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Atrial Rhythms

Atrial Rhythms

Cardiac conduction system

Cardiac conduction system

These are rhythms that originate somewhere in the atria other than the SA node. Causes include loss of SA node capability and atrial irritability. P waves in this category will have a different appearance than those beats generated from the SA node (can be notched, flattened, peaked, or sawtooth).

Wandering atrial pacemaker

Example Wandering atrial pacemaker

WAP (9.128)

· Rules: R-R slightly irregular ,

Rate 60-100bpm ,

P wave appearance changes with each beat ,

PRI varies but is usually

· Causes: Can be normal- seen in very young, very old, or athletic patients

· Clinical Picture: Usually asymptomatic

· Management: None needed

Premature Atrial Contractions (PAC’s)

It is a type of atrial ectopy caused by irritability. It is a single beat. It is important that you always identify the underlying rhythm and locate the ectopies throughout that rhythm.

Example of PAC

SR with PAC (5.3) (circled)

· Rules: Rhythm will appear irregular due to the ectopic beats interrupting.

Rate depends on underlying rhythm

P wave of the PAC will look different from the rest of the strip. It usually has a QRS following but can be blocked.

PRI 0.12-0.20sec (PAC’s PRI may be longer or different from the others)

QRS <0.12sec

· Causes: fatigue, hypoxia, Digoxin toxicity, caffeine, ischemia, CHF, or ETOH

· Clinical Picture: irregular pulse, but usually asymptomatic

· Management: Treat the cause. Monitor as it can lead to atrial tachyarrythmias. Oxygen, monitor, IV.

Atrial Tachycardia (AT)

Because of its fast rate and supraventricular origin, atrial tachycardia usually gets interpreted as SVT (See SVT in next section)

· Rules:

Regular

150-250bpm

P wave is atrial in origin (not sinus) and may be lost or hidden in T wave due to the fast rate

PRI 0.12-0.20sec

QRS <0.12sec

· Causes: Excessive amount of catecholamines like epinephrine, norepinephrine, and dopamine, or Digoxin toxicity

· Clinical Picture: Rapid, regular pulse. May show symptoms of decreased cardiac output like, dizziness, fatigue, short of breath, syncope. May have chest pain or palpitations

· Management: O2, monitor, IV. Vasovagal maneuvers, carotid massage, drug therapy like Ca channel blockers, Beta-blockers, antiarrhythmics, or cardioversion.

Atrial Flutter (A-Flutter)

Example of Atrial flutter

(12-16) aflutter (5.41)

· Rules: Usually regular but can be irregular

Atrial rate is usually 250-350bpm, ventricular rate can vary

P waves are upright and sawtooth

PRI –not applicable

QRS <0.12sec

· Causes: CAD,Rheumatic heart disease, hyperthyroid, MI

· Clinical Picture: If there is a rapid ventricular response- patient may have symptoms of decreased cardiac output like, dizziness, fatigue, short of breath, syncope and palpitations. Can lead to CHF.

· Management: Oxygen, monitor, IV. Treat the cause. Anticoagulant therapy is initiated due to increased risk of clots (the rapid atrial contraction causes turbulence in the blood which the body thinks is an injury- this causes platelets to collect at the site of the turbulence causing clots). If there is RVR, drug therapy such as Ca channel blockers, beta-blockers, and antiarrhythmics like Digoxin, Corvert, or Amiodarone can be used. Atrial pacing and cardioversion are options if patient becomes unstable.

Atrial Fibrillation (A-Fib)

Example of A-Fib

afib (5.29)

· Rules: Totally irregular.

If ventricular rate 100 “Rapid ventricular response”

No true P waves are produced in this rhythm, just fibrillatory waves

PRI unmeasurable

QRS <0.12sec

· Causes: MI, Digoxin toxicity

· Clinical Picture: Irregular pulse, may have symptoms of decreased cardiac output like, dizziness, fatigue, short of breath, syncope and palpitations. Can lead to CHF.

