Ravilya_Pediatrics_ Cardiology Medication

Front 1

Most potent pulmonary vasodilator:
Other dilators are

Back 1

Most potent pulmonary vasodilator: oxygen. Other dilators are alkaline pH, nitric oxide, low CO" and vasoactive substances

Front 2

A child has improved significantly with digoxin therapy for VSD with failure, grown normally, andgained weight. Would you increase the doses for weight gain?

Back 2

A child has improved significantly with digoxin therapy for VSD with failure, grown normally, andgained weight. Would you increase the doses for weight gain? No. Try to discontinue medication if clinical condition permits.

Front 3

A child is receiving digoxin. EKG reveals prolonged PR intervals. How do you manage patient? (important)

Back 3

A child is receiving digoxin. EKG reveals prolonged PR intervals. How do you manage patient? (important) A delay in administering next doses or a reduction in dosage should be considered. Digoxin should not be withheld, if patient's clinical condition is normal. However, serum digoxin level should be obtained, and hypokalemia and hypercalcemia should be excluded because they canexacerbate digoxin toxicity. (A normal level in aninfant is2-4 ng/ml andinolder children 1-2 ng/ml.)

Front 4

Ideal time obtaining blood to measure a digoxin level (important):

Back 4

Ideal time obtaining blood to measure a digoxin level (important): immediately before next dose and at least 4 hours after last dose to achieve tissue-plasma equilibrium.

Front 5

A child develops arrythmia after digoxin therapy:

Back 5

A child develops arrythmia after digoxin therapy: digoxin toxity must be ruled out, and next dose should not be given to patient. (

Side-effects of chronic furosemide therapy for congestive heart failure (important): hypokalemia and contraction of extracellular fluid volume resulting in a "contraction alkalosis." Management: postassium supplementation, discontinue furosemide, resume spironolactone which is a potassium-sparing diuretic. Acombination ofspironolactone and chlorothiazide canbeused. Isolated chlorothiazide therapy is less effective. Please remember, furosdemide is most commonly used diuretic in congestive cardiac failure.

Front 6

Side-effects of chronic furosemide therapy for congestive heart failure (important):

Back 6

Side-effects of chronic furosemide therapy for congestive heart failure (important): hypokalemia and contraction of extracellular fluid volume resulting in a "contraction alkalosis." Management: postassium supplementation, discontinue furosemide, resume spironolactone which is a potassium-sparing diuretic. A combination of spironolactone and chlorothiazide can be used. Isolated chlorothiazide therapy is less effective. Please remember, furosdemide is most commonly used diuretic in congestive cardiac failure.

Front 7

Most important sign of digoxin toxicity in children(important):

Back 7

Most important sign of digoxin toxicity in children(important): arrythmia. Any kind of arrythmia can occur, but atrial arrythmia is most common in infants. Other signs of toxicity include visual symptoms, diarrhea, dizziness, and less frequently nausea, vomiting; hypokalemia and hypercalcemia exacerbate digitalis toxicity. TREATMENT: first discontinue digoxin; give Digiband (digoxin-specific Fab antibodies) is preferred therapy.
(a)
Potassium for hypokalemia
(b)
Diphenylhydantoin for arrythmia of supraventricular origin
(c)
Lidocaine for ventricular arrythmia of supraventricular origin
(d)
Cardioversion for ventricular flutter and fibrillation



Drug that most commonly causes cardiotoxicity: doxorubicin or adriamycin. It produces cardiomyopathy months or even years after therapy. It causes (L) ventricular and (L) atrial enlargement. Doxorubin plus radiation therapy cause more damage to heart.
103.
How to diagnosis digoxin toxicity: it is mostly a clinical diagnosis supported by EKG. Do notuseserum levelasprimarymeans of diagnosis. Levels above 2.0 ng/ml in older children and above 4.0 ng/ml increase risk of toxicity. Serum digoxin level is useful in impaired renal function, inadequate response to standard doses, noncompliance, suspected toxicity, excessive ingestion of digoxin, anddruginteractin such asquinidine.
104.
Side effect ofisoproterenol: myocardial ischemia andnecrosis (newborns)

Front 8

Drug that most commonly causes cardiotoxicity:

Back 8

Drug that most commonly causes cardiotoxicity: doxorubicin or adriamycin. It produces cardiomyopathy months or even years after therapy. It causes (L) ventricular and (L) atrial enlargement. Doxorubin plus radiation therapy cause more damage to heart.

Front 9

How to diagnosis digoxin toxicity:

Back 9

How to diagnosis digoxin toxicity: it is mostly a clinical diagnosis supported by EKG. Do not use serum level as primary means of diagnosis. Levels above 2.0 ng/ml in older children and above 4.0 ng/ml increase risk of toxicity. Serum digoxin level is useful in impaired renal function, inadequate response to standard doses, noncompliance, suspected toxicity, excessive ingestion of digoxin, and drug interactin such asquinidine.

Front 10

Side effect of isoprotereno

Back 10

Side effect of isoproterenol: myocardial ischemia and necrosis (newborns)

Front 11

A premature infant with bronchopulmonary dysplasia (BPD) receiving corticosteroid therapy: what may develop

Back 11

A premature infant with bronchopulmonary dysplasia (BPD) receiving corticosteroid therapy: may develop transient hypertrophic cardiomyopathy, which usually resolves rapidly with discontinuation ofcorticosteroid

Front 12

First effect seen when digoxin is used:

Back 12

First effect seen when digoxin is used: reduced heart rate and then prolonged P-R interval. Digoxin toxicity also causes vomiting, diarrhea, depression, diplopia, blurred vision, yellow or green vision, andphotophobia. TREATMENT: discontinue digoxin; give Digiband (digoxin-specific Fab antibodies

Front 13

Side-effects of indomethacin:

Back 13

Side-effects of indomethacin: oliguria, increased serum urea nitrogen and creatinine, low platelet and platelet dysfunction, GI bleeding, ulcers, GI perforations, high BP, edema, oliguria, renal failure, high K, andbone marrow suppression.

Front 14

Most common complication of prostaglandin 1

Back 14

Most common complication of prostaglandin 1 (important for Board examination): apnea. Please remember, elevated prostaglandin levels can cause hypertrophic pyloric stenosis. For patients who develop apnea, endotracheal intubation is indicated.