9/18/2014

Cardiovascular System

Anatomy & Physiology

Beryl Ben C. Mergal, RN, MSN

DEVOTIONAL

Quiz #1
Label the Different Parts of the Heart.

Integration of Faith and

Learning

Proverbs 4:23
Keep thy heart with all
diligence; for out of it
are the issues of life..

Anatomy of the Heart

Location and Structure

Hollow, Muscular
Organ
Delivers oxygenated
blood to body through
arteries
When blood returns
through veins, pumps
it to lungs to be
reoxygenated

Lies obliquely in chest,

behind sternum in
mediastinum.
Located between the
lungs in front of spine.
Varies in size
depending on the
persons body size.
Estimated around 5 in
long and 3.5 in wide.

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Location and Structure

Location and Structure

MEDIASTINUM
-the central section
of the thorax
(chest cavity)
2/3 lies left of
MSL

Changes in the Heart

In older adult, becomes slightly smaller
and loses contractile strength and
efficiency.
By 70, cardiac output at rest has
diminished by about 30% to 35% in
many people.

Q: What is Oxygenation?
transport of O to all body
parts & the removal of CO.
Q: 4 Components of this Process:
1. Hgb O2 carrier
2. Blood vessels transporting network
3. Heart the pump
4. Lungs oxygenate blood

The flat, broader part.

The blunt rounded point of

the cone

Major Function of the

Cardiovascular System
Circulation of blood
_________
Delivery of O, nutrients,
_______
hormones & enzymes to
the body
Removal of CO and
________
other products of metabolism

Physiology of Oxygenation
1. Ventilation
2. Alveolar Gas
Exchange (oxygen
uptake or external
respiration)
3. 02 Transport &
Delivery
4. Cellular Respiration
3.

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1. Ventilation

Regulators of Ventilation
1. respiratory control centers in
the pons & medulla oblongata.
2. changes in the concentration of
pH & CO2 in the bodys fluid

The 1st step in the process of oxygenation.

The movement of air into and out of the lungs
for the purpose of delivering fresh air into the lungs
alveoli.

2. Alveolar Gas Exchange

3. Decrease in blood O2
concentration (hypoxemia)

2. Alveolar Gas Exchange

Once fresh air reaches the lungs alveoli, the 2nd step in
the process of oxygenation begins.
OXYGEN UPTAKE (external respiration) the exchange
of O2 from the alveolar space into the pulmonary capillary
blood.

3. O2 Transport & Delivery

3 FACTORS INFLUENCE THE CAPACITY OF
BLOOD TO CARRY O2:

1. The amount of O2 dissolved in

plasma
2. The amount hemoglobin
3. The tendency of hemoglobin to

bind with O2

4. Cellular respiration
Gas exchange at the cellular level
(also called internal respiration)
takes place via diffusion in response to
concentration gradient.
O2 diffuses fr the blood to the tissues,
while CO2 moves fr the tissues to the
blood
Then blood is reoxygenated by the lungs

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4. Cellular respiration

Heart Wall

Three Layers
1. Epicardium outermost layer and made up of
squamous epithelial cells

Gaseous Exchange

Heart Wall

Three Layers
2. Myocardium middle and thickest layer.
Made up of Myocardial cells.
Nodal cells - for pacemaker functions.
Purkinje cells-found in bundle of His, Left Bundle
Branch(LBB) & Right Bundle Branch(RBB).

Heart Wall

Heart Wall

Three Layers
3. Endocardium innermost layer, consisting of thin layer
of endothelial tissue that lines heart valves and
chambers.

Pericardium
Fluid-filled sac that envelops heart and acts as tough,
protective coating.
Consists of fibrous pericardium (tough, white, fibrous
tissue) and serous pericardium (two layers
<parietal,visceral>)

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Heart Wall

Heart Wall

Pericardium
Pericardial space separates the visceral and parietal layers
and contains 10-20ml of thin, clear, lubricating
pericardial fluid.

The 4 Heart Chambers

Functions of the Pericardial Fluid

Protects & cushions the heart & great vessels.
Provides barrier to infectious processes in
adjacent structures.

