INTEGRATED BIOLOGICAL BASES

Cardiovascular System I

WEEK 1
Review Structures

Base

 Broad, flat base, or posterior surface of the heart

 Directed towards the right shoulder

Apex

 Points inferiorly toward the left hip

 Apical pulse – caused by your beating hearts apex where it touches the chest wall
o Found between the 5th and 6th rib just below the nipple
 Formed by the left ventricle

Atria

 The receiving chambers

o The right and left atria

STRUCTURE = small, wrinkled, protruding appendages called auricles (increase atrial volume)

 Right atrium – two basic parts:

o Smooth-walled posterior part
o Anterior portion that has bumbles of muscle tissue that forms ridges in the walls
o Posterior and anterior part are separated by a C-shaped ridge
 Left atrium
o Mostly smooth and pectinate muscles are found in the auricles
o In a fetal heart  has an opening called the foramen ovale

FUNCTION = receiving chambers for blood returning to the heart from the circulation

 Small and thin=walled chambers because they need to contract minimally to push blood to the
ventricles
 Blood enters the right atrium through THREE veins
o Superior vena cava: returns blood from body regions superior to the diaphragm
o Inferior vena cava: returns blood from body areas below the diaphragm
o Coronary sinus: collects blood draining from the myocardium
 Blood enters the left atrium though FOUR pulmonary veins
o Makes up most of the hearts base
o Transport blood from the lungs back to the heart
o Seen in the posterior view of the heart

Ventricles

 The ventricles make up most of the volume of the heart

 Discharging chambers  the pumps of the heart

STRUCTURE

 Right ventricle forms most of the hearts anterior surface

  Left ventricle forms most of hearts posteroinferior surface (back and below)
 Features:
o Trabeculae carneae: irregular ridges of muscle that mark the internal walls of the
ventricular chambers
o Papillary muscles: play a role in valve function

FUNCTION

 Thick walls = ventricles contract and propel blood out of the heart into the circulation
 Right ventricle
o Pumps blood into the pulmonary trunk
 Sends blood to the lungs where gas exchange occurs
 Left ventricle
o Pumps blood into the aorta
 Largest artery in the body – pumps the blood to the rest of the body

Pericardium

 Pericardium: double walled sac that encloses the heart

STRUCTURE

 Fibrous pericardium: loosely fitting superficial part of the sac

o Made up of tough, dense connective tissue
 Serous pericardium: thin, slippery, two-layer serous membrane that forms a closed sac
around the heart
o Parietal layer: lines the internal surface of the fibrous pericardium
o Pericardial cavity: between the parietal and visceral later and is contains a film of
serious fluid (space)
 Do not like when this later fills up
o Visceral layer: inner most layer of the pericardium; is directly covering your heart
 Also known as the epicardium

FUNCTION (4)

 Fibrous pericardium
o Protects the heart (cushion)
o Anchors it to surrounding structures
o Prevents overfilling of the heart with blood
 Prevents from overfilling or stretching – can overcompensate but it wont do it
quickly
o Prevents friction
 The serous membrane (lubricated by the fluid in the parietal layer) glides
smoothly past one another and allows the heart to work in a relatively friction
free environment
Wall Layers

 The heart wall is richly supplied with blood vessels

STRUCTURE

 Composed of three layers =

o Epicardium: the visceral later of the serous pericardium
 Can be infiltrated with fat
o Myocardium: composed mainly of cardiac muscle
 Middle layer
 Forms bulk of the heart
 Supported by connective fissure fibres that reinforce the later internally and
anchors the cardiac muscle fibres
o Endocardium: glistening white sheet of endothelium that is resting on a thin
connective tissue later
 “Inside the heart”
 Located on the inner myocardial surface – lines all heart chambers
 Smooth surface because if it wasn’t then platelets would stick to it and form
blood clots.

