ch 20 heart and neck vessels Flashcards

1
Q

system consists of the heart (a muscular pump) and the blood vessels

A

cardiovascular (CV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

is the area on the anterior chest directly overlying the heart and great vessels

A

precordium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

heart and great vessels are located between the lungs in the middle third of the thoracic cage

A

(mediastinum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

lies behind the right ventricle and forms the apex and slender area of the left border.

A

left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

lies to the right and above the right ventricle and forms the right border

A

right atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

is located posteriorly, with only a small portion, the left atrial appendage, showing anteriorly.

A

left atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

blood vessels are arranged in two continuous loops, the

A

pulmonary circulation and the systemic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

“top” of the heart is the

A

base

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

bottom” is the

A

apex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

During contraction the apex beats against the chest wall, producing an
- fifth intercostal space, 7 to 9 cm from the midsternal line.

A

apical impulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

lie bunched above the base of the heart.

A

great vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

return unoxygenated venous blood to the right side of the heart

A

superior and inferior vena cava

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

leaves the right ventricle, bifurcates, and carries the venous blood to the lungs

A

pulmonary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

return the freshly oxygenated blood to the left side of the heart

A

pulmonary veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

carries it out to the body

A

aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

is a tough, fibrous, double-walled sac that surrounds and protects the heart
-two layers that contain a few milliliters of serous pericardial fluid. This ensures smooth, friction-free movement of the heart muscle.

A

pericardium (heart wall has numerous layers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

is adherent to the great vessels, esophagus, sternum, and pleurae and is anchored to the diaphragm.

A

pericardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

is the muscular wall of the heart; it does the pumping

A

myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

is the thin layer of endothelial tissue that lines the inner surface of the heart chambers and valves.

A

endocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

two atrioventricular (AV) valves separate the

A

atria and the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

right AV valve is the

A

tricuspid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

left AV valve is the

A

bicuspid or mitral valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

are anchored by collagenous fibers (chordae tendineae) to papillary muscles embedded in the ventricle floor.

A

valves’ thin leaflets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

open during the heart’s filling phase, or diastole, to allow the ventricles to fill with blood

A

AV valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

, the AV valves close to prevent regurgitation of blood back up into the atria.
-papillary muscles contract at this time so the valve leaflets meet and unite to form a perfect seal without turning themselves inside out.

A

pumping phase, or systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

are set between the ventricles and the arteries

-. Each valve has three cusps that look like half moons

A

semilunar (SL) valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

are the pulmonic valve in the right side of the heart and the aortic valve in the left side of the heart. They open during pumping (systole), when blood ejects from the heart.

A

SL valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

between the vena cava and the right atrium or between the pulmonary veins and the left atrium. For this reason abnormally high pressure in the left side of the heart gives a person symptoms of pulmonary congestion, and abnormally high pressure in the right side of the heart shows in the distended neck veins and abdomen.

A

no valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

first passive filling phase is called

A

early or protodiastolic filling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

active filling phase is called

A

presystole, or atrial systole, or sometimes the atrial kick

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

atrial systole occurs during

A

ventricular diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

ventricular walls contract. This contraction against a closed system works to build pressure inside the ventricles to a high level

A

(isometric contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

closure of the semilunar valves causes the second heart sound

A

(S2) and signals the end of systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

all four valves are closed, and the ventricles relax

A

(called isometric or isovolumic relaxation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

pressures in the right side of the heart are much lower than those of the left side because less energy is needed to pump blood to its destination, the

A

pulmonary circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

first heart sound the mitral component (M1) closes just before the tricuspid component (T1). And with(diastole) S2, aortic closure (A2) occurs slightly before pulmonic closure (P2).

A

Events in the Right and Left Sides. (left side close before right)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

occurs with closure of the AV valves and thus signals the beginning of systole.
-mitral component of the first sound (M1) slightly precedes the tricuspid component (T1), but you usually hear these two components fused as one sound. You can hear S1 over all the precordium, but usually it is loudest at the apex.

A

first heart sound (S1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

occurs with closure of the semilunar valves and signals the end of systole. The aortic component of the second sound (A2) slightly precedes the pulmonic component (P2). Although it is heard over all the precordium, S2 is loudest at the base

A

second heart sound (S2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

That means that during inspiration, intrathoracic pressure is decreased. This pushes more blood into the vena cava, increasing venous return to the right side of the heart, which increases right ventricular stroke volume. The increased volume prolongs right ventricular systole and delays pulmonic valve closure.

Meanwhile on the left side, a greater amount of blood is sequestered in the lungs during inspiration. This momentarily decreases the amount returned to the left side of the heart, decreasing left ventricular stroke volume. The decreased volume shortens left ventricular systole and allows the aortic valve to close a bit earlier. When the aortic valve closes significantly earlier than the pulmonic valve, you can hear the two components separately

A

split S2.(affected by respiration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

volume of right and left ventricular systole is just about equal, but this can be affected by respiration.

