1. Jan Bazner-Chandler CPNP, CNS, MSN, RN
Cardiac Lecture
Jan Bazner-Chandler
CPNP, CNS, MSN, RN

2. Cardiac
Ball & Bindler

3. Focused Health History
Family history of defects / early cardiac disease / siblings with defects
Maternal history of stillborns or miscarriages
Congenital anomalies / genetic anomalies / fetal alcohol syndrome / Down Syndrome and Turner Syndrome
Maternal exposure to rubella

4. Focused Health History
Heart murmur
Tires while eating
Low weight for height
Sweats while eating (diaphoretic)
Cyanosis, worsens with feeding or activity level
Irritable weak cry

5. Focused Health History
In the older child additional symptoms may include:
Chest pain
Decreased activity level
Syncope
Slight of build

6. Focused Physical Assessment
General appearance
Integumentary system
Face, nose, and oral cavity
Thorax and lung
Cardiovascular system

7. Heart Sounds

8. Heart Murmurs
These sounds are produced by blood passing through a defective valve, great vessel, or other heart structure.
Murmurs are classified by: intensity, location, radiation, timing, and quality.

10. Pulses
Alert:
Weaker pulses or lower blood pressure in the lower extremities may indicate coarctation of the aorta (COA)
Bounding pulses can indicate a patent ductus arteriosus (PDA) or aortic insufficiency.

11. Vital Signs
Heart rate: tachycardia in the absence of fever, crying, or stress may indicate cardiac pathology.
Tachypnea, even with rest, chest retractions indicate respiratory distress, possibly resulting from congestive heart failure

12. Knee-chest Position Nurse puts infant in knee-chest
position Whaley & Wong
Child with a cyanotic heart
defect squats (assumes a knee-chest position) to relieve
cyanotic spells. Some times called “tet” spells Ball & Bindler

14. First Breath Pulmonary alveoli open up
Pressure in pulmonary tissues decreases
Blood from the right heart rushes to fill the alveolar capillaries
Pressure in right side of heart decreases
Pressure in left side of heart increases
Pressure increases in aorta

15. Treatment Modalities Palliative procedures Pulmonary artery banding
Shunts
Corrective procedures

16. Diagnostic Test Chest x-ray to define silhouette of the heart.
Heart size, shape, pulmonary markings, and cardiomegaly.
Electrocardiogram ECG or EKG to define electrical activity of the heart.
Echo-cardiogram to visualize anatomic structures.
Non-invasive

17. Cardiac Conduction

19. Echo-Cardiogram

20. Cardiac Catheterization
An invasive test to diagnose or treat cardiac defects.
Visualizes heart and vessels.
Measures oxygen saturation of chambers.
Measures intra-cardiac pressures.
Determines muscle function and pumping action of the heart.

22. Toxicity to Dye
Watch for signs of toxicity to the dye used during the procedure.
Increased temperature
Urticaria
Wheezing
Edema
Dyspnea
Headache
*Allergy response

23. Pre-cardiac Catheterization
Assess vital signs with blood pressure.
Hemoglobin and hematocrit
Pedal pulses
NPO
Hold digoxin
IV if child is polycythemic

24. Post-cardiac Catheterization
Vital sign, with apical pulse, and blood pressure q 15 minutes for first hour.
Apical pulse for 1 minute to check for bradycardia or dysrhythmias.

25. Post-cardiac Catheterization
Assess pulses below the cath site.
Record quality and symmetry of pulses.
Assess temperature and color of affected extremity.
Check dressing for bleeding or hematoma formation.

26. Home Care Instructions
Keep dressing in place for 24 hours.
Keep site dry and clean.
Observe site for redness, swelling, drainage, or bleeding.
Check temperature.
Avoid strenuous exercise.
Acetaminophen for pain.
Keep follow-up appointment
Pre-procedure medications as ordered.

28. Left to Right Shunt
Pressures on the left side of the heart are normally higher than the pressures in the right side of the heart. If there is an abnormal opening in the septum between the right and left sides, blood flows from left to the right.

29. Left to Right Shunt

30. Clinical Manifestations
The infant is not cyanotic.
Tachycardia due to pushing increased blood volume.
Cardiomegaly due to increased workload of the heart.

31. Clinical Manifestations
Dyspnea and pulmonary edema due to the lungs receiving blood under high pressure from the right ventricle.
Increased number of respiratory infections due to blood pooling in the the lungs promoting bacterial growth.

32. Right to Left Shunts
Occurs when pressure in the right side of the heart is greater than the left side of the heart.
Resistance of the lungs in abnormally high
Pulmonary artery is restricted
Deoxygenated blood from the right side shunts to the left side

33. Right to Left Shunt Hole in septum + obstructive lesion =
Deoxygenated blood from the right side of the heart shunts to the left side of the heart and out into the body.

