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Cardiology > NCC Content > Flashcards

NCC Content Flashcards

1
Q

When can the fetal heartbeat be heard?

A

At 6 weeks

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2
Q

describe the four stages of cardiac formation

A
  1. Elongates & twists to right - if it doesn’t twist correctly, result can be dextrocardia
  2. Separates the atria and ventricles
  3. Formation of valves: mitral and tricuspid
  4. Great vessel formation: aorta, pulmonary arteries and vein
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3
Q

What does S1 represent?

A

Closing of the tricuspid and mitral valves at the end of atrial systole (aka the start of systole)

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4
Q

Where is S1 best auscultated?

A

Fifth intercostal space at the left midclavicular line or LLSB

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5
Q

What does S2 represent?

A

Closure of the aortic and pulmonic valves at the end of ventricular systole (aka start of diastole)
should be split until PVR is significantly lower!!

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6
Q

Where is S2 best auscultated?

A

At the ULSB

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7
Q

What are the semilunar valves?

A

Aortic valve

Pulmonary valve

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8
Q

Which side of the heart is dominant in fetal circulation?

A

The right heart is dominant - pumps 2/3 of combined ventricular output

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9
Q

What is one important function of the foramen ovale?

A

Allows oxygenated blood to bypass right ventricle and go to left side of heart (atrium) to eventually be delivered to the brain

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10
Q

What factors contribute to the closing of the PDA?

A

Oxygen, prostaglandins

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11
Q

What is cardiac output?

A

The volume of blood ejected by the heart in one minute

CO= stroke volume x heart rate

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12
Q

When do the PDA and the PFO usually close?

A 
PDA = 15-48 hrs of life
PFO = functionally closes soon after birth, structurally not closed until about 1 month of age
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13
Q

What is stroke volume?

A

The difference between the ventricular end diastolic volume and the end systolic volume

It is affected by preload, contractility and afterload

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14
Q

What is preload?

A

Volume of blood entering the ventricles

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15
Q

What is afterload?

A

The resistance that the left ventricle must overcome to circulate blood

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16
Q

What is contractility (inotropy)?

A

The speed of ventricular contraction

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17
Q

What factors affect contractility?

A

Catecholamines cause an increase

Acidosis/hypoxia cause a decrease

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18
Q

What does blood pressure represent?

A 
Systole = pressure on the walls of the vessels at the end of each heart contraction
Diastole = pressure on the walls of the vessels immediately before each contraction
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19
Q

Explain a widened pulse pressure with a PDA

A

Blood runs off into the pulmonary artery during diastole

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20
Q

Explain a narrow pulse pressure

A

Can indicate pericardial tamponade, intravascular depletion, or an ecmo pt

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21
Q

What is the definition of shock?

A

A state of inadequate circulatory blood volume

-Results in decreased perfusion and oxygenation to tissues - lactic acidosis - heart failure

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22
Q

3 types of shock

A

Hypovolemic: loss of volume
Cardiogenic: heart failure d/t tamponade, tension pneumo, CHD, etc.
Distributive: sepsis, toxins

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23
Q

Compensated vs. Uncompensated shock

A

Compensated: BP still normal; want to treat during this stage if possible
Uncompensated: hypotensive; occurs cause is untreated, much harder to reverse at this point

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24
Q

Where is the PMI best palpated?

A

Along lower left sternal border in the 5th intercostal space

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25
Q

What does S3 represent?

A

Extra sound that may be normal in the newborn related to ventricular filling

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26
Q

What does the S4 represent?

A

Rare, myocardial disease

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27
Q

Characteristics of a benign murmur.

A
  • FT infant may have murmur at 24-48 hrs d/t PDA closing

- systolic murmur

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28
Q

Characteristics of a pathologic murmur.

A
  • continuous?

