Functional Human Physiology for the Exercise and Sport Sciences The Cardiovascular System: Cardiac Function Jennifer L. Doherty, MS, ATC Department of.

Functional Human Physiologyfor the Exercise and Sport Sciences

The Cardiovascular System: Cardiac Function

Jennifer L. Doherty, MS, ATC

Department of Health, Physical Education, and Recreation

Florida International University

Overview of the Cardiovascular System

3 components The Heart Blood Vessels Blood

The Heart Atria Ventricles Interatrial Septum Interventricular

Septum Atrioventricular valves Semilunar valves

Overview of the Cardiovascular System

Blood Vessels Arteries Arterioles Capillaries Venules Veins

Blood Erythrocytes Leukocytes Platelets Plasma

The Path of Blood Flow Through the Heart and Vasculature

Pulmonary Circuit Blood flow between

the lungs and heart Supplied by the Right

side of the heart

Systemic Circuit Blood flow between

the rest of the body and heart

Supplied by the Left side of the heart

The Path of Blood Flow Through the Heart and Vasculature Right Atrium

Receives deoxygenated blood from the body

Blood passes through the Right AV (tricuspid) valve Enters the Right Ventricle

Right Ventricle Pumps blood into the Pulmonary Circuit

Blood passes through the Pulmonary Semilunar valve

Enters the Pulmonary Trunk → Pulmonary arteries → Lungs

The Path of Blood Flow Through the Heart and Vasculature Left Atrium

Receives oxygenated blood from the Lungs

Blood passes through the Left AV (bicuspid) valve Enters the Left Ventricle

Left Ventricle Pumps blood into the systemic circuit

Blood passes through the Aortic Semilunar valve Enters the Aorta → Arteries → Arterioles → Capillaries →

Venules → Veins

The Conduction System of the Heart

Autorhythmicity Ability of the heart to generate electrical signals that

trigger cardiac muscle contractions in a periodic manner

Autorhythmic cells (2 types) Coordinate and provide a rhythmic heartbeat Repeatedly and spontaneously depolarize neurons

1) Do not rely on external nervous stimulation Pacemaker Cells

Initiate action potentials, which establish the heart rhythm Conduction Fibers

Transmit action potentials throughout the heart

Conduction pathways Depolarization spreads throughout the heart

very rapidly facilitating a coordinated contraction pattern

Intercalated disks Form junctions between adjacent cardiac muscle

fibers Contain a high concentration of gap junctions for

rapid transmission of the action potential

The Conduction System of the Heart

Initiation and Conduction of an Impulse During a Heartbeat Action Potential is initiated at the

Sinoatrial (SA) Node Sinoatrial (SA) Node

Small cluster of cells in the right atrial wall, just inferior to the entrance of the superior vena cava

Fastest spontaneous depolarization rate:1) Approximately 70 - 80 bpm (normal resting heartbeat)

Establishes the normal pacemaker of the heart 1) Called Sinus rhythm

Initiation and Conduction of an Impulse During a Heartbeat

Action Potential travels from the SA Node toward the AV Node

Travel along Internodal pathways System of conduction fibers that run along

the walls of the atria to the AV Node

Travel along Interartrial pathways System of conduction fibers that run along

the walls of the atria to the cardiac muscle

Initiation and Conduction of an Impulse During a Heartbeat The impulse is conducted to the cells of the AV

Node Atrioventricular (AV) Node

Located in the interatrial septum just above the tricuspid valve.

Spontaneously depolarizes

AV delay Slight delay in conduction due to the smaller diameter of

these conduction fibers Allows the atria to finish contracting before the ventricles

depolarize and contraction

Impulse travels from the AV Node through the Atrioventricular (AV) Bundle

Compact bundle of muscle fibers Located in the interventricular septum Also called the Bundle of His

After the slight AV delay, the action potential passes rapidly through the AV bundle since it has large fibers

The depolarization then passes to the bundle branches


The impulse travels to the Right and Left Bundle Branches

Located in the interventricular septum Conduct the impulse to the right and left

ventricles

They pass the depolarization impulse rapidly to the Purkinje fibers.


Initiation and Conduction of an Impulse During a Heartbeat The impulse travels from the Bundles

Branches to the Purkinje Fibers Purkinje Fibers

Large diameter, rapid conduction fibers Spread the impulse to the ventricular myocardium

Responsible for approximately simultaneous excitation of the ventricles which is essential for efficient pumping

Total time elapsed between excitation of SA node and ventricular depolarization is about 0.22 sec

Electrical Activity in the Heart

Cardiac Contractile Cells Resting membrane potential in cardiac cells is

approximately -90 mV Cardiac action potentials

Depolarization causes the opening of Ca++ voltage-gated channels

1) Affects membrane potential

2) Triggers cardiac muscle contraction Special K+ voltage-gated channels close in response

to depolarization 1) Reduces membrane permeability to potassium

Spread of Action Potentials through the heart – Phases of the Action Potential

Phase 0: Depolarization Causes Na++ voltage-gated channels to open Increases permeability to Na++ Na++ ions follow their electrochemical gradient into

the cell Membrane potential becomes more positive


Phase 1: Repolarization Na++ voltage-gated channel inactivation gates

close 1) Decreases permeability to Na++

K+ voltage-gated channels close (in response to depolarization)

1) Decreases the flow of K+ out of the cell

Ca++ voltage-gated channels open 1) Increases permeability to Ca++

2) Ca++ flows into the cell


Phase 2: Plateau K+ channels stay closed Ca++ channels stay open

1) Ca++ influx prolongs depolarization

Membrane remains depolarized The purpose of the plateau phase is to prevent

tetany (prolonged contractions) that would interfere with the pumping ability of the heart

