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PEDS > week 6 > Flashcards

week 6 Flashcards

1
Q

Cardiovascular problems - distal impacts

A
  • growth and development
  • learning
  • cognitive function
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2
Q

Anatomy of the heart - pathway of blood through the heart

A
  • superior vena cava, inferior vena cava (deoxygenated)
  • right atrium
  • tricuspid valve
  • right ventricle
  • pulmonary artery
  • lungs
  • pulmonary veins (oxygenated)
  • left atrium
  • mitral valve
  • left ventricle
  • out aortic valve
  • to the body
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3
Q

blood flow in utero

A
  • placenta helps facilitate blood flow
  • umbilical vein - provides O2 blood into superior vena cava via ductus venosus
  • O2 blood mixes with deoxygenated blood –> heart –> septum bipases non aerated blood into left atrium and left ventcicle
  • umbilical arteries take deoxygenated blood from aorta
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4
Q

Blood moves through the body…

A

by pressure (blood moves away from pressure)

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5
Q

Fetal structures of cardiovascular (3)

A
  • foramen ovale
  • ductus arteriosus
  • ductus venosus
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6
Q

Foramen ovale

A

small hole between R and L heart
allows oxygenated blood to the left side of the heart

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7
Q

Ductus arteriosus

A

connects pulmonary artery to aorta
shunts deoxygenated blood from RV to descending aorta bypassing nonaerated lungs

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8
Q

Ductus venosus

A

shunts oxygenated blood from umbilical to Inferior vena cava bypassing the liver

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9
Q

Causes of congenital heart disease

A

cardiac development begins on 18th day of life, completed by 45th = environmental influences during this time
- 90% are multifactorial causes (genetic and environmental)

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10
Q

Gestational and perinatal history - cardiac (2)

A

maternal infection
maternal medications

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11
Q

Gestational and perinatal history - cardiac - maternal infection (2)

A
  • rubella in 1st trimester
  • HIV in late pregnancy
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12
Q

Gestational and perinatal history - cardiac - maternal medications (2)

A
  • amphetamines
  • phenytoin/progesterone/warfarin/valpro acid
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13
Q

Cardiovascular assessment - respirations (3)

A
  • rate depth effort
  • dry unproductive cough presence
  • mild/moderate/severe WOB
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14
Q

Cardiovascular assessment - pulse (2)

A
  • rate rhythm quality
  • compare pulse sites (upper/central/lower extremities)
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15
Q

Cardiovascular assessment - blood pressure (2)

A
  • is it within normal range for age
  • compare upper and lower extremities
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16
Q

Cardiovascular assessment - colour (4)

A
  • pale/dusky/cyanosis (blue better than grey)
  • compare colour in peripheral and central locations
  • does crying help or worsen the colour
  • pulse ox
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17
Q

Cardiovascular assessment - cap refill

A

press 3 seconds come back in 3 seconds

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18
Q

pulse assessment - babies

A

brachial pulse is easiest
dorsal foot
femeral

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19
Q

Cardiovascular assessment - heart auscultation (4)

A
  • auscultate for heart sounds, quality, loud/soft, distinct/muffled
  • any extra heart sounds
    • normal is S1 (lub) S2 (dub)
    • S3S4 abnormal
    • murmurs abnormal (location radiation timing
      quality)
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20
Q

Cardiovascular assessment - fluid status

A
  • edema (periorbital, facial, peripheral)
  • abdominal distension
  • palpate liver for hepatomegaly (liver margin)
  • monitor I/Os for fluid status
  • cap refill (press 3 seconds comes back 3 seconds)
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21
Q

Cardiovascular assessment - activity and behaviour

A

exercise intolerance

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22
Q

Increased pulmonary blood flow - types of defects (3)

A
  • patent ductus arteriosus
  • arterial septal defect
  • ventricle septal defect
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23
Q

Increased pulmonary blood flow - clinical manifestations (8)