FUNCTION

 The myocardium = muscle heart

o Contracts the heart
o Branching cardiac muscles are tethered to one another by crisscrossing connective
tissue fibers and arranged in cardiac muscle bundles
Valves (AV vs SL)

 Blood flows through the heart in ONE direction

o From atria to ventricles and out the greater arteries
 There are FOUR valves that enforce the “one way traffic”
o (1) Atrioventricular valves (AV) – tricuspid valve and mitral valve
o (2) Semilunar valves (SL) – aortic valve and pulmonary valve
 Location of heart sounds:
o You are hearing the turbulence after the valves close

FUNCTION (2)

 Prevent backflow of blood

 Open and close in response to pressure

S2 = best heart at aortic

S1 = best heart at mitral

1. Atrioventricular Valve (AV)  atrium + ventricular
 There are 2 – one located at each atrial-ventricular junction
 Main function  to prevent backflow into the atria when the ventricles contract

STRUCTURE

 Right AV = tricuspid valve

o Three flexible cusps (flaps of endocardium reinforced by connective tissue cores)
 Left AV = mitral valve
o Two cusps
o Sometimes called bicuspid valve
 Each AV valve flap is attached to a chordae tendineae (tiny white collagen cords) and anchor to
the muscles protruding from the ventricular wall
o Also known as “heart strings”

FUNCTION

 When the heart is relaxes the AV valve flaps are OPEN

 Blood flows into the atria and then through the OPEN AV valve into the ventricles below
 When ventricles contract (compressing the chamber) the intraventricular pressure rises, which
forces the blood against the valve flaps and the valve CLOSES
o The chordae tendineae anchor the valve flaps in their CLOSE position
 KEY – when the heart is relaxed AV is OPEN; when the heart contacts AV is CLOSED

2. Semilunar (SL) Valves

 There are 2 – aortic and pulmonary valves

 Guard the bases of the large arteries issuing from the ventricles
o Aorta and pulmonary trunk

STRUCTURE

 Each SL valve has THREE cusps

 Shaped like a crescent moon  semilunar = half moon

FUNCTION

 Prevent back flow into the aorta and pulmonary

 The SL valves open and close in response to different pressures
o When the ventricles CONTRACT and intraventricular pressure rises above the pressure in
the aorta and pulmonary trunk – the SL valves are forced OPEN and blood rushes
through them
 o When ventricles RELAX and the blood flows back toward the heart the cusps and
CLOSES the valves
 Decrease pressure then the valves close; pressure increases and valves open

KEY – when the heart is relaxed SL is CLOSED;

when the heart contacts SL is OPEN

AV Open and Closed

 A-V Valves OPEN and allow blood to flow from atria into ventricles when ventricular pressure is
lower than atrial pressure
o Occurs when ventricles are relaxed  chordae tendineae are slack and papillary muscles
are relaxed
 A-V Valves CLOSE preventing backflow of blood into atria
o Occurs when ventricles contract, pushing valve cusps closed, chordae tendineae are
pulled taut and papillary muscles contract to pull cords and prevent cusps from everting
Directional Flow

 Blood flows from the atrium to the ventricle

and then to the lungs OR the rest of the
body
 Left side of the heart is the systemic circuit
pump
 Right side of the heart is the pulmonary
circuit pump
 Veins carry oxygen poor blood to the heart;
arteries carry oxygen rich blood from the
heart
 Equal volumes of blood are pumped into the
systemic and pulmonary circuits but the two
ventricles have unique work loads
o Pulmonary circuit
 Served by right ventricle
 Short, low-pressure
circulation
o Systemic circuit
 Left ventricle
 Long pathway through the
whole body and encounters
about 5 times as much
friction/resistance to blood
flow
o Function difference is revealed in the anatomy of the two ventricles
 The walls of left ventricle are 3 times thicker than those of the right ventricle
 Its cavity is almost circular
 The right ventricle cavity is flattened into a crescent shape that partially encloses
the left ventricle
 Like a hand loosely grasping a clench fist
 The left ventricle can generate much more pressure than the right and has a far
more powerful pump
 Normal Intracardiac Pressures
Less
pressure= Mean ((mmHg) Range (mmHg)
less muscle Right Atrium 4 0-8
Right Ventricle Increase muscle
Systolic 24 15-28 size = harder to
More muscle End-diastolic 4 0-8 contract
to deal with Left Atrium 8 4-12
high pressure Left ventricle
 Systolic 130 90-100
End-diastolic 7 4-12
Coronary Circulation

