Download CARDIOVASCULAR SYSTEM

Dr. Vince Scialli
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CARDIOVASCULAR SYSTEM
REV. 12/20/06
Functions
Transport system
Keeps blood continuously circulating
Ensures continual supply of nutrients to cells ~ O2
Prevents build up of body wastes ~ CO2
Components
Heart ~ transport system pump
Blood Vessels ~ delivery routes
Blood ~ transport medium
THE HEART
Size of a fist ~ 3-4 inches wide . . . 5-6 inches long . . . 1LB
Located in Mediastinum ~ within Pericardial Cavity
Medial thorax cavity ~ 2nd & 5th intercostal space
Anterior to vertebrae ~ Posterior to sternum
Rests on diaphragm ~ Tilted at 45o . . . 60% left of midline
Base points to right shoulder ~ Apex points to left hip
Point of Maximal Intensity ~ Left side between 5th & 6th rib
Point where apex contacts thoracic wall ~ Loudest
Heart ~ Chapter 20~5/1/2017
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HEART LAYERS
Pericardium
Epicardium - - - - - I
Myocardium
I - - - HEART WALL
I
Endocardium - - - - -
PERICARDIUM
Double walled sac ~ completely encloses heart
1.
Parietal Pericardium ~ “Fibrous” pericardium
Tough, dense loose fitting CT outer layer
Protects & anchors the heart
Prevents overfilling of the heart
Forms Pericardial Sac ~ pericardial cavity
2.
Visceral Pericardium ~ “Epicardium”
Thin “serous” membrane ~ secretes serous fluid
Contacts parietal pericardium externally
Contacts the outer layer of myocardium internally
1st heart wall layer ~ Outermost
Heart ~ Chapter 20~5/1/2017
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Pericardial Cavity
Fluid filled area between Parietal & Visceral pericardium
Provides lubrication & cushion effect
Pericarditis ~ inflammation of the pericardium
Cause: Bacteria, virus, trauma or tumors
Symptoms:
Reduced serous fluid production
Increased friction
Adhesions & impeded heart activity
Pericardial friction rub ~ crackling sound
Deep sternal pain
Determine Cause: treat symptoms
Excess Fluid in pericardial cavity
Cardiac Tamponade ~ heart compression
Muffled heart sounds on auscultation
Treatment: by aspiration
drain excess fluid ~ lifesaving
Heart ~ Chapter 20~5/1/2017
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HEART WALL ~ Layers of Heart Muscle
1. Epicardium
~ outer surface of heart muscle
Visceral pericardium ~ attaches to myocardium
Composed of mesothelial cells & aerolar tissue
2.
Myocardium ~ thick Cardiac Muscle layer
Bulk of the heart ~ Cardiac muscle tissue
Forms Atria & Ventricle Walls ~ heart chambers
Primary contracting muscle
Intercalated Discs ~ desmosomes & gap junctions
Hold cells together
Allow transport of ions & action potentials
3.