A
  • tachypnea
  • tachycardia
  • murmur
  • congestive heart failure
  • poor weight gain
  • diaphoresis
  • periorbital edema
  • frequent respiratory infections
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24
Q

Decreased pulmonary blood flow - types of defects (4)

A
  • pulmonary stenosis
  • tetralogy of fallot
  • pulmonary atresia
  • tricuspid aterisia
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25
Q

Decreased pulmonary blood flow - clinical manifestations (4)

A
  • cyanosis
  • hypercyanotic episodes
  • poor weight
  • polycthemia
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26
Q

Obstructions to systemic blood flow - types of defects (5)

A
  • coarctation of aorta
  • aortic stenosis
  • hypoplastic left heart syndrome
  • mitral stenosis
  • interrupted aortic arch
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27
Q

Obstructions to systemic blood flow - clinical manifestations (5)

A
  • diminished pulses
  • poor colour
  • delayed cap refill
  • decreased U/O
  • congestive heart failure may occur with pulmonary edema
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28
Q

Mixed defects - dependent on the mixing of pulmonary and systemic blood - types of defects (4)

A
  • transposition of great arteries
  • total anomalous pulmonary venous connection
  • truncus arteriosus
  • double outlet right ventricle
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29
Q

Mixed defects - dependent on the mixing of pulmonary and systemic blood - clinical manifestations (4)

A
  • cyanosis
  • poor weight gain
  • pulmonary congestion
  • congestive heart failure may occur with increased shunting
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30
Q

Arterial septal defect (ASD) - what

A
  • 5-10% of defects
  • more in females
  • sometimes late presentation - 5 years
  • septum formed weeks 4-6
  • before birth patent foramen ovale
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31
Q

Arterial septal defect (ASD) - pathophysiology

A
  • at birth, left atrium pressure elevates and closes patient foramen oval
  • if it doesn’t close, there is a L to R shunt
  • RA dilation
  • RV volume overload
  • increase fluid to lungs
    larger ASD = bigger flow = worse syumptmos
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32
Q

Arterial septal defect (ASD) problems

A
  • Right atrium dilation
  • right ventricle volume overload
  • increase flow to lungs
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33
Q

Arterial septal defect (ASD) - larger ASD

A

bigger asd = bigger flow - worse symptoms

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34
Q

Arterial septal defect (ASD) - pressure

A
  • pressure from left to right = blood stays in pulmonary circulation
  • decreased perfusion to rest of body
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35
Q

Arterial septal defect (ASD) - clinical presentation (4)

A
  • usually asymptomatic
  • may present with congestive heart failure (5% <1 year…. cardiomyopathy, failure to thrive, Afib
  • pulmonary edema (rarely pulmonary hypertension)
  • may lack symptoms until late teens (fatigue SOBOE)
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36
Q

Arterial septal defect (ASD) - management

A
  • 87% close spontaneously by 1 year
  • congestive heart failure = digoxin, diuretics, fluid restriction
  • cath lab closure (umbrella type device)
  • surgical (stitch closure or patch)
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37
Q

Arterial septal defect (ASD) - complications (5)

A
  • sinus node dysfunction
  • 1st degree heart block
  • bleeding
  • tamponade
  • residual shunts
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38
Q

Ventricular septal defect - what

A
  • most common - 20% of defects
  • mostly males
  • Downs syndrome and other trisomies
  • isolated defect
  • associated with simple defects - ASD, patent ductus arteriosus
  • associated with complex defects - TGA, TET, Truncus, DORV
  • more pressure involved**
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39
Q

Ventricular septal defect - diagnosis (how and type)

A
  • echo/ultrasound determines diagnosis and severity
  • septum develops 4-8 weeks gestation
  • birth = no shunting due to equal pressures of RV and LV
  • 4-6 weeks significant L to R shunt
  • perimembraenous - right below aortic valve
  • muscular (swiss cheese closer to apex)
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40
Q

