ANATOMY & PHYSIOLOGY
HEART
Supplemental module prepared by
DR. JEANNETTE R. ABELLA
HEART– muscular organ that is essential for life because
it pumps blood throughout the body.
Like a pump that forces water to flow through a pipe –
heart contract forcefully to pump blood through the
blood vessel
– at rest approximately pumps 5L of blood per minute.
During short period of vigorous exercise it increase
several fold.
If the heart loses its pumping ability even for a few
minutes blood flow will stop and life will be in danger
HEART – two pumps in one
RIGHT SIDE – pumps blood to the lungs and back to the
left
LEFT SIDE – pumps blood to all other tissue and back to
the right
RIGHT – pulmonary circulation
LEFT– systemic circulation
FUNCTION
1.GENERATES BLOOD PRESSURE
– Responsible for blood movement thru blood vessel
2. ROUTING BLOOD
– Separates systemic and pulmonary circulation and
ensures flow of oxygenated blood.
3.ENSURES A ONE WAY FLOW
– function of the valves
4. REGULATING BLOOD SUPPLY – HR and force of
contraction matches the changing metabolic need of
tissues
rest exercise,= increase HR
SIZE/FORM/LOCATION
SIZE - The heart is slightly larger than a closed fist.
FORM – has a blunt cone shape, the blunt rounded
point is the apex and the larger flat portion on opposite
end base.
APEX – most inferior part and is directed ANTERIORLY
and to the left (found deep to the 5th ICS )
LOCATION
BASE – superior and slightly posterior
>most superior portion of the base is deep to the 2nd
ICS
– Heart is located in the thoracic cavity between the
lungs.
-in the MEDIASTINUM
is important to know where the heart sound is
accurate knowledge of the heart position
Important:
1. Placing of stethoscope
2. Placing of electrodes on ECG
3. Perform CPR
ANATOMY
PERICARDIAL CAVITY – space containing the heart.
PERICARDIUM OR PERICARDIAL SAC – is a double
layered closed sac that surrounds the heart.
-anchors it within the mediastinum
SEROUS PERICARDIUM
a. PARIETAL PERICARDIUM – lines the fibrous
pericardium
b. VISCERAL PERICARDIUM OR EPICARDIUM – portion
covering the heart surface
Both are continuous with each other where GREAT
vessels ENTER and LEAVE the heart.
PERICARDIAC FLUID – produced by serous pericardium
to help reduce friction as heart moves within the
pericardial sac
READINGS
PERICARDITIS- inflammation of the serous pericardium
with accumulation of fluid
CARDIAC TAMPONADE- fluid or blood accumulating
causing compression on the heart
EXTERNAL ANATOMY
ATRIA – (L)&(R) –entrance or chamber, located at the
base of the heart
VENTRICLES (L) & (R)- extends from the base towards
the apex
CORONARY SULCUS – extends around the heart,
separating the atria from the ventricles.
2 SULCI – which indicate the divisions between the right
and left ventricles, extends inferiorly from the coronary
sulcus.
ANTERIOR INTERVENTRICULAR SULCUS – extends
inferiorly from the coronary sulcus on the anterior
surface of the heart
POSTERIOR INTERVENTRICULAR SULCUS- the other
extend inferiorly form the coronary sulcus on the
posterior surface of the heart.
6 LARGE VEIN -carry blood to the heart
SUPERIOR VENA CAVA- carry blood to the right atrium
INFERIOR VENA CAVA-carry blood to the right atrium
4PULMONARY VEINS- carry blood from the lungs to the
left atrium.
2 LARGE ARTERIES
PULMONARY TRUNK-arise and splits into the right and
left pulmonary arteries
-which carry blood to the lungs
AORTA-exit the heart and carries blood from the left
ventricle to the body.
BLOOD SUPPLY TO THE HEART
CORONARY ARTERIES- supply blood to the wall of the
heart.
1.LEFT CORONARY ARTERY- originates on the left side
of aorta.
-it branches supply much of anterior wall of the heart
and most of the left ventricle.
