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NURS 406 > Exam 2: Cardiovascular Dysfunction > Flashcards

Exam 2: Cardiovascular Dysfunction Flashcards

1
Q

Fetal circulation differs from neonatal circulation in what ways

A
  • The process of gas exchange
  • Pressures within the systemic and pulmonary circulations
  • Existence of anatomical structures
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2
Q

How is cardiovascular dysfunction diagnosed?

A
  • Electrocardiography (ECG/EKG)
  • Chest radiography
  • Echocardiography
  • Cardiac MRI
  • Cardiac Catheterization
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3
Q

Differentiate between the two major groups of CV dysfunction

A
  1. Congenital heart disease: present at birth
  2. Acquired cardiac disorders: occurs after birth and seen with a normal heart or in the presence of congenital heart defects
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4
Q

Cardiovascular Dysfunction: History and Physical

A
  • Family history
  • Prenatal history
  • Birth history
  • Inspection, plantation/percussion, and auscultation
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5
Q

Risk Factors for Congenital Heart Disease

A
  • Maternal alcohol/illicit drug use

- Congenital disorders: Down syndrome or Turner syndrome

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6
Q

Assessment of Cardiac Function: Murmurs

A
  • Heart sounds that reflect the flow of the heart

- 80% of children have an innocent murmur at some point

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7
Q

Assessment of Cardiac Function: History

A
  • Poor feeding
  • Rapid breathing
  • Sweating with feeds
  • Poor weight gain
  • Headaches/fainting
  • Exercise intolerance
  • Chest pain/palpitations
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8
Q

What is the most common heart defect?

A

Ventricular septal defect

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9
Q

Congenital Heart Disease

A
  • Major cause of deaths in 1st year of life
  • Cause unknown
  • Often associated with chromosomal abnormalities
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10
Q

Ductus Arteriosus (PDA)

A
  • Connects aorta and pulmonary system
  • Closes 4-6 weeks (if open >6 weeks -> defect)
  • Closes d/t pressure changes when infant takes first breath
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11
Q

Foramen Ovale

A
  • Opening between right atrium and left atrium.
  • Closes: birth - 2 weeks
  • If it stays open: atrial septum defect
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12
Q

Ductus Venosus

A
  • Close: within a couple of hours
  • Alway automatically closes, never becomes a defect
  • Changes in circulation after first breath d/t pressure changes
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13
Q

LA and LV

A

Higher pressure

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14
Q

RA and RV

A

Lower pressure

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15
Q

Review Fetal Circulation!

A

Watch videos on YouTube

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16
Q

Cardiac Testing involves

A
  • Radiologic: CXR (size and blood flow pattern)
  • Electrocardiography: electrical activity
  • Echocardiography: Most frequently used; non-invasive
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17
Q

Cardiac Catheterization: Provides information on

A

Invasive procedure

  • Oxygen saturation
  • Pressure changes
  • CO
  • Anatomic abnormalities
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18
Q

Cardiac Catheterization: Nursing Responsibility

A
  • Pulses
  • Temperature and color of affected extremity
  • VS: HR, BP (hypotension may indicate hemorrhage)
  • Monitoring dressing
  • Fluid intake (adequate hydration)
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19
Q

Cardiac Catheterization: Post Procedure Management

A
  • Maintain straight extremity for 4-6 hours
  • Resume usual diet
  • Tylenol or Tylenol with codeine for pain
  • No strenuous exercise for several days
  • Monitor dressing frequently
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20
Q

Cardiac Catheterization: Dressing Management

A
  • Occlusive dressing applied post catheterization
  • Leave dressing on until next day to prevent bleeding and infection.
  • Once dressing is removed, keep site clean and dry.
  • If bleeding occurs, apply direct continuous pressure.
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21
Q

Heart Failure

A
  • Inability of the heart to pump an adequate amount of blood to the systemic circulation at normal filling pressures to meet the body’s metabolic demands
  • Can have Congenital heart disease or a normal structure (can result from excessive workload on a normal heart)
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22
Q

Heart Failure: Classification of Causes

A
  • Volume overload
  • Pressure overload
  • Decreased contractility
  • High CO demands
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23
Q

Heart Failure is divided into 3 groups

A
  1. Impaired myocardial function
  2. Pulmonary congestion
  3. Systemic venous congestion
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24
Q

What is one of the earliest signs of heart failure? **

A

-Tachycardia (heart compensates by increasing

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25
Q

What is a late sign of heart failure?**

A

Gasping and grunting respirations (latest signs are related to respirations)

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26
Q

What is a major concern of heart failure?

