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Notes Module 5 - Cardiovascular Disorders I. Etiology and Pathophysiology of Fetal to Newborn Circulation: A. Three Fetal Circulation Shunts Ductus venosus – a structure that shunts blood past the portal circulation Foramen ovale – an opening between the right and left atria of the heart Ductus arteriosus – a vessel between the aorta and the pulmonary artery that shunts blood from the PA to aorta * Shunts should close in several days after delivery. B. Fetal Circulation: 1. Main blood flow: Placenta Umbilical Vein Liver Ductus Venosus Inferior VenaCava Right Atrium Foramen Ovale (by pass going to lungs for oxygenation)Left Atrium Left Ventricle Aorta Body 2. Secondary blood flow: Right Atrium Right Ventricle Pulmonary Artery Ductus Arteriosus (bypass going to the lungs because the blood is already oxygenated) Aorta Body 3. Third route of blood flow – very minimal amount Right Atrium Right Ventricle Pulmonary Artery Lungs (needs to perfuse the lungs and upper body with oxygen) Left Atrium Left Ventricle Aorta Body C. Changes in Circulation at Birth The umbilical arteries and vein and the ductus venosus become non-functional Decreased pulmonary vascular resistance and increased pulmonary blood flow Increase in pressure of the left atrium, decrease pressure in right atrium, causing closure of foramen ovale. Pulmonary resistance is less than systematic resistance so there is leftto-right shunting resulting in closure of the ductus arteriosus. II. Congestive Heart Failure: Definition: CHF is inability of the myocardium to circulate enough oxygenated blood to meet the demands of the body. When the heart fails, cardiac output is diminished. Heart rate, preload, contractitility, and afterload are affected. Peripheral tissue is not adequately perfused. Congestion in lungs and periphery develops. Etiology and Pathophysiology: Congenital defects – allow blood to flow from the left side of the heart to the right so that extra blood is pumped to the pulmonary system rather than through the aorta when the ventricle contracts. Obstructive congenital defects – restricts the flow of blood so the heart hypertrophies to work harder to force blood through the narrowed structures. The hypertrophied muscle becomes ineffective. Other defects which weaken the heart muscle. Compensatory Mechanisms: Stimulation of the sympathetic nervous system which releases norepinephrine from the adrenals. This stimulates blood vessels to constrict and an increase in the heart rate. Tachycardia increases venous return to the heart which stretches the myocardial fibers and increases preload. Only successful for short period of time. Increased renin and ADH secretion caused by decrease renal perfusion. Resultant increase in Na and H2O retention to increase fluid to the heart and leading to edema. Assessment: Clinical Manifestations related to cause: I. Pulmonary Congestion Infant tires easily especially with feedings Tachypnea, dyspnea, orthopnea Retractions with respiratory distress, grunting, nasal flaring Wheezing, rales, rhonchi Easy fatigue – especially during feedings, tires with play Restlessness, apprehension, irritable * earliest signs are mild resting tachpnea, difficulty with feeding II. Impaired Cardiac Output Tachycardia, diminished pulses Extremities cool, mottled, pallor Capillary refill > 2 seconds Diaphoretic / sweating Hypotension III. Systemic venous congestion Hepatomegaly, Edema - appears first in face and eyes (periorbital); then peripheral Weight gain IV. High metabolic rate FTH (failure to thrive) Slow weight gain Goals of treatment: Improve cardiac function - increase contractility, make the heart work more efficiently/ Reduce afterload Reduce volume overload, Remove accumulated fluid and Na Decrease cardiac demands Decrease oxygen consumption Therapeutic Interventions and Nursing Care: Improve Cardiac Function- increase contractility and reduce afterload Medication Therapy a. Cardiac glycosides –improves ventricular contraction and decreases heart rate and work load. Main drug given is Digoxin. Nursing Care: Make sure have correct medication. Do not confuse with Digitoxin. Usual type: Digoxin Elixir (0.05 mg/ml). Assess heart rate prior to administration. Hold dose if: infant pulse < 100; child pulse is <80; adolescent pulse is < 60 * If pulse is greater than 100 BPM – GIVE the medication. Two nurses check dosage Assess digoxin levels – normal is 1.0 – 2.0 mg./ml Parent teaching – see p. 1262 Know signs of digitalis