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cardiovascular exam 3 Flashcards

1
Q

in a healthy heart what is usually the PMI?

A

left ventricular impulse

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2
Q

what is the left ventricular impulse generated by?

A

generated by the movement of the ventricular apex against the chest wall during contraction

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3
Q

normal descriptors of left ventricular PMI

A

-location= fourth or fifth intercostal space at the midclavicular line
-diameter= discrete, or <2 cm
-amplitude= brisk and tapping
-duration= <2/3 of the systol

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4
Q

hyperkinetic ventricular impulse

A

from transiently increased stroked volume- does not necessarily indicate heart disease

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5
Q

sustained ventricular impulse

A

increased afterload, from chronic pressure load

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6
Q

diffuse ventricular impulse

A

increased preload; ventricular dilation from chronic volume overload

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7
Q

conditions that can accentuate S1

A

tachycardia, mitral stenosis

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8
Q

conditions that can diminish S1

A

-1st degree heart block, left bundle branch block, and myocardial infarction
-also can be caused by mitral valve closure occurring before ventricular contraction- this is seen in severe aortic regurgitation

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9
Q

what can cause varying S1

A

1-complete heart block
2-totally irregular rhythm (atrial fibrillation)

*mitral valve closure varies in loudness

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10
Q

what causes split S1

A

-delayed closure of tricuspid valve
-best heard along lower left sternal border

-more prominent split of S1 than normal occurs in right bundle branch block *must be distinguished from s4 and early systolic click

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11
Q

effect of respiration on physiologic splitting of S2

A

-normal splitting accentuated by inspiration which increases interval between a2 and p2
-splitting disappears on expiration

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12
Q

what is the diameter of the pmi in supine patients?

A

1-2.5 cm

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13
Q

when might the pmi be located on the right side of the chest?

A

dextrocardia

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14
Q

what is a PMI greater than 2.5 cm indicative of?

A

left ventricular hypertrophy, hypertension, dilated cardiomyopathy

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15
Q

where might the PMI be in COPD patients?

A

PMI may be in the xiphoid or epigastric area due to right ventricular hypertrophy

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16
Q

because of their location the mitral and tricuspid valves are often called what?

A

atrioventricular valves

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17
Q

what are the aortic and pulmonary valves often called?

A

semilunar valves bc valve leaflets are shaped like half moons

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18
Q

what do s3 and s4 sounds mean in adults

A

pathologic

correlated with systolic and diastolic heart failure

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19
Q

what heart sound correlated to an abrupt decelration of inflow across from the mitral valve?

A

s3

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20
Q

what heart sound corresponds to increased left ventricular end diastolic stiffness which decreases compliance?

A

s4

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21
Q

what sound does closure of the mitral valve and tricuspid valve in the right side of the heart produce?

A

s1

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22
Q

what accompanies the opening of aortic valves in some conditions?

A

an early systolic ejection sound

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23
Q

what does maximal left ventricular pressure normally correspond to?

A

systolic blood pressure

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24
Q

what produces the heart sound S2

A

aortic valve closure, as well as the closure of the pulmonic valves

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25
Q

when might the opening of the mitral valve be audible as a pathologic opening snap (OS)?

A

if the valve leaflet motion is restricted, as in mitral stenosis

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26
Q

when do right side cardiac events occur relative to the left side?

A

usually occur slightly later than those on the left

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27
Q

which component of S2 is normally louder and why?

A

A2, bc high pressure in aorta

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28
Q

does splitting of s1 vary with respiration?

A

no

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29
Q

what are heart murmurs attributed to?

A

they are attributed to turbulent flow and usually indicate valvular heart disease

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30
Q

what causes regurgitation?

A

when valves close abnormally

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31
Q

muscular contraction is as follows

A

first the atria then the ventricles

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32
Q

cardiac output

A

Stroke volume x heart rate

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33
Q

what are the two common manifestations of heart failure determined by?