MoRe to the Right heart,

Less to the Left

A

affected by respiration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Normally diastole is a silent event. However, in some conditions ventricular filling creates vibrations that can be heard over the chest. These vibrations are S3. S3 occurs when the ventricles are resistant to filling during the early rapid filling phase (protodiastole)(1st part of filling). This occurs immediately after S2, when the AV valves open and atrial blood first pours into the ventricles

A

Third Heart Sound (S3). (extra heart sound)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

S4 occurs at the end of diastole, at presystole, when the ventricle is resistant to filling. The atria contract and push blood into a noncompliant ventricle. This creates vibrations that are heard as S4. S4 occurs just before S1.

A

S4(extra heart sound)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

turbulent blood flow and collision currents

- gentle, blowing, swooshing sound that can be heard on the chest wall

A

Murmurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q
  1. Velocity of blood increases (flow murmur) (e.g., in exercise, thyrotoxicosis)
  2. Viscosity of blood decreases (e.g., in anemia)
  3. Structural defects in the valves (a stenotic or narrowed valve, an incompetent or regurgitant valve) or unusual openings occur in the chambers (dilated chamber, septal defect)
A

Conditions resulting Murmurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q
  1. Frequency (pitch)—Heart sounds are described as high pitched or low pitched, although these terms are relative because all are low-frequency sounds, and you need a good stethoscope to hear them.
  2. Intensity (loudness)—Loud or soft
  3. Duration—Very short for heart sounds; silent periods are longer
  4. Timing—Systole or diastole
A

Characteristics of heart Sound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

node near the superior vena cava initiate an electrical impulse. (Because the SA node has an intrinsic rhythm, it is the “pacemaker.”)

A

sinoatrial (SA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

across the atria to the AV node low in the atrial septum.

A

AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

conduction system

A

bundle of His

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

conduction system

A

the right and left bundle branches, and then through the ventricles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

P wave—Depolarization of the atria

A

electrocardiograph (ECG)// electrical impulse stimulates the heart to do its work, which is to contract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

PR interval—From the beginning of the P wave to the beginning of the QRS complex (the time necessary for atrial depolarization plus time for the impulse to travel through the AV node to the ventricles)

A

electrocardiograph (ECG)// electrical impulse stimulates the heart to do its work, which is to contract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

QRS complex—Depolarization of the ventricles

A

electrocardiograph (ECG)// electrical impulse stimulates the heart to do its work, which is to contract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

T wave—Repolarization of the ventricles

A

electrocardiograph (ECG)// electrical impulse stimulates the heart to do its work, which is to contract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

is volume—it is the venous return that builds during diastole. It is the length to which the ventricular muscle is stretched at the end of diastole just before contraction

A

Preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

the greater the stretch, the stronger is the contraction of the heart.

A

Frank-Starling law

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

is pressure—it is the opposing pressure the ventricle must generate to open the aortic valve against the higher aortic pressure. It is the resistance against which the ventricle must pump its blood

A

Afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

CV assessment

-vessels reflect the efficiency of cardiac function.

A

carotid artery and the jugular veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

as a pressure wave generated by each systole pumping blood into the aorta

A

pulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

is a central artery (i.e., it is close to the heart). Its timing closely coincides with ventricular systole.

A

carotid artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

is located in the groove between the trachea and the sternomastoid muscle, medial to and alongside that muscle

A

carotid artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

empty unoxygenated blood directly into the superior vena cava
-filling pressure and volume changes. Because volume and pressure increase when the right side of the heart fails to pump efficiently

A

jugular veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

larger internal jugular lies deep and medial to the sternomastoid muscle.
-not visible, although its diffuse pulsations may be seen in the sternal notch when the person is supine

A

internal jugular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

is more superficial; it lies lateral to the sternomastoid muscle, above the clavicle.

A

external jugular vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

venous pulse occur because of events in the right side of the heart (no valve in superior vena cava to right aterium)

A

jugular pulse has 5 components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

A wave reflects atrial contraction because some blood flows backward to the vena cava during right atrial contraction.

A

5 components of the jugular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

, is backflow from the bulging upward of the tricuspid valve when it closes at the beginning of ventricular systole (not from the neighboring carotid artery pulsation)

A

C wave, or ventricular contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

shows atrial relaxation when the right ventricle contracts during systole and pulls the bottom of the atria downward.

A

X descent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

occurs with passive atrial filling because of the increasing volume in the right atria and increased pressure

A

V wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

reflects passive ventricular filling when the tricuspid valve opens and blood flows from the RA to the RV.

