NU 454 Arrhythmias

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How does myocardial muscle differ from other muscles in the body?

Myocardial muscle differs from other muscle in that it contains its own conduction system. Although it is innervated by the autonomic nervous system, impulses are not needed to maintain the cardiac cycle. You don’t need the spinal cord to innervate the heart. It can generate a pulse by itself. It can operate without any other connection to the nervous system.


How does the autonomic nervous system affect the heart?

Autonomic nervous system controls the:

-rate of impulse formation

-the speed of conduction

-the strength of contraction

Two components of the ANS that affect the heart:

-vagus nerve of parasympathetic nervous system – when stimulated, heart rate decreases, decreases conduction, and decreases contraction.

-Sympathetic nervous system - when stimulated, has the opposite effect of the PSN – speeds up heart rate, conduction, and strengthens contraction.


What are the two types of cardiac cells and what are their characteristics?

There are two types of cardiac cells: Electrical and mechanical

Electrical – responsible for impulse formation and conduction


  1. Automaticity – ability of cardiac cells to initiate an electrical impulse on their own. Controlled by pacemaker cells in the SA node.
  2. Excitability – ability of cardiac cells to respond to an external stimulus such as a chemical, electrical, or mechanical sources.
  3. Conductivity – ability of cardiac cells to receive an electrical impulse and transmit that impulse to an adjacent cell.
  4. Refractoriness – inability of cardiac cells to respond to a new stimulus while contracting. This prevents arrhythmias!

Mechanical – muscle cells responsible for contraction

  1. Contractility – ability to respond mechanically to an impulse by contracting

What are the different forms of electrical activity usually interpreted from an EKG?

Waveform – a movement away from the baseline (isoelectric line) in either direction, positively or negatively

P wave: Indicates atrial depolarization, occurs prior to contraction. Contraction of the atrium should follow. Normal atrial depolarization length is .12. Should be nice and rounded, not notchy. Atrial repolarization is not shown on EKG.

QRS complex: Ventricular activation, indicates ventricular depolarization. Triggers the contraction of the ventricles. Normal length of QRS complex is .04-.12.

T wave: Indicates ventricular repolarization. Should be rounded, should not be high or tented. Abnormal electrolyte levels cause tall, tented T wave. An inverted T wave means ischemia!

ST segment: Indicates early ventricular repolarization. Should not be depressed more than 5 mm, might indicate ischemia. Remember to look at the patient. If elevated from baseline more than 1 mm, indicates a STEMI or unstable angina.

PR interval: The time from atrial activation to the onset of ventricular activation. Indicates AV conduction time – the time it takes to get form the atrium down to the ventricles. .12 - .2 is normal time for this interval.

QT interval: total ventricular activity and the recovery. Beginning of end of T wave. Normal time is less than .44

A U wave can indicate low or high K levels or hyperthyroidism. Don’t usually see it, but you can.

Heart rate can be easily calculated from the EKG strip:

  • When the rhythm is regular, the heart rate is 300 divided by the number of large squares between the QRS complexes.
    • For example, if there are 4 large squares between regular QRS complexes, the heart rate is 75 (300/4=75).
  • To be more specific, the heart rate is 1500 divided by the number of small boxes between the R waves. HR of 79 if 19 small boxes (1500/19)
  • The second method can be used with a regular or irregular rhythm to estimate the rate. Count the number of R waves in a 6 second strip and multiply by 10.
    • For example, if there are 7 R waves in a 6 second strip, the heart rate is 70 (7x10=70). This is fastest and most common
    • This is not as accurate if the rhythm is irregular, but will see it used many times, but is more accurate if it’s regular.

What are the "normals" for the various measurements listed above on EKG?

Rate – Normally 60-100, less is bradycardia, more is tachycardia

Rhythm – Measure distance btwn R waves to determine regularity of rhythm.

P wave – Should have one positive (upward) P wave to every QRS complex. Missing a P wave is a problem

PR interval – Measure from beginning of P wave to R wave. Should be .12-.20

QRS complex – Measure from baseline to baseline. Measure from the Q wave to S wave. Should be from .04-.12.

QT interval – Beginning of QRS complex to end of the T wave. From the Q to the end of the T. Should be less than .44.

ST segment – If have greater than 1 mm elevation, could mean STEMI or more than 5 mm depression, could mean ischemia.

