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Mosby's > Chapter 14 outline > Flashcards

Chapter 14 outline Flashcards

1
Q

Between what costal cartilage is the heart located?

A

behind the sternum between 3rd and 6th costal cartilage

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2
Q

What is the top and bottom of the heart called?

A

base (top) bottom (apex)

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3
Q

What is it called when your heart is positioned to the right instead of the left?

A

dextrocardia

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4
Q

if the heart and stomach are on the right and liver on the left it is called?

A

situs inversus (rare)

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5
Q

What is the double-walled fibrous sac with fluid in between the walls = low friction movement

A

pericardium

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6
Q

What is the outermost layer of heart

A

epicardium

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7
Q

What is the muscle layer responsible for pumping?

A

myocardium

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8
Q

What lines the chambers of heart and covers heart valves?

A

endocardium

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9
Q

Name the layers of the pericardium from outermost to inner most?

A

Epicardium ->Myocardium -> Endocardium

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10
Q

Name the four chambers of the heart, their thickness and what they do?

A

2 X atria (thin walled)-house blood returning from veins

2 X ventricles (thick walled) pump blood into arteries

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11
Q

The left and right chambers of the heart are separated by (blank), which is impenetrable to blood

A

interventricular septum

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12
Q

What are the two types of important valves of the heart and what do they do?

A

Atrioventricular
• Tricuspid = between right atrium and right ventricle
• Bicuspid/Mitral = between left atrium and left ventricle

Semilunar
• Pulmonic = between right ventricle and pulmonary artery
• Aortic = between left ventricle and aorta

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13
Q

Where is the tricupsid located?

A

between right atrium and right ventricle

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14
Q

Where is the bicuspid/mitral valve located?

A

between left atrium and left ventricle

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15
Q

Where is the pulmonic valves located?

A

between right ventrical and pulmonary artery

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16
Q

Where is the aortic valve located?

A

between left ventricle and aorta.

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17
Q

What happens during systole?

A

ventricles contract to eject blood into arteries ( aortic and pulmonary)

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18
Q

What happens during diastole?

A

atria contract to get blood into ventricles

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19
Q

During the S1 what do you hear and what happens?

A

lubb, tricuspid and mitral valves CLOSE as ventricle contracts

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20
Q

During the S2 what do you hear and what happens?

A

dubb  aortic and pulmonic valves CLOSE when ventricle is empty
• 2 components (not always distinguishable):
o A2 and P2
A2  aortic valve closes = happens first
P2  pulmonic valve closes = happens second

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21
Q

During the S3 what happens?

A

sound of blood rushing from atria to ventricles = not always heard

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22
Q

During S4 what happens?

A

atria fully contract to make sure no blood is left in atria = also not always heard

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23
Q

What is the path of impulse for a ECG?

A

SA (sinoatrial) Node -> AV (atrioventricular) Node -> Bundle of His -> Purkinje Fibers in ventricles

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24
Q

What does the ECG path of impulse allow for and how does the ventricular contraction move?

A

Atria contract before ventricles and contraction begins at apex and moves toward the base

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25
Q

What are ECG waves based on?

A

 Based on depolarization and repolarization of cardiac myocytes

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26
Q

Describe the ECG waves

A

 P Wave  atrial depolarization
 PR interval  time in between atrial depolarization and ventricular depolarization
 QRS complex  ventricular depolarization
 ST segment and T wave  ventricular repolarization
 U wave  small deflection seen after T wave
 QT interval  time between onset of ventricular depolarization and completion
of ventricular repolarization=pretty much systole

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27
Q

explain the path of blood flow for infants

A

• Umbillical cord  Liver  Right Atrium  Right Ventricle OR Left Atrium via foramen ovale

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28
Q

In an infant, if the blood moves to the right ventricle then it will move by way of (blank), cuz lungs arent functional.
What if it moves to the left atrium?

A

o If it goes to right ventricle -> ductus arteriosus instead of pulmonary artery b/c lungs aren’t yet functional -> joins aorta and goes to rest of body
o If it goes to the left atrium ->l eft ventricle -> aorta

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29
Q

In an infant, are the atria and ventricles the same size?

