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NSG 309 Peds
CH 22 - Cardiovascular
| Question | Answer |
|---|---|
| Fetal circulation | - Pulmonary blood vessels are constricted - Systemic blood vessels are dilated w/ low resistance - Large ductus arteriosus - Patent foramen ovale - Patent ductus venosus |
| Patent foramen ovale | opening between the heart's upper chambers (atria) to allow heart to bypass lungs during fetal development - congenital defect in infants if not closed |
| Patent ductus venosus | rare congenital vascular defect where the fetal ductus venosus fails to close after birth - allows blood to bypass fetal liver - connects umbilical vein to ICV |
| Neonatal circulation | - Pulmonary vasculature dilated - Increased vascular resistance/arterial pressure/systemic blood volume - Ductus arteriosus close 2-5 days post-birth - Foramen ovale closes -> blood flow reverses - Ductus venosus closes |
| Patent ductus arteriosus | - common congenital heart defect - connects aorta to the pulmonary artery -> O2 rich blood backflow from aorta to pulm artery - Increased pulmonary blood flow disorder - Tx with IV NSAID, surgical ligation |
| Cardiovascular assessment of peripheral vascular system | Skin: Color, pulse, turgor/edema (fluid status) - Activity - Capillary refill/pulse |
| assessment of Cardiovascular system | - HR and heart rhythm - Adventitious lung sounds - Heart sounds (S1/S2, murmurs, S3/S4) - Chest assessment |
| Cardiac output | - Rate dependent d/t decreased pressure and volume - High heart rate and low blood pressure at birth - HR decrease + BP increase with age the smaller the person the faster their hearts pump + breathe |
| Prostaglandin E | relax smooth muscle to prevent PDA closure - Needed when conditions require open PDA or blood mixing |
| NSAIDs | Indomethacin/Ibuprofen - Close PDA (block prostaglandin E) - Allows for smooth muscle contraction to close openings |
| Inotropes | Alter force of cardiac contractions to improve cardiac output - treatment for heart failure - Eg. Digoxin |
| Congenital defects causing increased pulmonary blood flow | - Patent ductus arteriosus - Atrial septal defect - Ventricular septal defect - Atrioventricular canal |
| Congenital defects causing decreased pulmonary blood flow | - Pulmonic stenosis - Pulmonic atresia - Tetrology of Fallot - Tricuspid atresia |
| Congenital defects causing systemic vascular obstruction | - Aortic stenosis - Coarctation of aorta - Mitral stenosis - Interrupted aortic arch |
| Congenital defects causing mixed blood flow | - Hypoplastic left heart syndrome - Transposition of great arteries - Truncus arteriosus - Total anomalous pulmonary venous return |
| Clinical presentations of increased pulmonary blood flow defects | - Elevated HR/RR - Increased URI - Diaphoresis - Heart murmur - Poor weight gain - Heart failure |
| Clinical presentations of decreased pulmonary blood flow defects | - cyanosis (hypercyanotic episodes) - Polycythemia |
| Hypercyanotic episodes | AKA "Tet spells" - rapid O2 sat drop - closely related to Tetrology of Fallot |
| Clinical presentations of systemic vascular obstruction defects | - Diminished pulse/poor capillary refill - Poor color - Heart failure - Pulmonary edema |
| Clinical presentations of mixed blood flow defects | - Cyanosis - Poor weight gain - Pulmonary congestion - Heart failure |
| Increased pulmonary blood flow defects pathophysiology | - O2 rich blood mixed with low O2 blood - Left to right shunting (high to low pressure) S/S: failure to thrive, edema, tachypnea, increased work of breathing, murmur, cardiomegaly - eg. PDA or ASD |
| Atrial septal defect pathophysiology | Opening between upper heart chamber causes increased pulmonary blood flow - Left to right shunting - small defects may close spontaneously Tx: surgical patch placement |
| Ventricular septal defect pathophysiology | Opening between lower heart chamber cause increased pulmonary blood flow -> heart failure - Left to right shunting - May spontaneously close Tx: inotropes (for heart failure), VSD patch (3-12 months) |
