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Cardiac Physiology and the ECG
Week 24 LOs
1. Outline the sequence of events in the cardiac cycle including the electrical sequence,
pressure changes and opening and closing of the valves
Cardiac Cycle
– cardiac events that occur from the beginning of one heartbeat to the beginning of the
next
– initiated by spontaneous generation of an action potential in the SV node → rapidly
through both atria → through the AV bundle → ventricles
– delay > 1/10 sec in passage of impulse from atria to ventricles, allowing atria to contract
ahead of ventricles, acting as primer pumps, with the ventricles then providing the
major source of power for moving the blood through the vascular system
- diastole – relaxation where heart fills with blood
- systole – contraction
Cardiac cycle in a nutshell:
–
–
initiated by spontaneous generation of an action potential in the SV node →
moves through atria and both atria contract:
o opening the AV valves
o pushing blood into ventricle
o
–
–
–
increase in ventricular volume (although ventricles have also been filling during
diastole)
o increase in atrial P and decrease in atrial vol
impulse moves → through the AV node (there is a delay here) → to the bundle of His
and then through the Purkinje fibres
ventricles contract:
o AV valves close
o semilunar valves open
o increase in ventricular P and decrease in vol
o increase in atrial P due to bulging of AV vales into atria
o blood flows into aorta and pulmonary artery
o high P in arteries causes the semilunar valves to snap shut
atria begin to fill again
in more detail:
Impulse Conducting System
 consists of specialized cells that initiate the heartbeat and electronically coordinate
contractions of the heart chambers
 SA (sinoatrial) node
o small mass of specialized cardiac muscle fibres in the wall of the right atrium
near the SVC
o initiates electrical impulse for contraction
 Atrioventricular (AV) node
o beneath endocardium in the inferoposterior part of the interatrial septum
 Bundle of His
o distal to AV node and perforates the interventricular septum posteriorly
o
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bifurcates within the septum into a broad sheet of fibers that continues over the
left side of the septum – left bundle branch and a compact cable-like structure
on the right – right bundle branch
Left bundle branch
o functionally divided into anterior and posterior fascicle and a small branch to
the septum
Purkinje Fibres
o subendocardial plexuses of both ventricles send distributing Purkinje fibres to
the ventricular muscle
o impulses within the HIS-Purkinje system – transmitted first to the papillary
muscles and then to the walls of the ventricles (so the papillary muscles contract
first) – this prevents regurgitation of blood through the AV valves
Atria function as primer pumps:
- 75% of blood that enters the atria from the great veins flows directly into the
ventricles
- the atrial contraction causes a 25% extra filling of the ventricles – thus they
function as primer pumps, ↑ing the pumping ability of the ventricles by 25%
Pressure changes in the atria – a, c and v waves (see figure above):
- a wave
o caused by atrial contraction
- c wave
o occurs when ventricles begin to contract
o caused partly by slight backflow of blood in atria
o mainly by bulging of AV valves back into atria due to ↑P in ventricles
- v wave
o occurs towards end of ventricular contraction
o results from slow flow of blood into the atria from the veins while the AV valves
are closed and the ventricles are contracting
o when ventricular contraction is over, AV valves open and stored blood flows
into the ventricles causing the v wave to disappear
Function of ventricles as pumps:
Diastole
- large amts of blood accumulate in the atria during ventricular systole,
- flows rapidly into the ventricles as soon as systole is over and AV valves open = period of
rapid filling of ventricles (see ventricular volume curve)
o first 1/3 of diastole – rapid ventricular filling
o middle 1/3 – slow filling of ventricles by blood from veins→ atria –→ ventricles
o last 1/3 – atria contract and force more blood into ventricles (~25%)
Systole
- Period of isometric contraction
 immediately after start of ventricular contraction – abrupt ↑ P
 causes AV valves to close
 slight delay (0.02-0.03 sec) before aortic and pulmonary semilunar valves are
pushed open against their P


