Chapter 13: Cardiac Rhythm Disturbances

Phase 0

-Depolarization begins once the myocyte receives an impulse from a neighboring cell -Na+ quickly enters the cells through fast Na+ channels, some Ca++ enters the cells through slow Ca++ channels and the K+ channels close -With all this Na+ and Ca++ entering the cell, it becomes more positively charged -The charge overshoots neutral, rising to about 130 mV -When a certain level is reached, depolarization of the entire cell occurs

Dropped Beats

-Dropped beats occur when the SA node fails to initiate an impulse resulting in a pause in the ECG rhythm -Usually, the SA node recovers and fires another impulse -If the SA node fails to fire, then an escape pacemaker from the atria, AV junction, or ventricles initiates an impulse

Treatment of Sinoatrial Exit Block

-No treatment is indicated provided the patient is asymptomatic -If the patient is symptomatic, treatment includes administration of atropine or temporary or permanent ventricular pacing

Sinus Arrest

-Occurs when the SA node transiently stops firing -Results in short periods of cardiac standstill until a lower-level pacemaker discharges or the SA node resumes its normal function -Most prominent characteristic is a pause in ECG rhythm -Produces an irregularity -Rhythm typically resumes its normal appearance after pause unless an escape pacemaker resumes the rhythm

Effects of Sinus Bradycardia

-Often insignificant and the patient is asymptomatic -Hypotension can result if the heart rate slows to the point where cardiac output drops sufficiently -Patients are less tolerant of rates < 45 BPM

Dysrhythmias

-Refers to any ECG rhythm that differs from normal sinus rhythm -Heartbeat may be slower or faster than normal, irregular, or conduction through the heart may be delayed or blocked -Sometimes the first clinical manifestation of a cardiac dysrhythmia is sudden death

How does the heart beat arise?

As an electrical impulse from the SA node

Triggered Beats

Occur when problems at the level of the ion channels in individual heart cells lead to partial repolarization Partial repolarization causes repetitive ectopic firing called triggered activity Depolarization produced by triggered activity is known as afterdepolarization and can bring about atrial or ventricular tachycardia Are relatively rare but can result from the action of antidysrhythmic drugs, cell injury, and other conditions

Sinoatrial Exit Block

Occurs when the SA node fires but conduction to the atria is delayed or blocked

Proarryythmia

Refers to the development of new or a more frequent occurrence of pre-existing dysrhythmias that are caused by antidysrhythmic therapy or drugs used to treat other conditions

underlying rhythm

Sinus rhythm may be what is referred to this means is the sinus rhythm is seen, but then there is another dysrhythmia or cardiac condition seen as well. For example, if there is a delay in conduction through the AV node (referred to as first degree AV block, in chapter 15) then we call it sinus rhythm with first degree AV block (Figure 11-9A). Similarly, if there are early beats, we call it sinus rhythm with early beats

Effects of Dysrhythmias

Some are of little consequence and simply annoying while others are life-threatening medical emergencies that can lead to cardiac arrest and sudden death Some dysrhythmias slow the heart rate decreasing cardiac output Others decrease the stroke volume by making the heart beat too fast (which decreases cardiac output by not allowing the heart to fill properly)

Symptomatic

Symptoms such as lightheadedness, dizziness, fainting, chest pain, shortness of breath, sweatiness, and/or pallor may be seen in dysrhythmias that cause decreased cardiac output

After the atria contracts ..

The impulse then activates the AV node but it is slightly delayed there allowing the atria to finish contracting and pushing any remaining blood from their chambers into the ventricles

After it enters the ventricles ...

The impulse then spreads through both ventricles via the Bundle of His, right and left bundle branches, and the Purkinje fibers, causing a synchronized contraction of the ventricles and thus, the pulse

Causes of Mechanisms of Dysrhythmias

increased parasympathetic tone myocardial hypoxia, injury and infarction increased automaticity reentry triggered beats proarrhythmia

Some impulses originating from the SA node fail to conduct to the ventricles resulting in ?

one or more dropped ventricular beats

Causes of Sinoatrial Exit Block

(See Chart)