A

Inability to feed (babies only eat, sleep and poop; can’t do them if there is an issue)

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27
Q

Heart Failure: Signs and Symptoms of Impaired Myocardial Function

A
  • Tachycardia
  • Sweating (inappropriate)
  • Decreased urinary output
  • Fatigue
  • Weakness
  • Restlessness
  • Anorexia
  • Pale, cool extremities
  • Weak peripheral pulses
  • Decreased blood pressure
  • Gallop rhythm
  • Cardiomegaly
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28
Q

Heart Failure: Signs and Symptoms of Pulmonary Congestion

A
  • Tachypnea
  • Dyspnea
  • Retractions
  • Flaring nares
  • Exercise intolerance
  • Orthopnea
  • Cough, hoarseness
  • Cyanosis
  • Wheezing
  • Grunting
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29
Q

Heart Failure: Signs and Symptoms of Systemic Venous Congestion

A
  • Weight gain
  • Hepatomegaly
  • Peripheral edema
  • Ascites
  • Neck vein distention
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30
Q

Heart Failure is most often caused by

A

Congenital Heart Defects: Shunt, obstruction or combination of both

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31
Q

Another symptom of heart failure is

A
  • Increased metabolic demands (requires additional calories to grow)
  • Increase work of the heart and increase breathing further increases demands
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32
Q

Heart Failure Management

A
  • Feeding
  • Limit/cluster care
  • Organize nursing activities around sleep and rest periods
  • Bed linen changing and complete bed baths done only when necessary
  • Limit crying episodes
  • Monitor for fever (could indicate infection)
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33
Q

Heart Failure: Feeding Management

A
  • Limit feeding time (30 minutes because after they will start to burn more calories than they are eating)
  • Small frequent feeds
  • Jaw and cheek support
  • Increase caloric density of formula
  • NG tube if needed (if can’t eat calories needed, with support, within time)
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34
Q

Pharmacological Management of Heart Failure

A
  • Digoxin
  • Diuretics: Furosemide (Lasix)
  • Vasodilators: ACE Inhibitors (Captopril and Enalapril); Beta-Blockers
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35
Q

Heart Failure Drugs: Digoxin

A

Strengthens the force of myocardial contractions.

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36
Q

Digoxin: Nursing Assessment

A
  • Apical heart rate checked prior to administering (infant: 90-110 or child: 70)
  • Count pulse for 1 full minute
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37
Q

Digoxin: Nursing Management

A
  • Double check dosage prior to giving
  • Hold dose if toxicity symptoms occur
  • If missed dose: do not give extra
  • If vomiting: do not repeat
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38
Q

Digoxin Toxicity Symptoms

A
  • Vomiting
  • Bradycardia
  • Neurological Disturbances
  • Visual Disturbances
  • Dysrhythmias
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39
Q

Heart Failure Drugs: Diuretics

A
  • To eliminate excess water and sodium.
  • Increased urine production
  • Reducing systemic and pulmonary congestion
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40
Q

Furosemide (Lasix): Nursing management/interventions

A
  • Potent loop diuretic
  • Risk for hypokalemia (potentiates digoxin toxicity)
  • Give potassium supplements and/or potassium rich foods.
  • Observe for signs of dehydration.
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41
Q

Heart Failure Drugs: Vasodilators

A
  • Relaxes smooth muscles

- Most commonly given: ACE-Inhibitors and Beta Blockers

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42
Q

Vasodilators: Vasodilation results in

A
  • Decreased pulmonary and vascular resistance
  • Decreased BP
  • Reduces afterload
  • Decreased RA and LA pressures
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43
Q

Vasodilators: Side Effects

A
  • Hypotension
  • Renal Dysfunction
  • Cough
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44
Q

What are complications of HF? **

A
  • Cardiomegaly

- Pulmonary edema

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45
Q

Furosemide: Monitor for S/S of hypokalemia

A
  • Muscle weakness and cramping
  • Confusion, irritability and restlessness
  • Inverted T waves or prominent U waves
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46
Q

Furosemide: Monitor for S/S of dehydration

A
  • Sunken fontanel
  • Non-elastic skin turgor
  • Dry mucous membranes
  • Decreased tears, UO and concentrated urine
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47
Q

Heart medications: Indomethacin

A
  • Antirheumatic
  • Alternative to surgery, allows closure of PDA
  • Action: inhibits prostaglandin synthesis
48
Q

Heart medications: Prostaglandin E1

A

Short term maintenance of PDA latency required for infants to maintain blood oxygenation and perfusion of the lower body

49
Q

Hypoxemia

A

Lower than normal arterial oxygen tension.