A

ejection fraction (the percentage of ventricular volume ejected during each heartbeat and is normally 60%)

*HF with preserved EF
*HF with reduced EF

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34
Q

preload

A

load that stretches the cardiac muscle before contraction

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35
Q

afterload

A

degree of vascular resistance to ventricular contraction

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36
Q

myocardial contractility

A

ability of the cardiac muscle to shorten when given a load

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37
Q

causes of decreased ventricular preload

A

exhalation, dehydration, pooling of blood in capillary bed of the venous system

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38
Q

factors affecting blood pressure

A

-LV stroke volume
-distensibility of aorta and the large arteries
-peripheral vascular resistance, particularly at the arteriolar level
-volume of blood in arterial system

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39
Q

jugular venous pressure

A

reflects right atrial pressure=central venous pressure and RV end diastolic pressure

*best estimated from right internal jugular vein

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40
Q

3 peaks of jugular venous pulsations

A

a= atrial contraction
c= carotid transmission
v= venous filling

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41
Q

when do abnormally prominent cannon A WAVES occur?

A

-they occur in increased resistance to right atrial contraction: ex; 1,2,3 degree AV block, supraventricular tachycardia, junctional tachycardia, pulmonary hypertension, and pulmoniv stenosis

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42
Q

when are A WAVES absent?

A

atrial fibrillation

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43
Q

when do increased v waves occur?

A

occur in tricuspid regurgitation, atrial septal defects, and constrictive pericarditis

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44
Q

what causes peripheral edema?

A

fluid build up that can be caused by the right ventricle not moving blood adequately

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45
Q

what is the end result of all heart disease?

A

pump malfunction

46
Q

the final category of heart disease is valvular heart disease. it usually presents without symptoms, but when symptoms are present they usually relate to…

A

a failing heart

47
Q

common or concerning symptoms of the cardiovascular exam

A

-Chest pain
-Palpitations
-Shortness of breath: dyspnea, orthopnea, or paroxysmal nocturnal dyspnea
-Swelling (edema)
-Fainting (syncope)

48
Q

describe the symptoms that my occur in acute aortic dissection

A

Anterior chest pain, often tearing or ripping and radiating into the back or neck

49
Q

describe common symptoms of WOMEN over 65 with acute coronary disorder

A

women, particularly those over age 65, are more likely to report atypical symptoms that may go unrecognized, such as upper back, neck, or jaw pain; shortness of breath; paroxysmal nocturnal dyspnea; nausea or vomiting; and fatigue, making careful history-taking especially important

50
Q

what is increasingly used to describe the clinical syndromes caused by acute myocardial ischemia, which include unstable angina, non–ST elevation MI, and ST elevation infarction

A

acute coronary syndrome

51
Q

serious dysrhythmias that do not produce palpitations

A

ventricular tachycardia

52
Q

Sudden dyspnea occurs in

A

pulmonary embolus, spontaneous pneumothorax, and anxiety.

53
Q

Orthopnea and PND (paroxysmal nocturnal dyspnea) occur in

A

left ventricular heart failure and mitral stenosis and also in obstructive lung disease

54
Q

dependent vs anasarca edema

A

Dependent edema appears in the lowest body parts: the feet and lower legs when sitting, or the sacrum when bedridden. Anasarca is severe generalized edema extending to the sacrum and abdomen.

55
Q

Ask, “Do you experience any nighttime episodes of sudden dyspnea that awakens you usually 1 or 2 hours after falling sleep, prompting you to sit up and stand up?” This is called

A

paroxysmal nocturnal dyspnea (PND)

56
Q

what is syncope?

A

a transient loss of consciousness followed by recovery

57
Q

The more concerning causes of syncope

A

The more concerning causes of syncope involve the heart not providing adequate blood flow to the brain, as occurs in end-stage heart failure and arrhythmias

58
Q

In the physical examination of the cardiovascular system, remember to answer the following questions to assess the integrity of the pump:

A

Is the forward pump function normal?
Is the heart normal in size?
Is there evidence of valvular heart disease?
is there pulmonary edema?

