1. Summary of the Cardiac Cycle
Assessed at the bedside by noting:
Peripheral pulse at radial artery (heart rate and force)
Systolic and diastolic blood pressure (will be discussed later)
Jugular venous pulse observation
Apex beat (displacement on the left identifies left V hypertrophy)
Heart sounds
When pathology is suspected more specialized tests are carried out:
Echocardiography (non-invasive): Observing movement of the valves and walls of the heart (valve lesions, myocardial infarction, cardiac hypertrophy of different origin)
Cardiac catheterization (invasive)

2. Heart Sounds. The common heart sound are:
The first heart sound is due to the closing of the AV valves
The second heart sound is due to the closing of the aortic and pulmonary valves

4. S1 S2 OS Opening Snap S3 S4 Heart Sounds Sound Characteristics
Associated events S1
First heart sound (sounds like “lub”) Two bursts, a mitral M1 and a tricuspid T1 components
Closure of mitral & tricuspid valves S2
Second heart sound (sounds like “dub”) An aortic A2 and a pulmonary P2 component
Closure of aortic and pulmonary valves OS
Opening Snap
Opening of a stenotic mitral valve S3
Third heard sound
Diastolic filling gallop or V or protodiastolic gallop S4
Fourth heart sound
Atrial sound that creates an atrial or presystolic gallop
Note that a physiological S3 sound is present in some normal individuals, particularly children. Occurs in early diastole with rapid filling of the ventricles; When present S4 coincides with atrial contraction but usually it is abnormal

5. Location of the sounds on the chest
Each valve is best heard by a stethoscope from 4 distinct areas:
Mitral valve: Mid clavicular line of the 5th left intercostal space
Tricuspid valve: 5th interspace at the left sternal edge
Aortic valve: 2nd interspace at the right sternal edge
Pulmonary valve: 2nd interspace at the left sternal edge

6. Heart Murmurs: Abnormal heart sounds heard on auscultation which are due to faulty valves.
Incompetence: Failure of the valve to seal properly (valve may be torn, perforated, affected by rheumatic fever or a failing heart may be enlarged) such that it becomes leaky allowing blood to regurgitate through it
Stenosis: The open valve is narrowed so that a higher pressure gradient is needed to drive blood through (cicatrization after rheumatic or other infection)
Defective valves can be congenital or acquired. Abnormal valve causes blood turbulence which sets up high frequency vibrations which are heard as murmurs through the stetoscope

7. Rheumatic
heart disease

8. Benign Systolic Murmur
Heart Murmurs (cont.)
Benign Systolic Murmur
Aortic stenosis: Systolic murmur. Due to narrowing of the aortic valve when the flow during ejection becomes turbulent. Heard during ejection (systolic murmur) as ejection waxes and wanes (a crescendo – decrescendo murmur). Loudest over aortic area
Aortic stenosis murmur

9. Mitral Stenosis
left atrial pressure is elevated with mitral stenosis  induce hypertrophy of the left atrial muscle.
Elevated left atrial pressure is reflected back into the pulmonary bed and, if high enough, causes pulmonary congestion and "shortness of breath.“
A diastolic murmur associated with turbulent flow through the stenotic mitral valve can often be heard.

10. A. The aortic valve opens at 2 and closes at 7
If a murmur was heard during C and D which increased then decreased in volume, which of the following valve defects is most likely to be present?
A) Aortic incompetence
B) Aortic stenosis
C) Mitral stenosis
D) Mitral incompetence
A. The aortic valve opens at 2 and closes at 7
B. The aortic valve opens at 3 and closes at 5
C. The mitral valve opens at 2 and closes at 5
D. The mitral valve closes at 3 and opens at 5
E. The mitral valve closes at 3 and opens at 7.

