Cardiovascular Physiology Flashcards
Why do we have a cardiovascular system?
- To provide oxygen and nutrients and remove wastes like carbon dioxide from cells
- Rapid system
- Provides a steep concentration gradient within the vicinity of every cell: important b/c in multicellular organisms as diffusion is too slow
Hemodynamics
The study of blood flow relates Ohm’s law to fluid flow
Relationship between blood flow, blood pressure, and resistance to blood flow
F=deltaP/R
How does blood flow?
From high pressure to low pressure
Hydrostatic Pressure
Blood hydrostatic pressure is the pressure that the volume of blood within our circulatory system exerts on the walls of the blood vessels that contain it
Do we Use Absolute Pressure or the Difference Between Pressures?
The pressure differences
-the pressure difference must be greater than the sum of all resistances to create flow
What Determines Resistance to Blood Flow?
Viscosity = friction between molecules of flowing fluid
Length + diameter = determines amount of contact between moving blood and stationary wall of vessel
Puiseuille’s Equation
R=8nl/pir^4 R= resistance to blood flow n= viscosity of blood l= and length of vessel r = radius of vessel
Functions of the Cardiovascular System
- To deliver oxygen and nutrients and remove waste products of metabolism
- Fast chemical signaling to cells by circulating hormones or neurotransmitters
- Thermoregulation
- Mediation of inflammatory and host defense responses against invading microorganisms
The Heart
The pump
Blood Vessels
The pipes
Blood
The fluid to be moved
Arterioles
Small branching vessels with high resistance
Capillaries
Transport blood between small arteries and venules; exchange of materials
Arteries
Move blood away from the heart
Veins
Move blood towards the heart
What type of pressure does this closed circulatory system generate?
It generates greater pressures
Anatomy of the heart
2 atria
2 ventricles
Septa
Atria
Thin-walled
Low-pressure chambers
Receive blood returning to the heart
Ventricles
Forward propulsion of blood
Interatrial Septum
Separates left and right atria
Interventricular Septum
Separates left and right ventricles
Pulmonary Circulation
- Blood to and from the gas exchange surfaces of the lungs
- Blood entering lungs=poorly oxygenated blood
- Oxygen diffuses from lung tissue to blood
- Blood leaving lungs=oxygenated
Heart Functions as Dual-Path How?
- Left side pumps highly oxygenated blood to the systemic system
- Right side pumps poorly oxygenated blood to the pulmonary circuit
Systemic Circulation
- Blood to and from the rest of the body
- Blood entering tissues=oxygenated blood
- oxygen diffuses from blood to body tissues
- blood leaving tissues=poorly oxygenated
Why are they Called Serial Circuits
Because these steps happen in sequence
Series Flow
Found in the cardiovascular system
-Pulmonary and circulatory circuits
Parallel Flow
Occurs in most organs
- each organ is supplied by a different artery
- independently regulate flow to different organs
Distribution of Blood Flow at Rest and During Exercise
The cardiovascular system must ensure adequate perfusion of capillaries supply the organs at rest, during exercise, or emergency situation
Pericardium
Fibrous sac surrounding the heart and roots of great vessels
Functions of the Pericardium
- Stabilization of the heart in the thoracic cavity
- Protection of the heart from mechanical trauma, infection
- Secretes pericardial fluid to reduce friction
- Limits over fillings of the chamber, prevents sudden distension
3 Layers of the Pericardium
- fibrous pericardium
Serous pericardium
-2. parietal
-3. visceral (epicardium)
Pericardial Cavity
Pericardial fluid decreases friction
Separates the parietal pericardium and the visceral pericardium
Fibrous Pericardium
Provides protection for the heart and stabilizes the heart in the thoracic cavity by attaching to structures in the chest
Parietal Pericardium
Lies underneath the fibrous pericardium and is attached to it
Visceral Pericardium
The innermost layer of the pericardial sac
Called the epicardium when it comes into contact with the heart muscle
Serous Layer
A layer composed of cells that secrete a fluid
Pericarditis
Inflammation of the pericardium
Cardiac Tamponade
Compression of the heart chambers due to excessive accumulation of pericardial fluid
decreases ventricular filling
Why is the left ventricle thicker than the right ventricle?
