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patho final > structural cardiac disorders > Flashcards

structural cardiac disorders Flashcards

1
Q

ductus venosus

A

structure in liver which allows most blood to bypass the liver and enter directly into the inferior vena cava

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2
Q

foramen ovale

A

opening between atria allowing some fetal blood to pass from right side of heart to left, bypassing right ventricle and lungs

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3
Q

ductus arteriosus

A

between the pulm artery and aorta which allows blood to bypass the lungs and enter directly into descending aorta

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4
Q

which side of the heart is more oxygenated and what %

A

left side- blood is returning from the lungs (about 95%)

right side- (72-80%)

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5
Q

atria pressure

A

thin walled chambers, low pressure

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6
Q

ventricle pressure

A

thicker walled with high pressure

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7
Q

left ventricle has what

A

the greatest presssure because it must pump blood into the high pressure systemic circulation

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8
Q

what is a cardiac shunt

A

an abnormal blood flow through the heart or great vessle

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9
Q

left to right shunt

A

oxygenated blood flow from the left side of heart goes to the right side, going through the lungs again

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10
Q

right to left shunt

A

less o2 blood goes from the right side of the heart to the left side skipping the lungs

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11
Q

what is a functional murmur

A

usually seen with stress in children and infants, mostly normal and goes away with age, usually not of great concern

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12
Q

what are the causes of congenital heart defects

A
  1. alcohol, antiseizure,
  2. maternal rubella
    3heredity
  3. diabetic mothers
  4. 10x greater change of siblings have defects
  5. environment
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13
Q

atrial septal defect

A

Left-> right

abnormal opening between atria leading to increased pressure and o2 on right side of heart

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14
Q

where do most of the atrial septal defects happen

A

90% occure at foramen ovale

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15
Q

clinical mani of atrial septal defect

A

usually asymptomatic

may show s/s of HF

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16
Q

ventricular septal defect

A

left-> right shunt

abnormal opening between the ventricles leading to increased pressure and o2 on R side of heart (RV)

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17
Q

clinical mani of ventricular septal defect

A
  1. usually asymptomatic (most close spontaneously)
  2. may see s/s increased volume or HF on R side
  3. most common CHD
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18
Q

patent ductus artheriosus

A

left-> right shunt
failure of fetal structure to close after birth

blood shunted from high pressure aorta to low pressure pulmonary artery

usually closes with higher o2 levels

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19
Q

clinical mani of patent ductus arteriosus

A

may see s/s of HF or increased volume of R side

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20
Q

coarctation of aorta

A

acyanotic heart disease

narrowing of aorta

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21
Q

what are the two types of coarctation of aorta

A
  1. pre-ductal

2. post ductal

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22
Q

pre-ductal coarctation of aorta

A

between the ductus arteriosus and subclavian artery (most severe)

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23
Q

post-ductal coarctation of aorta

A

distal to the ductus arteriosus

24
Q

clinical mani of coartation of aorta on the proximal side

A

increased pressure proximal to the defect causes

  1. high BP
  2. bounding pulses in upper extremities
  3. dizziness, headache, fainting,
25
Q

clinical mani of coarctation of aorta distal

A

decreased blood supply distal to defect causes:

  1. low BP
  2. decreased/absent femoral pulses
  3. muscle cramps, cool pale extremities
26
Q

cyanotic heart disease

A

right-left shunt
desaturated venous blood flows into the left side of the heart, bypassing the lungs because the pressure on the right side is greater than the left or the vessels are misplaced

27
Q

what are the 4 defects in tetralogy of fallot

A
  1. VSD- ventricle septal defect
  2. pulmonic valve stenosis
  3. overriding aorta (shift into right ventricle)
  4. R ventricle hyertrophy
28
Q

what are the clinical mani of tetalogy of fallot

A

(related to degree of pulm stenosis)

  1. Polycythemia
  2. anoxic spells
  3. increases systemic vascular resistance
  4. shunted physical growth
  5. murmer
  6. squatting
  7. clubbing
29
Q

what all happens with the tetralogy of fallot

A

increased pressure in the RV leads to right ventricle hypertrophy. Pulmonary valve stenosis and open VSD lead to blood being shunted into the overriding aorta and lV

30
Q

where does the pressure increase and move to in tetralogy of fallot

A

high pressure on right pushing to the left

31
Q

why does squatting help in tetralogy of fallot

A

increases systemic resistance thus increasing blood flow to the lungs and increase o2 to the tissues

32
Q

what are the cyanotic heart diseases

A
  1. tetralogy of fallot

2. transposition of the great vessels

33
Q

what is transposition of the great vessels?

