gFlashcards

heart begins to form (before brain). Blood circ begins. Primitive RBC’s circulate. Tubular heart beats by 24 days.

• Atrial divisions (heart chambers are present). Fetal heart beat detectable. Groups of blood cells identifiable.

• Development of heart complete. It will grow and refine in structure but it wont grow any new parts. Newborn heart is larger than adult (%). Doubles in size by 5 years. 4 times original size by 9.

presymptomatic phase of arteriosclerosis. 176 serum cholesterol puts a child at moderate risk.

-History of frequent respiratory infections. - Poor weight gain. (organic failure to thrive) - Exercise intolerance. - Dusky color or cyanosis. - Finger and/or nail clubbing. (picture page 1487). (from lont-term poor peripheral circulation) - the younger the symptoms appear the more severe the circulatory alteration.

Definition- Inability of the heart to pump adequate amount of blood to the systemic circulation to meet cellular and tissue needs. Can be structural (usually). 50% of kids with CHF are less than 1 month old. Mixed right and left side is common.

Decreased Cardiac output (usually structural defect) leads to compensatory mechanisms which lead to sympathetic nervous system circulation (increased HR and force. Increased venous return, tone, sweating) this all leads to decreased Cardiac output and decreased renal perfusion

Circulation- tachycardia (>160 beats resting). Gallop rhythm. Decreased blood pressure. Pale, cool extremities, generalized edema.

Tachypnea, moist and grunting respirations. Nasal flaring. Costal retractions. Orthopnea. Cyanosis, Wheezing, cough, gasping/grunting (late sign). Other- Sudden wt gain. Feeding and/or activity intolerance. Fatigue. Irritability. Excessive sweating (particularly of scalp due to sympathetic stimulation).

1. improve cardiac function. 2. Remove accumulated fluid and sodium.
2. Decreased Cardiac output (to reduce stress). 4. Improve tissue oxygenation. 5. Decreased oxygen consumption.

Lanoxin (digoxin). Narrow margin of safety. More incidence of toxicity with kids. Premies more susceptible. Has a short half-life and rapid onset so it goes away fast. (this is good).

Bradycardia, N/V. Diarhea, dysrythmias, excessive saliva (drooling), abd pain, decreased blood pressure, HA, Drowsiness, fatigue, confusion, vision changes (green-yellow halos around objects, blurred vision, light flashes, double vision). The problem with looking for symptoms is that 50% are less than one month old. They cant talk. These symptoms duplicate CHF anyway.

Adults .5-2.5 mcg/ml. Child- .8-2.0 mcg/ml (until around 12).

• Premie= 5mcg/kg/day. Fullterm infant= 8-10mcg/kg/day. 10yrs= .125mg/day.

less than 90bpm in infant,

reduce preload. Lasix, Diuril, aldactone. Watch for K levels. Furosemides and thiamides cause a decreased potassium level and low

enhances the effects of digoxin which leads to a higher risk of toxicity. Increased K will decrease digoxin effects

8-10/1000 live births have this. 2-3 times more common in premies. 90% of the causes are of unknown origin.

sibling or parent with congenital heart defect or chromosomal abnormalities. Downs (40-50) Any trisomal (like downs) 80%. Fetal ETOH syndrome=heart defects.

Mother who has had rubella or other viral infections. Mothers poor nutrition. ETOH. Greater than 40 years old. Insulin dependent diabetic. Ingestion of lithium (antipsychotic drug). It has a teratogenic effect.