Phase 3: Repolarization K+ voltage-gated channels open

1) Increases permeability to K+

2) K+ flows out of cell

3) Results in repolarization

Ca++ channels begin to close1) Ca++ is pumped back into the SR

2) Ca++ is pumped out of cell into the extracellular fluid



Phase 4: Resting Resting potential is re-established at -90 mV

Excitation-Contraction Coupling in Cardiac Muscle Fibers Action potential spreads along the cell

membrane and down T-tubules Causes Ca++ voltage-gated channels to

open SR Ca++ voltage-gated channels release Ca++

into the cytosol Membrane Ca++ voltage-gated channels allow

Ca++ from extracellular fluid to enter cell

Excitation-Contraction Coupling in Cardiac Muscle Fibers

Cardiac muscle has less extensive SRs compared to skeletal muscle

Therefore, cardiac muscle contraction depends heavily on Ca++ influx from the extracellular fluid

When depolarization occurs, Ca++ voltage-gated channels open

1) Allows influx of Ca++ from the extracellular fluid The strength of cardiac muscle contraction is

directly related to the amount of Ca++ that enters the cell from the extracellular fluid

Unlike skeletal muscle cells because it is able to store large amounts of Ca++ in the SR

Excitation-Contraction Coupling in Cardiac Muscle Fibers In cardiac muscle, the SR releases more

Ca++ with each action potential Called Calcium-induced calcium release

Ca++ binds to troponin shifting tropomyosin off of the myosin-binding sites on actin

Cross-bridge cycling occurs The all-or-none law applies to the entire functional syncytium in cardiac

muscle, not to individual muscle fibers as in skeletal muscle

Excitation-Contraction Coupling in Cardiac Muscle Fibers For cardiac muscle to relax, Ca++ must be

removed from the cytosol Ca++ is removed from troponin and

tropomyosin shifts back over the myosin-binding sites on action

The muscle fiber then relaxes

Recording the Electrical Activity of the Heart with Electrocardiograms

Electrocardiogram (ECG or EKG) A recording of the electrical changes that

occur in the myocardium during the cardiac cycle

A graphic representation of the electrical activity of the heart obtained by electrodes on the surface of the skin

Body fluids conduct the electrical activity that can be detected by the electrodes.

Recording the Electrical Activity of the Heart with Electrocardiograms Einthoven’s triangle Imaginary triangle formed by the leads of

the EKG Each lead has a (+) and (-) electrode

Detects the difference in surface electrical potential between the positive and negative electrodes

Waveforms of a Normal EKG

P wave P-R interval QRS complex T wave

Only electrical events of the heart, such as arrhythmias or conduction blocks, can be detected on an EKG

No information about the mechanical events of the heart are revealed by the EKG


P wave Marks depolarization of

the atria Includes the time in which

the SA node sends the electrical impulse toward the AV node

This depolarization spreads as a wave of impulses across both atria, causing them to contract


P-R interval Includes the time

required for the electrical impulse to spread from the atria, through the AV node, to the ventricles


QRS complex Represents depolarization

of the ventricles Leads to ventricular

contraction The wave is large

because the ventricles have thicker walls and therefore produce a greater electrical impulse


T wave Occurs as the

ventricles slowly repolarize


Repolarization of the atria

Occurs during ventricular depolarization and is obscured by the QRS complex

The Cardiac Cycle

Includes all events associated with the flow of blood through the heart during a single, complete heartbeat

During the cardiac cycle, pressure changes occur as the atria and ventricles alternately contract and relax

When a chamber of the heart contracts, there is an increase in blood pressure inside the chamber

When a chamber of the heart relaxes, there is a decrease in blood pressure inside the chamber

Blood always flows from regions of high pressure to low pressure

Mechanical events of the cardiac cycle are associated with changes in pressure and blood volume in the heart

The pressure differences cause opening and closing of heart valves that allow one-way blood flow through heart

Changes in pressure and blood volume correspond with electrical events on the EKG

The Cardiac Cycle

The Cardiac Cycle – 5 Aspects

Pump Cycle Phases of the pumping action of the heart

Periods of valve opening and closure Changes in pressure within the atria and

ventricles Changes in ventricular volume

Reflect the amount of blood entering and leaving the ventricle during each heartbeat

Heart sounds

The Pump Cycle

One complete cardiac cycle includes both contraction and relaxation of the atria and ventricles

Two main stages: Systole

Contraction of a heart chamber forcing blood out

Diastole Relaxation of a heart chamber allowing blood filling

Phases of the Pump Cycle: Phase 1: Mid-to-late Diastole Two components

Ventricular Filling Atrial Contraction

Phases of the Pump Cycle: Phase 1: Mid-to-late Diastole

Ventricular filling Ventricles are relaxed

Intraventricular pressure is low

AV valves are open Semilunar valves are closed Most ventricular filling is passive

Passive blood flow from the atria into the ventricles accounts for about 70 - 80% of ventricular filling

Phases of the Pump Cycle: Phase 1: Mid-to-late Diastole

Atrial contraction Occurs following SA node depolarization

Relatively little contribution to ventricular filling in normal, resting heart

Atria contract and compress blood in the atria Slight rise in atrial pressure Last squirt of blood into ventricles

Atria relax and are in atrial diastole for the rest of the cardiac cycle

Phases of the Pump Cycle: Phase 2: Systole Two components

Isovolumetric Contraction Ventricular Ejection

Atria are relaxed Ventricles are contracting

Increase in ventricular pressure Pressure gradient exists between the ventricles and

atria

Phases of the Pump Cycle: Phase 2: SystoleIsovolumetric Contraction Ventricular contraction Increased ventricular pressure