A

Y descent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

adapts to ensure adequate blood supply to the uterus and placenta, to deliver oxygen and nutrients to the fetus, and to allow the mother to function normally during this altered state

  • Blood volume increases by 30% to 50% during pregnancy, most rapid expansion occurring during the second trimester
  • arterial BP decreases in pregnancy as a result of peripheral vasodilation. The BP drops to its lowest point during the second trimester and rises after that.
A

CV system (pregnancy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

fetal heart functions early; it begins to beat at the

A

end of 3 weeks’ gestation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

is more horizontal in the infant than in the adult; thus the apex is higher, located at the fourth left intercostal space (Fig. 20.14). It reaches the adult position when the child reaches age 7 year

A

heart’s position in the chest (infant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

increase in systolic BP
-caused by thickening and stiffening of the large arteries, which in turn are caused by collagen and calcium deposits in vessel walls and loss of elastic fibers. This stiffening (arteriosclerosis) creates an increase in pulse wave velocity because the less compliant arteries cannot store the volume ejected.

A

isolated systolic hypertension (Aging)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

left ventricular wall thickness increases.

A

thickens as u age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

left ventricular wall thickness increases.

  • creates an increased workload on the heart
  • Diastolic BP may decrease after the fifth decade.1 Together with a rising systolic pressure, this increases the pulse pressure (the difference between the two).
A

thickens as u age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

No change in resting heart rate occurs with aging.

Cardiac output at rest is not changed with aging.

A

NO changes occur as u age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

decreased ability of the heart to augment cardiac output with exercise. This is shown by a decreased maximum heart rate with exercise and diminished sympathetic response. Noncardiac factors also cause a decrease in maximum work performance with aging: decrease in skeletal muscle performance, increase in muscle fatigue, increased sense of dyspnea. However, aerobic exercise conditioning modifies many of the aging changes in CV function.

A

CV alterations w/ ageing lifestyle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

presence of supraventricular and ventricular dysrhythmias increases with age. Ectopic beats are common in aging people; although these are usually asymptomatic in healthy older people, they may compromise cardiac output and BP when disease is present.

A

Dysrhythmias.//Aging adult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

may not be tolerated as well in older people
-myocardium is thicker and less compliant, and early diastolic filling is impaired at rest. Thus it may not tolerate a tachycardia as well because of shortened diastole.

A

Tachydysrhythmias ( shortened diastole= higher chance tachy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q
  • Prolonged P-R interval (first-degree AV block) and prolonged Q-T interval, but the QRS interval is unchanged.
  • Left axis deviation from age-related mild LV hypertrophy and fibrosis in left bundle branch.
  • Increased incidence of bundle branch block.
A

Age-related changes in the ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

is the leading cause of death in those ages 65 years and older

A

CVD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

—no current smoking, no obesity (i.e., BMI <30), physical activity at least once per week, and a healthy diet

A

four healthful factors (help reduce CVD )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

major form of CVD (Cardiovascular disease)

A

coronary artery disease (CAD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

contributes to CAD because it accelerates the process of atherosclerosis;
increases the workload on the heart, and it increases the oxygen demand on the heart already compromised by atherosclerosis.

A

hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

High levels of low-density lipoprotein (LDL, or the “bad” cholesterol) add to the lipid core of plaque formation in coronary and carotid arteries
-results in MI and stroke.

A

Serum Cholesterol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

women tend to have smaller coronary arteries than men

leading cause of death in women is CVD,

A

Sex and Gender Differences.

87
Q

Prodromal symptoms are those that are intermittent and resolve spontaneously
-most common prodromal symptom linked with ACS (acute cardiac symptoms) is fatigue.
Four prodromal symptoms linked with ACS are discomfort in the jaw or teeth, unusual fatigue, arm pain, and shortness of breath
- nausea, neck pain, right arm pain, jaw pain, dizziness, and syncope than are men

A

Women may not experience the crushing chest pain

88
Q

frequent urination @ night

A

Nocturia

89
Q

squeezing “clenched fist” sign is characteristic of angina

A

angina

90
Q

sweating, ashen gray or pale skin, heart skips beat, shortness of breath, nausea or vomiting, racing of heart
Diaphoresis, cold sweats, pallor, grayness.
Palpitations, dyspnea, nausea, tachycardia, fatigue.

A

cardiac symptoms

91
Q

occurs with heart failure. Lying down increases volume of intrathoracic blood, and the weakened heart cannot accommodate the increased load.

A

Paroxysmal nocturnal dyspnea (PND) (sensation of SOB that awakens after 1 or 2 hrs sleep)

92
Q

is the need to assume a more upright position to breathe

A

Orthopnea

93
Q

Sputum production, mucoid or purulent. Hemoptysis is often a pulmonary disorder but also occurs with mitral stenosis

A

cough up mucous (risk cvd)

94
Q

Fatigue from decreased cardiac output is worse in the

A

evening

95
Q

Cyanosis or pallor(ashen) occurs with MI or low cardiac output states as a result of

A

decreased tissue perfusion.