The left ventricle develops higher pressure so that it can pump blood around the entire circulatory system
Layers of the Heart Wall
Epicardium
Myocardium
Endocardium
Epicardium
Covers the outer surface of the heart
Acts as a protective layer
Connective tissues attach it to the myocardium
Myocardium
The muscular wall of the heart and lies underneath the epicardium
- contains muscle cells or myocytes which contract and relax as the heartbeats
- contains nerves and blood vessels
Endocardium
The innermost layer of the heart wall
- lines heart cavities and the heart valves
- a thin layer of endothelium which is continuous with the endothelium of the attached blood vessels
Myocytes
Cardiac heart muscle
- branched (Y) and joined longitudinally which allows for greater connectivity in the heart
- striated, one nucleus per cell, many mitochondria
Intercalculated Disks
Interdigitated region of attachment
-desmosomes and gap junctions
Desmosomes
Adhering junctions that hold cells together in tissues subject to considerable stretching
Mechanically couples one heart cell to another
Proteins involved: cadherins, plaques, intermediate filaments
Gap Junctions
Communicating junctions
Electrically couple heart cells, allowing ions to move between cells
-important for the spread of action potentials
Protein Involved: Connexion
How are Heart Muscles Arranged?
They are arranged spirally around the circumference of the heart
Why are Heart Muscles Arranged Spirally?
When the cardiac muscle contracts and shortens, a wringing effect is produced, efficiently pushing blood upwards towards the exit of major arteries
Valves
Thin flaps of flexible, endothelium-covered fibrous tissue attached at the base to the valve rings
- leaflets or cusps
- collagen
Valve Rings
Cartilage
Site of attachment for the heart valves
How do valves function?
Unidirectional flow of blood through the heart
Open and close passively due to pressure gradients
-forward pressure gradient opens the one-way valve
-backward gradient closes the one-way valve and it cannot open in the opposite direction
Atrioventricular Valves
Found between the atria and ventricles
Prevent backflow of blood into atria when the ventricles contract
Tricuspid and Bicuspid
Tricuspid Valve
Right AV valve
Three leaflets
Bicuspid Valve
Left AV valve
Two leaflets
AV Valve Apparatus
Chordae tendineae
Papillary Muscles
Chordae tendineae
Tendinous-type tissue
Extend from the edges of each leaflet to papillary muscle
Papillary Muscles
Cone-shaped muscles
Contraction of papillary muscle causes the chordae tendineae to become taut
-THIS HOLDS THE VALVE CLOSED
The Function of the AV Valve Apparatus
Prevents the eversion of the AV valves into the atria during contraction of the ventricles
Valves open and close due to pressure gradients, not from contraction and relaxation of the papillary muscles
Semilunar (arterial) Valves
Found between the ventricle and the artery which ejects its blood
No valve apparatus
Semilunar valves open due to pressure differences
-pulmonary valve
-aortic valve
Pulmonary Valve
Pulmonary trunk, right ventricle
3 cusps
Aortic Valve
Aorta
Left ventricle
3 Cusps
Cardiac Skeleton
Fibrous skeleton of the heart
- dense connective tissue
- includes the heart valve rings and the connective tissue between the heart valves
Cardiac Skeleton Function
Physically separates the atria from ventricles
Electrically inactive and blocks the direct spread of electrical impulses from the atria to the ventricles
Provides support for the heart, providing a point of attachment for the valves leaflets and cardiac muscle
Coronary Sinus
A collection of veins joined together to form a large vessel that collects blood from the myocardium of the heart
Coronary Circulation
The part of the systemic circulatory system and supplies blood to and provides drainage from the tissues of the heart
Coronary Arteries
Arteries supplying the heart
-aortic sinus is a dilation or out-pocketing of the ascending aorta
