Cardiovascular System II
Einthoven’s triangle and the cardiac vector
Electrocardiogram connections are termed “leads”.
The simplest connections, Leads I, II and III, define
a triangle. I like to think of this triangle as a box
containing the heart. Each lead is like a peephole
that lets us have a view of the heart in the box.
If the bulk of the flow of current around the heart
during ventricular depolarization is represented by
a vector that sums all the currents, this vector would
ordinarily point downward and to the left, pretty
much along the physical axis of the heart.
Lead I gives us a view of this vector pointing almost
directly away from us. Lead III shows the vector
pointing almost directly toward us, and Lead II gives
a side-on view.
Any 2 of leads I, II and III
can define the vector in 2
dimensions
Here, the relative
heights of the R
wave in leads I, II
and III are plotted on
the Einthoven
triangle to yield the
vector
The 12-lead EKG
• In modern clinical settings, EKG data is collected from
12 different leads
• The 3 augmented leads simply add a second triangular
box – if the standard Einthoven triangle and the
augmented lead triangle were drawn together, they
would form a 6-pointed star.
• The 6 precordial leads utilize an exploring electrode
that is placed at 6 points forming a ring around the left
chest. Each of these points acts as a keyhole through
which we can gain a different view of the cardiac vector,
allowing it to be visualized in 3 dimensions.
Axis deviations
• As a rule, the vector shifts away from
damaged, wasted or non-excited tissue
that does not generate current - a scar
from an old heart attack, for example.
• The vector shifts toward parts of the
ventricle that generate excessive current,
such as a hypertrophied ventricle or a
patch of freshly damaged muscle that is
electrically leaky.
Ventricular hypertrophy as a source of axis
deviation
• Systemic hypertension that overloads the
left ventricle over time will cause it to
hypertrophy, resulting in a left-axis
deviation.
• Long-term overload of the right ventricle
(pulmonary hypertension or an
interventricular shunt) will result in a rightaxis deviation.
What kind of axis shift is happening here?
This trace is from a 63 year old woman with long-term hypertension.
She also has a 1st degree AV block, as shown by the prolonged P-R
interval (>0.20 sec)
Bundle branch block as a source of axis deviation
• Ordinarily, the left ventricle is served by two
branches of the Bundle of His
• If one of these is damaged, a conduction delay
or conduction block results, causing excitation to
spread to that part of the ventricle more slowly,
causing both an axis shift toward the blockage
(i.e. a right axis shift for a right bundle block and
vice versa) and a broadening or splitting of the
QRS.
Arrhythmias
• Arrhythmias have 3 main causes
– Failure within the SA node or conducting
system
– Presence of an ectopic pacemaker (ectopic
means “wrong place)
– Abnormal pattern of spread of excitation
within the myocardium, or between the atria
and the ventricles
If the SA node fails, the AV node can take over
Sinoatrial nodal block, with AV nodal rhythm during the block perod
(Lead III). The SA node is driving the 1st and 2nd beats – see the P
waves. When the SA node drops out, the AV node becomes the
pacemaker –see no P waves - at a slower rate.
1st Degree AV block
In 1st degree AV block, conduction into the AV node is even slower than
usual, so the P-R interval is prolonged
2nd Degree AV Block
In 2nd degree AV block, conduction from the SA node to the AV node fails
entirely for some beats, so the heart skips a beat.
In case of complete AV conduction failure, a ventricular
pacemaker usually appears
Notice that there is no relationship between the SA rhythm and
ventricular contractions, and the shape of the QRS seems wrong
What is happening here?
PVC (= VPC)
This trace is from a 62-year old woman who had a heart attack some
years previously. Note that the QRS and T waves from the abnormal beat
are different from the normal beats (why?) and there is a compensatory
pause before the next normal beat (why?).
PVC = premature ventricular contraction. This patient is at risk to fall into
ventricular fibrillation if the PVC falls during the time interval in which
some, but not all of the ventricle has repolarized.