96
Q

Any swelling of your feet and legs

  • (help elevate legs)
  • Cardiac edema is bilateral; unilateral swelling has a local vein cause.
A

Edema. (risk cvd)

97
Q

—Recumbency at night promotes fluid resorption and excretion; this occurs with heart failure in the person who is ambulatory during the day.

A

Nocturia

98
Q

hypertension, elevated cholesterol or triglycerides, heart murmur, congenital heart disease, rheumatic fever (inflammation esp of heart, blood vessels n joints) or unexplained joint pains as child or youth, recurrent tonsillitis, anemia

A

(risk cvd)

99
Q

low-dose aspirin if the potential benefit of preventing MI outweighs the potential risk of GI bleeding, Vitamin D replacement is important; vitamin D deficiency increases risk

A

(risk cvd)

100
Q

antihypertensives, beta-blockers, calcium channel blockers, digoxin, diuretics, aspirin/anticoagulants

A

meds for ppl risk cvd

101
Q

note fatigue during feeding. Infant with heart failure takes fewer ounces each feeding; becomes dyspneic (difficulty breathing) with sucking; may be diaphoretic, then falls into exhausted sleep; awakens after a short time hungry again.
Cyanosis occurs in some congenital defects: tetralogy of Fallot or transposition of the great arteries.

A

screen for heart disease in infant

102
Q

Most causes are musculoskeletal pain and respiratory causes, including asthma.

A

children (cvd)

103
Q

Gestational hypertension

-associated symptoms: weight gain; protein in urine; swelling in feet, legs, or face

A

Pregnant Woman

104
Q

any known heart or lung disease: hypertension, CAD, chronic emphysema, or bronchitis
-Noncompliance (nt taking meds) may be related to side effects or lack of finances

A

Risk of CVD increases with advancing age

105
Q

, the person should be supine with the head and chest elevated between 30 and 45 degrees.

A

assess the jugular veins and the precordium

106
Q

the person can be sitting up

A

evaluate the carotid arteries

107
Q
  1. Pulse and BP (see Chapter 10)
  2. Extremities (see Chapter 21)
  3. Neck vessels
  4. Precordium
    - begin observations peripherally and move in toward the heart
A

performing a regional CV assessment, use this order

108
Q

is the condition in which pressure over the carotid sinus leads to a decreased heart rate, decreased BP, and cerebral ischemia with syncope. This may occur in older adults with hypertension or occlusion of the carotid artery.

A

Carotid sinus hypersensitivity

109
Q

feels small and weak (decreased stroke volume as in cardiogenic shock).

A

Diminished pulse

110
Q

feels full and strong in hyperkinetic states

A

Increased pulse

111
Q

indicates turbulence from a local vascular cause and is a marker for atherosclerotic disease. This increases the risk of transient ischemic attack (TIA) and ischemic stroke.
- blowing, swishing sound indicating blood flow turbulence; normally none is present.

A

bruit (Auscultate the Carotid Artery)

112
Q

(1) the angle of the jaw, (2) the midcervical area, and (3) the base of the neck. Avoid compressing the artery because this could create an artificial bruit, and it could compromise circulation if the carotid artery is already narrowed by atherosclerosis

A

Auscultate carotid artery at three levels:

113
Q

much the same but is caused by a cardiac disorder. Some aortic valve murmurs (aortic stenosis) radiate to the neck and must be distinguished from a local bruit

A

murmur sounds

114
Q

you can assess the central venous pressure (CVP) and thus judge the heart’s efficiency as a pump and the intravascular volume status

A

jugular veins

115
Q

is caused by local cause (kinking or aneurysm)

A

Unilateral distention of external jugular veins

116
Q

above 45 degrees signify increased CVP as with heart failure.

A

Full distended external jugular veins

117
Q

is a sustained forceful thrusting of the ventricle during systole. It occurs with ventricular hypertrophy as a result of increased workload. A right ventricular heave is seen at the sternal border; a left ventricular heave is seen at the apex

A

heave or lift

118
Q

(volume overload) displaces impulse down and to left and increases size more than one space. A diameter of ≥4 cm is likely a dilated heart.15 This occurs with heart failure and cardiomyopathy.

A

Left ventricular dilation (Cardiac enlargement)// check precordium

119
Q

with increased force and duration but no change in location occurs with left ventricular hypertrophy (enlargement of organ or tissue) and no dilation (pressure overload)

A

sustained impulse (Cardiac enlargement)// check precordium

120
Q

is a palpable vibration. It feels like the throat of a purring cat. The thrill signifies turbulent blood flow and directs you to locate the origin of loud murmurs. However, absence of a thrill does not rule out the presence of a murmur.

A

thrill (Palpate Across the Precordium)

121
Q

Second right interspace—

A

Aortic valve area

122
Q

Second left interspace—

A

Pulmonic valve area

123
Q

Left lower sternal border—

A

Tricuspid valve area

124
Q

Fifth interspace at around left midclavicular line—

A

Mitral valve area

125
Q

(1) note the rate and rhythm, (2) identify S1 and S2, (3) assess S1 and S2 separately, (4) listen for extra heart sounds, and (5) listen for murmurs.