A

yes

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30
Q

when does the ductus arteriosus and foramen ovale CLOSE?

A

at birth

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31
Q

By age (blank), ventricles are twice the size of the atria

A

1

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32
Q

Heart is more (blank) until age 7

A

horizontal

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33
Q

What type of women have increased plasma volume by 50% until 30 weeks and returns to normal after delivery?

A

pregnant

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34
Q

Do pregnant women have increased cardiac output?

By how much?

A

yes

30-40% and peaks about 30 weeks and returns to normal after delivery

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35
Q

What is significant about heart size in old people?
What is significant about the valves and SA node?
What happens to the myocardium?

A

decreases unless there is hypertension or heat disease
the left ventricle thickens
can fibrose or calcify
becomes stiff

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36
Q

What will you see on an ECG of an old person?

A

o Blocks, wave abnormalities, premature systole, left ventricular hypertrophy, or atrial fibrillation

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37
Q

Overall, what can you say about the heart of an older person?

A

• Efficient at resting levels BUT poor response during stress/exercise

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38
Q

What should you ask your patient if he/she complains about chest pain?

A 
onset and duration
character
location
severity
symptoms
treatment
fatigue
cough
difficulty breathing
loss of consciousness
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39
Q

If a child complains of chest pain what should you look for?
pregnant woman?
old person?

A
  • With children specifically  look for fatigue, shortness of breath, joint pain, and preferring to squat instead of sitting
  • With pregnant women specifically  look for dizziness when standing, shortness of breath (dyspnea), fainting (syncope)
  • With old people specifically  look for confusion, dizziness, palpitations, coughs and wheezes, chest tightness, leg edema
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40
Q

If a pnt complain of chest pain, ask about PMH for what?

A

 Cardiac surgery?
 Any rhythm disorder of the heart?
 Any rheumatic fever or swollen joints?
 Any chronic illnesses such as hypertension, hyperlipidemia, diabetes, thyroid problems, coronary artery disease, congenital heart issues?

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41
Q

What are common differential diagnoses of chest pain?

A

 Angina Pectoris  pressure or choking pain that relays to neck, happens more after strenuous exercise or in the cold, specific time of onset, relief with nitroglycerin
 Musculoskeletal  history of trauma, vague onset, relief with NSAID’s
 Gastrointestinal  history of indigestion, vague onset, relief with antacids

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42
Q

When you are inspecting the heart, where do you look for the apical impulse?

A

chest moves up at 5th intercostal space on left side

• Harder to see when obese or have large breasts

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43
Q

If you cannot find heart sounds then what problems could result?

A

could be extracardiac problem = problem with pleural or pericardial fluid

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44
Q

You should inspect skin and nail bed for (blank)

A

cyanosis

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45
Q

What is the normal capillary refill time?

A

2 seconds

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46
Q

When you palpate, where should you start?

A

at the apex, move up left border, move towards sternum, move down toward right border

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47
Q

When you palpate, what should you feel for?

A

apical impulse (if too forceful, could be increased cardiac output or left ventricle hypertrophy)

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48
Q

If the apical impulse is displaced to the right, it may be signs of (blank)

A

dextrocardia

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49
Q

If the apical impulse is faint it may be a sign of (blank)

A

pericardial or pleural fluid problem

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50
Q

What is the apical impulse indicative of?

A

S1

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51
Q

What else should you palpate for other than the apical impulse?

A

Feel for the thrill -> fine, rushing vibration in 2nd intercostal space
• If you can feel it = aortic or pulmonary stenosis, pulmonary hypertension, or atrial septal defect

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52
Q

While feeling for the apical impulse, you should also feel for pulse in (blank)

A

carotid artery (medial neck region)

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53
Q

Why do you percuss the heart?

A

to find the borders of heart (sound will change to resonant to dull at border)

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54
Q

What 5 areas should you ausucultate?

