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411 > Week 8 Heart Murmur > Flashcards

Week 8 Heart Murmur Flashcards

1
Q

What are the two main branches of the right coronary artery ?

A

Acute marginal

Posterior descending artery (PDA)

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2
Q

What does the left main coronary artery divide into ?

A

Left anterior descending artery

Left circumflex artery

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3
Q

How is the period of systole defined ?

A

Time between atrioventricular valve closure and semilunar valve closer

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4
Q

When is aortic pressure at its lowest ?

A

Late diastole

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5
Q

What happens to the mitral valve when LV pressure becomes greater than LA pressure ?

A

Mitral valve closes

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6
Q

What is the isovolumetric contraction time ?

A

Period of time during which the LV pressure increases but the LV volume remains constant.

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7
Q

Why does the LA pressure increasing transiently during IVCT

A

The mitral valve bulges into the LA

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8
Q

When does the aortic valve open ?

A

When the LV pressure > aortic pressure

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9
Q

When does the aortic valve close ?

A

When the LV pressure dips below that of the intrinsic aortic pressure

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10
Q

What is the incisura or dicrotic notch ?

A

The transient increase in aortic pressure caused by the abrupt closure of the aortic valve

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11
Q

What is the isovolumetric relaxation time ?

A

Period of time during which the LV pressure is decreasing but the LV volume remains constant

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12
Q

When does the mitral valve open ?

A

When the LV pressure dips below that of the LA

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13
Q

What causes S1 ?

A

Closure of the atrioventricular valves (mitral and tricuspid)

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14
Q

What causes S2?

A

Closure of the semilunar valves (aortic and pulmonary)

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15
Q

What is the time between S1 and S2 defined as ?

A

Systole

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16
Q

What is the time interval between S2 and S1 defined as?

A

Diastole

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17
Q

What causes S3 ?

A

Rapid cessation of blood flow in early diastole in the presence of volume overload

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18
Q

When does S3 occur ?

A

Early diastole

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19
Q

When does S4 occur ?

A

Late diastole

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20
Q

What causes S4 ?

A

Occurs in presence of a pressure overload ventricle: extra pressure and volume conferred by atrial constriction into stiff ventricle —> abnormal heart sound

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21
Q

What causes an ejection click ?

A

Abnormal opening of a semilunar valve

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22
Q

What causes an opening snap ?

A

Rheumatic mitral valve stenosis

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23
Q

What are the two components of S1 ?

A

M1 and T1

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24
Q

What are the 2 components of the second heart sound ?

A

A2 and P2

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25
Q

What two heart sounds can be identified separately on auscultation ?

A

A2 and P2: splitting of the second heart sound

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26
Q

Heart sounds from which side of the heart are heard first ?

A

Left

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27
Q

What happens to the Intra thoracic pressure on inspiration ?

A

Becomes negative

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28
Q

What happens when there is negative intrathoracic pressure ?

A

Pulmonary vascular resistance decreases
Volume of blood returning to right heart increases
More blood stays in pulmonary vasculature

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29
Q

What happens to the left side of the heart when there is increased right heart blood volume return ?

A

Left side pressure decreases as a result of decreased left side blood return (increased blood stays in pulmonary vasculature)

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30
Q

Why do the left sided heart valves close earlier during inspiration ?

A

Left sided pressures and blood volumes decrease

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31
Q

What happens to S2 split on inspiration ?

A

Increases

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32
Q

What 3 things cause a heart murmur ?

A

Increased flow through normal structures
Increased turbulent flow through abnormal and small orifices
Increased flow from a narrow proximal chamber to a dilated distal chamber

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33
Q

Which one causes a systolic murmur ?
A. Severe anemia
B. Aortic stenosis
C. VSD

A

All of the above

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34
Q

When does stenosis occur ?

A

When a valve cannot fully open

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35
Q

When does regurgitation occur?

A

When a valve cannot fully close

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36
Q

How do electrical signals travel through the heart ?

A

Sinus node —> AV node —> Bundle of His

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37
Q

When does the P wave occur ?

A

Late diastole

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38
Q

When does the QRS complex occur ?

A

End of diastole (electrical signal for ventricular contraction)

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39
Q

What wave is associated with LV relaxation ?

