Transcript [Recovered] @2 (vishdess1-PC`s conflicted copy

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)
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
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
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
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
Rheumatic
heart disease
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
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.
If a murmur
heard
during
C and
increased
A. Thewas
aortic
valve
opens
at D2 which
and closes
at 7then
decreased in volume, which of the following valve defects is
Thetoaortic
valve opens at 3 and closes at 5
mostB.
likely
be present?
C. The
mitral valve opens at 2 and closes at 5
A) Aortic
incompetence
B) Aortic
stenosis
D. The
mitral valve closes at 3 and opens at 5
C) Mitral
stenosis
E. The
mitral valve closes at 3 and opens at 7.
D) Mitral incompetence
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
• 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
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
Cardiac Cycle
Left ventricular pressure-volume changes during one
cardiac cycle
KEY
Left ventricular pressure (mm Hg)
EDV = End-diastolic volume
ESV = End-systolic volume
Stroke volume
120
D
ESV
80
C
One
cardiac
cycle
40
EDV
B
A
0
65
100
Left ventricular volume (mL)
135
Cardiac Cycle
KEY
EDV = End-diastolic volume
ESV = End-systolic volume
Left ventricular pressure (mm Hg)
120
80
40
A
0
65
Left ventricular volume (mL)
100
135
Cardiac Cycle
KEY
EDV = End-diastolic volume
ESV = End-systolic volume
Left ventricular pressure (mm Hg)
120
80
40
EDV
B
A
0
65
Left ventricular volume (mL)
100
135
Cardiac Cycle
KEY
EDV = End-diastolic volume
ESV = End-systolic volume
Left ventricular pressure (mm Hg)
120
80
C
40
EDV
B
A
0
65
Left ventricular volume (mL)
100
135
Cardiac Cycle
KEY
EDV = End-diastolic volume
ESV = End-systolic volume
Stroke volume
120
D
Left ventricular pressure (mm Hg)
ESV
80
C
One
cardiac
cycle
40
EDV
B
A
0
65
Left ventricular volume (mL)
100
135
Stroke Volume and Cardiac Output
• Stroke volume
– 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
Ejection Fraction – is the fraction of the enddiastolic volume that is ejected with each beat,
that is, it is stroke volume (SV) divided by enddiastolic volume (EDV),
is a commonly used measure of cardiac
performance.
stroke volume / end diastole volume X 100%,
normal range, 55-65%.
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
-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?
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)
CO
Cardiac output
(ml/min)
=
HR
Heart rate
(beats/min)
25
X
SV
Stroke
volume
(ml/beat)
Factors Affecting Cardiac OutputAll factors that control HR and SV will influence CO
physiology
26
Question time• Incorrect statement about effect of
Parasympathetic stimulation of the heart isA) 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.
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
Factors that Affect Cardiac Output
EXTRINSIC
INTRINSIC
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.
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 contractionA)True
B)False.
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.
Length-force relationships in intact heart:
a Frank-Starling curve
Optimal Length
Figure 14-28
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
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
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
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)
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)
sympathetic
Fig. 14. Effect of changes in myocardial contractility on the FrankStarling 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
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
Factors that affect stroke volume.
Pressure-Volume Loops Provide Information Regarding
Ventricular Performance
Normal P-V loop
Increased Afterload
Increased Preload
Increased Contractility
1. 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
Stroke volume
Stroke volume
Frank-Starling curve
In Heart Failure-
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
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
50
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
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
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 enddiastolic 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
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.
O2 consumption(VO2)
Arterial-venous O2 content
difference
Heart rate
Mean Pulmonary Capillary
Wedge Pressure
Right Ventricular Systolic
pressure
End-Diastolic pressure
Right Ventricular End
Diastolic volume
Patient
Normal
188 ml/min
5.3 ml/dl blood
200-250mL/min
3.0-5.0 ml/dl blood
122
25 mm Hg
60-100 beats/min
<15 mmHg
80 mm Hg
16 mm Hg
<28mmHg
<8mmHg
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