Myocardial Hypoxia, Injury, and Infarction

-An oxygen deprived myocardium is extremely susceptible to dysrhythmias -Pulmonary disorders that interfere with adequate intake of oxygen are major causes of dysrhythmias -Damage to portions of the heart's conduction system can result in blockage of impulse formation and/or conduction -Sometimes myocarditis can precipitate dysrhythmias

Phase 3

-Ca++ channels close and many K+ channels open allowing a rapid outflow of K+, causing the cell interior to become more negatively charged -Ca++ and Na+ are pulled out of the cell interior by Na+ and Ca++ pumps helping to achieve and maintain the very negative resting membrane potential of the myocyte

Phase 2

-Ca++ enters the cell through voltage-gated L-type Ca++ channels, prolonging the depolarization -This movement of Ca++ into the cell counteracts the potential change caused by the movement of K+ out of the cell -Ca++ then reacts with myosin and actin causing the cell to contract

How can bradycardia be brought on?

-Can be brought about by failure of the SA node. Escape pacemaker should arise from the AV node or ventricles but is likely to result in bradycardia -Can also be caused by AV heart block -Can also be seen when the atria repeatedly or chaotically depolarize and bombard the AV node so rapidly that not all the impulses are conducted through to the ventricles -If the number of atrial impulses reaching the ventricles falls to less than normal, it results in a slower than normal ventricular rate

Treatment for symptomatic sinus tachycardia is directed at treating the cause

-Continued monitoring is indicated with an underlying medical or traumatic condition -For patients experiencing myocardial ischemia, consideration may be given to additional treatments that will slow the heart rate or vasodilate the coronary arteries

Normal Sinus Rhythms (NSR)

-During normal heart activity, SA node acts as the primary pacemaker -NSR has a heart rate of 60 to100 BPM (in the average adult)

Early Beats

-Fire early, before the SA node has a chance to initiate the impulse -Can arise from anywhere in the heart, including the atria, AV junction, or ventricles -The R-R interval between the normal complex and premature complex is shorter than the interval between two normal complexes -Frequent premature beats may progress to atrial, junctional, or ventricular tachycardia or deteriorate into ventricular fibrillation

Tachycardia

-Heart rate greater than 100 beats per minute -Has many causes -Leads to increased myocardial oxygen consumption -Extremely fast rates can have an adverse affect on cardiac output -When it arises from the ventricles it may lead to a chaotic quivering of the ventricles called ventricular fibrillation

bradycardia

-Heart rate less than 60 beats per minute -Can occur for many reasons and may or may not have an adverse affect on cardiac output -In the extreme, it can lead to severe reductions in cardiac output and eventually deteriorate into asystole -Can arise from the SA node. Sometimes this is normal. Can also be caused by increased parasympathetic (vagal) tone or a variety of medical conditions

Treatment of Sick Sinus Syndrome

-However, because both bradydysrhythmias and tachydysrhythmias may be present, drugs to control the rapid heart rates may worsen bradydysrhythmia -For this reason, a pacemaker is implanted before drug therapy is begun for the tachydysrhythmia

Lead II

-Is the most commonly used lead for identifying dysrhythmias -Has an excellent view of normal conduction of the impulse through the heart

Effects of Sinoatrial Exit Block

-Is usually insignificant -Can be clinically significant when there is an extended pause or when there are frequent occurrences of the dropped P waves (and subsequent QRS complexes) -Can lead to decreased heart rate, a drop in cardiac output, and decreased blood pressure and tissue perfusion

Treatment of Dysrhythmias

-Many dysrhythmias require no treatment as they are either benign or resolve on their own -The method used to manage dysrhythmias depends on whether or not the patient is stable or unstable -Patients who are symptomatic are considered unstable because symptoms indicate decreased cardiac output -Several treatment options are available to treat dysrhythmias and are employed on the basis of the mechanism or etiology of the dysrhythmia -Commonly used treatments include physical maneuvers, electricity therapy, and the administration of certain medications

Causes of Sinus Tachycardia

-Often occurs with physical labor, exercise, pain, fear, excitement, anxiety, and where increased sympathetic stimulation occurs in response to the need for more oxygen and nutrients at the cellular level (see chart)

Effects of Sinus Tachycardia

-Often of no clinical significance -Can increase myocardial oxygen consumption which can aggravate ischemia (bringing on chest pain), and infarction, particularly in those with cardiovascular disease