All four heart valves are momentarily closed1) When ventricular pressure exceeds atrial pressure, the AV valves

close2) The semilunar valves remain closed until the ventricular pressure

exceeds the pressure in the pulmonary trunk or aorta

Once the ventricular pressure exceeds the pressure in the pulmonary trunk and aorta, the semilunar valves open

Blood is ejected from the ventricles

Ventricular Ejection Begins when the semilunar valves open Blood is pumped out of the ventricles and

into the pulmonary trunk and aorta Ventricular volume decreases

Phases of the Pump Cycle: Phase 2: Systole

Phases of the Pump Cycle: Phase 3: Early Diastole Begins as ventricular contraction stops Two components

Isovolumetric Relaxation Ventricular Filling Phase

Phases of the Pump Cycle: Phase 3: Early DiastoleIsovolumetric relaxation Begins with ventricular relaxation Decreased ventricular pressure

Semilunar valves close

During this time, atria have been in diastole Filling with blood Increased atrial pressure

Phases of the Pump Cycle: Phase 3: Early Diastole

Ventricular Filling In early diastole, the atrial blood pressure

begins to exceed the pressure in the ventricles The AV valves open Blood flows from the atria into the ventricles

Ventricular filling begins Mid-to-late Diastole (discussed earlier)

Ventricles are relaxed AV valves are open Semilunar valves are closed

Other Features of the Cardiac Cycle

Quiescent period Follows ventricular systole The entire heart is relaxed for ~ 0.4 sec

Atrial systole lasts ~ 0.1 sec Ventricular systole lasts ~ 0.3 sec Note that pressure gradients keep blood

moving one-way through heart and cause valve opening/closing

Heart Sounds The heart sounds are triggered by valve closure

and blood passing through the heart "Lub-Dup" produced by vibrations and turbulence

created by blood flow inside the heart First sound is lub.

Longer and louder Reflects AV valve closure Indicates the beginning of ventricular systole

Second sound is dup. Shorter and sharp Reflects semilunar valve closure Indicates the beginning of ventricular diastole

Cardiac Output and its Control

Heart Rate (HR) The number of ventricular contractions per

minute

Stroke Volume (SV) The amount of blood pumped out of the ventricle

with each contraction Stroke volume is usually about 80ml/beat at rest.

Cardiac Output and its Control

Cardiac Output (CO) The volume of blood pumped by each ventricular contraction

per minute CO = SV x HR Example (normal resting adult):

1) SV = 70 ml/beat and HR = 72 bpm2) CO = 70 ml/beat x 72 bpm = 5,040 ml/min or about 5 L/min

At rest, CO is ~ 5 L/min During stress such as exercise, the normal heart has the

capacity to increase CO by 4 - 5 times that of resting ~ 20 – 25 L/min

Athletes can increase CO by as much as 7 times that of resting ~ 35 L/min, This is known as the Cardiac Reserve

Variables that Determine CO

CO may be altered by changes in SV and/or HR

Direct Relationship

Heart Rate ↑ HR = ↑ CO; ↓ HR = ↓ CO

Stroke Volume ↑ SV = ↑ CO; ↓ SV = ↓ CO

Variables that Determine CO

Force of heart muscle contraction (contractility)

Factors that affect heart rate and contractility Extrinsic control: Factors from outside of the

heart Neural Input Circulating hormones (drugs, neurotransmitters, etc.)

Intrinsic control: Factors from within the heart Starling’s Law of the Heart

Factors Affecting CO: Changes in HR

Autonomic Control of HR Heart rate is influenced by 3 types of factors:

1) Sympathetic control

2) Parasympathetic control

3) Hormonal control

Fibers of the ANS project to almost every part of the heart:

SA node AV node Ventricular myocardium

The ANS regulates both HR and SV (contractility)


Sympathetic nervous system activation causes ↑ HR ↑ SV (contractility)

Sympathetic input to the heart Sympathetic cardiac nerves emerge from the

sympathetic trunk from thoracic region of spinal cord Provides innervations to the:

SA node AV node Ventricular myocardium

Neurotransmitter is norepinephrine


Parasympathetic nervous system activation causes

↓ HR ↓ SV (contractility)

Parasympathetic input to the heart The vagus nerve (X) emerges from the medulla

oblongata Primarily innervates the

SA node AV node

Neurotransmitter is acetylcholine

Sympathetic Control of HR

Increased sympathetic activity Increases action potential frequency Action potential is transmitted faster

Reduced delay of impulse conduction between the atria and ventricles

Shortens the time it takes for action potentials to travel through the ventricles

↑ HR ↑ CO

Parasympathetic Control of HR

Increased parasympathetic activity Vagus Nerve Stimulation

Decreases depolarization

Decreases action potential frequency Action potential is transmitted slower

Decreased conduction between atria and ventricles Lengthens the time it takes action potentials to travel

through the ventricles

↓ HR ↓ CO

Hormonal Control of HR

Epinephrine (Catecholemines)

Secreted by the adrenal medulla, usually in response to sympathetic nervous stimulation

Travels through the bloodstream to the heart Exerts minute-by-minute control Increases the frequency of action potentials

generated by the SA node, thus ↑ HR Increases speed of action potential conduction

through heart, thus ↑ HR

Hormonal Control of HR

Thyroid Hormones (Thyroxine) Causes proliferation of adrenergic receptors, the

binding sites for catecholamines resulting in: ↑ HR ↑ SV ↑ CO Decreased total peripheral resistance (when present in very

large amounts)