Ventricular septal defect - size and effect

A
  • pinpoint to large
  • 50% close by 2 years spontaneously
  • L to R shunt
  • smal defect = asymptomatic, large shunt - increased pulmonary vascular resistance
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41
Q

Ventricular septal defect - increased pulmonary vascular resistance (2)

A
  • high flow
  • increased pressure –> hypertrophy of pulmonary vessels
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42
Q

Ventricular septal defect - pathophysiology - how it causes damage

A
  • increased pulmonary flow = pulmonary edema (high PVR, RV hypertrophy, LA dilation, LV volume overload
  • ay be asymptomatic until 6 weeks when pulmonary vascular resistance (PVR) drops
  • after 2-3 PVR les than systemic
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43
Q

Ventricular septal defect - development through childhood (4)

A
  • small VSD may go undetected till pre school
  • small restrictive - pressure gradient - loud murmur during systole
  • 80% close spontaneously
  • pulmonary vascular obstructive disease in 15% by age 20 (large VSDs)
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44
Q

Ventricular septal defect - management for small shunt

A
  • asymptomatic =
  • conservative
  • closes spontaneously at 1 year of life
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45
Q

Ventricular septal defect - management for moderate shunt

A
  • digoxin
  • diuretics
  • fluid restriction
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46
Q

Ventricular septal defect - management for severe shunt

A
  • surgery recommended early
  • suture or patch repair via right atrium
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47
Q

Ventricular septal defect - congestive heart failure symptoms

A
  • feeding difficulties
  • fatigue
  • dyspnea, tachypnea, grunting
  • pulmonary hypertension
  • increased respiratory infections
  • FTT
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48
Q

Patent ductus arteriosus - what (fequency, sex, risks, comorbidities, size)

A
  • 10% of defects
  • more in females
  • maternal rubella, prematurity
  • 15% associated with VSD, coarction of A
  • connects the aorta to the pain Pulmonary Artery at its bifurcation
  • approx. 1cm by 1cm
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49
Q

Normal development of Patent ductus arteriosus (4)

A
  • birth = breathing increase in PO2
  • begins closing within 10-15 hours of birth
  • constricts by 24-72 hours
  • structural closure 2-3 weeks
  • fibrosed at 12 weeks
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50
Q

Patent ductus arteriosus - why it remains open (5)

A
  • premature
  • hypoxia
  • scaring of ductus due to rubella
  • acidosis
  • PGE’s (we want it to stay open)
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51
Q

Patent ductus arteriosus - pressure

A
  • blood shunts from aorta to lungs
  • L to R shunt = pulmonary over circulation (LA dilation, LV hypertrophy, recirculates to left, volume loads LV
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52
Q

Patent ductus arteriosus - large

A
  • congestive heart failure, cardiomegaly
  • apnea, resp failure, recurrent infections
  • systolic murmur at LT sternal border
  • bounding peripheral pulses, wide pulses pressures with large PDAs
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53
Q

Patent ductus arteriosus - management

A
  • CHF -> diuretics, fluid restriction, digoxin
  • advil = PGE inhibitor –> close shunt
  • surgical - suture ligation via L thoractomy, coil catheterization
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54
Q

Patent ductus arteriosus - diagnosis

A
  • echo - size, progression etc.
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55
Q

Atrial ventricular septal defect - what

A
  • 1-2% of all defects
  • insufficiency of AV valves burdens the RV
  • more common in downs syndrome
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56
Q

Atrial ventricular septal defect - types

A
  • incomplete
  • complete
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57
Q

Atrial ventricular septal defect - incomplete

A
  • 2 seperate AV valves, often with a cleft mitral valve
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58
Q

Atrial ventricular septal defect - complete

A

common AV valves (5 leaflets), ASD and VSD

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59
Q

Atrial ventricular septal defect - shunting (4)

