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87 Cards in this Set
- Front
- Back
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length of P wave
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0.06-0.12
- affected by conduction changes in atrium |
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PRI length
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0.12-0.20
- Disturbance in conduction usually in AV node, bundle of His or bundle branches, but can be in atria |
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QRS length
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< 0.12
- affected by Disturbance in conduction in bundle branches or in ventricles |
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ST segment length
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0.12
- affected by Disturbances usually caused by ischemia, injury, infarction |
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T wave length
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0.16
- Disturbances usually caused by electrolyte imbalances, ischemia, infarction |
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QT interval intrinsic length
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0.34- 0.43
- Disturbances usually affecting repolarization more than depolarization and caused by drugs, electrolyte imbalances, and changes in HR |
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SA node intrinsic rate (pace maker)
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60-100
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AV node intrinsic rate
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40-60
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Bundle of His, Purkinje fibers (Ventricles) intrinsic rate
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20-40
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Refractory period
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recovery period after stimulation
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Absolute refractory phase
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occurs when excitability is zero and heart tissue CANNOT be stimulated
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Relative refractory period
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occurs slightly later in cycle and excitability is more likely
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Full excitability
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heart is completely recovered
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Common causes of dysrhythmias- cardiac conditions and other
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Accessory pathways
Cardiomyopathy Conduction defects HF Myocardial ischemia, infarction Valve Disease Acid-base Alcohol Caffeine, tobacco Connective tissue disorders Drug effects Electrical shock Electrolyte imbalance Emotional crisis Herbal Hypoxia Metabolic conditions Near-drowning Poisoning Sepsis, Shock |
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Evaluation of Dysrhythmias
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Holter monitoring- records continuously while pt active, maintains diary
Event recorder monitoring- even time only Exercise treadmill testing- assesses cardiac rhythms during exercise Signal-averaged ECG- identified late potentials for risk of ventricular dysrhythmias Electrophysiology study- to eval tachydysr, heart blocks, brady, accessory pathways, and determines effectiveness of drugs |
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Emergency Assessment findings
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- irregular r and r
- tachycardia or bradycardia - increases or decreased BP (brain needs 90mmHg) - lowered O2 sat - pain: chest, neck, shoulder, back jaw (elderly and women have dif pain- jaw indigestion, anxiety, not feeling well) - dizziness, syncope - extreme restlessness, anxiety - feeling of impending doom - numbness, tingling of arms - weakness, fatigue - cold, clammy skin - decreased peripheral pulses - diaphoresis - pallor - palpitations - N/V |
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Emergency Interventions
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- Ensure ABC's
- O2 via nasal cannula or non-rebreather - Obtain baseline v/s - Obtain 12 lead ECG - Continuous ECG monitoring - Identify rate/rhythm/dysrhythmias - Establish IV access (2 Large bore) - Monitoring vitals, LOC, O2, cardiac rhythm - anticipate admin of meds - anticipate need for intubation or respiratory distress evident - prepare to initiate advanced cardiac life support |
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Sinus bradycardia
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- sinus node fires <60 bpm
- could be normal in athlete |
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Sinus bradycardia occurs in response to
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- Carotid sinus massage
- Hypothermia - Increased vagal tone - Admin of parasympathomimetic drugs - Hypothyroid - Increased ICP - Obstructive jaundice - Inferior wall MI |
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Clinical significance of sinus bradycardia
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- Hypotension
- Pale, cool skin - weakness - angina - Dizziness, syncope - shortness of breath |
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Treatment for Sinus bradycardia
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- Atropine (0.5 mg? will stimulate contraction- will create a stronger P wave- its AntiSLUD arrythmia drug)
- pacemaker may be required - if due to drugs, hold or discontinue |
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Sinus tachycardia
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Sinus node discharge >100bpm as a result of vagal inhibition
>150 is supraventricular or atrial tachycardia--> won't be able to see P wave anymore its so fast |
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Causes of Sinus tachycardia
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- exercise
- pain - hypovolemia - myocardial ischemia - HF - Fever - Certain drugs (epi, norepi, atropine, caffeine, theophylline, nifedipine, hydralazine, OTC cold remedies-pseudephedrine) |
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Clinical signs of tachycardia