Inadequate thyroid function can produce decreased HR, SV, and CO

Integration of Heart Rate Control

Three influences are active at all times: Sympathetic Parasympathetic Hormonal

Parasympathetic nervous control dominates the heart at rest Parasympathetic fibers are connected to the heart by the vagus nerve,

which exerts beat-by-beat control of the SA and AV nodes Parasympathetic fibers release acetylcholine

Vagal tone (suppressive effect) Acetylcholine inhibits the SA node and AV node Results in ↓ HR

Decreased parasympathetic input Allows sympathetic input to dominate Results in ↑ heart rate

Other Factors that Influence HR

Age. HR is fastest in fetus (140 - 160 bpm) HR gradually decreases through childhood and most of adult life The elderly commonly develop tachycardia

Gender. HR is faster in women (72 - 80 bpm) compared to men (64 - 72 bpm)

Physical fitness. Highly-fit individuals have lower resting HR due to increased vagal tone

and decreased sympathetic tone Body temperature.

Increased body temperature (hyperthermia) as in fever or strenuous exercise increases HR

Decreased body temperature (hypothermia) decreases HR Both conditions are associated with changes in metabolic rate of the

myocardium

Factors Affecting CO: Changes in SV

Ventricular Contractility The capacity of the ventricles to produce force

Preload Also called End Diastolic Volume (EDV) The amount of blood in the heart at the end of

ventricular filling Afterload

Also called End Systolic Volume (ESV) The pressure the ventricles must overcome to eject blood

out of the left ventricle

The Influence of Ventricular Contractility on SV

Contractility Any factor that causes an ↑ in contractility = ↑ SV (↑ CO) Any factor that causes a ↓ in contractility = ↓ SV (↓CO)

Control of Ventricular Contractility Sympathetic nervous system Hormonal

The Influence of Ventricular Contractility on SVSympathetic Nervous System Control Stimulation of cardiac muscle cells by sympathetic

fibers results in the release of norepinephrine Norepinephrine

Binds to beta adrenergic receptors on cardiac muscle cell membrane

Stimulates a second messenger (cyclic AMP) to open Ca++ channels on the membrane

↑ Ca++ = ↑ ventricular contractility ↑ SV ↑ CO

The Influence of Ventricular Contractility on SVHormonal Control Epinephrine circulating in the bloodstream

binds to beta adrenergic receptors on cardiac muscle cells

Epinephrine Stimulates second messengers (cyclic AMP) to open

Ca++ channels on the membrane ↑ Ca++ = ↑ ventricular contractility

↑ SV ↑ CO

Summary Contractility refers to force of contraction at any

given preload The more blood in the ventricles at beginning of

systole…1) The greater the force of contraction

2) the more blood ejected by the ventricles

Results: ↑ SV and ↑ CO ↓ Afterload (ESV)

The Influence of Ventricular Contractility on SV

The Influence of Preload (EDV) on SV

Starling’s Law of the Heart When the rate at which blood flows into the

heart from the veins (venous return) changes, the heart automatically adjusts its output to match the inflow.

Starling’s Law is based on the observed changes that occur in EDV and preload as a result of venous return

This observation is called the Starling Effect

Starling’s Law of the Heart

End diastolic volume (EDV) Determined by venous return, which is the

amount of blood returned to the heart Influenced by central venous pressure

↑ EDV = ↑ force of contraction (contractility) ↑ EDV = ↑ SV ↑ EDV = ↑ CO


Preload The amount of tension, or stretch, on the

ventricular myocardium The cardiac muscle fibers are stretched due to

the blood filling the chambers The effect of stretching ventricular walls = ↑

force of ventricular contraction This is an example of intrinsic control of the heart


Starling Curves Within normal limits, any factor that increases venous

return will result in: ↑ preload (EDV) ↑ force of contraction

Ultimately, ↑ SV


Starling Curves ↑ sympathetic input = ↑ SV ↓ sympathetic input = ↓ SV

The Influence of Afterload (ESV) on SVAfterload The pressure the left ventricle must exceed before the

aortic valve opens Indicates how hard the cardiac muscle must work to

push blood into the arterial system Must push blood against the mean (average) arterial pressure

1) ↑ mean arterial pressure = ↑ afterload (ESV) Must push blood against the total peripheral resistance

1) ↑ total peripheral resistance = ↑ afterload (ESV)

An Increased afterload (ESV) results in: ↓ SV ↓ CO

Heart Rate Abnormalities

Tachycardia HR > 100 bpm Causes:

Fever SNS stimulation Exercise Certain hormones Certain drugs

Bradycardia HR < 60 bpm Common in

endurance-trained individuals

Causes: Hypothermia PNS stimulation Certain drugs


The Cardiovascular System: Blood




The Functions of Blood

Distribution and transport Delivers oxygen from lungs and nutrients from gastrointestinal tract to entire

body Transfers metabolic waste products from cells to elimination sites (lungs

and kidneys) Transports hormones from endocrine glands to target organs

Maintenance of body temperature Absorbing and distributing metabolic heat Blood maintains temperature homeostasis with variable blood flow through

the skin

Regulation and maintenance of normal pH Buffers (proteins and ions) Maintenance of water content of cells with blood osmotic pressure Components of blood are involved in clot formation, thus preventing

excessive blood/fluid loss

Protection Blood carries components of the immune system to prevent infection

Overview: The Composition of Blood

Blood is a fluid connective tissue composed of: Organic (living) portion

Cells or formed elements1) Erythrocytes2) Leukocytes3) Platelets4) Plasma proteins

