Cardiodynamics and Blood Vessels

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

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

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) 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 S2 S3, S4 Loud sounds
Produced by AV valves S2 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 Physical Limits
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 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

Vasoconstriction and Vasodilation Affect Afterload on heart Peripheral blood pressure Capillary blood flow

From heart to capillaries, arteries change From elastic arteries To muscular arteries To arterioles

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

Muscular Arteries Also called distribution arteries Are medium sized (most arteries) Tunica media has many muscle cells

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

Aneurysm A bulge in an arterial wall Is caused by weak spot in elastic fibers Pressure may rupture vessel

Figure 21–2 Histological Structure of Blood Vessels

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
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

Capillary Structure Endothelial tube, inside thin basal lamina No tunica media No tunica externa Diameter is similar to red blood cell

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

Figure 21–4 Capillary Structure

Capillary Sphincter Guards entrance to each capillary Opens and closes, causing capillary blood to flow in pulses

Vasomotion Contraction and relaxation cycle of capillary sphincters Causes blood flow in capillary beds to constantly change routes

Structure and Function of 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

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

Venous Valves Folds of tunica intima Prevent blood from flowing backward Compression pushes blood toward heart

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 (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

Force (F) Is proportional to the pressure difference (P) Divided by R

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

Viscosity R caused by molecules and suspended materials in a liquid Whole blood viscosity is about four times that of water

Turbulence Swirling action that disturbs smooth flow of liquid Occurs in heart chambers and great vessels Atherosclerotic plaques cause abnormal turbulence

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 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

Figure 21–13 Short-Term and Long-Term Cardiovascular Responses

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

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

Vasomotor Tone Produced by constant action of sympathetic vasoconstrictor nerves

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

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

Figure 21–14 Baroreceptor Reflexes of the Carotid and Aortic Sinuses

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

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

Angiotensin II Responds to fall in renal blood pressure Stimulates Aldosterone production ADH production Thirst Cardiac output Peripheral vasoconstriction

Erythropoietin (EPO) Released at kidneys Responds to low blood pressure, low O2 content in blood Stimulates red blood cell production

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

Figure 21–16a The Hormonal Regulation of Blood Pressure and Blood Volume.

Figure 21–16b The Hormonal Regulation of Blood Pressure and Blood Volume.

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

Short-Term Elevation of Blood Pressure Hormonal effects Increase cardiac output Increase peripheral vasoconstriction (E, NE, ADH, angiotensin II)

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

Blood Flow to the Brain Is top priority Brain has high oxygen demand When peripheral vessels constrict, cerebral vessels dilate, normalizing blood flow

Stroke Also called cerebrovascular accident (CVA) Blockage or rupture in a cerebral artery Stops blood flow

Heart Attack A blockage of coronary blood flow Can cause Angina (chest pain) Tissue damage Heart failure Death

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

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

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

Cardiodynamics and Blood Vessels

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