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NUR 131 > TLO 2.2 Cardiovascular Child > Flashcards

TLO 2.2 Cardiovascular Child Flashcards

1
Q

Fetal Circulation

A

Ductus Venosis

  • smaller of the 2 branches of the umbilical vein as it empties into the inferior vena cava
  • allows blood to bypass the liver

Foramen Ovale

  • opening between the atria and the fetal heart that closes after birth
  • shunt between R and L atria

Ductus Arteriosus

  • connection between main pulmonary artery and the aorta in the fetus
  • allows blood to bypass lungs
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2
Q

Fetal circulation: placenta?

A

Gas exchange takes place in the placenta

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3
Q

Fetal Circulation

Oxygenated blood travels?

A

Umbilical Vein:
brings oxygenated blood to fetus
small amount is routed directly to liver

Ductus Venosus bypasses liver

Inferior Vena Cava

R Atrium:
Foramen Ovale (closes shortly after birth)
small opening in septum that shunts blood from right atrium to left atrium

Left atrium

Left ventricle

Aorta: circulates to brain and coronary arteries

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4
Q

Diagnostic test: BLOOD TESTS?

A

CBC

  • Hgb (measures O2 carrying capacity of RBC)
  • Hct (% of blood volume that’s RBC’s)
  • ESR (helpful in diagnosing inflammatory conditions)

Blood Culture

Arterial Blood Gasses (ABG’s): analyze oxygenation, ventilation and acid base balance

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5
Q

Fetal circulation

BLOOD RETURNING FROM UPPER BODY

A

Blood returning from upper body:
Right atrium- tricuspid valve

Right ventricle

Pulmonary arteries- small amount (8%) travels to lungs (not functioning). Most goes thru the Ductus Arteriosus (bypasses the lungs)

descending Aorta (perfuses organs and tissues of lower body)

2 umbilical arteries

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6
Q

Diagnostic Tests

ELECTROCARDIOGRAM (EKG)

A

Records electrical conduction of the heart

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7
Q

Diagnostic Tests

XRAY

A

Looks at lungs, heart, chest, diaphragm, ribs.

Posterior, anterior, lateral

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8
Q

Diagnostic Tests

ULTRASOUND

A

Sonogram or echocardiogram
Noninvasive procedure that visualizes and records information concerning cardiac structures including the position, size and movement of valves

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9
Q

Diagnostic Tests

CARDIAC CATHETERIZATION

A

Invasive test that detects abnormalities in the heart chambers, valves, and blood vessels

Types: diagnostic, interventional, electrophysiology

Measures pressures, oxygen levels in heart chambers
Visualizes heart structures and blood flow patterns
Radiopaque catheter is the visualizing aide used

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10
Q

Diagnostic Tests

MAGNETIC RESONANCE IMAGING (MRI)

A

Noninvasive, computer based procedure that provides information r/t anatomy, congenital defects, blood clots and infections, looks at soft tissues

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11
Q

Congenital Heart Defects
CONTRIBUTING FACTORS
S/S

A

Contributing factors:
maternal infections, alcoholism, drug use, dietary deficiencies, IDDM (insulin dependent diabetes mellites) and >40 years old

S/S:
dysrhythmias, cyanosis, pallor, heart murmurs, decreased BP, frequent respiratory infections and fatigue

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12
Q

Congenital Heart Defects

CLASSIFICATIONS

A

Anatomic abnormality

Hemodynamic abnormality

Tissue oxygenation abnormality

  • acyanotic (normal oxygenation)
  • cyanotic
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13
Q

Congenital Heart Defects

ACYANOTIC

A

Right to left shunting lesions that INCREASE pulmonary blood flow

  • patent ductus arteriosus***
  • arterial septal defect
  • ventricular septal defect
  • atrioventricular septal defect

Obstructive or stenotic or lesions that DECREASE cardiac outflow

  • pulmonary stenosis
  • aortic stenosis
  • coarctation of aorta (narrowing of aorta)***

***main ones on exam

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14
Q

Post cardiac catheterization complications?

A 
Acute hemorrhage at entry site
Low grade fever
Vomiting
Loss of pulse in catheterized extremity
Transient dysrhythmias
Rare: stroke, seizures, tamponade, death
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15
Q

Congenital Heart Defects

CYANOTIC

A

DECREASED pulmonary blood flow

  • tetralogy of fallot***
  • tricuspid atresia
  • pulmonary atresia

INCREASED pulmonary blood flow
-truncus arteriosus

MIXED lesions
-transposition of great vessels with VSD

***main one on exam

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16
Q

Congenital Heart Defect symptom?