Endocardium ~ thin inner lining
Continuous with cardiac blood vessels
Simple squamous epithelium & CT ~ “endothelium”
Lines Ventricles & Forms the Heart Valves
Fibrous Skeleton ~ NOT a part of the heart wall
Dense connective tissue cover . . . structure & support
Encircle Aorta, Pulmonary Trunk & Valves
Heart ~ Chapter 20~5/1/2017
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HEART CHAMBERS & GREAT VESSELS
Four Chambers
Left Atria
Upper Chambers ~ “Receiving”
Right Atria
Left Ventricle
Lower Chambers ~ “Pumping
Right Ventricle
Septum ~ Muscular Wall between chambers
Interatrial Septum ~ Separates R & L atria
Intervertricular Septum ~ Separates R & L Ventricle
Atrioventricular Valves ~ AV Valves
Fibrous Tissue between atria & ventricles
Permits flow of blood in one direction only
Right AV Valve ~ between right atria & right ventricle
Tricuspid Valve
Left AV Valve ~ between left atria & left ventricle
Mitral Valve or Bicuspid Valve
Heart ~ Chapter 20~5/1/2017
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ATRIA ~ also called “auricles”
Receiving Chambers ~ Receive blood returning to heart
Slight pumping capabilities ~ Pectinate Muscles
Small & thin walled
Fossa Ovalis
Shallow depression in inter-atrial septum
Was the Foramen Ovale ~ an opening between atria in the
fetal heart
Allows Fetal Blood to by-pass Lungs
Foramen Ovale ~ normally closes at birth
----> Atrial Septal Defect ~ if not closed
RIGHT ATRIUM
Receives “unoxygenated” blood via three veins
Superior Vena Cava ~ from upper body
Inferior Vena Cava ~ from lower body
Coronary Sinus ~ from myocardium itself
Receives “unoxygenated” blood from body
Pumps blood into Right Ventricle through Right AV Valve
Right AV Valve ~ Tricuspid Valve
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LEFT ATRIUM
Receives “oxygenated” blood from lungs via Pulmonary Veins
2
Right Pulmonary Veins
High in O2/Low in CO2
2
Left Pulmonary Veins
Pumps O2 blood to Left Ventricle via the Left AV Valve
Left AV Valve ~ Mitral or Bicuspid Valve
VENTRICLES
MAJOR Pumping Chambers ~ Large, thick muscle
Contraction of ventricles pumps blood out of heart
Papillary Muscles ~ papilla like muscles for valve control
Prevents AV valves from collapsing back into atria
RIGHT VENTRICLE
Right Atria opens to Right Ventricle via Right AV valve ~
Tricuspid Valve
Right Ventricle receives “unoxygenated” from right atria
Right Ventricle pumps “unoxygenated” blood via
“pulmonary trunk” to lungs to be oxygenated
Pulmonary Trunk ~ consists of Pulmonary Arteries
Left Pulmonary Artery ~ to left lung
Right Pulmonary Artery ~ to right lung
Heart ~ Chapter 20~5/1/2017
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LEFT VENTRICLE
Left Atria opens to the Left Ventricle via Left AV valve
Mitral Valve or Bicuspid Valve
Left Ventricle receives “oxygenated” blood from left atria
Left Ventricle pumps “oxygenated” blood to the body
via the Aorta ~ largest artery in body
Left Ventricle pumps “oxygenated” blood to heart itself
via the Coronary Arteries
Left Ventricular wall is 3x thicker than Right Ventricle
Left Ventricle is a much stronger pump ~ WHY ???
BLOOD PATHWAY THROUGH HEART & LUNGS
Heart is two “side-by-side” pumps (ventricles)
Pulmonary Circuit ~ Right Ventricle Pump ~ to lungs ↑ CO2
Short distance, low pressure system ~ 24 mmHg > 8 mmHg
Systemic Circuit ~ Left Ventricle Pump ~ to body ↑ O2
Long distance, high pressure system ~ 120 mmHg > 80 mmHg
Work load & pressure is much greater than Pulmonary Circuit
Resistance is 5x greater than in Pulmonary Circuit
Heart ~ Chapter 20~5/1/2017
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PULMONARY CIRCUIT ~ Lung Circuit
1.
O2 poor (high CO2) blood enters the right atrium via the
vena cava & coronary sinus
2.
Blood passes through the Right AV valve (Tricuspid
Valve) from right atrium to right ventricle
3.
Right ventricle pumps low O2 (but high CO2) blood to
lungs via Pulmonary Artery (Pulmonary Trunk)
4.
In lungs, blood exchanges CO2 for new O2 in pulmonary
capillary beds
5.
Oxygenated blood, high in O2 (low In CO2) is carried
back to the heart via Pulmonary Veins
Unique System: Arteries carry “unoxygenated” blood and
Veins carry “oxygenated” blood
SYSTEMIC CIRCUIT ~ Body Circuit
1.
O2 rich (low CO2) blood enters the left atrium via the
Pulmonary Veins
2.
Blood passes through the Left AV valve (Mitral or
Biscuspid Valve) from left atrium to left ventricle
3.
Left Ventricle pumps high O2 (but low CO2) blood to
body & heart itself via the Aorta & Coronary arteries
4.
Blood exchanges O2 and CO2 in tissue capillary beds.
O2 passes into tissue & CO2 passes into blood
5.