 Coronary circulation: the functional blood supply of the heart and the shortest circulation in
the body
o How the heart gets nourishment and removes waste

o Arterial supply = bring nutrients to body

o Venous supply = take nutrients away from body
 Coronary arteries
o The left and the right coronary arteries come from the base of the aorta and encircle the
heart in a coronary sulcus
o Coronary arteries: provide arterial supply of the coronary circulation
 Left coronary artery – runs toward the left side of the heart and divides into
two major branches:
 Anterior interventricular artery: follows the anterior interventricular
sulcus and supplies blood to the interventricular septum and anterior
walls of both ventricles
 Circumflex artery: supplies the left atrium and the posterior walls of
the left ventricle
 Right Coronary Artery – courses to the right side of the heart (right atrium
and almost all the right ventricle) and divides into two branches:
 Right marginal artery: serves the myocardium of the lateral right side
of the heart
 Posterior interventricular artery: runs to the heart apex where it
merges with the anterior interventricular artery and also supplies the
posterior ventricular walls
 Complete blockage of a coronary artery leads to tissue death and heart attacks
 Coronary arteries provide an intermittent, pulsating blood flow to the myocardium
 The coronary arteries lie in the epicardium and send branches inward to nourish the
myocardium
 Blood gets delivered when the heart is
relaxed
o Ineffective when ventricles are
contracting as they are compressed
by the contracting myocardium
 The left ventricle receives most plentiful
blood supply
 The heart requires about 1/20 of the body’s
blood supply

 Coronary veins
o After passing through the myocardium the venous blood is collected in the cardiac veins
 The paths roughly follow those of the coronary arteries
o The veins join to form an enlarged vessel called the coronary sinus
 Coronary sinus: empties blood into right atrium
 Found on the posterior aspect of the heart
o Coronary sinus has three large tributaries:
 Great cardiac vein – in the anterior interventricular sulcus
 Middle cardiac vein – in the
posterior interventricular
sulcus
 Small cardiac vein – running
along hearts right inferior
margin
Blood Flow

 Starts on outside of the cell

 If the diastole BP is too high, there can be a problem

 Systole – minimal blood flow

o Muscle contraction

 Diastole – lots of blood flow (most)

o Muscle relaxation

 Anastomoses: create new pathways

Cardiac Cycle

- Right side of the heart receives oxygen poor blood from body tissues
o Flows through the superior vena cava and inferior vena cava into the right atrium
o Flows through the tricuspid valve into the right ventricle
- Then pumps the blood to the lungs to pick up oxygen and dispel CO2
o Travels through the pulmonary semi lunar valve to the pulmonary truck
o Splits off into the pulmonary arteries to the lungs
- The left side of the heart receives the oxygenated blood returning from the lings
o Travels back into the left atrium through the 4 pulmonary veins
o The blood fills the left atrium and into the left ventricle after pushing through the
mitral valve
- Then pumps the blood throughout the body to supply oxygen to body tissues
 o Blood fills the left ventricle and then passes through the aortic semilunar valve to
the aorta
o The blood is pumped through the aorta to the body

Cardiac Cycle  Marked by a succession of pressure and blood volume changes

 Cardiac cycle: describes the mechanical events associated with blood flow through the heart;
includes ALL events associated with the blood flow through the heart during one complete
heartbeat
o One complete heartbeat = arterial systole and diastole followed by ventricular systole
and diastole
 EDV: end diastolic volume
o Occurs in ventricle after heart has filled (120mL)
o Maximum volume of blood the ventricles will contain in a cycle
 ESV: end systolic volume
o After ejection of blood (50mL)
o Blood that is remaining in the chambers after ejection
 Stroke Volume: difference between EDV and ESV EDV – EDS = SV
o Volume ejected from each ventricle, each beat

