Adult Echocardiography
Lecture Three
Cardiac Physiology
Harry H. Holdorf
Electrophysiology
• Normal Electrical Activation
– SA node (Special Neuromyocardial Cells-pacemaker
– AV node (electrical impulse
pauses to prevent
simultaneous contraction of
the atria and ventricles
– Bundle of His
– Bundle branches (right and
left)
– Purkinje fibers
• HINT: which is the fastest intrinsic rate?
SA NODE
Action Potential
• What is the absolute refractory
state?
– That period when a muscle
cell is not excitable
• From phase one until into phase
3
• The relative refractory period is
during phase 3 and the muscle
cell might contract if the stimulus
is strong.
• See next slide for chart.
Electro-cardiogram
• Normal complex
– P wave-atrial systole
– P-R interval – includes P-R
segment (from atrial to
ventricular depolarization)
– T wave – ventricular diastole
(repolarization)
– HINT: Know what P wave, PR interval, and T wave
represent
1 small box = 0.04 seconds
1 big box = 0.2 seconds
5 big boxes = 1 second
• What is the normal duration for
the QRS complex?
– 0.10 seconds
– Normal values
• R-R interval = 3 to 5 big boxes
(60-100 beats/minute
• QRS complex = less than 3 little
boxes (less than 0.12 seconds)
• PR interval = Less than 1 big
box (less than 0.2 seconds)
Mechanical Events
• Frank-Starling Law (Length –
Tension Relationship)
– Increased volume (preload) =
increased contractility (to a
physiologic limit).
– Increased myocardial fiber
length = increased tension
(rubber band theory)
Know Frank-Starling Law
As the ventricles become overfilled (to the right
on the curve beyond EDV = ~250 mL), the heart
becomes inefficient and stroke volume levels off.
• Acute AI is hyper-contractile
because we shift up the Starling
curve.
• Chronic AI is failure when we
drop off the end.
PRELOAD
Load (volume) exerted on the
ventricle at END DIASTOLE.
Determines force of contraction.
The greater the load the greater the
force of contraction (Frank-Starling
Law).
PRELOAD cont…
• Increased preload:
Mitral regurgitation
Tricuspid regurgitation
Pulmonic regurgitation
Aortic regurgitation
Ventricular and atrial septal
defects
Fluid Overload
HINT: Echo findings for Preload vs.
afterload: Preload = dilatation
Afterload = hypertrophy
Afterload
• Resistance against which the
ventricle must pump.
• Determines the tension the
myocardium must generate.
• INCREASE AFTERLOAD
– Hypertension
– Aortic Stenosis
– Pulmonic stenosis
Which test does not allow for the calculation of
ejection fraction?
A. 2D echo
B. Cardiac angio
C. Chest X-ray
D. Cardiac Nuclear study
LV Function Indicators
• Stroke Volume (SV)
SV = end diastolic volume (EDV) – end
systolic volume (ESV)
Normal varies with end diastolic
volume, heart rate, size (normal: 70110 ml).
Ejection Fraction (EF)
EF = SV/EDV x 100
Normal is > 55%
Cardiac Output (CO)
CO = SV x heart rate (HR)
Normal is 4-8 L/min
Calculate CO from SV and HR
Bernoulli Equation
Aliasing
• Occurs when the Doppler shift
exceed the Nyquist Limit
• Nyquist Limit = ½ of the PRF
(Pulse Repetition Frequency)
• A problem with higher velocities
in pulsed Doppler (spectral &
Color flow)
• Occurs sooner with higher
frequency transducers
NOTE: How does switching to a lower
frequency transducer affect aliasing?
Aliasing will occur at higher
velocities
Doppler Stroke Volume
SV = VTI (FVI) x CSA
– VTI is the velocity time
integral as calculated by
tracing the Doppler spectral
display (sometimes called the
“flow velocity integral or FI”). It
represents how far the blood
travels in centimeters with
each ejection. Normally, 12
cm for the mitral valve and 20
cm for the aortic valve.
Doppler signal in the left
ventricular outflow tract:
Velocity Time Integral (VTI)
• CSA is the cross-sectional area
• NOTE: What does VTI x CSA
equal?
– Doppler stroke volume
Maneuvers Altering Cardiac
Physiology SV, CO, IHSS, AS, MR, HR, BP, AR
• Breathing:
– Inspiration: Increases venous
return
– Expiration: Decreases venous
return
• Standing
– Decreases venous return, SV
• Squatting
– Increases venous return, SV
and CO. (Increases AR,
Decreases IHSS)
• Handgrip
– Increases HR, CO, arterial
pressure. (Decreases AS,
increases MR)
• Valsalva
– 2 main phases-strain and
release.
– During strain-decreases
venous return, SV and CO
– Most murmurs decrease
during straining, IHSS
increases
– During release-increase
venous return, CO, and BP
• Sit-ups
– Increases HR, CO and SV
• Amyl nitrate inhalation:
Vasodilator-decreases peripheral
resistance- increases HR, CO, and
SV (increases forward murmurs,
decreases AR/MR.
NOTE:
Does venous return increase or
decrease with inspiration?
Increases
• Inhalation of amyl nitrite causes:
– Decreased afterload
Vasodilator drops BP
Tachycardia response
• Increases stroke volume
• Increases heart rate
• Mitral valve velocity during
inspiration:
– decreases
A Wiggers diagram is a standard diagram used in
cardiac physiology named after Dr. Carl J. Wiggers.
