Arrhythmias (1)

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Arrhythmias Sherry Vickers, RN, MSN, CCRN
Evaluation of Arrhythmias
Electrophysiology Study (EPS) electrical stimulation to various areas of the atrium and ventricle http://www.hrsonline.org/patientinfo/symptomsdiagnosis/hearttests/epstudy/ Used to identify different mechanisms of tachy dysrhythmias as well as heart blocks, brady dysrhythmias and cause of syncope Holter monitor: pt. wears for 24-48 hours and keeps a diary of events Event monitor: recorder placed over chest during symptoms (use telephone) Only turned on when symptoms occur and then call to report symptoms Electrical cardioversion: For emergencies Example: When the pt is hemodynamically unstable Different mode that the defibrillator can do Sedate the pt because you are shocking them while they are awake. Versed- doesn’t get rid of pain, it just makes you not remember the pain. May mix it with Demerol. Diprivan (given by anesthesiologists) May do TEE to see if there are any clots in atrium, because you don’t want to shock someone with a clot because you can throw the clot.) Synchronized with R interval (so it doesn’t fire in the QT interval) HIT SYNC BUTTON

Sinus Bradycardia
Rate less than 60/min Signs and Symptoms: • Grey • N/V • Hypotension • weakness • Pale, cool skin • Angina • Dizziness/syncope • Confusion/disorientation (hypoxia) • SOB Treatment If pt. symptomatic give Atropine (increases the HR) and may need pacemaker If Atropine does not work: Pace pt externally

Sinus Tachycardia
Rate greater than 100/min Treat underlying cause

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• Fever, pain, anxiety, shock, hypoxia- body’s way of compensating, trying to speed up to get blood to tissues • If temp: Tylenol • If Pain: give pain meds Signs and Symptoms • Dizziness • Dyspnea • Hypotension (d/t dec CO) • Angina Treatment If symptomatic can give B-adrenergic blockers (metoprolol, atenolol) to slow the rate down

Premature Atrial Contractions
Ectopic focus that did not originate in the SA node Aggravation around the SA node Originates in the atrium (L or R) New onset: need to investigate why the pt is having them First thing to ask: DIET Causes: • • • • • • Stress Caffeine Tobacco Alcohol CAD COPD

Treatment: monitor. • • • • Don’t cause a lot of problems; we don’t really worry about them. They are just early beats. But you do need to count them, along with PVCs for heart rate! Could give Beta Blockers for treatment

BBB
QRS > 0.12 seconds New onset: need to know why L or R is determined by 12-lead Causes: • • • • MI CHF Heart disease Cardiomyopathy

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Treatment: Monitor unless new BBB

Atrial Flutter
Sawtooth-shaped flutter waves Causes: • CAD • Hypertension • lung disease

Atrial rate 250 to 350/min; ventricle rate varies (usually on the slow side) Need blood thinner (RISK FOR BLOOD CLOT) Increased risk for thrombus formation in the atria d/t stasis blood Coumadin to prevent strokes The high ventricular rates and loss of the atrial “kick” decreases CO which causes serious consequences such as HF (especially in pts with underlying heart disease) Treatment Rapid ventricular response: need to slow down Cardizem: reduces rate “Controlled A-fib/A-flutter”: been slowed by meds Drug Therapy: Cardizem, digoxin, Badrenergic blockers, Cordarone, Rythmol, Betapace Cardizem or Digoxin: May actually convert pt back to SR (mostly new onset)

Atrial Fibrillation
Total disorganization of the atrial electrical activity Intermittent or persistent Cause: CAD CHF Cardiomyopathy caffeine use stress cardiac surgery thyrotoxicosis Ineffective atrial contractions and/or rapid ventricular response will cause decreased CO

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May need cardioversion- called snyc mode, will see red dots on QRS to make sure it doesn’t fire during the resting period, because that can throw them into a lethal arrythmia) Thrombi can form in atrium (need blood thinner) TEE can assess for clots A-fib for longer than 48 hours warrants anti-coagulation therapy Coumadin for 3 wks prior and 4 wks after conversion therapy Treatment: Drug Therapy: Goals of treatment: Dec in ventricular response Rate control: Calcium channel Prevention of cerebral embolic events blockers, beta blockers, digoxin, Conversion to SR Multaq Cardizem Digoxin Cordarone Betapace If drug and cardioversion does not convert rhythm, Coumadin will be needed for lifelong treatment

Ablation therapy: Burn out area around the SA node (sometimes chosen over Coumadin therapy) Could be completely pacemaker dependent s/p procedure depending on how much is burned off Maze Procedure: A heart surgeon creates multiple cuts into the upper part of your hear in an intricate pattern, or maze. Surgeon then stitches the incisions together to produce scars which do not carry electrical signals

PVC’s
Premature Ventricular Contractions In heart disease, PVCs may reduce the CO and precipitate angina and HF depending on the frequency Cause: Stress Caffeine Hypoxia Hypokalemia MI Fever Exercise Treatment: Lidocaine (side effect- Lidocaine Crazies, messes with CNS, can become very confused) Cordarone Two PVCs (such as one facing up/one facing down, are called “multifocal” PVCs and are more alarming b/c heart is irritated in more than one spot) Two aggravated places in the ventricle, puts pt more at risk for lethal dysrhythmias

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New onset: look at pt to see if they are symptomatic, VS, electrolyte values (could be cause—Hypokalemia is biggest cause)

Ventricular Tachycardia
Patient can have a pulse or may not have a pulse Pt will probably lose the pulse within a matter of time Ventricles take control as pacemaker Causes dec CO and the possibility of developing V-fib Check patient may be artifact (DO NOT TREAT THE MONITOR) Chest physiology, Parkinson’s, brushing teeth can mimic it on the monitor Treatment: With a pulse Lidocaine or Cordarone Without a pulse defibrillate, CPR

