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)
2
Q
What does the left main coronary artery divide into ?
A
Left anterior descending artery
Left circumflex artery
3
Q
How is the period of systole defined ?
A
Time between atrioventricular valve closure and semilunar valve closer
4
Q
When is aortic pressure at its lowest ?
A
Late diastole
5
Q
What happens to the mitral valve when LV pressure becomes greater than LA pressure ?
A
Mitral valve closes
6
Q
What is the isovolumetric contraction time ?
A
Period of time during which the LV pressure increases but the LV volume remains constant.
7
Q
Why does the LA pressure increasing transiently during IVCT
A
The mitral valve bulges into the LA
8
Q
When does the aortic valve open ?
A
When the LV pressure > aortic pressure
9
Q
When does the aortic valve close ?
A
When the LV pressure dips below that of the intrinsic aortic pressure
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
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
12
Q
When does the mitral valve open ?
A
When the LV pressure dips below that of the LA
13
Q
What causes S1 ?
A
Closure of the atrioventricular valves (mitral and tricuspid)
14
Q
What causes S2?
A
Closure of the semilunar valves (aortic and pulmonary)
15
Q
What is the time between S1 and S2 defined as ?
A
Systole
16
Q
What is the time interval between S2 and S1 defined as?
A
Diastole
17
Q
What causes S3 ?
A
Rapid cessation of blood flow in early diastole in the presence of volume overload
18
Q
When does S3 occur ?
A
Early diastole
19
Q
When does S4 occur ?
A
Late diastole
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
21
Q
What causes an ejection click ?
A
Abnormal opening of a semilunar valve
22
Q
What causes an opening snap ?
A
Rheumatic mitral valve stenosis
23
Q
What are the two components of S1 ?
A
M1 and T1
24
Q
What are the 2 components of the second heart sound ?
A
A2 and P2
25
What two heart sounds can be identified separately on auscultation ?
A2 and P2: splitting of the second heart sound
26
Heart sounds from which side of the heart are heard first ?
Left
27
What happens to the Intra thoracic pressure on inspiration ?
Becomes negative
28
What happens when there is negative intrathoracic pressure ?
Pulmonary vascular resistance decreases
Volume of blood returning to right heart increases
More blood stays in pulmonary vasculature
29
What happens to the left side of the heart when there is increased right heart blood volume return ?
Left side pressure decreases as a result of decreased left side blood return (increased blood stays in pulmonary vasculature)
30
Why do the left sided heart valves close earlier during inspiration ?
Left sided pressures and blood volumes decrease
31
What happens to S2 split on inspiration ?
Increases
32
What 3 things cause a heart murmur ?
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
33
Which one causes a systolic murmur ?
A. Severe anemia
B. Aortic stenosis
C. VSD
All of the above
34
When does stenosis occur ?
When a valve cannot fully open
35
When does regurgitation occur?
When a valve cannot fully close
36
How do electrical signals travel through the heart ?
Sinus node —> AV node —> Bundle of His
37
When does the P wave occur ?
Late diastole
38
When does the QRS complex occur ?
End of diastole (electrical signal for ventricular contraction)
39
What wave is associated with LV relaxation ?
T wave (late systole)
40
What is the ejection fraction ?
Stroke volume/ left ventricular end-diastolic volume
| 55-65% is normal
41
What are the 3 determinants of stroke volume ?
Preload ~ LVEDV
After load
Contractility
42
What is afterload ?
Ventricular wall stress encountered during contraction that must be overcome in order to eject blood
43
Law of Laplace
Wall stress = (P x r)/(2h)
44
What is the effect of afterload on stroke volume ?
Increased afterload —> decreased stroke volume
45
Affect of contractility on stroke volume
Increased contractility —> increased stroke volume (to a point)
46
How much can cardiac output increase during exercise ?
5-7 times the normal amount
47
What is concentric hypertrophy ?
An increase in myocardial wall thickness secondary to chronic pressure overload
48
What is eccentric hypertrophy ?
An increase in cardiac chamber radius secondary to chronic volume overload
49
What can concentric hypertrophy result in ?