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- dizziness and hypotension (decreased CO)
- possible angina (increased myocardial O2 consumption) |
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Treatment for sinus tachycardia
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- Beta-adrenergic blockers to reduce HR and myocardial oxygen consumption
- vagal maneuvers if stable (cough, bare down) - Anipyretics to treat fever - Analgesis to treat pain - fluids |
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Premature Atrial Contraction (PAC)
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- ectopic focus in atrium but not SA node
- travels across atria by abnormal pathway - creates a distorted P wave - may stop, continue, or go normal once hits AV node |
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Causes of PAC
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- emotional stress
- caffeine, tobacco, alcohol - Hypoxia - electrolyte imbalance - COPD - CAD - Hyperthyroid disease - Valvular disease |
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Significance of PAC
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- in healthy heart it is not significant
- heart disease- may be warning for dysrhythmias |
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Treatment for PAC
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- Beta-adrenergic blockers
- reduce or eliminate caffeine |
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Paroxysmal Supreventricular Tachycardia (PSVT)
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- ectopic above Bundle if His
- repeated PACs that starts and stops abruptly - occurs when excitation of atria and one way block - Wolff-Parkinson-White syndrome (WPW) or preecitation - extra conduction or accessory pathways |
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Causes of PSVT
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- overexcitation
- emotional stress - deep inspiration - stimulants (tobacco, caffeine) - digitalis toxicity - rheumatic heart disease - CAD - Cor pulmonale |
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Treatment for PSVT
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vagal stimulation and Adenosine (rapid IV push followed by a flush)
Beta blockers (-lol) Calcium Channel Blockers (Cardizem) Amiodorone If doesn't work, cardioversion can be used If patient has Wolfe-Parkinson-White syndrom and keeps reoccuring then treatment is ablation of accessory pathways |
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Affects of Adenosine
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short half life
stops reentry so brief asystole is not uncommon but may have a heavy chest or tunnel vision, not feel good during this |
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Atrial Flutter orinign
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single ectopic focus
saw toothed |
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Atrial flutter is associated with
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CAD
HTN Mitral valve disease Pulmonary emobolus Chronic lung disease Cardiomyopathy hyperthyroid Digoxin, quinidine, epinephrine |
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treatment for atrial flutter
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increase AV block to slow ventricular response with:
Beta blockers, Calcium Channel Blockers, Antidysrhythmia drugs- amiodarone, propafenone, ibutilide Cardioversion Radiofrequency ablation- curative |
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Atrial fibrillation
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multiple ectopic foci- loss of effective atrial contraction
most common dysrhythmia Prevalence increases with age (3% >65yo) |
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Clinical Associations for Atrial fibrillation
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Rheumatic Heart disease
CAD Caardiomyopathy HF Pericarditis Thyrotoxicosis Alcohol intoxication Caffeine use Electrolyte dusturbance Cardiac surgery |
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Goals for tx of A-fibrillation
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- control ventricular rate
- prevent thrombus formation - convert to sinus rhythm |
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Treatments for A-fib
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To slow V-rate: Beta blockers, Calcium Channel blockers, digoxin
Conversion drugs: Amiodarone, propafenone (Rhthmol) DC Cardioversion to convert to NSR If pt has been in A-fib for longer than 48 hours: 3-4weeks of Coumadin is recommended first and for 4-6 weeks after successful cardioversion |
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Maze procedure
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Surgical procedure that stops A fbib by interupting the ectopic electrical signals that are responsible
scar tissue development changes direction to a controlled, different path (like a maze) Done with open heart surgery Use of cold (cryoablation) and heat (high-intensity ultrasound) can be used also |
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Junctional Dysrhythmias
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- Originates in AV node
- Node failed to fire or impulse is blocked at AV node - Impulse then moves retrograde from AV and produces an abnormal P wave just before, after, or inside of QRS * Can serve as an escape mecahnism for an SA node that has not been aeffective--> escape rhythms should not be supressed * If rhythms are rapid this could reduce CO and HF |
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Clinical Associations/causes of Junctional dysrhythmias
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CAD
HF Cardiomyopathy Electrolyte imbalance Inferior MI Rheumatic heart disease Digoxin, amphetamines, caffeine, nicotine |
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Treatment of junctional dysrhythmias
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- If symptomatic--> atropine
- Accelerated junctional rhythm and junctional tachycardia caused by digoxin toxicity--> hold digoxin - Beta Blockers, Calcium Channel Blockers, and amiodarone are used if it is not caused by digoxin toxicity ******DC CARDIOVERSION IS CONTRAINDICATED!!***** |
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Premature Ventricular Contractions (PVCs)