A

T wave (late systole)

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40
Q

What is the ejection fraction ?

A

Stroke volume/ left ventricular end-diastolic volume

55-65% is normal

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41
Q

What are the 3 determinants of stroke volume ?

A

Preload ~ LVEDV
After load
Contractility

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42
Q

What is afterload ?

A

Ventricular wall stress encountered during contraction that must be overcome in order to eject blood

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43
Q

Law of Laplace

A

Wall stress = (P x r)/(2h)

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44
Q

What is the effect of afterload on stroke volume ?

A

Increased afterload —> decreased stroke volume

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45
Q

Affect of contractility on stroke volume

A

Increased contractility —> increased stroke volume (to a point)

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46
Q

How much can cardiac output increase during exercise ?

A

5-7 times the normal amount

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47
Q

What is concentric hypertrophy ?

A

An increase in myocardial wall thickness secondary to chronic pressure overload

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48
Q

What is eccentric hypertrophy ?

A

An increase in cardiac chamber radius secondary to chronic volume overload

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49
Q

What can concentric hypertrophy result in ?

A 
Increase in myocardial oxygen consumption 
Increase in myocardial workload 
Decreased ventricular compliance 
Decrease in chamber cavity size 
Negative geometric remodelling 
Decreased stroke volume 
Impaired systolic function
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50
Q

Definition of congenital heart disease ?

A

Abnormal formation or function of the heart, present at or before birth

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51
Q

What are some possible environmental causes of CHDs ?

A

Alcohol exposures
Infections
Medications
Maternal conditions

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52
Q

What are some possible genetic causes of CHDs ?

A

Abnormal number of chromosomes (trisomy 21, Turner syndrome)
Microdeletions (22q.11)
Single gene syndromes

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53
Q

What is the most common congenital malformation ?

A

CHD

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54
Q

What is situs solitus, inversus, and isomerism ?

A

Normal position in the body
Reversed position in the body
Mixed up position in the body

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55
Q

When does pump malfunction occur ?

A

If muscle is defective
If there is inadequate filling
If there is too much fluid in the pump
If there is too much resistance to output

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56
Q

In prenatal diagnosis of CHDs what symptom complexes can be recognized ?

A

Heart rate and rhythm abnormality
Hydrops fetalis: edema of the whole body
Structural abnormality of the heart

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57
Q

What does congenital heart block cause ?

A

Decrease heart rate

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58
Q

What can valve insufficiency and myocardial dysfunction lead to ?

A

Edema of the whole body (hydrops fetalis)

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59
Q

When in pregnancy is an anomaly screen conducted in BC ?

A

18-20 weeks

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60
Q

Describe fetal circulation

A

Single circulation with oxygenator in the circuit

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61
Q

Describe transitional circulation

A

Equal R and L ventricular pressures

Circulatory bypass via PFO and PDA

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62
Q

Describe neonatal circulation

A

Two circulations in series
Pulmonary resistance starts to fall
Cardiac outputs must be balanced

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63
Q

What is the incidence of critical heart disease in neonates ?

A

3:1000

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64
Q

Describe the cyanotic symptom complex

A

Presence of reduced hemoglobin in the systemic circulation

Oxygen saturation of <95%

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65
Q

What can cause cyanosis ?

A

Intra-cardiac shunt

Transposition physiology

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66
Q

Signs of tetralogy of fallot

A

Reduced O2 sat (<80%)

Ejection systolic murmur

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67
Q

Describe the effect of transposition

A

2 circulations in parallel

Saturation 60%

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68
Q

Describe tricuspid atresia and its effects

A

Single ventricle —> mixing of venous return at atrial and ventricular level
Variable restriction to pulmonary blood flow
Cyanosis

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69
Q

Presentation of afterload problem in the newborn

A

Poor pulses

Respiratory distress and shock

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70
Q

Conditions that cause afterload problems

A

Aortic stenosis
Coarctation
Interrupted arch
Hypoplastic left heart syndrome

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71
Q

Presentation of preload problem in infants

A

Tachypnea
Poor feeding
Failure to thrive

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72
Q

Conditions that can cause preload problems in infants

A

Regurgitant valves
L-R shunt at VSD
L-R shunt at ductus

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73
Q

Presentation of complete mixing disorders in infants

A

High pulmonary blood flow

Minimal cyanosis

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74
Q

Conditions that can cause complete mixing in infants

A

Atrial- TAPVR (total anomalous pulmonary Venus return)
Single ventricle with no outlet obstruction
Arterial: truncus arteriosus