A

Auscultation

126
Q

occurs normally in young adults and children

A

sinus arrhythmia

127
Q

—An isolated beat is early, or a pattern occurs in which every third or fourth beat sounds early.

A

Premature beat

128
Q

—No pattern to the sounds; beats come rapidly and at random intervals as in atrial fibrillation

A

Irregularly irregular

129
Q

signals a weak contraction of the ventricles; it occurs with atrial fibrillation, premature beats, and heart failure

A

pulse deficit

130
Q

and thus serves as the reference point for the timing of all other cardiac sounds

A

S1 is the start of systole

131
Q

S1 is louder than S2 at the apex;

S2 is louder than S1 at the base.

A

distinguish S1 from S2 are:

132
Q

S1 coincides with the carotid artery pulse. Feel the carotid gently as you auscultate at the apex; the sound you hear as you feel each pulse is S1
-S1 coincides with the R wave (the upstroke of the QRS complex) i

A

S1 n carotid artery pulse

133
Q

with conditions that place an increased amount of tissue between the heart and your stethoscope: emphysema (hyperinflated lungs), obesity, pericardial fluid

A

both heart sounds are diminished

134
Q

means that you are hearing the mitral and tricuspid components separately.
-audible in the tricuspid valve area, the left lower sternal border. The split is very rapid, with the two components only 0.03 second apart

A

split S1 (normal)

135
Q

is associated with closure of the semilunar valve

A

S2

136
Q

is a normal phenomenon that occurs toward the end of inspiration in some people. Recall that closure of the aortic and pulmonic valves is nearly synchronous. Because of the effects of respiration on the heart described earlier, inspiration separates the timing of the two valves’ closure, and the aortic valve closes 0.06 second before the pulmonic valve. Instead of one DUP, you hear a split sound—T-DUP (Fig. 20.24). During expiration, synchrony returns and the aortic and pulmonic components fuse together. A split S2 is heard only in the pulmonic valve area, the second left interspace.

A

split S2

137
Q

is unaffected by respiration; the split is always there.

A

fixed split

138
Q

is the opposite of what you would expect; the sounds fuse on inspiration and split on expiration

A

paradoxical split (opp of split s2)

139
Q

(which is associated with mitral valve prolapse) is the most common extra sound

A

midsystolic click

140
Q

occur in diastole; either may be normal or abnormal

A

third and fourth heart sounds

141
Q

occurs with heart failure and volume overload;

A

S3 (ventricular gallop)

142
Q

occurs with CAD

A

S4 (atrial gallop)

143
Q

may occur with a healthy heart or with heart disease;

A

systolic murmur

144
Q

always indicates heart disease.

A

diastolic murmur

145
Q

Grade 1—Barely audible; heard only in a quiet room and then with difficulty
Grade 2—Clearly audible but faint
Grade 3—Moderately loud; easy to hear
Grade 4—Loud; associated with a thrill palpable on the chest wall
Grade 5—Very loud; heard with one corner of the stethoscope lifted off the chest wall; associated thrill
Grade 6—Loudest; still heard with entire stethoscope lifted just off the chest wall; associated thrill

A

Loudness. Describe the intensity of murmur

146
Q

. Describe the pitch as high, medium, or low. The pitch depends on the pressure and rate of blood flow producing the murmur.

A

Pitch of murmur

147
Q

is low-pitched and rumbling, whereas that of aortic stenosis is harsh

A

murmur of mitral stenosis& aortic stenosis

148
Q

is caused by increased blood flow in the heart (e.g., in anemia, fever, pregnancy, hyperthyroidism)

A

functional murmur

149
Q

S3 and S4 and the murmur of mitral stenosis sometimes may be heard only when on the

A

left side.

150
Q

grows softer with standing-to-squatting, and it grows loud­er with squatting-to-standing.15 HCM is an inherited thickening of the myocardium

A

murmur of hypertrophic car­dio­my­opathy (HCM)

151
Q

is a level of pulsation that is >3 cm above the sternal angle while at 45 degrees . This occurs with heart failure, cardiac tamponade, and constrictive pericarditis. (angle of Louis (sternal angle))

A

Elevated pressure

152
Q

heart failure is present, the jugular veins will elevate more than 4 cm and stay elevated as long as you push

A

perform the abdominojugular test (formerly hepatojugular reflux)

153
Q

(particularly in the skin), liver size, and respiratory status. The skin color should be pink to pinkish brown

A

extracardiac signs that may reflect heart status in infants

154
Q

most important signs of heart failure in an infant are persistent tachycardia, tachypnea, and liver enlargement. -Engorged veins, gallop rhythm, and pulsus alternans also are signs. Respiratory crackles (rales) are an important sign in adults but not in infants.