· Management: Oxygen, monitor, IV. Treat the cause. Anticoagulant therapy is initiated due to increased risk of clots (the rapid atrial contraction causes turbulence in the blood which the body thinks is an injury- this causes platelets to collect at the site of the turbulence causing clots). If there is RVR, drug therapy such as Ca channel blockers, beta-blockers, and antiarrhythmics like Digoxin, Corvert, or Amiodarone can be used. Atrial pacing and cardioversion are options if patient becomes unstable.

STOP! TIME FOR PRACTICE STRIPS ON VARIOUS ATRIAL RHYTHMS

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Sinus Rhythms

Sinus Rhythms

Normal Sinus Rhythm

Examples of NSR

Click to enlarge

· Rules: 

Regular

60-100bpm

P wave is uniform, upright ,and there is one in front of every QRS

PRI is 0.12-0.20 and constant

QRS <0.12

· Causes: Normal

· Clinical Picture: Asymptomatic

· Management: None needed

Sinus Bradycardia
Example of Sinus bradycardia

Click to enlarge

· Rules: Regular

<60bpm

P wave uniform, upright, and one before every QRS

PRI 0.12-0.20sec and constant

QRS <0.12sec

· Causes: Sleep, hypothyroid, drug effects like beta-blockers, Ca+ channel blockers, and antiarrythmics, MI, increased ICP, increased vagal tone (i.e.athletes).

· Clinical Picture: Often asymptomatic, but may show symptoms of decreased cardiac output like, dizziness, fatigue, short of breath, syncope

· Management: If symptomatic, may give drugs to increase HR, apply pacemaker, etc. Also use O2, monitor, IV.

Sinus Tachycardia

Example of Sinus tachycardia

(12-41)ST (4.23)

· Rules: Regular ,

<100bpm ,

P wave same as above ,

PRI 0.12-0.20sec, constant ,

QRS <0.12sec

· Causes: Stress, anxiety, dehydration, pulmonary embolus, fever, exercise, anemia, drug effects (caffeine, cocaine, nicotine), shock, MI, hyperthyroid

· Clinical Picture: Often asymptomatic, but depends on cause. May have palpitations, SOB, chest pain

· Management: Usually should try to treat the cause. Also Use O2, monitor, IV.

Sinus Arrythmia

Example of Sinus Arrhythmia

sinus arrythmia

Also called “Respiratory Sinus Arrhythmia”. Occurs when your heart rate cycles with your breathing. When you breathe in, your heart rate speeds up slightly. When you breathe out, your heart rate slows back down.

· Rules: R-R intervals vary; change with patient’s respirations ,

Rate usually 60-100bpm, but can be slower ,

P wave same as above , PRI 0.12-0.20sec, constant ,

QRS <0.12sec

· Causes: Usually a normal phenomenon. Common in children, young adults, and athletes.

· Clinical Picture: Irregular pulse but usually asymptomatic

· Management: Usually none needed

Sinus pauses and sinus arrest

Caused when the sinus node fails to generate an electrical impulse to stimulate the heart to beat. Many times both of these categories are lumped into one called “Pauses” when interpreting rhythms.

1) Sinus Pause/Sinus block

A sinus pause is followed by a delayed, next sinus beat only.

Example of Sinus pause/Sinus block

sinoatrial block

· Rules: Irregular due to pause. Pause must be followed by a sinus beat.

Length of the pause is usually the same as or a multiple of the distance between two other P-P intervals.

Rate is usually normal but depends on the underlying rhythm.

P waves are uniform, upright, and before every QRS.

PRI 0.12-0.20sec, constant

QRS <0.12sec

· Causes: acute MI, medication effects like Digitalis, and other antiarrhythmics, CAD, myocarditis, CHF, increased vagal tone

· Clinical Picture: May show symptoms of decreased cardiac output like, dizziness, fatigue, short of breath, syncope

· Management: Usually treat the cause. Use O2, monitor, IV.

2) Sinus Arrest

A pause, however, many times is followed by an escape beat. This is called sinus arrest as the sinus node is taking too long to beat again needs help from the AV node.