50
Q

Cyanosis occurs if

A
  • SaO2 <85%

- Hgb not bound to oxygen reaches 5g/dL

51
Q

What are two physiologic changes of hypoxemia?

A
  1. Polycythemia

2. Clubbing

52
Q

What are 3 types of cardiac defect display cyanosis?

A
  • Obstruction of pulmonary blood flow
  • Mixing of arterial and venous blood flow
  • Transposition of the great arteries
53
Q

What are long term effects of hypoxemia?

A
  • Smaller stature
  • Poor weight gain
  • Dyspnea on exertion
  • Poor exercise intolerance
54
Q

Classification of Congenital Heart Defects

A
  1. Increased pulmonary blood flow
  2. Decreased pulmonary blood flow
  3. Obstruction to blood flow out of the heart
  4. Mixed blood flow
55
Q

Congenital Heart Disease Classifications: Increased pulmonary blood flow

A
  • Blood flows from the left ventricle (high pressure) to the right ventricle (low pressure)
  • Increased blood flow on the right side of the heart (Includes Patent Ductus Arteriosus or Ventricular Septal Defect**)
  • Increased pulmonary blood flow
56
Q

Congenital Heart Disease Classifications: Decreased pulmonary blood flow

A
  • Obstruction of pulmonary blood flow
  • Difficulty exiting the right side of the heart via the pulmonary artery
  • Increased pressure in the right side of the heart
  • Desaturation of blood
  • Usually appears cyanotic and hypoxemia
  • Includes Tetralogy of Fallot**
57
Q

Ventricular Septal Defect

A
  • Abnormal opening between the right and left ventricle
  • Frequently associated with other defects
  • Possible spontaneous closure in the 1st year of life.
58
Q

Ventricular Septal Defect Characteristics

A
  • Increased blood volume is pumped into the lungs (right ventricular hypertrophy)
  • Heart failure is common
  • Characteristic murmur
59
Q

Patent Ductus Arteriosus

A

-Failure of the fetal ductus arteriosus to close (usually closes in the first few weeks of life)

60
Q

Characteristics of Patent Ductus Arteriosus

A
  • Increased pulmonary congestion
  • Increased workload on the left side of the heart
  • Possible left ventricular hypertrophy
61
Q

Patent Ductus Arteriosus Management

A

-Indomethacin (prostaglandin inhibitor): closes patent ductus in infants and newborns

62
Q

Tetralogy of Fallot: Classic Form includes four defects

A
  1. ventricular septal defect
  2. pulmonary stenosis
  3. overriding aorta
  4. right ventricular hypertrophy
63
Q

Characteristics of Tetralogy of Fallot in Infants

A
  • Acutely cyanotic at birth
  • Characteristic murmur
  • Blue spells or tet spells: acute episodes of cyanosis and hypoxia when the infants O2 requirements exceed the blood supply (usually during feeding or crying)
64
Q

Tetralogy of Fallot Treatment

A

-Multiple surgeries required

65
Q

Congenital Heart Disease Classifications: Obstruction of Blood Flow

A
  • Blood exiting the heart meets an anatomical narrowing
  • Pressure in the ventricle and the great artery before the obstruction is increased
  • Location of narrowing is usually a valve
  • Exhibit signs of heart failure
  • Includes Coarctation of the aorta and aortic stenosis**
66
Q

Aortic Stenosis

A

Narrowing or structure of the aortic valve

67
Q

Characteristics of Aortic Stenosis

A
  • Resistance to blood flow in left ventricle
  • Decreased CO
  • Left ventricular hypertrophy
  • Pulmonary vascular resistance
  • Characteristics murmur
68
Q

Symptoms of Aortic Stenosis

A
  • Hypotension
  • Tachycardia
  • Poor feeding
69
Q

Coarctation of the Aorta

A

-Narrowing near the insertion of the ductus arteriosus

70
Q

Characteristics of Coarctation of the Aorta

A
  • Increased pressure proximal and decreased pressure distal the defect
  • 4 extremity blood pressures
71
Q

