Rhythm Interpretation and Dysrhythmias Ch. 39

12-Lead EKG

Printout of the heart's electrical activity viewed from 12 different angles as seen in 12 different leads

What is a lead?

electrocardiographic picture of the heart's electrical activity

Rhythm Strip

Printout of only one or two leads at a time

Isoelectric line

Baseline where every wave starts and comes back

Rhythm regularity is determined by

comparing R-R intervals

R-R interval

Distance between consecutive QRS complexes

Regular rhythm

Irregular rhythm (A-Fib)

Regular Rhythm w 1 abnormal beat

Regular but interrupted by premature beats

Regular but interrupted by pauses

Artifact (pt could be moving/ coughing)

Heart rate is determined by

# of QRS complexes per minute

Atrial rate is determined by

# of P waves per minute

6 second strip method

count the # of complexes within 6 seconds and multiply by 10

Large block method

Count the # of big blocks between QRS complexes then divide into 300.

Ex. 300/3.5= 86

Little Block Method

Count the # of little blocks between QRS complexes and divide into 1500.

Ex. 1500/11= 136

Normal Intervals

PR Interval= 0.12-0.20 secs

QRS Interval= <0.12 secs

QT Interval= 0.34-0.43 secs

Normal Sinus Rhythm (NSR)

Rate: 60-100

P waves: upright, matching previous ones

PR: 0.12-0.20 secs

QRS: < 0.12 secs

Sinus Bradycardia

Rate: <60

Cause: Vagal stimulation of vagus nerve, MI, Digoxin toxicity, well-trained athlete

Manifestations: Dizziness, pallor, weakness, syncope, diaphoresis, hypotension

Treatment: Atropine (if symptoms & given IV), O2, pacemaker, hold and meds that are bradycardia inducing

Anticholinergics (Atropine)

Action: bind w muscarinic receptors to block cholinergic effects on the heart and smooth muscles of the bronchi and intestines

Uses of Anticholinergics (Atropine)

Bradycardia, cardiopulmonary resuscitation

Nursing considerations when giving Anticholinergics (Atropine)

tachycardia, restlessness, irritability, hallucination, delirium, increased intraocular pressure, urinary retention, dilated pupils, decreased salivation and gastric secretions, decreased GI motility

CAN'T SEE, SPIT, SHIT

Contraindications associated with giving Anticholinergics (Atropine)

Given in narrow closure glaucoma, caution with renal and liver dysfunction, and various GI/ intestinal disorders

A patient's cardiac rhythm is sinus bradycardia with a heart rate of 34 beats/minute. If the bradycardia is symptomatic, the nurse would expect the patient to exhibit?

Shortness of breath (SOB)

Sinus Tachycardia

Rate: 101-160

Cause: Atropine, emotions, PE, MI, CHF, fever, vagus nerve inhibition, thyrotoxicosis

Manifestations: Decreased Cardiac Output

Treatment: Treat cause if symptomatic/ at risk for myocardial damage. Vagal maneuvers, consider beta-blockers

Atrial Dysrhythmias are a problem in what wave of an EKG

P wave

Premature Atrial Contraction (PAC)

Causes: stress, fatigue, caffeine, tobacco, alcohol, hypoxia, electrolytes

Manifestations: palpitations, "skips a beat"

Treatment: monitoring, withhold stimulants, beta blockers

Supraventricular tachycardia (SVT)/ Atrial tachycardia

Rate: 151-220

P waves: differ from NSR P's

Causes: stress, fatigue, caffeine, tobacco, alcohol, hypoxia, electrolytes, digoxin toxicity, heart disease

Clinical significance: Decrease CO, hypotension, dyspnea, angina

Treatment: Vagal maneuvers, calcium channel blockers, beta-blockers, amiodarone, oxygen, adenosine, cardioversion> ablation.

The primary function of adenosine is

Reset pt. HR and electrocontractility of the heart

Antidysrhythmic meds (adenosine)

Action: slows electrical conduction time through AV node

Uses: SVT

Side effects: Bradycardia or cardiac arrest, tachycardia, facial flushing

How do you administer Adenosine?

Rapid IV push (1-2 secs), followed by rapid normal saline flush, half life= 10 secs

Have crash cart in room with ECG monitoring

Nursing considerations: Monitor ECG continuously

Atrial flutter

Rate: 200-350

Cause: Pulmonary embolus, valvular heart disease, lung disease, thyrotoxicosis, heart failure

Clinical sig: Decreased cardiac output, heart failure, clots

Treatment: calcium channel blockers and/or beta-blockers first, adenosine, antiarrhythmics (amiodarone, flecainide) cardioversion, ablation (tx of choice)

Atrial fibrillation= (irregular/blood clot)

Can be paroxysmal or persistent

Most common type of dysrhythmia

Rate: 350-600

Cause: MI, lung disease, valvular heart disease, hyperthyroidism

Clinical sig: Decreased cardiac output, blood clots causing stroke or pulmonary embolus

If duration <48 hours: Digoxin, calcium channel blockers, beta-blockers, amiodarone, cardioversion

If duration >48 hours: Anticoagulation , TEE, cardioversion

Cardiac Glycosides (Digoxin)

Digoxin

Action: Positive inotropic effect (increases contractility) & negative chronotropic effect (decreases HR) causing an increase in cardiac output (CO)

Use: CHF & Atrial dysrhythmias (Atrial Fib, atrial flutter)

Side effects of Cardiac Glycosides (Digoxin)

Nausea

Loss of usual appetite

Headache

Administration consideration for Cardiac Glycosides (Digoxin)

Never give IM: can cause tissue irritation/sloughing

Watch for Digoxin Toxicity

Lots of drug interaction

Cardiac Glycosides (Digoxin) toxicity increases with?