MAIN EVENTS

 Ventricular filling (mid to late diastole)  periods of relaxation; passive

o Ventricular filling:
 Ventricles are filling up with blood from the atrium
 Pressure in the heart is low at this point
 Blood returning to heart is flowing passively through
 OPENS AV valves into ventricles
o Atrial contraction:
 Atrium contracts pushing the blood into the ventricles through the AV valves
 AV valve = open
 SL valve = closed

 Ventricular systole (atria to diastole)

o Isovolumetric contraction phase:
 Atria relax, ventricles begin contracting
 Pressure builds up in ventricles cause AV valves to close (ALL VALVES CLOSED)
o Ventricular ejection phase – stoke volume
 Semi lunar valves open
 Blood rushes from the ventricles into the aorta and pulmonary trunk
 Pressure in aorta reaches about 120 mmHG
 AV valve = closed Will always still have
 SL valve = open some blood left after
“emptying” because
 Early Diastole you don’t want
o Isovolumetric relaxation: bubbles
  Ventricles relax
THEN REPEAT  Blood remaining is no longer compressed, and pressure drops
 Closes the semilunar valves
 AV valve = open
 SL valve = closed
Ventricular Volumes

 what happens on the left happens on the right

Ventricular Pressures
Complete Cardiac Cycle – ECD and Heart Sounds

- What you hear is the turbulence

around the valves closing

- This is everything together 

AV valves close = “LUB”  S1

Semi lunar valves close = “DUB”  S2

Possible to have S3 and S4 if extra

volume and problems with the heart

Cardia Output

 Definition: amount of blood ejected by each ventricle in one minute

Stroke volume and heart rate are regulated to alter cardiac output

CO = SV x HR

o CO = cardiac output
 UNITS: L/min
o SV = stroke volume
 UNITS: mL/beats
 The volume of blood pumped out by one ventricle with each beat
 Correlates with the forced of ventricular contraction
o HR = heart rate
 UNITS: beats/min

 average CO = 70 x 75 = 5250 mL/min OR 5.25 L/min

 Why? – gives us an idea of the supply and demand on a persons cardiac system

 Cardiac Reserve: difference between minimum CO and maximum CO at rest

o Nonathletic people – cardiac reserve is typically 4 or 5 times the resting CO
o Trained athletes during competition – cardiac reserve may reach 7 times the resting CO

When max CO = CO at rest  major cardiac arrest

Influences of Stroke Volume

 Preload – amount ventricles are stretched by contained blood

 Contractility – cardiac cell contractile force due to factors other than EDV
 Afterload – back pressure exerted by blood in the large arteries leaving the heart

o Can work together OR separately to affect the SV

o Creates capacity to meet the demands of the body

PRELOAD : Degree of Stretch of Heart Muscle

 Preload: the degree to which cardiac muscle cells are stretched just before they contract
o Controls stroke volume
 Stretch required on ventricles to accept volume of pressure
 Pressure to fill decreases after each time – similar to blowing
up a balloon for the first time

 Higher preload = higher stoke volume

Frank-Starling Law of the Heart

 Relationship between preload and stroke volume

o Definition: The more muscle is stretched, the greater the force of contraction; with
more blood, more force of contraction results…within limits

 Effects on Preload

PRELOAD STRETCH
CONTRACTILITY

 Contractility: Cardiac cell contractile force due to factors other than EDV
 Inotropic state of the myocardium – normal
o Ability for myocardium to contract
 Ability of cardiac muscle to shorten when electrically stimulated

