Chapter 19: Physiology of the Cardiovascular System - PowerPoint PPT Presentation

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Chapter 19: Physiology of the Cardiovascular System


Chapter 19: Physiology of the Cardiovascular System – PowerPoint PPT presentation

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Title: Chapter 19: Physiology of the Cardiovascular System

Chapter 19 Physiology of the Cardiovascular
  • Major Function of the CV System Transportation
  • Transportation depends on flow of blood through
  • - Blood flow through capillaries must be
  • Continuous ? To meet cells 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
  • 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.)
  • 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
  • Location in the right atrium along the
    interatrial septum
  • Location originates in the AV node, spreads down
    the interventricular septum in 2 branches - L R
  • 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
    (LR branches) to purkinge fibers ? ventricles
  • 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 hearts electrical activity (graphic
  • 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 hearts 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
  • Clinical significance
  • EKG can show problems related to the spread of
    nerve impulses over the conduction system

Cardiac Cycle
  • 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
  • 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
  • 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
  • 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

  • Blood flows because of a pressure gradient
  • 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 Newtons
    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
  • 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
  • In practice, CO is computed by Ficks 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

Arterial Blood Pressure
  • Relationship between arterial blood volume and
    blood pressure.

Factors That Affect Stroke Volume
  • Starlings law of the heart (Frank-Starling
  • 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
  • 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
  • Ex. aortic baroreceptors and carotid
  • 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.)
  • 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
  • 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
  • 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 19-17)
  • Vasomotor control mechanism muscles in walls of
    arteriole may constrict (vasoconstriction) or
    dilate (vasodilation), thus changing diameter of
  • 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
  • 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
  • Vasomotor pressoreflexes
  • Initiated by change in aterial blood pressure
  • The change stimulates aortic and carotid
  • 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

  • Venous return amount of blood returned to the
    heart by the veins (venous blood deoxygenated
  • 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)
  • Venous pumps help to overcome the influence of
    gravity to maintain the pressure gradient of
  • 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
  • Total blood volume changes in total blood volume
    change the amount of blood returned to the heart
  • HOW?
  • Capillary exchange governed by Starlings 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
  • Antidiuretic hormone mechanism
  • Involves secretion/release of ADH (water
  • 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

  • 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

  • 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
  • (Poiseuilles Law) Minute volume Pressure
    gradient (mean arterial BP - central venous BP) ?
  • 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
  • 2. PR can decrease circ (allows less blood to
  • 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

  • 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 19-31)
  • Blood flows fastest in arteries, slowest in
  • Venule cross-sectional area is smaller than
    capillary cross-sectional area, causing blood
    velocity to increase in venules and veins

  • Pulse alternate expansion and recoil of an
    artery (Figure 19-32)
  • 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
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