The Heart Chambers

RA receives deoxygenated blood returning
from body.
LA receives oxygenated blood from lungs.
RV receives deoxygenated blood from RA,
pumping it to the lungs for reoxygenation.
LV receives oxygenated blood from LA,
pumping it into the systemic circulation.
ATRIA are reservoirs for ventricles (thinner
walls than ventricles).

Which chamber is the thickest & why?

RA 2mm

LA 3mm

Q: What separates the

heart chambers?

Septum (a muscular wall)

RV 3-5mm

LV 13-15mm

1. INTERATRIAL septum
separates the atria
2. INTERVENTRICULAR septum
separates the ventricles

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The Heart Valves

Chordae Tendinae

Atrio-ventricular
valves:AV valves
1. Tricuspid
2. Mitral or bicuspid

Small tendinous cords

anchored to the
papillary muscles that
holds the cusps or
leaflets of the valves.
Prevents the cusps
from bulging
backward into atria
during ventricular
contraction.

Semi-lunar valves:
1. Pulmonary
2. Aortic valves

The Heart Valves

The Heart Valves

AV Valves
Tricuspid valve separates RA fr RV; mitral
valve separates LA fr LV.
Closure of AV valves associated with S1
sound.

The Heart Valves

Ventricular Diastole

Semilunar Valves
Pulmonic valve, located where pulmonary
artery meets right ventricle.
Aortic valve, located where left ventricle
meets aorta.
Closure of semilunar valves associated with
S2 sound.

ATRIOVENTRICULAR VALVES OPEN

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Ventricular Systole

Q: What causes the valves to

open and close?
Increased pressure within the ventricles
during ventricular systole causes the
pulmonic and aortic valves to open,
allowing ejection of blood into the
pulmonary and systemic circulation.
Loss of pressure as the ventricular
chambers empty causes the valves to
close.

SEMILUNAR VALVES OPEN

Atrial and Ventricular

Pressure

Blood Flow to the Heart

Pulmonary Circulation
Mitral
Valve

Systemic
Circulation

Circulation through the Heart

Circulation through the Heart

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Coronary Blood Supply

Main coronary arteries
lie on surface of heart.
Heart receives its
blood supply almost
entirely through
coronary arteries.

Coronary Blood Supply

Coronary Blood Supply

Right Coronary Artery
Supplies blood to right
atrium, right ventricle,
and inferior wall of left
ventricle.
Posterior descending
artery supplies posterior
wall of left ventricle.

Coronary Blood Supply

Left Coronary Artery

Left Coronary Artery

Splits into two major

branches: left anterior
descending, left circumflex.
Left anterior descending
supplies blood to anterior
wall of left ventricle,
anterior interventricular
septum, bundle of His,
right bundle branch, and
anterior fasciculus of left
bundle branch.

Left circumflex provides

blood to lateral wall of left
ventricle and left atrium.

Coronary Blood Supply

Coronary Circulation

Heart receives its

blood supply during
ventricular relaxation
or diastole.

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Coronary Blood Supply to the

Heart

Cardiac Veins
About 75% of total
coronary venous blood
flow leaves left
ventricle by way of
coronary sinus.

The Circulation of Blood

TERMINAL
ARTERIOLE

The artery, capillary and vein and

its layers.

POSTCAPILLARY
VENULE

CAPILLARY
BED

CAPILLARY
TUNICA EXTERNA
TUNICA MEDIA
VALVE

TUNICA INTIMA
LUMEN

TISSUE CELLS
PRECAPILLARY
SPHINCTER

TRUE
CAPILLARIES

VASCULAR
SHUNT

Arteries
DIAMETER

LOCATION

ELASTIC

>1 cm

aorta
w/ extensive ELASTIC
Pulmonary
FIBERS at tunica media
common
Serve as pressure
carotid
reservoir
subclavian
Propels blood onward
common iliac
even if the LV is relaxed

0.1 10 mm

VEIN

Arterioles

TYPES

MUSCULAR

ARTERY

DESCRIPTION

Brachial (in
w/ more SMOOTH
the arm)
MUSCLE at tunica media
Radial (in the Capable of greater
forearm
vasoconstriction &
vasodilation.

Diameter: 10-100 micrometer

w/ high proportion of vascular
smooth muscles.

offer the greatest resistance to

blood flow.
a change in diameter affects
blood pressure.