T wave – if elevated more than ¾ the size of the QRS complex, could mean hyperkalemia. If inverted, means ischemia.


What do the terms "polarized," "depolarized," and "repolarized" mean?

Polarized – Also called the “resting membrane potential” is when there is no electrical activity occurring in the heart. Inside of cell has high K+ (and Ca++) and low Na+ (and Cl-), and is in a negative state (relaxed). Before the heart can mechanically contract and pump blood, cardiac cell depolarization must occur.

Depolarized (electrical activation) – When the cardiac cell is stimulated, the cell is said to “depolarize”. The rapid shift of Na from outside the cell to inside the cell, and K to outside the cell. Now the inside of cell has high Na and low K, and is in a positive state (contracted). Depolarization occurs in every cardiac cell, from those in the endocardium to the epicardium. On EKG, P wave represents atria depolarization. QRS represents ventricular depolarization.

Repolarized (deactivation) – The cell has returned to its negative resting level. This causes the cells to separate (relax). On the ECG, the ST segment represents “early” ventricular repolarization, and the T wave represents complete ventricular repolarization. There is the shift of Na back outside the cell, and K back inside, this occurs slowly, causing the polarized (relaxed) state. Relaxation phase.


What is the pathway of an impulse through the heart's electrical conduction system?


  • SA node (60-100 bpm) - in R upper atrium is where normal cardiac impulse begins. It’s the pacemaker. It has automaticity, generates an impulse by itself.
  • Impulse is then transmitted across the atrium causing the atrium to contract, and landing in the AV node
  • AV node (40-60 bpm)- at bottom of R atrium
  • From AV node, impulse travels down the Bundle of His, down R and L bundle branches, exiting through Purkinje fibers (15-40 bpm) to stimulate the ventricle to contract.

What is the electrophysiology of arrhythmias?

Arrhythmias can be initiated by disorders of impulse formation. If the SA node fails to fire or is too slow, an alternate pacemaker from another site will fire.

Also, these secondary pacer sites may fire ahead of the SA node. These beats, whether early or late, come from an “ectopic” focus from somewhere in the atria, ventricle, or AV nodal area.

Arrhythmias can be caused by several things. Treatment depends on symptoms and causes.


How do we evaluate dysrhythmias? What are some reasons to obtain an EKG on a patient?

In addition to continuous ECG monitoring, whether bedside or telemetry, there are other ways to evaluate dysrhythmias.

  • Electrophysiology (EPS) testing and ablation – The introduction of several electrode catheters into the right side of the heart. Different areas of the heart are electrically stimulated to purposefully induce a dysrhythmia. When problem areas are identified they are ablated.
  • Holter monitor – A patient wears a monitor for 24 hrs. and keeps a diary of activites and symptoms, which are compared to the ECG strips.
  • Event monitor – doesn’t record continuously, only records when pt is symptomatic.

Reasons to obtain an ECG reading for a patient:

  • to monitor hear rate, rhythms, or dysrhythmias
  • to diagnose a problem such as ischemia, injury, or infarction

If monitoring for rate and rhythm is all that is required, a cardiac monitor using 2 or 3 leads is sufficient. For diagnostic purposes of ischemia or infarction, a 12 lead is needed.


What are the characteristics of sinus arrhythmia?

Description: Irregular rhythm that originates in SA node; rate rises and falls with respirations; common in children,

ECG Characteristics:

  • Rate: 60-100
  • Rhythm: irregular w/respirations
  • P wave: precede each QRS
  • PR interval: normal
  • QRS complex: normal

Therapy: None


What are the characteristics of sinus bradycardia?

Description: decrease in the rate of discharge from the SA node and follows normal conduction pathways; may be normal in some, like athletes or drug induced (digoxin, beta-blockers, calcium channel blockers, narcotics); also may be caused by increased vagal tone (vomiting, rising ICP, carotid pressure, straining to poop) or injury to myocardium very common with acute MI, especially inferior and posterior

ECG Characteristics:

  • Rate: <60 bpm
  • Rhythm: normal
  • P wave: normal
  • PR interval: normal
  • QRS complex: normal


  • Eliminate any known cause
  • If asymptomatic, no therapy. Athletes can have this.
  • If symptomatic (dizziness, weak pulses, syncope, SOB, possibly chest pain, confusion, palor, sx of low cardiac output, decrease in O2 sat, increased respirations, etc.), Always End Danger Pronto! Use Atropine first, then can give Epinephrine, if BP is dropping you give them Dopamine, then may put in a Pacemaker.