A
  • aortic valve (2nd right intercostal space along sternum)
  • Pulmonic Valve  second left intercostal space along sternum
  • Second pulmonic area  third left intercostal space along sternum
  • Tricuspid area  fourth left intercostal space along sternum
  • Mitral area  fifth left intercostal space along midclavicular line
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55
Q

It is always louder at the (blank) of the heart and softer at the (blank)

A

apex, base

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56
Q

This is for which S?
Ask patient to hold breath upon expiration
• Louder at apex, quieter at base
• Possible for splitting to occur (because there are 2 valves – tricuspid and mitral) but RARE
• If too loud  blood velocity is increased
o Anemia, fever, hyperthyroidism, anxiety, exercise
• If too soft  possible blockage
o Increased overlying fat, systemic or pulmonary Htn, fibrosis and calcification of mitral valve

A

S1

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57
Q

This is for which S?
Ask patient to inhale deeply and try to hear split S2 (best heard in pulmonic valve area)
o With the splitting, A2 (aortic) is before P2 (pulmonic)
o Easier to detect in young patients
o Possible Pathology
 Wide Splitting  delay in split = pulmonic stenosis or pulmonary Htn
 Fixed Splitting  unaffected by respiration = septal defects
 Reversed Splitting  P2 before A2 = heard during expiration instead of inspiration
• Louder at base, quieter at apex
• If too loud 
o Systemic or pulmonary Htn
• If too soft 
o Increased overlying fat, aortic or pulmonic stenosis

A

S2

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58
Q

This is for which S’s
Here it sometimes, don’t hear it other times = it just depends
• S3 is very quiet b/c it is atrium passively filling the ventricle
o Sounds like Ken-TUCK-y
• S4 is the atrium forcefully contracting to fill ventricle
o Often times confused with a Split S1 because it occurs at the end of diastole (right before S1 is supposed to occur)
o Sounds like TEN-nes-see
o When loud  ALWAYS indicative of pathology
• Both are louder in left lateral decubitus position

A

 For S3 and S4

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59
Q 
What occupies both systole and diastole 
•	3 distinct components contribute to sound:
o	Atrial systole 
o	Ventricular systole 
o	Ventricular diastole 
	More distinct at APEX 
	Cause?
•	Inflammation of pericardial sac causes roughening of parietal and visceral surfaces
A

pericardial friction rub

60
Q

 CLICK sound early in diastole

 More distinct at APEX

A

Prosthetic mitral valve

61
Q

 CLICK sound early in systole

A

prosthetic aortic valve

62
Q

(blank) is a term used to define the failure of the mitral and tricuspid valvs or the pulmonic and aortic valves to close simulataneously.

A

splitting

63
Q

fixed splitting is unaffected by (blank)

A

respiration

63
Q

fixed splitting is unaffected by (blank)

A

respiration

64
Q

paradoxic splitting occurs when closure of the aortic valve is (blank)

A

delayed

64
Q

paradoxic splitting occurs when closure of the aortic valve is (blank)

A

delayed

65
Q

o For the valves, sound depends on material used for prosthetic
 Animal tissue =
 Pacemaker = NO SOUND

A

QUIET

65
Q

o For the valves, sound depends on material used for prosthetic
 Animal tissue =
 Pacemaker = NO SOUND

A

QUIET

66
Q

What are heart murmurs?

A

 Prolonged heart sounds that usually sound like “whooshing”
 Could have backflow of blood due to faulty valve  regurgitation

66
Q

What are heart murmurs?

A

 Prolonged heart sounds that usually sound like “whooshing”
 Could have backflow of blood due to faulty valve  regurgitation

67
Q

What is the most common cause of heart murmurs?

A

anatomic disorder of heart valves

67
Q

What is the most common cause of heart murmurs?

