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Dysrhythmias (slides 1-78)

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cdunbar4's version from 2016-12-03 17:18

Terms and such

Question Answer
Automaticityimpulse is spontaneous; any myocardial cell can initiate electrical impulse
Excitabilityaka "action potential" - cells are electrically stimulated
Conductivitycells are conductors (hand-off) of the transmission of impulse
Contractilityresponds mechanically to the stimulation; cells get stimulated and turn it into a contraction.
Left and right vagus nervesparasympathetic ↓'s stuff
Nerve fibers of SNS↑ stuff
Autonomic nervous system controlsrate of impulse formation, speed of conduction and strength of contraction
1 big box time0.2 seconds
1 teeny weeny box time (TWB)0.04 seconds
How do you calculate the BPM if you just count the little boxes?There are 1500 little boxes in a minute so...count the # of little boxes b/t 2 R-waves & divide the # to get BPM
Another way to determine heart rate by counting R waves?Count R-waves for 6 seconds X 10
Normal sinus rhythmfollows normal conduction pattern; sinus fires 60-100bpm
What does "sinus" mean?electrical signal starts at SA node
ECG lead placement/prep of skinClip excessive hair with scissors; gently rub skin with dr ygauze until slightly pink; if skin is oily, wipe with alcohol first; if diaphoretic, apply skin protectant before placing the electrode
What is an artifact?A distortion of the baseline and waveforms seen on the ECG; if one occurs, check for secure connections of the leads
Telemetry monitoringobservation of pt's HR & rhythm at a site distant from the patient
Evaluation of DysrhythmiasHolter monitoring; event recorder monitoring; exercise treadmill testing; signal averaged ECG; electrophysiologic study
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Waves and Intervals TBL 36-2

Question Answer
P wave descriptiontime for the passage of electrical impulse through the atrium causing atrial contraction (should be upright)
P wave normal duration0.06-0.12
P wave source of possible variationdisturbance in conduction within the atria
PR interval descriptionmeasured from beginning of P wave to beg. of QRS complex; represents the time taken for impulse to spread through the atria, AV node & bundle of His, Purkinje fibers to a point immediately preceding ventricular contraction
PR interval normal duration0.12-0.20
PR interval source of possible variationdisturbance in conduction usually in AV node, bundle of His or bundle branches, but can be in atria as well
QRS interval descriptionmeasured from beg. to end of QRS complex; represents time taken for depolarization of both ventricles
QRS normal duration0.12 seconds
QRS source of possible variationdisturbance in conduction in bundle branches or in ventricles
ST segment descriptionmeasured from S wave of QRS complex to the beg. of the T wave; represents the time b/t ventricular depolarization & re-polarization; should be isoelectric (flat)
ST segment normal duration0.12
ST segment source of possible variationdisturbances usually caused by ischemia, injury or infarction
T wave descriptionrepresents time for ventricular repolarization; should be upright
T wave normal duration0.16
T wave source of possible variationdisturbances usu caused by electrolyte imbalances, ischemia, or infarction
QT interval descriptionmeasured from beg. of QRS complex to end of T wave; represents time taken for entire electrical depolarization & repolarization of ventricles
Normal Sinus Rhythm you want a 1:1 ratio of which waveforms?P:QRS should be "married"
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SINUS Brady/Tachy