What are the characteristics of sinus tachycardia?


  • increase in rate of discharge from SA node with normal conduction
  • causes –.fever, anxiety, hypovolemia, pain, hypotension, hyperthyroidism, drugs, exercise, nicotine, caffeine, smoking, epinephrine, dopamine, anemia

ECG Characteristics:

  • Rate >100
  • Rhythm Normal
  • PR interval Normal
  • QRS complex Normal


  • Identify and treat underlying cause
  • If associate with AMI, may use beta-blockers to control rate

What are the characteristics of a premature atrial contraction?


A contraction that originates in an ectopic (abnormal) focus within the atrium in a location other than the sinus node. (Remember, if from the SA node, will have a normal looking P wave).

Causes: Caffeine, alcohol, stress, fatigue, hypoxia, tobacco, electrolyte imbalances, CAD, COPD, valve diseases

ECG Characteristics:

  • Rate: normal (varies based on frequency of PACs)
  • Rhythm: irregular
  • P wave: none or different looking
  • PR interval: Normal
  • QRS complex: normal


Treat any underlying cause if possible.

Remove any triggers for PACs

May give Beta blockers

May signal a worse type of atrial dysrhythmia.

Depends on symptomology


What are the characteristics of supraventricular tachycardia (narrow complex tachycardia?

Impulse originates in atrial area but not in control by SA node.

Rate>140 to 220; regular; P waves unidentifiable (buried in in T wave)

Narrow QRS complexes

Problem: Low cardiac output d/t rapid rate (heart cannot fill completely)

Causes: Cocaine, ETOH, Caffeine, and other stimulants (cold meds); stress; thyroid or pulmonary disease, P emboli, heart failure, atherosclerosis

Treat: ABCDE

  • Adenosine / Ablation: When giving Adenosine, always have a crash cart available. It causes asystole for a few seconds before hopefully returning to normal sinus. Can be ablation therapy by cardiac cath which is the preferred method. Can also do it surgically. For both, make them NPO for 8 hours, get consent, and start an IV.
  • BB-Corgard
  • CCB-Cardizem; Possible Cardioversion- a synchronized shock on the R wave. Can be emergency or can schedule one. Must have consent, NPO for 8 hours, hold digoxin, and sedate them usually with Versed.
  • Digoxin
  • Excitation (vagal stimulation)

If unstable (symptomatic, having problems): defibrillate the person

If stable (rate is fast, but still awake and relatively asymptomatic): cardiovert (Adenosine or Cardioversion)


What are the characteristics of paroxysmal supraventricular tachycardia?

Description: Originates in ectopic focus anywhere above the bifurcation of bundle of His. Run of repeated premature beats usually initiated by a PAC. Paroxsmal means that it comes and goes.

Causes: stress, overexertion, stimulants, drugs, rheumatic heart disease, dig toxicity, CAD, cor pulmonale

ECG characteristics:

Rate: 150-220

Rhythm: regular or irregular

Pwave: often hidden

PR interval: (if they have a P wave) sometimes it’s short or normal

QRS complex: look normal with fast rate

Causes decreased CO symptoms

Therapy: Same thing as SVT


What are the characteristics of atrial flutter?

Description:The SA node is replaced as the pacemaker by an extremely irritable focus within the atrium which stimulates the atria to contract at a very fast rate (200-350 times per minute). After 2-4 times trying to get an impulse through, the AV node finally gets an impulse through. Looks like a sawtooth.

ECG Characteristics:

  • Rate: atrial rate is 200-350, ventricular rate varies
  • Rhythm: usually looks regular
  • P wave: have flutter waves, called F waves or sawtooth pattern
  • PR interval: can’t measure, don’t have one
  • QRS complex: normal

Clinical significance: Depends on the rate. If the rate has slowed down enough that it causes bradycardia, it’s a problem. If the heart rate and CO is normal, it’s fine.

Therapy: If CO is low, can do cardioversion. Usually, just watchful waiting. But it can turn into atrial fibrillation.


What are the characteristics of atrial fibrillation?