Inorganic (non-living) fluid matrix Plasma

The liquid part of the blood Composed of water and a mixture of organic and

inorganic substances 92% water 7% plasma proteins < 1% other material Electrolytes, buffers, nutrients, gases, hormones, wastes,

etc. Functions of plasma:

Transports nutrients and gases Regulates fluid and electrolyte balance Helps maintain stable pH

Plasma

Plasma

Very similar to interstitial fluid, except with far more proteins

Proteins remain in the plasma and cannot easily move into the interstitial space because of the structure of blood vessels

Serum Plasma without plasma proteins

Plasma Proteins

Functions: Maintain plasma osmotic pressure

Very important for maintaining blood volume

Maintain proper blood pH Accomplished through buffering action Able to take on and give up hydrogen ions

Clotting Immunity

Albumins Comprise 55% of plasma proteins Functions:

Maintain osmotic pressure Transport hormones and fatty acids in the blood

Globulins Comprise 36% of plasma proteins Functions:

Transport iron, fats, and fat-soluble vitamins in the blood. Gamma globulins function as antibodies in providing immunity

Fibrinogen Comprises 7% of plasma proteins The largest plasma proteins, but least numerous Function:

Clotting

Plasma Proteins - 3 Groups

Formed Elements

All blood cells are the formed elements: Erythrocytes (RBC) Leukocytes (WBC) Platelets

Synthesized in bone marrow In children, the marrow of all bones produce blood cells In adults, only the marrow of the flat bones of the skull,

sternum, pelvis, and the long bones of the upper limbs produce blood cells

Erythrocytes (RBC)

The RBC is one of the most specialized cell type in the body

Adapted exclusively to produce and carry hemoglobin (Hb)

Hb comprises ~ 1/3 of the RBC’s total weight In an adult male, there are 5 - 6 million

RBCs/mm3 ~ 30 trillion RBCs circulating in blood

Women and children have about 4.5 - 5 million RBCs/mm3

Erythrocytes (RBC) - Characteristics

Tiny size (8 microns) and flexible Able to pass through the narrow lumen of the smallest

blood vessels Flexible, biconcave disks

Thinner in the center than around edges Provides a large surface area, which aids gas diffusion in

and out of the RBC No nucleus or other organelles

Unable to synthesize proteins, grow, or reproduce Glucose is the only fuel source for RBCs

Do not use any of the oxygen they carry

Hemoglobin (Hb)

Hb is the oxygen carrying component of RBCs Hb binds reversibly to oxygen

Hemoglobin is found in two forms: Oxyhemoglobin

Gives blood its bright red color. Hb + O2 —> HbO2

Deoxyhemoglobin Has a dark red color and gives veins a bluish tint HbO2 —> Hb + O2

Hemoglobin (Hb) Hb is composed of 4 globin molecules

Each globin molecule contains a heme group

Globin Molecule The protein portion of the Hb molecule Composed of four polypeptide chains Each of the 4 globin chains is bound to a heme group

Heme Group The non-protein pigment containing iron [Fe2+] Heme is the red part of red blood cells Each heme can bind reversibly with one oxygen molecule

1) Thus, each Hb molecule can carry four molecules of O2

Leukocytes (WBC) Represent only ~ 1% of total blood volume

But, WBCs are a crucial component of the immune system WBCs are similar to RBCs in the following ways:

Synthesized in bone marrow WBCs are unlike RBCs the following ways:

Contain a nucleus and organelles Do not contain hemoglobin Not always contained in blood vessels

1) Diapedesis WBCs are able to move in and out of blood vessels with amoeboid

motion

2) Chemotaxis WBCs follow a chemical trail leading to the site of tissue damage

Leukocytes (WBC) – 2 Groups

Classified based on structure and function Granulocytes

Lobed nuclei Obvious cytoplasmic granules Very short average life span, about 12 hours

Agranulocytes Spherical or oval nuclei Lack obvious cytoplasmic granules Relatively long life span, greater than 12 hours

Platelets (Thrombocytes)

Anucleate cell fragments Incomplete cells Formed from the fragments of a larger cell, a

megakaryocyte 1) Magakaryocytes are derived from stem cells in bone marrow

Brief life span of about 10 days Contain many cytoplasmic granules

These granules are loaded with enzymes

Function: Stop bleeding through the process of hemostasis

Platelets and Hemostasis

Stop bleeding in small blood vessels or in superficial cuts by:

Physically plugging breaks in blood vessel walls Releasing chemicals that promote blood clotting

Involves 3 phases that occur in rapid sequence: Vascular Spasm Platelet Plug Formation Formation of a Blood Clot

Vascular Spasm (Vasospasm)

The contraction of smooth muscle in the walls of small blood vessels resulting in vasoconstriction

Lasts only short time, around 20 - 30 minutes at most Within 20 – 30 minutes, a platelet plug has formed

Vasoconstriction results in: Narrowing of the lumen Increased resistance to blood flow Reduced blood loss

Vascular Spasm may be stimulated by: Damage, breaking or cutting of a blood vessel The release of local pain receptors

Platelet Plug Formation

Normally, platelets do not stick to each other or to blood vessel walls

Platelets do stick; however, to the rough edges of a damaged blood vessel

Platelets are attracted to the collagen in the vessel wall that is exposed when the vessel is damaged

2 components to platelet plug formation: Platelet adhesion Platelet aggregation

Platelet Plug FormationPlatelet adhesion Platelets adhere to the rough edges or underlying

endothelium of a damaged blood vessel

Von Willebrand factor (vWf) Protein secreted by magakaryocytes, platelets, and

endothelial cells lining blood vessels It is present in plasma and accumulates at the site of blood

vessel damage It binds to the exposed collagen of a damaged blood vessel Causes platelets to attach to the damaged area as well

Activates platelets Causes platelets to swell, become sticky, and develop spiky

projections

Platelet Plug FormationPlatelet Aggregation Occurs as the platelets begin to release chemical mediators

ADP, thromboxane A2, epinephrine, and serotonin ADP

Causes the platelets to aggregate, forming a platelet plug Aggregated or accumulated platelets stimulate the secretion of

more ADP, a positive feedback loop ADP also causes the release of thromboxane A2

Thromboxane A2

Formed from arachidonic acid, which is found in the membranes of platelets

Slows blood flow and attract platelets to the area Epinephrine, serotonin, and thromboxane A2 act as

vasoconstrictors to continue the vascular spasms.