59
Q

key components of the cardiovascular exam

A

-Note general appearance and measure blood pressure and heart rate.
-Estimate the level of jugular venous pressure.
-Auscultate the carotids (bruit) one at a time.
-Palpate the carotid pulse including carotid upstroke (amplitude, contour, timing) and presence of a thrill.
-Inspect the anterior chest wall (apical impulse, precordial movements).
-Palpate the precordium for any heaves, thrills, or palpable heart sounds.
-Palpate and locate the PMI or apical impulse.
-Palpate for a systolic impulse of the right ventricle, pulmonary artery, and aortic outflow tract areas on the chest wall.
-Auscultate S1 and S2 in six positions from the base to the
apex.
-Identify physiologic and paradoxical splitting of S2.
-Auscultate and recognize abnormal sounds in early diastole, including an S3 and OS of mitral stenosis and an S4 later in diastole.
-Distinguish systolic and diastolic murmurs, using maneuvers when needed. If present, identify their timing, shape, grade, location, radiation, pitch, and quality.

60
Q

A growing literature documents the poor reliability of clinic blood pressure measurements

A

Multiple averaged measurements improve precision, especially when using automated home and ambulatory blood pressure readings, which are more reliable, accurate, and better correlated with cardiovascular outcomes than clinic readings

61
Q

how is the JVP best assessed

A

from pulsations in the right internal jugular vein, which is directly in line with the superior vena cava and right atrium

62
Q

movement of JVP vs carotid pulse

A

The dominant movement of the JVP is inward, coinciding with the x descent.34 In contrast, the dominant movement of the carotid pulse, often confused with the JVP, is outward

63
Q

JVP levels fall and rise with

A

JVP falls with loss of blood or decreased venous vascular tone and increases with right or left heart failure, pulmonary hypertension, tricuspid stenosis, AV dissociation, increased venous vascular tone, and pericardial compression or tamponade.

64
Q

effect of JVP and position of pt

A

but your ability to measure the height of the column of venous blood, or JVP, differs according to how you position the patient.

65
Q

distinguishing internal jugular and carotid pulsations

A

INTERNAL JUGULAR PULSATIONS
-Rarely palpable
-Soft biphasic undulating quality, usually with two elevations and characteristic inward deflection (x descent)
-Pulsations eliminated by light pressure on the vein(s) just above the sternal end of the clavicle
-Height of pulsations changes with position normally dropping as the patient becomes more upright
-Height of pulsations usually falls with inspiration

CAROTID PULSATIONS
-Palpable
-A more vigorous thrust with a single outward component
-Pulsations not eliminated by pressure on veins at sternal end of clavicle
-Height of pulsations not effected by position
-Height of pulsations not affected by inspiration

66
Q

bruit

A

a murmur-like sound arising from turbulent arterial blood flow. Ask the patient to stop breathing for ∼10 seconds, then listen with the diaphragm of the stethoscope, which generally detects the higher-frequency sounds of arterial bruits better than the bell

67
Q

it is important to auscultate the carotid arteries prior to palpating the carotid pulse.

A

As the presence of carotid atherosclerosis could potentially narrow the carotid arteries

68
Q

The most feared complication of carotid artery palpation

A

is the dislodgment of an atherosclerotic plaque, which could result in stroke.

69
Q

do Bruits
correlate with clinically significant underlying disease

A

no

70
Q

Carotid artery stenosis causes ∼_____% of ischemic strokes and ______ the risk of coronary heart disease

A

10, doubles

71
Q

A tortuous and kinked carotid artery may produce a

A

unilateral pulsatile bridge

72
Q

causes of decreased pulsations include

A

decreased stroke volume from shock or MI and local atherosclerotic narrowing or occlusion.

73
Q

why should you never palpate both carotid arteries at the same time?