Cardiac Veins
Collect poorly oxygenated blood and empty it into the coronary sinus, which returns blood to the right atrium
Systole (Contraction)
Myocardial blood flow almost ceases and the right and left ventricle are contracting
Diastole (Relaxation)
Myocardial blood flow peaks as the ventricles are not contracting
Coronary Artery Disease
Caused by atherosclerosis of the coronary arteries supplying blood to the heart tissues
Atherosclerosis
Arteries supplying blood to the heart become hardened and narrow due to plaque in the arterial walls
Plaque
Fat, cholesterol, calcium, and other substances in the blood
Angina
Chest pain or discomfort
Blood flow to the heart muscle is reduced
Myocardial Infarction
Heart attack
Blood supply to the heart is completely blocked; muscle dies
Cardiac Syncytium
When myocytes communicate with each other
-set of cells that act together; the heart resembles a single, enormous muscle cell
Functional Syncytium
If one cell is excited, the excitation spreads over both ventricles (or atria)
-atrial syncytium and a ventricular syncytium
All or nothing property
Cardiac Muscle
Action potentials lead to contraction of heart muscles
Two types of myocytes:
-contractile cells
-conducting cells
Automaticity
The heart contracts or beats rhythmically as a result of action potentials that it generates itself
Contractile Cells
Mechanical work of pumping, propelling blood
Generates pressure to move blood
do not initiate action potentials
Conducting Cells
Initiates and conducts the action potentials responsible for contraction of the contractile myocytes
Part of the conducting system of the heart
-are in electrical contact with each other and the cardiac contractile cells through the gap junctions
Components of the Conducting System
Sinoatrial node Internodal pathways Atrioventricular node Bundle of His Bundle branches; left and right Purkinje fibres
Cardiac Skeleton and Conduction
Non-conducting, no action potentials travel across it
Physically separates the atria from the ventricles, stimuli cannot cross from the atria to the ventricles through the cardiac skeleton
Sinoatrial Node
Cardiac Pacemaker
Initiates action potentials
-sets heart rate
The cardiac skeleton isolate the atrial and ventricular myocardium
Internodal Pathways
The stimulus passed to contractile cells of both atria and to the AV node
Atrioventricular Node
100 msc delay
delay ensures atria depolarize and contract before the ventricles
Contraction of the ventricles would close the AV valves, preventing blood flow from the atria into the ventricles
Allows the ventricles time to fill completely before they contract
Excitation of the Ventricles
AV node and Bundle of His are the only electrical connection between atria and ventricles
Left and right branches travel along the interventricular septum and make contact with Purkinje fibres
Purkinje Fibres
Large number, diffuse distribution, fast conduction velocity
Left and right ventricular myocytes depolarize and contract nearly simultaneously
Pathway of Excitation
SA node - Internodal pathways - AV node - Bundle of His - Right and left branches - Purkinje fibres - Ventricular myocardium
Wolff-Parkinson-White Syndrome
There is an extra connection in the heart called an accessory pathway
-the accessory pathway is an abnormal piece of muscle that connects directly between the atria and ventricles
-electrical signals bypass the AV node and move from the atria to the ventricles faster than usual
-transmits electrical impulses abnormally from the ventricles back to the atria
Rapid heart rate or arrhythmias
Fast Action Potentials
Found in:
Atrial myocardium
Ventricular myocardium
Bundle of His, Bundle Branches, Purkinje fibres
Slow Action Potentials
Found in:
Sinoatrial node
Atrioventricular node
The Cardiac Action Potential
Phases of the cardiac action potential are associated with changes in the permeability of the cell membrane mainly to Na+, K+, and Ca2+ ions
