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The Cardiovascular System:
Heart Location
• The heart is located in the center of the chest in
an area called the mediastinum.
Heart Wall
• Fibrous Pericardium –
outer most layer.
– tough and prevents heart
from overfilling.
• Epicardium – Outermost
layer
– visceral layer of the
serous pericardium
– They are separated by
the fluid-filled pericardial
cavity
• Myocardium – cardiac
muscle layer forming the
bulk of the heart.
• Endocardium – endothelial
layer of the inner
myocardial surface.
– Deepest layer that is
continuous with the
lumen of the heart and
arteries.
Atria of the Heart
• Atria are the
receiving chambers
of the heart
• Blood enters right
atria
– Superior vena cava
– inferior vena cava
– coronary sinus
• Blood enters left
atria via pulmonary
veins
Ventricles of the Heart
• Ventricles eject
blood from the
heart
– Right ventricle
pumps blood into
the pulmonary
trunk which will go
to the lungs.
• Left ventricle
pumps blood into
the aorta which will
go to the rest of
the body
Atrioventricular Heart Valves
•
•
Heart valves ensure unidirectional blood flow
through the heart
Atrioventricular (AV) valves lie between the atria
and the ventricles
–
–
•
•
Tricuspid Right
Bicuspid (Mitral) Left
AV valves prevent backflow of blood into the atria
when ventricles contract
Chordae tendineae anchor AV valves to papillary
muscles
–
First heart sound (LUB) when valves close
• During diastole there is less pressure in the in ventricle. AV Valves
open and filling the ventricle.
• During systole the AV valves prevent the back flow of blood into the
atrium.
– Failure to prevent the blood from going back into the atria (systolic heart
murmur)
Semilunar Heart Valves
• Aortic semilunar valve lies between the left
ventricle and the aorta.
• Pulmonary semilunar valve lies between
the right ventricle and pulmonary trunk
– Semilunar valves prevent backflow of blood
into the ventricles.
• Second heart sound (DUB) when valves
close.
Figure 19.9b
• During ventricular systole the semilunar valves allow blood
to be ejected from the ventricles into the aorta and
pulmonary trunk.
• During diastole they prevent the back flow of blood back
into the ventricles.
– Failure to prevent the backflow of blood into the ventricles (diastolic
murmur)
• Cardiac muscle is short and striated.
• Ability to beat independent of
stimulation from the nervous
system.
– ANS
• Functional syncytium:
– intercalated discs connect
cardiac cells which allow free
passage of ions.
– This allows the spread of action
potentials from one myocyte to
another.
• The result is a coordinated
contraction that moves the
blood out of the heart.
Cardiac Muscle Cell Metabolism
• Aerobic respiration
– Large mitochondria
Rich in myoglobin
and glycogen
• Organic fuels:
– fatty acids,
glucose, ketones
• Fatigue resistant
Intrinsic Conduction System
•
•
•
•
•
Autorhythmic cells: cells that spontaneously generating action
potentials without any influence from the CNS.
Main pacemaker of the heart is the (SA node)
Sinoatrial node (SA node) sets cardiac heart rate. 
Atrioventricular node (AV node) leads into Bundle of His 
which splits into branch bundles
Purkinjie fibers carry the impulse to the ventricular myocardium
Sequence of Cardiac Excitation
• Note bundle branch and Purkinje fibers connection to
both the ventricular myocardium and papillary muscles
– This is important when considering how the ventricular
myocardium and AV valves can function in a coordinated
fashion.
Action Potential of Myocyte
Cardiac Cycle
• Cardiac cycle refers to all events
associated with blood flow through the
heart
– Systole – contraction of heart muscle
• Forces blood out of the ventricles
• This is felt when you take someone’s pulse
– Diastole – relaxation of heart muscle
• Ventricles relax allowing the heart to fill with blood
Blood Flow Through The Heart
Phases of the Cardiac Cycle
•
Ventricular filling – mid-to-late diastole
–
–
–
•
At the beginning of the cycle, the semilunar valves are
closed and the entire heart is in diastole.