Question Answer
Sinus Bradycardia: when is this a normal rhythm?Sinus node fires <60bpm; may be normal rhythm if aerobically trained athletes or during sleep
Sinus Brady: clinical association, occurs in response to:carotid sinus massage (Vagal massage); hypothermia; ↑ vagal tone; admin. of parasympathomimetic drugs (BB's, CCB's)
Sinus Brady occurs in disease states such as: ↑ ICP; inferior wall MI; hypothyroidism; hypoglycemia; obstructive jaundice
Sinus Brady clinical significancedepends on how the patient tolerates it hemodynamically
S/S sinus bradypale, cool skin; hypoTN; weakness; angina; dizzy/syncope; confused; disoriented; SOB
Sinus Brady Pharm Treatment for symptomsAtropine (anticholinergic) to reduce the slowing impact of the PNS so things speed up!
Other treatment sinus bradyPacemaker; if bradycardia is due to drugs, may need to hold or change the dosages
Sinus TachycardiaDischarge rate from the sinus node is increased as a result of vagal inhibition or sympathetic stimulation and is >100bpm
Sinus Tachy Clinical Associationsphysiologic stressors: exercise, pain, hypovolemia, MI, HF, fever, anemia, hypoTN, hypoxia, hypoglycemia, fear, hyperthyroidism, lots of drugs
ECG for Sinus TachyNormal P wave, PR interval and shape/duration; only the rate is increased (more QRS complexes)
Sinus Tachy clinical significancedepends on pt's tolerance of ↑HR; Sx: dizzy, dyspnea, hypoTN d/t ↓CO----↑myocardial O2 consumption may lead to angina
Sinus Tachy treatmentsTreat underlying etiology; adenosine IV; hypovolemia→↑fluids; vagal maneuvers (bear down)
Sinus Tachy BB's used toreduce HR & myocardial oxygen consumption
Sinus Tachy: antipyretics and analgesics are used for fever and pain
Sinus brady P waveone sinus P wave present before each QRS <0.11 seconds
Sinus brady PR IntervalNormal 0.12-0.20 seconds
Sinus brady QRSnormal or prolonged as a result of other conditions
Sinus brady R/Rrate <60; usually 40-60 bpm; regular rhythm
Tx for sinus brady if pt. is symptomaticatropine 0.5mg to 1mg IV (repeated 3x q5 min if necessary, check BP)
Sinus tachy P wavepresent before each QRS <0.11 seconds
sinus tachy PR intervalnormal 0.12-0.20 seconds
sinus tachy QRSnormal or prolonged as a result of other conditions
sinus tachy r/r100-160bpm; regular rhythm
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Aflutter and Afib

Question Answer
Atrial Flutteratrial tachy dysrhythmia identified by recurring, regular, sawtooth-shaped flutter waves on ECG; 4:1 flutter waves with each ventricular response
atrial flutter originates from a single _______ focusectopic
Clinical associations/usually occurs with:CAD, HTN, mitral valve disorders, PE, chronic lung disease, cardiomyopathy, hyperthyroidism
What drugs does atrial flutter usually occur with?Digoxin, quinidine, epinephrine
Clinical Significance: atrial flutterhigh atrial rates >100 and loss of the "atrial kick" can decrease CO & precipitate HF, angina
Atrial flutter has risk forstroke d/t stagnant blood (more in than out) thrombus formation
Primary treatment goal atrial flutterslow ventricular response by ↑ AV block
Drug treatment atrial flutterCCB's; BB's (epi, etc.)
_____________ may be used to convert atrial _______ to sinus rhythm emergently & electivelyElectrocardioversion; flutter
Other treatment for atrial flutterantidysrhythmia drugs to convert atrial flutter to sinus rhythm or to maintain sinus rhythm (amiodarone, propafenone)
Atrial flutter fixed ratio of flutter waves/QRS: 2:1, 3:1, atrial rate 250-350bpm
Afibtotal disorganization of atrial electrical activity d/t multiple ectopic foci => loss of effective atrial contraction
Two types afibparoxysmal or persistent
Clinical Association afibin pt's with HD, RHD, cardiomyopathy, HTN heart disease, CHF, pericarditis & alcohol
Acute associations: afibstress, caffeine, cardiac surgery, thryotoxicosis, electrolyte disturbances
Complications from aifib↓CO d/t ineffective atrial contractions (loss of kick) & rapid ventricular response; thrombi; embolus can develop and travel to brain
Primary treatment goal afib↓ VENTRICULAR RESPONSE to <100bpm, prevent stroke & try to get back to sinus rhythm
Drugs for rate control: afibBB's (metoprolol), CCB's (diltiazem), digoxin (↓'s conduction of impulses through AV node); coumadin for long-term anticoagulation
Electrocardioversion may be considered for afib, what drugs are used for maintenance?amiodarone & ibutilide
If in afib for >48 hours=>warfarin 3wks b4 cardioversion & 4wks post
Other treatments afibcatheter ablation, maze procedure (surgeon makes many small incisions (a maze) which become scare tissue & do not conduct)
Difference b/t cardioversion and defibrillationcardioversion synchs with T Wave to get normal 1:1 ratio (pt. given conscious sedation), defib is trying to get ventricles to wake up
Aflutter P waveV-shaped "Flutter" or F waves sawtooth appearance; PR Interval is not measurable
QRS AflutterNormal 0.10 seconds or less
Aflutter R/Ratrial rate is 250-400; ventricular rate varies; irregular or regular rhythm
Aflutter/Afib drug txTreatment aimed toward controlling the ventricular rate→diltiazem, BB's CCB's, Dig, Amiodarone, anti-coagulants or cardioversion
Afib P wavewavy fibrillatory or fwaves. May also see flutter waves in mixed rhythm (fib-flutter)
Afib PR interval and QRS complexPR not measurable QRS is normal 0.10 seconds or less
Afib R/Ratrial rate >400, ventricle rate varies, irregular rhythm
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The BLOCKS