A

the pulm artery and aorta are flipped.

  1. aorta leaves the RV
  2. pulm leaves the LV
34
Q

what must happen to people with transposition of the great vessels in order to live

A

must have a defect present to allow communication between the 2 circulations in order to live!
(sometimes they will make a hole)

35
Q

what are the clinical mani of transposition of great vessels

A

(depends on size and type of associated defects)
1. cyanotic manis

Congestive heart failure:

  1. tachy
  2. tachypnea
  3. cardiomegaly
  4. helatomegly
36
Q

when do infants develop S/S of transposition of the great vessels

A

no symptoms for first few hours until the PDA closes

37
Q

what is pedicarditis

A

inflammation of the pericardial mem and formation of a pericardial effusion

38
Q

pericarditis can be

A

acute or chronic

39
Q

what is the cause of pericarditis

A 
infection
injury
immune response, 
metabolic disorders
neoplasms
40
Q

what is the patho of pericarditis

A

pericardial mems become inflamed and roughened

an exudate usually developes

41
Q

what are the mani of pericarditis

A
  1. sudden onset of anterior/back pain
  2. dysphagia (trouble swallowing)
  3. weakness, malaise, restlessness, anx
  4. fatigue, exercise intolerance
  5. fever, tachy
  6. pericardial friction rub
  7. cardiac tamponade (cardiac compression and decreased CO)
42
Q

what is cardiomyopathies

A

disease of the myocardium itself affecting the pumping ability of the heart because the fibers cannot contract well

degeneration of myocardial fibers

43
Q

what causes cardiomyopathies

A

cost are idiopathic, we dont really know

may be secondary to toxins, infections, immunological disorders, nutritional disorders (alcoholism) and genetics

44
Q

what are the 3 categories of cardiomyopathies

A
  1. dilated (congestive)
  2. hypertrophic
  3. restrictive
45
Q

dilated cardiomyothies

A

enlarged heart due to degeneration of the heart fibers, balloons out

46
Q

hypertrophic cardiomyothies

A

VENTRICULAR septum hypertrophy, and LV hypertrophy leads to altered shape of chambers and poorly coordinated contractions

47
Q

restrictive cardiomyothies

A

myocardial fibers become infiltrated with abnormal substances (TOXINS) causing ventricular dysfunction

doesn’t allow LV to stretch and squeeze

48
Q

clinical mani of dialated cardiomyopathies

A

both RVF and LVF

immense cardiomegaly (large heart)

49
Q

clinical mani of hypertrophic cardiomyopthies

A

mostly LVF

50
Q

clinical mani of dilated cardiomyopathies

A

RVF and LVF

51
Q

mani of LVF and RVF cardiomyopathies

A

LVF:

  1. DOE
  2. orthopnea
  3. fatigue
  4. fluid in lungs

RVF:

  1. liver congestion
  2. edema
  3. JVD (jugular venous congestion)
52
Q

what are the causes of valve diorders

A
  1. inflammation, infections
  2. trauma (HTN)
  3. degenerative
  4. connective tissue disorders
53
Q

stanosis (valve)

A

doesnt open fully

valve orifice (opening) is narrowed and constricted

flow through that valve is impeded

increases pressure and workload of the chamber that is trying to eject blood through that valve

54
Q

regurgitation (incompetence, insufficiency)

A

valve leaflets fail to close completely

blood can leak back through the valve when it is supposed to be closed

increases volume to pump because some is coming back in

55
Q

with regurgitation, what has an increases workload

A

increased workload of both the chamber getting more volume and chamber trying to pump out

56
Q

manifestations of aortic valve stenosis

A

increased pressure, workload, hypertrophy of LV

narrowed pulse pressure

SYSTOLIC murmur

57
Q

mani of aortic valve regurgitation

A

increased volume to pump

LV volume overload due to backflow

LV hypertrophy, increased LV workload

DIASTOLIC MURMUR

patho final (3 decks)

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