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Arterioles

Capillaries

The ff can cause

vasoconstriction or vascular
smooth muscle contraction:
1. Epinephrine
2. Norepinephrine
3. Angiotensin II

Microscopic vessels (microcirculation)

Diameter: 4-10 micrometer
Consist of tunica intima or
endothelium
Function: allows exchange of
materials between blood & tissues.
Exchange vessels

Capillaries

Venules

High BP results to the ff:

1. rupture fragile capillaries
2. force solute-containing
fluids out into the interstitial
space.

Angiogeneis
angio = blood vessel
genesis = production
Growth of new blood vessels
- during wound healing
- during endurance exercise
training

Diameter: 10-100 micrometer

Function:
collect blood from capillaries &
deliver it to veins
w/ phagocytic WBCs

Veins
Diameter: 0.1 mm - >1mm
characterized by high volume &
low pressure
Function: volume storage
contain 70% of the circulating
blood volume
w/ valves

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Cardiac Physiology

Autonomic
Innervation of the
Heart
Sympathetic nerve
stimulation causes
release of
norepinephrine, which
increases heart rate
and accelerates AV
node conduction.

Autonomic
Innervation of the
Heart

Role of Baroreceptors and

Chemoreceptors in Response to Blood
Loss

Parasympathetic
Nerve stimulation
causes release of
acetylcholine, which
slows heart rate and
conduction through
the AV node.

Control of Blood
Pressure by
Baroreceptors
Baroreceptors are
stretch receptors in
the wall of some blood
vessels. They are
involved in the
control of arterial
pressure through the
discharge of impulses
to the cardiovascular
centre when there is
distension due to a
change in the blood
pressure.

Control of Blood
Pressure by
Chemoreceptors
They are sensitive to
any change in the
chemical composition
of the blood, such as a
decrease in oxygen
level and pH of the
blood or an increase
in the carbon
dioxide level.

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Effects of Blood Pressure to the

Heart

Chemoreceptor Stimulation
and the Hearts Response
Decreased Blood O2
Increased CO2
Decreased blood Ph

Decreased
Parasympathetic
Stimulation

Increased
Sympathetic
Stimulation

Increased
Heart Rate
Increased SV
Increased BP

Transmission of Electrical
Impulses

Transmission of Electrical
Impulses

In order for the heart to contract and pump

blood to the rest of the body, an electrical
stimulus needs to occur first.
Generation and transmission of electrical
impulses depend on the four key
characteristics of cardiac cells:
automaticity, excitability, conductivity
and contractility.

Four Key Cell Characteristics

1. Automaticity cells ability to
spontaneously initiate an electrical
impulse.
2. Excitability cells ability to respond to
an electrical impulse.
3. Conductivity cells ability to transmit
an electrical impulse from cell to another.
4. Contractility cells ability to contract.

Cardiac Conduction System

Impulses travel from
SA node (hearts
pacemaker) through
internodal tracts and
Bachmans bundle to
AV node.
From AV node,
impulses travel through
bundle of His, bundle
branches, and to
Purkinje fibers.

Cardiac Conduction System

1. Sinoatrial Node

(SA Node)

Located in the RA where

the superior vena cava joins
the atrial tissue mass.
Pacemaker of the heart.
Generates impulses about
60-100 b/min (resting
conditions).
Impulses travel on specific
path but dont travel in
backward or retrograde
direction.

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Cardiac Conduction System

2. Atrioventricular Node

(AV

Node)

Located in the inferior right

atrium near ostium of the
coronary sinus.
Does not possess
pacemaker cells but the
surrounding tissue does.
AV node conducts impulses
to the ventricles.
Firing rate of 40-60 b/min.

Cardiac Conduction System

Cardiac Conduction System

3. Bundle of His
Divided into 2 branches ;
RBB & LBB
RBB extends down the right
side of the interventricular
septum and through the
right ventricle.
LBB extends down the left
side of the interventricular
septum and through the left
ventricle.
Firing rate 30-40 b/min

Cardiac Conduction System

4. Purkinje Fibers
Composed of a diffuse
muscle fiber network
beneath the endocardium
that transmits impulses
quicker than any other part
of the conduction system.
Usually doesnt fire unless
SA and AV nodes fail to
generate or when impulse is
blocked in both BB.
Firing rate 20-40 b/min