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75
Q

Recognition of CHF in children

A 
Heart failure symptoms 
Asymptomatic murmur 
Most common: 
Ejection murmur off AS or PS
Regurgitant murmur of VSD 
Uncommon: 
Muscle dysfunction 
Coarctation
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76
Q

Criteria for characterizing heart murmurs

A 
Location 
Radiation 
Cardiac cycle
Duration 
Intensity
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77
Q

Patent foramen ovale remains open in what percentage of adults

A

~30%

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78
Q

How common is VSD In live birth CHDs

A

32% of patients

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79
Q

Important examinations for recognizing CHDs

A 
Growth charts
RR
Work of breathing 
Mucous membranes 
O2 sat 
BP, HR 
Precordial impulse 
Heart sounds 
Perfusion, pulses
Liver, lungs
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80
Q

Common tests for CHDs

A

ECG
Echocardiogram

Others: 
Exercise testing 
CXR 
Cardiac catheterization 
CT 
MRI
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81
Q

What can cardiac catheterization measure ?

A

Intra-cardiac pressures and blood flow

Angiography to define structural abnormalities

82
Q

Which layer of the mesoderm forms the cardiac precursor cells

A

Splanchnic

83
Q

What do cardiac precursor cells form ?

A

1st and 2nd heart fields

84
Q

Where do the cardiac precursor cells arise from?

A

Splanchnic mesoderm if the head (cranial) end

85
Q

Describe the arrangement of the 1st heart field

A

Arranged in a crescent shape: cardiac crescent

86
Q

Describe the 2nd heart field

A

Cardiac cells that arise in the same region as the 1st heart field at a slightly later time, and form endocardial tubes

87
Q

When do the endocardial tubes form ?

A

Day 19

88
Q

When do heart tubes fuse together ? And what do they form ?

A

Day 21

Endothelium

89
Q

What is the result of incomplete lateral folding ?

A

Anterior body wall defects

90
Q

How does cephalocaudal folding move the Heart ?

A

Brings heart from the head to the thorax

91
Q

What does lateral folding do ?

A

Brings the two heart tubes together to fold in the midline to make a single tube

92
Q

When do cephalocaudal and lateral folding happen in relation to each other ?

A

Simultaneously

93
Q

What is the first organ to function ?

A

Heart

94
Q

When does the heart start to beat and when does it start to fold ?

A

Day 22 and day 23

95
Q

What does the myocardium form from ?

A

2nd heart field

96
Q

What is the outflow end of the heart fixed into ?

A

Aortic arches

97
Q

What is the inflow end of the of the heart fixed to ?

A

Veins that are coming into the heart

98
Q

Why does cardiac looping occur ?

A

The Heart is. Fixed on the inflow and outflow end so when it lengthens it is forced to bend (loop)

99
Q

What does the bulbus cordis develop into ?

A

Outflow channels (aorta and pulmonary trunk)

100
Q

What does the primitive ventricle develop into ?

A

R & L ventricles

101
Q

What does the primitive atria develop into ?

A

R & L auricles

102
Q

What does part of the right atrium and SVC develop into ?

A

Coronary sinus

103
Q

Where does the bulbus cordis move during cardiac looping ?

A

Inferiorly and right

104
Q

Where does the primitive ventricle move during cardiac looping ?

A

Left

105
Q

Where does the primitive atrium move during cardiac looping ?

A

Superiorly and posteriorly

106
Q

Where does the sinus venosus move during cardiac looping ?

A

Posterior and superiorly

107
Q

What will happen if normal folding of the heart doesn’t occur?

A

Development of the heart will not continue

108
Q

When does cardiac looping occur ?

A

Day 23-28 (week 4)

109
Q

What are some consequences of abnormal cardiac rotation ?

A

Dextrocardia and situs inversus

110
Q

The growth of what is responsible for atrioventricular partitioning

A

Posterior and anterior endocardial cushions

111
Q

Aorticopulmonary septum contributes to the formation of what ?

