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52 Cards in this Set
- Front
- Back
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Pediatric cardiovascular disorders are divided into 2 groups
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Congenital: Anatomic abnormalities present @ birth that result in abnormal cardiac function
Acquired: Processes that occur after birth. Result from infections, autoimmune responses, environmental factors & familial tendencies |
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Congenital Heart Disease
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VSD: Ventricular Septal Defect – 30 %
PDA: Patent Ductus Arteriosus – 15% Pulmonic Stenosis – 8% ASD: Atrial Septal Defect – 7% Coarctation of the Aorta – 6% Aortic Stenosis – 5% |
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Diagnostic Tools
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Echocardiograph: (ECHO) Use of high frequency sound waves to produce an image of cardiac structures
Electrocardiograph (EKG) Graphic measure of electrical activity of heart Holter monitor 24-72 hour continuous ECG recording used to assess for ongoing dysrhythmias MRI: Noninvasive imaging technique used to evaluate vascular anatomy outside of heart (Ex: coarctation of the aorta) |
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Prenatal Circulation
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Blood carries 02 & nutrition from mom through the umbilicus via the large umbilical vein
Oxygenated blood enters the heart through the inferior vena cava at a higher pressure than the blood entering through the superior vena cava. This forces most of the blood into a different pattern: through the foramen ovale into the LA. It then goes into the LV. This allows the better oxygenated blood (from mom) to be pumped through aorta into head & upper extremities Blood from the head & upper extremities enters the RA from the superior vena cava and is then directed downward into the RV. This blood is pumped through the pulmonary artery, where the major portion is shunted to the descending aorta via the patent ductus arteriosus (commonly called the PDA) This means that only a small amount of blood actually flows to & from the nonfunctioning lungs. |
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Circulation
Changes @ Birth
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The placental blood flow stops with the clamping of the umbilicus...
The lungs expand from the first breath... Now we need blood with oxygen going to the lungs! This causes abrupt and pronounced changes in hemodynamics! |
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Changes in the hemodynamics of the heart at birth:
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Patent foramen ovale closes with pressure changes
PDA starts to close with presence of increased oxygen concentration in blood. Circulation is now “normal” |
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Classification of Congenital Cardiac Defects
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Defects with increased pulmonary blood flow
(Left to right shunt of blood) Defects with obstruction to blood flow from ventricles Defects with decreased pulmonary blood flow (right to left shunt of blood) Defects with mixed blood flow...Both saturated & de-saturated blood mix within heart or great arteries |
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Defects With Increased Pulmonary Blood Flow
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ASD (Atrial Septal Defect)
VSD (Ventricular Septal Defect) AVC (Atrioventricular Canal Defect) PDA (Patent Ductus Arteriosus) |
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Defects With Increased Pulmonary Blood Flow...With all of these defects:
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Intra-cardiac communication in septum or abnormal connection between great arteries
High pressure leads to blood flow that shunts from left to right sides of heart AND to increased pulmonary blood flow |
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ASD or VSD =Atrial or Ventricular septal defects
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Description: Abnormal opening between the atria or ventricles
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ASD/VSD: Clinical Malifestations, Px, Tx
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Clinical Manifestations:
ASD… not as serious… may be asymptomatic VSD may develop CHF. Always a murmur Treatment: Surgical closure if no spontaneous closure during first year or if cardiac fxn significantly disrupted Prognosis: ASD always good (mortality < 1%) VSD depends on the location, size, & number of openings… (Single defect <5% mortality; multiple defects have mortality risk >20%) |
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AVC Defect=
Atrioventricular Canal Defect
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Description:
Consists of a low ASD and a high VSD Clinical Manifestation: Moderate to severe CHF. Murmur. Treatment: Surgical repair with patch closure Prognosis: Operative mortality is < 10%. Potential problem later with mitral regurgitation. |
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PDA=
Patent Ductus Arteriosus
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Description:
Failure of the ductus arteriosus to close within the first weeks of life. Clinical Manifestation: May be asymptomatic or have signs of CHF Treatment: Surgical closure Prognosis: Very good with less than 1% mortality risk. |