 INCREASE CONTRACTILITY  Positive tropic agents increase the ability to shorten

o EXAMPLES:
 Calcium
 Epinephrine
 Digoxin
 DECREASES CONTRACTILITY  Negative tropic agents limit the ability to shorten
o EXAMPLE
 Calcium channel blockers
 Anesthetics
 Potassium
 Decreased oxygen
 Acidosis

AFTERLOAD

 Afterload: back pressure exerted by blood in the large

arteries leaving the heart
 Resistance the heart must pump against – Pushing open
the door against a strong wind

 On the other side of semilunar valves

 Increase resistance due to hypertension

 Increased afterload requires increased contraction

AFTERLOAD CONTRACTION

 Decreases afterload:
 o Diuretics
o Vasodilators

Regulation of Cardiac Output

Cardiac Muscle Cells

 Cardiac muscle is also known

as striated involuntary muscle
 Can only be found in one
organ of the body – the heart
 These cells form the bulk of
the wall of the heart and
shares features with both
smooth and skeletal muscles

 Mitochondria takes up 25% of

the space of a muscle cell
o Bigger because of the need for increase energy
  Do not want cells separating – want them all connected
 Has smooth ER but it is modified

Comparison of the Three Muscle Types

Skeletal Smooth Cardiac

Appearance under Striated Smooth Striated
light Microscope *

Fiber Arrangement Sarcomeres No sarcomeres Sarcomeres

Location Attached to bones Forms the walls of Heart muscle

hollow organs and
tubes

Tissue Morphology * Multinucleate; large; Uninucleate; small Uninucleate; shorter

cylindrical fibers spindle-shaped fibres branching fibres

Internal Structure T-tubule and No t-tubules; T-tubule and

sarcoplasmic reticulum sarcoplasmic reticulum sarcoplasmic reticulum
(SR)

Fiber Proteins Actin, myosin; troponin Actin, myosin; Actin, myosin; troponin
and tropomyosin tropomyosin and tropomyosin

Control *  Ca2+ and troponin  Ca2+ and  Ca2+ and troponin

 Fibres independent calmodulin  Fibers electrically
of one another  Some fibres linked via gap
 Ca2+ from SR electrically linked junctions
via gap junctions;  Ca2+ from ECF and
others independent SR
 Ca2+ from ECF and
SR

Contraction Speed Fastest Slowest Intermediate

Contraction Force of Not graded Graded Graded

Single Fiber Twitch

Initiation of Requires ACh from Stretch, chemical Autorhythmic

Contraction * motor neuron signals. Can be
autorhythmic

Neural Control of Somatic motor neuron Autonomic neurons Autonomic neurons

Contraction
 Hormonal Influence None Multiple hormones Epinephrine
on Contraction

Factors that INCREASE muscle

contraction:

- Catecholamines
- Digoxin
- Increased afterload
- stress

Sarcomeres Identify the intercalated disks

 The basic contractile unit of muscle fibres – basic unit of muscle contraction
o Very carefully arranged
 Contain two types of myofilaments = actin and myosin
 Cardiac sarcomeres branch in a variety of areas
 Rich blood supply
 Within each sarcomere there is a significant number of mitochondria
o Reflection of the energy output required
 The muscle fibers have T-tubules and
some sarcoplasmic reticulum
 Arranged differently than skeletal
muscle fibers and this is important
because:
 o Much of the calcium that enters the sarcoplasm during contractions enters from outside
the cell through the t-tubules rather than from storage

 Contains 2 types of myofilaments – actin and myosin

 Structural proteins hold the myosin filaments together along the M line and actin along the z

line
 Myofilaments form a geometric pattern in which each myosin filament interacts with 6 actin
filaments
 One myosin molecule contains 2 rod segments and a 2 sided head unit
o Myosin head has limited range of motion
o Binding sites to ATP and actin
 Actin filament consists of double chain of actin molecules and regulatory proteins – tropomyosin
and troponin