2. RIGHT CORONARY ARTERY- originates on the right
side of the heart and supplies most of the wall of right
ventricle
CORONARY ARTERIES
LEFT CORONARY → LEFT MARGINAL → ANTERIOR IV
ARTERY
RIGHT CORONARY → RIGHT MARGINAL → POSTERIOR
IV ARTERY
CIRCUMFLEX ARTERY → CONNECTS RIGHT & LEFT
CORONARY ARTERIES
BLOOD SUPPLY TO THE HEART
IN SKELETAL MUSCLE - blood flowing thru arteries to
the skeletal muscle gives up about 25% of its oxygen.
-the percentage of O2 blood release to skeletal muscle
increases up to 70% or more- DURING EXERCISE
CARDIAC MUSCLE
-percentage of O2 can not increase substantially during
exercise
-Cardiac muscle is therefore very DEPENDENT on an
increasing rate of blood flow than the coronary arteries
above its RESTING level to provide an ADEQUATE O2
supply during EXERCISE.
READ ON:
CORONARY ARTERY DISORDERS
Thrombus-coronary thrombosis (block)
Infarct MI- dead tissue
Streptokinase- to break or to block old clots
TPA (tissue plasminogen activator) thrombin breaks
blood clots
ATHEROSCLEROTIC LESIONS
ANGINA PECTORIS- chest pain
ANGIOPLASTY- balloon
CORONARY BYPASS- leg veins
CARDIAC VEINS- drain blood from the cardiac muscle
they are nearly parallel to the coronary arteries and
most carry blood from cardiac muscle to the CORONARY
SINUS
CORONARY SINUS (vein)- large veins located within the
coronary sulcus on the posterior
Blood flows from the coronary sinus into the right
atrium
Some small cardiac veins drain directly into the right
atrium
CARDIAC VEINS
CARDIAC MUSCLES → CARDIAC VEINS → CORONARY
SINUS → R.A.
POSTERIOR LEFT VENTRICLE → MIDDLE CARDIAC VEIN
RV →SMALL CARDIAC VEIN
LV → GREAT CARDIAC VEIN
INTERNAL ANATOMY
HEART CHAMBERS:
HEART – muscular pump consisting of 4 chambers
ATRIA – receive blood from veins
-function primarily as reservoirs where blood returning
from veins collect before it enters the ventricles.
Contraction of the ATRIA forces blood into the
ventricles to complete ventricular filling
HEART CHAMBERS
RIGHT ATRIUM – 2 major opening
1. Superior Vena cava- SVC
2. Inferior vena cava- IVC
- Large veins that enters the heart from various parts of
the body
-Smaller coronary sinus enters the right atrium from
the wall of the heart.
LEFT ATRIUM – has 4 openings that receive the 4
pulmonary veins from the lungs.
INTERATRIAL SEPTUM – partition consisting of cardiac
muscles that separates the 2 atria (IAS)
VENTRICLES – major pumping chambers
-eject blood into the arteries and force it to flow
through the circulatory system.
ATRIA open into the VENTRICLES each ventricle has
one large outflow route superiorly near the midline of
the heart.
2 VENTRICLES
RIGHT VENTRICLE – opens to the pulmonary trunk
LEFT VENTRICLE – opens into the aorta.
INTERVENTRICULAR SEPTUM – separates the 2
ventricles from each other (IVS)
VENTRICLES
LEFT THICKER THAN RIGHT– generates greater pressure
when it contracts, the pressure increase to approximate
120mmhg.
RIGHT VENTRICLE contracts the pressure increase
approximately 1/5 of the left ventricle pressure
RIGHT AND LEFT VENTRICLES – pumps nearly same
volume of blood.
HEART VALVES
ATRIOVENTRICULAR (AV) – between atrium and
ventricle and on the left & right side of the heart
TRICUSPID VALVE – between right atrium and right
ventricle (3 cusps)
BICUSPID/MITRAL – between left atrium and left
ventricle (2 cusps)
HEART VALVES- Allow blood to flow from the ATRIA
→VENTRICLES
But prevent it from flowing back into the atria.
PAPILLARY MUSCLES – cone shape muscular pillar on
each ventricle
CHORDAE TENDINAE- strong thin strings, connective
tissue where papillary muscles are attached to free
margins of the cusps of AV valves.