A
  • atrial level is a L to R direction (LV to RA, incompetent mitral and tricuspid valve)
  • L to R shunt to PVR drops so increased PVR over time
  • risk of pulmonary vascular obstructive disease by 1 year
  • shunt depends on : size of defect, PVR, AV valve competency
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60
Q

Atrial ventricular septal defect - volume load

A
  • loads right and left side of heart
  • CHF around 1-2 months, pulmonary hypertension, FTT
  • varying degrees of AV regurgitation (BAD, not getting closing of valves = leaking and back up and fluid retension)
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61
Q

Atrial ventricular septal defect - ventricle sized

A
  • balanced
  • unbalanced
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62
Q

Atrial ventricular septal defect - balanced

A
  • ventricles of equal size
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63
Q

Atrial ventricular septal defect - unbalanced

A

one ventricle larger than the other

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64
Q

Atrial ventricular septal defect - management (2)

A
  • digoxin and diuretics
  • antibiotics to prevent endocarditis
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65
Q

Atrial ventricular septal defect - surgery (complete vs incomplete)

A
  • 3-6 months for complete AV
  • 1-2 years for incomplete
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66
Q

Atrial ventricular septal defect - incomplete surgery

A
  • patch ASD and suture cleft in the mitral valve
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67
Q

Atrial ventricular septal defect - complete

A
  • pericardial patch repair of ASD and VSD and repair of cleft mitral and tricuspid valves (1 or 2 patch repair)
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68
Q

Atrial ventricular septal defect - post op

A
  • push volume slowly, use of inotropes
  • at risk for heart block, pulmonary edema, poor function
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69
Q

Right ventricular outflow tract obstructions

A

not getting oxygen or blood to pulmonary system
ex - tetralogy of fallot

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70
Q

Tetralogy of Fallot (4)

A
  • pulmonary artery obstruction
  • overriding aorta
  • VSD
  • right ventricular hypertrophy
  • worse with crying (increases PVR –> Ted spells = purple)
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71
Q

Intervention for ted spells

A

put knees to chest

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72
Q

Left ventricular outflow obstructions example

A
  • coarctation of the aorta
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73
Q

Coarctation of the aorta

A
  • picked up in utero or at a well baby clinic (as decreased PVR starts)
  • easily missed early on, picked up later
  • decreased cap refil and pulse to feet
  • gradient between BP in preductal (right arm) and postductal (legs)
  • PGEs to keep duct open, two IVs at all times, then surgery, balloon dilations (cath lab)
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74
Q

Kawasaki’s disease - what (3)

A
  • leading cause of aquired heart disease
  • most children who contract illness are less than two years, 80% less than 5
  • a generalized vasculitis of unknown etiology (attack coronary arteries)
75
Q

Kawasaki disease - complications (7)

A
  • coronary artery abnormalities (coronary aneurisms)
  • 25% if untreated….
    • may resolve or persist
    • may lead to thrombosis
    • evolve into segmental stenosis (narrowing)
    • or rarely rupture
  • cause of death = myocardial infarction
76
Q

Kawasaki disease - child presentation

A

child is always miserable = keep them calm

77
Q

Kawasaki disease - primary diagnosis criteria (3)

A
  • fever persisting at least 5 days
  • fever generally high and spiking (often to 40º)
  • persists in untreated patients for one to two weeks or longer
78
Q

Kawasaki disease - patient population

A
  • Japanese descent
  • typically male
  • COVID –> MISC have similar findings
79
Q

Kawasaki disease - presence of (5)

A

34

80
Q

Kawasaki disease - diagnosis criteria (5)

A

4 of 5 of the following
- polymorphic exanthem (~5 days after fever onset)
- bilateral conjunctival injection
- changes in lips and oral cavity
- Desquamation of the fingers and toes (1-3 weeks after fever onset)
- cervical lymphadenopathy

81
Q

Polymorphic exanthem

A

skin eruption of the trunk and extremities (several forms)
rash usually appears within five days of fever onset