A

signs of heart failure in an infant

155
Q
  • Cardiac enlargement, shifts to the left.
  • Pneumothorax, shifts away from the affected side.
  • Diaphragmatic hernia, shifts usually to right because this hernia occurs more often on the left.
  • Dextrocardia, a rare anomaly in which the heart is located on right side of chest.
A

The apex is displaced with:

156
Q

Persistent tachycardia is >200 beats/min in newborns or >150 beats/min in infants.
-Expect the heart rhythm to have sinus arrhythmia

A

infants n neonate tachycardia range

157
Q

Bradycardia is <90 beats/min in newborns or <60 beats/min in older infants or children
-Expect the heart rhythm to have sinus arrhythmia

A

infants n neonate bradycardia range

158
Q

S2 has a higher pitch and is sharper than S1. Splitting of S2 just after the height of inspiration is common, not at birth but beginning a few hours after birth.

A

infants s1,s2

159
Q

indicates atrial septal defect

A

Fixed split S2 (infants)

160
Q

Murmurs in the immediate newborn period do not necessarily indicate congenital heart disease. They are relatively common in the first 2 to 3 days because of fetal shunt closure. These murmurs are usually grade 1 or 2, are systolic, accompany no other signs of cardiac disease, and disappear in 2 to 3 days

A

Murmurs in the immediate newborn are normal

161
Q

are associated with: harsh murmur quality, location (right upper sternal border, left lower sternal border, apex), and timing (pansystolic, diastolic, or continuous)

A

Congenital defects in infants if murmur is absent

162
Q

apical impulse is sometimes visible in children with thin chest walls
-any obvious bulge or any heave—these are not normal.?

A

children

163
Q

to the left of the sternum with a hyperdynamic precordium signals cardiac enlargement. The bulge occurs because the cartilaginous rib cage is more compliant.

A

precordial bulge

164
Q

occurs with right ventricular enlargement; an apical heave occurs with left ventricular hypertrophy.

A

substernal heave

165
Q

is common in children. It occurs in early diastole, just after S2, and is a dull soft sound that is best heard at the apex.

A

Physiologic S3 (Children)

166
Q

—caused by turbulence of blood flow in the jugular venous system—is common in healthy children and has no pathologic significance. It is a continuous, low-pitched, soft hum that is heard throughout the cycle, although it is loudest in diastole.

A

venous hum (Children)

167
Q

is a benign murmur heard just above the clavicles.
-slightly harsh, early or midsystolic, often louder on the left, and will disappear completely by carotid artery compression.

A

carotid bruit

168
Q

that are innocent (or functional) in origin are very common through childhood (often termed Still’s murmur).

A

Heart murmurs (child)

169
Q

is BP ≥140/90 mm Hg on two separate measures without proteinuria, starting after 20th week of pregnancy. This returns to baseline by 12 weeks after delivery.

A

Gestational hypertension

170
Q

usually lowest in the left lateral recumbent position, a bit higher when supine, and highest when sitting

A

Gestational hypertension

171
Q

Inspection of the skin often shows a mild hyperemia in light-skinned women because the increased cutaneous blood flow tries to eliminate the excess heat generated by the increased metabolism.
-Palpation of the apical impulse is higher and lateral compared with the normal position because the enlarging uterus elevates the diaphragm and displaces the heart up and to the left and rotates it on its long axis.

A

Pregnant Woman

172
Q

An exaggerated splitting of S1 and increased loudness of S1 are common, as is a loud, easily heard S3. An ejection systolic murmur is common; heard at left sternal border; grade 1, 2 or 3 in intensity.
-Murmurs of aortic valve disease cannot be obliterated.

A

Pregnant Woman

173
Q

from breast vasculature is termed a mammary souffle

-heard in the 2nd, 3rd, or 4th intercostal space;

A

continuous murmur

174
Q

gradual rise in SBP is common with aging; the DBP stays fairly constant with a resulting widening of pulse pressure.

A

Aging Adult

175
Q

chest often increases in anteroposterior diameter with aging
-makes it more difficult to palpate the apical impulse and hear the splitting of S2. The S4 often occurs in older people with no known cardiac disease. Systolic murmurs are common, occurring in over 50% of aging people

A

Aging Adult/ heart

176
Q

is associated with heart failure and is always abnormal over age 35 year
-Occasional premature ectopic beats are common and do not necessarily indicate underlying heart disease.

