Cardiac Flashcards

1
Q

Gastrulation

A

cardiac development - the arrangement of the 3 germ layers

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2
Q

Heartbeat begins & blood pumping

A

at 22-23 days of life and begins pumping blood during week 4

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3
Q

Complete cardiac development

A

occurs at 6 weeks - disorders of this embryological age include transposition, dextrocardia

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4
Q

Maternal Diabetes and CHD

A

Diabetes prior to conception increases risk by 2-4x; Elevated insulin levels result in hypertrophic cardiac tissue,
common CHD: transposition, VSD, cardiomyopathy

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5
Q

Rubella and CMV r/t CHD

A

PDA, ASD, VSD

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6
Q

SLE r/t CHD

A

fetal and neonatal complete congenital heart block and dilated cardiomyopathy

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7
Q

Maternal influenza r/t CHD

A

Right ventricular outflow tract obstruction

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8
Q

Male infants more likely CHD

A

COA, aortic stenosis, TGV, hypoplastic left heart

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9
Q

premature infants r/t CHD

A

PDA, ASD, VSD

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10
Q

weak pulses

A

shock, myocardial failure, or left outflow obstructions

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11
Q

bounding pulses

A

cardiac runoff (surplus), aortic insufficiency, systemic to pulmonary shunts (left to right)

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12
Q

continuous bruit murmur over fontanelle and liver

A

AV malformation

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13
Q

CHD associated with Trisomy 21

A

AV Canal, VSD, PDA, ASD-1 and -2, TF

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14
Q

CHD associated with Trisomy 18 (Edwards syndrome)

A

VSD, polyvalvular disease, ASD, PDA

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15
Q

Trisomy 13 (patau’s syndome)

A

PDA, VSD, ASD, Coarctation, AS, PS

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16
Q

3 physiological states of CHD

A
  1. low cardiac output
  2. Congestive Heart failure
  3. Cyanosis
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17
Q

Low Cardiac Output

A

defect that obstructs flow of blood out of heart or when heart is unable to pump effectively

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18
Q

Management of Low Cardiac Output

A

Correct heart rate (increase)
fluid administration
correct acid base imbalance
Meds to improve heart function

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19
Q

Signs of Low Cardiac Output (8)

A

pale, mottled skin
decreased LOS
Decrease UOP
Cap Refil >3 seconds
hypoglycemia
metabolic acidosis
increased serum lactate
Weak pulses

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20
Q

Signs of CHF (8)

A

flaring
tachypnea
retractions
tachycardia
pulmonary edema
cool, clammy skin
diaphoresis
fatigue

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21
Q

Management of CHF

A

Meds (diuretics)
Limit fluid administration
Resp. Support
Improve Nutrition
Temperature Control

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22
Q

Congestive Heart Failure

A

occurs when there is a defect that causes an increase in blood to the lungs

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23
Q

Cyanosis (in relation to CHD)

A

When the defect causes a decrease in blood flow to the lungs

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24
Q

Differentiating Cyanosis (Respiratory or Cardiac)

A

Respiratory - cyanosis decreases with crying, improves with O2 admin, signs of resp. distress present
Cardiac - cyanosis increases with crying, doesn’t improve with O2 admin, tachypnea but no signs of distress