A

may decreased bf to brain and induce syncope

74
Q

what might pressure on the carotid sinus cause?

A

bradycardia or drop in BP

75
Q

when is the carotid pulse thready and when is it bounding

A

The carotid pulse is small, thready (barely detectable), or weak in cardiogenic shock; the pulse is bounding in aortic regurgitation.

76
Q

Pulsus alternans almost always indicates

A

severe left ventricular dysfunction.

77
Q

pulsus alternans

A

In pulsus alternans, the rhythm of the pulse remains regular, but the force of the arterial pulse alternates because of alternating strong and weak ventricular contractions

78
Q

what is the effect on cardiac upstroke seen in aortic stenosis?

A

it is delayed

79
Q

what position might accentuate pulsus alternans?

A

the upright position

80
Q

Paradoxical pulse or pulsus paradoxus

A

is a greater-than- normal drop in systolic blood pressure during inspiration.

81
Q

paradoxical pulse is found in

A

is found in pericardial tamponade, a life-threatening condition. It is also (more commonly) found in acute asthma and obstructive pulmonary disease. It also occurs in constrictive pericarditis and acute pulmonary embolism.

82
Q

To assess the PMI and extra heart sounds such as S3 or S4

A

ask the patient to turn to the left side—the left lateral decubitus position, which brings the ventricular apex closer to the chest wall. To bring the left ventricular outflow tract closer to the chest wall and improve detection of aortic regurgitation, have the patient sit up, lean forward, and exhale.

83
Q

The relative intensity of S1 and S2

A

S1 is usually louder than S2 at the apex; S2 is usually louder than S1 at the base.

84
Q

sounds before and after cardiac upstroke

A

Since the carotid upstroke always occurs in systole immediately after S1, sounds or murmurs coinciding with the upstroke are systolic

sounds or murmurs following the cartoid upstroke are diastolic

85
Q

when is palpation less useful?

A

Palpation is less useful in patients with a thickened chest wall (obesity) or increased AP diameter (obstructive lung disease).

86
Q

palpating s1 and s2

A

To palpate S1 and S2, using
firm pressure, place your right hand on the chest wall. With your left index and middle fingers, palpate the carotid upstroke to identify S1 and S2 just before and just after the
upstroke. S1 and S2 are usually not palpable

87
Q

palpating s3 and s4

A

position the patient in the left lateral
decubitus position, then palpate the cardiac apex gently with one finger as the patient exhales and briefly stops breathing. By marking an X on the apex, you may be able to palpate these brief early and late diastolic ventricular movements that are synchronous with pathologic third and fourth heart sounds.

88
Q

situs inversus totalis

A

the heart, trilobed lung, stomach, and spleen are on the right, and the liver and gallbladder are on the left.

89
Q

dextrocardia with situs inversus

A

a rare congenital transposition of the heart, the heart is situated in the right chest cavity and generates a right-sided apical impulse. Use percussion to help locate the heart border, the liver, and stomach.

90
Q

describing the apical impulse

A

It is always best to describe the apical impulse in relation to the midsternal or midclavicular line, or the anterior axillary line if the apical impulse is displaced

91
Q

palpable S2,
also known as a “pulmonary artery tap,” points to

A

increased pulmonary artery pressure from pulmonary hypertension.

92
Q

auscultating with the bell vs diaphragm

A

The diaphragm. The diaphragm is better for picking up the relatively high- pitched sounds of S1 and S2, the murmurs of aortic and mitral regurgitation, and pericardial friction rubs. Listen throughout the precordium with the diaphragm, pressing it firmly against the chest.

The bell. The bell is more sensitive to the low-pitched sounds of S3 and S4 and the murmur of mitral stenosis. Apply the bell lightly, with just enough pressure to produce an air seal with its full rim. Use the bell at the apex, then move medially along the lower sternal border.

93
Q

fundamental prerequisite for identifying
events in the cardiac cycle.