- diastolic

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29
Q

VSD murmur

A

Harsh pansystolic LLSB

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30
Q

PDA murmur

A

Continuous machinery

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31
Q

Truncus Arteriosus murmur

A

Harsh systolic with single S2

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32
Q

Valvular stenosis murmur

A

Loud ejection click

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33
Q

PPS murmur

Persistent pulmonic stenosis?

A

Radiates to axillae and back

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34
Q

EKG changes with hyperkalemia

A

Peaked T waves

Widened QRS

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35
Q

EKG changes with hypokalemia

A

Prominent U waves

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36
Q

EKG changes with hypercalcemia

A

Short QT interval

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37
Q

EKG changes with hypocalcemia

A

Prolonged QT interval

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38
Q

SVT is caused by….

A

Dual firing at the AV node

By definition, HR sustained > 220 bpm

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39
Q

SVT treatment

A
  1. Ice/Vagal maneuver
  2. Adenosine (digoxin or propranolol also options)
  3. Cardioversion
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40
Q

What is the biggest risk factor for CHD?

A

Family history of CHD

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41
Q

What % of infants with chromosomal abnormalities have CHD?

A

30%

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42
Q

When does the heart begin and finish developing?

A

Starts between 3rd and 7th week of gestation
Completed at 10 weeks
1st organ to function in utero

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43
Q

What is the most common CHD?

A

VSD (20-25%)

44
Q

What are the acyanotic heart defects?

A
  • ASD
  • VSD
  • PDA
  • AV canal
45
Q

Characteristics of acyanotic heart defects.

A
  • L to R shunt
  • cardiomegaly
  • increased pulmonary vascular markings
  • CHF when PVR drops (6-8 weeks of life)
46
Q

Characteristics of symptomatic PDA

A
  • hypotension d/t systemic steal
  • oliguria
  • respiratory distress
47
Q

PDA management in preterm infant

A

Conservative: fluid restriction and diuretics

Hemodynamically-significant PDA: ibuprofen/indomethacin, surgical ligation

48
Q

PDA management in term infant

A

Typically let it close on its own

If still open later, can having coiling procedure at 3 months

49
Q

Characteristics of ASD

A

Oxygenated blood from left atrium to right atrium, back to right ventricle and into the lungs

  • rarely get CHF or show symptoms
  • systolic ejection murmur
  • increased volume and work of RV leads to RV hypertrophy
50
Q

Management of ASD

A

75% resolve within first year of life
-treat CHF if symptomatic
Intractable CHF: surgical repair is necessary

51
Q

Characteristics of VSD

A

L-to-R shunting via ventricular septum causing increased pulmonary blood flow

  • harsh pansystolic murmur
  • left ventricle can become hypertrophied from overworking
52
Q

Management of VSD

A

Small or perimembranous: usually resolves by itself
Large or muscular: causes CHF in 6 to 8 weeks, needs repair

Mild VSD: fluid restriction, diuretics, digoxin
Moderate to severe VSD: pulmonary banding, suturing or patching of defect

53
Q

Characteristics of AV canal

A

-most common in Trisomy 21
Complete = 1 valve
Partial = mitral regurgitation?

54
Q

Management of AV canal

A

Treat CHF

  • PA banding
  • ASD, VSD closure and reconstruction of valve
55
Q

symptoms of CHF

A

(When the heart is no longer able to pump adequate amounts of blood to meet the needs of the body)

  • tachycardia, tachypnea
  • sudden weight gain or poor weight gain
  • poor feeding
  • hepatomegaly
  • arrhythmias
  • cardiomegaly
56
Q

What is Eisenmenger syndrome?

A

Occurs typically when an undiagnosed CHD with a left to right shunt causes enough significant damage to the lung tissue and heart that the shunt reverses and becomes right to left thus making the patient cyanotic

57
Q

Name the obstructive lesions.

A
  • aortic stenosis
  • pulmonary stenosis
  • coarctation of the aorta
58
Q

Characteristics of pulmonary stenosis.