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•
•
•
•
•
•
The X axis is used to plot time, while the Y axis
contains all of the following on a single grid:
Blood pressure
– Aortic pressure
– Ventricular pressure
– Atrial pressure
Ventricular volume
Electrocardiogram
Arterial flow
Heart sounds
By illustrating the coordinated variation of these
values, it becomes easier to illustrate the
relationship between these values in the cardiac
cycle.
Cardiac Cycle
(Wiggers Diagram)
b. Mitral valve closure
C. Aortic valve opens
e. Aortic valve closure
f. Mitral valve opens
• Know isovolumetric timing with
the ECG
– After R wave = isovolumic
contraction
– After T wave = isovolumic
relaxation
• Know the duration of IVRT and
IVCT
– 70 msec
• The duration of isovolumetric
relaxation time will be increased
with:
– Bradycardia
• Between which heart sounds will
the murmur of aortic stenosis be
heard?
– S1 –S2
• During the cardiac cycle, this
event NEVER happens:
– Ao valve is open & mitral
valve is open
– Both are closed during ISO-V
The truth about the cardiac cycle
1. Normal arterial pressure is
approx. 120/80 mmHg. Thus,
the aortic pressure lives high
2. Normal left arterial pressure is
approximately 10 mmHg. Thus,
the atrial pressure lives low.
3. The left ventricular pressure
bounces between aortic and
atrial. High and low.
4. The valve that lives between the
left ventricle and the aorta is the
aortic valve. The aortic valve
lives high.
5. The valve that lives between the atrium
and the left ventricle is the mitral valve.
The mitral valve lives low.
6. The magic word is “COCO’. Close,
open, close, open.
7. When a normal valve is open, there is
very little pressure difference between the
chambers on either side of the valve.
So, when the aortic valve is open, the LV
and aortic pressures are nearly identical.
When the mitral valve is open ,the atrial
and LV pressures are nearly identical.
HEMODYNAMICS
• Pulmonary
– Low pressure
– Low resistance
– RV wall is thin
– Low O2 content in artery
• Systemic
– High pressure
– High resistance
– LV wall is thick
– High O2 content in artery
Hemodynamics continued
Components
• Pulmonary
– Pulmonary artery
– Arteries
– Capillaries
– Veins
• Systemic
– Aorta
– Arteries
– Arterioles
– Veinules
– Veins
– Vena Cava
• Arteries
– Elastic, thick walled blood
vessels
– Expand during systole, then
recoil during diastole to keep
blood moving forward
• Veins
– Thin walled blood vessels that
collapse easily
– Able to expand rapidly to
accommodate large volumes
of blood
– Contain the majority of
circulating blood
Blood
• 54% of blood volume is plasma
• 45% of blood volume is red
blood cells (erythrocytes)
• 1% of blood volume is white
blood cells (leukocytes) and
platelets (thrombocytes)
Normal pressures
More normal pressure
ranges
•
•
•
•
•
•
•
RA = 8/5
Ao = 120/80
PA = 25/10
RV= 25/0
LV = 120/0/12
LA = 10/12
PCW = 10
Normal atrial pressures are about 6 mm
Hg in the right atrium and 10 mm Hg in the
left atrium. Other than that, the right –
sided pressures are approx. 1/5th of the left
sided pressures.
• Think Tank:
– What are normal pressures in
the pulmonary artery?
• 25/10
Normal O2 Saturations
• Oxygenated
blood,
95%
saturated (pink blood) starts in
the
pulmonary
veins
and
continues to the end of the
systemic arteries.
• Deoxygenated
blood,
75%
saturated (blue blood) starts in
the systemic veins and continues
to the pulmonary arteries.
• Where is the O2 saturation the
lowest?
– Coronary sinus
• Know O2 saturation in pulmonary
veins is 95% and Pulmonary
arteries is 75%
Cardiac Catheterization
• Angiography
– Contrast medium injected
while cineangiography film
records results (vessel
narrowing, regurgitation,
shunts, ejection fraction).
– LV angiogram also called
ventriculography, selective
angiography, or
angiocardiography.
• NOTE: Best cath technique for
LV function?
– LV angiogram
Cardiac Output
• Fick method measures O2
consumption divided by the
difference in O2 content between
arterial and pulmonary system.
•
Angiography technique multiples the stroke volume by
the heart rate.
•
Oximetry
– Measures O2 saturation in various chambers (able
to detect shunts by changes in O2 saturation).
– Shunt size is calculated by the difference between
pulmonary and systemic blood flow.
Cath Gradients
• Pressure waveforms for Aortic
Stenosis, Mitral Stenosis, Mitral
regurgitation
• What is PWC (Pulmonary
Capillary Wedge) measuring?
– Left atrial pressure
SEP = Systolic Ejection Period
DFP = Diastolic Filling Period
PCW = Pulmonary Capillary
Wedge (from a Swan-Ganz
Catheter
Aortic Stenosis
• To determine AS, where are
catheters placed?
• One in the LV and one in the Ao
or one in the LV and Pulled Back
across the AoV or one catheter
with two separate sensors.
• See LV and Ao tracings.
• The aortic valve lives between
the LV and Ao.
• If LV pressure is higher than Ao
pressure in systole (they should
track together), this is Aortic
Stenosis.
End Lecture Three
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