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- etopic focus in ventricles
- premature occurrence of a wide and distorted QRS complex - Multiifocal, unifocal, ventricular bigeminy, ventricular trigeminy, couples, triplets, R on T phenomena |
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PVC clinical association/causes
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- stimulants (caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol)
- Digoxin - Electrolyte imbalance - Hypoxia - Fever - Disease states (MI, mitral valve prolapse, HF, CAD) - May occur after coronary artery clot with thrombolutic therapy in acute MI (reperfusion dysrhythmias) -may occur following plaque reduction after percutaneous coronary intervention |
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PVC significance
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- normal heart: usually benign
- heart disease: may decrease CO and precipitate angina or HF --monitor pts reseponse to PVC --often don't generate a sufficient ventricular contraction to result in a peripheral pulse --Assess apical-radial pulse rate to determine if pulse deficit exists - represents ventricular irritability |
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Treatment for PVCs
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depends on cause:
- oxygen for hypoxia - electrolyte replacement - Beta Blockers, procainamide, amiodarone, lidocaine |
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Ventricular tachycardia
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- a run of 3 or more PVCs
- monomorphic- same voltage level from same foci - polymorphic- dif voltage heights - nonsustained- in and out of v-tach, like a dialysis pt) * Considered life threatening because of decreased CO and the possibility of deterioration to ventricular fibrillation |
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Clinical associations of V-tach
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MI
CAD Electrolyte imbalance Cardiomyopathy Mitral Valve prolapse Long QT syndrome Digitalis toxicity CNS disorders |
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Clinical significance of V-tach
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Stable- pt has a pulse
Unstable- pulseless Sustained VT --> severe decrease in CO |
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Decreased CO S/S
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- hypotension
- pulmonary edema - decreased cerebral blood flow - cardiopulmonary arrest - LOC, unresponsive, no pulse, BP changes |
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Treatment for V-tach
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- must be rapid
- must have prophylactic tx after to prevent reoccurance - V-fib may develop |
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Treatment for Monomorphic V-tach
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If hemodynamically stable (pulse) and presents with Left V function--> IV procainamide, sotalol, amiodarone, or lidocaine
If hemodynamically unstable with poor LV function: IV amiodarone or lidocaine followed by cardioversion |
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Treatment for polymorphic VT
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With normal baseline QT interval: Beta blockers, lidocaine, amiodarone, procainamide, sotalol
- cardioverion is used if drug therapy is ineffective sometimes polymorphic can be casued by magnesium imbalance If have prolonged baseline QT interval- IV magnesium, isoproterenol, phenytoin, lidocaine, or antitachycardia pacing *Drugs that prolong QT interval should be discontinued - Cardioversion if rhythm not converted |
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QT prolonging drug examples
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- Droperidol
- Erythromycin - Dofetilide - Citalopram (Celexa) - Chlorpromaxzine (Thorazine) |
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Torsades de Pointes
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poly morphic
"twisting of the points" associated with prolonged QT interval of the underlying rhythm |
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V tach without a pulse treatment
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* life threatening!
- CPR and rapid defibrillation ** first drug of choice is epinephrine |
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Accelerated Idioventricular Rhythm (AIVR)
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- can develop when SA or AV nodes become less than that of ventricular ectopic pacemaker (irritabilityd
- rate is between 40-100 bpm |
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Treatment of AIVR
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- can be escape mechanism or digitalis toxicitiy
If become symptomatic (hypoTN, angina) --> atropine can be (use cautiously with wider blocks) ** no amiodarone or anything that slows ventricular rate If acute MI- usually self limiting and well tolerated - temporary pacing may be requires |
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Clinical associations/causes of V-fib
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- Acute MI, CAD, cardiomyopathy
- may occur during cardiac pacing or catheterization - May occur with coronary reperfusion after fibrinolytic therapy - Accidental electric shock - Hyperkalemia - Hypoxia - Acidosis - Drug toxicity |
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Treatment for V-fib
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Immediate CPR and ACLS
Difibrillation and definitive drug therapy |
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Asystole
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no electrical activity, no contraction or CO
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Asystole associations
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- Advanced cardiac disease
- Severe cardiac conduction system disturbance - End stage HF |
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Asystole treatment
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CPR, ACLS (intubation, epi)
***NO ATROPINE, external pacing is not appropriate (theres no electrical activity to pace!) |
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Pulseless Electrical Activity (PEA)