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DEFECT CLASSIFICATION 2:
OBSTRUCTION TO BLOOD FLOW FROM
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Coarctation of the Aorta
Pulmonary & Aortic Stenosis (AS & PS) |
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Coarctation of the Aorta
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Description:
Localized narrowing near the insertion of the ductus arteriosus. Aorta appears pinched. Clinical Manifestation: Higher blood pressure to upper extremities than to lower. Decreased pulses to the lower. Treatment: Surgical treatment the norm. Balloon angioplasty may be tried first. Prognosis: Good with < 5% mortality |
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Pulmonic &
Aortic Stenosis
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Description: Narrowing of the pulmonic or aortic valve…
Clinical Manifestation: AS more symptomatic than PS Poor feeders, weak pulses, tachycardia PS may be asymptomatic or with mild cyanosis Treatment: Surgical correction usually. Balloon angioplasty may be tried first. Prognosis: Good. AS may develop valvular regurgitation. Balloon Angioplasty For Defects With Obstructed Blood Flow Out Of Heart |
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DEFECT CLASSIFICATION 3:
DECREASED PULMONARY BLOOD FLOW
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Tetralogy of Fallot (TOF)
Tricuspid Atresia |
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Tetralogy of Fallot (TOF)
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Description:
Includes 4 distinct defects: 1.VSD... 2.PS... 3.Overriding aorta Aorta positioned right over VSD instead of over the left ventricle 4.Right ventricular hypertrophy Thickening of the wall of the right ventricle Clinical Manifestation: Symptomatic in infancy. Murmur! May be acutely cyanotic @ birth or may develop worsening cyanosis over the first year. “Blue spells” described by parents. “Squatting” behavior with play in toddlers |
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Tetralogy of Fallot (TOF): Tx and Px
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Treatment: Complete repair is needed. Often infants have to undergo a partial repair called a Blalock-Taussig procedure initially.
Prognosis: Good. Operative mortality for complete repair is < 5%. CHF may occur post-op. |
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Tricuspid Atresia
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Description:
Failure of the tricuspid valve (ri-tri remember) to develop, so… No communication from RA to RV Blood flows thru a patent foramen ovale or ASD Clinical Manifestation: Cyanosis is seen in newborn period. Older children have signs of chronic hypoxemia with clubbing. Treatment: Surgical procedure. Prognosis: Surgical mortality varies. Post-op complications include dysrhythmias, pleural & pericardial effusions & ventricular dysfunction. |
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DEFECT CLASSIFICATION 4:
MIXED DEFECTS
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Complex cardiac anomalies!!!
Clarified as mixed because ALL involve mixing of 02 saturated systemic blood with the de-saturated pulmonary blood flow. Transposition of the Great Arteries (TGA) or Transposition of the Great Vessels (TGV) [same thing] Truncus Arteriosus (TA) Hypoplastic Left Heart Syndrome (HLHS) |
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Transposition of the Great Vessels
TGA or TGV… vessels are backwards!
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Description:
The pulmonary artery leaves the LV The aorta exits from the RV No communication between the systemic & pulmonary circulations which means… oxygenated blood not getting to body. Clinical Manifestations: Depends on size & type of defect. Children with minimum communication are severely cyanotic & depressed at birth. Symptoms of CHF. Cardiomegaly presents a few weeks after birth. Treatment: Surgical Repair. Prognosis: Operative mortality is 5-10%. Later risk of dysrhythmias & ventricular dysfunction. |
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Truncus Arteriosus
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Description: Failure of normal septation & division of pulmonary artery & aorta, resulting in a single vessel that overrides both ventricles
Blood from both ventricles mixes in the common great artery, causing desaturation and hypoxemia. Clinical Manifestation: Moderate to severe CHF, cyanosis, poor growth, murmur Treatment: Surgical repair Prognosis: Mortality is > 10%. Future operations always required for complete repair |
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Hypoplastic Left Heart Syndrome (HLHS) *the one you DON’T want your baby to have
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Description:
Complete underdevelopment of L. side of heart (L vent, Aortic valve & aorta) Therefore, L side of heart can’t maintain circulation R side of heart must maintain BOTH systemic & pulmonary circulation Foramen ovale & ductus arteriosus act as a shunt to help initially Once they close… baby dies Clinical Manifestation: Severe symptoms in 1st week of life. Progressive deterioration. Treatment: Prostaglandin given to prevent closure of PDA. Transplantation or 3 stage surgery: Norwood procedure, Hemi-Fontan procedure, then Fontan procedure |
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Transplantation..