Ventricular Fibrillation
Heart is quivering! NO CO No pulse Occurs in acute MI and myocardial ischemia, and in chronic diseases (HF and cardiomyopathy) Could occur during cardiac cath (d/t stimulation of the ventricle) Coronary reperfusion s/p fibrinolytic therapy Unresponsive, pulseless, apneic state Causes: MI Hyperkalemia hypoxia Treatment: CPR and immediate defibrillation (as soon as possible) The quicker defibrillulated the better the chances of survival

Torsades de Pointes
Life-threatening dysrhythmias which may result from: Hypokalemia Hypomagnesemia an overdose of tricyclic antidepressant or antidysrythmic drugs Alcoholics and QT prolongation are most likely the pts (pts on cordarone) Magnesium is the pharmacologic treatment

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First degree AV Block
PR interval > 0.20 seconds (prolonged conduction) No treatment monitor. If new onset need to wonder why. Causes: MI Ischemic heart disease Some drugs (beta-blockers, Dig toxicity) Could be a warning sign, if beta-blocker induced subsequent doses could cause more blocks Usually asymptomatic No treatment Monitor for any new changes in heart rhythm

Second degree AV Block Type I
PR interval gradually prolongs until a QRS is not conducted after a P wave Wenckebach WARNING May be a warning sign for more serious AV conduction disturbances Not always symptomatic CV status, N/V Same s/s as bradycardia (d/t low HR) Bradycardia is more likely to become symptomatic when hypotension, HF, or shock is present Causes: Digoxin toxicity B-blockers MI Ischemic cardiac disease If continued without treatment, could result in Type II block Usually result of myocardial ischemia or infarction Usually transient and well tolerated Treatment: If symptomatic atropine or pacemaker Especially if history of MI

Second degree AV Block Type II
PR interval constant, impulse not conducted after a P wave Impulse doesn’t make it to the ventricles Often progresses to third degree block Poor prognosis Decreased HR frequently results in dec CO with subsequent hypotension and myocardial ischemia

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Cause: Rheumatic heart disease MI Digoxin toxicity Treatment: If symptomatic: pacemaker atropine

Third degree

No impulses from the atria are conducted to the ventricles DIVORCE The ventricles are not communicating with eachother Atria are stimulated and contract independently from the ventricles Results in dec CO with subsequent ischemia, HF, and shock Syncope could result from severe bradycardia or even periods of asystole Causes: CAD Myocarditis Cardiomyopathy heart surgery MI Sick sinus syndrome Treatment: Drug therapy: Inc HR and support BP until pacing is established If due to Calcium channel blocker toxicity treat with Calcium chloride if symptomatic: atropine pacemaker Don’t keep giving a med that might be causing this

Asystole

No electrical activity Total absence of ventricular electrical activity Make sure none of the leads have come off Should be assessed in more than one lead V-fib may masquerade as asystole Causes: MI cardiac trauma Advanced cardiac disease Prolonged arrest without resuscitation 5 H’s and 5 T’s

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Hypokalemia Hyperkalemia Cardiac Tamponade Treatment: CPR ACLS Intubation Epinephrine atropine Not recommended to shock anymore, shows that it does not improve mortality rates.

Pacemakers
External- use defibrillator pads; pt will need sedation (transcutaneous pacing) Epicardial: Heart surgery Pt’s who have had CABGs Temporary- sheath placed into internal jugular vein or femoral vein by MD Permanent- placed in surgery or cath lab

Permanent Pacemaker Care
Do not allow patient to sleep or turn on right side- can pull leads in heart off, and then the leads will fire off randomly wherever they are in the heart • Regardless of where the pacemaker was placed • Will have an immobilizer that will hold the arm in place  Dependent on side (R side, R arm will be immobilized) Do not raise affected arm (side pacemaker is placed) a month to six weeks Keep HOB elevated for first 24 hours THEY CANNOT LAY FLAT Stay in bed until bed rest is up (usually first 24 hours) Do not wear pull over shirts for first month (got to raise arms) Keep immobilizer on until MD DC’s order- keeps affected arm immobilized Wires in the heart can come loose very easily Could take months for the skin to grow around the wires to anchor them Prophylactic antibiotic treatment as well as post-op Chest x-ray to check lead placement and rule out pneumothorax Monitor insertion site (bleeding or infection) EKG monitoring PPM DC Home Instructions • • • • • Do Do Do Do Do not not not not not lift anything heavier than a fork or newspaper- month or so do yard work, use a push mower, tractor, or hedge clippers remove steri-strips (let them fall off) wear tight clothes get wet until MD says O.K.

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• • • • • • • • • Do not allow child to hit or use rifle on that side No MRIs- ever, have CT instead Can use microwaves Do not have cell phone in breast pocket over PPM Do not lean directly over open hood of running car (produces an electrical field)- forever Will set off metal detectors (keep card on person) Know lowest rate set for PPM if pulse falls below call MD (need to check pulse regularly) Carry ID card with you at all times Pacemakers and leads get recalled all the time

Defibrillation
Monophasic Defibrillators- 360 Joules Biphasic Defibrillators- 150-200 Joules Don’t have to use as much energy, b/c the current is given in two different ways Automatic external defibrillators (AED) Implantable Cardioverter-Defibrillator (ICD) Synchronized Cardioversionmay be used for emergency or nonemergency must have sync button on when in use TX of v-fib or v-tach ***** T WAVE May see a peaked T with hyperkalemia Inverted T wave may suggest myocardial ischemia

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