A

Membranous interventricular septum

112
Q

When does the atrioventricular septum form ?

A

Day 228 - day 42

113
Q

When does the foramen ovale form ?

A

Day 28 - day 46

114
Q

What two septums form to leave the foramen ovale ?

A

Septum primum and septum secundum

115
Q

What is the septum primum ?

A

A muscular septum which forms from the dorsal part of the roof of the primitive atrium
Grows downward toward fusing endocardial cushions
Flexible

116
Q

What is the septum secundum ?

A

Grows from the ventral part of the roof of the primitive atrium
Grows towards the endocardial cushions
Sturdy

117
Q

When does the interventricular septum form ?

A

Day 28-46

118
Q

How does the interventricular septum grow?

A

Grows upward from the midline floor of the primitive ventricle

119
Q

When does the aorticopulmonary septum form ?

A

Day 35-56

120
Q

How does the separation of the bulbus cordis and truncus arteriosus start ?

A

3 ridges that appear at the sides of the bulbus and truncus

121
Q

What happens with the right and left conotruncal ridges during heart development ?

A

Widen and fuse together in a spiral separation between pulmonary trunk and aorta

122
Q

When does the interventricular septum form (membranous portion)?

A

Day 42-56

123
Q

What is the membraneous portion of the inter-ventricular septum an extension of ?

A

Aorticopulmonary septum

124
Q

What are the 4 steps involved in the sequential segmental analysis approach ?

A
  1. Determine cardiac sidedness and cardiac position
  2. Morphological identification of the cardiac chamber and great arteries
  3. Analyze the connections and relations
  4. Assess the associated anomalies of each segment
125
Q

What happens with blood when there is an ASD present in the heart ?

A

Mixing of systemic and pulmonary blood
Left - Right shunt
—> dilated right atrium, ventricle and pulmonary artery

126
Q

What interventions are available for an ASD ?

A

Surgical closure using a patch

Interventional catheterization

127
Q

Characterization of Tetralogy of Fallot

A

Cyanotic

  • VSD
  • over riding aorta
  • pulmonary stenosis
  • right ventricular hypertrophy

Key feature: anterior deviation of the infundibular septum
Shunt can be either direction depending on relative pressure

128
Q

When is intervention generally taken with tetralogy of fallot ?

A

Neonatal - 6 months

Determined by severity of outflow tract obstruction

129
Q

What is the most common cyanotic heart defect presenting in neonates ?

A

Transposition of Great arteries

130
Q

What happens to the circulation connection with TGA ?

A

Connected in parallel rather than in series
Aorta connected to right ventricle
Pulmonary artery connected to left ventricle
—> oxygenated blood flows to lungs

131
Q

What is critical for survival in patients with TGA ?

A

Mixing of blood (ASD, VSD, PDA)

132
Q

What surgical repair is done for patients with TGA ?

A

Arterial switch operation

133
Q

What is coarctation of the aorta ?

A

Narrowing of the aorta

134
Q

How does BP present in patients with coarctation of the aorta ?

A

Reduced BP in femoral pulse (legs)

Elevated BP in arms

135
Q

What can be prescribed to keep a PDA open temporarily ?

A

Prostaglandin E1

136
Q

How can coarctation of the aorta be repaired ?

A

Cardiac catheterization:
Stent inflated by balloon placed over area of narrow
Surgical:
Cut area of narrowing and anastomose the 2 ends together

137
Q

What is truncus arteriousus ?

A

Lesion characterized by single arterial vessel that gives rise to the systemic, pulmonary and coronary circulations.
Single semilunar valve present

138
Q

Repair of truncus arteriosus

A

VSD closed with patch: truncal valve arises from left ventricle —> new aortic valve
Valved conduit is used to create a path from the right ventricle to the pulmonary arteries

139
Q

What is hypoplastic left heart syndrome ?

A

Critically underdeveloped left side of the heart:
Single ventricle anatomy
PFO —> left to right obligate shunting
Some blood will shunt through PDA to supply aorta

140
Q

Management of hypoplastic left heart syndrome

A 
Prostaglandin E1 to keep PDA open temporarily 
Then 3 major surgeries: 
Norwood procedure 
Bidirectional Glenn connection 
Fontan surgery
141
Q

What is the Norwood procedure and when is it performed ?

