Chapter 13 Cardiac Arrhythmias & ECG Interpretation

Cardiac Arrhythmias and Their Electrocardiographic Interpretation

• Abnormal heart rhythms can cause heart malfunction
• Atria beat synchronization with the ventricles is no longer guaranteed
• Purpose of the chapter, discussion around the physiology of common cardiac arrhythmias and their effects on heart pumping and diagnosis by electrocardiography.
• Underlying cause is usually abnormalities in the rhythmicity-conduction system of the heart:
  • Abnormal rhythmicity of the pacemaker
  • Shift of the pacemaker from the sinus node to another location in the heart
  • Blocks in differing locations of of the impulse through the heart
  • Abnormal pathways of impulse transmission through the heart
  • Spontaneous generation of spurious impulses in almost any part of the heart

Abnormal sinus rhythms

Tachycardia

• This means fast heart rate, which is usually more than 100 beats/min in an adult.
• An ECG recorded from a patient with tachycardia is normal except for the heart rate
• Time intervals between QRS complexes, usually around 150 beats/min instead of the normal 72 beats/min.
• Some causes of tachycardia:
  • Increased body temperature
  • Dehydration
  • Blood loss anemia
  • Stimulation of the heart by the sympathetic nerves
  • Toxic conditions of the heart
• The heart rate usually increases about 10 beats/min for each degree Fahrenheit increase in body temperature (with an increase of 18 beats/min for each degree Celsius), up to a body temperature of about 105°F (40.5°C)
• The heart rate may decrease, higher temperature results in progressive debility of the heart muscle
• Fever causes tachycardia because an increased temperature increases the rate of metabolism of the sinus node, which in turn directly increases its excitability and rate of rhythm
• Sympathetic nervous system excitation from certain causes
  • Severe blood loss, sympathetic reflex stimulation of the heart
  • The heart rate may increase to 150 to 180 beats/min
  • Weakening of the myocardium increases the heart rate
  • The weakened heart does not pump blood into the arterial tree to a normal extent, causing reductions in blood pressure and eliciting sympathetic reflexes

Bradycardia

• Means a slow heart rate, usually less than 60 beats/min
• In athletes hearts are larger and stronger, enabling them to pump large volumes even during rests
• feedback circulatory reflexes or other effects cause bradycardia

Vagal Stimulation

• Reflex stimulates the vagus nerves that releases acetylcholine at the vagal endings in the heart, causing parasympathetic effects
• An example is patients with carotid sinus syndrome
• External pressure on the neck causes baroreceptor reflex which triggers acetylcholine effect causing decreased signal rate
• Sometimes this powerful reflex temporarily stops the heart leading to loss of consciousness (syncope)

Sinus Arrhythmia

• The heart rate increases and decreases during normal respiration, and in deep respiration it increases.
• Results from circulatory conditions altering the strengths of sympathetic and parasympathetic nerve signals being sent to the heart sinus node
• Respiratory type of sinus arrhythmia mainly from spillover of signals from the medullary respiratory center into the adjacent vasomotor center when the subject breathes in and out
• Altering the number of impulses being transmitted through the sympathetic and vagus nerves to the heart.

Heart block within the intracardiac conduction pathways

Sinoatrial Block

• The impulse from the sinus node is blocked before it enters the atrial muscle
• There is sudden cessation of P waves, resulting in standstill of the atria
• Ventricles pick up a new rhythm but the impulse usually originates spontaneously in the atrioventricular (A-V) node reducing S-T complex
• Myocardial ischemia affects, inflammation or infection of the heart, or side effects from medications, may be observed in conditioned athletes

Atrioventricular Block

• Impulses ordinarily pass from the atria to the ventricles through the A-V bundle, also known as the bundle of His
• Conditions that decrease the rate of impulse conduction in this bundle or block the impulse entirely:
  • Ischemia of the A-V node or A-V bundle fibers delays or blocks conduction from the atria to the ventricles
  • Coronary insufficiency causes ischemia of the A-V node and bundle
  • Compression of the A-V bundle by scar tissue or by calcified portions of the heart blocks conduction from the atria to the ventricles
  • Inflammation of the A-V node or A-V bundle depresses conduction from the atria to the ventricles
  • Extreme stimulation of the heart by the vagus nerves in rare cases blocks impulse conduction through the A-V node
  • Degeneration of the A-V conduction system is sometimes seen in older patients
  • Medications like digitalis or beta-adrenergic antagonists can impair A-V conduction

Incomplete Atrioventricular Block

• First-Degree Block is identified by a Prolonged P-R Interval.
• The usual lapse of time between the beginning of the P wave and the beginning of the QRS complex is about 0.16 second when the heart is beating at a normal rate
  • The P-R interval usually decreases in length with a faster heartbeat and increases with a slower heartbeat
  • Generally, when the P-R interval increases to more than 0.20 second, there is prolonged conduction
  • First-degree block is defined as a delay of conduction from the atria to the ventricles but not actual blockage of conduction
  • The P-R interval seldom increases above 0.35 to 0.45 second because, by that time, conduction through the A-V bundle is depressed
  • One can measure the P-R interval to determine the severity of some heart diseases

