care of patients with dysrhythmias c36 med
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| cardiac dysrhythmias | abnormal rhythms of the heart's electrical system that can affect ability to effectively pump oxygenated blood throughout the body.
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| automaticity | pacing function - ability of cardiac cells to generate electrical impulse spontaneously and repetitively. normally primary pacemaker cells (sa node, av junction) some conditions cause independent impulses creating dysrhythmia.
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| excitability | ability of non-pacemaker cells to respond to impulse from pacemaker cells and depolarize
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| depolarization occurs when... | the normally negatively charged cells within heart develop a positive charge
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| conductivity | ability to transmit impulse from cell membrane to cell membrane
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| contractility | ability of atrial and ventricular muscle cells to shorten their fiber length in response to impulse, so blood can be pushed out. mechanical activity of the heart.
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| sinoatrial node (SA node) location | close to surface of right arium near junction with superior vena cava.
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| SA node purpose | primary pacemaker. can spontaneously and rhythmically generate impulses and has greatest degree of automaticity.
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| changes in heart rate at the SA node from | sympathetic and parasympathetic NS
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| What does the P wave represent on an EKG? | atrial depolarization led by the SA node impulse moving over the atrial muscle, which causes atrial muscle contraction.
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| Atrioventricular junctional area consists of? | transitional cell zone, AV node and bundle of his.
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| location of AV node | beneath right atrial endocardium, between tricuspid valve and ostium of cornoary sinus.
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| Transitional cell function in AV junction | delay impulses in AV node. PR segment. allows atria to contract and ventricles to fill.
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| bundle of his location | in the interventricular septum
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| purkinje cells make up the.. | bundle of his, bundle branches and terminal purkinje fivers.
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| purkinje cell purpose | rapid conduction of impulses through ventricles, lading to ventricular depolarization and contraction
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| ECG pattern in relationship to isoelectric line | isoelectric line is neutral no flow in heart after complete depolarization and after complete repolarization. above line is positive deflection. below is negative deflection.
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| P wave of EKG | atrial depolarization
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| PR segment | time impulse going through AV node and to purkinje fibers
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| PR interval | from beginning of Pwave to end of PR segment. time of atrial depolarization and impulse delay in AV node and travel time to purkinje fibers. normally 0.12 to 0.20 seconds (5 small blocks)
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| QRS complex | ventricular depolarization.
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| Q part of QRS complex | usually small. if large - myocardial necrosis.
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| QRS duration | time required for depolarization of both ventricles. measured from beginning of qrs complex to the jpoint (junction where qrs complex ends and st segment begins). from 0.04 to 0.10 seconds (up to 3 blocks).
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| ST segment | normall isoelectric line. represents early ventricular repolarization. from j point to start of t wave. amplitude measured at 1.5 to 2 mm after j point. should be between 1mm and -0.5 mm from line.
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| T wave | after ST segment. represents ventricular repolarization. usually +, rounded and slightly asymmetric.
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| U wave | after t wave if present. shows slow repolarization of ventricular purkinje fibers. suggests electrolyte abnormality
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| QT interval | total time required for ventricular depolarization and repolarization. measured from beginning of QRS complex to the end of the T wave. varies depending on age, gender and HR.
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| Artifact | interference on monitor/rhythm strip, looks like wandering or fuzzy baseline. caused by patient movement, loose/defective electrodes, improper grounding or faulty ecg equipment. assess patient to differentiate artifact from actual lethal rhythms
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| 6 second strip method | method to estimate HR using ECG monitor. count numer of QRS complexes in 6 seconds and multiply by 10.
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| big block method | method to estimate HR using ECG monitor. count big blocks bw same point on any two successive QRS complexes and divide into 300. if little blocks left, add 0.2 for each big than divide by 300.
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| memory method | estimate HR on ECG by memorizing sequence: 300,150,100,75,60,50,43,37,33,30. find QRS on dark line rep. 0.2 second or a big block. count backwards to next qrs. each dark line is a memorized #. most used in hospitals for calc. hr for reg. rhythms.
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| 6 steps to analyze ecg rhythm strip | determine HR, determine Heart rhythm, analyze p waves, measure pr interval, measure QRS duration, interpret rhythm.
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| HR determination by ECG preferred method for irregular rhythms | 6 second strip method.
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| To assess regularity of atrial rhythm assess the ____ intervals, by... | PP, placing one caliper point on p wave and the other point on the precise spon on the next p wave. move caliper from p wave to pwave along entire strip to determine regularity of rhythm.
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| To assess regularity of ventricular rhythm assess the ___ intervals | RR
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| 5 questions to ask self when analyzing P waves | present? regular? P wave for each QRS? smooth, rounded and upright or inverted? all P waves similar?
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| To measure the PR interval using a caliper | one caliper point at beginning of P wave and other point at end of the PR segment. normally 0.12 and 0.20 second. should be constant.
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| 3 questions to ask self when analyzing PR interval | interval greater than 0.20? less than 0.12? constant across stripo?
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| To measure the QRS duration with a caliper | one caliper point at beginning of QRS complex other at j point. normally between 0.04 and 0.10 second. constant through strip.
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| normal sinus rhythm (NSR) | originates from SA node and rate: 60-100 bpm - rhythm: regular - p waves: present, consistent, 1 p wave b4 each QRS segment. - PR interval: 0.12 to 0.2 second and constant - QRS duration: 0.04 to 0.1 second and constant
PR interval: 0.12 to 0.20 s
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| sinus arrhythmia | same as NSR except irregularity in PP and RR intervals. greater than 0.12 second (3 small block) usually due to respiration
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| reasons for dysrhythmia | disturbance in relationship between electrical conductivity and mechanical response of myocardium. disturbance in impulse formation, disturbance in impulse conduction, combination of several mechanisms.