11. The Atrial and Central Venous Pressure (CVP) waves
Since there are no valves between the jugular veins (JV), v. cavae ant the RA, the right JV are communicated with the RA.
Changes in pressure in the RA produces a series of pressure changes which are reflected in the central veins and recorded from the JV: a, c and v waves.
CVP is the pressure in the vein at the entrance of the RA
a wave is due to increase in pressure caused by atrial systole
av descent (minimum) is due to relaxation of the right atrium and closure of the tricuspid valve
c wave is caused in the RA by the tricuspid valve bulging back into the atrial chamber as it closes. In the internal JV the c wave (c = carotid) is caused partly by expansions of the carotid artery

12. X descent is a sharp fall in the pressure caused by atrial relaxation
v wave. As the atria fill, A pressure rises producing v wave (v = ventricular systole which is occurring at the same time)
Y descent is a fall in pressure due to the rapid emptying of the atria after the AV valve opens
Fig. 13. Jugular venous pressure changes caused by cardiac cycle

13. Clinical examination of the JVP
JP of the internal jugular vein can be assessed by expecting the right side of the neck of a recumbent subject(45 degrees). Two sudden venous collapses (the X and Y descent) should be seen and measured externally on the right side of the neck- positive JVP
In right-side cardiac failure there is a positive JVP due to accumulation of blood into the failing RV and RA

14. Cardiac Cycle
Left ventricular pressure-volume changes during one cardiac cycle A B C 65
100
135
Left ventricular volume (mL)
120 80 40
EDV
ESV D
Stroke volume
KEY
EDV = End-diastolic volume
ESV = End-systolic volume
One
cardiac
cycle
Left ventricular pressure (mm Hg)
Another way to describe the cardiac cycle is with a pressure-volume graph, shown in Figure above.
This figure represents the changes in volume (x-axis) and pressure (y-axis) that occur during one cardiac cycle.
The flow of blood through the heart is governed by the same principle that governs the flow of all liquids and gases: flow proceeds from areas of higher pressure to areas of lower pressure. When the heart contracts, the pressure increases and blood flows out of the heart into areas of lower pressure.
Figure represents pressure and volume changes in the left ventricle, which sends blood into the systemic circulation.

15. Cardiac Cycle A 65
100
135
Left ventricular volume (mL)
120 80 40
KEY
EDV = End-diastolic volume
ESV = End-systolic volume
Left ventricular pressure (mm Hg)
The cycle begins at point A. The ventricle has completed a contraction and contains the minimum amount of blood that it will hold during the cycle-end systolic volume(ESV). It has relaxed, and its pressure is also at its minimum value. Blood is flowing into the atrium from the pulmonary veins.

16. Cardiac Cycle A B 65
100
135
Left ventricular volume (mL)
120 80 40
EDV
KEY
EDV = End-diastolic volume
ESV = End-systolic volume
Left ventricular pressure (mm Hg)
Once pressure in the atrium exceeds pressure in the ven­tricle, the mitral valve between the atrium and ventricle opens (Fig , point A). Atrial blood now flows into the ventricle, increasing its volume (point A to point B). As blood flows in, the relaxing ventricle expands to accommodate the entering blood. Consequently, the volume of the ventricle increases, but the pressure in the ventricle goes up very little.
The last portion of ventricular filling is completed by atrial contraction. The ventricle now contains the maximum volume of blood that it will hold during this cardiac cycle (point B). Because maximum filling occurs at the end of ventricular relax­ation (diastole), this volume is called the end-diastolic volume (EDV). In a 70-kg man at rest, end-diastolic volume is about 135 mL, but this value varies under different conditions.

17. Cardiac Cycle A B C 65
100
135
Left ventricular volume (mL)
120 80 40
Left ventricular pressure (mm Hg)
EDV
KEY
EDV = End-diastolic volume
ESV = End-systolic volume
When ventricular contraction begins, the mitral valve closes. With both the AV valve and the semilunar valve closed, blood in the ventricle has nowhere to go. Nevertheless, the ventricle continues to contract, causing the pressure in this chamber to increase rapidly during isovolumic contraction (B —> C in Fig ).