A

anatomic disorder of heart valves

68
Q

What are these causes of?
• 1) Increased speed of blood flow (could be from anemia or pregnancy)
• 2) Structural defects that reroute blood flow (myocardial septum defect)
• 3) Weak contraction
• 4) Blockage in blood flow of vessels near heart (such as aorta)
• 5) Aortic valve stenosis
• 6) Ruptured chordae tendineae in mitral valve
• 7) Forceful left ventricle contraction (more common in children)
• 8) Obstructive diseases in cervical arteries  atherosclerotic carotids OR fibromuscular hyperplasia

A

heart murmurs

68
Q

What are these causes of?
• 1) Increased speed of blood flow (could be from anemia or pregnancy)
• 2) Structural defects that reroute blood flow (myocardial septum defect)
• 3) Weak contraction
• 4) Blockage in blood flow of vessels near heart (such as aorta)
• 5) Aortic valve stenosis
• 6) Ruptured chordae tendineae in mitral valve
• 7) Forceful left ventricle contraction (more common in children)
• 8) Obstructive diseases in cervical arteries  atherosclerotic carotids OR fibromuscular hyperplasia

A

heart murmurs

69
Q

What is the difference between benign and innocent heart murmurs?

A

innocent, particularly in children or young athletes = NO structural anomaly at all even though benign may have one

69
Q

What is the difference between benign and innocent heart murmurs?

A

innocent, particularly in children or young athletes = NO structural anomaly at all even though benign may have one

70
Q

How are heart murmurs characterized?

A

 1) Timing and Duration  ex: Early systolic = begins with S1, decrescendos, and ends before S2
 2) Pitch  can be high, medium, or low  High pitch = use diaphragm, low pitch = use bell
 3) Intensity  5 Grades of “loudness”
 4) Pattern  Crescendo or decrescendo
 5) Quality  what does it sound like?
 6) Location and Radiation  sound usually transmitted in direction of blood flow from the affected valve!
 7) Respiratory  does breathing change it?

70
Q

How are heart murmurs characterized?

A

 1) Timing and Duration  ex: Early systolic = begins with S1, decrescendos, and ends before S2
 2) Pitch  can be high, medium, or low  High pitch = use diaphragm, low pitch = use bell
 3) Intensity  5 Grades of “loudness”
 4) Pattern  Crescendo or decrescendo
 5) Quality  what does it sound like?
 6) Location and Radiation  sound usually transmitted in direction of blood flow from the affected valve!
 7) Respiratory  does breathing change it?

71
Q

• Narrowed mitral valve = obstructed flow from left atrium to left ventricle
• Often seen with mitral regurgitation
• Causes? Rheumatic fever OR cardiac infection
• Findings
o Low-frequency diastolic
o Heard at apex
o Palpable thrill
o S1 is increased  makes sense because this valve needs to close to produce S1 sound!

A

mitral stenosis

71
Q

• Narrowed mitral valve = obstructed flow from left atrium to left ventricle
• Often seen with mitral regurgitation
• Causes? Rheumatic fever OR cardiac infection
• Findings
o Low-frequency diastolic
o Heard at apex
o Palpable thrill
o S1 is increased  makes sense because this valve needs to close to produce S1 sound!

A

mitral stenosis

72
Q

• Narrowed aortic valve due to calcification
• Causes? Rheumatic heart disease OR atherosclerosis
• Findings
o Mid-frequency midsystolic
o Heard at left sternal border
o Palpable thrill
o S2 is very quiet or absent  make sense because this valve needs to close to produce S2 sound and it can’t close properly due to calcification 

A

aortic stenosis

72
Q

• Narrowed aortic valve due to calcification
• Causes? Rheumatic heart disease OR atherosclerosis
• Findings
o Mid-frequency midsystolic
o Heard at left sternal border
o Palpable thrill
o S2 is very quiet or absent  make sense because this valve needs to close to produce S2 sound and it can’t close properly due to calcification 

A

aortic stenosis

73
Q 
•	Fibrous ring inferior to aortic valve
•	Can become worse with time 
•	HARD to differentiate this from aortic stenosis 
•	Findings
o	Fills systole 
o	Heard at apex 
o	Palpable thrill 
o	Multiple waves felt at apical impulse 
o	Split S2, hear S3 and S4
A