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| key features of sustained tachydysrhythmias and bradydysrhythmias | chest discomfort, pressure/pain - may radiate to jaw, back or arm. dizziness, synocope, palpiations, change in pulse, pulse deficit, SOB, dyspnea, tachypnea, crackles, orthopnea, s3 or s4, JVD, weakness, diaphoresis, nausea, dec Urine, delayed cap. refill
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| Reasons tachydysrhythmias are serious | shorten diastolic time and therefore coronary perfusion time, initially inc CO and BP - contintued rise in HR dec ventricular filling time bc shortened diastole, dec SV thus CO and BP dec. less perfusion, inc work of heart, inc myocardial oxygen demand
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| symptoms of tachydysrhythmia | palpitations, chest discomfort, restlessness, anxiety, pale, cool skin, syncope (blackout) from hypotension
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| symptoms of heart failure | dyspnea, lung crackles, distended neck veins, fatigue and weakness
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| reasons bradydysrhythmias are serious | coronary perfusion pressure may dec. if HR is too slow to provide adquate CO and BP
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| premature complexes | early rhythm complexes occurring when cardiac cell or group, other than SA node, becomes irritable and fires an impulse before next sinus impulse is produced.
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| bigeminy | exists when normal and premature complexes occur alternately in repetitive 2 beat pattern, w/ a pause after each premature complex so that complexes occur in pairs.
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| trigeminy | repeated 3 beat patter, usually as two sequential normal complexes followed by premature complex and a pause. repeating in triplets
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| quadrigeminy | repeated 4 beat pattern, usually as 3 sequential normal complexes followed by premature complex and pause, with same pattern in four beat pattern
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| escape complexes (rhythms) | when SA node fails to discharge or is blocked or when sinus impulse fails to depolarize ventricles bc of an AV nodal block.
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| incidences of dysrhythmias increase with ___ | age
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| excessive vagal stimulation may result from | carotid sinus massage, vomiting, suctioning, valsalva maneuvers, ocular pressure/pain.
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| premature atrial complex (PAC) | atrial tissue becomes irritable. ectopic focus fires impulse before next sinus impulse is due.
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| causes of atrial irritability | stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine or alcohol, drus (catecholamines, sympathomimetics, amphetamines, digitalis or anesthetic agents.
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| paroxysmal supraventricular tachycardia (PSVT) | intermittent rhythm. suddden premature complex such as PAC and terminated suddenly with or without intervention
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| atrial fibrillation occurances and causes | most common dysrhythmia. risk factors: hypertension (biggest), diabetes, being male, CHF, vavular disease. temporary episodes can be caused by alcohol, surgery, electrocution, MI, pericarditis, pulmonary embolism, myocarditis
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| atrial fibrillation | multiple rapid impulses from many atrial foci deplarize atria in disorganized manner at rate of 350 to 600 times per min. chaotic rhythm no clear p waves, no atrial contractions, loss of atrial kick, irregular ventricular response.
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| atrial flutter | rapid atrial depolarization occurring at rate of 250 to 350 times per minute. AV node block impulses that reach ventricles as protection.
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| idioventricular rhythm | ventricular nodes pace ventricles. usually less than 40/min. rhythm of dying heart.
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| pulseless electrical activity | no palpable pulse, no perfusion even though on monitor. patient is hypotensive and in shock. may require cpr
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| causes of PEA | (pulseless electrical activity) hypovolemia, hypoxia, acidosis, hyperkalemia/hypokalemia, hypothermia, drug overdose, tension pneumothorax, coronary/opulmonary thrombosis, cardiac tamponde.
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| nonsustained ventricular tachycardia | 3+ successive PVCs (premature ventricular complexes)
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| ventricular fibrillation | electrical chaos in ventricles and is life threatening. patient first becomes faint, loses conciousness, pulseless, apneic (no breathing). no bp, no heart sounds, respiratory/metabolic acidosis, seizures. death if not ended within 3 mins.
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| emergency care for ventricular fibrillation | defibrillate patient.
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| ventricular asystole | ventricular standstill. complete absence of a ventricular rhythm. no impulses in ventricles, no depolarization, no qrs complex, no contraction, no CO, no pulse, respirations or bp. Full cardiac arrest.
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| emergency care for ventricular asystole | cpr - assess other ecg lead to ensure rhythm is asystole and not fine VF (which would req. defib). do not shock asystole. manage airway, admin o2, epinephrine and atropine.
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| atrioventricular blocks | when supraventricular impulses are excessively delayed or totally blocked in av node or intraventricular conduction system.
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| degress of atrioventricular heart blocks | first degree av bock, sinus impulses eventually reach ventricles. second degree heart block, some sinus impulses reach ventricles but others don't because blocked. third degree heart block (complete) none of the sinus impulses reach ventricles.
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| bundle branch block (BBB) | conduction delay or block within one of the two main bundles of his branches. underlying rhythm is usually sinus in origin.
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| temporary pacing | nonsurgical intervention that provides timed electrical stimulus to heart when impulse initiation or conduction system of heart is defective. stimulus spreads throughout heart to depolarize, then contraction and CO.
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| asynchronous (fixed-rate) pacing mode | used when patient is asystolic or profoundly bradycardic. used until patients heart rate catches up.
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| aneurysm | ballooning portion of ventricular wall.
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