Pressure in the heart blood is lower than in the vena
cavas and pulmonary veins resulting in the movement
of blood into the atria
As pressure in the atria now exceed ventricular
pressure the AV valves are open allow blood to flow
from the atria into the ventricles.
Atria systole occurs (SA) node initiates
depolarization of both atria
–
–
Represented by the P-wave on an EKG
Both atrium contract forcing atrial blood into already
filled ventricles. (End Diastolic Volume)
Phases of the Cardiac Cycle
• Ventricular systole
• Atria relax( repolarization)
• There is a slight delay prior to the initiation of the AV node.
– (pr-segment)
• This allows atrial blood time to enter the ventricles
• AV node sends action potential → to the bundle of His → branch
bundles → perkinje fibers depolarizing both ventricles leading to
the ventricle myocardium to contract.
– QRS complex on EKG
• This results in rising ventricular pressure causing the closing of
AV valves (LUB) 1st heart sound
• Isovolumetric contraction phase
• (The ventricles are contracting with all 4 valves closed )
• This allows ventricular pressure to increase rapidly.
Phases of the Cardiac Cycle
• Ventricular ejection phase: semilunar valves open once
pressure in the ventricles exceed the pressure in the aorta
and the pulmonary trunk.
– Blood will now flow out of the heart.( Stroke Volume)
– ST segment on EKG
• Isovolumetric relaxation – early diastole
– Ventricles relax represented by the T-wave on the EKG
– Backflow of blood in aorta and pulmonary trunk closes
semilunar valves making the second heart sound ( Dub)
– This marks the end systolic volume (ESV)
Cardiac Output
• The cardiac output is a measure of cardiac function.
• Cardiac functions changes based on the demands that are
placed on it.
• The heart must:
– Deliver vital nutrients such as O2, hormones and all the fuels
sources body as quickly as they are used.
– Remove CO2, urea, lactic acid… from the cells of the body
as quickly as they are produced.
– Vigorous activities will increases systemic and cardiac O2
demands while producing more CO2 that will need to be
expired.
– During strenuous activities the bodies cardiac output will
increase dramatically to meet these demands.
Cardiac Output (CO)
• HR= is the number of heart beats per minute
• EDV = amount of blood collected in a ventricle during
diastole.
• ESV = amount of blood remaining in a ventricle after
contraction
• SV = is the amount of blood pumped out by a ventricle
with each beat
– SV = end diastolic volume (EDV) minus end systolic volume
(ESV)
• CO is the amount of blood pumped by each ventricle in
one minute
– CO is the product of heart rate (HR) and stroke volume (SV)
Cardiac Output
• Normal Cardiac Output
– CO (ml/min) = HR (75 beats/min) x SV (70
ml/beat)
– CO = 5250 ml/min (5.25 L/min)
• Exercise CO can increase 7 fold
– HR (160 beats/min) x SV (220 ml/beat)
– CO = 35200 ml/min (35.25 L/min)
External Regulation of Heart Rate:
Autonomic Nervous System
• Sympathetic nervous system (SNS) stimulation
is activated by stress, anxiety, excitement, or
exercise (Fight and Flight) increase both heart
rate and force of contraction.
• Parasympathetic nervous system (PNS)
stimulation is mediated by acetylcholine and
opposes the SNS which reduces the heart rate
and force. (rest and restoration)
Extrinsic Innervation of the Heart
Regulation of HR
• The sympathetic cardiac nerve originating from
the cardioacceleratory center in the medulla of
the brain releases the neurotransmitter
norepinepherine (adrenergic agent) onto the
cells of the SA node
– causes an increase in the frequency of action
potentials in the SA node leading to an increase in
HR.
• What gates would you open to increase the frequency of
action potentials?
