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Telemetry Test 52 Questions with Verified Answers,100% CORRECT

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Telemetry Test 52 Questions with Verified Answers Action potential - CORRECT ANSWER the graphic representation of cellular electrical events, describes the changes in intracardiac voltage that lead... to impulse formation and conduction and, ultimately, to cardiac contraction Automaticity - CORRECT ANSWER the ability to initiate impulses spontaneously Conductivity - CORRECT ANSWER the ability to conduct an impulse along the cell membrane Contractility - CORRECT ANSWER the ability to contract in response to a stimulus Depolarization - CORRECT ANSWER a change in the resting electrical state of the cardiac cell. the inside of the cell becomes more positive and impulse is spread through the heart Excitability - CORRECT ANSWER the ability of cells to respond to a stimulus Two types of refractory period - CORRECT ANSWER absolute refractory period Relative refractory period Absolute refractory period - CORRECT ANSWER the cardiac cell is unable to accept or respond to a stimulus relative refractory period - CORRECT ANSWER a stronger than normal impulse may stimulate the cardiac cell to depolarize repolarization - CORRECT ANSWER return of the cardiac cell to the resting membrane state the inside of the cell becomes more negative resting membrane potential - CORRECT ANSWER the electrical charge across the cardiac cell membrane between impulses, generally about -70 mV threshold - CORRECT ANSWER the electrical level at which the cell will continue to depolarize without additional stimulus, generally about -60 mV sinoatrial node (SA node) - CORRECT ANSWER located high in the right atrium, near the junction of the superior vena cava. it is the primary pacemaker of the heart with normal rate of automaticity of 60-100 bpm internodal atrial pathways - CORRECT ANSWER conduct the impulse from the SA node through the right atrium musculature to the AV node. consists of three tracts: Bachmann's tract, Wenckebach's tract, and Thorel's tract atrioventricular node (AV node) - CORRECT ANSWER located low in the right atrium, adjacent to the inter-atrial septum delays impulse from atria to allow atrial contraction and synchronizes atrial contribution to ventricular pumping impulse is then sent to the ventricles via the bundles of His, normally the AV node is the only structure that is capable to conducting impulses to the ventricles. the AV node can serve as a backup pacemaker. inherent rate of automaticity is 40-60 bpm Bundle of His - CORRECT ANSWER arises from the AV node and conducts impulse to bundle branch system bundle branch system - CORRECT ANSWER pathways that arise from the Bundle of His. composed of Right Bundle Branch and Left Bundle Branch right bundle branch (RBB) - CORRECT ANSWER a direct continuation of the bundle of His. transmits impulse down right side of the interventricular septum to the myocardium of the right ventricle left bundle branch - CORRECT ANSWER separates into three fascicles left posterior left anterior septal fascicle left posterior fascicle - CORRECT ANSWER transmits impulse over posterior and inferior endocardial surface of the left ventricle left anterior fascicle - CORRECT ANSWER transmits impulse over anterior and superior endocardial surfaces of the left ventricle purkinje fibers - CORRECT ANSWER arises from distal portion of bundle branches, transmits impulses into subendocardial layers of both ventricles; provides for the depolarization; followed by ventricular contraction and ejection of blood out of ventricles. intrinsic rate of 20 to 40 bpm isoelectric line: - CORRECT ANSWER flat line between complexes p wave - CORRECT ANSWER indicates that the impulse originated at the SA node and the atrial are normally depolarized duration: 0.10 seconds PR interval - CORRECT ANSWER represents the time required for the electrical impulse to travel from the SA node, through the atria, AV node, bundle of his, bundle branches and purkinje fibers measured form the beginning of the P wave to the beginning of the QRS complex duration: .12-.20 seconds QRS complex - CORRECT ANSWER represents the time required for the electrical impulse to depolarize the ventricles measured from the Q wave where the line leaves baseline to the S where the line returns to the baseline duration: 0.04-.10 seconds ST segment - CORRECT ANSWER represents the end of ventricle depolarization and beginning of ventricular repolarization measured from the end of the QRS complex and ends with the onset of the T wave duration: .08 seconds T wave - CORRECT ANSWER represents the latter phase of ventricular repolarization measured from the beginning as the deflection slopes upward from the ST segment and ends with the line returning to baseline amplitude: <5mm QT interval - CORRECT ANSWER represents the time between the onset of ventricular depolarization and the end of ventricular repolarization measured from the beginning of the QRS complex to the end of the T wave where the line returns to baseline duration: .30-.40 (varies with heart rate) U wave - CORRECT ANSWER represents the repolarization of the purkinje fibers usually not seen on the EKG may be found with electrolyte disturbances sinus rhythms - CORRECT ANSWER sinus simply means that the rhythm is produced by electrical impulses formed within the SA node (also called the sinus node) determinants of sinus rhythm - CORRECT ANSWER P wave must be singular and present before each QRS complex P wave must be upright and of normal morphology in leads I and II. p wave may be upright, inverted or biphasic in Lead II PR interval and QRS must be constant and of normal duration normal sinus rhythm - CORRECT ANSWER mechanism: normal cardiac rhythm significance: normal cardiac rhythm clinical features: rate: 60-100 rhythm: regular p waves: 1 occurs before each QRS complex, normally shaped PR Interval: 0.12-0.20 seconds QRS complex: 0.04-0.10 seconds QT interval: less than 1/2 of the R-R interval mechanism of sinus tachycardia - CORRECT ANSWER normal response to metabolic needs: exercise, anxiety, fear disease processes: MI, PE, CHF; heart rate responds to compensate for reduced stroke volume, hypoxia, hypovolemia, hyperthyroidism significance of sinus tach - CORRECT ANSWER tachycardia increases work of the heart and oxygen consumption, which may lead to heart failure, ischemia, and increased size of infarction risks associated with tachycardia depend on etiology. the risk is low if the etiology is stress, anxiety, fear, or physical activity. the risk increases if the etiology is hypoxemia, heart failure, or cardiac disease clinical features of sinus tach - CORRECT ANSWER rate: 100-150 rhythm: regular P waves: 1 occurs before each QRS complex, regularly shaped PR interval: normal QRS interval: normal symptoms: may lead to angina, dyspnea treatment of sinus tach - CORRECT ANSWER investigate and treat underlying cause pharmacologic interventions: oxygen, pain/fever relievers, beta-blockers, calcium channel blockers sinus bradycardia mechanism - CORRECT ANSWER vagal stimulation, normal in athletes, during sleep and inactivity disease: early MI, inferior wall MI, increased ICP, hypoparathyroidism, hypothermia drugs: digitalis, propranolol, morphine clinical significance of sinus brady - CORRECT ANSWER reduced cardiac output resulting in decreased coronary and cerebral blood flow leading to angina, syncope or heart failure slowly discharging SA node may allow a more rapidly discharging ectopic focus to take over role of cardiac pacemaker, predisposing patient to atrial and ventricular dysrhythmias including ventricular ectopy clinical features of sinus brady - CORRECT ANSWER rate: less than 60 rhythm: regular P waves: 1 occurs before every QRS complex, regularly shaped PR interval: normal QRS complex: normal symptoms: fatigue, angina, dyspnea, syncope, hypotension treatment of sinus brady - CORRECT ANSWER only treat if symptomatic! atropine if symptomatic cardiac pacing avoid medications with known bradycardic effects (digitalis, morphine, beta-blockers) Supraventricular tachycardia (SVT) mechanism - CORRECT ANSWER a narrow complex tachycardia or atrial tachycardia which originates in the atria and is so fast the origin cannot be determined clinical significance of SVT - CORRECT ANSWER increased rate will cause increase in myocardial oxygen demands creating ischemia for those with heart disease the ability to tolerate the increased rate will determine the urgency of treatment clinical features of SVT - CORRECT ANSWER rate: 140-220 bpm rhythm: regular p waves: difficult to find due to rate PR interval: cannot measure but if slowed the PR will vary depending on the location of the stimuli in the atria QRS complex: normal symptoms: fatigue, angina, dyspnea, syncope, hypotension treatment for SVT - CORRECT ANSWER cardiovert if unstable decrease rate with beta blocker, calcium channel blockers, or prainamide First degree AV block mechanism - CORRECT ANSWER progress of the impulse slows because of a prolonged conduction delay at the AV node thus increasing the time for the impulse to reach the ventricles diseases: ischemia, myocardial infarction, infection, vagal stimulation, hyperthyroidism, rheumatic fever, hyperkalemia, and congenital abnormality medications: side effect of digoxin, beta and calcium channel blockers, quinidine and procainamide clinical significance of first degree - CORRECT ANSWER usually clinically asymptomatic, symptoms are more likely to be present if underlying rhythm is bradycardia. can be a warning sign of advancing heart block especially when acute myocardial infarction is present clinical features of first degree - CORRECT ANSWER rate: normal to fast rhythm: regular p waves: present, normal, and P wave precedes every QRS QRS: present, normal duration <.12 seconds PR Interval: prolonged > 0.20 seconds and remains constant with QRS complex measuring normal second degree type 1 mechanism - CORRECT ANSWER conduction impulse is conducted normally to the AV node but each successive impulse has more and more difficulty passing through the AV node, until finally an impulse does not pass through diseases: usually a transient phenomenon often caused by increased vagal tone, acute infections, MI medications: side effect of digoxin, beta and calcium channel blockers, quinidine and procainamide clinical significance of second degree type 1 - CORRECT ANSWER self limiting, transient and reversible and seldom serious but can advance to a higher degree of heart block. patients are usually asymptomatic unless underlying rhythm is bradycardia clinical features of second degree AV block type 1 - CORRECT ANSWER rate: atrial rate usually regular ventricular rate irregular secondary to progressive lengthening of PR rhythm: irregular p waves: present, more P waves than QRS; p waves proceed each QRS, except for blocked beat QRS: present, normal duration <.12 seconds PR Interval: progressive prolongation of PR interval until QRS is dropped treatment of second degree AV type 1 - CORRECT ANSWER monitor patients hemodynamic status. pacemaker on stand-by for rapid use (1st choice) or atropine as second choice bradycardia [Show More]

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Telemetry Exam ( 33 Sets) Questions with Verified Answers,100% CORRECT

Telemetry Exam 68 Questions with Verified Answers,Telemetry Exam 39 Questions with Verified Answers,Cardiac- Telemetry Exam 72 Questions with Verified Answers,Telemetry Exam 60 Questions with Verified...

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