Transcript 5/14/13 Lecture 3 Blood vessels and cardiodynamics

Cardiodynamics and Blood Vessels
Muse s13 Bio238 Lecture #3
5/16/13
The Conducting System
 The Role of Calcium Ions in Cardiac
Contractions
 Contraction of a cardiac muscle cell is
produced by an increase in calcium ion
concentration around myofibrils
The Conducting System
 The Role of Calcium Ions in Cardiac
Contractions
 20% of calcium ions required for a contraction
 Calcium ions enter plasma membrane during plateau phase
 Arrival of extracellular Ca2+
 Triggers release of calcium ion reserves from sarcoplasmic
reticulum
The Conducting System
 The Role of Calcium Ions in Cardiac
Contractions
 As slow calcium channels close
 Intracellular Ca2+ is absorbed by the SR
 Or pumped out of cell
 Cardiac muscle tissue
 Very sensitive to extracellular Ca2+ concentrations
The Conducting System
 The Energy for Cardiac Contractions
 Aerobic energy of heart
 From mitochondrial breakdown of fatty acids and
glucose
 Oxygen from circulating hemoglobin
 Cardiac muscles store oxygen in myoglobin
The Cardiac Cycle
 Phases of the Cardiac Cycle
 Within any one chamber
 Systole (contraction)
 Diastole (relaxation)
The Cardiac Cycle
Figure 20–16 Phases of the Cardiac Cycle
The Cardiac Cycle
 Blood Pressure
 In any chamber
 Rises during systole (ventricular compression) 120
 Falls during diastole (vessel elasticity)
60
 Blood flows from high to low pressure
 Controlled by timing of contractions
 Directed by one-way valves - not perfect seals
The Cardiac Cycle
 Cardiac Cycle and Heart Rate
 At 75 beats per minute
 Cardiac cycle lasts about 800 msecs
 When heart rate increases
 All phases of cardiac cycle shorten, particularly
diastole
The Cardiac Cycle
Figure 20–17 Pressure and Volume Relationships in the Cardiac Cycle
The Cardiac Cycle
 Heart Sounds
 S1
 Loud sounds
 Produced by AV valves
 S2
 Loud sounds
 Produced by semilunar valves
 S3, S4
 Soft sounds
 Blood flow into ventricles and atrial contraction
The Cardiac Cycle
 Heart Murmur
 Sounds produced by regurgitation through
valves
The Cardiac Cycle
Figure 20–18 Heart Sounds
Cardiodynamics
 Cardiac Output
 CO = HR X SV
 CO = cardiac output (mL/min)
 HR = heart rate (beats/min)
 SV = stroke volume (mL/beat)
Cardiodynamics
 Factors Affecting Cardiac Output
 Cardiac output
 Adjusted by changes in heart rate or stroke volume
 Heart rate
 Adjusted by autonomic nervous system or hormones
 Stroke volume
 Adjusted by changing EDV or ESV
Cardiodynamics
Figure 20–20 Factors Affecting Cardiac Output
Cardiodynamics
 Factors Affecting the Heart Rate
 Autonomic innervation
 Cardiac plexuses: innervate heart
 Vagus nerves (X): carry parasympathetic preganglionic fibers
to small ganglia in cardiac plexus
 Cardiac centers of medulla oblongata:
– cardioacceleratory center controls sympathetic
neurons (increases heart rate)
– cardioinhibitory center controls parasympathetic
neurons (slows heart rate)
Cardiodynamics
 Autonomic Innervation
 Cardiac reflexes
 Cardiac centers monitor:
– blood pressure (baroreceptors)
– arterial oxygen and carbon dioxide levels
(chemoreceptors)
 Cardiac centers adjust cardiac activity
 Autonomic tone
 Dual innervation maintains resting tone by
releasing ACh and NE
 Fine adjustments meet needs of other systems
Cardiodynamics
Figure 20–21 Autonomic Innervation of the Heart
Cardiodynamics
 Effects on the SA Node
 Sympathetic and parasympathetic stimulation
 Greatest at SA node (heart rate)
 Membrane potential of pacemaker cells
 Lower than other cardiac cells
 Rate of spontaneous depolarization depends on