Description: Multiple ectopic focus sites involved that are discharging impulses throughout the atrium. The atria muscle is unable to respond in a uniform way, this leads to a “quivering” effect rather than a true contraction of the atria. The impulses pass through the AV node at irregular intervals, creating an irregular ventricular rhythm. Vent. rates greater than 100 bpm are considered rapid or uncontrolled. This is called a fib with RVR (rapid ventricular rate). Has a bigger chance of clotting and creating an embolus. This is called unstable a fib. Most common dysrhythmia over the age of 65.

Causes: CAD, RHD, Cardiomyopathy, HF, alcohol, thyroid problems, caffeine, electrolyte imbalance, postop problems.

ECG Characteristics:

  • Rate atrial rate can’t be determined usually, but can be as high as 350-600 if counted. Ventricular rate varies. 60-100 is controlled response, over 100 is RVR, less than 60 is SVR.
  • Rhythm Irregularly irregular
  • P wave fibrillating waves (squiggly lines) or can look flatline
  • PR interval can’t measure
  • QRS complex normal

Clinical Significance: Can sometimes co-exist w/ atrial flutter. Causes decreased CO and the threat of coagulation causing a thrombus and CVA. A fib causes 20% of CVAs. If they go into a fib, call the doctor.

Therapy: Rate control, can give Ca channel blockers, beta blockers, digoxin, Eliquis, Coumadin, Pradaxa, and Xarelto (to prevent coagulation). Can cardiovert them, after could hang amiodarone or cardiazem. Can also do radiofrequency ablation therapy. Can do maze therapy – usually done while doing open heart surgery. They make an incision in the electrical area of the heart, scarring prevents the abnormal electrical discharges.


What are the characteristics of junctional dysrhythmias?

Dysrhythmias that originate in the area of the AV node, primarily because the SA node fails to fire of the signal is blocked. This causes a slow rhythm bc the SA node isn’t working.

ECG Characteristics:

  • Rate will be slow! Usually 40-60 bpm.
  • Rhythm Regular
  • P wave Abnormal – inverted, might come after the QRS, or absent
  • PR interval - none
  • QRS complex - normal

Therapy: Treat any underlying cause if possible. Can give atropine to fix it.


What are the characteristics of first-degree heart block?

Description:Every impulse is conducted to the ventricles but duration of AV conduction is prolonged. Only difference btwn normal sinus and 1st degree heart block is that the PR interval is prolonged. Always will be over .20.

Causes: Inferior MI, CAD, Rheumatic fever, hyperthyroidism, vagal stimulation, drugs such as dig, BB, CCB.

ECG Characteristics:

  • Rate normal
  • Rhythm regular
  • P wave normal
  • PR interval - always greater than .20
  • QRS complex - normal

Therapy: None, except removing the underlying cause. Don’t do anything for it, watch and see if it progresses to a high degree block.


What are the characteristics of Type 1 second-degree heart block?


Conduction defect at level of AV node. Sinus impulse transmission through AV node takes longer with each successive impulse until and impulse fails to be conducted to the ventricles. ECG shows a progressively lengthening PR interval, followed by a dropped QRS complex and a pause. This sequence is repeated in a cyclic manner. Can cause palpitations.

Frequent causes – usually result of ischemia or infarction of AV node secondary to blockage of R coronary artery. Can also be due to dig and BB. HF also causes it.

ECG Characteristics:

  • Rate – atrial rate is normal, ventricular rate may be bradycardic due to a dropped beat.
  • Rhythm – ventricular and atrial rates are going to be irregular
  • P wave normal
  • PR interval – progressively lengthening until there’s a drop in the QRS
  • QRS complex - normal

Therapy: Atropine or pacemaker if symptomatic of CO.


What are the characteristics of Type 2 second-degree heart block?


  • more serious than Type I
  • Constant PR intervals on conducted beats, variable blocked QRS (2:1, 3:1, etc.). may occur w/varying ratios.

Causes: Anterior or inferior MI, drug toxicity, RHD, CAD

ECG Characteristics:

  • Rate – atrial rate might be normal, ventricular rate depends on degree of block, usually bradycardia
  • Rhythm – regular atrial rate, ventricular rate is irregular
  • P wave normal
  • PR interval probably prolonged, consistent and constant for every beat, not progressively getting longer like Type 1
  • QRS complex – usually greater than .12

Therapy: Usually worried about Type 2 going into Type 3 block. If symptomatic, they’ll have sx of decreased CO. Treatment is a temporary pacemaker until an underlying cause an be determined. If pacemaker isn’t available, give them atropine. Pacemaker might be permanent.