HEART VALVES
When ventricles RELAX – blood flows from the ATRIA
into the VENTRICLES and the valves are pushed open
into the ventricle
When ventricles CONTRACTS –blood pushes the valves
back toward the atria and the AV closes as the cusps
meet
FUNCTIONS OF THE HEART VALVES
BICUSPID/MITRAL OPENS – cusps are pushed by blood
into the ventricles
PAPILLARY MUSCLE – relax
CHORDAE TENDINAE – tension is DECREASE
blood from left atrium left ventricle.
SEMILUNAR VALVES
AORTIC VALVES– closed cusps of valve overlap pushed
by blood in the aorta towards the ventricles
No blood flow –from aorta into the ventricle
BICUSPID VALVE CLOSES – cusps of valves overlap as
they are pushed by blood toward left atrium
No blood flow – from the ventricle into the atrium
Papillary m. – contracted
Chordae tendinae – tension increase preventing
bicuspid valve from opening into the left atrium
Aortic Semilunar valve –cusps of valve are pushed by
blood toward the aorta
- blood flows from left ventricle to the aorta
Ventricular contraction – by pulling the chordae
tendinae attached to the valve cusps, the papillary m.
contracts and prevents the valves from opening into the
atria
AORTIC & PULMONARY TRUNK
Semilunar valves – consisting of 3 pockets like semi
lunar cusps.
* When ventricles contract the blood flowing out of the
ventricles pushes against each valves, folding the cusp
to open
HEART VALVES
When ventricles relax blood flows back from the aorta
or pulmonary trunk toward the ventricle the pockets
of the cusps causing them to bulge toward and meet in
the center of the aorta or pulmonary trunk closing the
vessels and keeping blood from flowing back into the
ventricles.
CARDIAC SKELETON
Skeleton of the heart - fibrous connective tissue
consisting mainly of fibrous rings around the valves
Provide a solid support for the valves
This connective tissue serves as electrical insulation
between the atria and ventricles
Also provide rigid site of attachment for the cardiac
muscle
HISTOLOGY
Heart wall composed 3 layer of tissues
1.EPICARDIUM (VISCERAL PERICARDIUM) – thin serous
membrane forming the smooth outer surface of the
heart.
Consist of simple SQ epithelium overlaying a layer of
loose connective tissue and fat.
2.MYOCARDIUM – thick middle layer of cardiac muscle
cells responsible for the ability of the heart to contract.
3.ENDOCARDIUM – smooth inner surface of the heart
chambers
SIMPLE SQ epithelium over layer of connective tissue
Allows blood to move easily through the heart.
HEART VALVE – is formed by a fold of endocardium of
connective tissue between the 2 layers
VENTRICLES – modified by ridges and columns of
cardiac m. on the surface of the interior wall.
ATRIA – smaller ridges found
CARDIAC MUSCES – are elongated branching cells that
contain 1 or 2 centrally located nuclei
Cardiac muscle cell contains
Actin & Myosin myofilaments - responsible for
contraction
Actin and myosin – organized to form SACROMERES
joined end to end to form MYOFIBRILS
CARDIAC MUSCES
ATP provides energy for contraction
ATP production depends on O2 availability
MITOCHONDRIA- ATP production
Extensive capillary network- provides adequate O2
Large O2 debt results in muscular fatigue and
cessation of cardiac control
Cardiac muscle cells are organized into spiral bundles or
sheet
Intercalated disks – specialized cells that bound them
end to end and laterally
GAP JUNCTIONS – are specialized C.M. structures in the
intercalated disks
-Reduce electrical resistance between cells
-Allows A.P. for pass easily from cell to adjacent cell
ELECTRICAL ACTIVITY
Action potential in cardiac muscle like in skeletal m. and
neurons it has DEPOLARIZATION & REPOLARIZATION
PLATEAU PHASE
–present in cardiac muscle
it is a period of SLOW REPOLARIZATION which prolongs
A.P.