NOTE: Patients with sinus arrest may have a history of syncope, near syncope, and/or falls.

sinus arrest

· Rules: Irregular due to pause.

Pauses will vary in length and are usually more than one PQRST complex long.

Rate varies depending on underlying rhythm.

P waves uniform, upright, and one before every QRS

PRI 0.12-0.20sec, constant

QRS <0.12sec

· Causes: hypoxia, MI, high potassium, Digoxin toxicity, medication effects like Beta-blockers and Ca+ channel blockers

· Clinical Picture: May show symptoms of decreased cardiac output like, dizziness, fatigue, short of breath, syncope

· Management: Usually treat the cause. Use O2, monitor, IV.

Facts

JUST WHAT IS "SICK SINUS SYNDROME"??

It occurs as a bradycardia with episodes of sinus arrest, sinoatrial block, and atrial fibrillation. Caused by partial destruction of the SA node from things like an MI. Can cause prolonged pauses in heart rate and rhythm and syncope. Many patients with sick sinus syndrome end up receiving a pacemaker.

STOP! TIME FOR PRACTICE STRIPS ON VARIOUS SINUS RHYTHMS

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How to Read, Measure, and Interpret Rhythm Strips

1  Waves and Measuring

Electrodes and leads

Assure good contact with the skin- may need to clean or shave areas before attaching

Electrode: actual equipment you place on the patient

Lead: The view you are seeing of the heart. Most common lead used in telemetry is Lead II. In this view of the heart, imagine there is a camera at the apex (bottom of the ventricles) of the heart looking up toward the top of the atria of the heart. Positive inflections (above isoelectric line) on the EKG represent current going toward the lead/camera and negative inflections (below isoelectric line) represent current going away from the lead/camera.

Graph paper and how to measure

EKG graph

Direction, magnitude, and duration of electrical flow can be measured.

Direction and magnitude (voltage) are measured by the horizontal lines. (For example- in the picture above, the QRS goes up, down, then up. How many boxes, or horizontal lines it goes up and/or down measures its direction and magnitude).

Duration is measured by the vertical lines. For example, in the picture above, the P wave rises and falls. How many boxes, or vertical lines it takes for it to rise and fall is its duration or length).

Voltage

The strength of the current. The stronger the current, the further away from the isoelectric line (the horizontal line from which every wave goes above or below) the deflection will be.

Causes of low voltage: electrodes have come off or worked loose from patient due to sweat, dried gel, or a disconnected wire.

NOTE: Sometimes, if a patient's QRS complexes are too small, it can cause the "low heart rate" alarm to sound on the monitor. This is because they are too small for the monitor to detect. When this happens, turn up the "amplitude" or "gain" on the monitor to make them bigger.

Duration (time and measurement)

EKG paper

(Click on picture left to enlarge)

Large box = 0.20 sec (heavy lines)

Small box = 0.04 sec (lighter lines)

Cardiac Cycle and Corresponding Waves, Intervals, and Segments

EKG

Terminology Definitions for the Cardiac Cycle:

Wave- Deflections above or below the isoelectric line

Interval- Area between and sometimes including waves

Segment- Straight line or area of electrical inactivity between waves

P wave- 1st wave of the cycle. Represents atrial depolarization

PR Interval (PRI)- Includes P wave and PR segment (includes everything from the beginning of the P wave to the Q wave). Represents the atrial depolarization and the slower conduction through the AV junction.

QRS Complex- Larger due to the muscle mass involved. Represents ventricular depolarization.

Complexes may not always look the same from patient to patient:

QRS's

ST Segment- Connects QRS complex and T wave. Starts at end of QRS and beginning of T wave. Sometimes difficult to determine exact beginning and end. Represents the time period that the ventricles are depolarized. It is isoelectric.

T Wave- Represents ventricular repolarization

Refractory Periods

Refractory periods

a) Absolute Refractory- the period when the cells are depolarized or repolarizing; when charges are not equal on inside and outside of cell. Occurs during QRS and T wave cardiac cycle.

b) Relative Refractory- This is a short period of time when the cell is not absolutely refractory. Occurs on the downslope of the T wave. Enough cells have returned to their original positions that, given a strong enough impulse, the cell can be depolarized again. This results in abnormal depolarization. Several undesirable arrhythmias can result from this depolarization including ventricular tachycardia and ventricular fibrillation.