A
  • obstruction of blood flow to lungs
  • may be valvular (90%), subvalvular or supravalvular
  • usually associated with large VSD or ASD which facilitates mixing of blood
  • need PDA to then get blood to the lungs
  • harsh systolic ejection murmur
59
Q

Pulmonary stenosis on x-Ray

A

Decreased pulmonary markings

Usually normal heart size

60
Q

Characteristics of aortic stenosis

A
  • obstruction of blood flow to the body
  • valvular, supravalvular (associated with William’s syndrome) or subvalvular
  • peripheral pulses are weak and threads
  • narrow pulse pressure in severe AS
61
Q

Is PS or AS more concerning?

A

AS - because there is limited blood getting to the body

62
Q

Characteristics of COA

A
  • narrowing in upper part of aortic arch (most commonly at the point where the ductus arteriosus joins the aorta)
  • strong pulses in upper extremities compared to lower extremities
  • Severe cases: LV pressure overload
  • Loud S3 gallop usually present
  • Mild=headaches; moderate=CHF; severe=shock
63
Q

Management of COA

A
  • treat CHF (digoxin and lasix)
  • prostaglandins
  • surgery: anastomosis, grafting, balloon angioplasty
64
Q

What kind of shunt has to exist to cause cyanosis?

A

Right to left

65
Q

Name the cyanotic heart lesions.

A 
TGA
TOF
Truncus
Tricuspid atresia
TAPVR

Ebstein’s anomaly
Single ventricle
Pulmonary atresia

66
Q

Characteristics of TGA

A
  • survival dependent on some communication between two circuits (VSD, ASD, PDA)
  • amount of blood flows into and out of the pulmonary circulation must be equal (important with all cyanotic mixing lesions)
  • patient will have hypoxia and cyanosis
67
Q

What is the most common cyanotic heart lesion in the newborn period?

A

TGA

68
Q

TGA on x-Ray

A

Egg on string

69
Q

TGA management

A
  • prostaglandin dependent: PDA is needed for systemic perfusion
  • balloon septostomy
70
Q

What is the most common cyanotic heart disease in general?

A

TOF

71
Q

Name the 4 abnormalities in TOF

A
  1. VSD
  2. Right ventricular hypertrophy
  3. Right ventricular outflow obstruction
  4. Overriding aorta (aortic override of the ventricular septum)
72
Q

Is TOF ductal dependent?

A

Not usually - only if pulmonary stenosis is significant or if pulmonary atresia is present

73
Q

Blue Tet characteristics

A

-amount of cyanosis depends on how much deoxygenated blood is shunting right to left through VSD (less blood to lungs = increased cyanosis) which is determined by degree of pulmonary stenosis

74
Q

Pink Tet characteristics

A
  • oxygenated blood shunts left to right through VSD which can result in excessive pulmonary blood flow
  • pink tets have mild pulmonary stenosis
75
Q

TOF on x-Ray

A
  • boot shaped heart (represents concave main PA segment with upturned apex secondary to right ventricular hypertrophy
  • variable pulmonary vascular markings r/t degree of pulmonary stenosis
76
Q

Management of TOF

A
  • treat CHF
  • provide O2 to relax pulmonary bed
  • if O2 sats remain
77
Q

TOF sat goal

A

75-85%

78
Q

TOF murmur

A

Systolic ejection murmur

79
Q

TAPVR characteristics

A

-pulmonary veins drain oxygenated blood directly or indirectly into the right atrium instead of the left atrium

80
Q

TAPVR on xray

A

snowman

81
Q

What is the Blalock-Taussig shunt?

A

subclavian is connected to pulmonary artery

-fixes TOF

82
Q

What shunt has to exist in TAPVR?