“Unoxygenated blood”, low in O2 (high in CO2) is carried
back to the heart via the Vena Cava & Coronary Sinus
where it enters the right atrium
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HEART VALVES
Allows blood to flow in one direction through heart circulation
Prevents back flow against normal path of circulation
ATRIOVENTRICULAR VALVES ~ AV Valves
Prevents back flow of blood from ventricles into atria
during ventricular contraction ~ systole
Valves close during ventricular contraction
Right AV Valve ~ tricuspid ~ three flaps
Left AV Valve ~ bicuspid ~ mitral valve ~ two flaps
Chordae tendineae ~ NO collapsed umbrella effect
Tendon that anchor valve flaps to papillary muscle
SEMILUNAR VALVES
Each valve has three cusps shaped like “half-moons”
Prevents back flow of blood from Aorta & Pulmonary
Artery into Left & Right Ventricles during ventricular
relaxation ~ diastole
Valves open with ventricular contraction ~ systole
Valves close with ventricular relaxation ~ diastole
Aortic Valve ~ prevents back flow into Left Ventricle
Pulmonic Valve ~ prevents back flow into Right Ventricle
Heart ~ Chapter 20~5/1/2017
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VALVE PATHOLOGY ~ Valvular Heart Disease
Increases cardiac workload ~ regurgitation or resistance
Caused by: aging, bacteria, virus, or rheumatic fever
“Vegetative Endocarditis” ~ valve inflammation
Valve Insufficiency ~ leaky valves ~ MOST COMMON
Mitral Valve Insufficiency ~ Left sided failure
Tricuspid Valve Insufficiency ~ Right sided failure
Valve Stenosis ~ valves narrow ~ Do Not open properly
Congenital Defects ~ Hereditary
Heart ~ Chapter 20~5/1/2017
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CORONARY CIRCULATION ~ Blood supply to the heart muscle
Provides nourishment & O2 to myocardium itself
Eliminates waste & CO2
CORONARY ARTERIES ~ branch off base of the Aorta
1.
Left Coronary Artery ~ supplies left atrium & left ventricle
“The Widow Maker”
2.
Right Coronary Artery ~ supplies right atrium & right ventricle
Unique: Coronary arteries deliver blood when heart is
relaxed. This is opposite most of arterial system
Coronary arteries compress during systole
Aortic valve flaps block entry of blood into coronary arteries
Coronary blood flow occurs during diastole
CARDIAC VEINS
Empty into Coronary Sinus
Empties unoxygenated blood from heart muscle itself
into right atrium
It drains:
Heart ~ Chapter 20~5/1/2017
Great cardiac vein
Middle cardiac veins
Small cardiac vein
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CORONARY ARTERY DISEASE ~ CAD
Coronary Ischemia ~ reduced circulation to myocardium
Reduces O2 flow to heart muscle itself
Angina pectoris ~ Thoracic Pain or “choke chest”
Deficient blood supply to myocardium
Due to: vasoconstriction caused by stress
Stress induced spasms of coronary arteries
Atherosclerosis ~ hardening of arteries
Treatment: nitroglycerin ~ vasodilators ~ angioplasty
Myocardial Infarction ~ “coronary or heart attack”
Severity depends upon tissue damage & location
Left side more severe than right side ~ why???
Involves complete or partial blockage of coronary artery
Lack of oxygen > death of tissue > scar tissue in heart
muscle > conduction disturbances
Treatment:
drugs, catheter, angioplasty
Stent ~ permanent implanted catheter
By-pass surgery ~ Last Invasive Option
Heart ~ Chapter 20~5/1/2017
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CARDIAC PHYSIOLOGY
Cardiac Muscle versus Skeletal Muscle ~ Both are striated
Skeletal ~ fibers are independent of one another
Cardiac ~ cardiac muscle cells interlock ~ gap junctions
Intercalated Discs ~ allow ion passage from cell to cell
Myocardium cells behave as a single coordinated unit
Skeletal muscle cells ~ 2% mitochondria by volume
Cardiac muscle cells ~ 25% mitochondria by volume ~ energy
Cardiac muscle cells have high resistance to fatigue
Skeletal cells ~ both aerobic & anaerobic respiration
Cardiac cells ~ aerobic respiration only ~ continuous O2
Skeletal muscle ~ Dependent on nervous system
BOTH Voluntary & Involuntary Neural Control
Cardiac muscle ~ Involuntary & self-excitable
Intrinsic ~ “Automaticity” ~ Autorhythmicity ~ Pacemaker
Skeletal ~ all muscle fibers contract as a single motor unit
Cardiac ~ contracts in a sequential rhythmic wave-like motion
Refractory period (resting) ~ much longer in cardiac muscle
Prevents heart stoppage ~ pumps continuously
Allows complete emptying of chambers
Heart ~ Chapter 20~5/1/2017
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MECHANISM OF CARDIAC MUSCLE CONTRACTION
Same for cardiac & skeletal muscle ~ MINOR VARIATIONS
1.