What are the characteristics of third-degree heart block (complete heart block)

Description: AKA atrioventricular dissociation

  • NO impulses from atria are conducted to ventricle- they beat independent of each other
  • conduction defect is below the AV node
  • The most serious heart block you can have

Causes: Severe CAD, MI, myocarditis, CM, dig, BB, CCB

ECG Characteristics:

  • Rate; Atrial is usually 60-100; ventricular varies, if AV node is controlling it’s 40-60, Perkinjie fibers make it 15-40
  • Rhythm regular
  • P wave normal, but all over the place and not in relation to the QRS
  • PR interval is inconsistent, no relationship to the QRS
  • QRS complex can be normal if block is above the bundle of HIS. Wide if below the bundle of HIS

Therapy: Always symptomatic with third degree block. Best treatment is pacemaker, if not available, give atropine. Typically, have a permanent pacemaker put in. Can also give epinephrine to increase heart rate and BP. Could also give dopamine and Lecophed to increase BP. If they have a CCB toxicity, give Ca Chloride.


What is the only thing you should know about intraventricular conduction blocks?

The QRS is greater than .12 or they look like rabbit ears.


What are the characteristics of premature ventricular contractions?

Description: Arise from an irritable focus in either ventricle. It occurs earlier than the expected sinus impulse and has a wide, bizarre looking QRS with a T wave usually in the opposite direction. Is not a basic rhythm, occur in conjunction with another rhythm.

Causes- hypoxia and hypokalemia (two major ones). Other electrolyte imbalances, stress, stimulants (caffeine, nicotine, alcohol), cardiac ischemia, MI, HF.

They may or may not produce palpable pulse

Treatment depends on cause & symptoms. Most don’t require antidysrhythmics. If more than 6 in a minute, it’s cause for concern. Can give procainenide, BB, amiodarone if symptomatic.

Always assess the pulses with PVCs! Watch the patient for signs of decreased CO.

Types of PVC’s:

  • Bigeminy – every other beat is a PVC
  • Trigeminy – every third beat is a PVC
  • Couplet – two consecutive PVCs
  • Unifocal – PVC’s that look alike and come from the same focus.
  • Multifocal– PVC’s that come from different foci and look different.
  • R-on-T –PVC falls on the T wave of the preceding beat. PVC fires during relative refractory period of vent repolarization often precipitates VT/VF.

What are the characteristics of ventricular rhythms?

Ventricles are the hearts least effective pacemaker. Innate rate of 20-40 (rate below the AV node, bundle of HIS, R/L bundle, purkinjes). Can originate from any part of the ventricle and does not usually follow normal pathway so QRS wide.

Ventricles assume responsibility if:

- SA/AV fails

- Impulse is blocked

- Rate from SA is slower than ventricular rate

- Irritable site in the ventricle produces early beat or rapid rhythm.


What are the characteristics of ventricular tachycardia?

Description: Occur with 3 or more PVC’s in immediate succession.

Nonsustained – lasts less than 30 sec

Sustained - lasts longer than 30 sec, causes decreased CO or no CO at all. Can be lethal

May occur with or without pulses and may be stable or unstable.

Monomorphic VT - QRS complexes have same shape, size and direction

Polymorphic VT - QRS gradually changes back and forth (Torsades with long QT)

Causes: MI, CAD, electrolyte abnormalities (K, Mg, Ca), CM, mitral valve prolapse, a long QT (usually caused by drugs like procainamide), CNS disorders, cardiac disease.

ECG Characteristics:

  • Rate 150-200 bpm
  • Rhythm regular or irregular
  • P wave may not be seen (buried in QRS, may be retrograde),
  • occur independent of QRS
  • PR interval not measurable
  • QRS distorted, greater than 0.12, RR regular or irregular.

VT Treatment:

Unstable(pulseless): ACLS (treat like VF) CPR & Defib, then identify cause!

Stable (pulse): Treat quickly even if nonsustained as may recur or develop VF.

Preserved LVEF: IV antidysrhythmics (procainamide, amio, lido)

Poor EF/low BP amio/lidocaine

Identify cause!


What are the characteristics of polymorphic VT?