Artifact and Interference

Artifact

Causes: Muscles tremors, patient movement, loose electrodes, effect of other electrical equipment in the room

2  Analyzing Rhythm Strips

One can analyze and measure rhythm strips using two methods- calipers or pencil and paper.

EKG capilers

Calipers: The more accurate method. Used by placing one of the sharp ends on the beginning of the area you are measuring, the other sharp end on the end of the area you are measuring. The calipers will also stay stretched to this width.

Bring the calipers down to a blank area on the graph paper and count the boxes between the sharp ends. Calipers are also useful for measuring R-R or P-P intervals and PRI interval consistency.

Pencil and paper: Use this method when calipers are not available. Take a piece of paper and hold it up to the rhythm strip. Draw a line on the paper where you want to begin and end measuring. Then do the same thing as

CaliperB

with the calipers: bring the paper down to a blank area on the graph and count boxes between the lines on your paper or compare , R-R intervals, etc..

Major Rhythm Categories

Sinus- Originating from the sinus node (intrinsec rate 60-100 beats per minute)

Atrial- Originating from elsewhere in the atria

Junctional- Originating from the AV junction
(intrinsec rate 40-60 beats per minute)

Ventricular- Originating from the ventricles
(intrinsec rate 20-40 beats per minute)

Rhythm Rules (Clues)

Each arrhythmia has been shown to have its own set of clues or rules. However, it is a gray area. No rules are 100% at all times. Use them only as guidelines.

types of irregularity

1) Regularity

a) How to Measure

Check the R-R interval across ENTIRE strip. Should be constant throughout.

NOTE: In slower rates, it may/can occasionally be off by one small square.

b) Three Types

Regularly Irregular- there is a pattern (Example: an interrupting beat every third beat)

Basically Irregular- regular with an interrupting beat or two

Totally Irregular- No pattern at all

2) Rate

a) How to Measure- several ways to calculate but depends on regularity

Telemetry Heart Rate Calculation Methods

MethodHow to
Key Points
Small Box Calculation
Count the number of small boxes between two consecutive R waves and divide into 1500
.Most accurate
·Time consuming
·Used only in regular rhythms
R Wave Calculation
Count the number of R waves in a 6-second strip and multiply by 10
.Not always accurate
.Should be used for quick estimates
Large Box Calculation
Count the number of large boxes between two consecutive R waves and divide into 300
.Not very accurate with fast rates
.Used only with regular rhythms

Large Box Scale Memorization
Memorize this scale:
1 large box = 300bpm
2 large boxes = 150bpm
3 large boxes = 100bpm
4 large boxes = 75bpm
5 large boxes = 60bpm
6 large boxes = 50bpm
.See above

Other rules for rate calculation:

Premature beats: When regular rhythms have (PVC, PAC, etc)- those beats are NOT included in the rate calculation. Use a calculation technique other than counting the R waves.
More than one rhythm per strip: When a strip has more than one rhythm on it, you have two possible options.
1- You can calculate the rate of each rhythm using a technique other than counting R waves.
2- Get another strip from the patient's monitor that has only one rhythm on it- I prefer to do the latter.

3) P wave

Characteristically, if they are “sinus”, they are smooth, rounded, uniform, and upright. They come before the QRS but can be hidden (i.e. may be hidden by T wave in tachycardia)

4) PR Interval

Measure for normal range: 0.12sec to 0.20sec

5) QRS Complex

Measure for normal : <0.12sec

Ventricular vs. Supraventricular

Supraventricular indicates that the impulse originated in the SA node, atria, or AV junction. Check the width of the QRS complex, if it is less than 0.12sec, it is likely supraventricular.

REMEMBER: Greater than 0.12sec may indicate that it is ventricular in origin, but it may also mean obstruction above the ventricles (i.e. Bundle Branch blocks).

