Life’s Progression through

Cardiac Physiology
Understanding the Normal
Physiology of the Heart as it Changes
through the Life Span
 Overall Design of the Heart
• Atrial fibers are divided into superficial & deep
• Superficial fibers spread over 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”
 Cardiovascular Review
• Anatomy - Skeletal vs Cardiac Muscle
• Sarcoplasmic/tubular system T tubules = transmit
Action Potential rapidly from the sarcolemma to
all 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
 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 a
contraction
 Cardiac Review
• 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
 Cardiac Muscle Tissue
• The actual structure of the cardiac muscle is
also unique and represents it’s 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
 CV Review
• Cardiac mm Vs Skeletal mm
– Fibers connected by intercalated discs forming
the SYNCYTIUM (one fiber depolorized , AP
spreads to all fibers, the whole syncytium
contracts not just one fiber)
 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 it’s own!
Ventricle Design is Different
• There are 3
layers of cardiac
muscle that will
overlap each
other from the
R to L ventricle
• This unique
design is part of
it’s functional
operation
 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-V
Node, Bundle Branches and Purkinje fibers
• The rates will become progressively slower
from the S-A to the Purkinje fibers
 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 heart
muscle over time & weaken heart function
 Cardio dynamics
• Preload pressures is the degree of stretching
experienced during ventricular diastole
• It is significant since it affects the ability of
the heart muscle to produce tension
• Much like the relationship between actin
and myosin in skeletal muscle for tension
• It is limited to myocardial connective
tissues, cardiac muscle and pericardial sac
 Cardio Dynamics
• End diastolic volume (EDV) - amount of
blood in ventricle at the end of diastole
• End systolic volume (ESV) – amount of
blood remaining at the end of vent. systole
• Stroke Volume (SV) is the amount of blood
pumped out of the ventricle on each beat,
EDV – ESV = SV
• Ejection Fraction is SV as a % of EDV
 Cardio Dynamics
• Frank-Starling Principle is the relationship
between the amount of ventricular 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 & L ventricular filling
• The body will retain fluids to increase this
effect for stretching the heart from more CO
 Cardiac Output (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
 Additional Factors
• Contractility is the force produced during a
contraction
• Drugs or factors that increase this force is
referred to as a “positive inotropic action”
• Those factors that decrease this force is
referred to as a “negative inotropic action”
• This is caused by assisting or blocking CA++
movement & metabolism of the cardiac cells
 Changes in Ion Concentrations
• Hypercalcemia – elevated CA++ will cause
cardiac cells to be highly excitable
• Hypocalcemia – low levels of CA++ will
cause weaker contractions & slower HR
• Hyperkalemia – elevated K+ cause weak
contractions and irregular heart beats
• Hypokalemia – low K+ lowers the rate of
contractions and hyperpolarizes the cells
 Changes in the Heart Over 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
Changes in the Heart Over 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 (20’s-30’s)
• Higher blood pressures create more afterload
• Weaker atriums create less preload
• Arteries become more rigid as we age also !!!
Understanding Cardiac Conditions
• The overall normal structure of the heart is
well designed for it’s function
• There is both a mechanical and electrical
component of the normal heart
• Aging and various disease processes can
effect the ultimate function of the heart
• Understanding these components is needed
to successfully implement physical therapy
 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
 Structures Continued
• Mediastinum, base heart occupies the right chest
and apex lies primarily in the left chest
• Papillary mm: arise from myocardial surface of
ventricles & attach to chordae tendin.
• Chordae tendineae: tendinous attachments from
papillary muscle to tricuspid and mitral valves.
Helps prevent eversion of valves into the atria
during systole
 Heart Chambers
• Atria (thin, low pressure)
– RT = venous blood from superior vena 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 for ventricular output
 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
 CV Review
• Cardiac conduction system
– SA node (pacemaker) = possesses fastest
inherent rate of AUTOMATICITY
– Internodal atrial pathways (SA node through