Treatment of Sinus Dysrhythmia

-Provided the patient is asymptomatic, usually no treatment is needed -If unrelated to respirations, consideration may be given to treating the underlying cause

Increases Automaticity

-Results from stimulation of the sympathetic nervous system -Causes the cells to spontaneously depolarize more quickly -The resulting heart rhythm depends on where the impulse originates -If it is the SA node, the rhythm remains normal but faster than 100 beats per minute -If it is an ectopic focus, any number of dysrhythmias may ensue May cause a single, occasional early beat or it can produce a sustained abnormal rhythm -Sustained rhythms produced by an ectopic focus in the atria or atrioventricular junction are less dangerous than those that arise from the ventricles

Sinus Dysrhythmia

-Same as NSR except there is a patterned irregularity -Described as a cycle of "slowing, then speeding up, then slowing again" -The beat-to-beat variation produced by irregular firing of the SA node usually corresponds with the respiratory cycle and changes in intrathoracic pressure -Heart rate increases during inspiration and decreases during expiration

Increased Parasympathetic Tone

-Stimulation of the parasympathetic nervous system causes the heart rate to slow and impulse conduction through the AV node to be prolonged -Can lead to bradycardia, sinus arrest and/or AV heart block

Electrical Therapy

-Synchronized cardioversion -Defibrillation -Pacing

SA Node Depolarization

-Through the property of automaticity, the heart's pacemaker cells spontaneously depolarize -They have what can be described as an unstable resting membrane potential

Effects of Sinus Dysrhythmias

-Usually of no clinical significance and produces no symptoms -In some patients and conditions it may be associated with palpitations, dizziness, and syncope

Phase 1

-Voltage-gated Na+ channels close, and a small number of the K+ channels open stopping the fast inflow of Na+ and allowing some K+ to move out of the cell -Chloride (Cl-) ions enter the cell -These ion movements lower the positive charge inside the cell somewhat

Types of Dysrhythmias

-bradycardia -tachycardia -early (premature) beats -dropped beats, or QRS complexes -irregular rhythms

Dropped QRS Complexes

-can occur from a partial or intermittent block at the AV junction -can also occur when a premature beat arises from the atria but fails to conduct to the ventricles -This is seen as more P waves than QRS complexes and R-R intervals that are longer wherever there is a dropped ventricular beat

fibrillation

-form of reentry Results when there are multiple micro-reentry circuits in the heart chambers and they are quivering due to chaotic electrical impulses -Atrial fibrillation occurs in the atria -Ventricular fibrillation occurs in the ventricles

Symptomatic patients of Sinus Arrest

-may be treated with administration of atropine or temporary or permanent ventricular pacing -Reasons to pace include the development of an AV junctional or ectopic ventricular pacemaker that is slow enough to result in such problems as syncope, CHF, angina, or frequent ventricular ectopic beats -As needed, drugs affecting SA node discharge or conduction, such as beta-adrenergic blockers, calcium channel blockers, and digoxin, should be discontinued

Five Types of Tachycardia

-narrow QRS complex regular rhythms, -wide QRS complex regular rhythms, -narrow QRS complex irregular rhythms, -wide QRS complex irregular rhythms, -wide QRS complexes of unknown origin. Being able to differentiate between the five types of tachycardia will help determine what type of treatment should be employed

Asymptomatic patients of Sinus Tachycardia

-require no treatment -However, patient should be encouraged to abstain from triggers such as alcohol, caffeine, and nicotine

From the SA node where does it spread?

Across the atria depolarizing the tissue and causing the atria to contract

Effects of Sick Sinus Syndrome

Although many types are symptom free, patients may present with Stokes-Adams attacks, fainting, dizziness or lightheadedness, palpitations, chest pain, shortness of breath, fatigue, headache, and nausea

Effects of Sinus Arrest

Becomes clinically significant with an extended pause or when there are frequent occurrences of the pause or arrest -Can lead to a drop in cardiac output and decreased blood pressure and tissue perfusion There is also a danger that SA node activity will completely cease and an escape pacemaker may not take over pacing

Causes of Sinus Dysrhythmias

Can occur naturally in athletes, children, and older adults (look at chart)