18. Cardiac Cycle A B C 65
100
135
Left ventricular volume (mL)
120 80 40
EDV
ESV D
Stroke volume
KEY
EDV = End-diastolic volume
ESV = End-systolic volume
One
cardiac
cycle
Left ventricular pressure (mm Hg)
Once ventricular pressure exceeds the pres­sure in the aorta, the aortic valve opens (point C). Pressure con­tinues to increase as the ventricle contracts further, but ventric­ular volume decreases as blood is pushed out into the aorta (C - D).
The heart does not empty itself completely of blood each time the ventricle contracts. The amount of blood left in the ventricle at the end of contraction is known as the end-systolic volume (ESV)
The ESV (point D) is the minimum amount of blood the ventricle contains during one cycle. An average ESV value in a person at rest is 65 mL, meaning that nearly half of the 135 mL that was in the ventricle at the start of the contrac­tion is still there at the end of the contraction.
At the end of each ventricular contraction, the ventricle begins to relax. As it does so, ventricular pressure decreases. Once pressure in the ventricle falls below aortic pressure, the semilunar valve closes, and the ventricle again becomes a sealed chamber. The remainder of relaxation occurs without a change in blood volume, and so this phase is called isovolumic relaxation (Fig , D —> A). When ventricular pressure finally falls to the point at which atrial pressure exceeds ventricular pressure, the mitral valve opens and the cycle begins again

20. Stroke Volume and Cardiac Output
Amount of blood pumped by each ventricle during one cardiac cycle
EDV – ESV = stroke volume. (135 mL - 65 mL = 70 mL)
Cardiac output
Volume of blood pumped by each ventricle per minute(not the total amount of blood pumped by the heart)
CO = HR  SV
CO = 72 beats/min x 70 mL/beat 
= 5040 mL/min (or approx. 5/L min) Average = 5 L/min
What is the purpose of blood remaining in the ventricles at the end of each contraction? For one thing, the resting end-systolic volume of 65 mL provides a safety margin. With a more force­ful contraction, the heart can decrease its ESV, sending addi­tional blood to the tissues. Like many organs of the body, the heart does not usually work "all out.“
For the average contraction in a person at rest:
135 mL - 65 mL = 70 mL, the normal stroke volume
Stroke volume is not constant and can increase to as much as 100 mL during exercise. Stroke volume, like heart rate, is regu­lated by mechanisms we discuss later in this chapter.
assess the effectiveness of the heart as a pump-CO.
Average total blood volume is about 5 liters. This means that, at rest, one side of the heart pumps all the blood in the body through it in only one minute!
During exercise, cardiac output may increase to L/min. Homeostatic changes in cardiac output are accom­plished by varying the heart rate, the stroke volume, or both. Both local and reflex mechanisms can alter cardiac output, as you will see in the sections that follow.

21. Ejection Fraction – is the fraction of the end-diastolic volume that is ejected with each beat, that is, it is stroke volume (SV) divided by end-diastolic volume (EDV),
is a commonly used measure of cardiac performance.
stroke volume / end diastole volume X 100%, normal range, 55-65%.
Of the ~120 ml of blood in each ventricle (EDV) just prior to ejection, only about 70 – 80 ml (stroke volume) is ejected during ventricular systole and the residual end-systolic volume (ESV) is ~ 50 ml. From this one can calculate the ejection fraction which is SV/EDV. In this example it is 80/120 = 0.67 (or 67%). The ejection fraction is measured clinically.

22. Measurement of cardiac output by the Fick principle
‑The Fick principle can be expressed by the following equation:
Cardiac output =
_____O2 Consumption ______
[02]pulmonary vein -- 02]pulmonary artery

23. ‑The equation can be solved as follows:
1. Oxygen consumption for the whole body can be measured.
2. Pulmonary vein [02] can be measured in a peripheral artery.
3. Pulmonary artery [02] can be measured in mixed systemic venous blood.
‑For example, a man has a resting O2 consumption of 250 ml/min, a peripheral arterial O2 content of 190 ml/L of arterial blood, and a 140ml /L of venous blood. What is his cardiac output?

