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8/8/2019 Function Cardiac
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Lifes Progression through
Cardiac Physiology
Understanding the Normal
Physiology of the Heart as it Changes
through the Life Span
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Overall Design of the Heart
Atrial fibers are divided into superficial & deep
Superficial fibers spread ov
er both R & L atria Deep fibers are confined to their respective
areas for the R or L atrium
Function of this is to provide a last minute push
of blood into the ventricles near the end of
filling, otherwise known as the Atrial kick
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Cardiovascular Re
view
Anatomy - Skeletal vs Cardiac Muscle
Sarcoplasmic/tubular system T tubules = transmit
Action Potential rapidly from the sarcolemma toall fibrils in muscle
Sarcoplasmic reticulum = houses calcium ions.
Action Potential across the T tubules causing
the release of CA++ from reticulum to the
fibrils resulting in a muscle contraction
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CV review
Sarcotubular system
T tubules = transmit AP rapidly from
sarcolemma to all fibrils in mm.
Sarcoplasmic reticulum = houses calcium ions.
Action Potential across the T tubules causes
release of CA++ from reticulum, resulting in acontraction
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Cardiac Rev
iew Contractile unit (Sarcomere). Muscle fibers
composed of fibrils
Each fibril is divided into filament
Each filament is made up of contractile proteins
Contractile proteins consist of
ACTIN, MYOSIN, TROPONIN, TROPOMYOSIN
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Cardiac Muscle Tissue The actual structure of the cardiac muscle is
also unique and represents its function
Muscle cells form attachments either parallel
or obliquely to each other
There is a greater amount of mitochondria
Sarcoplasmic reticulum is less abundant
Cells are much more dependent upon oxygen
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CV Review
Cardiac mm Vs Skeletal mm
Fibers connected by intercalated discs forming
the SYNCYTIUM (one fiber depolorized , APspreads to all fibers, the whole syncytium
contracts not just one fiber)
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Cardiac Muscle Tissue The aerobic dominance shows greater blood
vessel ratios to muscle cells
Aerobic dominance indicates need for good
supply of fatty acids as the fuel for ATP
Most important, is that each cardiocyte possess
the ability for intrinsic spontaneous rhythm
In other words, the heart will beat on its own!
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Ventricle Design is Different
There are 3
layers of cardiac
muscle that will
overlap eachother from the
R to L ventricle
This unique
design is part ofits functional
operation
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Myogenic Rhythms Some cardiocytes will become differentiated
into becoming the pacing and conducting
cells of the heart They form the Sino-Atrial Node, S-A Node,
other form the Atrio-Ventricular Node, A-VNode, Bundle Branches and Purkinje fibers
The rates will become progressively slowerfrom the S-A to the Purkinje fibers
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Cardio dynamics Afterload pressures is what the ventricles
have to contend with as they evacuate the
blood from the chambers (systolic pressure)
The cardiac muscle is designed to typically
work effectively against those pressures
However, high pressures will strain the heartmuscle over time & weaken heart function
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Cardio dynamics Preload pressures is the degree of stretching
experienced during ventricular diastole
It is significant since it affects the ability ofthe heart muscle to produce tension
Much like the relationship between actin
and myosin in skeletal muscle for tension It is limited to myocardial connectivetissues, cardiac muscle and pericardial sac
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Cardio Dynamics End diastolic volume (EDV) - amount of
blood in ventricle at the end of diastole
End systolic volume (ESV) amount ofblood remaining at the end ofvent. systole
Stroke Volume (SV) is the amount of blood
pumped out of thev
entricle on each beat,EDV ESV = SV
Ejection Fraction is SV as a % of EDV
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Cardio Dynamics Frank-Starling Principle is the relationship
between the amount ofventricular stretching
and contractile force of the heart muscle Starling basically said, more in = more out
Essentially, the ventricles are in a series with a
balance between the R & Lventricular filling The body will retain fluids to increase this
effect for stretching the heart from more CO