Congenital Heart Disease Classifications: Mixed Blood Flow

A
  • Survival depends on the mixing of blood from the pulmonary and systemic circulation in the heart chambers
  • Some degree of heart failure
  • Pulmonary congestion occurs
  • Cardiac output decreased
  • Includes: Hypoplastic left heart syndrome and Transposition of the Great Vessels**
72
Q

Transposition of the Great Vessels

A
  • No communication between the systemic and pulmonary system (pulmonary artery leaves the left ventricle; aorta leaves the right ventricle)
  • Cardiomegaly is evident
73
Q

Transposition of the Great Vessels: What must be present for survival?

A

A septal defect or a patent ductus arteriosus must be present for survival.

74
Q

Hypoplastic Left Heart

A
  • Underdevelopment of the left side of the heart (Hypoplastic left ventricle, aortic atresia)
  • Condition is fatal without intervention
75
Q

Characteristics of Hypoplastic Left Heart

A

Mild cyanosis and heart failure until PDA closes

76
Q

Treatment for Hypoplastic Left Heart

A
  • Prostaglandin E1 given to maintain ductal patency

- Multi-stage surgical treatment is used.

77
Q

Signs and Symptoms of Patent Ductus Arteriosus

A
  • Characteristic machine like murmur
  • Widened pulse pressure/bounding pulses
  • May or may not show signs of HF
78
Q

Tetralogy of Fallot Characteristics in Children

A
  • Squatting: compensatory mechanism to increase BF to heart
  • Increased cyanosis
  • Clubbing fingers
  • Poor growth
79
Q

Signs and Symptoms of Coarctation of the Aorta**

A
  • BP higher in upper extremities than lower
  • Bounding pulses in arms
  • Weak/absent femoral pulse
  • Cool lower extremities
  • Epistaxis from HTN
80
Q

Infective Endocarditis

A
  • Infection of the valves and inner lining of the heart (microorganisms grow in system and causes turbulence)
  • Can damage or destroy heart valves
81
Q

Infective Endocarditis: Treatment

A
  • High dose IV ABT for 2-8 weeks

- Prophylactic ABT for certain patients (amoxicillin, clindamycin or azithromycin)

82
Q

Infective Endocarditis: Clinical Manifestations

A
  • Unexplained low-grade, intermittent fever
  • Feeding difficulties
  • Tachycardia
  • Respiratory distress
  • Heart failure
  • Symptoms of septicemia
83
Q

Rheumatic Fever

A
  • Inflammatory disease that involves the joints, skin, brain, serous surfaces and the heart.
  • Self limiting
84
Q

Rheumatic Fever occurs after

A

Pharyngitis (strep throat)

85
Q

Rheumatic Fever:Most Significant Complication

A

Cardiac valve damage

86
Q

How is Rheumatic fever diagnosed?

A

Multiple lab tests

87
Q

What are clinical manifestations of Rheumatic Fever?

A
  • Fever (low grade spikes in the late afternoon)
  • Carditis: inflammation of the endocardium (most often the mitral valve)
  • Polyarthritis
  • Erythema marginatum: red, painless skin lesion over trunk and then spreads with central clearing
  • Subcutaneous nodules

From mentor study guide:

  • Arthralgia
  • Chorea
  • Prolonged P-R Interval
  • Elevated erythrocytes sedimentation rate or (+) C-reactive protein level
88
Q

Rheumatic Fever Treatment

A
  • Penicillin
  • Cephalosporin or macrolides if allergy
  • If valve replacement, prophylactic antibiotics prior to dental procedures
89
Q

Rheumatic Fever Management

A
  • Control joint pain and inflammation: massage, alternating hot & cold applications
  • Carditis: limit physical exercise, aspirin or corticosteroids (DO NOT ADMINISTER BEFORE DIAGNOSIS B/C IT MASKS POLYARTHRITIS)
  • Seizure precautions if child is experiencing chorea.
90
Q

Kawasaki Disease

A
  • Acute systemic vasculitis
  • Unknown cause: associated with organism or toxin
  • Leading cause of acquired heart disease
  • Self limiting (resolves in 6-8 weeks)
91
Q

Kawasaki Disease: If not treated

A

-20-25% develop cardiac problem

92
Q

Kawasaki Disease: Diagnosis

A
  • No specific diagnostic test.