A 
Increased pulse
Increased respirations
Retarded growth
Fatigue
URI
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17
Q

Acyanotic congenital heart defects examples (left to right shunt)

A

Right to left shunt:
Patent ductus arteriosus**
Arterial septal defect
Ventricular septal defect

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18
Q

Acyanotic congenital heart defects

S/S, RISKS

A 
Increase fatigue
Heart murmurs
Increase risk of endocarditis
CHF
Growth retardation
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19
Q

Patent Ductus Arteriosus (acyanotic)

What is it?

A

Ductus arteriosus fails to close at birth causing oxygenated blood to be shunted into pulmonary circulation.
Results in increased pulmonary blood flow

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20
Q

Patent Ductus arteriosus (acyanotic)

S/S

A 
Continued loud murmur
Pallor
Widened pulse pressure
Feeding problems
Resp infections
Cardiomegaly
CHF
Pulmonary edema
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21
Q

Patent Ductus Arteriosus (acyanotic)

TREATMENT

A 
Treat CHF (right, left, complete)
Right: edema, enlarged liver
Left: pulmonary edema
Complete: polycythemia (blood cancer, thickening of cell, slowing flow)
-CVA (heart attack)
Mediations:
Digoxin
Diuretics
O2
Pain meds
Rest

Surgical repair usually done by 1 yr

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22
Q

Coarctation of the Aorta (acyanotic)

what is it?

A

Narrowed aorta obstructs the outflow from left ventricle causing increased left ventricular pressure.
Pulmonary blood flow is normal

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23
Q

Coarctation of the Aorta (acyanotic)

S/S

A 
Decreased circulation to lower extremities (low B/P in lower extremities)
Growth retardation
Fatigues
HA
Epistaxis (nose bleed)
Leg cramps
Cardiomegaly
CHF
Metabolic acidosis
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24
Q

Coarctation of the Aorta (acyanotic)

TREATMENT

A

Digoxin
Diuretics
Prostaglandin E: dilates narrowed vessels
Balloon dilation
Surgical repair usually done at 2-4 years old

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25
Q

Cardiovascular disorders

Two major Groups

A

Congenital heart disease

Acquired heart disorders

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26
Q

Congenital Heart Disease defined with examples

A

Anatomic abnormalities present at birth that result in abnormal cardiac function

Clinical consequences: 2 broad categories

  • congestive heart failure
  • hypoxemia
  • genetic-trisomy 21 (Down Syndrome) incidence= 50%
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27
Q

Acquired Heart Disorders define with examples

A

Disease processes or abnormalities that occur after birth

  • infection (Rheumatic fever)
  • autoimmune responses (Kawasaki disease)
  • environmental factors
  • familial tendencies
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28
Q

Tetralogy of Fallot (cyanotic)

what is it?

A

Right to Left shunting of blood causes decreased pulmonary blood flow and decreased oxygen in systemic circulation

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29
Q

Tetralogy of Fallot

4 defects?

A

Ventricular Septal Defect
Pulmonary Stenosis
Overriding of the Aorta
Right ventricular Hypertrophy

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30
Q

Assessment of Child (family history)

A

Parent of sibling has heart defect

Frequent fetal loss

SIDS

Sudden death in adults

Hereditary conditions

  • Marfan syndrome: pectus excavatum, arachnodactyly, dilation of aorta
  • Cardiomyopathy: hypertrophic cardiomyopathy
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31
Q

Physical assessment of child: General appearance

A 
General appearance
Weight (gain or loss)
Activity level
Skin color
Effort of breathing
Audible breath sounds
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32
Q

Physical assessment: suspected cardiac disease inspection

A

Nutritional state: failure to thrive, poor weight gain

Color: cyanosis (common with CHD), pallor, poor perfusion

Chest deformities: enlarged heart can cause deformity

Pulsations: visible pulsations of the neck veins

Respiratory excursion: ease or difficulty of resp (brady, tachy, dyspnea)

Clubbing of fingers: associated with cyanosis and chronic hypoxia

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33
Q

Heart Murmurs: causes?

A 
S.P.A.M.S.
Stenosis of a valve
Partial obstruction
Aneurysms
Mitral regurgitation
Septal defect
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34
Q

Heart Murmurs: types?