 Resting membrane potential
 Rate of depolarization
 ACh (parasympathetic stimulation)
 Slows the heart
 NE (sympathetic stimulation)
 Speeds the heart
Cardiodynamics
Figure 20–22 Autonomic Regulation of Pacemaker Function
Cardiodynamics
 Hormonal Effects on Heart Rate
 Increase heart rate (by sympathetic
stimulation of SA node)
 Epinephrine (E)
 Norepinephrine (NE)
 Thyroid hormone
Cardiodynamics
 Factors Affecting the Stroke Volume
 The EDV: amount of blood a ventricle contains at the
end of diastole
 Filling time:
– duration of ventricular diastole
 Venous return:
– rate of blood flow during ventricular diastole
Cardiodynamics
 The Frank–Starling Principle
 As EDV increases, stroke volume increases
 Physical Limits
 Ventricular expansion is limited by
 Myocardial connective tissue
 The cardiac (fibrous) skeleton
 The pericardial sac
Cardiodynamics
 End-Systolic Volume (ESV)
 The amount of blood that remains in the
ventricle at the end of ventricular systole is
the ESV
Cardiodynamics
 Effects of Autonomic Activity on Contractility
 Sympathetic stimulation
 NE released by postganglionic fibers of cardiac nerves
 Epinephrine and NE released by suprarenal (adrenal)
medullae
 Causes ventricles to contract with more force
 Increases ejection fraction and decreases ESV
Cardiodynamics
 Effects of Autonomic Activity on
Contractility
 Parasympathetic activity
 Acetylcholine released by vagus nerves
 Reduces force of cardiac contractions
Cardiodynamics
 Hormones
 Many hormones affect heart contraction
 Pharmaceutical drugs mimic hormone actions
 Stimulate or block beta receptors
 Affect calcium ions (e.g., calcium channel
blockers)
Cardiodynamics
 Heart Rate Control Factors
 Autonomic nervous system
 Sympathetic and parasympathetic
 Circulating hormones
 Venous return and stretch receptors
Cardiac Reserve
The difference between resting and maximal cardiac output
Cardiodynamics
Figure 20–24 A Summary of the Factors Affecting Cardiac Output
Classes of Blood Vessels
 Arteries
 Carry blood away from heart
 Arterioles
 Are smallest branches of arteries
 Capillaries
 Are smallest blood vessels
 Location of exchange between blood and interstitial fluid
 Venules
 Collect blood from capillaries
 Veins
 Return blood to heart
Blood Vessels
 The Largest Blood Vessels
 Attach to heart
 Pulmonary trunk
 Carries blood from right ventricle
 To pulmonary circulation
 Aorta
 Carries blood from left ventricle
 To systemic circulation
Blood Vessels
 The Smallest Blood Vessels
 Capillaries
 Have small diameter and thin walls
 Chemicals and gases diffuse across walls
Blood Vessels
 The Structure of Vessel Walls
 Walls have three layers:
 Tunica intima
 Tunica media
 Tunica externa
Blood Vessels
 The Tunica Intima
 Is the innermost layer
 Includes
 The endothelial lining
 Connective tissue layer
 Internal elastic membrane:
– in arteries, is a layer of elastic fibers in outer margin of
tunica intima
Blood Vessels
 The Tunica Media
 Is the middle layer
 Contains concentric sheets of smooth muscle in loose
connective tissue
 Binds to inner and outer layers
 External elastic membrane of the tunica media
 Separates tunica media from tunica externa
Blood Vessels
 The Tunica Externa
 Is outer layer
 Contains connective tissue sheath
 Anchors vessel to adjacent tissues in arteries
 Contain collagen
 Elastic fibers
 In veins
 Contains elastic fibers
 Smooth muscle cells
 Vasa vasorum (“vessels of vessels”)
 Small arteries and veins
 In walls of large arteries and veins
 Supply cells of tunica media and tunica externa
Blood Vessels