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CardiacO
utput (CO
) CO is precisely regulated so that peripheral
tissues receive an adequate circulation under
various conditions cardiac reserve
SV can almost triple & HR can increase 250%
Cardiac output can increase 600 700 %
CO = 80 ml X 75 bpm = 6000 ml/min
That is an increase to 36,000 to 42,000 ml/min
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Additional Factors Contractility is the force produced during a
contraction
Drugs or factors that increase this force isreferred to as a positive inotropic action
Those factors that decrease this force is
referred to as a negativ
e inotropic action This is caused by assisting or blocking CA++movement & metabolism of the cardiac cells
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Changes in Ion Concentrations Hypercalcemia elevated CA++ will cause
cardiac cells to be highly excitable
Hypocalcemia low levels of CA++ willcause weaker contractions & slower HR
Hyperkalemia elevated K+ cause weak
contractions and irregular heart beats Hypokalemia low K+ lowers the rate ofcontractions and hyperpolarizes the cells
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Changes in the HeartOv
er Time There are a lower number of cardiocytes
Gradual invasion of fat & collagen tissues
This tends to make the heart less efficient
This will limit the potential for expansion
Pericardium may shrink with infections Endocardium will thicken to reduce filling
Heart valves will calcify & restrict flow
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Changes in the HeartOv
er Time Conductive system progressively looses SA
node cells & allows other cites to pace
Normal 1 capillary to 1 muscle ratio changes
CAD begins to show early in life (20s-30s)
Higher blood pressures create more afterload
Weaker atriums create less preload
Arteries become more rigid as we age also !!!
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Understanding Cardiac Conditions The overall normal structure of the heart is
well designed for its function
There is both a mechanical and electricalcomponent of the normal heart
Aging and various disease processes can
effect the ultimate function of the heart Understanding these components is neededto successfully implement physical therapy
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Structures of the Heart Endocardium: inner surface
Pericardium = fibroserous sac encloses the
heart and roots of great vessels in fluid.Protects heart from friction
Epicardium = Visceral layer of pericardium,
COVERS heart and great vessels
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Structures Continued Mediastinum, base heart occupies the right chest
and apex lies primarily in the left chest
Papillary mm: arise from myocardial surface ofventricles & attach to chordae tendin.
Chordae tendineae: tendinous attachments frompapillary muscle to tricuspid and mitral valves.Helps prevent eversion ofvalves into the atriaduring systole
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Heart Chambers
Atria (thin, low pressure)
RT = venous blood from superiorvena cava, inferior
vena cava & coronary sinus
LT = oxygenated blood heart from lungs via 4
pulmonary veins
70% flows passively from atria into
ventricle
Atrial contract forcefully (atrial kick) supplying
another 10-20% of blood forventricular output
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Heart Chambers Ventricles
RV = Deoxygenated blood into PA
LV = high pressure, ejects blood into systemic
circulation
Valves
AV = mitral (bicuspid), tricuspid (3 leaflets) Aortic = 3 valve cusps Pulmonic = 3 semilunar cusps
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CV Rev
iew Cardiac conduction system
SA node (pacemaker) = possesses fastest
inherent rate ofAUTOMATICITY Internodal atrial pathways (SA node through
RA to AV node)
Anterior tract (Bachmanns)
Middle tract (Wenckebachs)
Posterior tract (Thorels)
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CV Rev
iew Bachmans bundle (SA to LA)
AV node (40-60 beats)
Bundle of His
Bundle branch system = Rt. Lt
Purkinje system
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Cardiac Plumbing Coronary vasculature
RCA = SA node in 55% and AV node in 90%
of pts. RA and RV mm, inferiorpost wall ofLV, 80% hearts provides branch - Posterior
descending artery (located in interventricular
groove, supplies RV and inferior wall of LV
and posterior septum)
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Plumbing (continued) Left main coronary artery (LMCA)
LAD = anterior part of intervent. septum, ant.
Wall of LV, RBB, anteriorsuperior LBB
Circumflex (CF) = branch off CF called obtuse
marginal branch (OMB). CF supplies AV node
in 10%, SA node in 45% and lateral post.