A

some shunt needs to exist to move blood from the R to the L to supply the body
-usually mixing at the ASD level

83
Q

TAPVR treatment

A
  • manage CHF
  • surgical correction= pulmonary veins are connected to the left atrium and ASD is closed (done within first few weeks of life)
84
Q

Truncus arteriosus characteristics

A
  • only a single arterial trunk leaves the heart; it supplies pulmonary, systemic and coronary circulation
  • degree of cyanosis depends on amount of blood going to the lungs
85
Q

What is always present with truncus?

A

large VSD (almost serves as single ventricle)

86
Q

What genetic disorder is associated with truncus?

A

DiGeorge syndrome

87
Q

Truncus arteriosus management

A

-Rastelli operation= attempts to separate the common artery; conduit is placed from the right ventricle to the pulmonary artery, VSD is closed

88
Q

Tricuspid atresia characteristics

A
  • tricuspid valve is absent

- RV and PA are hypoplastic with decreased pulm blood flow due to underuse

89
Q

What opening is necessary for survival in tricuspid atresia?

A

-ASD, VSD or PDA necessary to get blood to the lungs

90
Q

Surgical correction for tricuspid atresia

A
  1. B-T shunt
  2. Glenn (connect SVC to pulmonary artery)
  3. Fontan (connect IVC to pulmonary artery)
    - all blood that should be going to right side of heart is going to lung after these procedures
91
Q

pulmonary atresia characteristics

A

no blood flow from right ventricle to pulmonary circulation

92
Q

What shunt is required in pulmonary atresia to survive?

A
  • communication at atrial level (PFO/ASD)

- PDA must be present to get blood to the lungs!!

93
Q

Epstein’s Anomaly characteristics

A
  • abnormal development of tricuspid valve; hypoplastic right ventricle d/t tricuspid valve placement, but RV is also overworked
  • sits deep in right ventricle and is dysplastic, allowing blood to regurgitate back to right atrium
  • results in decreased blood flow to the lungs and cyanosis
94
Q

Epstein’s anomaly on xray

A

-extremely large heart (“wall to wall”); considered diagnostic for EA

95
Q

Epstein’s anomaly management

A
  • prostins to get blood to lungs
  • treat CHF
  • pulmonary artery banding
  • surgery?
96
Q

HLH characteristics

A
  • *left side of the heart is basically nonfunctional**
  • hypoplastic left ventricle
  • aortic valve atresia or stenosis
  • mitral valve atresia or stenosis
  • aortic arch is hypoplastic
97
Q

What shunts are necessary for survival with HLH?

A
  • must have PFO/ASD to allow LA to receive oxygenated blood

- must have PDA to ensure systemic circulation

98
Q

HLH presentation

A
  • cyanosis
  • signs/symptoms of CHF
  • poor perfusion:pulmonary over-circulation
  • severe metabolic acidosis
99
Q

HLH medical management

A
  1. prostins
  2. must balance circuit of pulmonary and systemic circulation
  3. keeps sats 75-85%
  4. avoid excessive pulmonary vasodilation (because that means not enough blood is going systemically)
100
Q

HLH surgical management

A
  • norwood: rebuild tiny ascending aorta
  • stage II: glenn
  • stage III: fontan
  • cardiac transplant
101
Q

What are is the “Rule of 4’s” in cardiac patients?

A
  • pH= should be 7.40 (acidosis=lactic acid build up=muscle fatigue=bad cardiac contractility and function)
  • CO2= in the 40s
  • HCT= at least 40
  • K= level in the 4 range (Na/K pump regulates influx of electrical impulses to regulate heart muscle contraction)
102
Q

Maternal Diabetes =

A
  • hypertrophic cardiomyopathy
  • TGA
  • VSD
103
Q

Maternal Lupus =

A

heart block

104
Q

Maternal Alcohol Abuse =

A

TOF

105
Q

Maternal Rubella =

A
  • PDA

- PPS

106
Q

Down syndrome =

A

-AV canal
-VSD
(40% have CHD)

107
Q

Turner syndrome =

A

-coarctation of the aorta

Cardiology (1 decks)

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