```
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
```
50
Definition of congenital heart disease ?
Abnormal formation or function of the heart, present at or before birth
51
What are some possible environmental causes of CHDs ?
Alcohol exposures
Infections
Medications
Maternal conditions
52
What are some possible genetic causes of CHDs ?
Abnormal number of chromosomes (trisomy 21, Turner syndrome)
Microdeletions (22q.11)
Single gene syndromes
53
What is the most common congenital malformation ?
CHD
54
What is situs solitus, inversus, and isomerism ?
Normal position in the body
Reversed position in the body
Mixed up position in the body
55
When does pump malfunction occur ?
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
56
In prenatal diagnosis of CHDs what symptom complexes can be recognized ?
Heart rate and rhythm abnormality
Hydrops fetalis: edema of the whole body
Structural abnormality of the heart
57
What does congenital heart block cause ?
Decrease heart rate
58
What can valve insufficiency and myocardial dysfunction lead to ?
Edema of the whole body (hydrops fetalis)
59
When in pregnancy is an anomaly screen conducted in BC ?
18-20 weeks
60
Describe fetal circulation
Single circulation with oxygenator in the circuit
61
Describe transitional circulation
Equal R and L ventricular pressures
| Circulatory bypass via PFO and PDA
62
Describe neonatal circulation
Two circulations in series
Pulmonary resistance starts to fall
Cardiac outputs must be balanced
63
What is the incidence of critical heart disease in neonates ?
3:1000
64
Describe the cyanotic symptom complex
Presence of reduced hemoglobin in the systemic circulation
| Oxygen saturation of <95%
65
What can cause cyanosis ?
Intra-cardiac shunt
| Transposition physiology
66
Signs of tetralogy of fallot
Reduced O2 sat (<80%)
| Ejection systolic murmur
67
Describe the effect of transposition
2 circulations in parallel
| Saturation 60%
68
Describe tricuspid atresia and its effects
Single ventricle —> mixing of venous return at atrial and ventricular level
Variable restriction to pulmonary blood flow
Cyanosis
69
Presentation of afterload problem in the newborn
Poor pulses
| Respiratory distress and shock
70
Conditions that cause afterload problems
Aortic stenosis
Coarctation
Interrupted arch
Hypoplastic left heart syndrome
71
Presentation of preload problem in infants
Tachypnea
Poor feeding
Failure to thrive
72
Conditions that can cause preload problems in infants
Regurgitant valves
L-R shunt at VSD
L-R shunt at ductus
73
Presentation of complete mixing disorders in infants
High pulmonary blood flow
| Minimal cyanosis
74
Conditions that can cause complete mixing in infants
Atrial- TAPVR (total anomalous pulmonary Venus return)
Single ventricle with no outlet obstruction
Arterial: truncus arteriosus
75
Recognition of CHF in children
```
Heart failure symptoms
Asymptomatic murmur
Most common:
Ejection murmur off AS or PS
Regurgitant murmur of VSD
Uncommon:
Muscle dysfunction
Coarctation
```
76
Criteria for characterizing heart murmurs
```
Location
Radiation
Cardiac cycle
Duration
Intensity
```
77
Patent foramen ovale remains open in what percentage of adults
~30%
78
How common is VSD In live birth CHDs
32% of patients
79
Important examinations for recognizing CHDs
```
Growth charts
RR
Work of breathing
Mucous membranes
O2 sat
BP, HR
Precordial impulse
Heart sounds
Perfusion, pulses
Liver, lungs
```
80
Common tests for CHDs
ECG
Echocardiogram
```
Others:
Exercise testing
CXR
Cardiac catheterization
CT
MRI
```
81
What can cardiac catheterization measure ?
Intra-cardiac pressures and blood flow
| Angiography to define structural abnormalities
82
Which layer of the mesoderm forms the cardiac precursor cells
Splanchnic
83
What do cardiac precursor cells form ?
1st and 2nd heart fields
84
Where do the cardiac precursor cells arise from?