STOP! TIME FOR PRACTICE STRIPS

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Commonly Used Cardiovascular Drugs

1.   Commonly Used Cardiovascular Drugs

a. Antiarrythmics- general classification with many branches.  Here are some commonly used ones:-

Amiodarone- works as alpha and beta blocker, Ca channel blocker, and increases refractory period, therefore slowing HR

Digoxin- slows conduction through the AV node, increases cardiac output.  Not for use in emergencies

Ibutilide Fumarate- slows conduction through the AV node- converts afib to SR

Isoproterenol- sympathomimetic- for use in heart blocks, cardiac arrest

Lidocaine- limits Na+ influx into heart cell leading to decreased irritability- used for ventricular tachyarrythmias

Sotalol- decreases HR, prolongs refractory period

Procainamide- prolongs refractory period, decreases automaticity

b. Beta-adrenergic receptor blockers

1)   Actions- blocks the heart cells’ beta-adrenergic receptors which usually accept signals from sympathetic nervous system.  These meds essentially block the effects of the sympathetic nervous system on the heart.  They decrease afterload, BP, HR, and irritability.

2)   Examples:  “-lol” suffix

Metoprolol, Propanolol, Carvedilol, Atenolol

c. Alpha-adrenergic receptor blockers

1)  Actions- blocks the alpha-adrenergic receptors usually found in arteries and smooth muscle.  Smooth muscle relaxer.  Decreases BP and afterload.  Sometimes also used for prostate issues.

2)   Examples: “-osin” suffix

Doxazosin, Prazosin, Tamulosin, Terazosin

d.Calcium channel blockers

1)   Actions- blocks the voltage-sensitive Ca+ channels in the heart and blood vessels.  Prevents Ca+ levels from increasing as much in the cells when stimulated leading to less contraction and slower conduction.  Decreases BP by decreasing CO and HR by slowed conduction.

2)   Examples:  various suffixes including  “-pine”

Amlodipine, Felodipine, Nifedipine, Verapamil, Diltiazem

e. Angiotensin-converting enzyme (ACE) inhibitors

1)   Actions- Prevents angiotensin-converting enzymes from converting angiotensin I to angiotensin II which is a vasoconstrictor.  Lowers afterload and BP.

2)   Examples:  “-pril” suffix

Captopril, Enalapril, Lisinopril, Qunipril, Ramipril

f. Angiotensin receptor blockers (ARB’s)

1)   Actions- Works similar to ACE except it simply blocks the receptors for the vasoconstrictor angiotensin II.  Vasoconstriction is prevented decreasing BP and afterload.

2)   Examples: “-sartan”

Losartan,  Irbesartan, Valsartan

g. Nitrates

1)   Actions- Systemic vasodilators.  Decreases afterload, BP, and relieves angina pain

2)   Examples

Nitroglycerin, Isosorbide mononitrate

h. Diuretics

1)    Actions- Works through different mechanisms depending on class of diuretic.  All essentially decrease preload and afterload by decreasing blood and extracellular fluid volume by excreting it through the kidneys.

2)   Examples:  various suffixes including “-ide”

Furosemide, Bumetanide, Hydrochlorothiazide, Spironolactone

i. Parasympathhetic antagonists (Anticholinergics)

1)    Actions- Blocks parasympathetic nervous system- increasing HR and BP.

2)   Examples- Atropine

j. Sympathomimetics

1)   Actions- Mimics the effects of the sympathetic nervous system causing peripheral vasoconstriction, coronary vasodilation, increased HR, and BP.

2)   Examples- Epinephrine, Norepinephrine, Dopamine

k. Adenosine

1)   Actions- causes transient heart block in the AV junction momentarily stopping the conduction to allow heart to restart and a different pacemaker to take over.  Usually used in supraventricular tachycardias.