Figure 21–1 Comparisons of a Typical Artery and a Typical Vein.
Blood Vessels
Figure 21–1 Comparisons of a Typical Artery and a Typical Vein.
Blood Vessels
 Differences between Arteries and Veins
 Arteries and veins run side by side
 Arteries have thicker walls and higher blood pressure
 Collapsed artery has small, round lumen (internal
space)
 Vein has a large, flat lumen
 Vein lining contracts, artery lining does not
 Artery lining folds
 Arteries more elastic
 Veins have valves
Structure and Function of Arteries
 Arteries and Pressure
 Elasticity allows arteries to absorb pressure waves
that come with each heartbeat
 Contractility
 Arteries change diameter
 Controlled by sympathetic division of ANS
 Vasoconstriction:
– the contraction of arterial smooth muscle by the ANS
 Vasodilatation:
– the relaxation of arterial smooth muscle
– enlarging the lumen
Structure and Function of Arteries
 Vasoconstriction and Vasodilation
 Affect
 Afterload on heart
 Peripheral blood pressure
 Capillary blood flow
Structure and Function of Arteries
 Arteries
 From heart to capillaries, arteries change
 From elastic arteries
 To muscular arteries
 To arterioles
Structure and Function of Arteries
 Elastic Arteries
 Also called conducting arteries
 Large vessels (e.g., pulmonary trunk and
aorta)
 Tunica media has many elastic fibers and few
muscle cells
 Elasticity evens out pulse force
Structure and Function of Arteries
 Muscular Arteries
 Also called distribution arteries
 Are medium sized (most arteries)
 Tunica media has many muscle cells
Structure and Function of Arteries
 Arterioles
 Are small
 Have little or no tunica externa
 Have thin or incomplete tunica media
 Artery Diameter
 Small muscular arteries and arterioles
 Change with sympathetic or endocrine stimulation
 Constricted arteries oppose blood flow
– resistance (R):
» resistance vessels: arterioles
Structure and Function of Arteries
 Aneurysm
 A bulge in an arterial wall
 Is caused by weak spot in elastic fibers
 Pressure may rupture vessel
Structure and Function of Arteries
Figure 21–2 Histological Structure of Blood Vessels
Structure and Function of Arteries
Figure 21–3 A Plaque within an Artery
Atherosclerosis
 Hardening of the arteries. -Cholesterol
rich fatty plaques stick to side walls of
artery and fill with calcium.
 When they burst can lead to inflammation
which occludes the artery.
 White blood cells can build up here and
contribute to inflammatory response
atherosclerosis
Structure and Function of Capillaries
 Capillaries
 Are smallest vessels with thin walls
 Microscopic capillary networks permeate all active
tissues
 Capillary function
 Location of all exchange functions of cardiovascular system
 Materials diffuse between blood and interstitial fluid
Structure and Function of Capillaries
 Capillary Structure
 Endothelial tube, inside thin basal lamina
 No tunica media
 No tunica externa
 Diameter is similar to red blood cell
Structure and Function of Capillaries
 Fenestrated Capillaries
 Have pores in endothelial lining
 Permit rapid exchange of water and larger solutes
between plasma and interstitial fluid
 Are found in
 Choroid plexus
 Endocrine organs
 Kidneys
 Intestinal tract
Structure and Function of Capillaries
Figure 21–4 Capillary Structure
Structure and Function of Capillaries
Figure 21–4 Capillary Structure
Structure and Function of Capillaries
 Capillary Sphincter
 Guards entrance to each capillary
 Opens and closes, causing capillary blood to
flow in pulses
Structure and Function of Capillaries
 Vasomotion
 Contraction and relaxation cycle of capillary
sphincters