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Anti-rejection drugs for the rest of their lives
Kept on prostaglandin until a new heart is found |
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Complications of Congenital Heart Disease
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Congestive Heart Failure
Definition: the inability of the heart to pump an adequate amount of blood to the systemic circulation at normal filling pressures to meet the metabolic demands of the body. Leads to: Volume overload Pressure overload Decreased contractility High cardiac output demand Hypoxemia |
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Compensatory Mechanisms in CHF and Tx
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Hypertrophy of heart muscle (muscle is working harder!)
Sympathetic nervous system is stimulated to try to increase contractility 4 Goals of Treatment: Improve cardiac function by increasing contractility Reduce preload by removing fluid & Na Decrease cardiac demands Improve tissue oxygenation |
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CHF Treatment Pharmacology
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Treatment Goal #1: Improve cardiac function by increasing contractility
Digitalis [usually digoxin (Lanoxin)] Angiotensin-converting enzyme (ACE) inhibitors Captopril, enalapril, etc Treatment Goal #2: Decrease pre-load by removing fluid & Na (diuretics) Lasix (drug of choice)… Causes excretion of Cl & K. Hypokalemia may precipitate digitalis toxicity. Diuril… Can cause hypokalemia & acidosis Aldactone (weak diuretic)… Potassium sparing. Frequently used with Diuril & Lasix. Treatment Goal #3: Decrease Cardiac Demand Maintain normal temperature Prevent infection Decrease stress Prevent skin breakdown Maintain adequate nutrition Treatment Goal #4: Improve Tissue Oxygenation Often involves 02 therapy Careful monitoring of signs & symptoms of decreased oxygenation “Blue spells” “Tet spells” |
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Digitalis
Nursing Implications
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Signs of Digoxin Toxicity in Kids
Nausea Vomiting Anorexia Bradycardia Dysrhythmia Age & Pulse Guidelines to Withhold Dose If a 1 min pulse is < 70 for a school age child If a 1 min. pulse is < 90 for a child 2-4 yrs Younger than that must be determined by the cardiologist Give digoxin 1 hr. before or 2 hrs. after feedings If a dose is missed and more than 4 hrs have elapsed, withhold dose & give next dose @ regular time. If less than 4 hrs, give dose. If a child vomits dose, do not give 2nd. If > 2 consecutive doses missed, notify practitioner. If child acts ill, notify practitioner. |
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Nursing Care CHF
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Treating Hypercyanotic Spells:
Infant held in knee chest position Calm Comforting Approach Administer 100% 02 by mask Morphine if needed |
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Maintaining Adequate Nutrition in Infants with CHD/CHF
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Problems:
Higher caloric needs because of increased metabolic rate Fatigue during feeding poor intake Interventions Fortify calories of formula by concentrating calories… add MCT oil or mix @ higher calorie count… 30 cal/oz rather that 20 cal/oz Feed infant by nipple for specified limited period (20-30 minutes), then gavage feed the remainder of the feeding through NG tube |
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Nursing Care:
Post-Op Surgical Care...family preparation
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NOTHING in pediatric nursing as anxiety producing as caring for a child post-op heart surgery
Specialized training before being allowed access to post-op care even in PICU Generalized knowledge about what to expect is important to provide care to families IV Lines: Peripheral line for infusion of fluids Central line: medications Venous pressure line inserted into the right subclavian or jugular vein to monitor central venous pressure Arterial line for direct measurement of arterial pressure Tubes: ET (endotracheal tube) in place for ventilatory assistance Chest tube to drain fluid from around heart and lungs Foley catheter Incisions: Median sternotomy: splits the sternum Lateral thoracotomy: extends from midaxillary line to scapula Mini-sternotomy: opens the lower half of the sternum. Less invasive. Being used more often than it used to be |
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Nursing Care:
Post-Op Surgical Care...Basics of care,
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Basics of Care:
Frequent VS… usually q 15 mins. Hypothermia right after surgery… Important to warm back up! Observation of cardiac rhythm & monitoring CVP & arterial line pressure Auscultation of breath sounds Monitoring of mechanical ventilation… Suctioning Monitoring & recording chest tube drainage. Analgesics… IV opioid infusions (usually morphine and fentanyl). Also toradol, oxycodone Other IV meds: Inotropic medication, digoxin, diuretics, antibiotics Blood transfusions Monitoring fluids… very finite… includes flushes for the art and CVP lines |
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Nursing Care:
Post-Op Surgical Care...complications
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Surgical Complications:
CHF: digoxin & diuretics Low CO: IV inotropic meds Tamponade (blood or fluid in the pericardial space constricting the heart): prompt removal of fluid by pericardiocentesis Atelectasis: chest physiotherapy, coughing, deep breathing Pulmonary edema: diuretics Pleural effusions: diuretics, chest tube Pneumothorax: chest tube Seizures: antieleptic drugs CVA, cerebral edema, neurologic deficits Infections: antibiotics Anemia: transfusion Postoperative bleeding: clotting factors, blood products |
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Acquired Cardiac Problems
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Bacterial/Infective Endocarditis
Rheumatic Fever Kawasaki Disease |
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Bacterial Endocarditis
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Also called Infective Endocarditis
What Is It? Infection of valves &/or inner lining of heart Source of Infection: Organisms can enter bloodstream from any site of localized infection, but the most common sites: from dental work the urinary tract (post catheterization) the heart (post cardiac surgery) bloodstream from IV catheters left in place too long Pathophysiology: Pathogen enters the bloodstream Settle into & grow on the endocardium Form vegetations, deposits of fibrin, & platelet thrombi May invade adjacent tissues, such as aortic & mitral valves May break off & embolize elsewhere, especially in the spleen, kidney, & CNS |
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Bacterial Endocarditis: s&s, dx, tx, prevention
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Signs & Symptoms : Slow, insidious onset
New Murmur (90%) Unexplained Fever (90%)…low-grade and intermittent Malaise, anorexia, weight loss, sweating Extracardiac emboli formation: Thin black lines under nails (called splinter hemorrhages), Petechiae on oral membranes Red painful nodes on pads of fingers & toes (Osler nodes) Diagnosis: Based on clinical manifestations EKG changes: prolonged P-R interval X Ray evidence of cardiomegaly Lab: Anemia, leukocytosis, elevated ESR, microscopic hematuria Treatment: High dose antibiotics IV for 2-8 wks. Choice of antibiotics based on blood culture. Blood culture is repeated periodically to assess effectiveness. Prevention Life-long prophylactic administration of antibiotics taken 1 hr. before dental procedures (risk for strep viridans) for those most at risk: Previous valve dysfunction Previous heart surgery Previous acquired cardiovascular disorder Drugs of choice: Amoxicillin, ampicillin, clindamycin, cephalexin, cefadroxil, azithromycin, & clarithromycin |
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Rheumatic Fever
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What Is It?
Poorly understood inflammatory disease Develops 2-6 weeks after group A Beta hemolytic streptococcal pharyngitis Self limited autoimmune disease affecting joints, skin, brain, & heart Cardiac valve damage most significant complication… Diagnosis: Criteria known as “Modifications of Jones Criteria” Involves the presence of 2 major manifestations OR One major manifestation & 2 minor manifestations (arthralgia & fever) Treatment: Eradication of streptococci Relief of symptoms Prevention of recurrences Drug of choice: PCN injections Includes monthly prophylaxis of IM PCN… usually until age 18 yrs.!!!! PO Prophylaxis before all dental work lifelong |
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Rheumatic Fever
Signs & Symptoms
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Major Manifestations”
Polyarthritis (swollen, hot painful joints) Carditis (tachycardia, cardiomegaly, new murmur, chest pain, EKG changes) Sydenham’s Chorea (sudden aimless, irregular movements of extremities, facial grimaces, speech disturbance, muscle weakness) Erythema Marginatum (erythematous macules with clear center & well marked border) |
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Vascular Dysfunction:
Kawasaki Disease
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What Is It?
