1. Cardiovascular Physiology

2. Functioning of Heart Mechanical Events Electrical Events
Automatic or involuntary
Electrical Events

3. Mechanical Events Cardiac cycle Four Phases One cycle = One beat
Isovolumic Contraction Time (IVCT)
Systole
Isovolumic Relaxation Time (IVRT)
Diastole

4. IVCT Immediately before systole All four valves closed
Volume remains the same in ventricle
Atrial volumes change
Pressure builds in ventricle

5. Systole Ventricular Pressure Rises Ejection AV valves closed
When pressure in ventricle is greater than the pressure in the great vessels the Semilunar valves open
Ejection
Begins at apex and goes up
AV valves closed
Pressure pushes against valves
Pressure in Great Vessels Rise
When pressure in the great vessels gets higher than pressure in the ventricle the Semilunar valves close
The closure of the semi lunar valves is the 2nd Heart Sound

6. IVRT Immediately before diastole All four valves closed
Volume remains the same in ventricle
Atrial volumes change
Atrial pressure rises
Pressure drops in ventricle

7. Diastole Atrial Pressure Early Diastole
When the atrial pressure gets higher than the ventricular pressure the AV valves open
Early Diastole
LV pressure at lowest
Rapid Filling Phase
“sucking effect” because of negative pressure
70-75% of filling
If heart abnormal may hear 3rd Heart Sound

8. Diastasis
As ventricular walls become stretched, flow slows down
Left ventricle and atrium pressure equalize out
Atrial Kick
Happens at end-diastole
30% of blood
Corresponds to “P” wave on EKG
4th Heart Sound in some abnormal hearts

9. End Diastolic Volume Pressure Increases
The amount of blood in the ventricles at this point
Largest amount of blood in the heart during entire cardiac cycle (measurements at End Diastole)
Pressure Increases
Pressure in the ventricles increases
Forces the AV Valves to close
Closure of the AV Valves is 1st Heart Sound

11. The Heart Must Have Volume and Pressure

16. Cardiac Function Supply and Demand
Heart’s job to provide us supply of oxygen
This is done through Cardiac Function
Systolic Function
Diastolic Function

17. Systolic Function
Definition - Ability of ventricles to efficiently eject blood out of the heart and into systemic and pulmonary systems
Decreased systolic function-indicator of heart disease

18. Diastolic Function
Definition – Ability of the ventricles to relax and fill. (referred to as ventricular relaxation and compliance)
Indicates whether the ventricular filling pressure or normal or increased (referred to as ventricular end diastolic pressure
Decreased diastolic function (Diastolic Dysfunction) precedes Systolic dysfunction

19. Diastolic Dysfunction
Definition – failure of the ventricles to relax and allow normal filling
Indicator of heart disease

20. Cardiac Function Components
Cardiac function dependant on several factors
Wall thickening
Wall motion
Chamber size
Ventricular end diastolic pressure

21. Wall Thickening and Wall Motion
Known as Contractility
Indicator of adequate coronary blood flow and oxygenation

22. Terminology Hyperkinetic Hypokinetic Dyskinetic Akinentic
Excessive wall motion
Hypokinetic
Decreased wall motion
Dyskinetic
Movement away from the center of the cavity. This may indicate myocardial infarction (MI)
Akinentic
Mo movement or thickening of the myocardium

23. Facts about Akinesis Akinesis may be indicator of hibernation or MI
Hibernation-ischemic segment that is akinetic but not infarcted. Can be reversed with restoration of blood flow
Echo can not differentiate between hibernation and MI. But chronic infarct may have thinning walls

24. Wall Motion Abnormality
Normal wall- concentrically thicken and contract approx 30% toward center of chamber during systole
If does not thicken or contract properly called wall motion abnormality (WMA)
WMA indicator of ischemic heart disease
Can be global or localized

25. Dysfunction
When myocardium become ischemic, ventricle will have abnormal relaxation (ability to accept blood and fill) This is called diastolic dysfunction
Ischemia will cause decreased systolic function (ability to pump blood effectively)
If severe may become akinetic or is can not compensate for increased pressure, may become dyskinetic

26. Chamber Size
Normal-should concentrically decrease in size during systole (contract)
During diastole- should concentrically increase in size (filling)
Measurements – several methods to quantify

27. Pressure
End diastolic pressures (EDP) corresponds to degree of fiber stretch in ventricles
The degree of fiber stretch depends on the quantity of blood in the chamber prior to contraction
The greater the amount of blood entering the chamber, the greater the contraction required to expel the blood (Frank-Starling Law)
EDP can be determined by examining flow through the valves with doppler

28. Cardiac Output
If you go for run your body’s demand for oxygenated blood increases
Your heart must meet the demand for oxygen with supply.
Can meet demand by increasing heart rate and/or stroke volume

29. Heart Rate Stroke Volume (SV)
The number of times the heart beats per minute (bpm)
Normal resting
Stroke Volume (SV)
Definition - the volume of blood ejected with each heart beat
Normal resting ml
SV depends on Left Ventricular End Diastolic Volume (LVEDV) and Heart Rate (HR)
The greater the LVEDV and/or HR; the greater the SV
The combination of HR and SV determine Cardiac Output (CO)