 Causes blood flow in capillary beds to
constantly change routes
Structure and Function of Veins
 Veins
 Collect blood from capillaries in tissues and organs
 Return blood to heart
 Are larger in diameter than arteries
 Have thinner walls than arteries
 Have lower blood pressure
Structure and Function of Veins
 Vein Categories
 Venules
 Very small veins
 Collect blood from capillaries
 Medium-sized veins
 Thin tunica media and few smooth muscle cells
 Tunica externa with longitudinal bundles of elastic fibers
 Large veins
 Have all three tunica layers
 Thick tunica externa
 Thin tunica media
Structure and Function of Veins
 Venous Valves
 Folds of tunica intima
 Prevent blood from flowing backward
 Compression pushes blood toward heart
Structure and Function of Veins
Figure 21–6 The Function of Valves in the Venous System
Blood Vessels
 The Distribution of Blood
 Heart, arteries, and capillaries
 30–35% of blood volume
 Venous system
 60–65%:
– 1/3 of venous blood is in the large venous networks of the liver,
bone marrow, and skin
Blood Vessels
Figure 21–7 The Distribution of Blood in the Cardiovascular
System
Hemorrhage!
When large amounts of blood is lost in a short time
Class II haemorrhage (15–30% total blood volume)
Blood Vessels
 Capacitance of a Blood Vessel
 The ability to stretch
 Relationship between blood volume and blood
pressure
 Veins (capacitance vessels) stretch more
than arteries
Blood Vessels
 Venous Response to Blood Loss
 Vasomotor centers stimulate sympathetic
nerves
 Systemic veins constrict (venoconstriction)
 Veins in liver, skin, and lungs redistribute venous
reserve
Pressure and Resistance
Figure 21–8 An Overview of Cardiovascular Physiology
Pressure and Resistance
 Pressure (P)
 The heart generates P to overcome resistance
 Absolute pressure is less important than pressure
gradient
 The Pressure Gradient (P)
 Circulatory pressure = pressure gradient
 The difference between
 Pressure at the heart
 And pressure at peripheral capillary beds
Pressure and Resistance
 Force (F)
 Is proportional to the pressure difference (P)
 Divided by R
Pressure and Resistance
 Measuring Pressure
 Blood pressure (BP)
 Arterial pressure (mm Hg)
 Capillary hydrostatic pressure (CHP)
 Pressure within the capillary beds
 Venous pressure
 Pressure in the venous system
Pressure and Resistance
 Viscosity
 R caused by molecules and suspended
materials in a liquid
 Whole blood viscosity is about four times that
of water
Pressure and Resistance
 Turbulence
 Swirling action that disturbs smooth flow of
liquid
 Occurs in heart chambers and great vessels
 Atherosclerotic plaques cause abnormal
turbulence
Pressure and Resistance
Pressure and Resistance
Pressure and Resistance
Pressure and Resistance
Figure 21–12 Forces Acting across Capillary Walls
Cardiovascular Regulation
 Tissue Perfusion
 Blood flow through the tissues
 Carries O2 and nutrients to tissues and organs
 Carries CO2 and wastes away
 Is affected by
 Cardiac output
 Peripheral resistance
 Blood pressure
Cardiovascular Regulation
 Cardiovascular regulation changes blood
flow to a specific area
 At an appropriate time
 In the right area
 Without changing blood pressure and blood
flow to vital organs
Cardiovascular Regulation
Figure 21–13 Short-Term and Long-Term Cardiovascular Responses
Cardiovascular Regulation
 Controlling Cardiac Output and Blood Pressure
 Autoregulation
 Causes immediate, localized homeostatic adjustments
 Neural mechanisms
 Respond quickly to changes at specific sites
 Endocrine mechanisms
 Direct long-term changes
Cardiovascular Regulation