Surface of LV via the OMB
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CV Rev
iew Veins = great cardiac vein, small cardiac vein,
thebesian.
Local Control Mechanisms: tissues ability tocontrol their own blood flow calledAUTOREGULATION.
There are 2 major hypotheses
1. Vasdilatory = rate of metabolism increase, O2is consumed higher rate, so decreased PaO2 soincrease in vasodilator substances (lactic acid
adenosine, carbon dioxide) to increase blood
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1. Vasdilatory = rate of metabolism increase, O2 is consumed
higher rate, so decreased PaO2 so increase in vasodilatorsubstances (lactic acid adenosine, carbon dioxide) to
increase blood supply
2. Oxygen demand theory = when O2 decreases, dilation of
vessels occur to increase flow to increase O2. As increasedmetabolism occurs, O2 use increases so decreased amt. O2
available and causes local vasodilatation
Autoregulation of blood flow:
Myogenic theory: arterial pressure rises, vessels stretch,
stimulates contract. of smooth mm. in vessels (feedback
mechanism), reducing blood flow back to normal. As
tension decreases, smooth mm. relax
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CV Rev
iew Metabolic theory: Arterial pressure rises, increase blood
flow brings nutrients to tissues and remove vasodilator
substances. Both cause vessels to constrict.
Autonomic regulation ofvessels
Adrenergic symp. NS fibers secrete norepinephrine to
nerve endings, causing VASOCONSTRICTION
Parasymp. NS secrete ACETYLCHOLINE (cholinergiceffect) so VASODILATION
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CV Rev
iew Stretch receptors: barorecptors
(pressoreceptors) located in aortic arch,
carotid sinus, venae cavae, pulmonary arteriesand atria
Sensitive to arterial pressure > 60 mm Hg
Activated by elevated BP
1. Stretch in artery to aortic arch via vagus to medulla andcarotid sinus via Herings nerve to glossopharyneal nerveto medulla
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CV Rev
iew2. Sympath. action inhibited3. Vagal reflex dominates
4. Results in decreased HR and contract., dilation of peripheral
vessels, decreased SVR, BP lowered to normal
Activated with decreased BP1. Decreased vagal tone
2. Symp. NS dominant
3. Results in increased HR & contract., vasoconstriction (preserving
blood flow to brain and heart)
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CV Rev
iew Factors that affect BP- HR, CO,SVR,arterial
elasticity, blood volume, blood viscosity, age,
body surface area, exercise, Na retention,emotions
Pulse pressure, MAP (calculate)
CO
= SV X HR
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Preload Due to number ofvariables
stretch - fiber length, volume
Increase preload by increasing vol. to ventricles
Increase preload stretches fibers causing more forceful
contraction so increase SV thus increase CO but also
ventricular work
Myocardial fibers reach a point of stretch beyond which it
can contract and SV and CO decreases SO
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Preload changes Increased preload mitral insufficiency, aortic insufficiency
increased volume
vasoconstricting drugs increase atrial kick
Decrease preload mitral stenosis
decreased volume vasodilating drugs
decreased atrial kick
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Frank-Starling Curv
e Intrinsic ability of the heart to adapt to
changing volumes of inflowing blood. The
greater the heart mm. is stretched duringfilling, the greater will be the quantity of
blood pumped into the aorta.
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Afterload
Resistance that must be overcome byventricles in order to open semilunarvalves
and propel blood. SVR = MAP-CVP
CO
Increase afterload- aortic stenosis, arteriolarvasoconstriction, hypertension, polycythemia,vasoconstricting drugs
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Afterload (cont.)