A

S3 (older adult)

177
Q

stable (no change in pain pattern within last 60 days)
-Pressurelike pain (e.g., tightness, squeezing, burning, heaviness that lasts 3-5 minutes precipitated by activity and often resolves with rest and/or nitroglycerin

location/radiation: Generalized substernal or retrosternal: can radiate to teeth, jaw, neck, one or both arms or shoulders; or there may be no pain and only associated symptoms

Possible Associated Symptoms:Diaphoresis, nausea, vomiting, dyspnea, fatigue

A

Angina pectoris://Cardiovascular (Ischemic)

178
Q

desc: Pressurelike discomfort often occurring at rest, unrelated to physical or emotional stress

location/radiation: Retrosternal: can radiate to jaw, neck, left arm, or shoulder

Possible Associated Symptoms:Palpitations(noticeably rapid, strong,or irregular heartbeat), syncope, or feelings of syncope

A

Prinzmetal or variant angina////Cardiovascular (Ischemic)

179
Q

desc:Heaviness; viselike, squeezing, crushing, tightness; vague, burning, constricting, or pressure; poorly localized pain lasting 20-30 minutes to hours and does not resolve with rest or nitroglycerin

location/radiation:Generalized substernal or retrosternal: can radiate to teeth, jaw, neck, one or both arms or shoulders; or there may be no pain and only associated symptoms

Possible Associated Symptoms: Indigestion-like feeling, nausea, vomiting, dizziness, flushing, perspiration, palpitations, dyspnea, fatigue

A

Acute coronary syndrome (ACS) (unstable angina, myocardial infarction)//Cardiovascular (Ischemic)

180
Q

desc:Sudden sharp and stabbing pain relieved often by sitting or leaning forward and worsens by lying down or with inspiration

location/radiation: Substernal, which can radiate to trapezius muscle region

Possible Associated Symptoms: Dry cough, muscle and joint aches, fever

A

Pericarditis(Cardiovascular (Nonischemic)

181
Q

desc: Sharp pain not associated with activity

location/radiation: Chest pain without radiation

Possible Associated Symptoms:Fatigue, light-headedness, dyspnea, irregular heartbeat, palpitations, exercise intolerance

A

Mitral valve prolapse(Cardiovascular (Nonischemic)

182
Q

desc: Sudden severe pain with change in location and/or tearing sensation lasting for hours

location/radiation: Anterior chest pain with radiation to the neck, jaw, or intrascapular region of the back

Possible Associated Symptoms: Mental status changes, limb pain and weakness, dyspnea

A

Aortic dissection(Cardiovascular (Nonischemic)

183
Q

desc:Cardiac-like chest pain with exertion

location/radiation: Chest region

Possible Associated Symptoms: Dyspnea, lower-extremity edema, fatigue

A

Pulmonary hypertension (secondary)//(Cardiovascular (Nonischemic)

184
Q

desc: Sharp, stabbing pain worsening with deep breaths

location/radiation: Pain can be experienced in chest, back, shoulder, or upper abdomen

Possible Associated Symptoms: Dyspnea, hemoptysis(coughing up blood), cough

A

Pulmonary embolism (Pulmonary)

185
Q

desc: Sharp or stabbing pain associated with cough

location/radiation: Mostly generalized to one side of chest but can have upper abdominal pain

Possible Associated Symptoms: Cough, fever, dyspnea, chills, sputum, myalgia, malaise

A

Pneumonia (Pulmonary)

186
Q

desc:Acute/sudden and sharp

location/radiation: Lateral region of the chest but can have referred pain to shoulder

Possible Associated Symptoms: Acute dyspnea, cough

A

Pneumothorax(Pulmonary)

187
Q

desc: May be angina-like; however, usually burning sensation with eating large meals reproduced by lying down and relieved by sitting up

location/radiation: Retrosternal region

Possible Associated Symptoms: Cough, regurgitation of food, abdominal pain

A

Gastroesophageal reflux (Gastrointestinal)

188
Q

desc: Crushing chest pain

location/radiation: Substernal

Possible Associated Symptoms: Dysphagia, sensation of object in throat or esophagus

A

Esophageal spasm(Gastrointestinal)

189
Q

desc: Sudden onset of pain that crescendos and can last for up to 20 minutes, usually after eating a fatty meal

location/radiation: Epigastrium or right upper abdomen that can radiate to right intrascapular region, shoulder, or back

Possible Associated Symptoms: Nausea, vomiting, anorexia, fever

A

Cholecystitis(Gastrointestinal)

190
Q

desc: Sudden dull, boring, steady pain unrelieved by lying supine; leaning forward or the fetal position may ease pain

location/radiation: Epigastrium or periumbilical pain radiating to back

Possible Associated Symptoms: Nausea, vomiting, anorexia, and sometimes diarrhea

A

Pancreatitis(Gastrointestinal)

191
Q

desc: Unilateral, burning, borelike pain

location/radiation: Chest region in dermatome distribution

Possible Associated Symptoms:Tingling, itching, burning

A

Herpes zoster//Dermatologic

192
Q

desc: Sharp, pleuritic-type pain worsens with deep breathing, palpation, or movement

location/radiation: Area from 2nd through 5th intercostal spaces; can radiate to arm, depending on where initial inflammation occurs

Possible Associated Symptoms: Chest tightness, warmth at area of pain

A

Costochondritis(Musculoskeletal/Neurologic)