34. Clinical Manifestations
Hypoxemia = the result of decreased tissue oxygenation.
Polycythemia = increased red blood cell production due to the body’s attempt to compensate for the hypoxemia.
Increase viscosity of the blood = heart has to pump harder.

35. Potential Complications
Thrombus formation due to sluggish circulation.
Brain abscess or stroke due to the un-oxygenated blood bypassing the filtering system of the lungs.

36. Heart Failure Major manifestation of cardiac disease
Under 1 year of age due to congenital anomaly
Over 1 year with no congenital anomaly may be due to acquired heart disease

37. Clinical Manifestations of HF
Systemic Venous Congestion
Weight gain, hepatomegaly, edema, jugular vein distension
Pulmonary Venous Congestion
Tachypnea, dyspnea, cough, wheezes
Compensatory Response
Tachycardia, cardiomegaly, diaphoretic, fatigue, failure to grow

38. Digoxin Therapy
Digoxin increases the force of the myocardial contraction.
Take an apical pulse with a stethoscope for 1 full minute before every dose of digoxin. If bradycardia is detected.
< 100 beats / min for infant and toddler
< 80 beats in the older child
< 60 beats in the adolescent
* Call physician before administering the drug.

39. Signs of Digoxin Toxicity
Bradycardia
Arrhythmia
Nausea, vomiting, anorexia
Dizziness, headache
Weakness and fatigue

40. Interventions Fluid restriction
Diuretics – Lasix (potassium wasting) or Aldactone (potassium sparing)
Bed rest
Oxygen
Small frequent feedings – soft nipple with supplemental NG for adequate calorie intake
Pulse oximeter
Sedatives if needed

41. Feeding Small frequent feedings
Soft nipple to easy energy needed to suck
24 calorie formula for added calories
NG feed if not taking in adequate calories to gain weight

42. Cardiac Heart Defects

43. Patent Ductus Arteriosus
PDA
Incidence 10%
One of the most common benign defects
Ductus normally closes within hours of birth
Connection between the pulmonary artery (low pressure) and aorta (high pressure)
High risk for pulmonary hypertension

44. PDA

45. Diagnosis and Treatment
Diagnosis by
Chest x-ray – enlarged heart and dilated pulmonary artery
Echo-cardiogram – show the opening between pulmonary artery and aorta

46. Treatment
Indomethocin given po – constricts the muscle in the wall of the PDA and promotes closure
Cardiac Catheterization – coil is placed in the open duct and acts like a plug
Closed heart surgery – small incision made between ribs on left hand side and PDA is ligated or tied and cut

47. Atrial Septal Defect ASD 10% of defects
Blood in left atrium flows into right atrium
Pulmonary hypertension
Reduced blood volume in systemic circulation
If left untreated may lead to pulmonary hypertension, congestive heart failure or stroke as an adult.

48. ASD

49. Diagnosis and Treatment
Diagnosis: heart murmur may be heard in the pulmonary valve area because the heart is forcing an unusually large amount of blood through a normal sized valve.
Echocardiogram is the primary method used to diagnose the defect – it can show the hole and its size and any enlargement of the right atrium and ventricle in response to the extra work they are doing.

50. Treatment Surgical closure of the atrial septal defect
After closure in childhood the heart size will return to normal over a period of four to six months.
No restrictions to physical activity post closure

51. Ventricular Septal Defect
VSD
30% of defects
Opening in the ventricular septum
Left-to-right shunt
Right ventricular hypertrophy
Deficient systemic blood flow

53. VSD Small holes generally are asymptomatic
Medium to moderate holes will cause problems when the pressure in the right side of the heart decreases and blood will start to flow to the path of least resistance (from the left ventricle through the VSD to the right ventricle and into the lungs)
This will generally lead to CHF

54. Diagnosis and Treatment
Diagnosis – heart murmur – clinical pearl a louder murmur may indicate a smaller hole due to the force that is needed for the blood to get through the hole.
Electrocardiogram – to see if there is a strain on the heart
Chest x-ray – size of heart
Echocardiogram – shows size of the hole and size of heart chambers

55. Treatment VSD
CHF: diuretics of help get rid of extra fluid in the lungs
Digoxin if additional force needed to squeeze the heart
FTT or failure to grow may need higher calorie concentration
Will need prophylactic antibiotics before dental procedures if defect is not repaired

56. Surgical Repair
Over a period of years the vessels in the lungs will develop thicker walls – the pressure in the lungs will increase and pulmonary vascular disease
If pressure in the lungs becomes too high the un-oxygenated blood with cross over to the left side of the heart and un-oxygenated blood with enter the circulatory system.
If the large VSD is repaired these changes will not occur.