Torsades De Pointes Polymorphic VT associated with certain medications and/or electrolyte disturbances (low magnesium) that cause a prolonged QT interval (R on T). May terminate spontaneously or quickly progress to VF. Need to look at in two leads to confirm

Polymorphic VT w/normal QT: Bblockers, antidysrhythmics, DCCV.

Polymorphic w/long QT: Antitachy pacing, Remove offending drugs, abx, other antidysrhythmics, DCCV


What are the characteristics of ventricular fibrillation?


A chaotic rhythm originating in the ventricles; no organized depolarization; myocardium quivers and no effective contraction as a result; the patient is unresponsive, apneic, and pulseless

Causes: Anterior MI, HF, CM, left heart cath procedure, reperfusion of coronary arteries after block, electrical shock, hyperkalemia, hypoxemia, acidosis, toxicity.

ECG Characteristics: none are discernible

  • Rate – not measurable
  • Rhythm – irregular and chaotic
  • P wave - none
  • PR interval - none
  • QRS - none


- ACLS guidelines, but defibrillation is required. The faster treatment is initiated, the better the prognosis.


What are the characteristics of asystole?

Description: No electrical activity, no depolarization, zero CO. Occurs in the presence of severe cardiac damage. Must confirm in at least two leads and no pulse is palpable. Don’t want to mistake for fine VF or disconnected lead.

Causes: Advanced CAD, conduction disorders, or HF.

ECG Characteristics: Not present

  • Rate
  • Rhythm
  • P wave
  • QRS


- ACLS guidelines: All you can do is give CPR and epinephrine


What are two highly fatal dysrhythmias and what are their characteristics?

PEA: Pulseless electrical activity – electrical activity is present, mechanical activity is absent. Usually due to hypovolemia. Always give a bolus of NS and start CPR, then give epinephrine.

SCD: Death due to cardiac event, mostly unknown cause.


What are some general principles of 12 lead electrode placement and management?

Proper electrode placement is essential in order to acquire accurate EKG strips. Most EKG monitor manufacturers have specific placement guidelines.

I, II, III, aVr, aVl, aVf – frontal (limb) leads

  • Lead II (w/three electrodes) is the same as standard lead II in a 12 lead EKG, it is the most common monitoring lead.

V1, V2, V3, V4, V5, V6 – precordial leads (chest)

  • Lead = View

Trouble shooting and tips

Change the electrodes as needed. Usually every day at the time of bath.

Make sure all electrical patient care equipment is grounded.

Be sure all the lead cables are intact. Some manufacturers require changing the cables periodically.

Be sure the patient's skin is clean and dry. Have to shave hair underneath to get a good connection.

Make sure the leads are connected tightly to the electrodes.

Patient movement frequently causes interference. For example, the action of brushing teeth may cause interference that mimics V-tach.


What is the primary EKG component of EKG monitoring when diagnosing ischemia or infarction?

ST segment is the primary component of the ECG that is being observed.

Ischemia – Inverted T wave or ST depression (usually 5 mm or more)

Injury – Elevated St segment more than 1 mm above baseline. Cardiac enzymes are negative.

Infarction-ST elevation, positive cardiac enzymes, eventually a pathologic Q wave that’s at least ¼ the size of the R wave.


What leads and coronary arteries are associated with the anterior, anterolateral, inferior, and lateral walls of the heart?


  • Leads V3 and V4 show ST segment elevation
  • Affects the Left anterior descending coronary artery


  • Leads V3, V4, V5, V6, I, and aVL show ST segment elevation
  • Leads II, III, and aVF show reciprocal ST segment depression
  • Affects left anterior descending coronary artery


  • Leads II, III, and aVF show ST elevation
  • Leads I and aVL show reciprocal ST depression
  • Affects right coronary artery


  • Leads I, aVL, V5, and V6 show ST elevation
  • Leads II, III, and aVF show reciprocal ST depression
  • Affects left coronary artery

What is the difference between rapid defibrillation and synchronized cardioversion? What is an implanted cardioverter defibrillator?

Rapid Defibrillation (<2min) – does not synchronize

Treats: Treatment of choice for v fib and v tach that’s pulseless. Always check the pulse after the rhythm is restored.

Synchronized Cardioversion (DCCV) – synchronized on the R wave: Treatment of choice for ventricular rhythms such as v tach w/ a pulse or supraventricular rhythm.

