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NNP Board Exam Review > Cardiac > Flashcards

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
Q

Hyperoxia test

A

Take radial arterial Blood gas (pre ductal) on room air
Admin 100% FiO2 for 10 minutes
Repeat ABG
PaO2 <150mmHg - Cardiac
PaO2 >150mmHg - Respiratory

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26
Q

Interventions for cyanotic cardiac defects

A

Maintain high hematocrit (to maximize o2 carrying capacity)
Fluid administration
admin of supplemental o2
prostaglandins to keep PDA open

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27
Q

S1

A

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

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28
Q

s2

A

sound of the semilunar ( aortic and pulmonary valves) closing
heard best at the base of the heart

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29
Q

s3

A

if heard, signified rapid or increased flow across the AV valves
commonly heard in premature infants with PDA

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30
Q

s4

A

always pathologic, heard in conditions characterized by decreased compliance or CHF

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31
Q

Ejection clicks

A

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

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32
Q

Systole

A

the period when the heart contracts and the heart chambers eject blood

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33
Q

Diastole

A

heart relaxes, and the chambers fill with blood

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34
Q

Grade I murmur

A

barely audible, audible only after careful auscultation

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35
Q

Grade 2 murmur

A

soft, but immediately audible

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36
Q

grade III murmur

A

of moderate intensity, but not associated with a thrill

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37
Q

grade IV murmur

A

louder (may be associated with a thrill)

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38
Q

Grade V murmur

A

Very loud, can be heard with the stethoscope rim barely on the chest

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39
Q

Grade VI murmur

A

extremely loud; can be removed with the stethoscope just slightly removed from the chest

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40
Q

systolic ejection murmurs

A

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

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41
Q

Continuous systolic or crescendo systolic murmur

A

usually Grade I-II/VI
best heard at upper left sternal border
caused by transient left-to-right flow through the DA

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42
Q

Pathologic murmurs heard in the delivery room

A

usually a result of stenosis or regurgitation

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43
Q

continuous murmur

A

occurs in 1/3 of premature neonates with a PDA

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44
Q

Hepatomegaly

A

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
Q

Blood pressure changes after birth

A

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
Q

Pulse Pressures

A

difference between systolic and diastolic pressures;
normal: term: 25-30
preterm: 15-25
widened pulse pressures indicate aortic runoff as in pDA

47
Q

ASD begins as a ___ to ___ shunt

A

left to right

48
Q

Eventually, in ASD, the ___ to ____ shunt causes _____ and eventually leads to ____

A

Eventually, in ASD the right to left shunt causes pressures to increase and eventually leads to pulmonary hypertension

49
Q

ASD signs and symptoms

A

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
Q

Ventricular Septal Defects

A

most common congenital heart defect; shunting left to right in the ventricles

51
Q

With large VSDs, there is overload in the ____ side of the heart resulting in:

A

right; pulmonary overcirculation, CHF, respiratory distress, and pulmonary edema; infants may also experience poor growth

52
Q

VSD presentation

A

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
Q

Arrthymias secondary to VSDs

A

PVCs, PACs, signs of RVH on EKG, tachycardia

54
Q

Dextrocardia

A

heart is on the right side of the body

55
Q

2 types of dextrocardia

A
  1. levocardia
  2. situs inversus
56
Q

Levocardia

A

heart is formed on the right side of the body, but no change in rotation of the heart

57
Q

Situs inversus

A

heart is formed on the right side of the body, heart is completely rotated to the right, aorta arches to the right

58
Q

Ebstein’s anomaly

A

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
Q
A

ebsteins anomaly

60
Q

ebstein’s anomaly presentation

A

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
Q

Ebsteins anomaly management

A
  • o2 administration
  • prostaglandins to increase pulmonary blood flow and relieve hypoxemia
    • sildenafil (vasodilator) to decrease right ventricular afterload
62
Q

Tetralogy of Fallot

A

4 related disorders:

  1. pulmonary stenosis
  2. VSD
  3. overriding aorta
  4. Right ventricular hypertrophy
63
Q