57. Coarctation of Aorta COA 7 % of defects
Congenital narrowing of the descending aorta
80% have aortic-valve anomalies
Difference in BP in arms and legs (severe obstruction)

59. Diagnosis and Treatment
In 50% the narrowing is not severe enough to cause symptoms in the first days of life.
When the PDA closes a higher resistance develops and heart failure can develop.
Pulses in the groin and leg will be diminished
Echocardiogram will show the defect in the aorta

60. Treatment
Prostaglandin may given to keep the PDA open to reduce the pressure changes
The most common repair is resection of the narrowed area with re-anastomosis of the two ends
Surgical complications – kidney damage due to clamping off of blood flow during surgery
High blood pressure post surgery – may need to be on antihypertensives
Antibiotic prophylactic need due to possible aortic valve abnormalities.

61. Tetralogy of Fallot (TOF)
6% of defects
Most common cardiac malformation responsible for cyanosis in a child over 1 year

63. TOF Four Components VSD
Pulmonary stenosis – narrowing of pulmonary valve
Overriding of the aorta – aortic valve is enlarged and appears to arise from both the left and right ventricles instead of the left ventricle
Hypertrophy of right ventricle – thickening of the muscular walls because of the right ventricle pumping at high pressure

64. Clinical Manifestations
Dependent on degree of right ventricular outflow obstruction.
Right-to-left shunt
Clubbing of digits
“tet” spells - treated by flexing knees forward and upward
Severe irritability due to low oxygen levels

65. Diagnosis Cyanosis Oxygen will have little effect on the cyanosis
Loud heart murmur
Echocardiogram – demonstrates the four defects characteristic of tetralogy

66. Treatment
If oxygen levels are extremely low prostaglandins may be administered IV to keep the PDA open
Complete repair is done when the infant is about 6 months of age
Correction includes
Closure of the VSD with dacron patch
The narrowed pulmonary valve is enlarged
Coronary arteries will be repaired
Hypertrophy of right heart should remodel within a few months when pressure in right side is reduced

67. Long Term Outcomes
Leaky pulmonary valve that can lead to pulmonary insufficiency
Arrhythmias after surgery
Heart block – occasionally a pacemaker is necessary
Periodic echocardiogram and exercise stress test or Holter evaluation

68. Aortic Stenosis 6% of defects
Aortic valve: has two rather than three leaflets. Leaflets are thickened or fused.
Obstruction of blood flow from left ventricle
Mild symptoms: dizziness, syncope, angina, fatigue
30% incidence of sudden death

70. Aortic Stenosis
Causes obstruction to blood flow between the left ventricle and aorta.
Most common form is obstruction of the valve itself
When the aortic valve does not open properly the left ventricle must work harder to eject blood into the aorta.
Left ventricular muscle becomes hypertrophied.

71. Diagnosis
Heart murmur or AS is a turbulent noise caused by ejection of blood through the obstructed valve.
Electrocardiogram is usually normal
Echocardiogram will show the obstruction and rule out other heart anomalies
Exercise stress test – provides information on impact of the stenosis on heart function

72. Treatment
Cardiac catheterization – balloon dilation of the narrowed valve.
Surgical valvotomy if the closed procedure does not work – often done when patient is older when severe calcium deposits further obstruct the valve.
Recurrent valve obstruction is a complication and if valve replacement is done too early the child may outgrow the valve.
Antibiotic prophylaxis especially if valve replacement

73. Hypoplastic Left Heart
One of the most complex defects seen in the newborn and the most challenging of all the congenital defects
All the structures on the left side of the heart are severely underdeveloped.
Mitral and aortic valves are either completely closed or are very small – left ventricle is tiny – aorta is small and often only a few millimeters in diameter

75. HLH Life threatening shock develops when the ductus arteriosis closes
Low oxygen saturations – will not increase with oxygen administration
Pulses will be weak in all extremities
Plan to deliver infant in a hospital capable of providing the aggressive treatment needed

76. Treatment
Three staged procedure to reconfigure the cardiovascular system
Norwood – right ventricle becomes the systemic ventricle pumping blood to the body
Glenn done at 3-6 months
Fontan done at 2 -3 years of age

77. Long Term Complications
Easily tiring when participating in sports or other exercises
Formation of blood clots – heparin or Coumadin use
Heart arrhythmias – pace maker
Cardiac failure

78. Bacterial Endocarditis
Infection of endocardial surface of the heart
History of CHD, Kawasaki Disease, Rheumatic Fever, or prosthetic valves are more susceptible to infection
Prophylactic antibiotics with dental care, throat, intestinal, urinary or vaginal infections or surgery.

80. Kawasaki Disease Acute-self limiting disease Generalized vasculitis
Peak incidence 6 months to 2 years
More common in males and Japanese

82. Clinical Manifestations
High fever
Conjunctivitis – no drainage
Strawberry tongue
Edema of hands and feed
Reddening of palms and soles
Lymph node swelling

84. Edema – Hands and Feet

85. Peeling Finger Tips

86. Blood Values
Elevated WBC
Elevated ESR
Elevated platelets

87. Interdisciplinary Interventions
Intravenous gamma globulin
High dose of ASA while in hospital
Low dose ASA upon discharge
Base-line echocardiogram to assess coronary artery status