Splanchnic mesoderm if the head (cranial) end
85
Describe the arrangement of the 1st heart field
Arranged in a crescent shape: cardiac crescent
86
Describe the 2nd heart field
Cardiac cells that arise in the same region as the 1st heart field at a slightly later time, and form endocardial tubes
87
When do the endocardial tubes form ?
Day 19
88
When do heart tubes fuse together ? And what do they form ?
Day 21
| Endothelium
89
What is the result of incomplete lateral folding ?
Anterior body wall defects
90
How does cephalocaudal folding move the Heart ?
Brings heart from the head to the thorax
91
What does lateral folding do ?
Brings the two heart tubes together to fold in the midline to make a single tube
92
When do cephalocaudal and lateral folding happen in relation to each other ?
Simultaneously
93
What is the first organ to function ?
Heart
94
When does the heart start to beat and when does it start to fold ?
Day 22 and day 23
95
What does the myocardium form from ?
2nd heart field
96
What is the outflow end of the heart fixed into ?
Aortic arches
97
What is the inflow end of the of the heart fixed to ?
Veins that are coming into the heart
98
Why does cardiac looping occur ?
The Heart is. Fixed on the inflow and outflow end so when it lengthens it is forced to bend (loop)
99
What does the bulbus cordis develop into ?
Outflow channels (aorta and pulmonary trunk)
100
What does the primitive ventricle develop into ?
R & L ventricles
101
What does the primitive atria develop into ?
R & L auricles
102
What does part of the right atrium and SVC develop into ?
Coronary sinus
103
Where does the bulbus cordis move during cardiac looping ?
Inferiorly and right
104
Where does the primitive ventricle move during cardiac looping ?
Left
105
Where does the primitive atrium move during cardiac looping ?
Superiorly and posteriorly
106
Where does the sinus venosus move during cardiac looping ?
Posterior and superiorly
107
What will happen if normal folding of the heart doesn’t occur?
Development of the heart will not continue
108
When does cardiac looping occur ?
Day 23-28 (week 4)
109
What are some consequences of abnormal cardiac rotation ?
Dextrocardia and situs inversus
110
The growth of what is responsible for atrioventricular partitioning
Posterior and anterior endocardial cushions
111
Aorticopulmonary septum contributes to the formation of what ?
Membranous interventricular septum
112
When does the atrioventricular septum form ?
Day 228 - day 42
113
When does the foramen ovale form ?
Day 28 - day 46
114
What two septums form to leave the foramen ovale ?
Septum primum and septum secundum
115
What is the septum primum ?
A muscular septum which forms from the dorsal part of the roof of the primitive atrium
Grows downward toward fusing endocardial cushions
Flexible
116
What is the septum secundum ?
Grows from the ventral part of the roof of the primitive atrium
Grows towards the endocardial cushions
Sturdy
117
When does the interventricular septum form ?
Day 28-46
118
How does the interventricular septum grow?
Grows upward from the midline floor of the primitive ventricle
119
When does the aorticopulmonary septum form ?
Day 35-56
120
How does the separation of the bulbus cordis and truncus arteriosus start ?
3 ridges that appear at the sides of the bulbus and truncus
121
What happens with the right and left conotruncal ridges during heart development ?
Widen and fuse together in a spiral separation between pulmonary trunk and aorta
122
When does the interventricular septum form (membranous portion)?
Day 42-56
123
What is the membraneous portion of the inter-ventricular septum an extension of ?
Aorticopulmonary septum
124
What are the 4 steps involved in the sequential segmental analysis approach ?
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
What happens with blood when there is an ASD present in the heart ?
Mixing of systemic and pulmonary blood
Left - Right shunt
—> dilated right atrium, ventricle and pulmonary artery
126
What interventions are available for an ASD ?
Surgical closure using a patch
| Interventional catheterization
127
Characterization of Tetralogy of Fallot
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
When is intervention generally taken with tetralogy of fallot ?
Neonatal - 6 months
| Determined by severity of outflow tract obstruction
129
What is the most common cyanotic heart defect presenting in neonates ?
Transposition of Great arteries
130
What happens to the circulation connection with TGA ?