Subaortic Stenosis

73
Q 
•	Fibrous ring inferior to aortic valve
•	Can become worse with time 
•	HARD to differentiate this from aortic stenosis 
•	Findings
o	Fills systole 
o	Heard at apex 
o	Palpable thrill 
o	Multiple waves felt at apical impulse 
o	Split S2, hear S3 and S4
A

Subaortic Stenosis

74
Q 
•	Narrowed pulmonic valve 
•	Cause? Congenital! 
•	Findings 
o	Mid-frequency Systolic 
o	S1, ejection click, soft or absent S2 
o	Palpable thrill
o	Radiates into neck
A

pulmonic stenosis

74
Q 
•	Narrowed pulmonic valve 
•	Cause? Congenital! 
•	Findings 
o	Mid-frequency Systolic 
o	S1, ejection click, soft or absent S2 
o	Palpable thrill
o	Radiates into neck
A

pulmonic stenosis

75
Q

• Narrowed tricuspid valve due to calcification
• Causes? Rheumatic heart disease OR congenital OR endocardial fibroelastosis (thickening of heart chambers b/c of too many elastic fibers = RARE)
• Findings
o Diastolic
o Resembles mitral stenosis BUT louder on inspiration
o Palpable thrill over right ventricle

A

tricuspid stenosis

75
Q

• Narrowed tricuspid valve due to calcification
• Causes? Rheumatic heart disease OR congenital OR endocardial fibroelastosis (thickening of heart chambers b/c of too many elastic fibers = RARE)
• Findings
o Diastolic
o Resembles mitral stenosis BUT louder on inspiration
o Palpable thrill over right ventricle

A

tricuspid stenosis

76
Q

• Incompetent mitral valve = backflow from left ventricle to left atrium
• Causes? Rheumatic fever, myocardial infarction, rupture of chordae tendineae (small tendons that hold heart valves in place)
• Findings
o High-frequency Holosystolic = hear it throughout whole systole = after S1 until S2
o VERY loud = may mask S2 sound!
o Heard best at apex, radiates to left axillary region

A

mitral regurgitation

76
Q

• Incompetent mitral valve = backflow from left ventricle to left atrium
• Causes? Rheumatic fever, myocardial infarction, rupture of chordae tendineae (small tendons that hold heart valves in place)
• Findings
o High-frequency Holosystolic = hear it throughout whole systole = after S1 until S2
o VERY loud = may mask S2 sound!
o Heard best at apex, radiates to left axillary region

A

mitral regurgitation

77
Q

• Efficient in early systole BUT prolapses into atrium in late systole = some blood flows back into left atrium!
• Can become more severe and lead to mitral regurgitation
• Findings
o LATE systolic
o Often preceded by “clicks”
o Heard best at apex when patient is UPRIGHT, not supine

A

mitral valve prolapse

77
Q

• Efficient in early systole BUT prolapses into atrium in late systole = some blood flows back into left atrium!
• Can become more severe and lead to mitral regurgitation
• Findings
o LATE systolic
o Often preceded by “clicks”
o Heard best at apex when patient is UPRIGHT, not supine

A

mitral valve prolapse

78
Q

• Incompetent aortic valve = backflow from aorta to left ventricle
• Causes? Rheumatic heart disease, Marfan syndrome, cardiac trauma, syphilis o.O
• Findings
o High-frequency early diastolic
 But can also hear low-frequency version = Austin-Flint murmur
o Heard best at apex when patient is sitting upright and leaning forward

A

Aortic Regurgitation

78
Q

• Incompetent aortic valve = backflow from aorta to left ventricle
• Causes? Rheumatic heart disease, Marfan syndrome, cardiac trauma, syphilis o.O
• Findings
o High-frequency early diastolic
 But can also hear low-frequency version = Austin-Flint murmur
o Heard best at apex when patient is sitting upright and leaning forward

A

Aortic Regurgitation

79
Q

• Incompetent pulmonic valve = backflow from pulmonary artery to right ventricle
• Causes? Pulmonary hypertension OR bacterial endocarditis
• Findings
o Almost impossible to distinguish from aortic regurgitation with just physical exam