Opening and closing of ion channels alters the permeability
Concentrations of Ions in the heart
[K+]in>[K+]out
[Ca2+]out>[Ca2+]in
[Na+]out>[Na+]in
Pacemaker Potential
Slow depolarization to threshold
Regular spontaneous generation of action potentials
Stages of Slow Action Potential
- Pacemaker potential
- K+ channels = progressive reductive in potassium permeability
- F-type cells = funny
- T-type cells = transient - Depolarization
- L-type channels = long-lasting - Repolarization
- K+ channels = potassium leaves cell
Summary of Slow Action Potential
Depolarization phase is slow due to slow movement of Ca2+
Pacemaker potential due to changes in movement of ions
AV node pacemaker current rises to threshold more slowly
Electrocardiograms
Graphic recording of electrical events
Electrical activity of the heart detected on the surface of the body
Voltage gradients in the heart may be as much as 100 mV, translated to charges of up to 1 mV on the skin surface
Used to diagnose heart problems
P-wave
Spread of depolarization across atria
-atria contract 25 msec after start of P-wave
First wave on ECG
QRS Complex
Spread of depolarization across ventricles
-atria repolarize simultaneously
When the ventricles are depolarizing, the atria are repolarizing
T-Wave
Ventricular repolarization
Normal ECG
P-wave always followed by QRS complex and T-wave
Partial AV Node Block
Every 2nd P-wave is not followed by a QRS complex
Complete AV Node Block
No synchrony between atrial and ventricular electrical activities
Ventricles driven by slower bundle of His
Cardiac Myocyte
Muscle cell of the heart
Intercalated Disk
Where the membranes of two adjacent myocytes are extensively intertwined; desmosomes and gap junction
Sarcolemma
Plasma or cell membrane of a muscle cell
Sarcoplasmic Reticulum
A special type of smooth endoplasmic reticulum which stores and pumps calcium ions
Cardiac Myocyte Structure
Contains myofibrils
Striated
T-tubules = invaginations of sarcolemma; transmit depolarization of membrane into interior of muscle cell
Excitation-Contraction Coupling in Cardiac Muscle
Calcium ions regulate the contraction of cardiac muscle
- calcium binds to ryanodine receptors, releasing calcium from the sarcoplasmic reticulum
- calcium dependent calcium release
Activation of Cross-Bridge Cycling by Calcium
Troponin = contains binding sites for calcium and tropomyosin, and regulates access to myosin-binding sites on actin Tropomyosin = partially cover the myosin-binding sites on actin at rest, preventing cross-bridges from making contact with actin
Steps in Cardiac contraction
- Excitation spreads along the sarcolemma
- Excitation also spreads to the interior of the cell by T-tubules
- During plateau phase of action potential, permeability of the cell to calcium increases
- Calcium enters through L-type Ca2+ channels in sarcolemma and T-tubules
- Calcium causes the release of calcium from sarcoplasmic reticulum through calcium-release channels
- Elevation of cytosolic calcium
- Calcium binds to troponin which unblocks active sites between actin and myosin
- Cross-bridge cycling and contraction of myofibrils
Excitation-contraction coupling in skeletal muscles
Physical coupling between DHP receptor and ryanodine receptor
Excitation-contraction coupling in cardiac muscle
L-type Ca2+ channel
-voltage-gate Ca2+ channel
Calcium-dependent calcium release
ECC in Cardiac Muscle - Relaxation Steps
- Influx of calcium stops as L-type Ca2+ channels close
- SR is no longer stimulated to release calcium
- SR takes up cytosolic calcium by Ca2+-ATPase
- Calcium removed from cell by Na+-Ca2+ exchanger
- Reduced calcium binding to troponin
- Sites for interaction between myosin and actin are blocked
- Relaxation of myofibrils
Refractory Period
Period of time in which a new action potential cannot be initiated Absolute Refractory Period -250 msec -no response to another stimulus -inactivation of Na+ channels Prevents tetanus