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25
Hyperoxia test
Take radial arterial Blood gas (pre ductal) on room air Admin 100% FiO2 for 10 minutes Repeat ABG PaO2 <150mmHg - Cardiac PaO2 >150mmHg - Respiratory
26
Interventions for cyanotic cardiac defects
Maintain high hematocrit (to maximize o2 carrying capacity) Fluid administration admin of supplemental o2 prostaglandins to keep PDA open
27
S1
closure of mitral and tricuspid valves during ventricular systole heard at apex Loud at birth decreases in intensity over 48 hours s1 is louder with increased cardiac output
28
s2
sound of the semilunar ( aortic and pulmonary valves) closing heard best at the base of the heart
29
s3
if heard, signified rapid or increased flow across the AV valves commonly heard in premature infants with PDA
30
s4
always pathologic, heard in conditions characterized by decreased compliance or CHF
31
Ejection clicks
snappy, high frequency sounds, if present can be heard after the first heart sound, commonly heard during the first 24 hours of life and are normal at that time, but always considered abnormal after 24 hours associated conditions : aortic or pulmonic stenosis, pulmonary artery, systemic or pulmonary hypertension, truncus arteriosus, TOF
32
Systole
the period when the heart contracts and the heart chambers eject blood
33
Diastole
heart relaxes, and the chambers fill with blood
34
Grade I murmur
barely audible, audible only after careful auscultation
35
Grade 2 murmur
soft, but immediately audible
36
grade III murmur
of moderate intensity, but not associated with a thrill
37
grade IV murmur
louder (may be associated with a thrill)
38
Grade V murmur
Very loud, can be heard with the stethoscope rim barely on the chest
39
Grade VI murmur
extremely loud; can be removed with the stethoscope just slightly removed from the chest
40
systolic ejection murmurs
the most common innocent murmur usually grade I-II/VI Best heard along the mid and upper left sternal border result of turbulent flow across pulmonary valve and associated with rapidly decreasing pulmonary resistance
41
Continuous systolic or crescendo systolic murmur
usually Grade I-II/VI best heard at upper left sternal border caused by transient left-to-right flow through the DA
42
Pathologic murmurs heard in the delivery room
usually a result of stenosis or regurgitation
43
continuous murmur
occurs in 1/3 of premature neonates with a PDA
44
Hepatomegaly
occurs with increased central venous pressure. A liver more than 3cm below the sternal border indicates right-sided heart failure in a term infant
45
Blood pressure changes after birth
BP decreases in the first 3-4 hours of life because of fluid shifts into and out of the vascular space; systolic pressure reaches a minimum at 3-4 hours and plateaus at 4-6 hours
46
Pulse Pressures
difference between systolic and diastolic pressures; normal: term: 25-30 preterm: 15-25 widened pulse pressures indicate aortic runoff as in pDA
47
ASD begins as a ___ to ___ shunt
left to right
48
Eventually, in ASD, the ___ to ____ shunt causes _____ and eventually leads to \_\_\_\_
Eventually, in ASD the right to left shunt causes pressures to increase and eventually leads to pulmonary hypertension
49
ASD signs and symptoms
often asymptomatic; large ejection murmur most common types: 1) secundum (assoc with Holt-Oram) 2) Primum (AV Canal assoc) 3) sinus venosus 4) coronary sinus MOST CLOSE BY AGE 2 surgery indicated for sinus venosus, secundum ASD
50
Ventricular Septal Defects
most common congenital heart defect; shunting left to right in the ventricles
51
With large VSDs, there is overload in the ____ side of the heart resulting in:
right; pulmonary overcirculation, CHF, respiratory distress, and pulmonary edema; infants may also experience poor growth
52
VSD presentation
acyanotic with a grade II, holosystolic harsh murmur located at the lower sternal border which may not be audible until PVR decreases; Larger VSDs may result in CHF symptoms; CXR may show normal - large heart size and increased pulmonary vascular markings;
53
Arrthymias secondary to VSDs
PVCs, PACs, signs of RVH on EKG, tachycardia
54
Dextrocardia
heart is on the right side of the body
55
2 types of dextrocardia
1. levocardia 2. situs inversus
56
Levocardia
heart is formed on the right side of the body, but no change in rotation of the heart
57
Situs inversus
heart is formed on the right side of the body, heart is completely rotated to the right, aorta arches to the right
58
Ebstein's anomaly
displaced tricuspid valve down into the right ventricle creates a small right ventricle = a decrease in ventricular output, = only allows an insignificant amount of blood into the pulmonary artery creating a **ductal dependent lesion** often accompanied by an ASD
59
ebsteins anomaly
60
ebstein's anomaly presentation
cyanosis dependent on degree of right-to-left atrial shunting; holosystolic murmur varying from grade I-VI low PaO2 on ABG (\<20) CXR abnormal for cardiomegaly and diminshed pulmonary vasculature EKG positive for abnormal P waves, SVT, and Right Bundle branch block May be associated with wolfe-parkinson-white syndrome, COA, ASD, and PA