A

Performed in 1st week of life in patients with hypoplastic left heart syndrome
Create new aorta from pulmonary artery and create anastomosis to the native aorta as the coronary arteries arise from this vessel, placing a shunt to supply lungs its limited amount of flow opening up the ASD so it is unrestrictive

142
Q

What is the bidirectional Glenn connection surgery and when is it performed ?

A

Performed at about 6 months in patients with HLHS

Disconnect SVC from heart and connect it directly to the pulmonary artery

143
Q

What is the Fontan surgery and when is it performed ?

A

Performed at 3-4 years in patients with HLHS

Disconnect the IVC from the heart and connect it directly to pulmonary artery

144
Q

What is the prevalence of CHD ?

A

8-11 per 1000 live births

145
Q

What is the leading cause of neonatal mortality ?

A

CHD

146
Q

What is the benefit of reducing a patients body temperature before heart surgery ?

A

Reduce the amount of oxygen needed —> safer

147
Q

When in fetal development does cardiac development occur ?

A

Weeks 4-7

148
Q

Describe fetal circulation

A

Oxygenated blood placenta —> UV through liver —> IVC —> RA —> PFO —> LA —> LV —> aorta —> brain and coronaries
SVC blood —> RA —> RV —> PA —> PDA —> descending aorta

149
Q

Describe postnatal circulation

A

Placenta eliminated —> increase SVR
Lung expansion —> decreased PVR
Increased PO2 —> further decrease in PVR —> increase in pulmonary blood flow —> increase LA pressure —> closure of PFO
Increased PO2 —> closure PDA

150
Q

What is CHD ?

A

Failure of myocardial oxygen supply to meet myocardial oxygen demand

151
Q

How does CHD present in infants ?

A

Tachypnea
Tachycardia
Diaphoresis
Hepatomegaly

152
Q

Why does CHD result in volume overload ?

A

Large communication between systemic and pulmonary circulations
Valvular regurgitant lesions

153
Q

Why does CHD lead to pressure overload ?

A

Obstruction to ventricular emptying

154
Q

What does a PDA connect ?

A

Aorta and pulmonary artery

155
Q

Are ASDs more common in females or males?

A

Female (~2-3x)

156
Q

What is the most common congenital cardiac anomaly

A

VSD

157
Q

How does coarctation of the aorta present in infancy vs older children ?

A

CHF

Hypertension

158
Q

Examples of cyanotic CHDs

A 
TGA 
Tetralogy of fallot 
Total anomalous pulmonary venous return 
Truncus arteriosus 
Single ventricle (HLHS)
159
Q

What is total anomalous pulmonary venous drainage ?

A

Anomalous drainage of the entire pulmonary venous circulation directly into the RA or via systemic veins connecting with the RA
Compensatory right to left shunt through PFO for survival
Surgical emergency

160
Q

How does high output failure present ?

A

Poor growth

161
Q

How does low output failure present ?

A

Poor perfusion

162
Q

What are the two most important objectives in the management of an infant/child with shunt physiology ?

A

Optimize growth and nutrition

Ensure developmental milestones

163
Q

How to optimize growth and nutrition in infants with fast breathing

A

Diuretics

Digoxin

164
Q

How to optimize growth and nutrition in infants with slow weight gain ?

A

Additional calories: 24 or 27 Kcal supplements

NG feeds

165
Q

How to optimize growth and nutrition in infants with mechanical heart problem ?

A

Surgery

166
Q

What 3 tests are used to determine why an infant is cyanotic ?

A

Hyperoxic test
CXR
Electrocardiogram

Pulmonary problem will improve with O2 therapy cardiac problem wont

167
Q

What shape is the heart with tetralogy of fallot ?

A

Boot shaped

168
Q

What can a fetal echocardiograph assess

A

Structure
Function
Heart rate and rhythm

169
Q

Intra cardiac shunts

A

Atrial septal defect
Ventricular septal defect
Atrio-ventricular septal defect

170
Q

Extra-cardiac shunts

A

PDA

Aorta pulmonary window

171
Q

Left to right shunts

A

ASD
VSD
AVSD
PDA

172
Q

Right to left shunts

A 
Eisenmenger syndrome (VSD, AVSD, PDA) 
Tetralogy of fallot
173
Q

Mixed cyanotic shunt

A

TGA

174
Q

What does the degree and direction of shunting depend on ?