82
Q

Bilateral conjunctival injection (5)

A
  • bulbar conjuntivae involved
  • limbic region spared
  • not usually associated with exudate
  • usually painless
  • aka redness of the eyes
83
Q

Kawasaki disease - changes in lips and oral cavity (3)

A
  • strawberry tongue
  • redness and cracking of lips
  • erythema of oropharyngeal mucosa (no ulcerative lesions)
84
Q

Desquamination of fingers and toes

A
  • acute distinctive changes in extremities (redness, swelling, induration of hands and feet)
  • 1-3 weeks after onset of fever
  • approx. 1-2 months after fever onset Beau’s lines (white lines on fingernails) may appear
85
Q

beau’s lines

A

white lines on fingernails

86
Q

Cervical lymphadenopathy (3)

A
  • at least one lymph node with diameter of 1.5cm or greater
  • usually unilateral
  • firm and slightly tender nodes
87
Q

Kawasaki disease - cardiac investigation findings

A
  • pancarditis (esp coronary arteries)
  • pericardial effusion (spontaneous resolve)
  • myocarditis +/- CHF
  • coronary artery abnormalities in 20-25% of patients
  • diffuse ectasia or coronary aneurisms
88
Q

Kawasaki disease - non-cardiac investigation findings (not including labs = 2)

A
  • often very irritable
  • arthritis and arthragia (first 2-3 weeks at knees ankles hips)
89
Q

Kawasaki disease - non-cardiac investigation findings - Labs (7)

A
  • elevated CRP
  • elevated WBC >15,000,
  • normocytic, normochromic anemia (normal number not normal amount at maturity)
  • platelets >450,000, p
  • pyuria (WBC in urine)
  • ALT >50
  • albumin <3
90
Q

Kawasaki disease - treatment (6)

A
  • not treated in 10 days, pts under 1yr have increased risk of coronary artery aneurisms
  • initial therapy = reduce fever and inflammatory features
  • treatment = helps prevent coronary artery abnormalities and myocardial ischemic injury
  • Long term therapy = avoiding coronary thrombosis (prevent platelet aggregation)
  • give an IVIG - antibodies to IV
  • high dose asprin orally (prevents platelets) first dose, lower for 6-8 weeks
91
Q

ECG’s - what they show (8)

A
  • HR and rhythm
  • abnormalities of conduction
  • muscular damage (ischemia)
  • hypertrophy
  • bundle branch blocks
  • electrolyte balance
  • drug effects
  • pericardial disease
92
Q

SA node

A

primary pacemaker, initiates impulses

93
Q

AV node

A

secondary pacemaker, conducts impulses

94
Q

Bundle of His

A

purkenje cells rapidly impulse transmission

95
Q

Purkenje fibres

A

rapid ventricular spread

96
Q

Conduction (5) - ECG

A

P-wave
PR interval
QRS
ST segment
T wave

97
Q

P-wave

A

contraction and depolarization of aorta

98
Q

PR interval

A

spread and delay of electrical impulse form SA node to AV node

99
Q

QRS

A

ventricular depolarization

100
Q

ST segment

A

baseline

101
Q

T wave

A

ventricular repolarization

102
Q

Normal sinus rhythm - origin

A

SA node

103
Q

Normal sinus rhythm - rhythm

A

regular +/-10%

104
Q

Normal sinus rhythm - rate

A
  • P to P
  • R to R
105
Q

Normal sinus rhythm - P waves

A
  • present upright and uniform
  • 1:1 conduction
106
Q

Normal sinus rhythm - PR interval

A

constant within age related norms

107
Q

Normal sinus rhythm - QRS

A

narrow, age related norms
QRS complexes are identical

108
Q

Sinus bradycardia - rate

A

less than 80 bpm in newborns
less than 60 bpm in children

109
Q

Sinus bradycardia - effect

A

rate dependent
- may decrease CO (low BP, dizzy, weak, decreased LOC, syncope, pale, underperfused)