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electrical activity on ECG but no mechanical activity in ventricles, no pulse
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Clinical associations with PEA
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- hypovolemia
- Hypoxia - Metabolic acidosis (hydrogen ions) - Hypothermia - Drug overdose - Cardiac tomponade - MI - Tension pneumothorax - Pulmonary embolus - Trauma (H's and T's) |
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Treatment of PEA
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- CPR, intubation, IV epi
- Atropine is used if ventricular rate is slow - Treatments is directed toward correction of the underlying cause PEA- push epi and figure out whats going on |
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Hs and Ts of PEA causes
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- hypovolemia
- Hypoxia - Hydrogen ions (acidosis) - Hyper/hypo kalemia - Hypothermia - Hypoglycemia (not a cause, but mimics everything bad) - tablets (overdose) - tamponade (cardiac) - Tension pneumothorax - Trauma - Thrombosis (MI or pulmonary) |
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Sudden Cardiac Death
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- death from cardaic cause
- usualy as a result of V- dysrhythmias (tach or fib) |
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Prodysrhythmias
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- Antidysrhythmic drugs cause dysrhythmias
- increased risk if severe LV dysfunction - digoxin and class IA, IC and III antidysrhythmia drugs - monitor in hospital |
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Treatment with antidysrhythmic drugs
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- first several days of drug therapy is vulnerable period for developing prodysrhythmias
- oral med regimens are initiated in a monitored hospital setting |
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Defibrillation
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depolarizes cells to allow SA node to resume as pacemaker, for V-fib and V-tach
- output measures in joules or watts per second |
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Recommended energy for initial chocks in defibrillation
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- Biphasic (+ and -)-- first and successive- 150-200 joules
- Monophasic (- only)-- initial shock of 360 joules |
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Choice of therapy for hemodynamically unstable ventricular or supraventricular tachydysrhythmias
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Synchronized cardioversion
-delivered on the R wave of the QRS complex - must turn on synchronizer |
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Implantable Cardioverter- Defribrillator (ICD) is appropriate for
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- pts that have survived synchronised cardioversion
- spontanwous sustained Vtach - syncope with inducible C-tach/fibrillation during EPS (?) - high risk for future life-threatening dysrhythmias |
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ICD
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Implantable Cardioverter-Defibrillator
- lead system placed via subclavian vein to endocardium - battery powered pulse generator implanted subcu approx 25sec after detecting VT or VF it delivers < 25 joules, if first not successful, recycles and delivers successive shocks - have antitach and antibrady pacemakers |
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ICD education
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* very important
- fear of body imae change - fear of recurrent dysrhythmias - pain with ICD discharge - anxiety about going home - encourage ICD support group |
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Pcemaker complications
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infection, hematoma at insertion site, pneumothorax
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Acute coronary Syndrome (ACS) ECG changes
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- in response to inschemia, injury, infarction
- seen in leads that face the area of involvement - recipricol (opposite) changes in leads facing opposite area |
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Ischemia ECG changes
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- ST segment depression and/or T wave inversion
- ST segment depression is significant if it is at least 1 mm (one small box) below the isoelectric line - Response to inadequate supply of blood and oxygen causing an electric disturbance in myocardial cells - one treated, ECG changes will resolve |
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Injury ECG changes
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- ST segment elevation is significant is >1mm above isoelectric line
- if tx is prompt and effective, may avoid infarction - if serum cardiac markers are present, an ST-segment-elevtion MI (STEMI) has coccured |
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Infarction ECG changes
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- Physiologic-- Q wave (small and narrow <0/04s in duration)
-- Pathologic-- deep and >0.03s in duration --> at least hald of the thickness of the heart wall is involved (Q wave MI), pathological Q wave may be present indefinitely _ T wave inversion related to infarction occurs within hours and may persist for months |
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Syncope
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- brief lapse in consciousness accompanied by a loss in postural tone (fainting)
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Cardiovasculr causes of syncope
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- Cardioneurogenic syncope or "vasovagal" syncope
- Primary cardiac dysrhythmias (tachys and bradys) |
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Noncardiovascular causes of syncope
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- hypoglycemia
- Hysteria - Unwitnessed seizure - Stroke - Vertebrobasilar transient ischemic attack |
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Diagnositc studies for syncope
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Enchocardiography
EPS HEad upright tilt table testing (BP, HR abnormal, and clinical symptoms) Holter monitor Event monitor.loop recorder |
