Ch. 7- Clinical Correlations For Heart

Front 1

Persistent truncus arteriosus (PTA)

Back 1

- caused by abnormal neural crest cell migration, partial development of AP septum
- results in one large vessel leaving heart and receiving blood from both RT and LT ventricles
- truncoconal septa and ventricular membranous septum do not form at all
- blood from both sides of heart mix and body and lungs receive partially oxygenated blood
- usually accompanied with VSD
- marked cyanosis (R-->L shunting of blood)

Hint 1

AP septum

Front 2

Ventricular septal defects (VSD)

Back 2

1) b/c of deficient development of proximal truncoconal swellings
2) failure of muscular and membranous ventricular septa to fuse
3) endocardial cushion defect
4) excessive perforation of muscular ventricular septum
- massive L-->R shunting of blood and pulmonary hypertension
- most common cardiac defect

Hint 2

or is it R-->L?
AP septum

Front 3

D-transposition of great arteries (complete)

Back 3

- abnormal neural crest cell migration such taht there is nonspiral development of AP septum
- results in aorta arising abnormally from RT ventricle and pulmonary trunk arising from LT ventricle --> systemic and pulmonary circulations completely separated from one another
- need accompanying shunt, like VSD, patent foramen ovale, or patent ductus arteriosus
- marked cyanosis (R-->L shunting of blood)

Hint 3

aorticopulmonary (AP) = truncoconal

Front 4

L-transposition of great arties (corrected)

Back 4

- aorta and pulmonary trunk are transposed and ventricles "inverted" so that anatomical RT ventricle lies on LT side and anatomical LT ventricle lies on RT side.
- major deviations offset one another so that pattern of blood flow is normal

Hint 4

AP septum

Front 5

Tetralogy of Fallot (TF)

Back 5

- skewed development of AP septum
- pulmonary trunk smaller than aorta
1) pulmonary stenosis
2) RT ventricular hypertrophy
3) Overriding aorta (rightward displacement of aorta)
- defects raise BP within right ventricle, causing its enlargement
4) Ventricular septal defect
= PROVE
- marked cyanosis , clinical consequences depend primarily on pulmonary stenosis

Hint 5

AP septum

Front 6

Atrial septal defects (ASDs)

Back 6

- septum secundum is too short to completely cover ostium secundum
- problem after birth b/c of massive shunting of blood from L-->R atrium
- may lead to enlargement of RT atrium, ventricle and pulmonary trunk
- associated with autosomal and sex chromosome aberrations, and trisomies

Hint 6

ASD

Front 7

Foramen secundum defect

Back 7

- caused by excessive resportion of septum primum, septum secundum, or both
- results in opening between RT and LT atria
- most common clinically significant ASD
- result in patent foramen ovale

Hint 7

ASD

Front 8

Common atrium (cor triloculare biventriculare)

Back 8

- ASD
- caused by complete failure of septum primum and septu secundum to develop
- result is one atrium is formed

Hint 8

ASD

Front 9

Probe patency of foramen ovale

Back 9

- ASD
- incomplete anatomic fusion of septum primum and septum secundum.
- usually of no clinical importance

Hint 9

ASD

Front 10

Premature closure of foramen ovale

Back 10

- ASD
- closure of foramen ovale during prenantal life
- results in hypertrophy of RT side of heart, underdevelopment of LT side of heart

Hint 10

ASD

Front 11

Persistent common AV canal

Back 11

- failure of fusion of dorsal and ventral AV cushions (inferior/superior)
- common AV canal never partitioned, large hole in center of heart
- tricuspid and bicuspid valves represented by one valve common to both sides of heart
1) causes L-->R shunting, enlarged RT atrium and RT ventricle
2) causes mitral valve regurgitation, enlarged LT atrium/ventricle