193
Q

desc: Sharp pain with moving, stretching, or pushing movements of the arms; palpation of area reproduces the pain

location/radiation: Area around the strained muscle, sternum, or ribs

Possible Associated Symptoms: Muscle spasm, crepitation, swelling, loss of strength

A

Chest wall muscle strain(Musculoskeletal/Neurologic)

194
Q

desc: Heaviness

location/radiation: Chest region

Possible Associated Symptoms: Fatigue, restlessness, withdrawal, weight gain or loss, depressed mood

A

Depression (Psychogenic)

195
Q

desc: Sharp pain

location/radiation:Chest region

Possible Associated Symptoms: Palpitations, dizziness, sweating, shaking, restlessness, fatigue, irritability

A

Anxiety(Psychogenic)

196
Q

Decreased cardiac output occurs when the heart fails as a pump and the circulation becomes backed up and congested.

A

Heart Failure

197
Q

(1) the heart’s inability to pump enough blood to meet the metabolic demands of the body;
(2) the kidney’s compensatory mechanisms of abnormal retention of sodium and water to compensate for the decreased cardiac output. This increases blood volume and venous return, which causes further congestion.

A

Signs and symptoms of heart failure come from two basic mechanisms

198
Q

(1) acute, as following a myocardial infarction when the heart’s contracting ability has been directly damaged; or (2) chronic, as with hypertension, when the ventricles must pump against chronically increased pressure.

A

Onset of heart failure maybe

199
Q

systolic dysfunction, in which the heart cannot contract properly, resulting in a low ejection fraction (the stroke volume divided by the end-diastolic volume, normally 60% to 80%)

A

Heart failure involve

200
Q

is a failure of the heart to relax fully between heartbeats; here the heart muscle wall is stiff and does not fill properly; there is low cardiac output but a normal ejection fraction.

A

Diastolic dysfunction

201
Q

(1) position of the atrioventricular (AV) valve at the start of systole,
(2) structure of the valve leaflets,
(3) how quickly pressure rises in the ventricle.

A

intensity of S1 depends on three factors

202
Q

Position of AV valve at start of systole—Wide open and no time to drift together
ex:Hyperkinetic states in which blood velocity is increased: exercise, fever, anemia, hyperthyroidism

A

Loud (Accentuated) S1

203
Q

Change in valve structure—Calcification of valve; needs increasing ventricular pressure to close the valve against increased atrial pressure
ex: Mitral stenosis with leaflets still mobile

A

Loud (Accentuated) S1

204
Q
  1. Position of AV valve—Delayed conduction from atria to ventricles. Mitral valve drifts shut before ventricular contraction closes it (First-degree heart block (prolonged PR interval))
  2. Change in valve structure—Extreme calcification, which limits mobility (Mitral insufficiency)
  3. More forceful atrial contraction into noncompliant ventricle; delays or diminishes ventricular contraction(ex:Severe hypertension—Systemic or pulmonary)
A

Faint (Diminished) S1

205
Q
  1. Position of AV valve varies before closing from beat to beat (Atrial fibrillation—Irregularly irregular rhythm)
  2. Atria and ventricles beat independently(Complete heart block with changing PR interval)
A

Varying Intensity of S1

206
Q

Mitral and tricuspid components are heard separately(normal but uncommon)

A

Split S1

207
Q
  1. Higher closing pressure(ex:Systemic hypertension, ringing or booming S2)
  2. Exercise and excitement increase pressure in aorta
  3. Pulmonary hypertension(Mitral stenosis, heart failure)
  4. Semilunar valves calcified but still mobile (Aortic or pulmonic stenosis)
A

Accentuated S2

208
Q
  1. A fall in systemic blood pressure causes a decrease in valve strength (shock)
  2. Semilunar valves thickened and calcified, with decreased mobility (Aortic or pulmonic stenosis)
A

Diminished S2

209
Q

 Ejection click

 Aortic prosthetic valve sounds

A

Early systolic: (

Systolic Extra Sounds)

210
Q

Midsystolic (mitral) click

A

Mid/late systolic:

211
Q
  1.  Opening snap

2.  Mitral prosthetic valve sound

A

Early diastole: Diastolic Extra Sounds

212
Q
  1.  Third heart sound

2.  Summation sound (S3 + S4)

A

Mid-diastole//Diastolic Extra Sounds

213
Q

1. Fourth heart sound

 2.Pacemaker-induced sound

A

Late diastole://Diastolic Extra Sounds

214
Q

Normally the opening of the AV valves is silent. In the presence of stenosis, increasingly higher atrial pressure is required to open the valve. The deformed valve opens with a noise: the opening snap. It is sharp and high pitched with a snapping quality. It sounds after S2 and is best heard with the diaphragm at the 3rd or 4th left interspace at the sternal border, less well at the apex.

A

Opening Snap