61
Ebsteins anomaly management
* o2 administration * prostaglandins to increase pulmonary blood flow and relieve hypoxemia * sildenafil (vasodilator) to decrease right ventricular afterload
62
Tetralogy of Fallot
4 related disorders: 1. pulmonary stenosis 2. VSD 3. overriding aorta 4. Right ventricular hypertrophy
63
The most common cyanotic heart defect
TOF
64
TOF presentation
ABG shows normal pH, normal Co2, pO2 depends on degree of right-to-left shunting a “boot shaped” heart on CXR CBC will show information about possible coinciding anemia or sepsis A large VSD lessens symptomatic CHF
65
TOF management
TOF maybe ductal dependent and require prostaglandins, surgical repair
66
TOF
67
Truncus Arteriosus
during embryology the outflow track fails to divide the pulmonary artery and aorta; So, there is one single trunk responsible for systemic and pulmonary circulation;
68
Truncus Arteriosus management
associated with extracardiac anomalies (PS, dysplastic valves, ect, aortic arch interruption), Associated with DiGeorge, pansystolic lower left sternal border murmur widened pulse pressures based on acidosis, murmur, CHF symptoms may be present depending on amount of pulmonary blood flow o2 may remain close to 85% until PVR decreases and pulmonary blood flow increases
69
Transposition of great arteries
deoxygenated blood returns to the Right ventricle, and circulated by the aorta, an oxygenated blood returns to the left ventricle and returns to the lungs via pulmonary artery; resulting in a parallel circuit ASD, PDA, and VSD provide opportunities for mixing blood more common in males PaO2 will be low if the septum is intact PG-E1 indicated; ductal dependent
70
TAPVR (Total anomalous Pulmonary Venous Return) types
4 types 1. Supracardiac (most common) - pulmonary blood returns oxygenated blood into the superior vena cava 2. infracardiac - pulmonary vein routes through the diaphragm and into the IVC 3. cardiac (routes pulmonary veins through coronary sinus or right atrium 1. mixed
71
TAPVR signs
“snowman sign” on CXR; presentation varies because of the different types; an obstructive TAPVR the result is venous congestion and decreased pulmonary flow; TAPVR may be asymptomatic INFRACARDIAC PRESENTS IN THE NEONATAL PERIOD
72
Tricuspid atresia
the right atrium and right ventricle are not connected due to agenesis of the tricuspid valve; resulting: right ventricular hypoplasia Pulmonary artery hypoplasia VSD Blood shunts across the ASD, goes to the lungs via left-to-right shunting via the PDA or VSD Relies on the presence of an ASD for survival PGE required (ductal dependent)
73
Prostaglandin E1 (Alprostadil) Use and Side Effects
to maintain ductus patency; larger ductus requires lower dose, small ductus requires higher dose; Major side effect: apnea other side effects: hypotension & tachycardia
74
Coarctation of the Aorta (interrupted aortic arch)
an obstruction or constriction of the aortic arch near the PDA; a ductal dependent lesion generally develops postnatally associated with Turners syndrome twice as high in males as in females more severe obstruction results in left sided heart failure or poor cardiac output
75
Signs of COA
diminshed femoral pulses; cardiomegaly on CXR and increased cardiac markings; ABG reflective of shunting
76
COA management
ductal dependent = PG E1 for infants with poor perfusion and signs of CHF continuous inotropes such as dopamine and dobutamine are suggested for cardiovascular support metabolic acidosis should be corrected;
77
Hypoplastic Left Heart
characterized by coinciding spectrum disorders: aortic valve atresia, mitral valve atresia, severe left ventricular hypoplasia, aortic hypoplasia and COA An ASD is required to mix blood and decrease pulmonary edema; Only available circulation is blood traveling from the PA through the DA to the aorta **critically ductally dependent to prevent systemic hypotension, acidosis, organ perfusion** associated with turner syndrome, trisomy 9, 13, 18, holt-oram, smith-lemli-ortiz, jacobsen
78
HLHS presentation
presents as cyanosis, tachynpea, with no murmur; perfusion and palpable pulses with diminish with ductal closure;
79
HLHS management
PG E1 to maintain patency, **avoid oxygen with HLHS because it is a vasodilator** volume expansion and inotropes help balance pulmonary circulation with system circulation; eventual surgery
80
AV Canal Defects
The endocardial cushion fails to form the center of the heart;
81
AV Canal Association
Trisomy 21
82
AV Canal presentation
Presents as desaturation and cyanosis due to right-to-left shunting until PVR decreases and flow is reversed as in CHF;
83
AV Canal management
addressing cyanosis with supplemental O2, care of CHF which may involve lasix, digoxin, and an afterload reducer; **avoid oxygen in the presence of CHF as it is a vasodilator and may increase pulmonary blood flow** surgical correction at 2-6 months
84
Aortic Stenosis
a valvular disease resulting in **left-sided outflow obstruction** if critical it results in decreased systemic output and cardiogenic shock males affected x3 than females