toxicity: (cardiac dysrrhythmia is first sign in children. Bradycardia, anorexia, nausea and vomiting, dizziness, weakness). b. ACE inhibitors / afterload-reducing agents: function by inhibiting conversion of angiotension I to II-results in arterial relaxation. By relaxing the arterioles it reduces the impedence to left ventricular ejection (afterload) and improve cardiac output. Capoten(Captoril) Vasotec Nursing care a. Promote rest b. Maintain oxygen therapy and evaluate oxygen saturation Remove Volume Overload / Accumulated Fluid & Na Medication Therapy Diuretics - main stay of therapy. Diuretics enhance renal secretion of sodium and water by reducing circulating blood volume and decreasing preload. o Furosemide (Lasix) – used for rapid diuresis Lasix – give (1mg/kg) IM or IV, check K+ level prior to IV administration because low K+ levels lead to increase chance of developing toxicity, monitor electrolytes, weigh daily, I&O o Chlorothiazide (Diuril) – used for maintenance diuresis o Zarozolyn (Thiazide type) o Spironolactone (Aldactone) Diet Therapy - Fluid restriction may be required, but with caution to prevent dehydration. Infants rarely require fluid restrict Nursing Care a. Measure intake and output – weighing diapers b. Observe for changes in peripheral edema and circulation c. If ascites present – take serial abdominal measurements to monitor changes. d. Skin care e. Turning schedule Decrease Cardiac Demands Reduce metabolic needs Limit physical activity Maintain body temperature Treat infections Minimize work of body o Small frequent feedings o If unable to consume an appropriate amount in 30 minutes of feeding, stop feeding. NG tube feedings may be considered. o Organize care Improve Tissue Oxygenation All previous measures Supplemental cool humidified oxygen Cardiac Disorders: Cardiac disorders in children are divided into two major groups: congenital heart disease and acquired heart disorders. III. Congenital Heart Diseases Main classifications of Congenital Heart Disease and Underlying Pathophysiology: 1. Defects that increase pulmonary blood flow Abnormal opening between cardiac chambers or greater arteries Increase volume overload on right side of heart Cardiac workload increases to compensate for volume overload Increased pulmonary blood flow Obstruction of blood flow from ventricles causes ventricular hypertrophy, dilation Major problem is congestive heart failure 2. Defects with decrease blood flow and mixed defects Narrowing or constriction of an opening (valve or vessel) obstructing blood flow Pressure rises in the area behind the obstruction Increase in cardiac workload Ventricular strain Obstruction on the left side of the heart can cause decrease perfusion to the body 3. Defects obstructing systemic blood flow Obstruction on the right side of the heart decreasing the amount of blood volume to the lungs Decreased oxygen saturation to the left side of the heart Cynanosis Defects that increase pulmonary blood flow 1. Patent Ductus Arterious PDA: Pathophysiology: Failure of the fetal ductus arterious to close completely at birth. Stimuli for closure include: Increased oxygen levels in the blood when the baby breaths normally Decreased prostaglandin levels Usually closes after birth Degenerates to a ligament When the ductus fails to close Oxygenated blood from the aorta returns through the PDA to the pulmonary arteries to the lungs Left to right shunting Increased cardiac workload on left side of the heart Increased pulmonary blood flow – congestive heart failure Signs and Symptoms: Continuous heart murmur – often the first indication of a congenital heart defect. Signs of congestive heart failure Increase in respiratory infections Therapeutic interventions Medication Therapy a. Intravenous Indomethacin (Indocin) - a prostaglandin inhibitor, to promote ductal constricture. 