Systole
Ventricular contraction and blood ejection
Diastole
Ventricular relaxation and blood filling
Cardiac Cycle
The cardiac cycle length is the period of time from the beginning of one heartbeat to the beginning of the next
- each heartbeat involves one ventricular systole and one ventricular diastole
- the heart spends most of its time is diastole
Isovolumetric Ventricular Contraction (systole)
All heart valves closed, blood pressure in the ventricles remains constant
Ventricular Ejection (systole)
Pressure in ventricles exceeds that in arteries, semilunar valves open and blood ejected into the artery
Stroke Volume (systole)
Volume of blood ejected from each ventricle during systole
Isovolumetric Ventricular Relaxation (diastole)
all heart valves closed, blood volume remains constant, pressure drops
Ventricular filling (diastole)
AV valves open, blood flows into ventricles from atria. Ventricles receive blood passively
Atria contraction (diastole)
occurs at the end of ventricular filling
Cardiac Cycle - Diagram
Review this
Pressure-volume curve
Pressure is generated when the muscles of the heart chamber contract as well as when a chamber fills with blood
Blood always flows from a region of higher pressure to a region of lower pressure
Valves open and close in a response to a pressure gradient
End-diastolic Volume (EDV)
Amount of blood in each ventricle at the end of ventricular diastole
End-systolic Volume (ESV)
Amount of blood in each ventricle at the end of ventricular systole
Stroke Volume
Volume of blood pumped out of each ventricle during systole
Stroke Volume Formula
SV=EDV-EDS (usually 70-75 mL)
Wigger’s Diagram
Understand this diagram that shoed the pressure and volume changes for the heart
Do the right side or the left side of the hear have lower pressure?
The right side has lower pressure than the left ventricle during systole
2 Heart Sounds
Lub = closure of AV valves - onset of systole
Dub = closure of semilunar valves - onset of diastole
The sounds result from vibrations caused by the passive closing of the valves
How does blood flow normally?
Laminar flow and makes no sound
-characterized by smooth concentric layers of blood moving in parallel down the length of a blood vessel
Abnormal Blood Flow
May be turbulent
- makes sounds = murmer
- stenosis
- insufficiency
Stenosis
Blood flows rapidly through a narrowed valve; leaflets do not open completely
Insufficient Valve
Blood flows backward through leaky valve; leaflets do not close completely
Sympathetic Innervation of the Heart
The entire heart, including the atria, ventricles, SA node, AV node
Parasympathetic Innervation of the Heart
Atria, SA node, AV node
Parasympathetic Stimulation of the SA Node
rate of depolarization decreases; heart rate decreases
Sympathetic Stimulation of the SA Node
rate of depolarization increases; heart rate increases
Parasympathetic Stimulation of the AV Node
Conduction decreases; increased AV node delay
Sympathetic Stimulation of the AV Node
Conduction increases; decreased AV node delay
Parasympathetic Stimulation of the Atrial Muscle
Decreased contractility
Sympathetic Stimulation of the Atrial Muscle
Increased contractility
Parasympathetic Stimulation of the Ventricular Muscle
No significant innervation; no effect
Sympathetic Stimulation of the Ventricular Muscle
Increased contractility
Cardiac Output (CO)
The amount of blood pumped by each ventricle in one minute
Cardiac Output Formula
CO = HR (heart rate) * SV (stroke volume)
Factors Affecting Cardiac Output
Heart rate
Stroke Volume
How do we alter heart rate?
Modifying the activity of the SA node
How do we alter stroke volume?
Altered by varying the strength of the contraction of the ventricular myocardium
- increased contraction = increased stroke volume
- decreased contraction = decreased stroke volume
Does the ventricles completely empty out after each contraction?