T-Tubules

 The T-tubules in cardiac cells

o Fewer in number
o Wider than in skeletal muscles
o Aligned with the z-discs

Arrangement
  Cardiac muscle fibres are very carefully arranged in many rod-like myofibrils
 The sarcomere organization has several different names
o M line – thick filaments linked by accessory proteins  myosin
o Z disks  actin
o H zone
o A band – thick and thin filaments overlap
o I band – thin filaments only
 Relationship between actin and myosin arrangements

Sliding Filament Theory

 DO NOT SHORTED BUT SLIDE PAST EACH OTHER

 Thin filament pulls them closer together and muscle contracts  H zone shortens

 Thick filament – has 2 binding sites

o 1) ATP
o 2) Actin

Matching Question – ONLINE MODULE

 Actin  thin filament

 Myosin  thick filament
 These two things bind on the head of this molecule  actin and ATP
 T-tubules  deliver calcium
 Basic unit of muscle contraction  sarcomere
  Prevents cells from separating during contraction  desmosomes
 Allows ions to pass from cell to cell and transmit current across the heart  gap junctions
 Actin filament contains double chain of actin molecules and these two proteins  troponin and
tropomyosin

Cardiac Markers

 Troponin: intracellular regulator protein; we measure this because it is a good indicator of

cardiac muscle damage  will tell us if significant amount of troponin is escaping into
circulation
o
 High troponin = loss of integrity of cell membrane, results in MI; plasma membrane is semi-
permeable and troponin regularly inside the cell
o Troponin T – most common; binds to myosin
Unique to
 Unique to cardiac muscles
heart
o Troponin I – inhibits binding of actin to myosin
 Unique to cardiac muscles
o Troponin C – binds to calcium
 Calcium is bound; used in other muscles

 CK (Creatine Kinase) – enzyme in muscle cell; can be released, when this happens there is
Mean the muscle damage
same o Used in Canada and US
thing
 CPK (Creatine Phosphokinase)
o Used in Europe
o Enzymes in muscle – damage when released

o Isoenzymes – CKMB (cardiac muscles) / CKMM (skeletal) / CKBB (brain)

 Old and not used often

 No IM injections for patients with cardiac issue

o Only IV because you are destroying skeletal muscles and CK will increase, and values
will be off

Cardiac Conduction System

 Remember difference between excitatory cells and muscular cells

 Heart muscle:
o Is stimulated by nerves and is self-excitable (automaticity) – don’t require outside
source
 o Contracts as a unit
o Has a long (250 ms) absolute refractory period
 Cardiac muscle contraction is similar to skeletal muscle contraction

 Cardiac muscle contraction – the molecular basis of muscle contraction

o Muscle contraction is initiated by stimulation of a motor nerve
o The action potential travels down the nerve to the motor end plate
o Spreads across sarcolemma and into T-tubule system
o The t-tubule membrane is depolarized which activates dihydropyridine receptor
o Calcium leaves the T-tubule, travels to sarcoplasmic reticulum and there it activates the
ryanodine receptor
o This opens the calcium channel which releases calcium into the cytoplasm
o Calcium bonds to troponin, causing troponin to shift and expose actin. Myosin binds to
actin
o Myosin ATP A's hydrolyzes ATP forming ADP and phosphate
o The release of phosphate changes the angle of head unit this causing a power stroke
which moves the actin filament. ADP is replaced by ATP
o Power strokes occur along all myosin filaments in sarcomere
o Calcium transports into endoplasmic reticulum by calcium pump
o Without calcium, troponin can resume its inhibitory position preventing myosin from
bonding to act  This allows actin filaments to slide back to resting position.

o In conclusion: Muscle contraction is caused by myosin-actin interactions, regulated by

calcium.

Pacemakers – SA node (has how action potential)

 Heart muscle is stimulated by nerves and is self-excitable (automaticity)  Can generate its
own impulse
 Contracts as a unit (atria contract together and ventricles contract together)
 Has a 250ms absolute refractory period (LONG!)