Hint 11

AV septum

Front 12

Ebstein's anomaly

Back 12

- caused by failure of posterior and septal leaflets of tricuspid valve to attach normally to annulus fibrosus
- instead displaced inferiorly into RT ventricle
- blocks access of blood to pulmonary orifice, allows blood to regurgitate into RT atrium
- result is R-->L shunting thru persistent foramen ovale

Hint 12

AV septum

Front 13

Atrioventricular septum (AV)

Back 13

- 4 cushions
- RT/LT endocardial cushion
- inferior/superior cushion
- end of week 6, inferior and superior cushions fuse--> septum intermedium
- divides common AV canal into RT and LT AV canals

Hint 13

AV septum

Front 14

Foramen primum defect

Back 14

- caused by failure of AV septum to fuse with septum primum
- results in condition which foramen primum is never closed and generally accompanied by abnormal mitral valve

Hint 14

AV septum

Front 15

Tricuspid atresia (hypoplastic right heart)

Back 15

- insufficient amount of AV cushion is available to form the tricuspid valve
- results in complete agenesis of tricuspid valve
- no communication between right atrium and right ventricle
- marked cyanosis accompanied by the following:
1) patent foramen ovale
2) IV septum defect
3) overdeveloped LT ventricle
4) underdeveloped RT ventricle

Hint 15

AV septum

Front 16

Membranous VSD

Back 16

- caused by faulty fusion of RT bulbar ridge/LT bulbar ridge/AV cushions
- opening between RT and LT ventricles allows free flow of blood
- large VSD initially associated with L-->R shunting, increased pulmonary blood flow, pulmonary hypertension
- L-->R shunting patients complain of excessive fatigue on exertion

Hint 16

IV septum

Front 17

Eisenmenger syndrome

Back 17

- uncorrected VSD, ASD, PDA
- all initially associated with L-->R shunting of blood, inreased pulmonary blood flow and hypertension
- later hypertension causes marked proliferation of tunica intima and tunica media, resulting in narrowing of lumens
- ultimately, pulmonary resistance become higher than systemic and cause R-->L shunting of blood and cyanosis

Hint 17

IV septum

Front 18

Muscular VSD

Back 18

- caused by single or multiple perforations in muscular IV septum

Hint 18

IV septum

Front 19

Common ventricle (cor triloculare biatriatum)

Back 19

- caused by failure of membranous and muscular IV septa to form

Hint 19

IV septum

Front 20

Postductal coarctation

Back 20

- occurs when aorta abnormally constricted
- found distal to the origin of left subclavian artery and inferior to ductus arteriosus
- clincally associated with increased BP in upper extremities, lack of pulse in femoral artery, high risk of cerebral hemorrhage and bacterial endocarditis
- collateral circulation involving: internal thoracic, intercostal, superior epigastric, inferior epigastric, external iliac arteries
- rib notching: dilaion of intercostal arteries erode lower border of ribs, seen in x-ray

Hint 20

arterial problems

Front 21

preductora coarctation

Back 21

- aorta constriction located superior to ductus arteriosus
- occurs in Turner syndrome (XO)

Hint 21

arterial problems

Front 22

patent ductus arteriosus (PDA)

Back 22

- when ductus arteriosus, connection between LT pulmonary artery and aorta, fails to close
- usually functionally closes within a few hours after birth via smooth muscle contractions --> ligamentum arteriosum
- causes L-->R shunting of O2 rich blood from aorta back into pulmonary circulation
- treated with prostaglandin synthesis inhibitors, acetylcholine, histamine, catecholamines to close DA

Hint 22

arterial problems

Front 23

Cardiac tamponade

Back 23

- rapid accumulation of fluid in pericadium
- fibrous pericardium not elastic
- acute pressure on the heart, causes compression of venous return, decreased diastolic capacity, reduced CO increased HR and venous pressure
- it is the resulting compression of the heart
- treated by pericardiocentesis