Dysrhythmias

Can originate from the SA node, atria, AV junction, or ventricles and can occur due to AV heart block

Relative Refractory Period

During the later phase of repolarization a sufficiently strong stimulus will depolarize the myocardium

Absolute Refractory Period

During this period, no stimulus, no matter how strong, will depolarize the cell -Helps assure the rhythmicity of the heartbeat -Assures that after contraction, relaxation is nearly complete before another action potential can be initiated -Prevents spasm-producing (tetanic) contractions in the cardiac muscle This period includes Phases 0, 1, 2, and part of phase 3

Causes of Increased Automaticity

Emotional stress or physical exercise, caffeine, amphetamines, ischemia, hypoxia, atrial stretching or dilation hyperthyroidism, or a myriad of other medical conditions, such as hypovolemia, congestive heart failure, etc

Identifying Dysrhythmias

Examination of the ECG rhythm on the ECG monitor must be done in a systematic, organized way

Sinus Bradycardia

Has all the characteristics of NSR but the heart rate is < 60 BPM

Sinus Tachycardia

Has same characteristics as NSR but has a rate >100 BPM

Nonpacemaker Myocyte Depolarization: Phase 4

In the polarized state, nonpacemaker myocytes have a resting membrane potential of -80 to -90 mV which remains stable until the cell is stimulated

Sick Sinus Syndrome

Is a group of abnormal rhythms that occur with malfunction of the sinus node -Bradycardia-tachycardia syndrome is one variant in which slow dysrhythmias and fast dysrhythmias alternate

Causes of Sick Sinus Syndrome

Is a moderately uncommon disorder (see chart)

Irregularity

Is caused by some type of dysrhythmia including: -early beats and dropped beats -dysrhythmias that speed up and slow down in a cyclical manner -those that originate from more than one site (sometimes from many sites) -some types of AV heart block

Reentry

Occurs when an electrical impulse reenters a conduction pathway rather than moving from one end of the heart to the other and then terminating -Some hearts have an accessory pathway located between either the right atrium and the right ventricle or the left atrium and the left ventricle -These accessory pathways allow electrical impulses to bypass the AV node and depolarize the ventricles -Some hearts have a dual conduction pathway through the AV node -Under the right circumstances, reentry can occur in both accessory pathways and dual conduction pathways through the AV node

Causes of Sinus Bradycardia

Often occurs naturally as body's way to conserve energy during times of reduced demand for blood flow (look at chart)

Causes of Sinus Arrest

Results from marked depression in SA node automaticity (look at chart)

sinus rhythms

Rhythms originating from the SA node are called sinus rhythms

What is the hearts primary pacemaker?

The SA node because it reaches its action potential more quickly that the other pacemakers cells.

Medications for slow heart rates

a drug that blocks the effects of the parasympathetic nervous system, such as atropine, may be initially used

Reentry circuits are responsible for

a number of dysrhythmias, including atrial flutter, most paroxysmal supraventricular tachycardia, and ventricular tachycardia

Depending on the timing, reentry can generate ..

a sustained abnormal circuit rhythm

Cardiac Output

can also be decreased when the atria don't contract properly or contract at all (eliminating the atrial kick which normally pushes blood into the ventricles

antidysrhythmics

can be used to suppress tachydysrhythmias and ventricular fibrillation

bradycardiac patient

may also be treated by directly stimulating the sympathetic nervous system through the use of drugs that have sympathomimetic properties, such as epinephrine or dopamine

Symptomatic patients of Sinus Bradycardia

may improve with the administration of atropine, transcutaneous pacing, or administration of an IV infusion of dopamine or epinephrine

Asymptomatic treatment of Sinus Arrest

no treatment

The most common symptom of dysrhythmias

palpitations, an abnormal sensation felt with the heartbeat

Asymptomatic patients of Sinus Bradycardia

require no treatment but should be monitored in case there is a progression of the bradycardia

Tachydysrhythmias

respond well to medications

Vagal maneuvers

stimulate the vagus nerve, sometimes resulting in slowed conduction of electrical impulses through the AV node -Gagging -Holding your breath and bearing down (Valsalva maneuver) -Immersing your face in ice-cold water (diving reflex) -Coughing

Bradydysrhythmias

well controlled with pacemakers