A positive feedback loop The cycle is initiated and results in rapid

formation of a platelet plug Within one minute, enough platelets have

accumulated at the injury site to form a platelet plug

The platelet plug reduces blood loss from small blood vessels, but a large blood clot may be required to completely stop bleeding

Platelet Plug Formation

Formation of a Blood Clot

Also called coagulation A blood clot is the result of many clotting

factors Most clotting factors are plasma proteins There are ~ 30 different clotting factors in the blood

that affect the coagulation process

Clot formation Depends on the balance between clotting factors

that promote clotting (procoagulants) and those that inhibit clotting (anticoagulants)

Procoagulants Enhance blood clotting, or coagulation Mostly produced by the liver

Anticoagulants Inhibit blood clotting Heparin

Produced by basophils Inactivates thrombin or prostaglandin 12

Prostaglandin I2 (PGI2) and nitric oxide (NO) Produced and continually released by healthy vascular endothelial

cells. Repel platelets, thus preventing platelet adhesion

Normally, anticoagulants dominate over procoagulants. But with vessel injury, procoagulant activity increases dramatically at the site of vascular damage resulting in blood clot formation.

Formation of a Blood Clot

Step 1. Prothrombin Activation Prothrombin activation may be accomplished via 2 pathways: Extrinsic pathway

It is a rapid, shortcut pathway that occurs within seconds if damage is severe

Coagulation factor III is released by damaged vessels Cascade of coagulation factors are activated, ultimately leading to the

activation of thrombin Intrinsic pathway

It occurs slowly, requiring several minutes Coagulant factor XII (also called Hageman factor) is activated Cascade of coagulation factors are activated, ultimately leading to the

activation of thrombin This is usually the slowest step in the clotting process

Formation of a Blood Clot: A 6 step process

Step 2. Conversion of Prothrombin to Thrombin Prothrombin activator

An enzyme that catalyzes a series of chemical reactions that convert prothrombin to thrombin

Prothrombin An inactive plasma protein produced in the liver

Thrombin The active from of an enzyme that converts fibrinogen to

fibrin

Formation of a Blood Clot:A 6 step process

Step 3. Conversion of Fibrinogen to Fibrin Occurs in a chemical reaction catalyzed by thrombin Fibrinogen

A soluble plasma protein that forms blood clots when activated by thrombin

Fibrin An insoluble, elastic protein composed of many

fibrinogen units joined end to end Fibrin forms a network of long threads, forming the

blood clot Fibrin threads trap blood cells, platelets, and plasma to

strengthen and stabilize the clot


Step 4. Clot Retraction After clot formation, the platelets begin to

contract Platelets contain actin and myosin

Retraction draws the injured edges of the blood vessel into close proximity

Prevents further blood loss Retraction squeezes serum out of the

platelets Platelets shrink after the blood clot forms


Step 5. Repair While the clot is retracting, platelets release

Platelet Derived Growth Factor (PDGF) PDGF stimulate fibroblasts and endothelial cells

Fibroblasts and endothelial cells in the vessel wall are stimulated by PDGF to:

Reproduce Repair the damaged blood vessel wall

Ultimately, the clot dissolves as the tissue heals


Step 6. Fibrinolysis Clot breakdown

Coincides with repair of the blood vessel wall Tissue plasminogen activator (tPA)

Released by blood cells or endothelial cells Converts plasminogen to its active form, plasmin

Plasminogen An inactive plasma protein enzyme

Plasmin Breaks down fibrin Inactivates certain coagulation factors Dissolves the blood clot

Occurs usually within a few days after the blood clot forms



The Cardiovascular System: Blood Vessels, Blood Flow, and Blood Pressure




Physical Laws Governing Blood Flow and Blood Pressure The goal of the cardiovascular system is to

maintain adequate blood flow through peripheral tissues and organs

General principles govern how pressure gradients and resistance affect blood flow

Pressure Gradients

Pressure Gradient Defined as the difference in pressure from one region of

the vascular system to another Specifically, it is the force exerted (per unit area)

by the blood against the inner walls of the blood vessels

Blood always flows from regions of high pressure to regions of low pressure

If there is no pressure gradient, no blood will flow Blood pressure is directly generated by the

pumping action of the heart.