  • Nonemergent: Consent, NPOx8hr, hold dig, sedate w/ Versed. If they have a fib, they’ll do a TEE to check for clots
  • Emergent: Just shock them w/o consent.
  • Cardio, Oh Say It Isn’t So! Consent, O2 sat monitor, Suction equipment, IV line, Intubation equipment (crash cart), Sedation (Versed) and analgesics

Implanted Cardioverter Defibrillator (ICD) – usually for someone who’s survived SCD or v tach/v fib

  • Teaching: Follow up appointments, S&s of infection, keep clean and dry for 4 days, avoid lifting arm, no driving or sex until cleared by HCP, no MRIs or diathermy (avoid magnets), notify airlines and transportation security, have an ICD ID (bracelet or card), call MC within 24 hours after they have a shock.

What is a pacemaker used for? What are the different methods of pacing? What

Pacemakers Used when the hearts own conduction system (SA Node is the pacemaker of the heart) is malfunctioning. Have a power source & wires that deliver current to the myocardium. Used to: override slow, abnormal rhythms


  • Bradycardia (heart blocks)
  • tachyarrhythmias
  • A-fib w/ SVR
  • After cardiac surgery
  • Sick sinus syndrome
  • When clinical findings are symptomatic

Methods of pacing:

TEMPORARY– power source outside the body

  • Trancutaneous (external)–Used in emergency to provide adequate HR & rhythm. Use two large (anterior/posterior) electrode pads. Warn pt!
  • Epicardial (internal)– A/V Pacing leads sewn to the epicardium during heart surgery and passed through chest wall. Prophylactic for brady/tachydysrhythmias postop.
  • *Always wear gloves when handling pacemaker wires!
  • Tranvenous (internal)- Pacing wire is advanced through a large vein (IJ or SC) into the R atrium and/or R ventricle (endocardial). Typically emergent and bridge to permanent of resolution of dysrhythmia. Watch for infection, pneumo, hematoma,

PERMANENT – power source subcutaneous over pectoral, leads threaded transvenously to R atrium and one or both ventricles


What are the different types of pacemakers?

Fixed vs Demand Pacers:

Fixed: pace rate is set by the HCP regardless of the pats intrinsic heart rate, fires at a constant rate

Demand: Preferred; pacer senses the pts intrinsic heart rate and will pace if the intrinsic signal is slower than the rate programmed; functions if HR goes below set rate.


Output: Amt of current delivered to myocardium

Rate: speed of impulse delivery from pacer

Sensitivity: ability to sense cardiac activity

Biventricular pacer: 3rd lead place in Lt ventricle; one in the R atrium, one in the R ventricle.

(both V have pacing wires unlike more common pacemakers, used primarily for HF pts)

Cardiac Resynchronization therapy (CRT) – paces both ventricles to improve ventricular function. Especially in HF population w/Intraventricular conduction delays. Combined w/ICD for maximum therapy.


What are some common pacemaker problems and complications?

1.F ailure to Sense - the pacemaker does not recognize normal beats and fires inappropriately. It may sense the wrong time and fire when it is not needed (causing VT).

  • Causes: damaged wire, low battery, dislodged lead (turn them on the left side), sensing is too low, fibrosis at the tip of the catheter or lead.
  • Actions: Call the doctor

2.Failure to Capture – the chamber has not responded to a pacing stimulus; on the ECG, the pacer spike is not followed by the appropriate complex

  • Causes: Same as failure to sense
  • Actions: Same as failure to sense

3 .Failure to pace –Absence of spike and no activity! Causes and Actions same as above

Pacer Complications:




*Lead doesn’t implant

*Perforated heart chamber

*Failure to function properly


What is the nursing management required for patients with pacemakers? Patient teaching?

Nursing Management:

  • EKG monitoring
  • Secure leads
  • Infection prevention
  • CXR
  • Keep replacement batteries nearby (for temporary)
  • Wear rubber gives to handle external leads

Patient Education:

  • F/U appointment
  • Monitor pulse (call if slow)
  • Infection; clean/dry for 4 days
  • Avoid lifting arm above shoulder; keep sling on for 1-2 weeks
  • Avoid MRI
  • ID card in wallet/ tell TSA
  • Microwave use is NOT restricted
  • Don’t drive or have sex until OK by HCP