A

The correct timing of systole and diastole

94
Q

diastolic vs systolic murmurs

A

Diastolic murmurs usually represent valvular heart disease. Systolic murmurs point to valvular disease but can be physiologic flow murmurs arising from normal heart valves

95
Q

Important Topics for Health Promotion and Counseling

A

-Challenges of cardiovascular disease prevention
-Health disparities in cardiovascular disease
-Assessing cardiovascular disease risk factors
Step 1: Screen for individual cardiovascular disease risk factors
Step 2: Calculate 10-year and lifetime global cardiovascular disease risk using a web-based calculator
Step 3: Address individual risk factors—hypertension, diabetes, dyslipidemias, metabolic syndrome, smoking, family history, and obesity

96
Q

where does a murmur best heard in the right intercostal space usually originate?

A

at or near the aortic valve

97
Q

how is the pitch of a murmur categorized?

A

high medium or low

98
Q

where does the murmur or aortic stenosis usually radiate?

A

it usually radiates down the neck in the direction or arterial flow especially on the right side

99
Q

where does the murmur or mitral regurgitation usually radiate?

A

it often radiates to the axilla supporting transmission by bone conduction

100
Q

right sided and left sided murmurs usually increase w what part of respiration?

A

right sided= inspiration

left sided= expiration

101
Q

what murmur is distinguished from all other murmurs by an increase in intensity during squatting-to- standing action (95% sensitivity, 84% specificity) and by a decrease in intensity during standing-to-squatting action (95% sensitivity, 85% specificity)

A

hypertrophic obstructive cardiomyopathy

102
Q

“the square wave” response

A

In patients with severe heart failure, blood pressure remains elevated and there are Korotkoff sounds during the phase 2 strain phase, but not during phase 4 release, termed “the square wave” response

103
Q

effect of isometric handgrip

A

increases the systolic murmurs of mitral regurgitation, pulmonic stenosis, and ventricular septal defect as well as the diastolic murmurs of aortic regurgitation and mitral stenosis

104
Q

transient arterial occlusion

A

Transient compression of both arms by bilateral blood pressure cuff inflation to 20 mm Hg greater than peak systolic blood pressure augments the murmurs of mitral regurgitation, aortic regurgitation, and ventricular septal defect

105
Q

murmurs differentiated from other systolic murmurs by augmentation of their intensity with handgrip and transient arterial occlusion

A

mitral regurgitation and ventricular septal defect

106
Q

important topics for cardiovascular health promotion and counseling

A

-Challenges of cardiovascular disease prevention
-Health disparities in cardiovascular disease
-Assessing cardiovascular disease risk factors
Step 1: Screen for individual cardiovascular disease risk factors
Step 2: Calculate 10-year and lifetime global cardiovascular disease risk using a web-based calculator
Step 3: Address individual risk factors—hypertension, diabetes, dyslipidemias, metabolic syndrome, smoking, family history, and obesity
-Promoting lifestyle changes and risk factor modification

107
Q

health behaviors of ideal cardiovascular health

A

Body mass index <25 kg/m2
Not smoking
Being physically active
Following a healthy diet

108
Q

health factors of ideal cardiovascular health

A

Untreated total cholesterol <200 mg/dL
Blood pressure <120/<80 mm Hg Fasting blood glucose <100 mg/dL

109
Q

screening for individual CV risk factors

A

Begin routine screening at 20 years for individual risk factors and for any family history of premature heart disease (age <55 years in first-degree male relatives and age <65 years in first-degree female relatives)

110
Q

causes of secondary hypertension

A

Causes include obstructive sleep apnea, chronic kidney disease, renal artery stenosis, medications, thyroid disease, parathyroid disease, Cushing syndrome, hyperaldosteronism, pheochromocytoma, and coarctation of the aorta

111
Q

risk factors of primary hypertension

A

risk factors include age, genetics, black race, obesity and weight gain, excessive salt intake, physical inactivity, and excessive alcohol use

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