Systemic Blood Pressure Expressed in terms of millimeters of mercury (mm Hg) Blood pressure of 120 mm Hg would be equal to the

pressure exerted by a column of mercury 120 mm high Systolic blood pressure (SBP)

The maximum blood pressure generated during ventricular contraction (systole)

Diastolic blood pressure (DBP) The lowest blood pressure that remains in the

arteries during ventricular relaxation (diastole)

Pressure Gradients

Pulse A physical event due to alternating expansion and

contraction of the arteries The pulse can be palpated at certain places on the body

where the arteries are close to the surface

Pulse pressure (PP) The arithmetic difference between SBP and DBP PP = SBP - DBP It is a calculated figure not a physical event

Pressure Gradients

Mean Arterial Pressure (MAP) The driving pressure in the arterial system that keeps

blood flowing A weighted average of systemic blood pressure to

account for the heart spending more time in diastole NOT the arithmetic average of SBP and DBP MAP = DBP + 1/3 (SBP - DBP)

Changes in MAP occur due to: Abnormal increases in blood volume

1) Increased salt intake Abnormal decreases in blood volume

1) Dehydration 2) Hemorrhage

Pressure Gradients

Any factor that alters blood volume will affect BP

The volume of the blood in the arteries is directly proportional to BP

A hemorrhage causing a loss in blood volume will cause a decrease in BP

The restoration of BP, such as during a blood transfusion, will increase the volume of blood thereby increasing BP

Pressure Gradients

Resistance in the Cardiovascular SystemPeripheral Resistance The force that opposes blood flow

Caused by friction between the blood and the walls of the blood vessel

In order for blood to flow, BP must be greater than the peripheral resistance

BP decreases as the distance from the left ventricle increases

The greatest decrease in BP occurs across the arterioles because these blood vessel offer the greatest resistance to blood flow

Blood pressure continues to decrease as blood flows through capillaries and the venous system

Sources of Peripheral Resistance

3 main sources of peripheral resistance Blood Viscosity

Refers to the "stickiness" or thickness of the blood

Vessel Length Vessel Radius

Blood viscosity

Blood viscosity is related to the density of blood cells in the plasma

There is a direct relationship between blood viscosity and peripheral resistance

↑ viscosity = ↑ peripheral resistance; ↓ viscosity = ↓ peripheral resistance

There is an inverse relationship between blood viscosity and blood flow (impedes blood flow)

↑ viscosity = ↓ blood flow; ↓ viscosity = ↑ blood flow

In healthy people, blood viscosity varies little Any condition that increases or decreases the concentration

of blood cells or plasma proteins may alter blood viscosity Anemia or hemorrhage = ↓ blood viscosity High altitude or dehydration = ↑ blood viscosity

There is a direct relationship between vessel length and resistance to blood flow

The greatest effect of vessel length on peripheral resistance is found in the blood vessels of the systemic circuit

Blood vessels in the pulmonary circuit are shorter (and more elastic)

Therefore, resistance to blood flow in the pulmonary circuit is lower in comparison to the systemic circuit

Vessel length does not vary much in adults

Vessel Length

Vessel diameter is associated with the amount of friction between the blood and the walls of blood vessel

Blood flowing close to the wall of the blood vessel is slowed due to friction

Blood flowing down the center of a blood vessel meets less friction, therefore blood flows faster

Large-diameter vessels offer less resistance to blood flow More blood is able to flow down the center of the blood

vessel Small-diameter vessels offer greater resistance to blood

flow More blood is in contact with the wall of the blood vessel

Vessel Diameter

Corresponds with the pressure in the right atrium

Central venous pressure is measured in the right atrium because all of the veins in the systemic circuit empty into this heart chamber

Blood pressure decreases as it flows out of the arterial circulation and into the venous circulation

Central Venous Pressure

Central Venous Pressure

Venous blood flow is maintained via: Respiratory pump

Depends on pressure changes in the ventral body cavity associated with breathing

It helps to move blood upward toward the heart Muscle pump

Even more important Skeletal muscle contractions function to “milk blood”

back to heart

Movement of Fluid Across Capillary Walls2 purposes: To exchange nutrients, gases, and

metabolic byproducts between blood and cells

This is impossible in arteries and veins because the vessel walls are too thick to allow rapid diffusion

To maintain normal distribution of the extracellular fluid

Movement of Fluid Across Capillary Walls Forces that drive movement of fluid in and

out of capillaries are called, Starling Forces

Capillary exchange is made possible by three forces at work simultaneously

Diffusion Filtration Osmosis

The most important method of capillary exchange Accounts for the exchange of oxygen and most nutrients such

as amino acids, fatty acids, and glucose, carbon dioxide, hormones, etc.

Diffusion occurs along the entire length of the capillary bed Solutes move down their concentration gradient from

areas of higher concentration to areas of lower concentration.

For example, oxygen and nutrients diffuse from the blood into cells

Conversely, carbon dioxide and metabolic waste products diffuse from the cells into the blood

The direction and magnitude of water movement across capillary walls depends on the balance between hydrostatic pressures and osmotic pressures

Diffusion

The movement of fluids through a capillary wall is due to hydrostatic pressure

The force exerted by a fluid pushing against a wall In capillaries, hydrostatic pressure is the capillary BP Capillary BP is influenced by:

Arterial pressures Venous pressures Resistance in the pre- and post-capillary sphincters

Filtration occurs primarily at the arterial end of the capillary where hydrostatic pressure is high, and decreases along the length of the capillary as hydrostatic pressure decreases

Filtration is a passive process accounting for movement of solutes such as ions

Filtration

Water movement from an area of lower solute concentration to an area of higher solute concentration

Occurs in response to oncotic pressure Osmotic pressure exerted by proteins

Plasma proteins (mainly albumin) are large, lipid insoluble particles that do not leave the blood in capillaries

Osmotic pressure in capillaries does not change along the length of vessels

Plasma proteins remain in the capillaries, exerting a fixed amount of osmotic pressure along its entire length

Plasma proteins create an osmotic pressure greater than the osmotic pressure of the interstitial fluid

Therefore, blood in the capillary has a greater attraction for water than does interstitial fluid

Osmosis

Starling Forces

Forces driving fluid into and out of the capillaries

These forces are balanced and counteracted by high capillary hydrostatic pressure and osmotic pressures

Net filtration pressure (NFP) The net effect of all the forces driving fluid across

the capillary walls NFP = (forces that promote filtration) - (forces that oppose filtration)

Starling Forces

Forces that promote filtration and drive fluids out of the capillary are:

Capillary hydrostatic pressure Interstitial fluid osmotic pressure

Forces that promote fluid absorption and pull fluids into the capillary are:

Capillary osmotic pressure Interstitial fluid hydrostatic pressure

Net Movement Usually more fluid leaves the capillary at the arterial end than

returns at the venous end Excess fluid is collected by the lymphatic system and returned

to the systemic circulation.