Question Answer
1˚ AV block every impulse is conducted to the ventricles, but duration of AV conduction is prolonged (PR interval >0.20 seconds)
1˚ AV block clinical associationsMI, CAD, Rheumatic heart fever, hyperthyroidism, vagal stimulation, Drugs: digoxin, BB's, CCB's, flecainide
1˚ AV block Clinical sig. and txusually asymptomatic (could be precursor to higher AV blocks); tx= usually just monitor and check medications
2˚ AV block Type 1(Mobitz I, Wenckebach)- GRADUAL/PROGRESSIVE lengthening of PR interval (prolonged AV conduction time) until QRS is blocked & cycle repeats
2˚ AV block Type 2(Mobitz II)- CONSTANT ↑PR interval & varying QRS blocks (some QRS' are missing, but every QRS is preceded by a P)
Where does 2˚ AV block usually occur?at AV node, but can occur at His-Purkinje system: Atria are normal, ventricles are slower
2˚ type I clinical associationsDrugs: dig, BB's; may be associated with CAD & other diseases that can slow AV conduction
2˚ type I clinical significanceusually a result of myocardial ischemia or infarction; almost always transient & well-tolerated; may be a warning signal of a more serious AV conduction disturbance
2˚ type I treatment if symptomaticatropine or a temporary pacemaker (EFFECTIVE if HR ↑'s, so if vent. rate increases then tx is working)
2˚ type I tx if asymptomaticmonitor with a transcutaneous pacemaker on standby
2˚ type II clinical associationsRheumatic HD; CAD; anterior MI; digitalis toxicity
2˚ type II clinical significanceoften progresses to 3 degree AV block and associated with a poor prognosis; reduced HR often results in ↓CO with hypoTN/myocardial ischemia to follow
2˚ type II treatmentif symptomatic (e.g. hypoTN, angina) b4 perm. pacemaker can be inserted, temporary transvenous or transcutaneous pacemaker
3˚ AV Heart BlockCOMPLETE heart block: no impulses from atria are conducted to ventricles, atria & ventricles beat independently
3˚ AV Heart Blocknormal P wave shape PR varied and no relationship b/t P & QRS complex
3˚ AV Heart Block placement of ectopic pacemakerabove or below the bifurcation of the bundle of His
3˚ AV Heart Block clinical associationssevere HD: CAD, MI, myocarditis, cardiomyopathy; systemic diseases (amyloidosis, scleroderma); Drugs: dig, BB's CCB's
3˚ AV Heart Block clinical sig.↓CO with ischemia, HF, shock to follow
3˚ AV Heart Block Treatment if symptomatictranscutaneous pacemaker until a temporary pacemaker can be inserted can be inserted
3˚ AV Heart Block DRUGS for Txatropine, epi (temporary measure to ↑HR & support BP until temporary pacing is initiated
1˚ ECG changes1 sinus P wave before each QRS (<0.11sec); prolonged PR Interval (>0.20sec) & remains constant; QRS is normal; Rate is usually sinus, regular rhythm
1˚ symptomsnone, may be a warning that 2-3rd blocks may follow; maybe D/C drugs that are causing AV block
2˚ ECG changes1 P before each QRS, PR Intervals progressively lengthen until a QRS is dropped (QRS is normal 0.11secs); rate is of underlying rhythm (usu sinus); Atrial rate > V rate; Irreg Ventricular rhythm
3˚ ECG changesSinus P waves present but NO relationship to QRS (P waves hidden in QRS or T wave); variable PR interval; QRS Normal <0.10, but can be wide >0.10; rate usu sinus Atrial rate > Vent rate; rhythm regular
3˚ ventricular rate is b/t 40-60 ifpaced by AV node or 30-40 if paced by ventricles. Atrial ventricular rhythm regular
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