110
Q

Sinus bradycardia - cause (7)

A
  • athletes
  • electrolyte imbalances (hypokalemia)
  • vagal stimulation
  • hypoxia
  • drugs (beta blockers, digoxin, etc)
  • hypothermia
  • increased ICP
111
Q

Sinus bradycardia - treatment

A
  • none, or treat the cause
  • oxygen
  • chest compressions for HR less than 60 bpm-
  • meds = epinephrine, atropine
  • pacing (transthoracic, transcutaneous, transesophogeal)
112
Q

Types of bradycardias (4)

A
  • sinus bradycardia
  • nodal (junctional) rhythm
  • second degree AV block
  • third degree AV block
113
Q

Sinus bradycardia - origin

A

SA node

114
Q

Sinus bradycardia - rhythm

A

regular

115
Q

Sinus bradycardia - rate

A

slower than normal for age

116
Q

Sinus bradycardia - PR interval

A

constant, age related norms

117
Q

Sinus bradycardia - QRS

A

narrow, age related norms

118
Q

Sinus bradycardia 0 p waves

A

present upright and uniform, 1:1 conduction

119
Q

bradycardias - general causes (2)

A

suppressed automaticity or conduction

120
Q

bradycardias - impacts (6)

A
  • decreased CO
  • decreased BP
  • decreased LOC
  • increased tissue hypoxia
  • increased anaerobic metabolism
  • increased acidosis
121
Q

Causes of bradycardias - specific (8)

A
  • hypoxia
  • SA node dysfunction
  • heart block
  • acidosis
  • hypothermia
  • increased vagal tone
  • hyperkalemia
  • drugs (digoxin)
122
Q

Sinus tachycardia - rate

A

> 160 bpm in infants (usually lower than 200)
140 bpm in children

123
Q

Sinus tachycardia - effect (2)

A

poor coronary filling, fatigue of myocardium

124
Q

Sinus tachycardia - causes

A
  • small stroke volume (tamponade, shock, CHF, hypovolemia)
  • symptomatic stimulation (pain anxiety infection exercise, respiratory failure, myocarditis/pericarditis, fever, drugs, anemia, cardiac disease, shock
125
Q

Sinus tachycardia - treatment (2)

A

treat cause
- if CO compromised = Digoxin, Ca channel blockers, beta blockers

126
Q

Types of tachycardia (5)

A
  • sinus tachycardia
  • supraventricular tachycardia (SVT)
  • ventricular tachycardia (VT)
  • Atrial fibrillation (Afib)
  • Atrial flutter
127
Q

Sinus tachycardia - origin

A

SA node

128
Q

Sinus tachycardia - rhythm

A

regular

129
Q

Sinus tachycardia - rate

A

p to p (age related norms

130
Q

Sinus tachycardia - R to R

A

faster than normal

131
Q

Sinus tachycardia - p wave

A

present upright uniform
1:1 conduction

132
Q

Sinus tachycardia - PR interval

A

constant age related norm

133
Q

Sinus tachycardia - QRA

A

narrow, age related norms

134
Q

Tachycardias - impacts (7)

A
  • decreased cardiac filling time
  • decreased stroke volume
  • increased O2 demand
  • decreased coronary artery diastolic filling time
  • decreased BP
  • increased hypoxia
  • increased acidosis
135
Q

Tachycardias - causes (7)

A
  • congenital
  • idiopathic
  • drug toxicity
  • surgical
  • hypoxia
  • acidosis
  • infectious and inflammatory
136
Q

SVT - what

A

rapid rate with normal QRS
- infants HR >220 bpm
- children HR >180 bpm

137
Q

SVT - P waves

A
  • may be buried in previous T wave and not visible
  • not a rounded smooth sinus p wave
138
Q

SVT - causes (9)