RA to AV node)
• Anterior tract (Bachmann’s)
• Middle tract (Wenckebach’s)
• Posterior tract (Thorel’s)
 CV Review
• Bachman’s bundle (SA to LA)
• AV node (40-60 beats)
• Bundle of His
• Bundle branch system = Rt. Lt
• Purkinje system
 Cardiac Plumbing
• Coronary vasculature
– RCA = SA node in 55% and AV node in 90%
of pts. RA and RV mm, inferiorpost wall of
LV, 80% hearts provides branch - Posterior
descending artery (located in interventricular
groove, supplies RV and inferior wall of LV
and posterior septum)
 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
 CV Review
• Veins = great cardiac vein, small cardiac vein, thebesian.
• Local Control Mechanisms: tissues ability to control
their own blood flow called AUTOREGULATION.
• There are 2 major hypotheses
1. Vasdilatory = rate of metabolism increase, O2 is
consumed higher rate, so decreased PaO2 so increase
in vasodilator substances (lactic acid adenosine,
carbon dioxide) to increase blood supply
1. Vasdilatory = rate of metabolism increase, O2 is consumed
higher rate, so decreased PaO2 so increase in vasodilator
substances (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 increased
metabolism 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
 CV Review
– Metabolic theory: Arterial pressure rises, increase blood
flow brings nutrients to tissues and remove vasodilator
substances. Both cause vessels to constrict.
• Autonomic regulation of vessels
– Adrenergic symp. NS fibers secrete norepinephrine to
nerve endings, causing VASOCONSTRICTION
– Parasymp. NS secrete ACETYLCHOLINE (cholinergic
effect) so VASODILATION
 CV Review
• Stretch receptors: barorecptors
(pressoreceptors) located in aortic arch,
carotid sinus, venae cavae, pulmonary arteries
and atria
– Sensitive to arterial pressure > 60 mm Hg
– Activated by elevated BP
1. Stretch in artery to aortic arch via vagus to medulla and
carotid sinus via Hering’s nerve to glossopharyneal nerve
to medulla
 CV Review
2. Sympath. action inhibited
3. Vagal reflex dominates
4. Results in decreased HR and contract., dilation of peripheral
vessels, decreased SVR, BP lowered to normal
• Activated with decreased BP
1. Decreased vagal tone
2. Symp. NS dominant
3. Results in increased HR & contract., vasoconstriction (preserving
blood flow to brain and heart)
 CV Review
• 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
 Preload
• Due to number of variables
– 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
 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
 Frank-Starling Curve
• Intrinsic ability of the heart to adapt to
changing volumes of inflowing blood. The
greater the heart mm. is stretched during
filling, the greater will be the quantity of
blood pumped into the aorta.
 Afterload
• Resistance that must be overcome by
ventricles in order to open semilunar valves
and propel blood.
• SVR = MAP-CVP
CO
• Increase afterload- aortic stenosis, arteriolar
vasoconstriction, hypertension, polycythemia,
vasoconstricting drugs
 Afterload (cont.)
• Decreased afterload - arteriolar vasodilators
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
 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
 Neurologic Control of the Heart
• Chemoreceptors = carotid and aortic bodies,
sensitive to changes in pH,PaO2,PaCO2
and cause changes in HR & RR via
stimulation vasomotor center in medulla
• Stretch receptors: Respond to pressure and
volume changes
Neurologic (cont.)
• Autonomic
– Sympathetic: Release norepin. Elicits 2
types of effects
• Alpha adrenergic = arteriolar vasoconstriction
• Beta adrenergic (B1)
– Increase SA node discharge - HR
(+ chronotropic)
 Neuro (cont.)
– Increases force of myocardial contraction (+
intropic)
– Accelerates AV conduction time (+
dromotropic)
– Parasympathetic: Rt vagus (affecting SA
node), Lt. Vagus (Affecting AV conduction) =
Release of acetylcholine
 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
 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
 Heart (cont.)
• Look up:
– Pressures in chambers
– Blood flow to the heart
– Subendocardial region: more vulnerable to
diminished flow than subepicardial region
• Collateral vessels
 Myocardial Ischemia
• Myocardial O2 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)
Coronary Artery Disease (CAD)
• Endothelial cells in the intima are mech. &
chemical injured. This changes structure of
cells, making more permeable to circulation
lipoproteins (Phase 1 CAD)
• Platelets adhere and aggregate to injury and
macrophages migrate to area. Lipoproteins
enter smooth mm. cells of intima and
promote “fatty streak” ( Phase 2 CAD)
 CAD (cont.)
• Repeated injury to endothelial cells lead to
“fibrofatty plaque”. It can protrude into
lumen and obstruct flow (Phase 3)