Autoregulation of Blood Flow within Tissues

Adjusted by peripheral resistance while cardiac
output stays the same

Local vasodilators:
– accelerate blood flow at tissue level
» low O2 or high CO2 levels
» low pH (acids)
» nitric oxide (NO)
» high K+ or H+ concentrations
» chemicals released by inflammation (histamine)
» elevated local temperature
Cardiovascular Regulation
 Vasomotor Tone
 Produced by constant action of sympathetic
vasoconstrictor nerves
Cardiovascular Regulation
 Reflex Control of Cardiovascular Function
 Cardiovascular centers monitor arterial blood
 Baroreceptor reflexes:
– respond to changes in blood pressure
 Chemoreceptor reflexes:
– respond to changes in chemical composition, particularly
pH and dissolved gases
Cardiovascular Regulation
 Baroreceptor Reflexes
 Stretch receptors in walls of
 Carotid sinuses: maintain blood flow to brain
 Aortic sinuses: monitor start of systemic circuit
 Right atrium: monitors end of systemic circuit
 When blood pressure rises, CV centers
 Decrease cardiac output
 Cause peripheral vasodilation
 When blood pressure falls, CV centers
 Increase cardiac output
 Cause peripheral vasoconstriction
Cardiovascular Regulation
Figure 21–14 Baroreceptor Reflexes of the Carotid and Aortic Sinuses
Cardiovascular Regulation
 Hormones and Cardiovascular Regulation
 Hormones have short-term and long-term
effects on cardiovascular regulation
 For example, E and NE from suprarenal
medullae stimulate cardiac output and
peripheral vasoconstriction
Cardiovascular Regulation
 Antidiuretic Hormone (ADH)
 Released by neurohypophysis (posterior lobe of
pituitary)
 Elevates blood pressure
 Reduces water loss at kidneys
 ADH responds to
 Low blood volume
 High plasma osmotic concentration
 Circulating angiotensin II
Cardiovascular Regulation
 Angiotensin II
 Responds to fall in renal blood pressure
 Stimulates
 Aldosterone production
 ADH production
 Thirst
 Cardiac output
 Peripheral vasoconstriction
Cardiovascular Regulation
 Erythropoietin (EPO)
 Released at kidneys
 Responds to low blood pressure, low O2
content in blood
 Stimulates red blood cell production
Cardiovascular Regulation
 Natriuretic Peptides
 Atrial natriuretic peptide (ANP)
 Produced by cells in right atrium
 Brain natriuretic peptide (BNP)
 Produced by ventricular muscle cells
 Respond to excessive diastolic stretching
 Lower blood volume and blood pressure
 Reduce stress on heart
Cardiovascular Regulation
Figure 21–16a The Hormonal Regulation of Blood Pressure and Blood
Volume.
Cardiovascular Regulation
Figure 21–16b The Hormonal Regulation of Blood Pressure and Blood
Volume.
Cardiovascular Adaptation
Cardiovascular Adaptation
 Short-Term Elevation of Blood Pressure
 Carotid and aortic reflexes
 Increase cardiac output (increasing heart rate)
 Cause peripheral vasoconstriction
 Sympathetic nervous system
 Triggers hypothalamus
 Further constricts arterioles
 Venoconstriction improves venous return
Cardiovascular Adaptation
 Short-Term Elevation of Blood Pressure
 Hormonal effects
 Increase cardiac output
 Increase peripheral vasoconstriction (E, NE,
ADH, angiotensin II)
Cardiovascular Adaptation

Long-Term Restoration of Blood Volume

Recall of fluids from interstitial spaces

Aldosterone and ADH promote fluid retention
and reabsorption

Thirst increases

Erythropoietin stimulates red blood cell
production
Cardiovascular Adaptation
 Blood Flow to the Brain
 Is top priority
 Brain has high oxygen demand
 When peripheral vessels constrict, cerebral
vessels dilate, normalizing blood flow
Cardiovascular Adaptation
 Stroke
 Also called cerebrovascular accident (CVA)
 Blockage or rupture in a cerebral artery
 Stops blood flow
Cardiovascular Adaptation
 Heart Attack
 A blockage of coronary blood flow
 Can cause
 Angina (chest pain)
 Tissue damage
 Heart failure
 Death
Cardiovascular Adaptation
 Blood Flow to the Lungs
 Regulated by O2 levels in alveoli
 High O2 content
 Vessels dilate
 Low O2 content
 Vessels constrict
The Systemic Circuit
Figure 21–20 An Overview of the Major Systemic Arteries
The Systemic Circuit
Figure 21–24a Major Arteries of the Trunk
Aging and the Cardiovascular System
 Three Age-Related Changes in Blood
 Decreased hematocrit
 Peripheral blockage by blood clot (thrombus)
 Pooling of blood in legs
 Due to venous valve deterioration
Aging and the Cardiovascular System
 Five Age-Related Changes in the Heart
 Reduced maximum cardiac output
 Changes in nodal and conducting cells
 Reduced elasticity of cardiac (fibrous) skeleton
 Progressive atherosclerosis
 Replacement of damaged cardiac muscle cells by
scar tissue
Aging and the Cardiovascular System
 Three Age-Related Changes in Blood Vessels
 Arteries become less elastic
 Pressure change can cause aneurysm
 Calcium deposits on vessel walls
 Can cause stroke or infarction
 Thrombi can form
 At atherosclerotic plaques