85
Aortic Stenosis Associations
associated with Williams syndrome
86
Aortic stenosis presentation
harsh midsystolic murmur audible with systolic ejection click; a palpable thrill at the suprasternal notch should be evident; pulse oximetry will show a gradient between the upper and lower extremities due to Right to left shunting management is PG E1 - if CHF - surgical procedure
87
PDA associations
more common in females and associated with chromosome 12;
88
PDA presentation
results from left-to-right shunting which may also decrease cardiac output and increase the workload of the left side of the heart presents with: upper Left quadrant loud machine like systolic murmur bounding pulses visible precordium widened pulse pressures worsening respiratory status due to pulmonary edema
89
CHF
r/t pressure overload (AS, COA), volume overload (L-R shunting in PDA, TA, TOF, VSD, AV canal, single ventricle, AVM), a combo of pressure and volume overload (IAA, COA with VSD, AS)
90
CHF presentation
tachypnea, sinus tach, hepatomegaly worsening CHF may include grunting, retractions; later symptoms include poor feeding and growth
91
CHF management
decrease o2 consumption (thermoneutral environment) o2 admin, fluid restriction, increased calories without volume, pharm: PG E1 if due to ductal dep., diuretics, inotropes, digoxin, afterload reducers
92
Dopamine
an endogenous catecholamine that produces a cardiovascular response to stimulate dopaminergic, alpha-adrenergic, beta-adrenergic and sertoninergic receptors to increase BP dose: 2 to 20 micrograms/kg/minute
93
Dobutamine
a cardioselective sympathomimetic amine with signficant alpha-adrenoreceptor mediated and Beta-adrenoreceptor mediated inotrope which reduces peripheral vascular resistance; works best for neonates with cardiac dysfuction and elevated pulmonary vascular resistance; Dobutamine added to Dopamine for infants with RDS improves BP
94
Epinephrine
an alpha and beta adrenergic agonist and sympathomimetic agent that increases BP and increases cerebral vascular blood flow
95
Milrinone
a phosphodiesterase 3 inhibitor which reduces afterload in neonates with CHD or with low cardiac output; shown to improve oxygenation of infants with PPHN
96
vasopressin
a synthetic antidiuretic hormone that impacts the cardiovascular system by vasoconstriction (works similar to dopamine)
97
Premature Atrial Contractions
early depolarization of the atria but are not from the sinus node; True PACs are followed by a QRS complex, Bigeminy refers to PACS every other beat generally asymptomatic
98
Atrial flutter
a type of reentry tachycardia via the atrial myocardium at the tricuspid valve; rate usually 300 to 600 bpm,
99
Atrial Fibulation
A Fib rare in neonates; a continuous dysrhythmia; associated with Ebstein anomaly, and wolfe-parkinson-white syndrome
100
Premature Ventricular Contraction
an early beat due to a spontaneous ventricular depolarization of the ventricles; if baby is asymptomatic, neg family history, and PVCs disapear with higher heart rates - considered benign
101
Ventricular Tachycardia
originates below the bundle of his; impacts hemodynamics and cardiac function may require intervention
102
complete AV heart block (3rd degree)
indicates a disfunctional AV node; making the atria and ventricles independent of one another associated with maternal SLE
103
Average BP for term infant (systolic, diastolic, MAP)
56-77 systolic 33-50 diastolic MAP 42-60
104
Fetal circulation: deoxygenated blood leaves the fetus and returns to the placenta via the \_\_\_\_\_\_\_\_\_\_\_.
umbilical arteries
105
Fetal circulation: Freshly oxygenated blood returns from the placenta to the fetus via __________ going into through the fetal ________ and then to the \_\_\_\_\_\_\_\_\_.
the umbilical vein fetal liver right atrium of the heart
106
Fetal circulation: From the right atrium, the blood shunts through the _______ into the ___________ and then is pumped into the ___________ and out of the ___________ to the rest of the body (brain first).
**PFO** into the **left atrium** and then **left ventricle** and out to the **aorta**
107
Fetal Heart pressures are higher on the _______ because \_\_\_\_\_\_\_\_
Right because the lung is collapsed, so pulmonary vascular resistance is very high!
108
After birth, pressures on the _____ side of the heart is higher because PVR decreases when \_\_\_\_\_\_\_\_\_.
Pressures on the Left side of the heart is higher because PVR decreases when the lung inflates.
109
D-transposition vs L-transposition
D-transposition (most common) occurs when the right ventricle emptys into the aorta which takes deoxygenated blood to the body and the left ventricle sends already oxygenated blood back to the lungs. Only opportunity for mixing are PDA, ASD, VSD L-transposition - not as common, but occurs when the the Left and right ventricles are swapped. It ends up being less symptomatic because the vessels empty to the right places but are side by side instead of the pulmonary artery looping through the aorta like normal.