A
  • fever
  • catecholamines
  • congenital heart disease
  • cardiac surgery
  • CHF
  • hypoxia
  • infection
  • electrolyte imbalance
  • idopathic
139
Q

SVT - origin

A

atria or junctional (common term)

140
Q

SVT - rhythm

A

regular

141
Q

SVT - rate

A

p to p but often not seen
R to R normal

142
Q

SVT - p wave

A

present upright and different than sinus, often not seen

143
Q

SVT - PR interval

A

constant, sometimes longer (in accessory pathways is shorter)

144
Q

SVT - QRS

A

narrow, age related norms

145
Q

SVT - treatment (3)

A
  • vagal stimulation (coughing gagging valsava knee to chest position suction ice to face carotid sinus massage (MD))
  • atrial overdrive pacing, cardioversion
  • adenosine, amiodarone, procainamide
146
Q

Adenosine

A

a drug that stops the heart momentarily

147
Q

Sinus arrythmia - rate

A
  • HR increases with inspiration
  • HR decrease with expiraciton
148
Q

Sinus arrythmia - effect

A
  • sign of good cardiac reserve
  • indicates heart is unger vagal contral and not sympathetic
149
Q

Sinus arrythmia - causes

A

normal varient in young and elderly
change in respiratory cycle -= change in intrathoracic pressure and change in sympathetic tone

150
Q

Sinus arrythmia - treatment

A

none unless due to increased ICP or respiratory obstruction

151
Q

Sinus arrythmia - origin

A

SA node

152
Q

Sinus arrythmia - rhythm

A

regularly irregular (fluctuates with resp cycle)

153
Q

Sinus arrythmia - rate

A

P to P, R to R age related norms

154
Q

Sinus arrythmia - p waves

A

present upright uniform, 1:! conduction

155
Q

Sinus arrythmia - PR interval

A

constant, age related norms

156
Q

Sinus arrythmia - QRS

A

narrow, age related norms

157
Q

Tetrology of Fallot - etiology (3)

A
  • multifactorial (genes and environment)
  • more common in trisomy 21 and others
  • advanced maternal age, alc use, poor nutrition, viral illness
158
Q

Tetrology of Fallot - structural abnormalities (4)

A

1) VSD
2) pulmonary stenosis
3) RV hypertrophy
4) overriding aorta

159
Q

Pulmonary stenosis - what

A

narrowing of pulmonary valve

160
Q

overriding aorta - what

A

an exist exists above both ventrivles

161
Q

Tetrology of Fallot - pathophysiology (6)

A

1) pulmonary stenosis = decreased deoxygenated blood into pulmonary circuit
2) increased RV pressure (increased blood volume form shunting from VSD and less exiting to pulmonary)
3) increased RV pressure –> RV hypertrophy (increased work load to pump blood past stenosis)
4) VSD causes blood to be shunted L to R (severe pulm. stenosis will cause R to L shunting)
5) overriding aorta straddles VSD (deoxygenated blood shunted from RV to exit heart via aorta from LV to systemic circulation
6) deoxygenated blood enters systemic circulation = decreased O2

162
Q

Tetrology of Fallot - initial symptoms

A
  • murmurs at left mid-upper sternal border with posterior radiation
  • Pre/post ductal SpO2 (decreased blood to R hand and both feet)
  • Cyanosis/Tet spell
163
Q

difference in pre and post ductal SpO2

A

pre - left hand
post = right hand and both feet

164
Q

Tet spell

A

when a baby with Tetrology of Fallot turns cyanotic in lips or nail beds when they cry

165
Q

Tetrology of Fallot - diagnosis (3)

A
  • chest X ray (RV hypertrophy, boot shaped heart, decreased pulmonary vascular)
  • echocardiograpm (visualize 4 structural defects)
  • electrocardiogram (RV hypertrophy = right axis deviation, prominant P waves = atrial enlargment)
165
Q

Tetrology of Fallot - diagnosis (3)

