated blood back to the heart
– 2 kinds:
• Respirations
• Skeletal muscle contractions
Mechanisms of Venous Pumps
– Respirations: Create pressure
changes that act as venous pumps
• During inspiration: pressure changes
cause blood to be pumped from
abdominal vena cava to thoracic vena
cava
• During expiration: pressure changes
cause blood to be pumped into the atria
– Skeletal muscle contractions:
promote venous return by
squeezing veins through a
contracting muscle and milking the
blood toward the heart
• Contraction: squeezes veins within 
pumps blood toward heart
• One-way valves in veins prevent
backflow
Total Blood Volume
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Total blood volume: changes in total blood volume
change the amount of blood returned to the heart
– HOW?
– Capillary exchange: governed by Starling’s law of
the capillaries (Figure 19-26)
• At arterial end of capillary, outward
hydrostatic pressure is strongest force; moves
fluid out of plasma and into intracellular fluid
• At venous end of capillary, inward osmotic
pressure is strongest force; moves fluid into
plasma from intracellular fluid; 90% of fluid
lost by plasma at arterial end is recovered
• Lymphatic system recovers fluid not recovered
by capillary and returns it to the venous blood
before it is returned to the heart
• Note: If lymphatic system operates normally
there is no net loss of blood volume resulting
from capillary exchange
Mechanisms that Change Total Blood Volume
• Mechanisms that change total blood volume most
quickly cause water to move into or out of the
plasma
• Antidiuretic hormone mechanism
– Involves secretion/release of ADH (water retention)
– Increases TBV and venous return
• Renin- Angiotension Mechanism
– Involves secretion of aldosterone (sodium retention
followed by water retention)
– Increases TBV and venous return
• Atrial natriuretic peptide mechanism
– Involves secretion of atrial natriuretic hormone (sodium
loss, followed by water loss)
– Decreases TBV and venous return
MEASURING BLOOD PRESSURE
• Arterial blood pressure
– Measured with a sphygmomanometer and
stethoscope; listen for Korotkoff sounds as
the pressure in the cuff is gradually
decreased (Figure 19-29)
– Systolic blood pressure: force of the blood
pushing against the artery walls while
ventricles are contracting
– Diastolic blood pressure: force of the blood
pushing against the artery walls when
ventricles are relaxed
– Pulse pressure: difference between systolic
and diastolic blood pressure
MINUTE VOLUME OF BLOOD
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The volume of blood circulating through the body per minute = minute blood volume
– Determined by magnitude of the blood pressure gradient and peripheral resistance
Caculated based on mathematical equation:
– (Poiseuille’s Law): Minute volume = Pressure gradient (mean arterial BP - central
venous BP)  Resistance
• MV = Minute Volume (volume of blood circulated per minute)
• BP = Blood Pressure
• PR = Peripheral Resistance
– PR Has 2 effects on circulation:
– 1. PR can increase circ (increases artery blood volume)
– 2. PR can decrease circ (allows less blood to flow)
Relation to arterial and venous bleeding
– Arterial bleeding: blood escapes from artery in spurts because of alternating increase
and decrease of arterial blood pressure
– Venous bleeding: blood flows slowly and steadily because of low, nearly constant
pressure
FACTORS THAT INFLUENCE THE FLOW OF BLOOD
VELOCITY OF BLOOD FLOW
• Velocity of blood is governed by the physical
principle that states when a liquid flows from
an area of one cross-sectional size to an area
of larger size, its velocity decreases in the
area with the larger cross section (Figure 1931)
• Blood flows fastest in arteries, slowest in
capillaries
• Venule cross-sectional area is smaller than
capillary cross-sectional area, causing blood
velocity to increase in venules and veins
PULSE
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Pulse: alternate expansion and recoil of an artery (Figure 1932)
Causes: LV contraction and relaxation & elasticity of artery
walls
Clinical significance: reveals important information regarding
the cardiovascular system, blood vessels, and circulation
Physiological significance: expansion stores energy released
during recoil, conserving energy generated by the heart and
maintaining relatively constant blood flow (Figure 19-33)
Pulse wave
– Spread of pulse through arteries, each LV contraction
starts a new pulse wave that spreads as a wave
throughout arteries
Where is the pulse felt?
– Superficial arteries that lie over a firm surface
– Examples: Radial artery, common carotid artery, brachial
artery
Venous pulse
– Detectable in large veins that lie near the heart
– Due to contraction/relaxation of the atria