Acute systemic vasculitis Occurs most frequently under age 5 yrs, with peak incidence in the toddler age group Cause is unknown! Thought to be infectious, but is not spread by person to person contact. Most cases occur in late winter & early spring. Without treatment, app. 20% of children develop cardiac sequelae (especially aneurysms) Pathophysiology: Principal area of involvement is cardiovascular system During initial stage of illness: extensive inflammation of the arterioles, venules, & capillaries Later progresses to the formation of coronary artery aneurysms in some kids |
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Kawasaki Disease:
Pick 5 for Diagnosis
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Fever 5 or more days
Bil. Conjunctivitis (no exudate) Strawberry tongue or fissures on lips Abdominal pain Rash Cervical Lymphadenopathy Peeling hands or feet or peripheral edema Swollen joints Vascular aneurysm Cardiac changes |
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Vascular Dysfunction:
Kawasaki Disease
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Acute phase:
Signs & Symptoms: Abrupt onset of high fever unresponsive to antibiotics to antipyretics, followed by development of other symptoms. Child VERY irritable during this stage |
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Nursing Care of Kawasaki
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Monitor cardiac status for development of CHF
Daily wts. & record I & O watching for dehydration. Administer IV gamma globulin (2G/Kg over 8-12 hrs) with frequent VS & monitoring for allergic reactions Shortens duration of fever Decreases risk of aneurysm formation High dose ASA (until fever subsides) Controls fever & joint pain Prevents clotting Low dose ASA ( for several weeks) Continues to prevent clotting during the time when coronary arteries might be enlarging Comfort measures: Irritability MOST challenging issue |
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Vascular Dysfunction:
Kawasaki Disease: Sub-acute phase
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Sub Acute Phase:
Begins with resolution of fever Lasts until all clinical signs have resolved This is the stage when child is MOST at risk for development of coronary artery aneurism (low dose ASA) Frequent EKGs to monitor myocardial & coronary artery status Irritability persists |
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Vascular Dysfunction:
Kawasaki Disease: Convalescent Phase
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Convalescent Phase:
All clinical symptoms have resolved Lab values indicating inflammatory response have not resolved (ESR) This phase is completed when lab values are normal Usually 6-8 weeks after onset |
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Kawasaki Complications
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Coronary artery aneurysm
1-2% mortality rate |
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Pediatric Hypertension
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Previously reported to affect only 0.3%-1.2% of children in the 1970’s & 1980’s
Now affects 5% of children Brady, T., Siberry, K., Solomon, B.: Pediatric Hypertension. Contemporary Pediatrics 2008;25:46. |
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Connection with childhood obesity
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Prevalence increases with BMI percentile
Obese children (BMI percentile >95%) are 3 times more likely to be hypertensive than non-obese children HTN is detectable in 30% of children with a BMI > 95% |
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Defining pediatric hypertension
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Hypertension =
Systolic BP (SBP) and/or Diastolic (DBP) measurements > 95th percentile repeated 3 times (see Harriet Lane for ranges) Pre-Hypertension = SBP and/or DSP between 90-95th percentile repeated 3 times (see Harriet Lane) Adolescents with BP > 120/80 |
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Linkage With Other Risk Factors
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HTN in children is linked to the same cardiovascular risk factors that are commonly recognized in adults:
Insulin resistance High triglycerides (LDL) Reduced high-density lipoprotein (HDL) |
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Staging and treating Pediatric HTN
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Stage 1 HTN:
BP readings 95-99th percentile Stage 2 HTN: BP readings > 99th Percentile These definitions guide treatment Stage 1: Weight reduction of about 10% body mass Anti-hypertensive medication IF: Child is symptomatic Has diabetes Has evidence of end organ damage Stage 2: Referral for complete evaluation Initiation of HTN medications, including: ACE inhibitors Beta blockers Calcium-channel blockers Angiotensin-receptor blockers Diuretics Goal: Target BP < 90th percentile |
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HTN Screening: Who & When & How?(AAP guidelines)
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All children > 3 years of age
All children < 3 years of age IF: History of prematurity History of congenital heart disease, kidney disease or genitourinary abnormality History of recurrent UTI or proteinuria Direct auscultation is superior to automated readings & correct cuff size imperative |