A

Systolic:

  • crescendo (increased during systole)
  • decrescendo (decreased during systole)

Diastolic:
-indicates pathologic disease

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35
Q

Physical assessment: palpation and percussion

A

Chest: PMI (point of maximum impulse), thrills, heart size
-a thrill is a vibration like movement of the chest wall caused by turbulent blood flow over a heart valve. It is palpable murmur

Abdomen: hepatomegaly or splenomegaly present

Peripheral pulses: rate, regularity, amplitude

Heart rate/rhythm: tachy, brady, regular/irregular

36
Q

Character of heart sounds: murmurs

A

Patent ductus arteriosus (PDA): continuous murmur machinery like sound

Coarctation of the aorta-systolic murmur accompanied by thrill

Tetralogy of Fallot: harsh systolic murmur

Atrial septal defect (ASD) systolic and diastolic murmur

37
Q

Tetralogy of Fallot (cyanotic)

S/S

A 
S/S:
Cyanosis (that worsens with age)
Squatting posture
Hypercyanotic Episodes (tet spells), preceded by crying, feeding and defecation, can lead to hypoxia/brain damage
Clubbing finger/toes
Squatting posture
Exertional dyspnea
Failure to thrive
Heart murmur
Increased RBC and Hct
38
Q

Patent Ductus Arteriosus

What is it?

A

Failure of the fetal ductus arteriosus to close within the first weeks of life
L to R shunt:
Blood flows from aorta to pulmonary artery
Results in increased workload on the Lt side of the heart
Increased pulmonary vascular congestions
Potential increased Rt ventricular pressure and hypertrophy

39
Q

Cyanotic Heart Defects Mnemonic

4-T’s

A

Tetralogy of Fallot** focus on this one

Truncus Arteriosus
Transposition of the Great vessels
Tricuspid Atresia

40
Q

Tetralogy Fallot
RISK
SURGICAL TREATMENT

A

Episodes of acute cyanosis and hypoxia
Anoxic after crying/feeding

Risk:
Emboli
Seizures
LOC
Sudden death following anoxic spell (without O2)

Surgical:
Palliative shunt (surgery contraindicated)
Preferred Modified Blalock Taussing shunt surgery
Complete repair 1st year of life

41
Q

Congestive Heart Failure diagnostic tests

A

Chest x-ray
EKG
Echocardiogram

42
Q

Congestive heart failure medical treatment

A

Digitalis glycoside (digoxin, Lanoxin): increase cardia output.

  • decrease heart size
  • decrease venous pressure
  • relief of edema
Check apical pulse for 1 minute
When do you hold these medications? HR?
Infants: <100
Children: <70
Adults: <60

Monitor for Digoxin(0.5-2) toxicity and hyperkalemia

43
Q

What is congestive heart failure?

A

Inability of the heart to pump and adequate amount of blood to the meet systemic circulation needs

44
Q

Congestive heart failure in children

WHAT ARE THE CAUSES?

A 
Secondary to structural abnormalities
Septal defects
Myocardial failure
Ventricle impaired
Excessive demands on the heart
-sepsis
-severe anemia
45
Q

Left sided congestive heart failure

A

Blood back up to the lungs=
Crackles in the lungs
Pulmonary congestion

46
Q

Right sided congestive heart failure

A 
Blood back up to the liver=
Hepatomegaly
Splenomegaly
Neck vein distention
Lower extremity edema
47
Q

Treating congestive heart failure mnemonic

A 
U.N.L.O.A.D.   F.A.S.T
Upright position
Nitrates (low dose, nitroglycerine)
Oxygen
Aminophylline (not used a lot anymore)
Digoxin (helps cardiac output)
Fluids (decrease)
Afterload (decrease)
Sodium restriction
Test (Dig levels, ABG's, K levels)
48
Q

Congestive heart failure ACE inhibitors med and what do they do?

A

Lisinopril
Captopril
Enalapril

Vasodilation occurs: decreased pulmonary and systemic vascular resistance
Decreased BP and reduction in afterload

49
Q

congestive heart failure

BETA BLOCKERS

A

Carvedilol and Coreg

  • decrease HR(<55-60) and BP(<90-100)
  • vasodilation
  • *must check apical pulse for 1 min and B/P prior
50
Q

congestive heart failure

DIURETICS

A

Lasix
Possible fluid restriction
Monitor K+ levels
Potassium supplements

51
Q

congestive heart failure

DECREASE CARDIAC DEMAND

A 
Limit physical activity (bed rest)
Maintain body temp
Treat infections
Reduce effort of breathing (HOB elevated)
Medication to sedate an irritable child

Improve tissue oxygenation: O2

52
Q

Rheumatic Fever S/S

A 
Fever
Fatigue
Migratory joint pain
Sub-q nodules over bony prominences
Erythema marginatum (abd skin rash)
Chorea (involuntary movement)

Rheumatic heart disease is a condition in which the heart valves have been permanently damaged by rheumatic fever. The heart valve damage may start shortly after untreated or under-treated streptococcal infection such as strep throat or scarlet fever

53
Q

What triggers Rheumatic Fever?

