Heart Functions: the MEA and the Frank Starling Law of the heart 2/14

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Transcript Heart Functions: the MEA and the Frank Starling Law of the heart 2/14

Heart Functions: The Frank Starling Law of the
heart
2/15 and 2/16
20 point quiz at end of class Monday: Bring scantron
Lab Exam is Thursday 7am-6pm
Open Lab Monday: 6am-8pm, Tuesday:6am-8pm
Wed:6am to about 1pm
• What happens to the MEA in left side or right side
hypertrophy?
• What is the Frank-Starling Law of the Heart?
• How does EDV determine SV in a healthy heart?
• How does EDV determine SV in an unhealthy heart?
• Where does fluid accumulate when the right and left
ventricles fail?
• Why does the fluid accumulate in these places?
• DON’T FORGET LECTURE QUIZ MONDAY: 20 points
over Heart/ECG
Could you do these calculations for lecture test or lab test?
Do the math at home with a ruler or box-method.
This or something like it will be on the next lecture exam
What letter would represent AV valve closure? A, B, C, D, E, F or G
What letter would represent the start of the atrial “kick” into the ventricles? A, B, C, D,
E, F or G
What is the cardiac output of this ventricle? Show Math.
This is lead II, what is wrong with this persons ECG?
Finger Pulses that are associated with ECG tell us ventricular ejection occurred
Lead II ECG Record
Finger Pulse amplitude is a function of stroke volume, if
ventricular filling is incomplete, ejection is smaller than normal and
finger pulse is small or non-existent (plusus alternans may occur).
What is this MEA? Anything wrong with it? Why?
Lead I
Lead II
Lead III
What are the three standard “LEADS” that folks use to look at
heart function? Lead I (RA- and LA+), Lead II (RA- and LL+) and
Lead III (LA- and LL+). These form a “perfect” triangle around the
heart that sits at the “exact” center of chest. Sort of…
MEAN ELECTRICAL AXIS (MEA) GIVES A MORE ADVANCED
CARDIAC DIAGNOSIS OF FUNCTION/PATHOLOGY.
• The mean electrical axis is the average direction of depolarization
in the heart.
• Einthoven’s Triangle: represents an equilateral triangle at the center of
chest. (remember the heart is shifted slight to left side)
• Dead heart tissue does not depolarize
• ECG Changes: Large R-wave becomes a small R-wave
• ECG leads can identify exact spot on heart where infarct or clot
is located with out cutting you open to look.
• MEA if aortic BP is 180/130:
– Left Ventricle works harder so it gets larger
– MEA shifts to Left Side= Left Shift
• MEA if you have emphysema (hard to drive blood through lung):
– RightVentricle must work much harder
– Pulm arterial pressure 20/480/30
– Right side gets more muscular Mass increasesECG Changes
This or something like it will be on the next lecture exam
What letter would represent AV valve closure? A, B, C, D, E, F or G
What letter would represent the start of the atrial “kick” into the ventricles? A, B, C, D,
E, F or G
What is the cardiac output of this ventricle? Show Math.
FRANK STARLING LAW OF THE HEART: “Energy of
contraction is proportional to the initial length of the cardiac
muscle fiber”. This explains how a heart can regulate its own
output based simply on venous return to the heart.
Normally the heart contracts at less than the ideal actin/myosin length
and preload! Curve: EDV (ml) vs Stroke Volume (ml)
However as the EDV is increased, the myocardium is stretched and the
actin/myosin orientation becomes closer to ideal (In healthy heart!)
Each “curve” is unique to conditions around heart: temp, CO2, etc.
As EDV↑…Contactility↑…SV↑….therefore CO goes up…SO WHAT?
 Heart moves more blood/beat for about the same ATP cost
 Cardiac Output can increase with no change in rate
 Adaptation can occur independently of nervous system
 VIP: Limits to System Exist
 With respect to cardiac reserve, why does your heart normally
work/function in “middle” of ascending part of curve, and not
at the top or back side of the curve?
The key is to ask where you are on the curve given the observed
EDV for a given systole, this lets you predict the SV for that systole:
Often Folks call this the ventricles “PRELOAD”
Frank-Starling curves are shifted by:
A “Shift” makes the heart pump a larger or smaller stroke volume.
A “Shift” creates a new F-S curve with a new shape.
Factors That Modify the “Shape” of F-S curves: Make myocardium
contract more/less forcefully
• Sympathetic stimulation:
•
Digitalis and calcium uptake inhibitors:
•
Hypercapnia/Hypoxia-
•
Body temperature-
•
Thin myocardial walls (alcoholic heart)-
•
Many more factors exist……
•
•
What determines where your heart is “Located” on a F-S Curve:
Answer: Preload and Stroke Volume
The original F-S Curve is modified based changes to myocardial function
caused by temperature, positive ionotropic drugs, myocardial infarct,…etc.
Frank Starling Curve Shifts Up when the heart needs to work harder (
Add Epinephrine) and Shifts Down when the heart starts to fail (add
Hypoxia or have an Infarct).
If Preload Changes on a Single Curve Stroke volume changes.
WHAT HAPPENS TO THE HEART WHEN IT FAILS?
In terms of the FS-curve, why will SV and cardiac output plummet?
1) Loss of myocardium due to infarctCan you generate force if the myocytes are dead?
2) EDV gets too large- ejection fraction small
3) Actin/myosin are over stretched- no traction
4) Contractility is reduced and SV is reduced- This is bad!
5) Cardiac Output Plummets!
Can you supply the heart with oxygen without CO?
Other Classic Problems:
• If heart hypertrophies (grows to big/thick)• If heart dilates (creates a large EDV, small SV and a thin wall)• During lung problems: emphysema, core pulmonare, etc….
• Problem:Law of Laplace: ^radius…^tension…^^^^work
• These examples can result in death from a loss in cardiac
reserve and a set or neurological responses that make the
original problem WORSE and lead to a heart attack.
A failing heart results in the accumulation of fluids (edema) in the lung or
body. With respect to Rt or Lt ventricular failure, where does the pressurized
fluid accumulate? Why? What could cause Rt/Lt Failure? Why might your
brain try to make the heart work even harder? Can it work harder?
WHAT ARE SOME MECHANISMS FOR IMPROVING VENOUS RETURN
IN A LOW PRESSURE (VENOUS) LOOP?
• Simple pressure gradient-Systemic vs. Pulmonary circuits
mmHg
mmHg
• Thoracic (Respiratory) Pumping by ribs/sternum
• Valsalva Maneuver and preload changes: heart attack risk
• Cardiac Suction: Negative Pressure in Atria or Ventricles
• Venous Return to Heart: Venous valves and skeletal muscle activity– Varicosities and Anal Hemorrhoids
• Gravity changes pressure: ±1.92 mmHg/inch of elevation or
depression
• If the top of your head is 15 inches higher than your head the BP at
the higher location would be decreased by 29 mmHg(15X1.92= 28.8mmHg)
• BP at brain is: (120-29)/(80-29)=91/51
• BP at foot is added! 40X1.92=77 mmHg 199/157
• If you are dizzy, why does laying down prevent you from passing out?
• Why does your sprained ankle hurt and swell more if you are standing
up?
Gravitational effects on
blood flow and pooling
are part of the reason we
are asked to lay flat when
we feel dizzy or why our
sprained ankles “throb”
and become swollen only
when we are standing up.
Remember:
+/- 1.92 mmHg pressure
for each Inch of elevation
or depression!
If the brain has no
pressure, there is no blood
being delivered!
Venous pumping provides a very simple and very effective way
to increase the return of venous blood to the heart?
(If venous return to atria causes the Preload to increase too!)