24. Cardiac output =
____250 ml/min _______
(190 ml / L arterial bl.‑ 140 ml/L of venous bl.) =
5000 ml/min or 5.0 L/min (typical value for a 70‑kg male)

25. Presentation InformationCO
Cardiac output
(ml/min) = HR
Heart rate
(beats/min) X SV
Stroke volume
(ml/beat)
Cardiac output (CO) is defined as the volume of blood
ejected from the heart per unit time. The usual resting values
for adults are 5 to 6 L/min, or approximately 8% of
body weight per minute.
Cardiac output is the product of heart rate (HR) and stroke
volume (SV), the volume of blood ejected with each beat:
CO SV HR (1)
Stroke volume is the difference in the volume of blood in
the ventricle at the end of diastole—end-diastolic volume—
and the volume of blood in the ventricle at the end of systole—
end-systolic volume.
CONFIDENTIAL

26. Presentation Information
Factors Affecting Cardiac Output- All factors that control HR and SV will influence CO
physiology
CONFIDENTIAL

27. Question time-
Incorrect statement about effect of Parasympathetic stimulation of the heart is-
A) Decreases heart rate by acting on SA node
B)Enhances potassium permiability hyperpolarizing the SA node membrane
C)Influences AV node decreasing its excitability,prolonging transmission through it.
D)Causes decrease in contractile strenght of ventricular muscle.

28. Factors Affecting Heart rate
Presentation Information
Factors Affecting Heart rate
1. Autonomic innervation
Sympathetic stimulus increases heart rate Ex. During fight or flight response
Parasympathetic stimulation decreases heart rate,dominant during resting conditions.
Balance of symp. & parasymp.
2. Hormones
Epinephrine : Increases heart rate
CONFIDENTIAL

29. Factors that Affect Cardiac Output
EXTRINSIC
INTRINSIC

30. A. Intrinsic regulation of stroke volume
Intrinsic regulation is due to the intrinsic ability of the heart to adjust its SV in responses to changes in the input (venous return/ EDV-?)
This property of the heart is called the Frank-Starling Law of the Heart. Simply stated the law says that within defined limits the heart will pump whatever volume of blood is received
This intrinsic control depends on the length- tension relationship of cardiac muscle.

31. Question time again-
In skeletal muscle the resting muscle length is approximately the optimal length at which maximal tension can be developed during a subsequent contraction-
A)True
B)False.

32. Fig. -. Frank-Starling Law of the heart
Fig. -. Frank-Starling Law of the heart. The graph illustrates the relationship between SV and changes in ventricular end-diastolic volume. The insets showing diagrammatic sarcomeres, illustrate the relationship between end-diastolic volume and myofilament overlap.

33. Optimal Length Length-force relationships in intact heart:
a Frank-Starling curve
Optimal Length
Figure 14-28

34. Preload and afterload of the heart
The force of contraction of cardiac muscle is dependent upon its preloading and afterloading
In vivo the preload is the degree to which the myocardium is stretched before it contracts
The afterload is the resistance against which blood is expelled (the blood pressure)
The Frank-Starling Law of the heart can be restated as: increasing preload increases the force of contraction

35. Factors affecting end-diastolic volume, e. g
Factors affecting end-diastolic volume, e.g. the degree to which cardiac muscle is stretched
Increase
Stronger atrial contraction
Increased total blood volume
Increased venous tone
Increased pumping action of skeletal muscle
Increased negative intrathoracic pressure
Decrease
Standing
Increased intrapericardial pressure(Cardiac tamponade)
Decreased ventricular compliance

37. B. Extrinsic Regulation of Stroke Volume
Any changes in the strength of cardiac contraction that occur independently of changes in EDV are referred to as changes in myocardial contractility
A change in myocardial contractility (Inotropism) is mechanistically different from the altered vigor of contraction seen with changes in muscle length
Changes in contractility are direct result of changes in the rate and extent of Ca2+ movement into the cytoplasm
Increased firing of cardiac sympathetic nerve results in  in both the rate (chronotropic action) and extent (inotropic action) of myocardial contractions

38. Relationship between contractility and intracellular Ca2+ : contractility is a result of cytoplasmic Ca2+ concentration. This is the result of both release of Ca2+ from the sarcoplasmic reticulum and influx of Ca2+ from the extracellular space. Increased Ca2+ results in activation of additional crossbridges (indicated in red)

39. Fig. . Changes in SV due to changes in contractility are mechanistically different from those occurring as a result of EDV. The two mechanisms can operate simultaneously to  SV (lower panel). EDV = end- diastolic volume; ESV = end-systolic volume; SV = stroke volume (Human Physiology)