 Autorhythmic cells:
o Initiate action potentials
o Have unstable resting potentials called pacemaker potentials
o Use calcium influx (rather than sodium) for rising phase of the action potential
o Approx. 1% cardiomyocytes have capacity to generate impulses

Pacemakers Action Potentials

  No flat lines
o Not waiting for something to get it going

Pacemaker Stimulation

 Epinephrine
o Increase heart rate, increases slope
o Increase time to get to action potential by changing the slow of pacemaker potential
 Acetylcholine
o Decreases slope
o Takes longer to reach threshold therefore slow down
 Manipulating threshold manipulates HR

Electrical Pathway
 Sinoatrial (SA) node – “ruling pacemaker” regulates heart rate
o 60-100 bpm is normal
 Atrioventricular (AV) node delays the impulse approximately 0.1 second
o Can rake over if the SA node stops working but only goes 40-60
 Bundle of His = Atrioventricular Bundle
o After electrical impulse is sent from the sinoatrial (SA) node to the atrioventricular (AV)
node, the bundle of his quickly transmits the impulse to the left and right bundle
branches and into the ventricles
 Resulting in a synchronized contraction pf the ventricles
o Located under the AV node
o Bundle branches split into 2 pathways going to each ventricle
 Purkinje Fibres or Network (Subendocardial conducting network)
o Completes the pathway through the interventricular septum
o Penetrates the heart apex, and then turns superiorly into the ventricular walls.

 Increase to 100 =tachy

 Below 60 = brady

 30-40  not enough for what our body needs

ECG – Electrocardiogram

 The electrical currents generated in and transmitted through the heart spread throughout the
body and can be detected with a device called an electrocardiograph.
 An electrocardiogram (ECG) is a graphic record of heart activity. An ECG is a composite of all
the action potentials generated by nodal and contractile cells at a given time.

P WAVE

- This is an example of a normal P wave, reflecting normal SA node firing and if the SA node fired
at a rate between 60 to 100bpm then this part of the rhythm would be considered normal sinus
rhythm.
What electrical activity is taking place:

What happens during this part of the cardiac cycle

Directly link this to the ECG waveforms

CONTRACTION

 Absolute – No impulse can go through, forces the heart to rest

 Calcium released as needed for contraction

PHYSIOLOGY OF CONTRACTION
PR INTERVAL

-
- Reflects the normal delay from the SA node to the AV node
- If the SA node fired at a rate between 60 to 100 then this part of the rhythm would be
considered normal sinus rhythm

PR INTERVAL

- Reflects the normal delay from the SA node to the AV node.

- Implications of a delay or block between the SA and AV node:

HEART BLOOCK – 1st Degree

{ The easiest to understand }

 Some level of blockage between the atria and when the electrical activity goes down into the ventricles
 On the ECG – a longer day between the first P wave and the QRS complex
HEART BLOCK – 2nd Degree

HEART BLOCK – 3rd Degree

ATRIAL FIBRILLATION -- not required to know

- Picture on left = normal sinus rhythm

o Reflects normal electrical pathways
 Sinus node or the SA node fires one firing at a time
 Depolarizes the entire atrium in a unit
 It moves down to the AV node
 Then to the rest of ventricular fibres
o Looking at the ECG you can see a small positive deflection right before the positive spike
 This is the P wave before the spike (orange arrows) and that is the normal
pathway
- Picture on right = atria are uncoordinated in its electrical activity (AFIB)
o A variety of electrical foci independently firing and only a couple get to the AV node
down into the ventricles
o Looking at the ECG you can see there is a variety of “bumps” before the upward spike
 There isn’t a coordinated effort or contraction
o Some people with the loss of an atrial kick will become compromised due to
decrease in cardiac output
Effects of Myocardial Ischemia, Injury, and Infraction on the ECG

 When you are looking at an ECG you are normally looking for abnormal electrical condition that occurs
in any areas of cardiac muscle damage
o Don’t have to know for purpose of course

NORMAL

INFRACTION

INJURY
ISCHEMIA