A.P. – in cardiac muscle approximately 200-500
millisecond to complete
Skeletal muscle- <2 milliseconds to complete
ACTION POTENTIAL
1.DEPOLARIZATION PHASE – rapid
2.REPOLARIZATION – rapid but partial early
3.PLATEAU – longer period of slow repolarization
4.FINAL REPOLARIZATION – end of plateau, more rapid
final takes place
Membrane potential returns to resting level
CHANGES -in membrane channels are responsible for
permeability changes that produce action potential
1.DEPOLARIZATION PHASE
Voltage gated Na+ channel- OPENS
K+ channel – CLOSE
Ca+ channel – begin to open
2. EARLY REPOLARIZATION AND PLATEAU PHASES
Na+ channel CLOSES
Some K+ channel OPENS, causing early repolarization
Ca+ channels OPEN produce plateau by slowing further
repolarization
3.FINAL REPOLARIZATION
Ca+ channels close
Many K+ channel open
Diffusion of Ca+ into the cell decreases
Diffusion of K+ out of the cell increases
There changes cause the membrane potential to return
to its resting level
REFRACTORY PERIOD – last about the same length of
time as the action potential in cardiac muscles
The prolonged A.P and refractory period – allow cardiac
m. CONTRACT
and almost COMPLETE RELAXATION to take place
before another A.P can be produced
REFRACTORY PERIOD
The long refractory period
1.Prevents TETANIC contractions
2.Ensure a rhythm of contraction and relaxation
SA node or Sino arterial node
Located in the superior wall of the right atrium
Initiates the contraction of the heart.
PACEMAKER- because it produced A.P at faster rate
than other areas of the heart
SA NODE
1.Larger # of voltage gated Ca+ channels some Ca+
channels open it diffuses to the cell causing
Depolarization
2. Additional channels open Na+ channel open
further depolarization quickly threshold is reached
and another A.P is produced
DRUGS:
Ca+ channel blockers – used to treat some types of
TACHYCARDIA and ARRYTHMIA because they block Ca+
channels and slow the A.P produce
ex. Nifedipine
CONDUCTION SYSTEM OF THE HEART
Conducted in the specialized cardiac muscle cells
1. SA node – A.P originates the spread over the right &
left atria causing them to contract.
2. A.V node – 2nd area of the heart, in the lower portion
of the right atrium
A.P reach the A.V node spread slowly then to the next
structure
3.AV bundle – specialized cell slow rate of A.P conducts
in the AV node allows the atria to complete their
contraction before A.P are delivered to the
interventricular septum
4. Left or Right bundle branches -Ventricles
5. Purkinje fibers – tips of the left and right bundle
branches conducting tissue forms many bundles of
purkinji fibers
6. Then pass to the apex and then to the cardiac muscle
of the ventricle walls
7. Relax then another A.P originates in SA node to begin
the next cycle of contractions.
ECTOPIC BEAT– when A.P originates in an area other
than the SA node
HR – slower than normal
ELECTROCARDIOGRAM – A.P conducted through the
heart during cardiac cycle produced by ELECTRICAL
CURRENT measured
ECG/ EKG-records of electrical events
Electrode place on the surface are attached to a
recording device that can detect small electrical
changes
Normal ECG consist of
1.P wave
2. QRS complex
3. T wave
ECG
1. P Wave – result from depolarization of the atrial
myocardium
– precedes the onset of ATRIAL CONTRACTION
2. QRS COMPLEX – results from depolarization of the
ventricles
– precedes ventricular contraction
3. T-WAVE – repolarization of ventricles
– precedes ventricular relaxation
ATRIAL REPOLARIZATION is not seen because it occurs
during QRS complex
4. PQ INTERVAL – time between the beginnings of P
Wave and beginning of QRS complex
PR INTERVAL – because Q wave is very small
During PQ – atria contract and begin to relax
END of PQ – ventricles begin to depolarize
5. QT INTERVAL – extends from beginning QRS complex
to the end of T WAVE
> Represents the length of time require for
VENTRICULAR DEPOLARIZATION and REPOLARIZATION
CARDIAC CYCLE
Heart is viewed as 2 separate pumps represented by
Right valves & Left valves of the heart
Primer pump – atrium
Power pump – ventricle
2 PUMPS
Primer pump – atrium
-because they complete filling of the ventricle with
blood
Power pump – ventricle
Because they produce major force that causes blood to
flow through the pulmonary and systemic circulation.