No
Factors Affecting Heart Rate
Increased sympathetic activity
-increase heart rate
Increased parasympathetic activity
-decreased heart rate
Effect of the Sympathetic System on Heart Rate
Increases the slope of the pacemaker potential (faster depolarization)
- increases HR
- increases F-type (allows Na+ to enter cell) and T-type (allows Ca2+ to enter cell) channel permeability
Effect of the Parasympathetic System on Heart Rate
Decreases the slope of the pacemaker potential (slower depolarization)
- decreases HR
- decreases F-type channel permeability (reduced Na+ in cell)
- hyperpolarizes cells (increases K+ permeability)
Sympathetic Stimulation on Pacemaker Potential
Pacemaker potential rises more quickly to threshold, or takes less time to reach threshold, increasing the heart rate
Parasympathetic Stimulation on Pacemaker Potential
Pacemaker potential rises more slowly to threshold, or takes more time, decreasing heart rate
3 Factors Affecting Stroke Volume
End-diastolic volume (EDV; preload)
Contractility of the ventricles
Afterload
Preload
Tension of load on myocardium before it begins to contract or amount of filling of ventricles at the end of diastole
-the ventricles will contract more forcefully when they have been stretched prior to contraction
EDV
The volume of blood in the ventricles at the end of ventricular diastole or the volume of blood in the ventricles after the ventricles have completed filling
Sympathetic Stimulation of Venous Smooth Muscle
Increases the return of blood to the heart through vasoconstriction, increasing filling of the ventricles
-sympathetic stimulation only, parasympathetic does no innervate venous muscle
Frank-Starling Mechanism
The relationship between EDV and SV
Main determinant of cardiac muscle fibre (sarcomeres) length is degree of diastolic filling: preload
Increase filling - increase EDV - increase cardiac fibre length - greater force during contraction and greater SV
Mechanism of the Length-tension Relationship
When the ventricle is filled more fully with blood, there is an increased force of contraction and a greater stroke volume
-stretches the heart = increases the sarcomere length
Contractility
The strength of contraction at any given EDV
A change in the contractility of the ventricles will alter the volume of blood pumped by the ventricles during systole
Sympathetic Stimulation and Contractility
The stroke volume is greater at any given EDV during sympathetic stimulation
More rapid contraction and more rapid relaxation
Ventricles ejecting more blood
Ejection Fraction
EF = SV/EDV
Mechanism of Sympathetic Effect on Contractility
Acts through a G protein coupled mechanism
Afterload
Tension (arterial pressure) against which the ventricles contract
-often called the load
As afterload increases, SV decreases
Any factor that restricts blood flow through arterial system will increase afterload
Endothelium
Smooth, single-celled layer of endothelial cells
Endothelium of vessels is continuous with endocardium of the heart
Physical lining that blood cells do not normally adhere to
Pressures in the Systemic and Pulmonary Circuits
Pressures in the systemic and pulmonary circuits generated from ventricular contraction decrease as the blood moves further along the circuit
Pulmonary vascular resistance is much lower the systemic total resistance
Arteries
Smooth muscle, elastic fibres, connective tissues
Muscular walls allow arteries to contract and change diameters
Elasticity permits passive changes in vessel diameter in response to changes in blood pressure
Elastic Arteries
Many elastic fibres, few smooth muscle cells
Expand and recoil in response to pressure changes
Muscular Arteries
Many smooth muscle cells, few elastic fibres
Distributes blood
Arterioles
1-2 layers of smooth muscle cells
Resistance vessels
Vasoconstriction
Contraction of arterial smooth muscle decreases the diameter of the artery
-decreased blood flow to organs
Vasodilation
Relaxation of arterial smooth muscle increases the diameter of the artery
-increased blood flow to organs
Functions of Arterioles
Regulate blood flow to organs
-capillary beds
Determine MAP
-resistance
Resistance in Arterioles
High resistance vessels due to their small size
- causes drop in mean arterial pressure (MAP)
- altering arteriolar diameter alters resistance and flow
Intrinsic or Basal Tone
Arteriolar smooth muscle is partially contracted in the absence of external factors
-other factors can increase or decrease the state of contraction to cause vasoconstriction or vasodilation