A

pulmonic regurgitation

79
Q

• Incompetent pulmonic valve = backflow from pulmonary artery to right ventricle
• Causes? Pulmonary hypertension OR bacterial endocarditis
• Findings
o Almost impossible to distinguish from aortic regurgitation with just physical exam

A

pulmonic regurgitation

80
Q

• Incompetent tricuspid valve = backflow from right ventricle to right atrium
• Causes? Pulmonary hypertension, bacterial endocarditis, cardiac trauma, or congenital
• Findings
o Holosystolic just like mitral regurgitation!
 How to differentiate?
• Heard at lower left sternal border rather than apex
• Look for pulmonary hypertension by feeling an impulse over second left intercostal space
• ALSO P2 (part of split S2) should be accentuated to try and compensate

A

Tricuspid Regurgitation

80
Q

• Incompetent tricuspid valve = backflow from right ventricle to right atrium
• Causes? Pulmonary hypertension, bacterial endocarditis, cardiac trauma, or congenital
• Findings
o Holosystolic just like mitral regurgitation!
 How to differentiate?
• Heard at lower left sternal border rather than apex
• Look for pulmonary hypertension by feeling an impulse over second left intercostal space
• ALSO P2 (part of split S2) should be accentuated to try and compensate

A

Tricuspid Regurgitation

81
Q

if an infant has right sided heart failure it will show signs of an (blank)

A

enlarged liver that is pushed inferiorly

81
Q

if an infant has right sided heart failure it will show signs of an (blank)

A

enlarged liver that is pushed inferiorly

82
Q

apical impulse shifted to right

A

diaphragmatic hernia

82
Q

apical impulse shifted to right

A

diaphragmatic hernia

83
Q

murmurs and tachycardia are common for the first 48 hours of infants lifes, they are typicall (blank)

A

systolic

83
Q

murmurs and tachycardia are common for the first 48 hours of infants lifes, they are typicall (blank)

A

systolic

84
Q

apical impulse shifted to right

A

dextrocardia

84
Q

apical impulse shifted to right

A

dextrocardia

85
Q

in, infants S2 has a high pitch and splitting is common, S3 and S4 can be heard … T or F

A

T

85
Q

in, infants S2 has a high pitch and splitting is common, S3 and S4 can be heard … T or F

A

T

86
Q

This is normal in who?
 Sinus arrhythmia  fast HR upon inspiration, slow HR upon expiration = NORMAL
 Heart rates can change quickly with stress or temperature change

A

Children

86
Q

This is normal in who?
 Sinus arrhythmia  fast HR upon inspiration, slow HR upon expiration = NORMAL
 Heart rates can change quickly with stress or temperature change

A

Children

87
Q

Does heart rate decrease or increase with age?

A

decrease

87
Q

Does heart rate decrease or increase with age?

A

decrease

88
Q

Most heart murmurs in children result from what?

A

congenital problems or rheumatic fever

88
Q

Most heart murmurs in children result from what?

A

congenital problems or rheumatic fever

89
Q

Who is this heard in?
 Increased blood volume and heart rate
• Hear split S1 and S2, along with S3 (late in pregnancy) but NO S4
 Heart is shifted upwards so apical impulse is also shifted upwards
 Systolic murmurs are common in the pulmonic area
 Should NOT see cyanosis

A

pregnant women

89
Q

Who is this heard in?
 Increased blood volume and heart rate
• Hear split S1 and S2, along with S3 (late in pregnancy) but NO S4
 Heart is shifted upwards so apical impulse is also shifted upwards
 Systolic murmurs are common in the pulmonic area
 Should NOT see cyanosis

A

pregnant women

90
Q 
Who am I describing?
	Try not to make them change positions to often 
	Heart Rate = Low 40’s to low 100’s 
	Apical impulse is harder to find 
	S4 is common!
A

old people

91
Q

 Infection of endothelial layer of heart and valves
 Pathology More common with valve defects OR when on IV drugs
 Symptoms  fever, fatigue, murmur, CHF
 Findings  Neurologic dysfunction, Janeway lesions (small hemorrhaging on palms and soles), Osler nodes (septic emboli on tips of fingers and toes)