BOTH ~ Increased Na+ permeability > Na+ influx into
cardiac cell > rising action potential > depolarization
2.
CARDIAC ONLY ~ Increased Ca+ permeability > Ca+ influx
into cardiac cell > “continued” depolarization
Plateau Effect ~ due to Ca+ influx ~ delays repolarization
3.
BOTH ~ K+ permeability decreases > K+ exits the cell >
repolarization & a resting membrane potential
INTRINSIC CARDIAC CONDUCTION SYSTEM ~ Nodal System
Ability of cardiac muscle to depolarize & contract is intrinsic
to the heart muscle
Contraction does not depend on stimuli from nervous system
Autorhythmic Cells ~ Pacemaker Cells ~ Nodal Cells
Specialized NON-contractile cells
Initiate & distribute impulses throughout heart
Continuously depolarize & spread throughout heart
Trigger rhythmic contractions ~ “milking effect”
Never stops depolarizing ~ NO REST
Heart muscle depolarizes in an orderly & sequential
manner . . . from atria to ventricles
Heart ~ Chapter 20~5/1/2017
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SEQUENCE OF ELECTRIC IMPULSE CONDUCTION
Autorhythmic Cells ~ Continuously fire & spread impulses
1.
Sino-atrial node ~ SA node
2.
Atrioventricular node ~ AV node
3.
Atrioventricular bundle ~ Bundle of His
4.
Right & Left Bundle Branches
5.
Purkinje Fibers ~ in ventricles ONLY
SINOATRIAL NODE ~ SA NODE ~ “the pacemaker”
Located in right atrial wall near inter-atrial septum
Generates approximately 75 impulses per minute
75X
Sets pace for heart contractions ~ “the pacemaker”
Pace = heart rate called “NORMAL sinus rhythm”
Sends IMPULSES via gap junctions in the “internodal”
pathway to BOTH the AV node & Left Atrium
ATRIOVENTRICULAR NODE ~ AV NODE
In inter-atrial septum ~ above right AV valve in right atrium
Delays impulses at AV node to allow atria to contract & fully
empty, and allow ventricles to fully fill
AV node Fires at 50 impulses per minute & passes impulses
to atrioventricular bundle (Bundle of His)
50X
Heart ~ Chapter 20~5/1/2017
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ATRIOVENTRICULAR BUNDLE ~ BUNDLE OF HIS
Located in lower portion of atrioventricular septum
Impulses pass between AV node & ventricle at 30X
Divides into right & left bundle branches in interventricular
septum
RIGHT & LEFT BUNDLE BRANCHES
Located in the interventricular septum down to heart apex
Supply impulses to both the right & left ventricles
PURKINJE FIBERS
Located in the inferior interventricular septum
Traverse the apex, then turns superior into the right & left
ventricular walls
Impulse wave of ventricular contraction start at the apex &
move upward
Stimulate papillary muscles which closes the AV valves
Heart ~ Chapter 20~5/1/2017
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CONDUCTION SYSTEM DYSFUNCTION
Autorhythmic Cells ~ can also serve as own “pacemakers”
SA node ~ fires impulses at
75x per min.