tension is ↑ing in the ventricular muscle, but no shortening of the muscle fibres
(contraction but no emptying)
= isometric/isovolumic contraction
-
Period of Ejection
 LV P >80mmHG and RV P> 8mmHg, the semilunar valves are opned and
ventricles empty
 70% in the first third of ejection time = period of rapid ejection
 30% in the next 2/3 = period of slow ejection
-
Period isometric relaxation
 end of systole, intraventricular P ↓ rapidly
 backflow of blood in aorta and pulmonary artery closes semilunar valves
 0.02-0.03 sec, the ventricular muscle relaxes but volume doesn’t ↓ - isometric
relaxation
 once P ↓s to diastolic levels, AV valves open and the ventricles begin to fill
again
Function of the valves
- Atrioventricular valves
 tricuspid and mitral prevent backflow of blood from ventricle to atrium during
systole
 semilunar valves (aortic and pulmonary artery) prevent backflow of blood into
ventricles during diastole
 open and close passively when there is forward and backward pressure
respectively
- papillary muscles
 attach to AV valves by chordae tendineae
 contract when ventricle walls contract but do not help valves to close
 pull the vanes of the valves backward to prevent bulging too far into atria during
ventricular contraction
- Aortic and Pulmonary valves
 high P in aorta and pulmonary vessels cause semilunar valves to snap shut
(compared to softer closing of AV valves)
 velocity of blood ejection through them is greater than AV valves – smaller
diameter
 therefore – much greater mechanical abrasion
Aortic Pressure Curve
- entry of blood into arteries – causes stretch and ↑ P to 120mmHg
- end of systole, after ventricle stops ejecting blood and aortic valve closes , elastic recoil
of arteries maintains high P in the arteries even during diastole
- blip in the P curve when valve snaps shut and backflow of blood is suddenly stopped
- aortic P then ↓ during diastole as blood flows through arteries into veins, to ~80mmHg
2. Explain the features of the normal ECG, identifying the electrophysiological events
which produce the P waves, PR interval, QRS complex (and why it is normally so brief
<0.1 sec), ST segment and T wave: explain why the ST segment is normally isoelectric,
and suggest electrophysiological changes in injured muscle which may result in ST
segment shifts
3. Display a familiarity with the normal ECG sufficient to be able to recognize gross
changes as abnormal, and to provide a basis for later learning of detailed ECG
interpretation
Normal ECG
 As the electrical impulse spreads through the heart, some electrical current spreads
through the surrounding tissue to the skin
 electrodes placed on opposite sides of the heart can measure the electrical potential
generated by the current
 The normal ECG consists of P waves, a QRS complex (often made up of 3 waves; Q, R
and S) and a T wave
 it is recorded onto standard paper traveling at a rate of 25mm/s, that is divided into
large squares 5mm wide (0.2 sec) each containing 5 small squares (0.04 sec)
 ECG machines are calibrated so the a current of 1mV moves the stylus vertically through
1cm (0.1mV =1mm=1 small square)
 Amplitude of deflection affected by
- myocardial mass
- net vector of depolarization
- thickness and properties of intervening tissues
- distance between electrode and myocardium
 Direction of deflection:
- depends on whether the electrical impulse is traveling towards or away from
the detecting electrode, i.e. the orientation of that electrode to the wave of
depolarisation
- towards = upwards (+ve) deflection from isoelectric line
- away = downwards (-ve)
- when the wave of depolarization is at right angles = equiphasic deflection

ECG Leads
- not a single wire connected to the body but a combination of two wires and
their electrodes on either side of the heart to make a complete circuit with the
ECG machine

Rate
-


one large square = 0.2s thus there are 5 large squares per second and 300 per
minute
if rhythm is regular, you can count the number of large squares between 2
consecutive R waves and divide this number into 300
if irregular, use the rhythm strip and count the number of QRS complexes in 10s
(i.e. 25cm of recording paper) and x6
Rhythm
- use prolonged reading from one lead (usu Lead II)
Cardiac Axis
- mean direction of the wave of ventricular depolarization in vertical plane
- zero reference point looks at the heart from the same position as Lead I, above
this axis is negative, below is positive
- normal range is -30° to 90°
- beyond -30° = left axis deviation and beyond 90° is right axis deviation
to determine the axis:
o
o
o
o
o
look at all 6 leads which look at the
heart in the vertical plane, i.e. I, II, III,
aVL, aVR and aVF
choose the one that is the closest to
equiphasic in the QRS complex – the
axis lies about 90° to the right or left
of this lead
look at the QRS complexes in the
leads adjacent to the equiphasic one
(on the hexaxial figure above)
if the lead to the left is positive, then
the axis is 90° to the equiphasic lead
towards the left
if the lead to the right is positive, then
the axis is 90° to the eqiphasic lead
towards the right
P wave
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
electrical potential generated by
depolarization of the atria before atrial
contraction
atria have relatively little muscle and
generate a single small P wave that
rarely exceeds 2.5 small squares
(0.25mV)
duration = < 3 small squares (0.12s)
PR interval (or PQ interval)