A

Group A Hemolytic Streptococcus is thought to trigger antibody formation and an autoimmune reaction (URI, otitis media infection, Impetigo)
Antibodies attack heart valves, causing rheumatic endocarditis

54
Q

Rheumatic fever: mitral valve

A

Mitral valve becomes inflamed and thickening making it difficult to close properly
Blood flow from L atria to L ventricle is decreased which may lead to CHF

55
Q

Rheumatic fever: inflammatory disease

A

Inflammatory disease of the collagen (connective tissue), which may cause permanent damage to heart
Common cause of heart diseases in children 5-15 years old from untreated or partially treated strept throat

56
Q

What causes Rheumatic fever?

A

Follows group A Beta-hemolytic streptococcal pharyngitis.
Most often in last school age children or adolescents.
Rheumatic fever develops 2-6 weeks after URI

57
Q

Rheumatic fever diagnosis

A 
Jones Criteria
Increased WBC
Fever
Increased ESR
Arthralgia
Recent streptococcal infection
Abnormal EKG
Heart Cath
58
Q

Rheumatic fever treatment

A

Prevent/treat CHF (Digitalis, Diuretics etc.)
Treat infection (antibiotics)
Streptococcal prophylaxis for 5 years or thru adolescence, whichever is greater to prevent further damage to valves
Surgery, repair or replace mitral valve

59
Q

Rheumatic fever nursing interventions

A

Complete bed rest to decrease workload of heart and activity restrictions with carditis
Monitor VS, I/O, weight
Gentle care r/t painful, swollen joints
Teach r/t disease, prophylactic antibiotics must be given before any dental or invasive procedure to decrease risk of endocarditis
Facilitate recovery and provide emotional support
Encourage rest and adequate nutrition
Prevention: throat culture, referrals for testing

60
Q

Kawasaki’s Disease clinical manifestations

A

Acute phase
Subacute phase
Convalescent phase

61
Q

Rheumatic Fever labs?

A

Erythrocyte sedimentation rate (ESR)
ASO or ASLO titer (looks for strep antibodies) in 80% cases
C-reactive protein- inflammatory immune response

62
Q

Kawasaki disease: what is it?

A

An acquired cardiovascular disorder

  • acute systemic vasculitis
  • unknown cause (non-contagious infection)
  • without treatment 15-25% develop coronary artery aneurysms
63
Q

Kawasaki’s disease diagnosis and criteria?

A

Diagnosis:
No specific diagnostic test
WBC, ESR, C-reactive increased in acute phase
Platelets increase in sub-acute phase

Criteria:
Fever (101-104) for 5 or more days
Unresponsive to antibiotics
Bilateral conjunctival inflammation without drainage
Erythema, dryness, fissures, or oral mucus membranes (strawberry tongue)
Peeling of hands and feet
Erythematous rash
Cervical lymphadenopathy (>1.5cm node)
64
Q

Kawasaki Disease Acute phase s/s

A

High fever >5 days
4 out of 5 criteria
Unresponsive to antibiotics and antipyretics
Very irritable

65
Q

Kawasaki disease medical treatment

A

Prevent or reduce damage to coronary arteries
-Large doses of IV Gamma globulin which reduce incidence of coronary artery abnormalities when given within the 1st 10 days of illness

Salicylate therapy (aspirin in high doses) to decrease fever and inflammation initially, then to decrease platelets for 6-8 weeks

  • acute phase: fever and anti-inflammatory
  • sub acute phase: low dose for antiplatelet action

Long term anticoagulants for moderate to large aneurysms

66
Q

Kawasaki disease prognosis?

A

Most fully recover after treatment
Morbidity with cardiovascular complications
Death rare: cause thrombosis
Coronary artery aneurysms: serious complication, 20-25% of children with untreated

67
Q

Kawasaki disease nursing interventions

A

Monitor cardiac status (CHF), I/O, VS, weight, low cholesterol diet, aspirin

Heart and lung assessment: CHF, murmurs

Monitor for allergies to IV globulin

Symptomatic relief, mouth care, lotions, liquids, soft foods, high calorie, low acid, bland and special skin care

Treat joint pain

Treat and keep record of fever

Quiet environment

Family support

No live vaccines for 11 months after treatment (MMR)

CPR for parents of child with cardiac involvement

68
Q

What is Sickle Cell anemia?

A 
Inherited disorder (both parents) that affects African Americans
Hemoglobin S replaces all or part of the normal hemoglobin
69
Q

Pathophysiology of Sickle Cell anemia?