– Force of contraction is also increased because of the
increased uptake of extra cellular calcium.
Regulation of HR
• Parasympathetic: Stimulation via (Vagus)
nerve originating from the cardio inhibitory
center in the medulla.
• This center releases the neurotransmitter
acetylcholine (cholinergic agent) onto the cells
of the SA node
– causes a decrease in the frequency of action
potentials in the SA node leading to a decrease in HR
• What gates would you open to decrease the frequency of
action potentials?
Frank-Starling Law of the Heart
• Preload : degree of
myocardial stretch is related
to the volume of blood in the
ventricles .The greater the
stretch on the ventricular
walls, the greater the force the
myocardium will contract thus
increasing stroke volume.
– Slower heart rate increase
ventricular filling time
(venous return) increasing
SV
• How will blood loss effect
heart rate and stroke volume?
Factors Affecting Stroke Volume
• Afterload – back pressure exerted
by blood in the large arteries
leaving the heart
– The greater the afterload the
harder the heart has to work to
eject blood.
• During diastole the coronary
arteries fill with blood as blood
recoils off the aortic semilunar
valves.
• Patients with chest pain (angina)
are not getting enough blood to
meet myocardial demand.
Blood Vessels
• Blood is carried in a closed system of vessels
that begins and ends at the heart
• The three major, and types of vessels are:
– arteries, capillaries, veins
• Arteries carry blood away from the heart, veins
carry blood toward the heart
• Veins transport blood back to the heart
– 65% of blood is located in the veins
• Capillaries contact tissue cells and directly serve
as site for gas exchange
Arteries
• Blood exits the ventricle into an artery
– Aorta: blood exits the left ventricle which delivers
blood into systemic circulation.
– Pulmonary trunk: de-oxygenated blood is carried to
the lungs (pulmonary circulation)
• Arteries become more numerous and smaller in
diameter as the get further from the heart.
– As the arteries become smaller in diameter they
become arterioles
• Arterioles flow into capillaries
Capillaries
• Capillaries are location for exchange of materials
between the blood and the cells of the body.
• These vessels are the smallest diameter and are the
most numerous.
Veins
• After leaving the capillaries, blood flows into venules
• As the blood continues to move towards the heart; the
venules converge into larger diameter vessels called
veins
• The veins merge into a single vein which returns the
blood back to the atria of the heart
– Superior Vena Cava above the diaphragm.
– Inferior Vena Cava below the diaphragm.
Structure of Blood Vessels
• Arteries and veins are composed of three
tunics:
– tunica interna, tunica media, and tunica
externa
• Lumen – central blood-containing space in
the center of the vessel
• Capillaries only have an endothelium layer
necessary for exchange of gases and
nutrients.
Generalized Structure of Blood Vessels
Tunics
• Tunica interna (tunica intima)
– Endothelial layer that lines the lumen of all vessels (inner
most layer)
• Tunica media (middle layer)
– Smooth muscle and elastic fiber layer, regulated by
sympathetic nervous system
– Smaller vessels have a more muscular layer than larger
vessels
• SNS causes vasoconstriction.
– (no stimulation ) results in vasodilatation of vessels
– This will affect blood pressure and distribution)
• Tunica externa (tunica adventitia)
– Collagen fibers that protect and reinforce vessels
– Larger vessels like the aorta have more to allow them to
deal with higher pressures
Blood Flow Through Capillary Beds
• There are 5-6 liters of blood and 60 thousand miles of
vessels in the circulatory system.
Capillary Beds
• Precapillary sphincter
shunt blood to where it
is need.
• Blood flow is regulated
primarily by the SNS
• If all the precapillary
sphincters were to open
simultaneously what
would happen?
– The answer will SHOCK
you!!.