Decreased afterload - arteriolarvasodilators
drugs, septic shock (late phase)
Excessive afterload causes increased LV
stroke work, decrease stroke volume,
increased MI O2 demand and may result in
LV failure
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Contractility
Increase contractility usually there is shift of curve
to the left and up
Increase in contractility Inotropic drugs - digitalis, epinephrine,
dobutamine
Increase HR Symp. stimulation via beta 1 receptors
Hypercalcemia
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Neurologic Control of the Heart
Chemoreceptors = carotid and aortic bodies,
sensitive to changes in pH,PaO2,PaCO2 and
cause changes in HR & RRvia stimulationvasomotor center in medulla
Stretch receptors: Respond to pressure and
volume changes
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Neurologic (cont.)
Autonomic
Sympathetic: Release norepin. Elicits 2
types of effects Alpha adrenergic = arteriolarvasoconstriction
Beta adrenergic (B1)
Increase SA node discharge - HR
(+ chronotropic)
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Neuro (cont.)
Increases force of myocardial contraction (+
intropic)
Accelerates AV conduction time (+dromotropic)
Parasympathetic: Rt vagus (affecting SAnode), Lt. Vagus (Affecting AV conduction) =
Release of acetylcholine
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Neuro (cont)
Decrease in SA node discharge - decreased HR can slow
conduction through AV tissue
Bainbridge Reflex: Stretch receptors in atria, large
veins and pulmonary arteries
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Heart
Aerobic organ so can easily undergo
irreversible damage with reduction in O2.
3 factors influencing O2 consumption
1. Tension time index (p. 15)
2. Contractile state of myocardium
3. Heart rate
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Heart (cont.)
Look up:
Pressures in chambers
Blood flow to the heart
Subendocardial region: more vulnerable to
diminished flow than subepicardial region
Collateral vessels
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Myocardial Ischemia
MyocardialO2 deprivation and inadequate
removal of metabolites secondary to decreased
perfusion. Most common pathologic process is narrowing of
coronary arteries (often proximal segments).
Nonatherosclerotic: inflammatory or autoimmune
processes. (Lupus, RA, diabetes)
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Coronary Artery Disease (CAD)
Endothelial cells in the intima are mech. &chemical injured. This changes structure of
cells, making more permeable to circulationlipoproteins (Phase 1 CAD)
Platelets adhere and aggregate to injury andmacrophages migrate to area. Lipoproteins
enter smooth mm. cells of intima andpromote fatty streak ( Phase 2 CAD)
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Myocardial Ischemia
Also have coronary artery spasms,embolism. Anemia & infections can also
increaseO
2 demand Contractile force & segment shortening are
reduced ABRUPT coronary occlusion.
Reduced high-energy phosphate supply
Cellular acidosis Both cause CA++ binding alterations
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Myocardial Infarction
NECROSIS of myocardial tissue due toloss of blood supply to myocardium
Important to determine: Location, severity
of narrowing, extent of collaterals, size of
vasc. Bed perfused, O2 needs ofmyocardium at risk.
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Myocardial Infarction
Color changes and infarcted mm. Is REMOVED
by mononuclear cells. Becomes scared, white &
firm. Types
Transmural = Full thickness
Subendocardial
Intramural
Subepicardial
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Types of Angina
1. Stable
2. Vasospastic
3. Unstable
ACUTE MIS
The atria and Rt. Vent. less incidence
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Acute MI
90% of transmural MI due toatherosclerosis. Occur most often in
proximal 2 cm of LAD and LCX andproximal and distal thirds of RC.
Nearly all transmural MI affect LV, 15%RV
Reflow to reperfusion to injured cells mayrestore viability but leave cells poorlycontractile (stunned) for up to 1 -2 days
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Cardiomyopathies
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Causes of Cardiac Dysfunction
Cardiomyopathy
Myocardial infarction
Arrhythmias, valve defects
Pulmonary hypertension
Pericardial or myocarditis
Aging
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Secondary causes of Cardiomyopathy
inflammatory
metabolic
toxic
infiltrative
fibroplastic
idiopathic
hematologic
hypersensitive
genetic
physical agents
acquired (misc)
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Prevalence of Cardiac
Dysfunction Greater than 2 million cases CHF
400,000 new cases annually
Costs range $15 to 28 Billion annually
1% prevalence in 50 to 59 year olds
Increases to 10% in 80 to 89 year olds
Left ventricular failure most common
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Break Time
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Pulmonary Heart Disease
RV VOLUME is larger than LV and EF is
lower. Afterload is lower, stroke work is
less ITP falls during inspiration which
INCREASES venous return to RV, shifts
septum toward the LV so decrease inLVEDV.
