click below
click below
Normal Size Small Size show me how
Cardiotonic drugs
pharm exam 3: drugs affecting cardiac circulation in heart failure
Questi | Answer |
---|---|
define automacity | ability to spontaneously initiate an electrical impulse without external stimuli (self-excitement) |
3 properties of the heart | automaticity; conductivity; refractoriness |
define conductivity | ability to transmit action potential from cell to cell |
where does conductivity exists | in heart muscles and electrical conductions system |
define refractoriness | people during cardiac cycle during which a stimulus fails to produce an action potential |
normal cardiac output volume | 4-8 L/minute |
What part of the heart does the sympathetic nervous system innervate? | all of the heart |
What part of the heart does the parasympathetic nervous system innervate? | AV node, atria, little in the ventricle |
hormones that affect cardiac output | epinephrine, norephinephrine, acetylcholine |
normal stroke volume | 70 mL/beat |
3 factors affecting stroke volume | preload, contractility, afterload |
define preload | ventricular filling |
define contractility | ventricular contraction |
define afterload | systemic vascular resistance |
define Starling's Law | degree of stretch = stretching the myocardial fibers during diastole will increase the force of contraction during systole |
Starling's Law describes the increase in... | preload |
inotropic drugs affect what factor in stroke volume? | contractility |
effects of + inotropic drugs | strengthens contractility |
effects of - inotropic drugs | decreases contractility |
chronotropic drugs affect what part of cardiac output? | heart rate |
effects of + chronotropic drugs | increases heart rate by increased impulses from SA node |
effects of - chronotropic drugs | decreases heart rate by decreased impulses from SA node |
dromotropic drugs influence what? | conduction |
effects of + dromotropic drugs | speeds conduction |
effects of - dromotropic drugs | slows conduction |
5 forms of heart problems | heart failure; hypertension, arrhythmia, angina, myocardial infarction |
define heart failure | heart is no longer pumping enough blood for metabolic demands of the body |
define hypertension | elevated BP |
What causes elevated BP in hypertension | blood volume is greater compared to space available inside blood vessels |
define arrhythmias | electrical conduction problems that occur when pathways malfunction |
define angina | chest pain; way of signaling that some of heart cells are not getting enough oxygen |
define myocardial infarction | damage to heart muscle due to ischemia (lack of oxygen) |
another name for cardiotonics | cardiac glycosides |
prototype for cardiotonic (cardiac glycosides) | digoxin (lanoxin) |
other names for digitalis | foxglove; cardiotonics; cardiac glycosides |
What was digitalis (foxglove) initially prescribed for? | dropsy (edema) |
primary action of digitalis (foxglove) | on the heart; duresis occurs following improved circulation |
dynamics of digoxin (Lanoxin) | more influx of calcium into cells |
How does digoxin increase force of contraction? | more complete systolic emptying; heart size decreases; increased kidney perfusion |
What happens when force of heart contraction is increased? | CO increases; systolic emptying is more complete; heart size decreases |
What causes duresis with digoxin? | increased kidney perfusion |
What property of digoxin allows for increased force of contraction? | + ionotropic = increased cardiac output |
How does digoxin increase vagal activity? | conduction through AV node is decreased and refractory time is prolonged |
What properties of digoxin allow for increased vagal activity? | - dromotropic; - chrontopic |
EKG signal seen with use of digoxin symbolizing increased vagal activity | prolonged p-r interval |
uses for digoxin | congestive heart failure; atrial dysrhythmias |
Kinetics of digoxin | po - absorption 2 hours IV - 10 minutes |
Why can digoxin lead to accumulation | widely distributed; bound to albumin in blood |
clinical manifestations of heart failure | weak, rapid heart rate; less than normal cardiac output; SOB |
Why is digoxin used in heart failure? | slows the heart and strengthens contraction |
Where is digoxin detoxified? | in liver; only small amount destroyed and excreted daily (leading to accumulation) |
Why is a loading dose required for digoxin? | blood protein must be saturated before blood concentration is stabilized |
define digitalization | use of a loading dose to achieve high plasma levels of digoxin quickly |
How long does it take to reach plateau drug levels if no loading dose of digoxin is given? | 6 days |
Loading dose varies with... | age, body size, health problems |
describe pediatric dose of digoxin | proportionally higher doses according to weight |
maintenance of digoxin | may take a week to reach state |
How does renal impairment affect digoxin levels | slows elimination |
percentage of patients who have digoxin toxicity | 10-25% of patients |
describe optimal dose of digoxin | close to toxic dose |
first symptoms of digoxin toxicity appears where? | vision, GI, cardiac |
vision symptoms of digoxin toxicity | blurred, double vision, yellow or green color changes, halos around objects |
GI symptoms of digoxin toxicity | anorexia, nausea, vomiting, diarrhea |
apical impulse rates in adult digoxin toxicity | 60 or less |
apical impulse rates in infants digoxin toxicity | 100 or less |
How long should you measure the apical impulse when digoxin toxicity is suspected? | 1 minute |
EKG changes seen in digoxin toxicity | prolonged p-r interval, shortening QT, T wave inversion, PVCs |
predispositions for digoxin toxicity | hypokalemia, hypocalcemia, vomiting, gastric suctioning, diuretics |
IV predisposition for digoxin toxicity | large amount of IV dextrose |
Why does a large amount of IV dextrose a predisposition for digoxin toxicity? | causes intracellular shift of potassium |
age predispositions for digoxin toxicity | young and old |
health alterations that predispose for digoxin toxicity | liver and kidney dysfunction |
normal potassium level | 3.5-5 |
normal calcium level | 8.5-10 |
nursing assessment diagnositc of digoxin toxicity | appearance (color/edema); tachycardia/bradycardia, dysrhythmia,m pulmonary rales, anorexia, visual distrubances |
What to monitor with digoxin toxicity | I&O; weight; apical pulse for one full minute |
Labs to draw with digoxin toxicity | potassium, calcium, kinetics |
When do you hold digoxin | adult apical impulse below 60; infant apical impulse below 90-110 |
When do you check calculation on digoxin? | prior to administration |
Antidote for digoxin | digoxin immune FAB (Digibind) |
What color is the bottle of digoxin for children? | green |
Teaching for digoxin use | how/when to call doctor; how to measure digoxin with children; daily weight may need increase in potassium rich foods/supplementation |
How much weight gain may indicate fluid retention? | 1-2 pounds |
1 kg = ?? lbs | 2.2 |
Human B-type natiuretic peptide prototype | nesiritide (natrecor) |
therapeutic use of nesiritide (natrecor) | acute heart failure |
what does nesiritide (natrecor) do? | recombinate DNA - identical to peptide secreted by ventricle with fluid and pressure overload |
Action of nesiritide (natrecor) | decreases preload/afterload; increases diuresis and secretion of sodium; decrease renin-angiotension-aldosterone and secretion of norephenephrie |
nesiritide (natrecor) onset | immediate |
Nursing considerations for nesiritide (natrecor) | give IV, bolus then separate IV; monitor urinary output |
Why is nesiritide (natrecor) given in separate IV? | not compatible with many drugs |
What to do in emergency situation while on neiritide (natrecor) | put patient on heart monitor |