Connected in parallel rather than in series
Aorta connected to right ventricle
Pulmonary artery connected to left ventricle
—> oxygenated blood flows to lungs
131
What is critical for survival in patients with TGA ?
Mixing of blood (ASD, VSD, PDA)
132
What surgical repair is done for patients with TGA ?
Arterial switch operation
133
What is coarctation of the aorta ?
Narrowing of the aorta
134
How does BP present in patients with coarctation of the aorta ?
Reduced BP in femoral pulse (legs)
| Elevated BP in arms
135
What can be prescribed to keep a PDA open temporarily ?
Prostaglandin E1
136
How can coarctation of the aorta be repaired ?
Cardiac catheterization:
Stent inflated by balloon placed over area of narrow
Surgical:
Cut area of narrowing and anastomose the 2 ends together
137
What is truncus arteriousus ?
Lesion characterized by single arterial vessel that gives rise to the systemic, pulmonary and coronary circulations.
Single semilunar valve present
138
Repair of truncus arteriosus
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
What is hypoplastic left heart syndrome ?
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
Management of hypoplastic left heart syndrome
```
Prostaglandin E1 to keep PDA open temporarily
Then 3 major surgeries:
Norwood procedure
Bidirectional Glenn connection
Fontan surgery
```
141
What is the Norwood procedure and when is it performed ?
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
What is the bidirectional Glenn connection surgery and when is it performed ?
Performed at about 6 months in patients with HLHS
| Disconnect SVC from heart and connect it directly to the pulmonary artery
143
What is the Fontan surgery and when is it performed ?
Performed at 3-4 years in patients with HLHS
| Disconnect the IVC from the heart and connect it directly to pulmonary artery
144
What is the prevalence of CHD ?
8-11 per 1000 live births
145
What is the leading cause of neonatal mortality ?
CHD
146
What is the benefit of reducing a patients body temperature before heart surgery ?
Reduce the amount of oxygen needed —> safer
147
When in fetal development does cardiac development occur ?
Weeks 4-7
148
Describe fetal circulation
Oxygenated blood placenta —> UV through liver —> IVC —> RA —> PFO —> LA —> LV —> aorta —> brain and coronaries
SVC blood —> RA —> RV —> PA —> PDA —> descending aorta
149
Describe postnatal circulation
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
What is CHD ?
Failure of myocardial oxygen supply to meet myocardial oxygen demand
151
How does CHD present in infants ?
Tachypnea
Tachycardia
Diaphoresis
Hepatomegaly
152
Why does CHD result in volume overload ?
Large communication between systemic and pulmonary circulations
Valvular regurgitant lesions
153
Why does CHD lead to pressure overload ?
Obstruction to ventricular emptying
154
What does a PDA connect ?
Aorta and pulmonary artery
155
Are ASDs more common in females or males?
Female (~2-3x)
156
What is the most common congenital cardiac anomaly
VSD
157
How does coarctation of the aorta present in infancy vs older children ?
CHF
| Hypertension
158
Examples of cyanotic CHDs
```
TGA
Tetralogy of fallot
Total anomalous pulmonary venous return
Truncus arteriosus
Single ventricle (HLHS)
```
159
What is total anomalous pulmonary venous drainage ?
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
How does high output failure present ?
Poor growth
161
How does low output failure present ?
Poor perfusion
162
What are the two most important objectives in the management of an infant/child with shunt physiology ?
Optimize growth and nutrition
| Ensure developmental milestones
163
How to optimize growth and nutrition in infants with fast breathing
Diuretics
| Digoxin
164
How to optimize growth and nutrition in infants with slow weight gain ?
Additional calories: 24 or 27 Kcal supplements
| NG feeds
165
How to optimize growth and nutrition in infants with mechanical heart problem ?
Surgery
166
What 3 tests are used to determine why an infant is cyanotic ?
Hyperoxic test
CXR
Electrocardiogram
Pulmonary problem will improve with O2 therapy cardiac problem wont
167
What shape is the heart with tetralogy of fallot ?
