TLO 2.2 Cardiovascular Child Flashcards
Fetal Circulation
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
Fetal circulation: placenta?
Gas exchange takes place in the placenta
Fetal Circulation
Oxygenated blood travels?
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
Diagnostic test: BLOOD TESTS?
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
Fetal circulation
BLOOD RETURNING FROM UPPER BODY
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
Diagnostic Tests
ELECTROCARDIOGRAM (EKG)
Records electrical conduction of the heart
Diagnostic Tests
XRAY
Looks at lungs, heart, chest, diaphragm, ribs.
Posterior, anterior, lateral
Diagnostic Tests
ULTRASOUND
Sonogram or echocardiogram
Noninvasive procedure that visualizes and records information concerning cardiac structures including the position, size and movement of valves
Diagnostic Tests
CARDIAC CATHETERIZATION
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
Diagnostic Tests
MAGNETIC RESONANCE IMAGING (MRI)
Noninvasive, computer based procedure that provides information r/t anatomy, congenital defects, blood clots and infections, looks at soft tissues
Congenital Heart Defects
CONTRIBUTING FACTORS
S/S
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
Congenital Heart Defects
CLASSIFICATIONS
Anatomic abnormality
Hemodynamic abnormality
Tissue oxygenation abnormality
- acyanotic (normal oxygenation)
- cyanotic
Congenital Heart Defects
ACYANOTIC
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
Post cardiac catheterization complications?
Acute hemorrhage at entry site Low grade fever Vomiting Loss of pulse in catheterized extremity Transient dysrhythmias Rare: stroke, seizures, tamponade, death
Congenital Heart Defects
CYANOTIC
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
Congenital Heart Defect symptom?
Increased pulse Increased respirations Retarded growth Fatigue URI
Acyanotic congenital heart defects examples (left to right shunt)
Right to left shunt:
Patent ductus arteriosus**
Arterial septal defect
Ventricular septal defect
Acyanotic congenital heart defects
S/S, RISKS
Increase fatigue Heart murmurs Increase risk of endocarditis CHF Growth retardation
Patent Ductus Arteriosus (acyanotic)
What is it?
Ductus arteriosus fails to close at birth causing oxygenated blood to be shunted into pulmonary circulation.
Results in increased pulmonary blood flow
Patent Ductus arteriosus (acyanotic)
S/S
Continued loud murmur Pallor Widened pulse pressure Feeding problems Resp infections Cardiomegaly CHF Pulmonary edema
Patent Ductus Arteriosus (acyanotic)
TREATMENT
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
Coarctation of the Aorta (acyanotic)
what is it?
Narrowed aorta obstructs the outflow from left ventricle causing increased left ventricular pressure.
Pulmonary blood flow is normal
Coarctation of the Aorta (acyanotic)
S/S
Decreased circulation to lower extremities (low B/P in lower extremities) Growth retardation Fatigues HA Epistaxis (nose bleed) Leg cramps Cardiomegaly CHF Metabolic acidosis
Coarctation of the Aorta (acyanotic)
TREATMENT
Digoxin
Diuretics
Prostaglandin E: dilates narrowed vessels
Balloon dilation
Surgical repair usually done at 2-4 years old
Cardiovascular disorders
Two major Groups
Congenital heart disease
Acquired heart disorders
Congenital Heart Disease defined with examples
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%
Acquired Heart Disorders define with examples
Disease processes or abnormalities that occur after birth
- infection (Rheumatic fever)
- autoimmune responses (Kawasaki disease)
- environmental factors
- familial tendencies
Tetralogy of Fallot (cyanotic)
what is it?
Right to Left shunting of blood causes decreased pulmonary blood flow and decreased oxygen in systemic circulation
Tetralogy of Fallot
4 defects?
Ventricular Septal Defect
Pulmonary Stenosis
Overriding of the Aorta
Right ventricular Hypertrophy
Assessment of Child (family history)
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
Physical assessment of child: General appearance
General appearance Weight (gain or loss) Activity level Skin color Effort of breathing Audible breath sounds
Physical assessment: suspected cardiac disease inspection
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
Heart Murmurs: causes?
S.P.A.M.S. Stenosis of a valve Partial obstruction Aneurysms Mitral regurgitation Septal defect
Heart Murmurs: types?
Systolic:
- crescendo (increased during systole)
- decrescendo (decreased during systole)
Diastolic:
-indicates pathologic disease
Physical assessment: palpation and percussion
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
Character of heart sounds: murmurs
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
Tetralogy of Fallot (cyanotic)
S/S
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
Patent Ductus Arteriosus
What is it?