60% successful in 1st 14 days Cardiac Catheterizaton / Transcatheter closure a. Coil placed that promotes occlusion of the ductus arteriosus b. Corrective measure that is less invasive than surgery Pre-care: History and Physical Lab work – EKG, ECHO cardiogram, CBC NPO Preprocedural teaching Post Care: Monitor vital signs Monitor extremity distal to the catheter insertion, Keep leg immobilized Vital signs Check for bleeding at insertion site, pressure dressing for first 24 hours. Measure I&O – force fluids. Fluids increase elimination of the contrast dye from the body. Surgical Intervention a. Open heart surgery / Surgical ligation of ductus via left thoracotomy incision. Pre-operative Nursing Care: 1. Extensively prepare the child and the parents for the experience demonstrate tubes and bandages and describe the scar the operation leaves 2. Teach coughing and deep breathing to the child 3. Conduct the child and the parents on a tour of the intensive care unit and introduce them to the staff 4. Observe the child for signs of infection 5. Make sure all laboratory tests are completed Post-operative Nursing Care 1. Maintain adequate pulmonary function o Keep patent airway o Patient should deep breathe and cough. Monitor use of IPPB. o Suction if necessary o Oxygen - adequate to cells o Chest suction for refilling lungs. Care of chest tubes o Check rate and depth of respirations o Check water-seal chest drainage 2. Maintain adequate circulatory functioning o Check vital signs o Replace blood where necessary o Check intake and output every hour 3. Provide for rest through organized care 4. Establish adequate hydration and nutrition; fluid and electrolyte balance 5. Take measures to prevent post-operative complications o Turn patient frequently o Skin care o Check extremities for occlusions of major vessels with blood clots: cyanosis, paleness of extremity, or coldness to the touch o Passive range of motion o Check dressing for signs of hemorrhage 6. Prepare for discharge 2. Atrial Septal Defect ASD: Pathophysiology: Involves defects that occur during the development of the atrioventricular canal with an opening located between the atriums. o A Patent foramen ovale happens in 20 percent of all births, a slit-like opening remains in the atrial septum. This defect is usually functional murmur and requires no surgical intervention. Left to right shunting through the defect Enlarged right atrium Increased pulmonary blood flow – congestive heart failure Signs and Symptoms: Frequently asymptomatic if there are no other abnormalities Signs of congestive heart failure may develop later in life Increased respiratory infections Therapeutic Interventions and Nursing care: Medical management a. Watched closely by cardiologist – assess for spontaneous closure in first year of life. Cardiac catheterization a. Amplatzer Septal Occluder. Small round mesh device loaded into the tip of a special catheter placed in heart via cardiac catheterization. Once it is in place the device is deployed and attaches to rim of tissue around defect. Tissue will eventually cover the device and close the defect. Surgical Intervention a. Surgical closure with sutures or patch 3. Ventricular Septal Defects VSD: Pathophysiology: Abnormal opening between the ventricles The majority of defects occur in the membranous septum of the ventricles, and severity is related to the size of the defect and amount of pulmonary blood flow. Left to right shunting. Blood flows from Left ventricle through defect to the right ventricle and re-circulated via pulmonary artery to the lungs causing increase in pulmonary congestion. Signs and Symptoms: Depend on the severity Tachypneic, diaphoretic, fatigues easily, underweight for age, tires before feeding completed. More severe have congestive heart failure Therapeutic Interventions and Nursing care: Usually requires no treatment – closes first few years of life. Treat the congestive heart failure Surgical a. Closure with sutures or patch via cardiopulmonary bypass surgery Defects with decrease blood flow and mixed defects 1. Pulmonic Stenosis Pathophysiology: Pulmonic stenosis - Lesion that obstructs the flow of blood from the right ventricle usually by narrowing of entrance to the pulmonary artery leads to right ventricular hypertrophy Aortic - Lesion that obstructs the flow of blood from the left ventricle usually by narrowing of entrance to the aorta which can lead to left ventricle hypertrophy. Signs and Symptoms Depend on severity Usually asymptomatic and have normal growth and development Can manifest EKG abnormalities with exertion Murmur Therapeutic Interventions: Medications Prostaglandins to keep the PDA open so some oxygenation can occur Cardiac catheterization a. Baloon valvuloplasty – special catheter with balloon end is passed through the heart into the defective valve and then balloon dilates stenotic valve. Stents may be placed also. Surgery a. Valvotomy 2. Tetralogy of Fallot: Pathophysiology: Most common cyanotic heart defect in children over 2 years of age. Contains these 4 anomalies: Ventricular septal defect Dextroposition of aorta so that it overrides the defect Hypertrophy of right ventricle Stenosis