Blood Flow in Response to Needs
• Arterioles shift blood flow with changing priorities
Systemic Blood Pressure
• The pumping action of the heart generates blood
flow through the vessels along a pressure
gradient, always moving from higher- to lowerpressure areas
• Pressure results when flow is opposed by
resistance
• Systemic pressure:
– Is highest in the aorta
– Declines throughout the length of the pathway
– Is 0 mm Hg in the right atrium
• The steepest change in blood pressure occurs in
the arterioles
Systemic Blood Pressure
Velocity of Blood Flow
Arterial Blood Pressure
• Systolic pressure – pressure exerted on
arterial walls during ventricular contraction
• Diastolic pressure – lowest level of arterial
pressure during a ventricular cycle
– Pulse pressure – the difference between systolic
and diastolic pressure
Baroreceptor regulation of BP
• Increased blood pressure stimulates the
cardioinhibitory center to stimulate the vagus
nerve to:
– Decrease heart rate, cardiac output, vasodilatation of
major vessels.
• The result is reduced peripheral resistance, and a lower BP
• Low blood pressure also stimulates the
cardioacceleratory center to:
– stimulates the SNS to constrict blood vessels
• Increase blood pressure, increase cardiac output and
peripheral resistance
Baroreceptor Reflexes
Capillary Blood Pressure
• Capillary BP ranges from 20 to 40 mm Hg
• Lower capillary pressure is desirable
because high BP would rupture fragile,
thin-walled capillaries.
• Low BP is sufficient to force filtrate out into
interstitial space and distribute nutrients,
gases, and hormones between blood and
tissues.
• The artery has a much thicker tunica media and
a large lumen
• The vein is much thinner and tends to collapse
Mechanisms of Venous Return
• Several factors affect venous pressure
gradient and venous return.
– Gravity drains blood from head and neck
– Skeletal muscle pump in the limbs
– Thoracic pump
• inhalation - thoracic cavity expands (pressure )
abdominal pressure , forcing blood upward
• central venous pressure fluctuates
– 2mmHg- inhalation, 6mmHg-exhalation
– blood flows faster with inhalation
Muscle Pump
Figure 20.19a
Valves Prevent Back Flow
Capillary Exchange Filtration and Reabsorption
• Hydrostatic pressure
– physical force exerted against a surface by a liquid,
(BP is an example)
• blood (hydrostatic) pressure drives fluid out of
capillary
• high on arterial end of capillary, low on venous end
– colloid osmotic pressure (COP) draws fluid into
capillary
• results from plasma proteins (albumin)- are maintained in the
vessel drawing fluid back into the blood via osmosis
• oncotic pressure = net COP (blood COP - tissue COP)
Hypotension
• Orthostatic hypotension – temporary low BP and
dizziness when suddenly rising from a sitting or reclining
position
• Chronic hypotension –
– poor nutrition: low protein diet = low albumin levels
• Insufficient osmotic gradient to draw water back into
circulatory system
– warning sign for Addison’s disease
• Decreased Aldosterone production
• Acute hypotension – important sign of circulatory shock
– Threat to patients undergoing surgery and those in
intensive care units
Hypertension
• Hypertension can increase both cardiac preload and
afterload. Hypertension maybe transient or persistent
Chronic hypertension (140/90 mmHg) damages the arterial
walls promoting atherosclerosis and increases energy
requirements of the heart.
• Hypertension :risk factors in include diet, obesity, age, race,
heredity, stress, smoking and identifiable disorders such as
endocrine disorders.
• What hormones might contribute to hypertension?
Antihypertensive Therapy
– Beta Blockers :Block sympathetic stimulation to Beta-1
receptors located on cardiac muscle. This lowers the heart
rate and contractility reducing myocardial demand.
Increases time in diastole which increases the perfusion
time of the heart. Reduces cardiac afterload.
– Diuretics increase electrolytes elimination such as sodium
in the urine. This reduces the blood volume which reduces
blood returning to the heart. The result is a reduction in
preload.