Cardiac Conduction Times

SA
(60-100/min)

AV
(40-60/min)

BUNDLE OF HIS
(30-40/min)

PURKINJE FIBERS
(20-30/min)

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Abnormal Impulse Conduction

Causes include:
Altered Automaticity
Retrograde Conduction of Impulses
Reentry Abnormalities and Ectopy

Major Electrolytes That Affect

Cardiac Function

1. K
2. Na
3. Ca

Depolarization & Repolarization

(Action Potential)
Depolarization and repolarization are
electrical activities which cause muscular
activity.
Depolarization- generation of an electrical
impulse by an electrical cell which then causes
the ions to cross the cell membrane and
causes the action potential.
Repolarization - is the return of the ions to
their previous resting state, which corresponds
with relaxation of the myocardial muscle.

2 Types Of Ion Channels:

1. Na-K pump
the fast sodium channels
2. Na-Ca pump
Slow Ca channels

Sodium-Potassium Pump

Sodium-Potassium Pump

moves Na ions back out of the

cell in exchange for an inward
movement of K ions & viceversa.
Both ions are moving against
a concentration gradient
the ratio is 3 Na : 2 K

powered by ATP

Digoxin blocks Na-K pump

Epinephrine & insulin
stimulate it, causing uptake
of K to cells.

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Sodium-Potassium Pump

The Na-K Pump

give glucose and insulin to

hyperkalemic patients
Epinephrine and insulin is
associated with hypokalemia

Sodium-Calcium Pump

POLARIZATION
resting potential

Calcium ions move into the cell to

activate contraction.
Moves Ca back into the ECF
The energy stored in the Na
gradient powers the movement of Ca.

DEPOLARIZATION
(action potential)

REPOLARIZATION
(the recovery phase)

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The Pacemaker Potential

The Cardiac Muscle Potential

Depolarization-Repolarization

Depolarization-Repolarization

Action Potential of a Cardiac Muscle

Action Potential of a Cardiac Muscle

Phase 0: Rapid Depolarization

Na moves rapidly into cell.
Ca moves slowly into cell.
Cell receives stimulus from a
neighboring cell.
Myocardical contraction occurs

Phase 1: Early Repolarization

Na channels close
Na stops flowing into the cell.
Cell is in absolute refractory
period (no stimulus, no matter
how strong, can excite the
cell).

Depolarization-Repolarization

Depolarization-Repolarization

Phase 2: Plateau Phase

Ca channels open
K channels close
Calcium continues to flow in.
Potassium continues to flow
out.
Cell is in absolute refractory
period (no stimulus, no matter
how strong, can excite the
cell).

Phase 3: Rapid Repolarization

Occurs as the cell returns to its
original state.
Ca channels close.
K flows out rapidly.
Active transport via the Na-K
pump begins restoring K to the
inside of the cell and Na to the
outside of the cell.
Cell is in relative refractory
period; however, strong
stimulus can depolarize it.

Action Potential of a Cardiac Muscle

Action Potential of a Cardiac Muscle

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Depolarization-Repolarization
Action Potential of a Cardiac Muscle

Basic Electrocardiogram

(ECG)

Phase 4: Resting Phase

Cell membrane is impermeable
to Na.
K moves out of the cell.
Cell is ready for another
stimulus.

The ECG machine is designed to recognise and

record any electrical activity within the heart.
A standard ECG is printed at 25mm per second or
25 small squares per second.

Basic Electrocardiogram

(ECG)

Basic Electrocardiogram

(ECG)

Normal Sinus Rhythm

The P Wave

Normal Sinus rhythm occurs when an impulse starts in

the sinus node and progresses to the ventricles through a
normal conduction pathway from Sinus Node, Atria, AV
node, bindle of His, to the bundle branches, and on to the
Purkinje fibers.

P wave - represents atrial depolarisation.

Location: precedes the QRS complex
Amplitude: 2-3 mm high
Duration: 0.06-0.12 sec

Basic Electrocardiogram

Basic Electrocardiogram

(ECG)

The PR Interval

PR Interval Tracks atrial impulse from atria to AV node,

bundle of His, and RBB and LBB.
Location: from beginning of P wave to the beginning of the
QRS complex.
Duration: 0.12-0.60 sec

(ECG)

The Q Wave

Q wave and represents depolarisation in the septum.