of the pulmonary artery Hemodynamics - a right to left shunt arises in this anomaly due to the position of the aorta and the hypertrophied right ventricle thus, partially unoxygenated blood is sent back to the systemic circulation through the VSD Signs and Symptoms: 1. Retarded growth and failure to thrive 2. Lack of energy 3. Frequent infections 4. Polycythemia 5. Clubbing of fingers 6. Squatting 7. Cerebral abscess 8. Blood pressure 9. Cardiomegaly 10. Cyanosis Therapeutic Interventions and Nursing Care: . Surgical Interventions 1. Palliative - Blalock-Taussig or Potts procedure, which increases blood flow to the lungs. Creates an artificial PDA. 2. Open-heart surgery for corrective treatment of pulmonary stenosis and vsd 3. Survival depends upon mixing of blood from pulmonic and systemic circulation 3. Transposition of the great arteries: The aorta arises from the right ventricle, and the pulmonary artery arises from the left ventricle - which is not compatible with survival unless there is a large defect present in ventricular or atrial septum. Nursing Diagnosis and Goals: Alternation in cardiac output: decrease R/T heart malformation Child will maintain an adequate cardiac output AEB: 1. RR (state specific highest and lowest range) 2. B/P (state specific highest and lowest range) 3. clear equal breath sounds 4. 5. 6. 7. 8. 9. 10. O2 sat as specified Monitor weight inappropriate weight gain (<30G/day), absence of puffy eye lids skin warm to touch capillary refill 2-3 seconds adequate urinary output (state amount, .5-2ml/kg/hr) or 0 > 60% of I Maintain S.G. 1.005-1.018 Absence of S & S of CHF as sited earlier Therapeutic Interventions and Nursing Care: V.S. Maintain Temp to avoid excessive 02 consumption Assess for S&S as listed above I&O, output > 60% of intake Assess Specific gravity of urine Administer Cardiac drugs Notify Dr. if any deterioration Elevate HOB 30% Check labs Organize care to provide periods of rest; provide outlets like dolls, reading Give small frequent feedings Assess and record child/family knowledge of participation in care including: meds, HOB elevated, rest periods, I&O, S&S of decreased cardiac output 4. Truncus arteriosus: A single arterial trunk arises from both ventricles that supplies the systemic, pulmonary, and coronary circulations. A VSD and a single, defective, valve also exist. Entire systemic circulation supplied from common trunk Defects Obstructing Systemic blood flow: 1. Coarctation of the Aorta Pathophysiology: Coarctation applies to any constriction /narrowing of the lumen of the aorta. Obstruction to left ventricular output impeding systemic blood flow Left ventricular hypertrophy Pressure in ventricle and great artery increased before obstruction decreased beyond obstruction Pulmonary edema Signs and Symptoms Increased B/P in upper extremities Decreased B/P in lower extremities. Radial pulses, full bounding pulses. Femoral or popliteal pulse weak or absent Leg pains occur under exertion, weakness or tingling in lower legs Fatigue Headache, nose bleeds Therapeutic Interventions Baloon dilation with possible stent placement of the coarctation Open heart surgery with surgical reconstruction of the aorta . 2. Hypoplastic left heart: May have various left-sided defects, including coarctation of the aorta, aortic valve & mitral valve stenosis or artresia IV. Acquired Cardiac Diseases A. Rheumatic Fever: Etiology and Pathophysiology: A systemic inflammatory (collagen) disease of connective tissue that usually follows a group A beta-hemolytic streptococcus infection. This disorder causes changes in the entire heart (especially the valves), joints, brain, and skin tissues. Assessment: Clinical Manifestations and Diagnostic tests: Jones Criteria – utilized for diagnosis. There is no single clinical pattern. Two major criteria, or one minor criteria are necessary for a positive diagnosis Major criteria: o Carditis, valvulitis o Polyarthritis – knees, ankles, hips, shoulders o Chorea o Erthyema marginatum o Subcutaneous nodules Minor criteria: o Fever o Arthralgia-large joints, usually knees, wrists, elbows o Previous rheumatic fever or rheumatic heart disease o Elevated erythrocyte sedimentation rate o Positive C-reaction protein o P-R interval prolonged o Antistreptolysin O titer - elevated Supporting Evidence o Recent scarlet fever o Positive throat culture for group A streptococci o Increased strep antibodies Therapeutic Interventions: Medication Therapy a. Antibiotic therapy for at least 5 years after attack with