Extrinsic Factors
Factors external to the organ or tissue; who body needs (MAP); nerves and hormones
Intrinsic Factors
Local controls; organs and tissees alter their own arteriolar resistances independent of nerves or hormones
Extrinsic Controls: Nerves
Sympathetic innervation
- NE causes vasoconstriction
- sympathetic tone can be increased or decreased
- regulating MAP by influencing arteriolar resistance throughout the body
- noncholingeric and nonadrenergic nerves cause vasodilation
Extrinsic Controls: Hormones
Epinephrine from adrenal medulla causes vasoconstriction or vasodilation
Local Controls: Active Hyperemia
Local control which acts to increase blood flow when the metabolic activity of an organ or tissue increases
Hyperemia = excess of blood flow in the vessels supplying an organ or tissue
Local Controls: Flow Autoregulation
Changes in arterial blood pressure alters blood flow to an organ
-changes in the concentration of local chemicals
Arterioles change their resistance to maintain constant blood flow in the presence of a pressure change
Constant metabolic activity
No nerves or hormones involved
May also be mediated by the myogenic response
-direct response of arteriolar smooth muscle to stretch
Reactive Hyperemia
Form of flow autoregulation
Occurs at constant metabolic rate
Occurs due to changes in the concentrations of local chemicals
Occlusion of blood flow = greatly decreases oxygen levels and increases metabolites = arterioles dilate = blood flow greatly increases once occlusion is removed
Capillaries
One endothelial cell thick
-no smooth muscle or elastic tissue
Exchange of material fluid between blood and interstitial fluid
Intercellular clefts = narrow water-filled space at the junctions between cells
Types of Capillaries
Continuous
Fenestrated
Sinusoidal
Continuous Capillaries
Endothelial cells form an uninterrupted tube, surrounded by complete basement membrane
Exchange of water, small solutes, lipid-soluble material, no exchange of blood and plasma proteins
Most tissues
tight junctions = low permeability
Pericytes
Lie external to the endothelium; may help stabilize the walls of blood vessels and help regulate blood flow through capillaries
Fenestrated Capillaries
Contains fenestrae (pores) that penetrate the endothelial lining Surrounded by complete basement membrane Rapid exchange of water and solutes Endocrine organs, choroid plexus, GI tract, kidneys
Sinusoid Capillaries
Discontinuous capillaries; flattened and irregularly shaped capillaries -large fenestrae and gaps between cells -basement membrane thin or absent Free exchange of water and solutes Live, bone marrow, spleen
Microcirculation
The circulation of blood through the smallest vessels in the body
- precapillary spincter
- metarteriole
Precapillary Sphincter
At entrance to a capillary Ring of smooth muscle Alters blood flow No innervation -respond to local factors
Metarteriole
Connects arterioles to venules
Contains smooth muscle cells
Change diameter to regulate flow
Diffusion
Movement of substance down its concentration gradient
- short distance to travel across a capillary
- moves down concentration gradient
Trancytosis
Use of vesicles to cross endothelial cells
-fused vesicle channel = endocytic and exocytic vesicles form a water-filled channel across the cell
Bulk Flow
Movement of protein-free plasma across the capillary wall
-distribution of extracellular fluid volume
Filtration
Movement of protein-free plasma from capillary to interstitial fluid
Reabsorption
Movement of protein-free plasma from interstitial fluid to capillary
Bulk Flow: Hydrostatic Pressure
Pressure that drive fluid movement in and out of the capillary
- capillary hydrostatic = pressure exerted on the inside of capillary walls by blood which favours fluid movement out of the capillary
- interstitial fluid hydrostatic pressure = fluid pressure exerted on the outside of the capillary walls by interstitial fluid which favours fluid movement into capillary (NEGLIGIBLE)
Bulk Flow: Colloid Osmotic Pressures
Pressures that drive fluid movement (bulk flow) into and out of the capillary
- blood colloid osmotic pressure = osmotic pressure due to non-permeating plasma proteins inside of the capillaries which favours fluid movement into the capillaries
- interstitial fluid colloid osmotic pressure = small amount of plasma proteins may leak out of capillaries into interstitial space which favours fluid movement out of capillaries (NEGLIGIBLE)