AV node
50x
AV Bundle & Purkinje fibers
30x
Pacemakers cannot dominate unless
faster pacemaker becomes non-functional
DEFECTS IN CARDIAC CONDUCTION – Arrhythmias
“irregular heart rhythms”
Diagnosed with electrocardiogram ~ EKG
Tachycardia ~ very rapid heart rate >100 beats per minute
Bradycardia ~ very slow heart rate < 60 beats per minute
Fibrillation ~ rapid or irregular contractions
Ventricular Fibrillation ~ heart is useless as a pump
Very dangerous & life threatening
Atrial Fibrillation~ not as serious as V-fib
Defibrillation ~ attempt to restore SA node firing
Atrial Flutter ~ Rapid, shallow atrial contractions
Heart ~ Chapter 20~5/1/2017
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DEFECTS IN CARDIAC CONDUCTION – Arrhythmias
Defective SA Node
SA node not firing properly ~ defective pacemaker
75X
Stimulates other pacemakers to fire abnormally
AV node may become new pacemaker
50X
Slower firing of ventricles occurs
Firing of ventricles without atrial contraction
Ectopic Beats ~ Abnormal pacemaker
Skipped Beats ~ not usually a problem if few
Premature Extra-systole ~ extra beats ~ not a
problem if few
Premature Ventricular Contractions ~ PVC’s
Defective AV Node
AV node does not pass through impulses to ventricles
“Total or partial heart block”
Ventricles beat at own intrinsic rate of
30 per minute which is too slow
30x
Causes inadequate circulation or LOW cardiac output
Corrected with external pacemaker implant
Heart ~ Chapter 20~5/1/2017
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ELECTROCARDIOGRAPHY
Study of the electrical currents transmitted through the heart
ELECTROCARDIOGRAPH
Instrument that monitors, amplifies & measures the
electric currents through the body generated by heart
ELECTROCARDIOGRAM ~ EKG or ECG
Graphic recording of all action potentials generated in
the nodes & contractile cells of the heart
EKG ~ Three distinguishable deflection waves
P QRS T COMPLEX
1.
P-wave ~ atrial contraction
Depolarization from SA node through atria
2.
QRS complex ~ ventricular contraction
Depolarization of ventricle prior to contraction
3.
T-wave ~ ventricular relaxation
Repolarization of ventricles
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ELECTROCARDIOGRAPHY
Two distinguishing interval measurements
1.
P-Q interval
Time from beginning of atrial stimulation to the
beginning of ventricular excitation
Atrial depolarization & atrial contraction
2.
Q-T interval
Time from beginning ventricular depolarization
through repolarization
Ventricular contraction ~ SYSTOLE
EKG DYSFUNCTION: Abnormal EKG
Several examples
In a healthy heart, the size, duration, & timing of the
deflection waves tends to be similar
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THE CARDIAC CYCLE ~ “Overlapping” Phases
One complete heart beat with pressure & volume changes
Contraction ---> Relaxation ---> Contraction
SYSTOLE ~ atrial & ventricular contraction ~ EMPTY
DIASTOLE ~ atrial & ventricular relaxation ~ FILLING
Blood flow controlled by pressure changes ~ HIGH ---> LOW
Blood volume & pressure on either sides of heart valves force
valves to open or close
Atrial Systole ~ atrial contraction (emptying) ~↑ atrial pressure
↓
Ventricular Diastole ~ ventricular relaxation & filling
LOW ventricular pressure ~ 80 mm HG in L. Ventricle
08 mm HG in R. Ventricle
↓
Ventricular Systole ~ ventricular contraction & emptying