CARDIAC CYCLE – refers to the respective pumping
process that begins with the onset of the cardiac muscle
contraction & ends w/ with the beginning of the next
contraction
PRESSURE CHANGES- produced within the heart
chambers as a results of cardiac muscles contraction are
responsible for blood movement
Because blood moves from areas of higher pressure to
areas of lower pressure.
CARDIAC CYCLE
ATRIAL SYSTOLE – refers to contraction of the 2 ARTRIA
VENTRICULAR SYSTOLE – contraction of the ventricles
ATRIAL DIASTOLE – refers to relaxation of the 2 ATRIA
VENTRICULAR DIASTOLE – relaxation of the 2 ventricles
CARDIAC CYCLE
Systole and Diastole – when used without reference to
atria or ventricles they refer to VENTRICULAR
contraction or relaxation.
Ventricle contain more muscle than atria and produce a
greater pressure which forces blood to circulate
throughout the vessels of the body.
Major events of cardiac cycle
1. As systole begins, contraction of the ventricle pushes
blood toward atria causing AV valve to CLOSE
2. When the pressure in the ventricle exceeds the
pressure in the pulmonary trunk and aorta semilunar
valves are forced OPEN the blood is ejected into the
pulmonary trunk and aorta
3. At the beginning of the ventricular diastole, the
pressure in the ventricles decreases the semilunar
valves CLOSE and prevent blood from flowing back into
the ventricles.
4. The pressure continuous to decline in the ventricles
until finally the AV valves OPEN and blood flows directly
from the atria into the relaxed ventricles.
5. During the previous ventricular systole, the atria were
relaxed and blood collected in them. When the
ventricles relaxed and the AV valves OPEN blood flows
into the ventricles and fill them to approximately 70% of
their volume.
6. At the end of ventricular diastole, the atria contract
and then relaxed. Atria systole forces additional blood
to flow into the ventricles to complete their filling.
-Semilunar valves remain closed
EVENTS :
ECG – indicates electrical events that cause contraction
and relaxation of atria and ventricles.
PRESSURE GRAPH – shows the pressure changes in the
left atrium, left ventricle, aorta resulting from atria
ventricular contractions & relaxation
Pressure changes on the right side not shown but
similar to the left side only lower
VOLUME GRAPH – presents the changes in the left
ventricle volume as blood flows into and out of the left
ventricle as a result of the pressure changes.
SOUND GRAPH – records the closing of valves caused by
blood flow
MAJOR CARDIAC ARRYTHMIA AND HEART RYTHYMS
TACHYCARDIA
HR > 100 heats per minutes
Elevated body temperature
Excessive sympathetic stimulation
Toxic conditions
BRADYCARDIA
HR<60 beats /min.