The Lymphatic System

A pump-less system that transports body fluids

Functions: Maintain fluid balance

Drains tissue spaces of excess interstitial fluid Defend body against disease (immunity)

Produces and maintains lymphocytes Transport dietary fats (digestion)

Carries lipids (and lipid soluble vitamins) from their site of absorption in the GI tract to the blood

Lymph and Lymphoid Tissue

Lymph Tissue fluid that has entered a lymph capillary Contains mostly water

Also contains other dissolved solutes that were diffused or filtrated out of the blood into the interstitial fluid

Interstitial fluid forms when plasma is filtered out of capillaries at the arterial end of capillary bed

Formation of Lymph About 3 L of excess fluid is formed per day

More fluid is filtered out of the capillaries than is reabsorbed by the capillaries

This fluid drains into the lymph capillaries and becomes lymph fluid Interstitial fluid has essentially the same composition as plasma, but

the interstitial fluid has a much lower concentration of plasma proteins

Lymph Function

Return leaked plasma proteins to blood circulation Without the lymphatic system, plasma proteins would

accumulate in the interstitial space Excess plasma proteins in interstitial spaces would exert

osmotic pressure causing a decrease in fluid absorption at the venous end of capillaries

Tissue edema or swelling would occur Normally, as excess interstitial fluid accumulates it pushes

against the outside of lymph capillaries, separating the flaps in the lymph capillary walls allowing fluid to enter

Once inside, the fluid pushes the flaps in the lymph capillary wall closed, preventing lymph from flowing back into the interstitial space

Lymph Transport Dependent on outside forces to move the lymph

The lymphatic system is pump-less The vessels are low pressure conduits like veins that require help

to move lymph through the system

Lymph flow Respiratory pump

1) Depends on pressure changes in the ventral body cavity associated with breathing

2) Increased intra-abdominal pressure squeezes the abdominal lymph vessels and moves the lymph toward the heart

Muscle pump 1) Skeletal muscle contractions function to “milk lymph” back to

heart

2) Lymphatic valves prevent the backflow lymph in the system

The Cardiovascular System: Regulation of Function

Extrinsic Control of Cardiovascular Function:

Accomplished through the regulation of Mean Arterial Pressure (MAP)

Two types of extrinsic control Neural Control of MAP Hormonal Control of MAP

Neural Control of MAP

Neural Control of MAP usually involves reflexes of the autonomic nervous system

Arterial Baroreceptor Reflexes Arterial Chemoreceptors

Arterial Baroreceptor Reflexes

Specialized mechanoreceptors Locations:

Aortic arch Carotid sinuses

Responsive to changes in arterial pressure Respond to stretch produced on the arterial walls

due to increased blood pressure The baroreceptors send signals to the cardiac

center in the medulla

Located in the carotid sinus Responive to changes in the level of O2 and

CO2 in the blood and cerebrospinal fluid Chemoreceptors signal the vasomotor center of

the medulla

Changes in the level of O2 and CO2 triggers the activation of either the cardioaccelerator reflex or the cardioinhibitory reflex

Arterial Chemoreceptors

Arterial Chemoreceptors

Cardioaccelerator reflex Activated by decreased levels of O2 (increased levels of CO2)

Sympathetic stimulation of the SA node increases HR The vasomotor center of the medulla stimulates vascular

smooth muscle vasoconstriction producing:1) Increased blood pressure 2) Increased venous return

Cardioinhibitory (Baroreceptor) Reflex Activated by increased baroreceptor activity and increased

levels of O2 (decreased levels of CO2) Results in decreased sympathetic stimulation of the SA node,

thereby decreasing HR and eliciting vasodilation to decrease BP

Hormonal Control of MAP

Hormones may produce direct effects on: The heart, or Vascular smooth muscle

Hormones may produce an indirect effect on blood volume

Hormones controlling MAP include: Epinephrine and Norepinephrine ADH (vasopressin) and the Renin-Angiotensin system

(aldosterone) Thyronine (T4) and Triiodothyronine (T3) Atrial Natriuretic Peptide (ANP)

Epinephrine and Norepinephrine

Increase HR Increase contractility (SV) Indirectly increases CO Increases total peripheral resistance

Stimulates vascular smooth muscle resulting in vasoconstriction

Increases central venous pressure Increases MAP

ADH (vasopressin) and the Renin-angiotensin system (aldosterone)

Produce vasoconstriction Increase blood volume Increase BP

Thyronine (T4) and Triiodothyronine (T3) Increase HR Increase contractility (SV) Results in increased BP

Atrial Natriuretic Peptide (ANP) Released by atrial cells and produces vasodilation Decreases blood volume Results in decreased BP

Other Hormones

Functional Human Physiology for the Exercise and Sport Sciences The Cardiovascular System: Cardiac Function Jennifer L. Doherty, MS, ATC Department of.

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