Filling Volume is the same in both ventricles
HIGH Ventricular Pressure
Aortic Blood Pressure = 120 mm HG
Pulmonary Artery Blood Pressure = 24 mm HG
Atria are in diastole & fill during ventricular systole
↓
Atrial Diastole ~ atrial relax & filling ~ LOW atrial pressure
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HEART SOUNDS
Two distinguishable heart sounds heard during each CYCLE
“LUB DUB” pause “LUB DUB” pause
Caused by closing of the heart valves
“Ascultate” with a stethoscope . . . LISTEN
Left AV valve ~ Mitral ~ Bicuspid
-
left 5th space
Right AV valve ~Tricuspid
-
right 5th space
near sternum
Aortic valve ~ Semilunar
-
right 2nd space
Pulmonic valve ~ Semilunar
-
left 2nd space
First Sound ~ S1
Closure of AV valves
Beginning of ventricular systole
Loudest & longest sound ~ “luuub”
Second Sound ~ S2 Closure of Semilunar valves
Beginning of ventricular diastole
Sharp and shortest sound ~ “dub”
Third & Fourth Heart Sounds ~ S3 & S4
Diastole ONLY
Faint & seldom detectable ~ weak sounds
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ABNORMAL HEART SOUNDS ~ “MURMURS”
Due to abnormal & turbulent blood flow in heart
VALVE DYSFUNCTIONS – most common
“Stenosis”
“Obstructions”
Aortic or Pulmonic Stenosis
Congenital Defects
“Insufficiencies”
“leakage”
Mitral Valve Prolapse ~ very common
Mitral Valve Insufficiency ~ left heart failures
Septal Defects – HOLES between chambers
VSD ~ ventricular septal defect
ASD ~ atrial septal defect
PDA ~ patent ductus arteriosus
TF ~ tetrology of fallot
NORMAL “functional” murmur ~ vibrating thin valve walls
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CARDIODYNAMICS
Movements & forces generated during cardiac contractions
Both Ventricle contractions eject equal amounts of blood
CARDIAC OUTPUT ~ CO
Blood volume pumped out by each ventricle in 1 minute
CO = Stroke Volume (SV) X Heart Rate (HR)
Heart rate & stroke volume change with body demands
Stroke Volume
=
Volume of blood pumped out by each
ventricle w/ each heart beat
Depends on: ventricular filling, contraction, & resistance
NORMAL SV = 70 ml per beat
Heart Rate
= Number of Heart Beats per minute
NORMAL HR = 75 beats per minute
Cardiac Output = 75 beats/min x 70 ml/beat = 5250 ml/min
1000 ml in one liter, therefore,
NORMAL CO = 5.25 liters/minute
NORMAL Adult Blood Volume = 1.4 gallons ~ 5 liters
Entire blood supply passes through each side of the heart
once each minute
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CARDIAC OUTPUT REGULATION
Cardiac Reserve = difference between resting & maximal
cardiac output
Normal Cardiac Output
= 5.25 liters/minute
Normal Cardiac Reserve
= 20-25 liters/minute
(5x)
Athletes Cardiac Reserve
= 35 liters/minute
(7x)
REGULATION OF STROKE VOLUME (SV)
SV =
difference between “end diastolic volume”
& “end systolic volume”
SV =
EDV minus ESV
End Diastolic Volume (EDV)
Amount of blood in the ventricles AFTER ventricular
diastole or filling
Depends on length of diastole & venous pressure
End Systolic Volume (ESV)
Amount of blood remaining in the ventricles AFTER
ventricular systole or emptying
Depends on force of contraction & arterial pressure
Each ventricle pumps out about 70 ml of blood or 60% of
it’s volume with each heart beat
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REGULATION OF STROKE VOLUME
3 FACTORS causing changes in either EDV or ESV
1.
2.
3.