Increase stroke volume in athletes
Excess vagus nerve stimulation
Non functional SA node
Carotid sinus syndrome
SINUS ARRYTHMIA
HR valves – 5% during respiratory cycle
Up to 30% during deep respiration
Occasionally caused by ischemia inflammation or
cardiac failure
cause not always known
PAROSYMAL ATRIAL TACHYCARDIA
Sudden increase HR to 95-150bpm for few seconds or
several hours
P wave precedes every QRS complex, P Wave inverted
and super imposed
Excess sympathetic stimulant
AbN increase permeability of cardiac muscular Ca++
ATRIAL FLUTTER
As many as 300 P waves/min. and 125 QRS
complexes/min. resulting in 2 or 3 P waves (atrial
contraction) for every QRS (venticular contraction)
ECTOPIC beats in Atria
No P waves, normal QRS and T waves
Irregular timing with ventricles constantly stimulated by
atria
Reduced ventricular filling
Increase change of fibrillation
Ectopic beats in atria
VENTRICULAR TACHYCARDIA SYSTOLE
Frequently causes fibrillation Cause closure of the AV valves
Often association with damage to AV node or Second – higher pitch occurs beginning of ventricle
ventricular muscle DIASTOLE and closure of semilunar valves
Valve usually DO NOT make sound when they open
HEART BLOCKS CLINICALLY
SA NODE BLOCK – no P wave, low HR result from AV VENTRICULAR SYSTOLE – occurs between the 1st and
node acting as peace maker 2nd heart sound
Normal QRS and T waves VENTRICULAR DIASTOLE – occurs between the 2nd and
Ischemia the 1st heart sound of the next beat
Tissue damage due to infarction Diastole – last longer so there is less time between 1st-
Sometimes unknown 2nd sound than between 2nd-1st sound

AV NODE BLOCKS MURMURS – are abnormal heart sounds usually as a

1. First degree – PQ interval results of faculty valves
> 0.2 sec. INCOMPETENT VALVES
Inflammation of AV bundle - fails to close tightly and blood leaks through the valves
2. Second degree – PQ interval when it close
0.25-0.45 SWISHING sound after the closure of the valve
Some p waves trigger QRS and other do not e.g. P/QRS MURMURS
ratio 2:1, 3:1, 3:2 STENOSED – narrowing of the opening
Excessive vagus nerve system Swishing sound proceeds closure of the stenosed valve
AV node damage If the BICUSPID valve is stenos then swishing sounds
3. Complete heart block proceeds the 1st Heart sound
P wave dissociate from QRS
Atria rhythm < 40bpm REGULATION OF HEART FUNCTION
Ischemia of AV node Cardiac Output -volume of blood pumped by either
Compression of AV bundle ventricle of the heart each minute
Stroke Volume-volume of blood pump per ventricle
PREMATURE CONTRACTION each time the heart contracts
PAC Premature Atrial Contraction Heart Rate - number of times the heart contracts each
occasional shortened interval between one contraction minute
and the succeeding contraction CO= SV x HR
Frequently occur in healthy person
Excessive smoothing UNDER RESTING CONDITION
Lack of sleep HR= 70 bpm
Too much caffeine SV= 70 ml/beat
CO=SV x HR
PREMATURE CONTRACTION = 70 ml/beat x 72 beats/min =
Premature ventricle contraction 5040ml/min
prolonged QRS VARIATIONS IN HR & SV
Exaggerated voltage because only 1 ventricle in ATHLETES- higher SV & lower HR at rest because
depolorized exercise increases the size of the heart
Possible inverted t wave NON ATHLETES- may have higher HR & lower SV
Increase probability of fibrillation During exercise HR increases to 190 bpm & SV at 115
Ectopic beat on ventricle ml/beat CO =22L/min approximately
lack of sleep
too much coffee During exercise HR increases to 190 bpm & SV at 115
irritability ml/beat CO =22L/min approximately
occasionally occurs with thrombosis ATHELETES- can increase CO to greater degree than non
athletes
HEART SOUNDS – the use of stethoscope was originally
for lungs and heart sounds CONTROL MECHANISM
2 MAIN HEART SOUNDS 1. INTRINSIC REGULATION- mechanism contained w/in
1ST – represented by LUBB the heart
2nd – represented by DUPP FORCE OF CONTRACTION related to DEGREE OF
First – lower pitch occurs at the beginning of ventricle STRETCH of cardiac muscles
AMOUNT OF BLOOD at the end of VENTRICULAR
DIASTOLE determines the DEGREE OF STRETCH
VENOUS RETURN -Amount of blood that returns to the
