Lab 19 Flashcards
1
Q
Every physical examination includes an assessment of the
A
cardiovascular system, in which the heart rate is counted, heart sounds are auscultated, and the blood pressure is measured
2
Q
Heart sounds are produced by
A
the closing of valves at certain points during the cardiac cycle.
3
Q
The first heart sound, called
A
S1,
4
Q
S1 is caused by the
A
simultaneous closure of the mitral and tricuspid valves when the ventricles begin to contract during isovolumetric contraction.
5
Q
The second heart sound, called
A
S2,
6
Q
S2 is caused by
A
is caused by simultaneous closure of the aortic and pulmonary valves as the ventricles begin to relax during isovolumetric relaxation.
7
Q
The process of listening to heart sounds is known as
A
auscultation (aws-kuhl-TAY-shun).
8
Q
Heart sounds typically are auscultated in four areas, each of which is named for the
A
valve that is best heard at that specific location.
9
Q
The position of each area is described relative to the
A
sternum and the spaces between the ribs, known as intercostal spaces.
10
Q
The first intercostal space is located between the
A
first and second rib, which is roughly inferior to the clavicle. From the clavicle you can count down to consecutive spaces to auscultate in the appropriate areas.
11
Q
The four areas,are as follows:
A
- Aortic area.; 2. Pulmonic area; 3. Tricuspid area. ; Mitral area
12
Q
- Aortic area.
A
The aortic area is the location where the sounds of the aortic valve are best heard. It is located in the second intercostal space (between ribs two and three) at the right sternal border (to the right of the sternum).
13
Q
- Pulmonic area.
A
The pulmonary valve is best heard over the pulmonic area, which is located at the second intercostal space at the left sternal border.
14
Q
- Tricuspid area.
A
The sounds produced by the tricuspid valve are best heard over the tricuspid area, which is found in the fourth intercostal space at the left sternal border.
15
Q
- Mitral area.
A
The mitral area is located in the fifth intercostal space at the left midclavicular line (draw an imaginary line down the middle of the clavicle).
16
Q
The following variables are evaluated during heart auscultation.
A
■■Heart rate.
17
Q
■■Heart rate.
A
The heart rate refers to the number of heartbeats per minute.
18
Q
If the rate is more than 100, it is termed
A
tachycardia (tak-ih-KAR-dee-uh).
19
Q
If the rate is below 60 beats per minute, it is termed
A
bradycardia (bray-dih-KAR-dee-uh).
20
Q
■■Heart rhythm.
A
The heart’s rhythm refers to the pattern and regularity with which it beats.
21
Q
Some rhythms are regularly irregular, in which the
A
rhythm is irregular but still follows a defined pattern.
22
Q
Others are irregularly irregular, in which
A
the rhythm follows no set pattern.
23
Q
■■Additional heart sounds.
A
Sometimes sounds in addition to S1 and S2 are heard, which could be a sign of pathology. These sounds are called S3, which occurs just after S2, and S4, which occurs immediately prior to S1.
24
Q
■■Heart murmur.
A
A heart murmur is a clicking or “swooshing” noise heard between the heart sounds. Murmurs are caused by a valve leaking, called regurgitation, or by a valve that has lost its pliability, called stenosis (sten-OH-sis).
25
stenosis
where a valve has lost its pliability
26
Heart sounds are auscultated with a
stethoscope (STETH-oh-skohp), which you will use in this unit.
27
Most stethoscopes contain the following parts (Fig. 19.2)
:
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■■Earpieces
are gently inserted into the external auditory canal and allow you to auscultate the heart sounds.
29
■■The diaphragm
is the broad, flat side of the end of the stethoscope. It is used to auscultate higher-pitched sounds and is the side used most often in auscultation of heart sounds.
30
■■The bell
is the concave, smaller side of the end of the stetho-scope. It is used to auscultate lower-pitched sounds.Note that sounds are not audible through both the bell and the diaphragm at the same time. Typically, the end can be flipped from one side to the other by simply turning it clockwise or counterclockwise. Before auscultating with either side, lightly tap the end to ensure that you can hear sound through it. If the sounds are faint or muted, turn the end to the other side and try again.
31
If the end of your stethoscope has only one side (the diaphragm), it works slightly differently.
In these stethoscopes, placing light pressure on the end as you are auscultating yields sounds associated with the diaphragm, while placing heavier pressure yields sounds associated with the bell. If you are trying to auscultate with the diaphragm and the sounds are faint, try decreasing the amount of pressure you are placing on the end. When you have completed the procedure, answer Check Your Understanding question 1 (p. 527).