Front 24

Surgical significance of transverse pericardial sinus

Back 24

- finger can be passed through sinus to aorta and pulmonary trunk
- can pass clamp or place ligature around vessels to divert or stop circulation of blood in large arteries during cardiac surgery

Front 25

Pericarditis

Back 25

- inflammation of the pericardium
- may result in:
1) cardiac tamponade
2) pericardial effusion
3) precordial and epigastric pain
4) pericardial murmur
5) pericardial friction rub
- symptoms of dysphagia, dyspnea, cough
- treated with steroids, paracentesis

Front 26

Pericardial effusion

Back 26

- accumulation of liquid in pericardial space
- from inflammation caused by acute pericarditis
- compresses heart, inhibiting cardiac filling
- englarged heart, water bottle appearance, faint heart sounds
- treated by pericardiocentesis
- causes cardiac tamponade

Front 27

Pericardiocentesis

Back 27

- surgical puncture of pericardial cavity for aspiration of fluid
- relieves pressure on heart
- needle inserted through 5th intercostal space left of sternum
- b/c of cardiac notch, needle misses pleura and lungs and goes into pericardium

Front 28

Pericardial friction rub

Back 28

- surface of pericardium becomes rough and resulting friction sounds like rustle of silk
- heard upon auscultation

Front 29

Cardiomegaly

Back 29

- slow increase in size of heart
- this slow increase is allowed by pericardium without pressure

Front 30

Levels of viscera in mediastinum

Back 30

- most pictures assume anatomical position, with body lying supine
- in this position, abdominal viscera push mediastinal structures superiorly
- in standing position, everything sags inferiorly under influence of pressure
- significance: movement of mediastinal structures must be considered during physical and radiological exminations

Front 31

Pulmonary stenosis

Back 31

- pulmonary valve stenosis: narrowing, valve cusps are fused, form dome of narrow central opening
- infundibular pulmonary stenosis: conus arteriosus underdeveloped, produce restriction of RT ventricular flow
- both may occur together, degree of hypertrophy of RT ventricle variable

Hint 31

valve disorder

Front 32

Cardiovascular accidents (CVA)

Back 32

- aka stroke
- when thrombi (clot) forms on wall of left atrium and then breaks off (becomes embolus), occlude artery in the brain
- affect vision, cognition, sensory, motor function of parts of body controlled by damamged area of brain

Front 33

Valvular heart disease

Back 33

- problems with valve disturb pumping efficiency of heart
- valvular heart disease
- produces stenosis (narrowing) or insufficiency
- increase workload for heart
- produce turbulence that produce vibrations that can be heard as murmurs or felt as thrills
- valves can be replaced by valvuloplasty with either artificial valve or xenografted valve

Front 34

Stenosis

Back 34

- failure of valuve to open fully, slowing blood flow from chamber
- increased workload for the heart
- produce turbulence that produce vibrations that can be heard as murmurs or felt as thrills

Hint 34

valve disorder

Front 35

Valvular insufficiency or regurgitation

Back 35

- failure of valuve to close completely
due to nodule formation (scarring) on cusps so edges don't meet
- allows variable amount of blood to flow back into chamber
- result in increased workload for heart
- produce turbulence that produce vibrations audible as murmurs and superficial vibratory sensations (thrills)

Hint 35

valve disorder

Front 36

Prolapsed mitral valve

Back 36

- valve exerts back into left atrium because leaflets are enlarged or floppy during systole
- blood regurgitates into left atrium when left ventricle contracts, producing characteristic murmur
- chest pain, palpitations, shortness of breath
- no treatment is needed

Hint 36

valve disorder

Front 37

aortic valve stenosis

Back 37

- most frequent valv abnormality
- results in left ventricular hypertrophy
- result of degernative calcification

Hint 37

valve disorder

Front 38

Myocardial infarction

Back 38

- sudden occlusion of major artery by embolus
- necrosis of mycardium b/c of local ischemia
- usually in coronary artery, arteriosclerosis of coronary arteries