Pre-load
Contractility
After-load
PRE-LOAD =
degree of heart muscle stretch in diastole
The greater the stretch, the greater the volume,
& force of contraction . . . to a point
Starling’s Law of the Heart
Venous Return ~ volume of blood flow return to heart
Increased volume of venous return
 EDV
Blood loss reduces venous return
 EDV
Filling Time ~ duration of ventricular diastole
Slower heart rate allows more filling time
 EDV
Rapid heart rate reduces filling time
 EDV
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CONTRACTILITY = force of contraction of ventricule muscle
Positive Inotropic Action ~ VERY POWERFUL  ESV
Extrinsic factors increase contractility which
increases ejection from heart ~ VERY POWERFUL
Ca+ influx into myocardial cell due to
sympathetic stimulation
 ESV
Sympathetic Stimulation ~ Epinephrine  ESV
Negative Inotropic Action
 ESV
Extrinsic factors decrease contractility which
decrease ejection from heart
Rising extra~cellular K+ ~ slows repolarization
Calcium blockers ~ prevents Ca+ from entering
Parasympathetic Stimulation ~ ACH
AFTERLOAD = back pressure exerted by blood in arteries
leaving the heart
Pressure the ventricles must overcome to open valves &
eject blood from the heart
Back pressure exerted on the Semilunar Valves
Hypertension ---->  ESV thus reducing SV
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EXTRINSIC REGULATION . . . OF CARDIAC OUTPUT
Cardiac Output =
Stroke Volume X Heart Rate
NORMALLY . . . stroke volume & heart rate remains constant
HR increases to compensate for lower stroke volume to
maintain cardiac output to tissues . . . if conditions change
NERVOUS & CHEMICAL EXTRINSIC REGULATORS
Autonomic Nervous System . . . Affects HR & Contractility
Reflex Cardiac Centers ~ located in Medulla Oblongata
---->
↑ HR
Cardio-inhibitory Center ~ parasympathetic ---->
↓ HR
Cardio-accleratory Center ~ sympathetic
Sympathetic Nervous System ~ affects SA & AV nodes
Increases heart rate, vasoconstriction, blood pressure
Increases force of heart contraction ~ positive inotropic
Stimulates Adrenal Medulla to secrete catecholamines in
response to stress ~ epinephrine/norepinephrine
Catecholamines & sympathetic cardiac nerves directly
stimulate the SA node, AV node & heart muscle
Enhances Ca+ penetration into heart cells ~ increasing
contractility ~ VERY POWERFUL POSITIVE INOTROPIC
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Parasympathetic Nervous System ~ main affects AV node
Slows the heart rate ~ VAGUS STIMULATION
Parasympathetic reflex center in medulla oblongata
senses need to slow the heart rate
Medulla sends inhibitory impulses to the heart via the
vagus nerve ~ X cranial nerve ~ VAGUS Nerve
Vagus nerve sends impulses to the SA & AV nodes
TO SLOW HEART RATE (DOMINANT INHIBITOR OF HR)
CHEMICAL REGULATION
HORMONES
Epinephrine ~  heart rate & contractility
Thyroxine ~ increases netabolism & heart rate
IONS
Electrolyte imbalances danger to heart
Sodium
Excess Na+ (hyper-natremia) inhibits Ca+ transport
into cells, thus Blocks Ca++ Plateau Effect
Calcium
Reduced Ca+ (hypo-calcemia) depresses the heart
contractility by Blocking Ca++ Plateau Effect
Increased Ca+ (hyper-calcemia) stimulates
contractility by Prolonging Ca++ Plateau
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Potassium
Excess K+ (hyper-kalemia) interferes with
depolarization, causing heart block & cardiac arrest
(Prevents Repolarization ~ Tetany)
Low K+ (hypo-kalemia) from potassium depleting
diuretics causes weak heart beat & arrhythmias
(Rapid or continued Repolarization)
DRUGS
Digitalis ~ positive inotrope ~ increases contractility
↑ SV
Used In Heart Failure
Beta Blockers ~ propanalol ~ negative inotrope
↓ SV & HR Used For Blood Pressure
Calcium Channel Blockers ~ negative inotrope
↓ SV & HR Used For Blood Pressure
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OTHER FACTORS AFFECTING HEART RATE
NORMAL
RATES
AGE
Fetus
Female
Male
Athletes
140-160
72-80
64-72
40-60
Tachycardia – “hurry heart”
HR > 100 beats per minute ~ could be normal
Could lead to fibrillation if > 180
Caused By:
 body temperature, exercise
Stress ~ sympathetic stimulation
Drugs ~ sympathomimetic drugs
Heart disease ~ conduction problems
Bradycardia – “slow heart”
HR < 60 beats per minute ~ could be normal
Could lead to heart block if < 55
Caused By:
 body temperature, inactivity