Boot shaped
168
What can a fetal echocardiograph assess
Structure
Function
Heart rate and rhythm
169
Intra cardiac shunts
Atrial septal defect
Ventricular septal defect
Atrio-ventricular septal defect
170
Extra-cardiac shunts
PDA
| Aorta pulmonary window
171
Left to right shunts
ASD
VSD
AVSD
PDA
172
Right to left shunts
```
Eisenmenger syndrome (VSD, AVSD, PDA)
Tetralogy of fallot
```
173
Mixed cyanotic shunt
TGA
174
What does the degree and direction of shunting depend on ?
Pressure difference between chambers
Relative compliance between chambers
Size of defect
175
Sequela of VSD left to right shunt
```
Pulmonary over circulation
Pulmonary hypertension
Left sided chamber dilation
Left sided chamber dysfunction
Clinical heart failure
Arrhythmias
```
176
What changes do you expect to see with O2 sat in VSD left to right shunt ?
Increased RV and PA O2 sat
177
Changes in O2 sat with PDA left to right shunt
Increased PA O2 sat
178
Outline the progression to Eisenmenger syndrome
Left to right shunting —> pulmonary over circulation —> pulmonary hypertension —> severe pulmonary hypertension —> pulmonary pressures exceed systemic pressures —> right to left shunting
179
Why does right to left shunting occur with tetralogy of fallot ?
Severe right ventricular outflow tract obstruction
180
Changes in O2 sat with right to left shunt in tetralogy of fallot
Decreased RV, LV and aortic O2 sat
181
Changes in O2 sat in TGA
Increased PA O2 sat
| Decreased aortic O2 sat
182
Sequela of aortic coarctation
```
Hypertension
Increased LV pressure
Distal hypoperfusion
Progressive LV dilation and dysfunction
Clinical heart failure
```
183
Long term progression of ASD
Progressive functional impairment through 3-5 decades
- arrhythmia
- RV dysfunction
- paradoxical embolic phenomena
- pulmonary vascular disease
184
When is the ideal time to intervene with ASD ?
First decade
185
Effects of moderate to large VSD
```
Volume loads
-LA, LV
-pulmonary vasculature
Pressure loads
-RV/PA depending on size/shunt
May become smaller or spontaneously close
```
186
Effects of large VSD
```
Pressure and volume loads
CHF, FTT
Infection
Pulmonary vascular disease
Eisenmenger syndrome
```
187
When is the decision to repair a VSD usually made by ?
4-6 months
188
What is pulmonary hypertension ?
Elevated pulmonary artery pressure
189
Which CHDs tend to result on pulmonary vascular disease (pulmonary hypertension) ?
VSD, PDA, TGA sometimes ASD
190
What is the difference between stenosis and coarctation ?
Both are partial obstruction to flow but stenosis is in valves coarctation is in vessels
191
What do obstructive lesions lead to ?
Chronic increased afterload
192
What does coarctation of the aorta lead to pressure load on ?
Ascending aorta
Aortic valve
LV
LA
193
Possible consequences of coarctation of the aorta
```
Chronic hypertension
LV hypertrophy
Cerebrovascular event
Dissection of the aorta
Infective endocarditis
Angina = LV failure
Morbidity from early teens
Associated aortic stenosis
```
194
Interventions for coarctation
Surgery
Angioplasty
Bicuspid aortic valve, aortopathy
195
Coarctation outcomes with older age at repair
Hypertension
Coronary artery disease
Vascular anomalies
196
What is a major issue with atrial repair in transposition ?
RV failure (CHF)
197
Effects of unoperated tetralogy of fallot
```
95% mortality by young adult years
Progressive cyanosis
Progressive right to left shunt
Erythrocytosis
Stroke, cerebral abscess, gout
```
198
Long term effects of tetralogy of fallot
Pulmonary valve regurgitation
Atrial arrhythmia
LV function
Ventricular arrhythmia and SCD
199
Risk of pregnancy with ASD, VSD, PDA
Low risk-less 1%
200
Risk of pregnancy with aortic stenosis, coarctation, unoperated tetralogy, severe pulmonic stenosis
Medium risk 5-15%
201
Risk of pregnancy in patients with complex coarctation and pulmonary hypertension ?
High risk 25-50 %