• Cont. process of narrowing then vessels

may hemorrhage and increase size of
plaque and the fibrofatty plaque may
rupture and form thrombus (Phase 4)
 Myocardial Ischemia
• Also have coronary artery spasms,
embolism. Anemia & infections can also
increase O2 demand
• Contractile force & segment shortening are
reduced ABRUPT coronary occlusion.
– Reduced high-energy phosphate supply
– Cellular acidosis
• Both cause CA++ binding alterations
 Myocardial Infarction
• NECROSIS of myocardial tissue due to
loss of blood supply to myocardium

• Important to determine: Location, severity

of narrowing, extent of collaterals, size of
vasc. Bed perfused, O2 needs of
myocardium at risk.
 Myocardial Infarction
• Color changes and infarcted mm. Is REMOVED
by mononuclear cells. Becomes scared, white &
firm.
• Types
– Transmural = Full thickness
– Subendocardial
– Intramural
– Subepicardial
 Types of Angina
1. Stable
2. Vasospastic
3. Unstable
• ACUTE MI’S
– The atria and Rt. Vent. less incidence
 Acute MI
• 90% of transmural MI due to
atherosclerosis. Occur most often in
proximal 2 cm of LAD and LCX and
proximal and distal thirds of RC.
• Nearly all transmural MI affect LV, 15%
RV
• Reflow to reperfusion to injured cells may
restore viability but leave cells poorly
contractile (“stunned”) for up to 1 -2 days
Cardiomyopathies
 Causes of Cardiac Dysfunction
• Cardiomyopathy
• Myocardial infarction
• Arrhythmias, valve defects
• Pulmonary hypertension
• Pericardial or myocarditis
• Aging
Secondary causes of Cardiomyopathy
• inflammatory • hematologic
• metabolic • hypersensitive
• toxic • genetic
• infiltrative • physical agents
• fibroplastic • acquired (misc)
• idiopathic
 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
Break Time
 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 in
LVEDV.
 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
 Pulmonary Circulation
• COMPLIANCE , Proportion of vessel 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.
 Cardiovascular Review Items
• Normal Electrophysiology
– Depolarization, Repolarization, Automaticity,
Bradycardia, Tachycardia
• Reentry
• Barrier, Unidirectional block, slow conduction
• Reentrant tachycardia (WPW,MI)
 Normal Electrophysiology
• Depolarization, Repolarization,
Automaticity, Bradycardia, Tachycardia
 Reentry
– Barrier, Unidirectional block, slow
conduction
– Reentrant tachycardia (WPW,MI)
 Types of Angina
1. Stable
2. Vasospastic
3. Unstable
• ACUTE MI’S
– The atria and Rt. Vent. less incidence
 Acute MI
• 90% of transmural MI due to
atherosclerosis. Occur most often in
proximal 2 cm of LAD and LCX and
proximal and distal thirds of RC.
• Nearly all transmural MI affect LV, 15%
RV
• Reflow to reperfusion to injured cells may
restore viability but leave cells poorly
contractile (“stunned”) for up to 1 -2 days
 Causes of Cardiac Dysfunction
• Cardiomyopathy
• Myocardial infarction
• Arrhythmias, valve defects
• Pulmonary hypertension
• Pericardial or myocarditis
• Aging
 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
 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?
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
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
 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
 Heart Tube beings to Change
• As more cells divide and grow, there is need
for more plumbing and pumping of the heart
• Lungs begin to develop but very little blood
is sent there, You’re getting 02 from Mom
• But, when you leave home, you had better
start breathing, so lungs, begin to expand !
• This causes a lower pressure gradient pulling
the blood into the lung tissues
 Stop the Shunting
• The change in pressure gradients stops the
shunting of blood away from the lungs
• This causes the patent structures to close, like
the Foreamen Ovale & Ductus Arteriosus
• This is usually completed within 3 months
• Cardiac tissues are now feeling the full effect
of their job with increased blood pressures
Break Time