1. Adult Echocardiography Lecture Three Cardiac Physiology
Harry H. Holdorf

2. Normal Electrical Activation
Electrophysiology
Normal Electrical Activation
SA node (Special Neuro-myocardial 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

4. What is the absolute refractory state?
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.

6. 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, P-R interval, and T wave represent

8. 1 small box = 0. 04 seconds 1 big box = 0
1 small box = 0.04 seconds 1 big box = 0.2 seconds 5 big boxes = 1 second

9. What is the normal duration for the QRS complex? 0.10 seconds
Normal values
R-R interval = 3 to 5 big boxes ( 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)

10. 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

11. As the ventricles become overfilled (to the right on the curve beyond EDV = ~250 mL), the heart becomes inefficient and stroke volume levels off.

12. 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).

13. 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

14. Resistance against which the ventricle must pump.
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?
2D echo
Cardiac angio
Chest X-ray
Cardiac Nuclear study

15. 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: 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

16. Bernoulli Equation

18. Occurs when the Doppler shift exceed the Nyquist Limit
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

19. 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.

20. Doppler signal in the left ventricular outflow tract: Velocity Time Integral (VTI)

21. CSA is the cross-sectional area
NOTE: What does VTI x CSA equal?
Doppler stroke volume

22. 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)

23. 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

24. 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

25. Inhalation of amyl nitrite causes: Decreased afterload
Vasodilator drops BP
Tachycardia response
Increases stroke volume
Increases heart rate
Mitral valve velocity during inspiration:
decreases

26. A Wiggers diagram is a standard diagram used in cardiac physiology named after Dr. Carl J. Wiggers.
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.

27. Cardiac Cycle (Wiggers Diagram)

28. b. Mitral valve closure C. Aortic valve opens e. Aortic valve closure f. Mitral valve opens

30. 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

31. 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

33. The truth about the cardiac cycle
Normal arterial pressure is approx. 120/80 mmHg. Thus, the aortic pressure lives high
Normal left arterial pressure is approximately 10 mmHg. Thus, the atrial pressure lives low.
The left ventricular pressure bounces between aortic and atrial. High and low.
The valve that lives between the left ventricle and the aorta is the aortic valve. The aortic valve lives high.

34. 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.

36. 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

37. Hemodynamics continued Components
Pulmonary
Pulmonary artery
Arteries
Capillaries
Veins
Systemic
Aorta
Arterioles
Veinules
Vena Cava

38. 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

39. 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)

40. Normal pressures

41. More normal pressure ranges
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.

42. What are normal pressures in the pulmonary artery?
Think Tank:
What are normal pressures in the pulmonary artery?
25/10

43. 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.

45. Where is the O2 saturation the lowest?
Coronary sinus
Know O2 saturation in pulmonary veins is 95% and Pulmonary arteries is 75%

46. 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

48. 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.

49. 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

50. 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.

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