Whilst the electrical stimulus passes through the bundle
of His, and before it separates down the two bundle
branches, it starts to depolarise the septum from left to
right.

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Basic Electrocardiogram

(ECG)

The R Wave

(ECG)

The S Wave

R wave represents the electrical stimulus as it passes

through the main portion of the ventricular walls
(Ventricular Depolarization).

Basic Electrocardiogram

Basic Electrocardiogram

(ECG)

The QRS Complex

S wave and represents depolarisation in the Purkinje

fibres.
The S wave travels in the opposite direction to the large R
wave because, the Purkinje fibres spread throughout the
ventricles from top to bottom and then back up through
the walls of the ventricles.

Basic Electrocardiogram

(ECG)

The ST Segment

QRS Complex represents depolarization of

ventricles.
Location: follows PR interval
Amplitude: 5-30 mm high (differs for each lead used)
Duration: 0.06-0.10 sec

The ST segment represents end of ventricular

depolarization and onset of ventricular
repolarization.
Location: extends from the S wave to the beginning of the
T wave.
Duration: 0.08 sec

Basic Electrocardiogram

Basic Electrocardiogram

(ECG)

The T Wave

T wave represents relative refractory period of

repolarization or ventricular recovery.
Location: follows ST segment
Amplitude: 0.5 mm in leads I, II, and III and up to 10 mm
in precordial leads
Duration: 0.06-0.12 sec

(ECG)

The QT Interval

QT Interval measures timed needed for ventricular

depolarizaton and repolarization.
Location: extends from beginning of QRS complex to the
end of the T wave.
Duration: varies; usually lasts 0.36-0.44 sec

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Basic Electrocardiogram

ECG Waveform
COmponents

(ECG)

The U wave

U wave represents repolarization of His-purkinje

system.
The U wave may not appear on an ECG. A prominent U
wave may be due to hypercalcemia, hypokalemia, or
digoxin toxicity.

Cardiac Contraction

The Physiology of the

CARDIAC CYCLE

Basic Phases of the Cardiac

Cycle
Relaxation

Atria Ventricles
AV Node delays impulses
travelling from Atria to
Ventricles.

Ventricular Systole
Contraction

Contraction
Filling

Ejection

SYSTOLE

Muscle contraction is
initiated by action potentials
that normally originate from
a pacemaker site (SA Node)
in the right atrium.
Action Potentials depolarize
cells, causing contraction.
Sequence of contraction

DIASTOLE

Systole
Begins with ventricular contraction.
Ends when ejection ceases.

Diastole
Begins when ejection ceases as ventricles relax
Ventricular filling begins after sufficient relaxation occurs.

Filled volume is the End

Diastolic Volume
Initiated by ventricular
depolarization (QRS of ECG
LVP increases
AV Valve Closes
LV contraction is initially
isovolumetric

Ejection
Outflow valves open
Repolarization (T wave of
ECG) initiates relaxation
causing ejection rate to
rapidly decline.
Residual volume after ejection
is End Systolic Volume

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Atrial Systole

Ventricular Diastole

(Contraction & Ejection)

Relaxation
Initiated by repolarization (T
wave of ECG)
LVP decreases
Outflow valves close (begins
diastole)
Initially Isovolumetric

Ejection
AV valves open when LV
pressure < atrial pressure.
Most ventricular filling occurs
before atrial contraction.
Maximal filled volume is enddiastolic volume.

Initiated by
depolarization (P wave
of ECG)
Occurs near end of
diastole
Atrial pressure
transiently increases (a
wave), forcing
additional blood into the
ventricles.
Accounts for 10% of
ventricular filling at
resting (up to 40%
during exercise)

Cardiac Cycle and its

Relationship to the ECG

Atrial Diastole

(Relaxation & Filling)

Blood continously
enters the atria, except
when transiently
impeded during atrial
systole.
Occurs throughout
ventricular systole and
diastole (until P wave of
ECG).
AV valves suddenly
open when LV pressure
< atrial pressure
(creating the v wave).

Average, Normal Intracardiac

and Vascular Pressures (mmHg)

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Stroke Volume
Ventricular Stroke volume is the difference
between ventricular end-diastolic volume
(EDV) and end-systolic volume (ESV).