32
A vascular examination is the portion of a physical examination that assesses the
health of the blood vessels.
33
Two other common tests include
auscultation of vessels; measuring capillary refill time
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auscultation of vessels to check for
noises called bruits (broo-eez) and
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measuring capillary refill time
capillary beds to refill.
36
Vascular disease in large vessels may lead to
turbulent blood flow through the vessel, producing a bruit.
37
Blood flows through arteries, which branch into successively
smaller arteries until they branch into arterioles.
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Arterioles then feed
capillary beds, known collectively as the
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microcirculation,
where gas, nutrient, and waste exchange takes place (Fig. 19.3).
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Capillary beds are then drained by
venules,
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which merge to form
veins.
42
Notice that capillary beds form
interweav-ing networks.
43
interweav-ing networks creates
This creates a large surface area for the rapid exchange of substances that occurs across capillary walls.
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Tissue Perfusion
The amount of blood that flows to a tissue through capillary beds is called tissue perfusion.
45
A tissue’s perfusion is tightly regulated—if it’s too low,_________ , and if it’s too high, ____________
the cells will get insufficient oxygen and nutrients and may die; the high pressure in the capillaries can force excess water out of the blood and into the interstitial fluid
46
A normal capillary refill time measures
1–3 seconds; a value greater than 3 seconds may signify some sort of pathology (but be aware that it may also just mean that the patient is cold).
47
How to measure capillary refill time
press each finger till it turns white, wait and count till fingers turn pink again
48
Blood pressure is defined as
the pressure exerted by the blood on the walls of the blood vessels.
49
Blood Pressure is determined by the following three factors:
cardiac output; peripheral resistance; blood volume
50
1. Cardiac output.
Cardiac output is the amount of blood each ventricle pumps in 1 minute.
51
Cardiac Output is a product of
It is a product of heart rate and stroke volume, or the amount of blood pumped with each beat.
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2. Peripheral resistance.
Resistance is defined as any impedance to blood flow encountered in the blood vessels.
53
Peripheral resistance is determined largely by
It is determined largely by the degree of vasoconstriction or vasodilation in the systemic circulation.
54
Vasoconstriction does what to resistance, and vasodilation does what to resistance
increases resistance; decreases resistance
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Other factors that influence resistance include
obstructions such as atheromatous plaques within the arteries.
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Resistance is highest
away from the heart in the body’s periphery, so it is often called peripheral resistance.
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3. Blood volume.
The amount of blood found in the blood vessels at any given time is known as the blood volume.
58
Blood volume is greatly influenced by
It is greatly influenced by overall fluid volume and is largely controlled by the kidneys and hormones of the endocrine system.
59
Note that cardiac output and peripheral resistance are factors that can be altered quickly to change
blood pressure.
60
Alterations to blood volume, however, occur
relatively slowly and generally require several hours to days to have a noticeable effect.
61
Arterial blood pressure is measured clinically and experimentally using instruments called a
sphygmomanometer (sfig-moh-muh-NAH-muh-ter) and a stethoscope.
62
This procedure yields two pressure readings:
1. Systolic pressure.; Diastolic pressure
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1. Systolic pressure
The pressure in the arteries during the period of ventricular contraction, called ventricular systole (SIS-toh-lee), is known as the systolic pressure (sis-TAHL-ik). This is the larger of the two readings, averaging between 100 and 120 mmHg.
64
2. Diastolic pressure.
The pressure in the arteries during ventricular relaxation, or ventricular diastole (dy-AEH-stoh-lee), is the diastolic pressure (dy-uh-STAHL-ik). This is the smaller of the two readings, averaging between 60 and 80 mmHg.
65
Arterial blood pressure is measured by
placing the cuff of the sphygmomanometer around the upper arm.
66
When the cuff is inflated, it compresses the
brachial artery and cuts off blood flow.
67
When the pressure is released to the level of the systolic arterial pressure, blood flow through the brachial artery resumes
but is turbulent.
68
This results in noises known as
Korotkoff sounds (koh-ROT-koff), which may be auscultated with a stethoscope.
69
The autonomic nervous system (ANS) exerts a great deal of control over blood pressure through its influence on
cardiac output, peripheral resistance, and blood volume.
70
Recall that the two divisions of the ANS are the
sympathetic nervous system (SNS) and the parasympathetic nervous system (PSNS).