Second-Degree Block

• When conduction through the A-V bundle is slowed enough to increase the - interval to 0.25 to 0.45 second, the action potential is sometimes strong enough to pass through the bundle into the ventricles and sometimes not strong enough to do so
  • there will be an atrial P wave but no QRS-T wave, therefore “dropped beats” of the ventricles There are two types of second-degree A-V block—Mobitz type I and II
  • Type I block is characterized by progressive prolongation of the P-R interval until a ventricular beat is dropped and is then followed by resetting of the - interval repeating
  • Type I block is almost always caused by abnormality of the A-V node, mostly benign
  • Type II block has a fixed number of non-conducted P waves for every QRS complex, as a 2:1 block for example, and the P-R interval remains fixed before the dropped beat
  • Type II Block is generally caused by an abnormality that requires implantation of a pacemaker to prevent Cardiac Arrest

Complete A-V Block

• Third-Degree Block happens when conditions causing poor conduction in node are severe, there is complete block
  • The ventricles spontaneously establish their own signal which causes atria to dissociate from the QRS-T complexes
  • In that case the atria are about 100 beats/min, whereas the 40 beats/min in the ventricles

Stokes-Adams Syndrome—Ventricular Escape

• Block of conductive signals causing a halt to impulse for just a few seconds or extended the period of time
  • Ventricles don't start right away usually from suppression- the driving system of impulses that are greater than rhythm can cause excitability
  • Afterword Purkinje distal to A-V node starts, generates signals rapidly acting as a pacemaker and leading to ventricular escape
  • If brain isn't active for long people faint- the ventricles escape causing blood and recovery
  • Prolonged states require pace makers

Incomplete Intraventricular Block

• Electrical Alternans occurs for partial block causing tachycardia because system can't respond quick enough, because conditions caused from system failing
• Prolonged states require pace makers

Premature Contractions

• Before a typical contraction
• It happens because abnormal impulses and odd times
• Ischemia- small calcified plaques attach irritations
• From Toxic factors like nicotine

Premature Atrial Contractions

• 1 atrial beat
  • Early P wave
  • Shortened interval
  • Near nodes
  • Longer pause for originating in medium, discharging at sinus node

PREMATURE VENTRICULAR CONTRACTIONS

• (PVCs) series of beats alternating with normal contraction shown as bigeminy altering ECG
  • Longer to reach impulse
  • High Voltage because impulses reach only 1 direction eliminating partial depolarization from reaching sinus node
  • Potential opposes to (QRS) Because of longer process

Vector Analysis of the Origin of an Ectopic Premature Ventricular Contraction

• Use of ectopic point location determine from axis using analysis
• The mean vector point to where the first point is located at focus

Disorders of Cardiac Repolarization

• Longer and delayed ventricular muscle can develop syndromes known for (LQTS)
• Can be triggered due the muscle

Paroxysmal Tachycardia

• Heart can discharge rapidly to all areas by focus
  • The rate in rapid and starts fast
  • Vagal is stopped from eliciting effects during regions
  • Drugs slow condition

Paroxysmal Atrial Tachycardia

• The study of ECG shows changes, with a inverted p wave causing a rate of 150/ bpm due irregular shape of atrium

A-V Nodal Paroxysmal Tachycardia

• Rhythm has normal (QRS-T) but missing the regular P waves because of conditions
• It startles people and causes a general unconcern

Ventricular Tachycardia

• Displayed from series of ventricular beats without the normal beats shown as (ECG) but has 2 reasons
  • Damage may have caused
  • It may involve lethal conditions- often causes rapid stimulating as discssed but other causes may include intoxication

Ventricular Fibrillation

• It disrupts or sends cardiac impulses off to stimulate different portions
  • Chamber dont expand just contract to the normal phase
• Ischemia- Electrical Shock- and of systems are all causes

Phenomenon of Re-entry Circus-Movements as the Basis for Ventricular FibrillationNormal impulses don't re-enter- but is a list of other reasons why signal does

• Pathway much Longer
• Pathways slowed down, not efficient
• A Short time to React

CHAIN REACTION MECHANISM OF FIBRILLATION

• With the re-entry series heart contracts in directions at all locations
• A Best way is electrical and applying current
  • It goes in all directions, causing all fibers to be in refractory stage. Then portions out of refractions- impulses only travelling but blocked

ELECTROCARDIOGRAM IN VENTRICULAR FIBRILLATION

• The heart shows irregularity, causing contractions without regular function and low voltage
• Voltage is Low, decays rapid requiring success- but in electric shock

VENTRICULAR DEFIBRILLATION

• A Fraction of a electric signals a action causes impulses from area simultaneously setting all the fibers
• Voltage is strong for short period from two sides to get results- it may require higher voltages if through chest

HAND PUMPING OF THE HEART

• Lack blood requires pumping, may work to assist
• CPR a common- causes trauma- to assist the brain

ATRIAL FIBRILLATION

• Contratry to the above atrial is the atria dont pump due the same reasons- lessens efficiency but the person can have it due not pumping

ELECTROCARDIOGRAM IN ATRIAL FIBRILLATION

• The irregular rhythms and rapid in atria cause fast heartbeat
• The signals are weak

ELECTROSHOCK TREATMENT OF ATRIAL FIBRILLATION

• Shocks can convert rhythm like it does in ventricular

CARDIAC ARREST

• No Spontaneously, due to hypoxia preventing electros Prolonged cases may benefit