A

bacterial endocarditis

92
Q

 Decrease in pulmonary or systemic circulation
 Pathology -> less flow to tissues, left or right sided, when diastolic -> because of too much glycated collagen = ventricles can’t dilate = happens with older diabetics that has not been well controlled
 Symptoms -> fatigue, shortness of breath, edema
 Findings ->Systolic = narrow pulse pressure, diastolic = wide pulse pressure

A

congestive heart failure

93
Q

 Inflammation of pericardium
 Pathology  May lead to cardiac tamponade
 Symptoms  Sharp chest pain aggravated by movement
 Findings  Hear a friction rub

A

pericarditis

94
Q

 Too much fluid in the pericardial sac
 Pathology  hard for heart to relax, impairs access of blood into the heart, caused by pericarditis or trauma
 Symptoms  anxiety, chest pain, shortness of breath, discomfort when moving, lightheadedness (syncope), pale skin, rapid breathing, palpitations, edema!
 Findings  Beck’s triad (heart sounds are muffled, hypotension, jugular venous distention)

A

cardiac tamponade

95
Q

 Enlargement of right ventricle b/c of pulmonary malfunction
 Pathology  chronic, usually caused by COPD = leads to pulmonary Htn = stress on right ventricle = hypertrophy = BAD!
 Symptoms  fatigue, cough
 Findings  wheezes and crackles, distended neck veins, cyanosis, loud S2

A

Cor pulmonale

96
Q

 Ischemic necrosis caused by blockage in flow to myocardium
 Pathology  usually affects left ventricle, caused by atherosclerosis and thrombosis
 Symptoms  Deep pain that radiates to neck, jaw, and arm, can be mild in older patients = bad because it goes unnoticed!
 Findings  Dysrhythmias, S4 is present, distant heart sounds

A

myocardial infarction

97
Q

 Inflammation of the myocardium
 Pathology  results from infectious agents, toxins, or autoimmune disorders such as amyloidosis
 Symptoms  fatigue, fever, palpitations, shortness of breath
 Findings  cardiac enlargement, murmurs, tachycardia

A

myocarditis

98
Q

 Problem with conduction of nerve impulses throughout heart
 Pathology  Can be ischemic, infiltrative, or rarely neoplastic, can be caused by certain drugs (ex: antidepressants)
 Symptoms  transient weakness, syncope (fainting), rapid or irregular heartbeat

A

conduction disturbances

99
Q

Syncope is caused by what?

A 
CANADA
	Cardiac (valve stenosis)
	Arteriovenous
	Nervous (autonomic problem)
	Anemia
	Drugs (alcohol, poisons, and diabetes as well)
	Altitude
100
Q

o Atrial contraction: ventricular contraction  4:1 (should be 1:1) =too much contraction

A

atrial flutter

101
Q

slow heart rate between 50 and 60 bpm -> not necessarily a problem

A

sinus bradycardia

102
Q

irregular atrial contraction

A

atrial fibrillation

103
Q

slow hear rate b/c disruption of conduction signal between atria and ventricles

A

heart block

104
Q

o Usually paroxysmal (transient) and due to some stimulus to the atria that is separate from the SA node  high heart rate

A

atrial tachycardia

105
Q

o High heart rate (>200 bpm), usually suggestive of heart failure = BAD prognosis 

A

ventricular tachycardia

106
Q

o Irregular ventricular contraction = BAD prognosis = may precede sudden death

A

ventricular fibrillation

107
Q

 We’re back to the overall 20 abnormalities!
 Arrhythmia caused by malfunction of SA node
 Pathology  secondary to hypertension, atherosclerosis, or rheumatic heart disease
 Symptoms  fainting, dizzy, seizures, palpitations
 Findings  Dysrhythmias as seen above! Can lead to CHF