- Monitor status with echocardiogram.

93
Q

Kawasaki Disease: Treatment

A
  • High dose IVIG

- Salicylate therapy

94
Q

Kawasaki Disease: Prognosis

A

-Most recover fully after treatment (except for cardiac complications)

95
Q

What are clinical manifestations of Kawasaki disease?

A
  • Changes in extremities: Erythema of palms and soles of feet; edema of hands and feet; peeling of fingers and toes
  • Polymorphous exanthem
  • Bilateral bulbar conjunctival injection without exudate (eyes red and swollen)
  • Erythema and cracking of lips
  • Strawberry tongue
  • Cervical lymphadenopathy
96
Q

Complications of Kawasaki Disease

A

-Cardiac involvement -> aneurysms can develop

97
Q

Hyperlipidemia

A
  • General term for excessive lipids

- Plays a role in developing atherosclerosis -> coronary artery disease

98
Q

Risks for Hyperlipidemia Includes

A
  • Family history
  • Cigarette smoking
  • Diabetes
  • Obesity*
  • Hypertension
  • Chronic inflammatory disease
  • Cancer
  • Transplantation
  • Congenital heart disease*
  • History of Kawasaki Disease*
99
Q

How is hyperlipidemia diagnosed?

A
  • Based on lab values

- In children: total cholesterol >200 mg/dl and LDL >130 mg/dl

100
Q

When should you not draw labs for hyperlipidemia?

A

Should not draw labs within 3 weeks of febrile illness.

101
Q

Treatment for Hyperlipidemia

A
  • Lifestyle modification
  • Diet modification: Food choices and Portion sizes
  • Medications are needed at times
  • Include the whole family
102
Q

Cyanosis in an anemic infant

A

Level of desaturation will be higher before cyanosis becomes apparent (lower hgb level from anemia means that a larger percentage of hgb must be desaturated before cyanosis becomes visible)

103
Q

Cyanosis in children with polycythemia

A

Appear cyanotic when a lesser amount of hgb is desaturated (higher hgb levels mean a smaller percentage must be desaturated before cyanosis is seen)

104
Q

Hypercyanotic Episode

A

-Dramatic event in children with cyanotic heart disease (often called test spells because they often occur in children with tetralogy of Fallot)

105
Q

When do hypercyanotic episodes usually occur?

A
  • Most frequent in 2 years of life

- Occurs mainly in the morning

106
Q

A hypercyanotic episode is preceded by

A
  • Crying
  • Feeding
  • Defecation
107
Q

Treatment for hypercyantoic episodes include

A
  • Calming infant
  • Knee to chest
  • O2
  • Morphine sulfate (vasodilates)
  • Phenylephrine (vasoconstricts)
108
Q

What should the nurse assess to identify cyanosis?

A
  • Know source of pulmonary BF for children with cyanotic heart disease
  • Baseline cyanosis and general appearance
  • Level of activity (including irritability)
  • Observe in natural light: skin, mucous membranes, conjunctiva, nail beds
  • General skin color
  • IV Line patently and air-> embolism
  • Smaller than peers -> may have clubbing, thickening/flattening of fingertips and toes (d/t polycythemia)
109
Q

Cyanosis interventions are directed toward

A
  • Stabilizing

- Preparing child for medical or surgical interventions

110
Q

Cyanosis Interventions include

A
  • Administration of Prostaglandin E1; vasodilator
  • Parent teaching
  • Monitoring fluid status
111
Q

Cyanosis Interventions: Administration of Prostaglandin E1: Vasodilators

A
  • Maintains ductal patency and restores pulmonary or systemic blood flow
  • Continuous IV Fusion
112
Q

Side Effects of Prostaglandin E1

A

Apnea (infants frequently require intubation)

113
Q

Cyanosis Interventions: Parent Teaching

A
  • Need simple thorough explanations
  • Help ID sources of emotional support and encourage communication
  • Stress importance of child interacting with environment as much as possible
  • Recognize illness that place child at risk for dehydration
114
Q

Children who are cyanotic are prone to

A
  • Respiratory Infections which increase cardiac workload, cyanosis and desaturations
  • Avoid crowded areas
115
Q

Cyanosis Interventions: Monitor fluid status

A
  • Prevents hemo-concentration

- I&O monitored and daily weights

NURS 406 (18 decks)

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