The most common cyanotic heart defect

A

TOF

64
Q

TOF presentation

A

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
Q

TOF management

A

TOF maybe ductal dependent and require prostaglandins, surgical repair

66
Q
A

TOF

67
Q

Truncus Arteriosus

A

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
Q

Truncus Arteriosus management

A

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
Q

Transposition of great arteries

A

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
Q

TAPVR (Total anomalous Pulmonary Venous Return) types

A

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
Q

TAPVR signs

A

“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
Q

Tricuspid atresia

A

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
Q

Prostaglandin E1 (Alprostadil) Use and Side Effects

A

to maintain ductus patency;

larger ductus requires lower dose, small ductus requires higher dose;

Major side effect: apnea

other side effects: hypotension & tachycardia

74
Q

Coarctation of the Aorta (interrupted aortic arch)

A

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
Q

Signs of COA

A

diminshed femoral pulses; cardiomegaly on CXR and increased cardiac markings;

ABG reflective of shunting

76
Q

COA management

A

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
Q

Hypoplastic Left Heart

A

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
Q

HLHS presentation

A

presents as cyanosis, tachynpea, with no murmur; perfusion and palpable pulses with diminish with ductal closure;

79
Q

HLHS management

A

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
Q

AV Canal Defects

A

The endocardial cushion fails to form the center of the heart;

81
Q

AV Canal Association

A

Trisomy 21

82
Q

AV Canal presentation

A

Presents as desaturation and cyanosis due to right-to-left shunting until PVR decreases and flow is reversed as in CHF;

83
Q

AV Canal management

A

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
Q

Aortic Stenosis

A

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
Q

Aortic Stenosis Associations

A

associated with Williams syndrome

86
Q

Aortic stenosis presentation

A

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
Q

PDA associations

A

more common in females and associated with chromosome 12;

88
Q

PDA presentation

A

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
Q

CHF

A

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
Q

CHF presentation

A

tachypnea, sinus tach, hepatomegaly

worsening CHF may include grunting, retractions;

later symptoms include poor feeding and growth

91
Q

CHF management

A

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
Q

Dopamine

A

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
Q

Dobutamine

A

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
Q

Epinephrine

A

an alpha and beta adrenergic agonist and sympathomimetic agent that increases BP and increases cerebral vascular blood flow

95
Q

Milrinone

A

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
Q

vasopressin

A

a synthetic antidiuretic hormone that impacts the cardiovascular system by vasoconstriction (works similar to dopamine)

97
Q

Premature Atrial Contractions

A

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
Q

Atrial flutter

A

a type of reentry tachycardia via the atrial myocardium at the tricuspid valve;

rate usually 300 to 600 bpm,

99
Q

Atrial Fibulation

A

A Fib rare in neonates; a continuous dysrhythmia; associated with Ebstein anomaly, and wolfe-parkinson-white syndrome

100
Q

Premature Ventricular Contraction

A

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
Q

Ventricular Tachycardia

A

originates below the bundle of his; impacts hemodynamics and cardiac function may require intervention

102
Q

complete AV heart block (3rd degree)

A

indicates a disfunctional AV node; making the atria and ventricles independent of one another

associated with maternal SLE

103
Q

Average BP for term infant (systolic, diastolic, MAP)

A

56-77 systolic

33-50 diastolic

MAP 42-60

104
Q

Fetal circulation: deoxygenated blood leaves the fetus and returns to the placenta via the ___________.

A

umbilical arteries

105
Q

Fetal circulation: Freshly oxygenated blood returns from the placenta to the fetus via __________ going into through the fetal ________ and then to the _________.

A

the umbilical vein

fetal liver

right atrium of the heart

106
Q

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).

A

PFO into the left atrium and then left ventricle and out to the aorta

107
Q

Fetal Heart pressures are higher on the _______ because ________

A

Right because the lung is collapsed, so pulmonary vascular resistance is very high!

108
Q

After birth, pressures on the _____ side of the heart is higher because PVR decreases when _________.

A

Pressures on the Left side of the heart is higher because PVR decreases when the lung inflates.

109
Q

D-transposition vs L-transposition

A

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.

NNP Board Exam Review (19 decks)

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