71
The SNS is the
“fight or flight” branch that helps the body to maintain homeostasis during situations such as exercise, emotion, and emergency.
72
SNS neurons release
Norepinephrine onto cardiac muscle cells to increase the rate and force of their contraction, which increases cardiac output.
73
SNS neurons also release
They also release norepinephrine onto the smooth muscle cells lining the walls of blood vessels, which triggers most blood vessels to constrict (note that some blood vessels, such as those serving skeletal muscles, dilate).
74
This vasoconstriction increases
peripheral resistance.
75
The combined effect of increased cardiac output and peripheral resistance leads to an
increase in blood pressure
76
.The PSNS is the
“rest and digest” branch of the ANS that helps the body to maintain homeostasis in between those bursts of sympathetic activity.
77
As you might expect, the PSNS has the opposite effects on
blood pressure as from the SNS.
78
Parasympathetic neurons release
acetylcholine onto cardiac muscle cells and slow the heart rate, which decreases cardiac output.
79
The vast majority of blood vessels aren’t innervated by PSNS neurons; however, blood vessels do dilate when
sympathetic stimulation stops
80
. So indirectly, vasodilation occurs when PSNS activity
increases, which decreases peripheral resistance.
81
Together, the decreased cardiac output and peripheral resistance cause a
decrease in blood pressure.
82
Peripheral artery disease (PAD), also called
peripheral vascular disease,
83
peripheral vascular disease,
is any disease of the arteries outside of the brain and coronary circuit. Although any of these vessels can be affected, it is the arteries of the lower limbs that tend to show the most symptoms of the disease.
84
There are many risk factors for PAD; some of the most common include
poorly controlled diabetes mellitus, atherosclerosis, cigarette smoking, and hypertension.
85
The ankle–brachial index (ABI) is a test that is used to assess the
severity of PAD.
86
The ABI compares the
systolic blood pressure in the legs (the “ankle” portion) to the systolic blood pressure in the arms (the “brachial” portion).
87
If an individual has PAD, the ankle pressure is generally
much lower than the brachial pressure, which reflects the fact that less blood is flowing to the lower limbs.
88
The ABI is obtained by
dividing the systolic pressure in the ankle by the systolic pressure in the arm.
89
Typically, the ABI is a decimal number because ankle pressure is slightly lower than the brachial pressure. This is because
the legs are farther from the heart than the arms, which causes a slight decline in blood pressure.
90
intermittent claudication
(temporary blockages to blood flow)
91
Note that in younger or more athletic persons, the ABI is often greater than 1. This is simply a result of
more muscle mass in the lower limb, which is difficult to completely compress with a sphygmomanometer cuff. This falsely elevates the ankle pressure, and so it appears higher than the brachial pressure.
92
Within the heart we find two populations of cardiac muscle cells:
pacemaker cells, contractile cells
93
pacemaker cells which account for
which account for about 1 percent of the total cells of the heart,
94
and contractile cells,
hich make up the remainder.
95
Pacemaker cells are unique because they
rhythmically, spontaneously depolarize and have action potentials.
96
It is their depolarizations that trigger the
contractile cells to depolarize and have action potentials.
97
There are three groups of pacemaker cells (Fig. 19.6):
■■Sinoatrial node. ; ■■Atrioventricular node. ;
98
■■Sinoatrial node.
We find the cells of the sinoatrial node (sy-noh-AY-tree-uhl), or SA node, in the superior portion of the right atrium. The SA node depolarizes about 60 times per minute and is the normal pacemaker of the heart.
99
■■Atrioventricular node.
The next cluster of pacemaker cells is collectively called the atrioventricular node, or AV node, which is located posterior and medial to the tricuspid valve. It depolarizes about 40 times per minute and acts as a backup pacemaker should the SA node stop pacing the heart.
100
■■Purkinje fiber system.
The final series of pacemaker cells is a group that is collectively called the Purkinje fiber system (pur-KIN-jee).
101
The system begins with an
atrioventricular bundle (AV bundle) in the inferior interatrial septum and the superior interventricular septum.
102
The AV bundle then splits into the
right and left bundle branches, which run down the right and left sides of the interventricular septum, respectively.
103
Near the apex of the heart, the bundle branches split into the
terminal branches, which fan out through the ventricles and contact ventricular contractile cells.
104
Together, these three groups of pacemaker cells make up what is known as the
cardiac conduction system.
105
This system is named as such because it represents a sort of
“hardwiring” of the heart.
106
cardiac conduction system allows
It allows depolarizations from pacemaker cells to spread extremely rapidly to other pacemaker cells and to contractile cells.