A

Irregular shape of the sickled cell blocks the microcirculation leading to occlusion

Absence of blood flow causes local hypoxia and leads to tissue ischemia and infarction

Increased RBC destruction

70
Q

Sickle Cell anemia diagnosis?

A

Usually not symptomatic until 4-6 months
Sickledex: accurate results in 3 minutes, high = active crisis
Hgb electrophoresis: to distinguish between trait or disease
Reticulocytes: increased r/t decreased life span of sickled RBC

71
Q

Sickle Cell Anemia crisis?

A

Vaso-occlusive: distal ischemia and pain, leg or joint pain, edema of hands and feet, priapism, CVA

Sequestration: pooling of blood in liver and spleen leads to hypovolemic shock

Aplastic: decreased RBC production= profound anemia

72
Q

Sickle cell anemia management

A

Prevent condition that lead to sickling crisis

Maintain hydration, oral and IV

Teach parents to seek treatment for all infections immediately

Prevent infection (flu and pneumonia vaccines
-spleen doesn't function properly and or may have been removed r/t prior complication, increases susceptibility to infections

Blood replacement to treat anemia

Antibiotics for infection

Complementary treatment: massage, relaxation

Splenectomy (atrophies after 6 years old)

73
Q

Sickle cell anemia prognosis?

A

Varies, most live into 50’s

Most at risk; children <5 years due to infection

74
Q

Sickle Cell nursing care

A 
Teach family to seek early medication treatment for fever >101.3
Recognize s/s of respirator problems
Adequate hydration
I/O and daily weight
Management of pain
Psychological support
Heat is soothing
NO cold compresses, enhances sickling
Bed rest
Monitor V/S, pulse ox
75
Q

hemophilia, what is it?

A

inherited bleeding disorder transmitted by an X linked recessive chromosome. Male disease transmitted by carrier females.
Impaired ability to form clot r/t abnormal clotting factors

76
Q

Hemophilia, 2 types

A

Type A, most common, deficiency of Factor 8

Type B, Christmas disease, deficiency of Factor 9

77
Q

hemophilia diagnosis

A

PT, factors: II, V, VII, X
PTT, factors: II, V, VIII, IX, X XI, XII
Other clotting tests

78
Q

Hemophilia treatment

A

Replace missing factors to prevent bleeding

Transfuse plasma concentrates or FFP (fresh frozen plasma) with missing factors

79
Q

Hemophilia S/S

A

Bleeding
Joint swelling, loss of function, pain
Tarry, black stools

80
Q

Hemophilia nursing care

A

Prevent and treat bleeding episodes
-RICE (rest, ice, compress, elevate), bed cradle, VS, check environment, soft toothbrushes/toys, medic alert tag, maintain weight (stress on joints)
-pain management
avoid rectal temperatures, can cause bleeding
-if muscle or joint injury occurs immobilize, elevate and apply ice to area, measure injury

81
Q

Immune Thrombocytopenic Purpuro (ITP), what is it?

A

Acquired hemorrhagic disorder
Characterized by:
-thrombocytopenia (excessive destruction of platelets)
- purpura (discoloration caused by petechiae beneath the skin)
**believe to be an autoimmune response to disease related antigens

82
Q

Hemophilia medical management

A

Primary treatment is replacement of the missing clotting factor
DDAVP: increases plasma factor VIII
Corticosteroids for hematuria, acute hemarthrosis and chronic synovitis
Aminocaproic acid (Amicar): prevents clot destruction
Children are treated at home, decrease complications
Family taught IV admin of AHF for >2-3 year old
Child learns procedure on self at 8-12 years old

83
Q

Immune Thrombocytopenia Purpura (ITP) diagnosis

A 
Clinical findings
Platelet count reduced
Bleeding time prolonged
No definitive test
Diagnosed r/t symptoms
Several tests to rule out other disorders such as lupus, leukemia, lymphoma
84
Q

Immune Thrombocytopenia Purpura (ITP) management

A 
Gamma globulin (increases platelet count)
Transfusion of RBC
Bleeding precautions (control bleeding)
-safety, limit activity
-restrict use of ASA, use Tylenol
Prednisone
Anti-D antibody (one dose over 5-10 min)
85
Q

Immune Thrombocytopenia Purpura (ITP) clinical manifestions

A

Easy bruising
Bleeding from mucous membranes
Hematomas over lower extremities

86
Q

immune Thrombocytopenia purpura (ITP) prognosis

A

usually self limiting

splenectomy may modify chronic disease and child will be asymptomatic

NUR 131 (38 decks)

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