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Electrocardiogram 1

Electrocardiogram lab

12 lead ecg may show: changes or damage to heart, i.e.: ischemia, infarction, enlargement.
p wave represents atrial depolarization
qrs wave electrical depolarization of the ventricles (ventricular contraction)
t wave ventricular depolarization, gets ready for next impulse/contraction.
pr interval represents time from atrial depolarization to the begging of ventricular depolarization (0.12-0.20 seconds)
qrs interval amount of time for ventricular depolarization (less than 0.12 seconds)
qt interval time measurement of ventricular activity (0.34-0.43 seconds). this can be prolonged due to effects of medications. (can cause serious heart rhythm disturbances)
medications the change the qt intervals lidocaine, pronestyle, amiodaroe.
u wave repolarization of purkinje fibgers.
normals sinus rhythem 60-100 bpm heart rate and intervals all normal. (shorter intervals = decreased cardiac output)
Common heart rates: normal sinus rhthym: 60-100 bpm sinus bradycardia: <60 bpm sinus tachycardia: 101-200 bpm paroxysmal supraventricular tachycardia extra beat in atrium): 150-200 bpm atrial fibrillation:350-600 beats junctional rhythm: 40-180 bpm (decreased cardiac ou
common heart rates continued: ventricular tachycardia: 150-250 bpm (w/ or w/o pulse, cardiac output is decreased) ventricular fibrillation: can not measure rate.
Sinus bradycardia: HR is less than 60 bpm. Don't let the pt. sit for long period of time. Give atropine (Increases heart contraction), pacemaker, or if cause by drugs, hold them.
S & S of sinus bradycardia pale, hypotension, angina, syncope, all intervals normal, decreased coronary perfusion, decreased bp --> mi and CHF, decreased cardiac output, dizziness.
sinus tachycardia: HR 101-200 bpm. decreased CO (because of decreased fill time) & coronary artery filling, increased O2 demand and workload of heart. give beta blockers (decrease force of contractions and rate), lopressor.
S & S of sinus tachycardia: dizziness, dyspnea, hypotension.
Paroxysmal supraventricular tachycardia (atrial) orgin: anywhere above the bundle of his. HR: 150-220 bpm. causes: CAD, digitalis toxicity.
S&S of paroxysmal supraventricular tachycardia hypotension, angina, dyspnea,.
treatment of paroxysmal supraventricular tachycardia adenosine, cardizem (slows down heart to see is there's a "p" wave), beta blockers, calcium channel blockers, amiodarone, vagal stimulation (valsalva maneuver and coughing)
Atrial flutter: Atrial rate: 200-350bpm. No measurable PR or QT intervals, caused by: CAD, HTN, mitral valve disease, pulmonary embolus, cardiomyopathy, high risk of CVA and CHF.
treatment for atrial flutter: calcium channel blockers, beta blockers, cardioversion, amiodarone, radio frequency ablation.
Atrial fibrillation: multiple impulses from the atria outside av node. irregular regular rhythm. HR 350-600 bpm. no p wave and no pr interval. Causes: CAD, rheumatic heart disease, heart failure, pericarditis,
treatment for atrial fibrillation: cardioversion, digoxin, cardizem, beta blockers, coumadin.
junctional dysrhythmias: oringinate in area of SA node due to failed AV node firing, junction becomes pacemaker. caused by: CAD, CHF, IWMI, cardiomyopathy. HR 40-60 bpm.
treatment for junctional dysrhythmias: if symptomatic, treat with atropine, beta and calcium channel blockers, amiodarone, and pacemaker.
Atrioventricular heart block 1st degree: prolonged PR intervals (SA node takes too long to fire to P wave) >.20 seconds. caused by: MI, CAD, digoxin toxicity, rheumatic fever, drugs (beta blockers, calcium channel blockers)
AV heart block 2nd degree: mobitz type 1- wenchebach . Not every P wave creates a qrs. P wave belong longer until QRS is dropped. caused by: impending complete heart block, MI, rheumatic fever, digoxin toxicity.
treatment of AV block 2nd degree: cardiac monitor and oxygen, atropine, temporary pacemaker if symptomatic bradycardia, temporary pacemaker,
av heart block 2nd degrreL mobitz type 2: conduction block in the av node or below the bundle of his. some qrs dropped, pr normal. can lead to 2rd degree HB. caused by: CAD, MI, Rheumatic heart disease, HR: 40-60 bpm.
treatment of 2nd degree/mobitz type 2: epinephrine or vasopressin IVP, hold digoxin, temporary pacemaker,
Av heart block 3rd degree complete heart block between the atria and ventricles. No relation between p waes and qrs complexes. independent pacemakers within atria and ventricles. HR: 30-40 bpm. caused by: severe heart disease, i.e: CAD, MI, cardiomyopathy, drug overdose.
treatment of 3rd block: oxygen, atropine, ephinephrine, dopamine, isuprel, temporary PM, permanent PM.
PVC's -doesn't produce pulse early qrs complex with no p wave. (ventricular tachycardia: 3 or more consecutive beats of PVC) worry that pt will go into v-tach or v-fib.
ventricular bigeminy: PVC occur with every other beat
ventricular trigeminy PRVC occur with every third beat
causes of PVC MI, CAD, CHF, Drugs (digoxin, epinephrine, hypoxia, fever, stress, hypokalemia, caffine, alcohol.
treatment of PVC: if greater than 10/min, start lidocaine or amiodarone IV drip, give oxygen, check potassium levels and replace if low.
ventricular tachycardia (continued PVC with no break) pulse or pulseless. rapid irregular rate with no p wave and wide bizarre beats from the ventricle. HR: 150-250 bpm. brief: with pulse, patien can tolerate. long: no pulse, immediate treatment.
Cause of ventricular tachycardia: MI, CAD, Respiratory failure, frequent PVCs.
treatment for ventricular tachycardia: always check for pulse first!!! with pulse: amiodarone, lidocaine, procainamide, cardioversion. without pulse: treat like v-fib, CPR, defibrillation, epinephrine, amiodarone, IV drip.
ventricular fibrillations No p, qrs, or t waves, no bp, no hr, no respirations, chaotic waves can lead to brain damage. caused by: MI, CHF, cardiomyopathy, electric shock, hypoxemia, acidosis, drug toxicity.
treatment for ventricular fibrillations: immediate CPR, defibrillation and advanced cardiac life support protocol, epinephrine, lidocaine, amiodarone, magnesium sulfate, procainemide follows ACLS protocol.
Ventricular asystole or cardiac standstill total absence of ventricular electrical activity. No pr or qrs complexes. No pulses, no bp, patient is unresponsive, pulseless, no respirations. (pretty much dead)
causes for ventricular asystole: acidosis, HF, hyperkalemia
treatment for ventricular asystole: CPR, O2, epinephrine, atropine, vasopressin, intubation, pacemaker, IV push drugs.
Created by: Lindsay515