107
The cells of the SA node
depolarize; these depolarizations spread through the atria via specialized atrial conducting fibers, and the atrial contractile cells depolarize.
108
2. The impulse reaches the AV node as
the atrial cells complete their action potentials and contract.
109
Conduction slows at the AV node, a phenomenon known as the
AV node delay, which allows the atria to depolarize and contract before the ventricles depoarize and contract.
110
The depolarization next propagates along the
Purkinje fiber system, first along the AV bundle.4.
111
The depolarization spreads down either side of the
interventricular septum along the right and left bundle branches.5.
112
The terminal branches trigger contractile cells of the ventricles to
depolarize, have action potentials, and contract.
113
The electrical activity of the heart can be examined by taking an
electrocardiogram, or ECG,
114
electrocardiogram, or ECG,
which is a recording of the changes that occur in the electrical activity of cardiac muscle cells over a period of time.
115
Electrical activity is recorded by placing electrodes on the surface of the skin that record the changes in
electrical activity.
116
The changes in electrical activity are visible on the ECG as
waves.
117
Note that if there is no net change in electrical activity, the line on the ECG is
flat.
118
However, even when the ECG is flat between waves, the cells of the heart are in some phase of an
action potential.
119
Also note that the ECG appears flat during pacemaker cell
action potentials.
120
This is because
there are so few pacemaker cells in the heart that their activity isn’t detectable with a standard ECG.
121
A standard ECG recording consists of five waves, each of which represents the
depolarization or repolarization of different parts of the heart.
122
The five parts of ECG
p wave; qrs complex; t wave; P-R interval; Q-T interval
123
■■P wave.
The initial P wave shows the depolarization of the cells of the right and left atria. It is fairly small because of the small number of cells in the atria. Note that the flat segment right before the P wave is when the SA node depolarization takes place.
124
■■QRS complex.
The QRS complex is actually a set of three waves that represent the depolarization of the right and left ventricles. The first wave is the Q wave, a downward deflection, the next is the R wave, a large upward deflection, and the last is the S wave, the final downward deflection. The large size of the QRS com-plex compared with the P wave results from the large number of ventricular cells.
125
■■T wave.
The small T wave is usually the final wave, and it represents the repolarization of the right and left ventricles.
126
The waves aren’t the only important landmarks of the ECG. In addition, we consider the
periods between the waves,
127
periods between the waves,
which show the spread of electrical activity through the heart and phases of the contractile cells’ action potentials.
128
We look at two types of periods:
intervals, segments
129
intervals,
which include one or more waves in the measurement,
130
and segments,
which do not include waves in the measurement.
131
One important interval is the R-R interval,
or the period of time between two R waves.
132
R-R interval represents the
the generation and spread of an action potential through the heart. It can be used to determine the heart rate, which we discuss shortly.
133
Another interval we examine is the P-R interval,
defined as the period from the beginning of the P wave to the beginning of the QRS complex. During the P-R interval, the depolarization from the SA node spreads through the atria to the ventricles via the AV node; this interval includes the AV node delay.
134
A final key interval is the Q-T interval,
the time from the beginning of the Q wave to the end of the T wave.
135
During the Q-T interval, the ventricular cells are
depolarizing and repolarizing.wn as a normal sinus rhythm, which means that the SA node is pacing the heart at a rate between 60
136
An important segment that we examine is the S-T segment,
which is between the end of the S wave and the begin-ning of the T wave. This segment is recorded during the ventricles’ plateau phase. Recall that there is no net change in electrical activity during this phase, and for this reason, the S-T segment is generally flat.
137
The normal pattern seen on an ECG is known as a
normal sinus rhythm
138
normal sinus rhythm means
that the SA node is pacing the heart at a rate between 60 and 100 minutes per minute
139
Any deviation from the normal sinus rhythm is known as
dysrhythmia or arrhythmia.
140
An electrocardiograph records the tracing at a standard speed of 25 mm/second. This allows us to
determine precisely the heart rate and the duration of the intervals we discussed. As you can see in Figure 19.7,
141
each small box on the ECG tracing measures
0.04s, and each large box measures 0.20s.
142
Five large boxes together measure
1 second.
143
Determining the duration of most intervals is simple—
just count the small or large boxes, and add the seconds together.
144
Calculating the heart rate is equally simple: count the number of large boxes, and divide
300 by this number. For example, if you count 4.2 boxes: 300/4.2 = 71 beats per minute.