30. Cardiac Output
Definition - the volume of blood pumped from the ventricle each minute
Calculated as stroke volume X heart rate
Normal 4-8 liters per minute ( l/min)
CO(l/min)= SV X HR

31. Cardiac Index
Cardiac index is the CO corrected for body surface area (BSA)
Normal 3-4 l/min2
BSA is the calculated surface area of the human body
Normal 1.73 m2 (but varies with size and age)
Mosteller formula
(Height [inches] X weight [lbs] / 3131)(1/2)

32. Review Equations
SV =EDV-ESV
CO = SV X HR
CI = CO / BSA
(hint…hint…)

33. Blood Pressure Reading that corresponds to pressure in arteries
Systolic
Diastolic
Reads as fraction
mmHg
Normal
60-90

34. The heart’s ability to increase the CO dependent on
Preload
Afterload
Inotropic Force
Chronotropic Force

35. Preload Preload-The volume (load) in the heart at the end of diastole
LVEDP-The degree of fiber stretch related to the quantity of blood in the chamber prior to contraction

36. Frank Starling Law
Frank Starling Law- (Length–Tension Relationship) The more blood that enters the heart during diastole (preload); the greater the force of contraction (systole) required to eject the blood
In other words…Increased myocardial fiber length means increased tension

37. Interval-Strength Relationship
The longer the interval between heartbeats; the stronger the contraction required to eject the blood
PVC
Increased preload requires stronger contraction to eject blood
This is called extrasystolic potentiation

39. Force-Velocity Relationship
The greater the force required to eject the blood; the slower the velocity of muscle fiber shortening

40. Facts About Preload
Preload is increase by any state of fluid overload, such as valvular regurgitation, ventricular septal defect (VSD), atrial septal defect (ASD), or Patent Ductus Arteriosus (PDA)

41. Valvular Regurgitation
Abnormal backwards flow through a “closed” valve that doesn’t close properly

42. Ventricular Septal Defect
A defect in the interventricular septum that allows abnormal flow between the left and right ventricle

43. Atrial Septal Defect
Defect in the interatrial septum that allows abnormal flow between the left and right atrium

44. Patent Ductus Arteriosus
When the Ductus Arteriosus (a connection between the aorta and pulmonary artery during fetal circulation) does not close properly at birth and remains patent (open)

45. The ductus arteriosus, shown encircled with suture on the specimen on the left, extends from the pulmonary artery ventrally to the aorta dorsally, bypassing the lungs in fetal circulation. After birth the blood oxygen tension increases, causing the ductus to constrict and eventually become the ligamentum arteriosum, shown encircled on the specimen on the right

46. Increased preload (volume) results in dilation of the heart chambers

47. Afterload Afterload- The resistance that the heart must pump against
The higher the resistance; the greater the contractility of the ventricles
The resistance can be anywhere in the circulatory system- not just in heart

48. Facts About Afterload
Afterload is increased by any state of pressure overload such as aortic stenosis, idiopathic hypertrophic subaortic stenosis, pulmonic stenosis, systemic hypertension, of pulmonary hypertension

49. Ventricular Outflow Tract Obstructions
Aortic stenosis, idiopathic subaortic stenosis, pulmonic stenosis are all forms of outflow tract obstructions

50. Systemic Hypertension
Definition-systolic B/P above 140 mmHg and a diastolic B/P above 90 mmHg on three consecutive readings

51. Pulmonary Hypertension
Definition- An increased systolic pulmonary artery pressure above 30

52. Increased afterload results in hypertrophy (thickening) of the myocardium because the myocardium is required to generate more tension in order to perform its task

53. Inotropic Force
Definition – Force of contraction (contractility of the heart muscle)

54. Chronotropic Force
Definition – Rate of contraction (heart rate)

55. Autonomic Nervous System
Involuntary nervous system
Controls tissues that are not under volunatary control
Heart
Smooth muscles
Glands
Responds to the metabolic needs of body
Sympathetic
Parasympathetic

56. Sympathetic Fight or Flight
Increases heart rate to give body extra oxygen it needs for “fight” or “flight”
Survival instinct

57. Parasympathetic Decreases heart rate by the vagus nerve (not Vegas)
Rest and digest system, functions with actions that do not require immediate reaction
A useful acronym to summarize the functions of the parasympathetic nervous system is
SLUDD(salivation,lacrimatation,urination, digestion and defecation).

58. Maneuvers That Alter Cardiac Physiology
Valsalva
Most common in echo
Bearing Down
Releasing
Amyl Nitrate
Small capsule that is broken and ask pt to inhale fumes
Decreased peripheral resistance which increased HR rate, SV and CO

59. Other Maneuvers Inspiration increases venous return, SV & CO
Expiration decreases venous return, SV & CO
Squatting increases venous return, SV & CO
Standing decreases venous return, SV & CO

60. The End