| Atrioventricular canal pathophysiology | Combined atrial + ventricular defect + abnormal AV valves - Partial vs complete defects - Possible bidirectional shunting - AKA endocardial cushion defect - Need lifelong ppx for infective endocarditis! Tx: Surgical repair (within 12 months) |
| Decreased pulmonary blood flow defects pathophysiology | Obstruction of blood flow to the lungs - Right to left shunting S/S: hypercyanotic spells, hypoxemia, polycythemia (compensation) - Eg. Pulmonic stenosis/atresia |
| Pulmonic stenosis pathophysiology | Right ventricular outflow obstruction - Subvalvular vs. valvular vs. supravalvular - Need lifelong endocarditis ppx Tx: Surgical intervention, CHF management |
| Pulmonary atresia pathophysiology | - Underdeveloped pulmonic valve -> hypoplastic right ventricle - Severe hypoxia risk Tx: prostaglandins (keep PDA open), palliative repair -> surgical repair |
| Tetralogy of Fallot pathophysiology | Dx requires 4 congenital defects - Pulmonic stenosis - RV hypertrophy - Overriding aorta - VSD - Possible open foramen ovale/ASD S/S: rapid O2 drop (d/t decreased systemic venous flow) Tx: surgical repair |
| Tricuspid atresia pathophysiology | - Incomplete tricuspid valve -> unconnected RA/RV - ASD present Tx: STAT prostaglandin, HF management, 3 stage surgical repair (3 separate surgeries at 3 separate ages of life) |
| Hypercyanotic spells | S/S: bluish or gray skin/nail/lip coloration Management: knee chest position, O2, IV fluid - morphine sulfate (IV/SC) -> decrease infundibular spasm - propranolol (IV/PO) -> lower HR |
| Infundibular spasm | - muscle under pulm valve - commonly seen in Tet spell |
| Coarctation of aorta pathophysiology | - aortic narrowing (systemic blood flow obstruction) - impaired perfusion when PDA closes S/S: high UE BP and low LE BP Tx: surgical repair |
| Aortic stenosis pathophysiology | - aortic valve narrowing (systemic blood flow obstruction) - Need exercise restriction Tx: surgical repair, balloon valvuloplasty |
| Transposition of great arteries pathophysiology | - Arteries connected to wrong ventricles - Must have another defect to keep blood flow/O2 mixing (cause mixed defect) Tx: Prostaglandins (keep PDA open until surgical repair) |
| Truncus Arteriosus pathophysiology | Single large artery w/ large VSD (mixed blood flow) - activity limitation Tx: HF treatment, surgical repair |
| Hypoplastic left heart syndrome | - Underdeveloped (hypoplastic) left side of heart (mixed blood flow) - Need open PDA Tx: Surgical repair |
| Nursing considerations for CV disorder | - appropriate pain intervention (esp. post op) - Adequate oxygenation (decrease cardiac output = decrease perfusion) - Monitor protein/vitamin intake w/ small frequent meals - OT/PT for motor milestones - Play/socialization w/ peers for psychosocial development - Provide emotional/psychosocial support using support groups/social workers PRN |
| Cardiac catheterization purpose | - Eval pressure/location of abnormal opening; pressure in structures; O2 sat in chambers - Repair - Commonly R side cath w/ contrast media (femoral vein -> RA) |
| Cardiac cath pre-op | - Consent - NPO status 4-6+ hours - Iodine/shellfish allergy check - Assess skin around groin - Baseline VS + O2 sat - Mark pedal pulse - Administer sedation/analgesics - Void on call (if potty trained) |
| Cardiac cath post-op | - VS check Q15m x 4hr -> Q30m x 4hr -> Q1h x 4h-> Q4h x 16h - Apical pulse (check arrhythmia/tachycardia) - Low BP = hemorrhage - Assess peripheral pulse/LOC/color + warmth of extremities - Pressure dressing x 24hr - Pressure 1" above site if bleeding + call MD - Post op mobility restriction: decrease leg movement + hip flexion for 4-6 hrs - I/Os (contrast = diuretic) - Glucose check for possible hypoglycemia |
| Contrast dye | - Function as diuretic (important in infants) - Nephrotoxic in nature - Fluids for clearing dye |
| Heart failure | - usually d/t structural/functional impairment |
Created by:
sleepingbear