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Transcript
2- Heart rate, heart sound and murmurs.
Objectives:
1. Describe the heart rate.
2. Explain the mechanism of the heart sounds.
Heart rate:
It is number of heart beat. The contraction of atria (atrial systole) is followed by
contraction of the ventricle (ventricular systole). SA node able to generate action
potential with rate of 60 – 100 beats/minute in young adult. When SA node does
not generate action potential, AV node generates it at rate of 40 – 60 beats /minute
and Purkinje fiber at rate of 20 – 40 beats /minute. Increase in heart rate will
reduces the duration of ventricular diastole and so reduce the time available for
ventricular filling that will reduce the stroke volume.
cardiac cycle:
The cardiac events that occur from the beginning of one heartbeat to the
beginning of the next are called cardiac cycle. If the heart rate is 75 beats/minute,
the duration of cardiac cycle is 0.8 second (0.5 s for diastole, 0.3 s for systole).
Increased heart rate leads to decrease in cardiac cycle time (systole and diastole),
but a decrease in diastolic time is more. It is not beneficial to body to increase heart
rate above 200 beats / minute, because lowering diastolic time will not leave
sufficient time to fill the ventricle, so this will decrease stroke volume. The
cardiac cycle starts by atrial systole followed by ventricular systole then by
diastole of the whole heart. A normal heart rate is varies between 60 and 100
beats/min. which is called normocardia. a fast heart rate, more than 100
beats/min. is called tachycardia. a heart rate less than 60 beats/min. is called
bradycardia.
Effects autonomic nervous system on heart rate:
Figure 6 shows the effect of sympathetic and parasympathetic on heart rate.
Stimulation of the sympathetic nervous system activates B1 receptors in the SA
node by norepinephrine which increases inward Na ion current, and increases the
rate of phase 4 depolarization. That mean the SA node is depolarized to threshold
more frequently (increase heart rate).
Stimulation of parasympathetic nervous system activates muscarinic receptors by
acetylcholine (Ach) in the SA node which decreases inward Na ion current and
decreases the rate of phase 4 depolarization. That mean SA node is depolarized to
threshold less frequently (decreased heart rate).
Figure (6): Effect of autonomic nervous system on the heart (Ganong's review
of medical physiology 2010)
Effect of Body temperature on heart rate: Increase temperature as occur in
fever, increases permeability of the cardiac muscle membrane. During fever the
heart rate increases approximately 10 beats/min. per one C°. Decrease temperature
causes greatly decreased heart rate. Contractile strength of the heart often is
enhanced by a moderate increase in temperature, but prolonged elevation of the
temperature exhausts the metabolic system of the heart and causes weakness.
Factors increase heart rate:
1-Decreased activity of baroreceptors.
2- Inspiration.
3- Excitement.
4- Anger.
5- Painful stimuli.
6- Hypoxia.
7- Norepinephrine.
8- Exercise.
9- Epinephrine.
10- Fever.
11- Thyroid hormone
Factors decrease heart rate:
1- Increased activity of baro-receptors.
2- Expiration.
3- Grief.
4- Stimulation of pain fiber in trigeminal nerve.
5- Increased intracranial pressure.
Heart sound
When the stethoscope is placed on the chest wall over the heart, two sounds are
normally heard during each cardiac cycle (1st & 2nd heart sounds). One does not
hear opening of the valve because this is slowly developing process that normally
makes no noise. When the valve close, the vanes of the valves and the surrounding
fluid vibrate under the influence of the sudden pressure in all directions through the
chest.
1-First heart sound: When the ventricles contract, first heart sound is heard by
closure of the A-V valves. Vibration is low in pitch and relatively long. The valves
bulge backward toward the atrium until the chordae tendineae abruptly stops the
back bulging.
2-Second heart sound: When the aortic and pulmonary valves close at end of
systole, they close rapidly and vibrate for short period of higher pitch.
The duration of the 1st. heart sound (0.14 second), is longer than the second heart
sound (0.11 second); this is because the semilunar valves are tauter than AV
valves, so they vibrate for short period than do AV valves. The first heart sound
has a lower frequency (pitch) which is 25-45 Hz than second heart sound (50 Hz),
this is because the tautness of the semilunar valves in comparison with much less
taut AV valves. Second heart sound is single during expiration, while the interval
between aortic and pulmonary valve closure during inspiration is frequently long
enough for the second sound to be re-duplicated (physiological splitting) because
during inspiration, the venous return increases, so there will be a delay in filling
the right ventricle and delay in the closure of the pulmonary valve.
Third heart sound: It has duration of 0.1 second, not heard normally by
stethoscope. It is physiological sound in children and in young adult. It occurs in
the middle third diastole, caused by rapid ventricular filling and is probably due to
vibration set up by the in- rush of blood. it is caused by the vibrations of the
ventricular walls, follows the opening of AV valves. It is a low-pitched sound and
can be heard after the S2. It is heard in normal heart; in children and in adult during
exercise. It is also heard in anemia, and AV valve regurgitation.
Fourth heart sound: Normally not heard with stethoscope, but by
phonocardiogram, because it has low frequency (20 Hz). It occurs immediately
before the first heart sound at late diastole. This sound occurs due to atrial
contraction. it is caused by inrush of blood into the ventricle. It is not heard in
normal hearts but occurs during ventricular overload as in severe anemia,
Thyroitoxicosis (hyperthyroidism) or in reduced ventricular compliance and in
hypertension. See figure7.
The third and fourth sounds are low frequency. They give a characteristic gallop
rhythm. Both sounds are best heard with the bell of the stethoscope at the cardiac
apex.
Figure (7): Heart sounds (Ganong's review of medical physiology 2010)
Murmurs
Murmurs or bruits are abnormal sound heard in various parts of CVS. Normal
blood flow is laminar and non-turbulent (silent) up to critical velocity. Above this
velocity and beyond an obstruction, blood flow is turbulent (creates sound). Blood
flow speeds when an artery or a heart valve is narrowed. The major cause of
cardiac murmur is the disease of the heart valves. When the orifice of a valve is
narrowed (stenosis), blood flow through it is accelerated and turbulent. When a
valve is incompetent, blood flow backward through it (regurgitating) that
accelerates flow. The timing (systole or diastole) of murmur due to stenosis or
regurgitation of any particular valve can be predicted from knowledge of
mechanical events of cardiac cycle. Murmur due to disease of a particular valve
can generally be heard well when the stethoscope is over that valve. See figure 8.
Figure (8): Turbulent blood flow (Ganong's review of medical physiology 2010)
The time of murmurs are listed below table.
Table (1): Show type of valve, abnormality and timing of murmur.
Valve
Abnormality
Timing of murmur
Aortic or pulmonary
Mitral or tricuspid
Stenosis
Systolic
Insufficiency
Diastolic
Stenosis
Diastolic
Insufficiency
Systolic