40. sympathetic
Fig. 14. Effect of changes in myocardial contractility on the Frank-Starling curve. The curve shifts downward and to the right as contractility is decreased. The major factors influencing contractility are summarized on the right (dashed lines indicate portions of the curve where maximum contractility has been exceeded). W.Ganong. Review of Medical Physiology

41. Afterload and Cardiac Performance
Presentation Information
Afterload and Cardiac Performance
Afterload: all the factors that impede fiber shortening, in this case it would be all the factors that impede the ejection of blood from the ventricle. What the heart has to pump against
Volume of blood in the arterial circulation
Pressure in aorta at onset of ejection (DAP)
Compliance of aorta
Size of outflow orifice
CONFIDENTIAL

42. Factors that affect stroke volume.

43. Pressure-Volume Loops Provide Information Regarding Ventricular Performance
Figure shows a plot of left ventricular pressure as a
function of left ventricular volume. One cardiac cycle is
represented by one counterclockwise circuit of the loop. At
point 1, the mitral valve opens and the volume of the ventricle
begins to increase. As it does, diastolic ventricular
pressure rises a little, depending on given ventricular diastolic
Compliance.
The less the pressure rises with the filling of the ventricle,
the greater the compliance. The volume increase between
point 1 and point 2 occurs during rapid and reduced ventricular
filling and atrial systole. At point 2,
the ventricle begins to contract and pressure rises rapidly.
Because the mitral valve closes at this point and the aortic
valve has not yet opened, the volume of the ventricle cannot
change (isovolumetric contraction). At point 3, the aortic
valve opens. As blood is ejected from the ventricle, ventricular
volume falls. At first, ventricular pressure continues
to rise because the ventricle continues to contract and build
up pressure—this is the period of rapid ejection in Figure
. Later, pressure begins to fall—this is the period of reduced
ejection in Figure . The reduction in ventricular
volume between points 3 and 4 is the difference between
end-diastolic volume (3) and end-systolic volume (4) and
equals stroke volume.
At point 4, ventricular pressure drops enough below aortic
pressure to cause the aortic valve to close. The ventricle
continues to relax after closure of the aortic valve, and this
is reflected by the drop in ventricular pressure. Because the
mitral valve has not yet opened, ventricular volume cannot
change (isovolumetric relaxation). The loop returns to
point 1 when the mitral valve opens and, once more, the
ventricle begins to fill.

44. Increased Preload
Normal P-V loop
Increased Afterload
Increased Contractility

46. The figure below shows pressure volume loops for two situations
The figure below shows pressure volume loops for two situations. When compared with loop A, loop B demonstrates
(A) Increased preload
(B) Decreased preload
(C) Increased contractility
(D) Increased afterload
(E) Decreased afterload

48. Frank-Starling curve
In Heart Failure-
Stroke volume
Stroke volume

49. Which of the following would cause a decrease in stroke volume, compared with the normal resting value?
(A) Reduction in afterload
(B) An increase in end-diastolic pressure
(C) Stimulation of the vagus nerves
(D) Electrical pacing to a heart rate of 200 beats/min
(E) Stimulation of sympathetic nerves to the heart

50. Myocardial Hypertrophy
Presentation Information
Myocardial Hypertrophy
Concentric
Cross sectional area of a muscle increases when repeatedly exposed to an elevated work load over a sustained period of time
In cardiac muscle this can be the result of increased wall tension caused by increased preload or increased after load .
eccentric
CONFIDENTIAL