A

Pressure difference between chambers
Relative compliance between chambers
Size of defect

175
Q

Sequela of VSD left to right shunt

A 
Pulmonary over circulation 
Pulmonary hypertension 
Left sided chamber dilation 
Left sided chamber dysfunction 
Clinical heart failure
Arrhythmias
176
Q

What changes do you expect to see with O2 sat in VSD left to right shunt ?

A

Increased RV and PA O2 sat

177
Q

Changes in O2 sat with PDA left to right shunt

A

Increased PA O2 sat

178
Q

Outline the progression to Eisenmenger syndrome

A

Left to right shunting —> pulmonary over circulation —> pulmonary hypertension —> severe pulmonary hypertension —> pulmonary pressures exceed systemic pressures —> right to left shunting

179
Q

Why does right to left shunting occur with tetralogy of fallot ?

A

Severe right ventricular outflow tract obstruction

180
Q

Changes in O2 sat with right to left shunt in tetralogy of fallot

A

Decreased RV, LV and aortic O2 sat

181
Q

Changes in O2 sat in TGA

A

Increased PA O2 sat

Decreased aortic O2 sat

182
Q

Sequela of aortic coarctation

A 
Hypertension 
Increased LV pressure 
Distal hypoperfusion 
Progressive LV dilation and dysfunction 
Clinical heart failure
183
Q

Long term progression of ASD

A

Progressive functional impairment through 3-5 decades

  • arrhythmia
  • RV dysfunction
  • paradoxical embolic phenomena
  • pulmonary vascular disease
184
Q

When is the ideal time to intervene with ASD ?

A

First decade

185
Q

Effects of moderate to large VSD

A 
Volume loads 
-LA, LV 
-pulmonary vasculature 
Pressure loads 
-RV/PA depending on size/shunt
May become smaller or spontaneously close
186
Q

Effects of large VSD

A 
Pressure and volume loads 
CHF, FTT
Infection 
Pulmonary vascular disease 
Eisenmenger syndrome
187
Q

When is the decision to repair a VSD usually made by ?

A

4-6 months

188
Q

What is pulmonary hypertension ?

A

Elevated pulmonary artery pressure

189
Q

Which CHDs tend to result on pulmonary vascular disease (pulmonary hypertension) ?

A

VSD, PDA, TGA sometimes ASD

190
Q

What is the difference between stenosis and coarctation ?

A

Both are partial obstruction to flow but stenosis is in valves coarctation is in vessels

191
Q

What do obstructive lesions lead to ?

A

Chronic increased afterload

192
Q

What does coarctation of the aorta lead to pressure load on ?

A

Ascending aorta
Aortic valve
LV
LA

193
Q

Possible consequences of coarctation of the aorta

A 
Chronic hypertension 
LV hypertrophy 
Cerebrovascular event 
Dissection of the aorta 
Infective endocarditis 
Angina = LV failure 
Morbidity from early teens 
Associated aortic stenosis
194
Q

Interventions for coarctation

A

Surgery
Angioplasty
Bicuspid aortic valve, aortopathy

195
Q

Coarctation outcomes with older age at repair

A

Hypertension
Coronary artery disease
Vascular anomalies

196
Q

What is a major issue with atrial repair in transposition ?

A

RV failure (CHF)

197
Q

Effects of unoperated tetralogy of fallot

A 
95% mortality by young adult years 
Progressive cyanosis 
Progressive right to left shunt 
Erythrocytosis 
Stroke, cerebral abscess, gout
198
Q

Long term effects of tetralogy of fallot

A

Pulmonary valve regurgitation
Atrial arrhythmia
LV function
Ventricular arrhythmia and SCD

199
Q

Risk of pregnancy with ASD, VSD, PDA

A

Low risk-less 1%

200
Q

Risk of pregnancy with aortic stenosis, coarctation, unoperated tetralogy, severe pulmonic stenosis

A

Medium risk 5-15%

201
Q

Risk of pregnancy in patients with complex coarctation and pulmonary hypertension ?

A

High risk 25-50 %

411 (16 decks)

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