A
  • chest X ray (RV hypertrophy, boot shaped heart, decreased pulmonary vascular)
  • echocardiograpm (visualize 4 structural defects)
  • electrocardiogram (RV hypertrophy = right axis deviation, prominant P waves = atrial enlargment)
166
Q

Tetrology of Fallot - nursing priorites (6)

A
  • managing tet spells
  • risk for blood clots
  • risk of endocarditis
  • maintaining O2
  • patient family education
  • fluid balacne
167
Q

Tet spell - Assessment findings (3)

A
  • SpO2 - drastic decrease
  • Respirations - increase in rate and depth
  • skin colour - may appear cyanotic
168
Q

Tet spell - treatment (6)

A
  • knee to chest position (increase systemic vascular resistance= increased blood to lungs)
  • administer o2
  • IV fluids - improve preload and pulmonary blood flow
  • narcotics
  • beta blockers*
  • vasoconstrictors*
169
Q

Endocarditis (Tetrology of Fallot) - assessment findings (5)

A
  • elevated WBC (if infection is cause)
  • Anemia
  • increased temp, respiratory rate, pulse
  • blood culture positive
  • chest x ray = heart inflammation
170
Q

Endocarditis (Tetrology of Fallot) - treatment (3)

A
  • prophylactic antibiotic treatment
  • health teaching on aseptic techniques
  • extra caution surrounding high risk procedures (ex dental surgery)
171
Q

Tetrology of Fallot - treatment options (3)

A
  • non-surgical (rare)
  • palliative surgery
  • complete surgical repair
172
Q

Tetrology of Fallot - non surgical treatment (3)

A
  • manage symptoms
  • poorer outcomes or death
  • will need surgery by 6 months to 1 year (not sustainable)
173
Q

Tetrology of Fallot - palliative surgery (3)

A
  • less invasive surgery, not open heart
  • small tube placed between aorta and pulmonary artery to provide blood flow to lungs
  • allow babies to grow strong enough for a complete surgical repair later
174
Q

Tetrology of Fallot - complete surgical repair

A
  • open heart surgery
  • close VSD with patch, open obstructed pathway between RV and pulmonary artery
  • most often done before an infant 1 year old
  • prognosis excellent, following cardiologist necessary
175
Q

Tetrology of Fallot - medication spotlight

A
  • antibiotics
  • narcotics
  • beta blockers
  • digoxin
  • loop diuretic
176
Q

coarctation of the aorta

A

present at birth
- narrowing or constriciton of descending aorta by a ridge formed by thickening of medial wall, tissues of aortic wall folding in

177
Q

coarctation of the aorta - pathophysiology

A
  • narrowing of aorta –> LV working harder to pump blood through body
178
Q

coarctation of the aorta - severe narrowing symtoms (7)

A
  • tachypnea
  • problems eating (poor weight gain)
  • irritability
  • sleepiness and lethargy
  • generalized mottling
  • pale or gay skin colour, cyanosis
  • heart failure and shock
179
Q

coarctation of the aorta - mild symptoms (7)

A
  • chest pain
  • cold feet/legs
  • dizziness, faintness
  • decreased stamina
  • poor growth/failure to thrive
  • pounding headache
  • SOB-
  • can be asymptomatic
180
Q

coarctation of the aorta - diagnosis

A
  • echocardiogram
  • chest X ray
  • ECG
  • CT scan
  • CT angiogram
  • MRI
  • hyperoxia
  • 4 limb BP
  • blood tests
181
Q

coarctation of the aorta - surgery

A
  • interposition graft
  • end-to-end anastomosis
  • patch augmentation
  • subclavian flap repair
  • ascending to descending aorta bypass graft
  • balloon angioplasty
  • transcatheter stent therapy
182
Q

coarctation of the aorta - other interventions (non surgical) (3)

A
  • antihypertensives
  • vasodilators
  • promoting healthy lifestyle/preventing complications
183
Q

fuck

A

me

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