Certain drugs ~ negative inotropes
Parasympathetic stimulation ~ VAGUS
Head trauma
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CARDIAC OUTPUT DYSFUNCTION
Occurs when the balance between venous return & cardiac
output are impeded
If heart cannot pump blood coming in . . . Back-up “venous
congestion” occurs ~ increasing hydrostatic pressure
CONGESTIVE HEART FAILURE
Occurs when pumping efficiency & cardiac output is so low
that the circulation is inadequate to meet tissue needs
Pathology:
weakened, soft, or stressed myocardium
Caused By:
Coronary atherosclerosis > hypoxia > ischemia
Persistent high blood pressure
Large Afterload & Resistance > greater
work load for ventricle > enlarged ventricle
Hypertrophy ~ enlarged heart
Multiple myocardial infarcts ~ heart attacks
Scar tissue replaces normal muscle
Causes Conduction problems
Sudden Death Cardiomyopathy ~ Athletes
Dilated or flabby ventricle
Causes Impaired ventricular contractility
Heart ~ Chapter 20~5/1/2017
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Dr. Vince Scialli
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CONGESTIVE HEART FAILURE
LEFT SIDED FAILURE
If left side backs up, venous congestion is in the lungs
Pulmonary congestion > Pulmonary edema (Lung Fluid)
RIGHT SIDED FAILURE
If right side backs up, venous congestion is in the organs
Peripheral congestion > edema or ascites
Fluid in Abdomen or Fluid in Lower Limbs
Treatment of CHF: Digoxin ~ slows rate and ↑ contraction
Diuretics ~ remove excess fluids
Reduce after load ~ BP medication
Heart Transplant ~ last resort
Heart ~ Chapter 20~5/1/2017
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Dr. Vince Scialli
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CONGENITAL HEART DEFECTS ~ most common Birth Defects
BY-PASS DEFECTS ~ SHUNTS
Occurs when Openings in fetus heart do not close at birth
Mixing oxygen-poor blood with oxygen-rich blood
Dilutes overall O2 in arterial blood
Left ventricle is dominant since fetal circulation by-passes the
lungs ~ left ventricle pressure is higher
Foramen Ovale ~ opening between left & right atrium
Allows blood entering the right heart (atrium) to move
directly to left atrium ~ by-passing fetus lungs
Atrial Septal Defect
L ----> R
Ductus Arteriosus ~ connects the pulmonary trunk & aorta
Allows blood from right heart to by-pass the lungs & be
pumped directly into the aorta
PDA ~ Patent Ductus Arteriosus
L ----> R
Ventricular Septal Defects ~ diagnosed later in life
Hole in wall between ventricles fails to close
L ----> R
Oxygenated blood from left ventricle overwhelms right
ventricle
Heart ~ Chapter 20~5/1/2017
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Dr. Vince Scialli
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CONGENITAL HEART DEFECTS
STENOSIS DEFECTS ~ Strictures
Stenosis of valves causing blood flow resistance &
restriction - - - - > heart overload
Pulmonic Stenosis ~ diagnosed later in life
Aortic Stenosis ~ Coarctation of the Aorta
Tetralogy of Fallot ~ Multiple Defects
Pulmonary Stenosis
VSD
Aorta branches off both ventricles
Right ventricular after load (overload)
AGE DYSFUNCTIONS
(Not Covered in Lecture)
CARDIAC RESERVE DECLINE
Aged heart less capable of responding to sudden
or prolonged stress ~ less contractility & stretch
Sympathetic control less efficient ~ weaker heart
Decline in maximum heart rate capability & contractility
Heart ~ Chapter 20~5/1/2017
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Dr. Vince Scialli
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AGE DYSFUNCTIONS
FIBROSIS of cardiac muscle
Cardiac cells replaced by scar tissue as they die with age
Contractility is reduced ~ Stroke volume is decreased
Arrhythmias & conductivity problems occur
VALVE SCLEROSIS & thickening
Caused by stress of blood flow . . . over the years
Mitral Valve Insufficiency ~ due to enlarged heart
ATHEROSCLEROSIS ~ Coronary Artery Disease
Blood vessel walls become harder & thicker with age
“Occludes” coronary arterieies ~ Coronary Thrombosis
Myocardial ischemia ~ cuts off O2 supply to muscle
Myocardial Infarction ~ tissue death = Heart Attack
Predisposing Risk Factors
Genetics & male . . . Inactivity
Diet: cholesterol, animal fat, high salt, diabetic
Smoking, stress, obesity, high blood pressure
Heart ~ Chapter 20~5/1/2017
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