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Cardiac Anatomy, Physiology, and Conduction System

1. Cardiac Anatomy and Physiology

a. Heart Anatomy

Anatomy of the Heart  (texasheartinstitute.org)

Anatomy of heart

1) Chambers

a. Atria -Top, smaller chambers – Receive blood from the vena cava and pulmonary vein and squeeze into the ventricles

b. Ventricles -Bottom larger chambers that receive blood from the

atria and squeeze it into the pulmonary artery and aorta

2) Valves

a. Aortic/pulmonic

Aortic- between L ventricle and aorta

Pulmonic- between R ventricle and pulmonary artery

b. Tricuspid, Mitral

Tricuspid- between R atrium and ventricle

Mitral (Bicuspid)- between L atrium and ventricle

3) Mechanical vs Electrical

Mechanical -physical contraction or squeeze in response to electrical stimulation. Mechanical does not work without electrical.

Electrical -signals that tells the heart to beat.

b. Direction of Blood Flow

Anatomy of the Heart (texasheartinstitute.org)

Anatomy of heart

1) Body -Vena cava - R atrium - Tricuspid valve - R ventricle - Pulmonic valve - Pulmonary artery - lungs - pulmonary veins - L atrium - Mitral (Bicuspid) valve - L ventricle - Aortic valve - Aorta - Body

2) Preload vs Afterload

Preload - amount of blood coming back to heart

from venous system. Affected by blood volume and venous blood pressure

Afterload - Amount of resistance met by the heart muscle upon contraction. Affected mainly by dilation or constriction of peripheral arterial system and blood pressure

Here's a tip for understanding the difference between preload and afterload: Preload refers to volume; afterload refers to pressure.

c. Cardiac output

Part of the mechanical function of the heart. Think of the heart as an electrical water pump. A water pump must have all of the following to work properly: the pressure or “squeeze” is must be adequate, the timing must be accurate (has time to fill between squeezes), it must have water to pump, and it must be given adequate energy and electricity. The pump can be affected by both electrical and mechanical issues. The heart works the same way- it must have a strong enough squeeze to get the blood where it needs to go, the atria and ventricles must squeeze at the right time so each can fill appropriately, the heart must have blood in it to pump, and the heart muscle itself must be given enough oxygen and electricity to squeeze- if any of the above components are off- the result can be low cardiac output.

d. Electrophysiology

1) Heart cell automaticity

The heart cell can discharge an electrical current without an external stimulus. All nerves to the heart could be cut and it would still continue to beat. It accomplishes this by changing its membrane permeability through the sodium pump

2) Electrolytes' Role

Sodium pump

Sodium Pump-new-2

a) Sodium and Potassium: The two main electrolytes involved: sodium (Na+) and potassium (K+). Both are positively charged atoms, but not equally charged. Sodium has a stronger positive charge than potassium. This has to do with the physical makeup of the atoms themselves. In the heart cell, at rest, the outside is (+) and the inside is relatively (-) compared to the outside. At rest, the number of positive charges outside the cell equals the number

of negative charges inside. The cell is POLARIZED; there is NO electrical current. The cell is in a “ready” state.

b) Calcium: Calcium's role in the heart is contributing to contractility (the force of contraction) and signal transduction. Calcium levels and the calcium-sensitive proteins inside the heart cells determine the force of the contraction. Calcium acts like a stimulator- stimulating the interactions between the heart muscle filaments causing contraction and generating force. The more calcium in the cell the stronger the force. Once the signal passes, the channel letting the calcium in closes and the cells pump the calcium out and away from the muscle filaments. This removes the stimulus and allows the muscles to relax.

3) Depolarization and Repolarization

Sodium pump

Sodium Pump-new-2

Depolarization: The heart cell produces its electrical current by changing its outer charge to negative. It does this by modifying its membrane, pulling sodium into the cell, and allowing potassium to exit. The cell is no negative on the outside and positive on the inside. The difference in charges causes an electrical current which gets passed from cell to cell along the conduction pathway. This is called depolarization.

Repolarization: Occurs after depolarization when the positive and negative charges return to their original state. (Sodium returns to the outside of the cell and potassium returns to the inside). Cells are then only POLARIZED and ready for another stimulus when each positive charge on the outside is balanced with a negative charge on the inside.