measured from beginning
of P wave to first deflection
of QRS complex
 time between onset of
atrial depolarization and
onset of ventricular
depolarization normal
duration = 3-5 small
squares (0.12-0.20s)
 PR segment = brief return
to isoelectric line after P
wave – time when the impulse is conducted through the AV node, the bundle of His and
bundle branches and the Purkinje fibres
QRS complex
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electrical potential generated by depolarisation of the ventricles before they contract
the depolarisation wave spreads throughout the ventricles before they contract
P wave and QRS complex are both DEPOLARISATION WAVES
duration measured in lead with widest complex and should be < 2.5 small squares
(0.10s), due to rapid depolarization of the ventricles
wave of depolarization spreads through the interventricular septum, through the bundle
of His and bundle branches and to the ventricular myocardium via the Purkinje fibres
left side of septum depolarizes first then right
the wave of depolarization then reaches the endocardium at the apex of the heart and
then travels to the epicardium, spreading outwards in all directions
depolarization of the RV and LV produces opposing electrical vectors but the LV
dominates as the left side of the heart has greater muscle mass than the right
ST segment
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period between the end of ventricular depolarization and the beginning of
repolarisation
starts at the J point (wherer QRS terminates) and ends at the start of the T wave
should be isoelectric and level with the adjacent TP segment and fairly flat (although
may slope upwards)


there is no reading on the ECG when the muscle is completely repolarised or
depolarized, current only flows through the ventricles ( and thus to the body surface)
when part of the muscle is depol (-ve) and part repol (+ve)
thus the ST segment should be isoelectric as all ventricular muscle is depolarised
T wave

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
electrical potential generated when the ventricles repolarise – REPOLARISATION WAVE
normally asymmetrical with more gradual slope in the first half
orientation usually corresponds with the QRS complex
symmetrical inverted T waves – suggestive of ischaemia, but asymmetrical inverted T
waves are frequently non-specific
QT interval
 measured from the start of the QRS complex to the end of the T wave = total time for
depolarization and repolarisation of the ventricles
 lengthens as the heart rate slows
 between 0.35 and 0.45 s
ST elevation
 indication of acute myocardial injury – usually due to a recent infarction or to
pericarditis
 leads in which elevation occur indicate the part of the heart that is damaged anterior
damage seen in V leads and inferior in lead III and VF
 pericarditis is not usually localized so elevation occurs in all leads
 part of the heart remains partially or totally depolarized all the time (-ve) and current
flows between this depolarized part and polarized parts of the heart all the time, even
between heartbeats
 ischaemia is the most common cause as not enough nutrients are present in the
coronary blood for the heart muscle to maintain normal membrane repolarization
4. Practice the skills of recording and interpreting an ECG
Assessing An ECG:
The Rhythm:
 Is there a P- wave for each QRS complex (sinus rhythm)?
 Atrial Rhythm: Measure the P-P intervals between consecutive P waves. The interval should
be reproducible with only small variations for respiration
 Ventricular Rhythm: Measure the intervals between two consecutive R waves from the QRS
complexes. If not present you can use the Q or S waves consecutively. The R-R interval
should occur regularly.
 Determine if there is irregularity, if it is regularly irregular or irregularly irregular.
Calculate The Rate:
 Always check the pulse to correlate with the heart rate on the ECG.
 300/no of large squares between consecutive R waves
Evaluate The P Wave
 P waves present?
 Are they of similar size and shape?
 Do they have normal configuration?
o Peaked/tall: Right atrial hypertrophy.
o Notched/broad: Left atrial hypertrophy.
 Does every P wave have a QRS complex
Check The PR Interval:
 start of P wave to start of QRS complex
 3-5 small squares (0.12-0.2s)
 Is the interval constant?
Check the QRS complex:
 start of the R wave to the end of the S wave
 < 0.10 seconds (2.5 squares)
 Are all QRS complexes the same size and shape?
 Does a QRS complex occur after every P wave?
ST segment:
 Is it isoelectric? The ST segment should be level with the rest of the baseline.
T Wave:
 Check the shape:
o Peaked in hyperkalaemia
o Flat, prolonged in hypokalaemia
 Inverted T waves: Normal in leads V1 and aVR.
The Cardiac Axis
 See above
5. Practice the skills of recording and interpreting an ECG
Recording an ECG
 10 wires with electrodes attached to skin (need good contact so may have to shave
chest)
 one electrode is attached to each limb and 6 to the anterior chest wall
 right leg (RL) electrode is ‘earth’
 10 electrodes: V1-V6, aVL, aVR, aVF, RL
 12 leads: V1-V6 and aVL, aVR, aVF and I, II and III
Position of the six chest electrodes for
standard 12 lead electrocardiography.
V1: right sternal edge, 4th intercostal
space;
V2: left sternal edge, 4th intercostal
space;
V3: between V2 and V4;
V4: mid-clavicular line, 5th space;
V5: anterior axillary line, horizontally
in line with V4; V6: mid-axillary line,
horizontally in line with V4
Anatomical relations of leads in a standard 12 lead electrocardiogram
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II, III, and aVF: inferior surface of the heart
V1 to V4: anterior surface
I, aVL, V5, and V6: lateral surface
V1 and aVR: right atrium and cavity of left ventricle
Vertical and horizontal perspective
of the leads. The limb leads “view”
the heart in the vertical plane and
the chest leads in the horizontal
plane