heart
PRELOAD- degree to w/c the ventricular walls are
stretched at the end of diastole
THEREFORE if the VR is high the heart fills a greater
volume & stretches the muscle producing a high
PRELOAD
If PRELOAD is high there is a greater force of
contraction
So if the VR is low= PRELOAD is low= CO is low
STARLINGS LAW- relationship of the PRELOAD & SV,
having major influence to CO
EXERCISE
VR is high= PRELOAD is high= SV is high = CO is high
High CO is needed in to supply O2 to exercising skeletal
muscles
AFTERLOAD- pressure against w/c the ventricles must
pump blood
HYPERTENSION
AFTERLOAD is high because of increase AORTIC
PRESSURE during contraction of the ventricles
HEART- must do more to pump blood from the LV to the
AORTA= increase WORK LOAD on the heart can lead
to HEART FAILURE
WORK LOAD
If there is low AFTER LOAD = less WORKLOAD
AFTERLOAD influences CO less than PRELOAD
AFTERLOAD must increase substantially before it
decreases the volume of pumped blood by a healthy
heart
READ ON:
HEART FAILURE
Right sided SYSTEMIC HYPERTENSION
Left sided PULMONARY HYPERTENSION
2. EXTRINSIC REGULATION- external mechanisms of the
heart
a. NERVOUS-influence through ANS
SYMPATHETIC & PARA SYMPATHETIC
both innervates the heart & have major effect on the SA
NODE
PARA= <HR & SV SYMPA= > HR & SV
BARORECEPTOR REFLEX
Plays an important role in regulating the heart
REFLEX: sensory receptor control center effector
BARORECEPTORS- stretch receptors
Monitor BP in the AORTA & walls of INTERNAL CAROTID
arteries w/c carries blood to the brain
BARORECEPTOR REFLEX
CHANGE IN BP change in stretch of blood vessel walls
change in pressure
AP transmitted nerve fibers stretch receptors
medulla oblongata Brain
CARDIOREGULATORY CENTER- brain
CARDIOREGULATORY CENTER- Medulla oblongata
Receives & integrates AP from baroreceptors control
of AP in the sympathetic & parasympathetic nerves
extends from the BRAIN & S.C. to the HEART
- also effect sympathetic stimulation of the ADRENAL
GLANDS
2. EXTRINSIC REGULATION
b. HORMONES- EPINEPHRINE & NOREPINEPHRINE
-Released from the ADRENAL GLANDS
Increasing SV & HR
REGULATION
If BP is high baroreceptors stimulated send AP along
Medulla oblongata Cardioregulatory center (+) para
sympathetic &
(-) sympathetic stimulation of the heart Decreasing HR
& SV= BP to decrease normal BP
Decrease BP less stimulation of baroreceptors (-)
feed back to medulla oblongata (-) para sympathetic &
(+) sympathetic stimulation increase in HR & SV
increase BP
It may also stimulate ADRENAL GLAND
ADRENAL MEDULLA EPI & NOREPINEPHRINE
increasing HR & SV further increasing BP towards
normal
c. EMOTIONS- integrated in the cerebrum & can
influence the heart
Excitement , Anxiety, Anger can affect the
Cardioregulatory center causing (+) sympathetic
stimulation & increasing CO
Depression can (+) parasympathetic stimulation &
decreases CO
EPI & NOREPINEPRHINE
May be released in response to Exercise, Excitement &
Stress influencing heart function
-bind to receptors causing increase HR & SV
CHEMORECEPTORS sensitive to changes in PH & CO2
<PH= >CO2 sympa= higher HR & SV
CHANGES IN EXTRACELLULAR CONC.
1.Excess extracellullar K+ = decease HR & SV
Normal conduction of AP is blocked & death results
2.Excess Ca+ arrythmic contraction
3.Low Ca+ = Decreasa HR & SV
BODY TEMPERATURE
Affects metabolism in the heart
Increase Temperature= higher HR
Decrease temperature = slower HR
SURGERY to decrease temperature intentionally to
lower, heart rate & metabolism of the heart
EFFECTS OF AGING
Minor at rest, obvious during exercise in response to
age related diseases
1. 70 y.o –CO low to 1/3 due to decrease reserve
strength of the heart
2. HYPERTROPHY- LVH age related due to increase
afterload or pressure from the aorta
ATHEROSCLEROSIS
EFFECTS OF AGING
3. Decrease maximum HR by 85 y.o. & CO decrease to
30-60%
4. High tendency of aortic semilunar valves to be
stenosed or incompetent due to less flexibility & Ca+
deposits
5. Increase arythmias- SA node & AV bundle
replacement
EFFECTS OF AGING
6. Coronary artery disease & heart failure 10% over 80
y.o.
SUGGESTION: regular aerobic exercise