A

sick sinus syndrome

108
Q

 4 cardiac defects  ventricular septal defect, pulmonic stenosis, dextroposition of aorta, right ventricular hypertrophy
 Pathology  need surgical correction after first spell
 Symptoms  dyspnea (shortness of breath), exercise intolerance, poor growth, can have SPELLS (paroxysmal dyspnea, loss of consciousness, central cyanosis)
 Findings  systolic murmur, if not treated can lead to clubbing of fingers and toes, precordial prominence

A

tetralogy of fallot (infants and children only)

109
Q

 Infants and children ONLY
 Opening between left and right ventricles
 Pathology  30-50% close on their own within first 2 years of life
 Symptoms  recurrent respiratory infections, if large VSD  poor breathing and growth, can lead to CHF
 Findings  arterial pulse is small, holosystolic loud murmur

A

Ventricular septal defect (VSD) Infants and children

110
Q

Infants and children ONLY
 Failure of ductus arteriosis to close at birth
 Pathology  blood destined for pulmonary arteries goes to aorta too = stress on right ventricle
 Symptoms  if small, no symptoms. If large, dyspnea (shortness of breath) when exerted
 Findings  harsh, continuous murmur, wide pulse pressure

A

patent ductus anteriosis

111
Q

 Infants and children ONLY
 Congenital defect in division between left and right atria
 Symptoms  usually asymptomatic but possible for adults to develop CHF
 Findings  brief diastolic murmur, wide split S2

A

atrial septic defect

112
Q

 Systemic connective tissue disease occurring after STREPTOCOCCAL infection or skin infection
 Pathology  lots of stuff  usually problems with mitral or aortic valve leading to stenosis, most common between age 5 and 15  treatment is antibiotics
 Symptoms  fever, inflammation of joints, rash, chest pain, palpitations, fatigue, dyspnea
 Findings  murmurs that usually show mitral or atrial regurgitation, friction rub, CHF
 Remember that this is the cause of A LOT of murmurs! Detect early and you’re good 
• To differentiate this, run an antibody test for the strep bacteria

A

Infants and children only!!! Acute rheumatic fever

113
Q

 Infants and children ONLY
 Inflammation of arteries throughout the body, including coronary arteries
 Pathology  affects lymph nodes, skin, and mucous too, usually affects children under age of 5
 Symptoms  high fever, conjunctivitis (inflammation of eyelids), inflamed lips, lymphadenopathy, erythema (redness of skin), joint pain, tachycardia
 Findings  diagnosis is made if most of the above symptoms are seen!

A

kawasaki disease

114
Q

 Caused by deposition of cholesterol and lipids on arterial walls
 Pathology  leads to thickening of vascular wall = narrowing of lumen = less blood flow
 Symptoms  angina, dyspnea, palpitations
 Findings  family history is common, see dysrhythmias and CHF

A

atherosclerotic heart disease (old people)

115
Q

OLD PEOPLE ONLY
 Already went over this! Leaky mitral valve = blood flow from left ventricle into left atrium
 Symptoms  dyspnea, edema, decreased exercise tolerance
 Findings  high pitched murmur radiating to axilla, may hear S3

A

mitral regurgitation

116
Q

 Old People!
 Pain caused by myocardial ischemia
 Pathology  occurs when your cardiac myocytes are receiving less O2 than they require!
 Symptoms  pain radiating to neck, jaw, and left arms, dyspnea, fatigue, syncope, diaphoresis (excessive sweating)
 Findings  not definitive  see hypertension, tachycardia, and diaphoresis. Look at risk factors and see if patient has them  COPD, HTn, abnormal pulsations

A

angina

117
Q

Old People!
 Deposition of Amyloid (a fibrillary protein produced by chronic inflammation or a neoplastic disease) into heart
 Pathology  reduced heart contraction, possible CHF
 Symptoms  palpitations, edema, fatigue, low exercise tolerance
 Findings  Arrhythmia, dilated neck veins, hepatomegaly, thickened ventricles

A

senile cardiac amyloidosis

118
Q

 Old People!
 LAST ONE 
 Thickening and calcification of aortic valve
 Usually asymptomatic except for midsystolic murmur

A

aortic sclerosis

Mosby's (7 decks)

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