no residual heart disease such as Penicillin or erythromycin b. ASA for joint symptoms and relieve pain c. Protection through use of antibacterial prophylaxis - penicillin Nursing Interventions ** It is important that nurses teach measures in prevention of Rheumatic fever. Teach parents that if child has a strep infection – emphasize the importance of giving entire course of antibiotics and do not discontinue because child feels better. Assess compliance to medication therapy Bed rest Prevention further infection 2. Subacute Bacterial Endocarditis / Ineffective Endocarditis: Etiology and Pathophysiology: An infectious disease which involves abnormal heart tissue, particularly rheumatic lesions or congenital defects. Microorganisms grow on the endocardium, forming vegetations, deposits of fibrin, and platelet thrombi. The lesion may invade adjacent tissues such as aortic and mitral valves. Assessment: Clinical Manifestations: Insidious onset of symptoms Fever Lethargy General malaise Anorexia Splenomegaly Retinal hemorrhages Heart murmur – 90% Diagnosis: Blood cultures Therapeutic Interventions and nursing care: Medication Therapy 1. Large dose of Antibiotic therapy – Penicillin, Amoxicillin, Clindmycin Nursing Care 1. Bed rest 2. Teach to notify dentist prior to dental work. C. Kawasaki Disease: Etiology and Pathophysiology: Also known as mucocutaneous lymph node syndrome, is an acute systemic inflammatory illness. Multisystem vasculitis – inflammation of blood vessels in the body especially the coronary arteries with antigen-antibody complexes. Does not appear to be contagious, however there is often a preceding upper respiratory tract infection. Cause is unknown, although it is associated with an immunologic response to infectious agents. Complications include: CHF, aneurysms, coronary thrombosis Assessment: Clinical Manifestations: Three phases of the disease: 1. ACUTE PHASE - 10 to 14 days- characterized by: Rapid onset of fever that persists for more than 5 days (generally 38.3-39.9 C or 101-104F) and does not respond to antibiotic treatment. Bilateral conjunctivitis lasting 3-5 weeks Rash on day 5 of illness, usually macular spreading from extremities to trunk Cervical lymphadenopathy Irritability, lethargy Anorexia, possibly; diarrhea, hepatic dysfunction Acute pericarditis Hands and feet are edematous and red. Red throat 2. SUBACUTE PHASE - 10-25 days - fever disappears and most symptoms resolve, characterized by Continued irritability Anorexia, diarrhea Arthritis and arthralgia Lip cracking and peeling – strawberry tongue Desquamation of the extremities palms and soles Cervical lymphadenopathy with large nodes Possible coronary aneurysms, with potential for thrombosis formation. 3. CONVALESCENT PHASE - 25-60 days. Disease is self-limiting, the signs of illness decrease and disappear. Transverse lines called Beau’s line form on the nails Lasts until the erythrocyte sedimentation rate returns to normal and all S&S of the illness disappear Diagnostic tests: ECG, Echocardiogram CBC, WBC increased PT- elevated ESR- elevated SGOT, SGPT- both elevated RT hepatic dysfunction IgA, IgG, and IgM elevated Therapeutic Interventions and Nursing Care: Medication Therapy – given to decrease aneurysm formation and fever a. Aspirin therapy – 100 mg/kg/day in four doses until fever resolved, then doses decrease for 6-8 weeks or until aneurysms gone. b. Gamma globulin - High dose IV (IVGG) Nursing Interventions 1. Monitor VS including B/P 2. Assess oral mucous membranes and lubricate the lips, and give small frequent feedings of soft, bland foods and liquids. 3. Assess body rash and extremities and provide skin care 4. Give antipyretics as ordered 5. Monitor I & O 6. Decrease stimulation 7. Provide comfort measures - cool compresses and tepid sponge baths - passive ROM to facilitate joint movement Discharge Teaching 1. Aspirin for anticoagulant therapy, interventions for elevated temp. 2. Skin care and comfort measures 3. F/U for ECGs, echocardiograms, CXR every 3 months for 1 year 4. Call Dr. if: chest pain, SOB, dizziness, change in behavior, not eating or drinking, illness, or any other concerns. Summary for all heart disorders: General Principles that apply to all heart conditions: 1. 2. 3. 4. Encourage normal growth and development Counsel parents to avoid overprotection Deal with parents’ concerns and anxieties Educate parents about conditions, tests, planned treatments, medications 5. Assist parents in developing ability to assess child’s physical status