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
Cyanotic Heart Defects Mnemonic
4-T’s
Tetralogy of Fallot** focus on this one
Truncus Arteriosus
Transposition of the Great vessels
Tricuspid Atresia
Tetralogy Fallot
RISK
SURGICAL TREATMENT
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
Congestive Heart Failure diagnostic tests
Chest x-ray
EKG
Echocardiogram
Congestive heart failure medical treatment
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
What is congestive heart failure?
Inability of the heart to pump and adequate amount of blood to the meet systemic circulation needs
Congestive heart failure in children
WHAT ARE THE CAUSES?
Secondary to structural abnormalities Septal defects Myocardial failure Ventricle impaired Excessive demands on the heart -sepsis -severe anemia
Left sided congestive heart failure
Blood back up to the lungs=
Crackles in the lungs
Pulmonary congestion
Right sided congestive heart failure
Blood back up to the liver= Hepatomegaly Splenomegaly Neck vein distention Lower extremity edema
Treating congestive heart failure mnemonic
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)
Congestive heart failure ACE inhibitors med and what do they do?
Lisinopril
Captopril
Enalapril
Vasodilation occurs: decreased pulmonary and systemic vascular resistance
Decreased BP and reduction in afterload
congestive heart failure
BETA BLOCKERS
Carvedilol and Coreg
- decrease HR(<55-60) and BP(<90-100)
- vasodilation
- *must check apical pulse for 1 min and B/P prior
congestive heart failure
DIURETICS
Lasix
Possible fluid restriction
Monitor K+ levels
Potassium supplements
congestive heart failure
DECREASE CARDIAC DEMAND
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
Rheumatic Fever S/S
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
What triggers Rheumatic Fever?
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
Rheumatic fever: mitral valve
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
Rheumatic fever: inflammatory disease
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
What causes Rheumatic fever?
Follows group A Beta-hemolytic streptococcal pharyngitis.
Most often in last school age children or adolescents.
Rheumatic fever develops 2-6 weeks after URI
Rheumatic fever diagnosis
Jones Criteria Increased WBC Fever Increased ESR Arthralgia Recent streptococcal infection Abnormal EKG Heart Cath
Rheumatic fever treatment
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
Rheumatic fever nursing interventions
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
Kawasaki’s Disease clinical manifestations
Acute phase
Subacute phase
Convalescent phase
Rheumatic Fever labs?
Erythrocyte sedimentation rate (ESR)
ASO or ASLO titer (looks for strep antibodies) in 80% cases
C-reactive protein- inflammatory immune response
Kawasaki disease: what is it?
An acquired cardiovascular disorder
- acute systemic vasculitis
- unknown cause (non-contagious infection)
- without treatment 15-25% develop coronary artery aneurysms
Kawasaki’s disease diagnosis and criteria?
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)
Kawasaki Disease Acute phase s/s
High fever >5 days
4 out of 5 criteria
Unresponsive to antibiotics and antipyretics
Very irritable
Kawasaki disease medical treatment
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
Kawasaki disease prognosis?
Most fully recover after treatment
Morbidity with cardiovascular complications
Death rare: cause thrombosis
Coronary artery aneurysms: serious complication, 20-25% of children with untreated
Kawasaki disease nursing interventions
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
What is Sickle Cell anemia?
Inherited disorder (both parents) that affects African Americans Hemoglobin S replaces all or part of the normal hemoglobin
Pathophysiology of Sickle Cell anemia?
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
Sickle Cell anemia diagnosis?
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
Sickle Cell Anemia crisis?
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
Sickle cell anemia management
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)
Sickle cell anemia prognosis?
Varies, most live into 50’s
Most at risk; children <5 years due to infection
Sickle Cell nursing care
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
hemophilia, what is it?
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
Hemophilia, 2 types
Type A, most common, deficiency of Factor 8
Type B, Christmas disease, deficiency of Factor 9
hemophilia diagnosis
PT, factors: II, V, VII, X
PTT, factors: II, V, VIII, IX, X XI, XII
Other clotting tests
Hemophilia treatment
Replace missing factors to prevent bleeding
Transfuse plasma concentrates or FFP (fresh frozen plasma) with missing factors
Hemophilia S/S
Bleeding
Joint swelling, loss of function, pain
Tarry, black stools
Hemophilia nursing care
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
Immune Thrombocytopenic Purpuro (ITP), what is it?
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
Hemophilia medical management
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
Immune Thrombocytopenia Purpura (ITP) diagnosis
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
Immune Thrombocytopenia Purpura (ITP) management
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)
Immune Thrombocytopenia Purpura (ITP) clinical manifestions
Easy bruising
Bleeding from mucous membranes
Hematomas over lower extremities
immune Thrombocytopenia purpura (ITP) prognosis
usually self limiting
splenectomy may modify chronic disease and child will be asymptomatic