SV = EDV - ESV
In a normal heart, EDV-ESV is the same
volume of blood as ejected into the aorta
during each systole.

Stroke Volume

3 Factors Determine Stroke Volume

1. PRELOAD the vol of
blood in the ventricles at
the end of diastole,
before the next
contraction. (Lewis, et al 2008)

proportional to the
end-diastolic volume
(EDV).

Q: Factors AFFECTING
Preload
b. Ventricular compliance
the elasticity when blood enters
ventricle.
Conditions that elasticity:
When muscle thickens =Hypertrophy
increased fibrotic tissue within the
ventricle = after MI
cardiac tamponade

Stroke Volume

3 Factors Determine Stroke Volume

1. PRELOAD
the distending force
that stretches the
ventricular muscle during
ventricular relaxation

(Woods, 2010).

Can be compared to
the stretching of a rubber
band.

Q: Factors AFFECTING
Preload

a. Venous return
the vol of blood that enters
the ventricle during diastole.
Conditions venous return:
Fluid overload

Frank Starlings Law of

the Heart

The > the volume,

the > the stretch of the
cardiac muscle,
the > the force of
contraction to accomplish
emptying.

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Frank Starlings Law of the

Heart

Has physiologic limit

Overstretching of the
cardiac muscle fibers
eventually results in
ineffective contraction.

Conditions that Decreases

Preload

Hemorrhage
Fluid shifting to 3rd space
vasodilation

Conditions that Increases

Preload

Stroke Volume

CHF
Renal disease
Vasoconstriction
Hypervolemia
Regurgitation of cardiac valves

2. CONTRACTILITY

Q: Why do you think blockage of coronary

arteries affect the hearts contractility?

Q: What are the substances

that increases contractility?

3 Factors Determine Stroke Volume

the forcefulness of

contraction of ventricular
muscle fibers.

Q: WHAT will happen if

contractility is poor?
Poor contractility =
reduction of CO

positive inotropic agents.

1. Dopamine
2. Dobutamine
3. Dopexamine
4. Epinephrine (adrenaline)
5. Isoprenaline (isoproterenol)
6. Norepinephrine
7. Digoxin
8. Digitalis
9. Insulin

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Q: What are the substances

that decreases contractility?

negative inotropic agents.

1. Beta blockers
2. Calcium channel blockers
a) Diltiazem
b) Verapamil
c) Clevidipine
3. Class IA antiarrhythmics such as
a) Quinidine
b) Procainamide
c) disopyramide
4. Class IC antiarrhythmics such as
a) Flecainide

Stroke Volume

3 Factors Determine Stroke Volume

Stroke Volume

3 Factors Determine Stroke Volume

3. AFTERLOAD
the force that the
ventricles must generate
to eject blood.
Amount of pressure left
ventricle must work
against to eject blood
during systole.

Determinants of LV AFTERLOAD

Resistance

3. AFTERLOAD
Factors Affecting Afterload
1. Diameter of the aorta &
pulmonary artery.

Systemic Vascular
Resistance (SVR)

2. Opening and competence of

the pulmonary & aortic valves.

HPN
Aortic Valve
Stenosis

The FORCE

Determinants of RV AFTERLOAD
Resistance

The FORCE

Pulmonary vascular
resistance (PVR
CONGESTED
LUNGS
Pulmonic Valve
Stenosis

Ejection Fraction
Ejection Fraction (EF) is the fraction of
blood ejected by the ventricle relative to its
filled volume (end-diastolic volume).

EF is a measure of the ability of the heart

to eject blood.
EF is normally about 0.55-0.65 (55%-65%)

PULMONARY
EMBOLISM

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Cardiac Output
Cardiac Output is the amount of blood the
left ventricle pumps into the aorta per
minute.

=
Normal cardiac output is 4-8L per
minute, depending on body size.

Sample Computation
(Compute the SV, EF & CO)
HR = 70/min

End diastolic volume

End systolic volume

= 120 ml
= 50 ml

Ejection volume (stroke volume) =

Ejection fraction = 70ml/120ml =

70 ml
58%

(normally 60%)
If heart rate (HR) is 70 beats/minute, what
is cardiac output?
Cardiac output
= HR x SV
= 70/min * 70 ml
= 4900ml/min

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