51. Changes in the radius of the ventricles (curvature of the ventricle) can affect ventricular pressure (Laplace’s Law) and efficiency of the heart as a pump
The pressure generated in a sphere is directly proportional to the wall tension (T) developed, and inversely related to the radius of the sphere (r) (Law of Laplace)
P = 2T/r
In normal conditions, during ejection phase of cardiac cycle the volume of blood in the V falls, and the r of the V decreases. As the radius falls, the tension in the V walls is more effective in ventricular pressure
In chronic cardiac failure the contractility is reduced and the heart becomes less effective as a pump and dilates radius of the ventricles and reduces its curvature, and ejection gets more difficult as it proceeds
As related to the heart, this law means that the amount of pressure generated in the ventricle is directly proportional to the tension (force) developed in the ventricular muscle. The greater the force generated by the ventricles, the greater the tension in the walls and the greater the pressure of the blood inside. However, when the radius of the ventricle chamber is large, the amount of tension developed is less and so the pressure developed in the ventricle is less. So, as the heart becomes more and more dilated the ventricles are not so effective in converting tension into ventricular pressure which reduces the efficiency of the heart as a pump.
Conversely, the smaller the radius, the less tension is needed to raise the ventricular pressure.
Ventricular distension has advantages and disadvantages
The Laplace effect and Frank-Starling mechanism act in opposition. Distension of the ventricle raises its contractile force through the Frank-Starling mechanism but reduces the pressure generated by a given force through Laplace’s Law. In a healthy heart, the gain in contractile energy by the Starling mechanism greatly outweighs the Laplace effect. In moderate to severe heart failure, the cardiac distension has stretched the myocardial fibres so much that the heart is on the plateau of the Starling curve.
Laplace’s Law and Heart Failure
The failing heart is often grossly dilated which means that its radius is enlarged. Conversion of tension into ventricular pressure then is adversely affected. Laplace’s law states that to reach the normal ventricular systolic pressure, the heart has to contract with a greater force i.e. it has to exert a greater contractile tension and it needs more oxygen. Such a heart is less efficient as a pump. An important therapeutic goal in heart failure is to reduce cardiac distension and this is achieved by diuretics which lower the cardiac filling pressure.

52. Point Y in the figure below is the control point. Which point
corresponds to a combination of increased contractility and increased ventricular filling?
(A) Point A
(B) Point B
(C) Point C
(D) Point D
(E) Point E

53. Summary of the regulation of Cardiac Output
The Cardiac output is the volume of blood pumped by each ventricle and equals the product of heart rate and stroke volume
Heart rate is  by stimulation of the sympathetic nerves to the heart (NE) and by epinephrine (E); it is  by stimulation of the parasympathetic nerves to the heart
Stroke volume is increased mainly by an  in end-diastolic volume (the Frank-Starling mechanism) and by an  in contractility due to sympathetic-nerve stimulation or to epinephrine. Afterload can also play a significant role in certain situations

54. Swollen legs
A 47 year old woman was brought to the hospital because of severe shortness of breath and swelling of her lower body. Over the last year *she had noticed periods of shortness of breath while doing her housework (exertional dyspnea). She also had shortness of breath while lying down (orthopnea). The patient often awoke at night with a sensation of not getting enough air and she had to sit or stand to obtain relief (paroxysmal nocturnal dyspnea). #More recently she noticed swelling first of her lower extremities and then of her lower abdomen. The swelling was
worse through the day and decreased overnight. She reported awakening three to four times a night to urinate. The patient did not remember any ill health before these problems began.
Physical examination revealed a woman sitting up in bed in mild to moderate respiratory distress. Her blood pressure was 100/70, pulse was 120 and weak. Respirations were 26 per minute and labored. There was jugular venous distension, even while she was sitting. Palpation of the sternum revealed a restrosternal lift. Auscultation of the heart revealed an opening snap and a long diastolic rumble at the apex. Auscultation of the lungs revealed crackles halfway up the lungs. There was also severe lower extremity edema. During her hospitalization, as part the work-up, the following studies were done.

55. Arterial-venous O2 content difference 5.3 ml/dl blood
Patient
Normal
O2 consumption(VO2)
188 ml/min
mL/min
Arterial-venous O2 content difference
5.3 ml/dl blood
ml/dl blood
Heart rate
122
beats/min
Mean Pulmonary Capillary Wedge Pressure
25 mm Hg
<15 mmHg
Right Ventricular Systolic pressure
End-Diastolic pressure
80 mm Hg
16 mm Hg
<28mmHg
<8mmHg
Right Ventricular End Diastolic volume
140 ml/m2
60-88mL/m2
Use the data in the table above to calculate cardiac output and ejection fraction
· Evaluate the mean electrical axis of the heart using the ECG shown overleaf