Hypokalemia

Signs & Symptoms: Headache, Visual disturbances, Nausea, Diarrhea, Vomiting

Nursing care for someone who is taking Cardiac Glycosides (Digoxin)

Assess BP, HR, ECG

Assess serum drug level

Monitor K, Mg, Ca levels

Monitor I&O along w daily weights

Teach S&S of toxicity

Potassium Channel Blocker Antidysrthmic (Amiodarone)

Action: Blocks potassium from re-entering cell to repolarize causing a prolonged refractory period and decrease automaticity

Uses: Vtach, Vfib, SVT, Atrial Fib, Atrial Flutter

Side effects: dizziness, fatigue, hypotension, bradycardia, nausea/vomiting, ataxia, paresthesia

How to administer Potassium Channel Blocker Antidysrthmic (Amiodarone)

May take with food (stay consistent if you take it w food or not)

Avoid grapefruit juice and direct sunlight

Avoid alcohol, caffeine, and tobacco

Nursing Considerations for Potassium Channel Blocker Antidysrthmic (Amiodarone)

Monitor BP, HR, and ECG

Monitor liver and thyroid function

Assess for pulmonary & neuro toxicity

Report HR <60

Ventricular dysrhythmias

HR ranges 0-250

Most lethal of all rhythms

Most will cause symptoms of decreased cardiac output

Premature ventricular contraction (PVC) (AKA: BIG NASTY)

Ventricular bc QRS is affected

Cause of Premature ventricular contraction (PVC) (AKA: BIG NASTY)

Heart disease, hypokalemia, hypoxia, hypomagnesemia, stimulants, caffeine, stress

Clinical Sig: reduced CO, angina

Treatment for Premature ventricular contraction (PVC) (AKA: BIG NASTY)

Treat cause (supplemental oxygen/potassium), amiodarone, procainamide, beta blockers

A patient has a diagnosis of acute myocardial infarction, and his cardiac rhythm is sinus bradycardia with 6 to 8 premature ventricular contractions (PVCs) per minute. The pattern that the nurse recognizes as the most characteristic of PVCs is ?

A wide, distorted QRS complex

Monomorphic ventricular tachycardia

QRS complexes that are the same shape, size, and direction

Polymorphic Ventricular Tachycardia (Torsades de Pointes)

constant change on QRS complex (usually Mg problem)

Causes of Ventricular Tachycardia

MI, CAD, hypoxia, hypokalemia, hypomagnesemia, stimulants

Clinical Sig: pulse (stable VT) or no pulse, Dec CO, Shock, unconsciousness, death

Treatment for Ventricular Tachycardia

Treatment w pulse: procainamide, amiodarone, lidocaine

Treatment wo pulse: CPR & rapid defibrillation (only if DEAD)

Treatment for Polymorphic VT: Mg, isoproterenol, cardioversion

Cardioversion (MUST HAVE A PULSE)

Used for supraventricular dysrhythmias and VT w pulse

Usually small shock w less electricity bc pt is alive

Requires synchronization w cardiac cycle= must have PULSE

Ventricular fibrillation

Pulseless, unresponsive, apneic (death if untreated)

Cause of Ventricular fibrillation

MI, hypoxia, hypokalemia, hyperkalemia, drowning, OD, accidental electric shock

Treatment for Ventricular fibrillation

Immediate CPR, defibrillation, epinephrine, amiodarone, oxygen

Defibrillation (MUST BE PULSELESS)

Larger shock= more electricity

NOT synchronized

Treatment of choice for Vfib and pulseless Vtach

3 ways to deliver a shock

1. Monitor/defibrillator

2. AICD (implanted)

3. AED

Asystole (pulseless & DEAD)

Pt. is dead but must go in room to verify

Cause and treatment for Asystole

Cause: Hypoxia, advanced cardiac disease, severe cardiac conduction problem, end stage heart failure

Treatment: CPR, epinephrine, O2

Pulseless Electrical Activity (PEA)

Electrical activity can be observed on the ECG, but no mechanical activity of the ventricles is evident, pt has no pulse

Poor prognosis unless underlying cause is quickly identified and treated

Pacemakers

Electronic devices implanted into or attached to a patient

Sends out electrical signal causes heart to depolarize

Used to maintain reasonable HR in pt who's HR is too slow

Can pace atrium, ventricle, or both

Indications for pacemakers

Symptomatic sinus bradycardia

Junctional rhythms

Slow ventricular rhythms

AV blocks

Tachydysrhythmias

3 ways to pace w a pacemaker

1. Transcutaneous pacing (thru skin)

2. Transvenous pacing (catheter in heart)

3. Permanent pacer (implant)

Temporary pacemakers

Used when dysrhythmia is likely to last only a few days

Most common types: Transvenous & Transcutaneous

Pulse generator at bedside

Permanent Pacemaker

Used when dysrhythmia is thought to be permanent

Implanted surgically

Can be used to pace atrium, vernticle, or both

Components: Battery (last 5-10 yrs), pacing catheter

Cardiac resynchronization therapy (CRT)

Pacing technique that paces both ventricles to promote ventricular function in HF pts

Pacing: Atrial, Ventricular, Dual Chamber

Dual chamber: both atrial and ventricular are paced

Implantable cardioverter defibrillator (ICD)

Treatment for life-threatening ventricular arrhythmias

Lead system placed via subclavian vein to endocardium

Pulse generator is implanted over pectoral muscle

Batteries must be changed ab every 5-10 years