4) Refractory periods

Depolarization cannot occur unless cell charges are returned to their original position. While the cell is depolarized, it is “refractory” meaning it cannot accept another impulse.

e. Indications for Telemetry Monitoring

2. Cardiac Conduction System

a. Path of a Normal Impulse

Cardiac conduction system (acssurgery.com)

Cardiac conduction system

Sinoatrial (Sinus) node - Atrioventricular node - Bundle of His - L & R Bundle branches - Purkinje fibers

b. The Pacemakers

1) Three pacemakers (impulse initiating) sites
Sinoatrial (SA) node
Atrioventricular junction (AV node)
Ventricles

2) Inherent rates
Each site has an inherent rate range. Note: It is possible for those rates to exceed and/or fall below this. Use these ranges as clues and not concrete rules.
SA node: 60-100bpm
AV junction: 40-60bpm
Ventricles: 20-40bpm
The fastest inherent rate available will become the pacemaker of the heart and override everything else. Since the SA node is the fastest- it is usually the pacemaker. If for some reason the SA node fails, the AV node has the next highest inherent rate.

c. Irritability and Escape
There are two reasons the SA node will not be the pacemaker of the heart.

Irritability: Sites sometimes get irritable due to drugs, electrolyte imbalance, hypoxia, injury, etc. and discharge impulses at a faster rate than the SA node.

Escape: Escape rates and rhythms are the “safety nets” of the heart. If the SA node slows to less than 60 (due to drugs, injury, etc) the next pacer will kick in.

NOTE: Irritability will ALWAYS be faster than escape.

REMEMBER: THE SITE THAT INITIATES IMPULSES AT THE FASTEST RATE WILL USUALLY BECOME THE PACEMAKER.

d. Nervous System Influence (Autonomic)

Autonomic Nervous system

Autonomic Nervous System

1) Sympathetic branch (Fight or flight)
a) Areas of the heart influenced
Atria and ventricles
b) Effects
Increased rate

Increased conduction through the AV node
Increased irritability
2) Parasympathetic branch (Rest and digest)
a) Areas of heart influenced
Atria ONLY
b) Effects
Decreased rate
Decreased conduction through the AV node
Decreased irritability
c) Vagus Nerve
Parasympathetic stimulation of the heart is controlled by the vagus nerve.
1) Branches
The right vagus goes to the SA node. If R vagus is over stimulated, may cause bradyarrythmias.
The left vagus goes to the AV node. If L vagus overstimulated, atrioventricular blocks may occur.
2) Activation
Activation of the vagus nerve typically causes lower heart rate, blood pressure, or both.
Activation is caused by stimuli such as vomiting/BM’s, carotid sinus massage, Valsalva manuever, or pain from any cause. Stress can also cause activation when parasympathetic system overcompensates for such a strong sympathetic response- causing vasovagal syncope d/t sudden drop in HR/BP.

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Course Objectives and Disclosures

Title:  UnderstandingEKG Online Clinical Telemetry Course   ONA ID# 17161

Author:  Melissa L. Campagna, RN, BSN

Purpose of this course:  To provide licensed healthcare professionals with information regarding how to interpret EKG readings and care for telemetry patients in a clinical setting.

Who is this course for?  

This course is designed for all licensed healthcare professionals with a focus on those working in areas with telemetry-monitored patients such as ICU, surgery, special procedures, endoscopy, interventional radiology, and basic telemetry hospital units.

Learning objectives:

1) Describe the normal cardiac anatomy and physiology of cardiac conduction.

2) Identify cardiac medication classes and their uses.

3) Identify basic normal EKG waveform morphology and be able to measure and analyze each wave and segment.

4) Describe the distinguishing features of, clinical picture of, and associated treatments for each basic dysrhythmia.

Disclosures:

Author Melissa Campagna, planner Vincent Campagna, and content expert Patricia Hyland have disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

This continuing nursing education activity was approved by the Ohio Nurses' Association (OBN-001-91), an accredited approver by the American Nurses' Credentialing Center's Commission on Accreditation.

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