– Ca+ channel blockers: decrease the amount of
intracellular Ca2+. The reduction in intracellular Ca2+
promotes relaxation of the myocardium and muscles
within the artery walls. The result is decreased ventricular
contractility, SV and arterial blood pressure. This will
reduce the afterload thus reducing cardiac workload.
– Nitroglycerin: promotes rapid vasodilation which can
reduce both preload and afterload. This is the drug of
choice if someone is complaining of chest pain.
Which Medication Is This?
Healthy Vessel
Atherosclerosis
Arteriosclerosis
Markers for Atherosclerosis.
• Inflammation plays a major role in the pathophysiology of
atherosclerosis.
• HDL/ LDL ratios and total triglycerides levels also give
vital information on risk of developing atherosclerosis
– Low HDL’s and high LDL and triglycerides are a
dangerous cholesterol profile
• Markers of inflammation such as high-sensitivity Creactive protein are associated with sudden cardiac
death.
Effects of Prolonged Hypertension
Angiogram
Myocardial Infarction
• Progression of coronary
artery disease
– Leads to reduced blood
flow to myocardium.
• Angina will result
• Thrombus breaks off
– Embolism travels until it
blocks the flow of blood
distal to the clot.
– Acute damage to
endothelium causes
inflammatory response that
occludes lumen.
• Lack of blood=lack of
O2
(hypoxia)=myocardial
muscle death
Angina and the Elderly
Congestive Heart Failure (CHF)
• Congestive heart failure (CHF) is caused by:
– Coronary atherosclerosis, high blood
pressure, multiple myocardial infarcts
– Look at the anatomy to figure out why you
have the symptoms and what part of your
heart is involved.
– Can be:
• Right sided
• Left sided
• Biventricular
Left Sided Heart Failure
• Left ventricle is not able to pump the blood out
as fast as it returns from the lungs. Blood backs
up to the lungs.
– Presents as fatigue and SOB with minimal exertion
as the blood backing up to the lungs.
– Orthopnea (need to be upright) Drowning in own
fluids while lying down
– Crackles in the lung bases( water in lungs)
– Cyanosis ( blue lips, and nail beds) results from
impaired pulmonary gas exchange from fluid overload
in lungs.
– Tachycardia from heart working harder.
• deliver less oxygen to tissues
• rising levels carbon dioxide
Right Sided Heart Failure
When the right side is pump blood out as fast as it
returns it will back up in both vena cavas.
Clinically you will see :
– Organomegoly: organs become swollen from blood
backing up into the inferior vena cava.
– Abdominal ascites and rapid weight gain from the
veins that would normally drain the abdomen.
– Pitting Edema usually in the both legs as blood backs
up the IVC.
– Distention of jugular vein as SVC backs up into
jugular vein
Other Causes of Edema
•  Capillary filtration from chronic  capillary BP leads
to  Capillary reabsorption.
– Hypoproteinemia (oncotic pressure  blood albumin)
– Cirrhosis and famine may lead to reduced albumin
production
– Hypertension results in excessive albumin lose in the
blood.
• Kidney failure: Not able reabsorb solutes needed to
maintain proper osmotic balance in the blood.
– Swelling will be bilaterally
• Obstructed lymphatic drainage: swelling is usually
only on the affected side.
Cerebral Vascular Accident
CVA
• Ischemic Stroke:
– Thrombus occludes
blood flow to specific
areas of the brain
causing tissue death.
• Hemorrhagic Stroke
– Ruptured blood vessel
causes blood to pool
in the cranium placing
pressure on the brain.
Cardiovascular/Respiratory
Screen
•
•
•
•
•
•
•
•
•
•
•
•
•
Shortness of breath
Chest ,back and L arm Pain
Heart palpitations
Syncope(Fainting)
Fatigue/ Weakness
Cough/ Sputum
Edema / weight gain
Cyanosis (lips,nails,skin)
Nausea
Dizziness
Changes in heart rate
Change in Respiratory Rate
Changes in distal pulses