In fibrillation, the myocardium stops acting as a
unit
• In the fibrillating myocardium, excitation does not pass
over the myocardium as a wave front, but continuously
circles back to reenter areas that had already recovered
from their refractory period. This is usually due to the
presence of some damaged tissue that conducts
excitation very slowly. Once it starts, the heart does not
recover a normal rhythm spontaneously.
• Defibrillation synchronously excites the whole
myocardium, making it all refractory at the same time.
This may reestablish a normal conduction pattern.
Mechanical Aspects of the
Heart Cycle
Review of cardiac structures
Beware of some confusing
multiple names.
I will refer to the tricuspid
and mitral valves simply as
the AV valves. Sometimes
the mitral valve is referred
to as the bicuspid valve.
The pulmonary and aortic
valves are sometimes
referred to as the semilunar
valves.
Events of the heart cycle
• Late diastole: AV valves are open – blood is flowing into the
ventricles under venous pressure (diastasis or passive filling).
Pulmonary and aortic valves are closed.
• Atrial contraction (atrial systole): adds an additional amount of blood
to the ventricles – the contribution is trivial except during exercise
• AV delay: allows atrial contraction to be complete
• Ventricular systole: immediately causes closure of AV valves,
causing 2nd heart sound. Vent. Systole can be divided into
– an initial period of isovolumetric contraction during which all heart valves
are closed,
– followed by a period of blood ejection, during which pulmonary and
aortic valves are open,
– then pulmonary and aortic valves close (2nd heart sound), leading to a
period of isovolumetric ventricular relaxation.
When ventricular pressure drops below venous pressure, the AV valves
reopen and passive filling begins again.
Pressure and volume
changes in the heart
cycle
A must-know, mustunderstand slide.
The pressure values are
for the left ventricle and
aorta– values for the right
ventricle and pulmonary
arteries would be about
1/3 as great
The mechanical task of the heart
• The heart fills under low pressure of venous blood
(preload) -1 – +3 mmHg – it’s not a good suction pump,
so venous values cannot and should not go far in the
negative direction.
• The heart ejects blood against the high pressure of
arterial blood (afterload) average value about 100
mmHg.
• As averaged over times longer than a few beats, the
cardiac output of each ventricle must equal the venous
return to that ventricle, and the cardiac output of each
ventricle must match that of the other, or a physiological
catastrophe would occur. Intrinsic regulatory properties
of the healthy heart muscle prevent this catastrophe.
Determinants of Cardiac Performance
• Heart rate: determined by balance of chronotropic
effects of adrenergic and cholinergic inputs
• Intrinsic heart contractility or inotropic state: determined
by the state of health of the myocardium, the inotropic
effects of autonomic inputs, and anything else that
affects the peak Ca++ level reached in the cytoplasm
during activation.
• End-diastolic ventricular volume – which determines the
preload of the ventricule
• Aortic or pulmonary arterial pressure, which determines
the afterload of the ventricle.
Performance characteristics of the
isolated heart
• The first step towards understanding the
performance of the CV system is to study
the performance of the heart in isolation.
• These experiments were carried out by
Frank for the frog heart and Starling for the
dog heart.
The effect of the preload: the Frank-Starling Law
says the heart pumps out what comes in
These cardiac function
curves are basically about
the relationship between the
length of cardiac muscle
fibers and their force
development: over the
normal operating range of
ventricular end-diastolic
volumes, increasing volume
increases force, which
increases stroke volume,
which increases cardiac
output.
The curves reflect the
performance of the isolated
heart, in the absence of the
vascular system.
Cardiac function curves reflect the limits of potential
performance – they don’t determine actual performance
The inotropic state of the heart
merely determines the range of
possible cardiac outputs – for
example, the maximum cardiac
output for the heart in the
absence of any positive inotropic
effect is 10 L/min; with maximal
sympathetic input it rises to
almost 25 L/min. As we will see,
the actual cardiac output in any
real-life situation is determined
by the interaction of the heart
and the vascular system, and
not by the heart alone.
Cardiac performance versus the afterload
+ sympathetic input
No input
Parasympathetic
input or disease
This curve shows that the
ventricle is rather
insensitive to afterload,
maintaining a constant
output until arterial
pressure reaches a value
at which the heart is simply
not strong enough to open
the aortic valve.