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RT Ventricle & Pulmonary
Circulation Decrease in LV preload and increase in
afterload result in insp. Decrease in BP
(Pulsus Paradoxus) PP is usually less than 10 mmHg but
increases with pts with obstructive lung
disease
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Pulmonary Circulation
COMPLIANCE , Proportion ofvessel NOT
perfused. Normal pul circulation can increase
2.5-3 fold before increase in PAP (Fig 7-2) RESISTANCE, PVR is increased with hypoxia
(vasoconstriction), low and high lung volumes.
VENT-PERFUSION MATCHING = normally
there is physiologic dead space. Vent. but under
perfused.
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Cardiovascular Review Items
Normal Electrophysiology
Depolarization, Repolarization, Automaticity,
Bradycardia, Tachycardia
Reentry Barrier, Unidirectional block, slow conduction
Reentrant tachycardia (WPW,MI)
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Normal Electrophysiology
Depolarization, Repolarization,
Automaticity, Bradycardia, Tachycardia
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Reentry
Barrier, Unidirectional block, slow
conduction
Reentrant tachycardia (WPW,MI)
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Types of Angina
1. Stable
2. Vasospastic
3. Unstable
ACUTE MIS
The atria and Rt. Vent. less incidence
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Acute MI
90% of transmural MI due toatherosclerosis. Occur most often in
proximal 2 cm of LAD and LCX andproximal and distal thirds of RC.
Nearly all transmural MI affect LV, 15%RV
Reflow to reperfusion to injured cells mayrestore viability but leave cells poorlycontractile (stunned) for up to 1 -2 days
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Causes of Cardiac Dysfunction
Cardiomyopathy
Myocardial infarction
Arrhythmias, valve defects
Pulmonary hypertension
Pericardial or myocarditis
Aging
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Prevalence of Cardiac
Dysfunction Greater than 2 million cases CHF
400,000 new cases annually
Costs range $15 to 28 Billion annually
1% prevalence in 50 to 59 year olds
Increases to 10% in 80 to 89 year olds
Left ventricular failure most common
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It All Begins with the Heart Fetal Development
Structural differences of cardiac muscle
Responses to blood volume & growth
Conductive nature of the cardiac tissues
Importance of HR x SV = CO
How does all this respond to the aging process?
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Impact of Growth on Cardiac System
Physical changes due to growth
Changes in stroke volume & blood volume Metabolic tissue changes cardiac response
Dietary & Lifestyle influences on the
cardiovascular system over time
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Aging Effects on the Cardiac System
Histological changes to the cardiac tissues
Culminating effects of chosen lifestyles Afterload & Preload pressures on the heart
Potential impact on functional tolerances
Overall influences of lifespan modifications
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It Starts with the Hearts
Is the 1st functioning system in the embryo!
Begins to form in the 3rd week of gestation
Due to the fact that as cells divide, simple
diffusion does not work, call the plumber!
Heart begins to pump in a tube fashion the
oxygen, nutrients & remove CO2, wastes
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Heart Tube beings to Change
As more cells divide and grow, there is needfor more plumbing and pumping of the heart
Lungs begin to develop but very little bloodis sent there, Youre getting 02 from Mom
But, when you leave home, you had betterstart breathing, so lungs, begin to expand !
This causes a lower pressure gradient pullingthe blood into the lung tissues
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Stop the Shunting
The change in pressure gradients stops the
shunting of blood away from the lungs
This causes the patent structures to close, likethe Foreamen Ovale & Ductus Arteriosus
This is usually completed within 3 months
Cardiac tissues are now feeling the full effectof their job with increased blood pressures
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Break Time