Bulk Flow: Net Exchange Pressures
When net filtration pressure is positive = favours filtration
When net filtration pressure is negative = favours absorption
Net Filtration and Net Reabsorption Along the Capillary
Transition point between filtration and reabsorption lies closer to venous end of capillary
-more filtration that absorption
Distribution of Blood Volume
60% of blood volume is in the venous system
A lot of blood is found in the liver, bone marrow, and skin
Veins
Expand and recoil passively with changes in pressure
High capacitance vessels as can store large amount of blood
Highly distensible at low pressure and have little elastic recoil
Reservoir for blood
Venous Valves
Low pressure system
Composed of two leaflets or folds = prevents the backflow of blood into the capillaries
-blood flows in one direction only
Compartmentalize blood
Varicose Veins
Valves do not function properly when vein walls weaken, stretch
Blood pools and vessels distend
Mechanisms for Venous Return
Smooth muscle in veins -innervated by sympathetic neurons Skeletal muscle pump -compresses veins -venous pressure increases, forcing more blood back to the heart Respiratory pump -inspiration causes an increase in venous return -breathe deeper=blood to heart faster
Venous Return and Frank-Starling Law
Increased venous return results in increased stroke volume through the Frank-Starling mechanism
Lymphatic System Components
Lymphatic capillaries
Lymph vessels
Lymph nodes
Lymph Capillaries
Single layer of endothelial cells
Large water-filled channels permeable to all interstitial fluid components
IF enters lymphatic system through capillaries by bulk flow
Closed end tubes
Lymph Vessels
Formed from convergence of lymphatic capillaries
One-way valves
Empty into venous system
IF is called lymph once it enters the lymph vessels
Lymph Nodes
Immune response
Mechanism of Lymph Flow
Return of fluid from interstitial fluid to blood
Mechanism
-lymphatic vessels have smooth muscle; responsive to stretch
-sympathetic nervous system
-skeletal muscle contractions
-respiratory pump
Arterial Blood Pressure
Determined by the volume of blood in the vessels and the compliance of a vessel
Large arteries function as pressure reservoirs due to elastic recoil
-not as compliant as veins
Compliance
Ability to distend and increase volume with increasing transmural pressure
The greater the compliance of a vessel, the more easily it can be stretched
Systolic Pressure
Maximum blood pressure during ventricular systole
Diastolic Pressure
Minimum blood pressure at the end of ventricular diastole
Systolic/Diastolic Pressure
120/80 mmHg
Normal blood pressure
Pulse Pressure
Systolic - diastolic
Hypertension
Chronically increased arterial blood pressure
Hypotension
Abnormally low blood pressure
Mean Arterial Pressure
The pressure driving blood into the tissues averaged over the cardiac cycle
-ensures organ perfusion
Pulse pressure decreases as distance from heart increases
-pressure pulses disappear at level of arterioles
-smooth flow at capillaries
MAP decreases as distance from heart increases
The largest drop in pressure occurs across the arterioles (high resistance vessels)
MAP Formula
MAP = CO * TPR
- TPR=total peripheral resistance
- can be determined by total arteriolar resistance
TPR
The combined resistance of all of the systemic vessels
Short-Term Regulation of MAP
Seconds to hours
Baroreceptors reflexes
Adjusts CO and TPR resistance by ANS
Long-Term Regulation of MAP
Adjust Blood Volume
Restore normal salt and water balance through mechanisms that regulate urine output and thirst
Arterial Baroreceptors
Carotid sinus and aortic arch baroreceptors
Respond to mean arterial pressure and pulse pressure
Respond to changes in pressure when walls of vessel stretch/relax
-degree of stretching is directly proportional to pressure
Baroreceptor Action Potential Frequency
Rate of discharge is proportional to the mean arterial pressure
Increase in MAP increases rate of firing of baroreceptors
Decrease in MAP decreases rate of firing of baroreceptors
Respond to changes in pulse pressure
The Medullary Cardiovascular Center
Located in the medulla oblongata
Receives inout from baroreceptors
Alter vagal stimulation (parasympathetic) to the hear and sympathetic innervation to heart, arterioles, and veins
Baroreceptors adapt to sustained changes in arterial pressure
Chemoreceptors
Respond to O2 and pH levels in blood
- affect respiration and blood pressure through the cardiovascular center
- aortic and carotid bodies
