EXAM 2- BASIC DYSRHYTHMIAS WITH 100% CORRECT ANSWERS.

what do you do if artifacts occur on an ECG? check connections in equipment rhythm starts in the SA node, 60-100 BPM, normal conduction pathway normal sinus rhythm Brainpower Read More Previous Play Next Rewind 10 seconds Move forward 10 seconds Unmute 0:02 / 0:15 Full screen normal P wave length .06-.20 the time of passive of impulse through the atria, causing atrial depolarization (atrial contraction) P wave normal PR interval length .12-.20 time taken for the impulse the spread through the atria, AV node, and bundle of HIS, bundle branches, & purkinje fibers, right up until ventricular contraction. (atrial contraction -> beginning of ventricular contraction) PR interval normal QRS length <.12 time taken for depolarization of both ventricles (systole- ventricular contraction) QRS normal ST segment length .12 time between ventricular depolarization and repolarization; should be isoelectric. (end of systole -> beginning of diastole) ST segment normal T wave length .16 ventricular relaxation (diastole) T wave is K or Na higher inside the cell? K is K or Na higher outside the cell? Na what happens with depolarization of a cell? Na influx into cell normal QT .34-.43 time taken for entire depolarization/repolarization of ventricles (ventricular contraction + relaxation) (ventricular diastole + systole) QT the ability of a cardiac cell to fire spontaneously without being activated automaticity the ability of a cell to become depolarized; determined by the length of time after depolarization that they can be restimulated (the refractory periods) excitability SA node is firing <60 BPM P, QRS, T all normal regular rhythm sinus bradycardia is sinus bradycardia ever normal? yes- it's only significant when symptomatic symptoms of sinus bradycardia syncope, chest pain, pale/cool skin, hypotension, weakness, angina, dizziness, confusion, SOB SA node firing >100 BPM regular rhythm normal P and QRS QT <0.35 (shortened) sinus tachycardia the nurse knows that exercise, fever, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, myocardial ischemia, HF, hyperthyroid, and anxiety can all cause sinus tachycardia why may sinus tachycardia cause angina? inc O2 consumption in the heart sinus tachy Tx vagal stimulation, beta blocker, adenosine, CCB sinus brady Tx atropine (anticholinergic) (if that doesn't work- dopamine, epi) atrial tachydysrhymia recurring, regular, COARSE, SAWTOOTH-SHAPED waves caused by one single point in the R atrium regular rhythm PR interval unmeasurable QRS normal may see some AV block atrial flutter what is the risk with an atrial dysrhythmia? loss of atrial kick, so drop in CO (can cause HF); risk for clot formation (stroke/PE because of blood stasis) what is an atrial dysrhythmia pt given prophylactically and why? warfarin to prevent clots atrial flutter/fibrillation Tx CCB, BB, electrical cardioversion, amiodarone total disorganization of electrical activity due to multiple ectopic places firing inappropriately. loss of effective atrial contraction and loss of atrial kick. P waves replaced by chaotic FINE waveforms irregular rhythm PR unmeasurable atrial fibrillation prolonged time of AV conduction, could be caused by RCA MI . takes longer for a signal to get from SA -> AV, causing bradycardia and a drop inCO AV block ectopic stimuli on ventricles fire prematurely. early QRS with no P waves. irregular rhythm wide QRS: >.12 seconds large T wave in the opposite direction of the QRS. compensatory pause afterward PVC all PVCs going in the same direction; it's the same spot firing unifocal PVCs going in different directions; multiple spots are firing multifocal PVC every other HB bigeminy PVC every 3rd HB trigeminy PVC every 4th HB quadrigeminy 2 consecutive PVCs couplet 3 consecutive PVCs triplet more than 3 consecutive PVCs ventricular tachycardia if a PVC or cardioversion stimulation falls on the T wave of a preceding beat; a signal has been sent at the relative refractory phase. this is the _________ phenomenon, and the pt is at risk for _________ or ___________ R on T; VF, VT are PVCs always harmful? only harmful if symptomatic PVC symptoms (drop in CO causes:) angina, HF PVC Tx BB, procainamide, amiodarone a pt in V-tach is at risk for drop in CO, v-fib, death ventricular rate 150-250 regular or irregular rhythm P wave buried in QRS PR unmeasureable distorted, widened QRS: >.12 sec T wave in opposite direction of QRS ventricular tachycardia how does v-tach drop CO? less ventricular diastole filling time, no atrial contraction a pt in VT is at risk for V-fib a pt in V-tach is unresponsive. the priority intervention is CPR, defibrillation unmeasureable HR irregular, chaotic rhythm invisble P wave PR unmeasureable QRS unmeasureable ventricles are just quivering; many locations are firing all at once. no ventricular contraction is happening. ventricular fibrillation why is v-fib lethal? no CO v-fib Tx CPR, life support, defibrillation, epinephrine or vasopressin when is defibrillation appropriate? VF, pulseless VT where are paddles placed for defibrillation? front/back; R upper sternum under clavicle and left of left nipple at mid-ax line