Lecture 7 - Arrhythmias 1 Flashcards
Sinoatrial (SA) or Sinus Node
dominant center of automaticity (dominant pacemaker) which initiates cardiac electronic impulse
generate sinus rhythm
paces heart at resting Tate of 60-100 bpm
Intranodal pathways
3 pathways going into right atrium
Bachmann’s bundle will connect right to left atrium
Atrioventricular (AV) node
known as junction box, delays SA node signal
area of specialized tissue that conducts normal electrical impulse from atria to the ventricles
Bundle of His
Transmits electrical impulses form the AV node to the point of the apex of the fascicular branches (bundles of specialized muscle fibers)
Bundle of His + AV Node =
AV Junction
between the Atria and ventricles lies a fibrous AV ring that will not permit electrical stimulation - hole in this can cause arrhythmia
K+ conc is….
higher inside cell
has greater effect on membrane potential because its more permeable
Na+ conc is….
higher outside cell
Nodal tissue action potential…..
slow, Ca2+ dependent
Rhythmic tissue action potential…..
Fast, Na+ dependent
5 phase of action potential of ventricular system
Phase 0 = Rapid depolarization, Na rushes in
Overshoot potential = results in brief initial repolarization or phase 1
Phase 1 = Partial repolarization, related to K+ efflux
Phase 2 = Plateau phase, increased influx of Ca2+, low efflux of K+
Phase 3 = Rapid depolarization, large K+ efflux, reduction of Ca2+/Na+ influx
Phase 4 = Resting membrane potential (-80/90)
Threshold potenital = juncture of phase 4-0, where rapid Na+ influx is initiated
Properties of Electrical Conduction System
Excitability Conductivity Contractility Automaticity Lusitropy Autonomic nervous system control
Excitability
ability of cardiac tissue to respond to adequate stimuli by generating an action potential followed by a mechanical contraction
Bathmotropy
The influencing of the excitability of cardiac muscle
can be + or -
Factors affecting Excitability
RMP lvl
Threshold lvl
Behavior of Na+ channel
Refractory periods
Absolute refractory period
interval of AP during which no stimulus, regardless of its strength, can induce another impulse
Relative refractory period
interval of AP during which an impulse of significant magnitude may be elicited
Supranormal Period
Period at end of the action potential were an impulse can be generated by weaker than normal stimuli
Conductivity
Property of the cardiac muscle that allows the impulse to travel along tissue
Dromotropy
The influencing of the conductivity of cardiac muscle
inc conduct = +
dec conduct = -
Contractility
capacity of shortening in reaction to an appropriate membrane depolarization
Inotropy
The influencing of contractility
Automaticity
Ability of cardiac muscle to spontaneously depolarize in a regular constant manner
normally started by SA node
Chronotropy
Influencing of automaticity
Overdrive suppression basic idea
every tissue in heart has an inherent pacemaker
if SA node stops, another tissue will control HR
P wave
Represents atrial depolarization
PR interval
atrial depolarization plus the normal AV nodal delay
QRS complex represents
Represents ventricular depolarization
atrial repolarization is occurring simultaneously and the atrial T wave is hidden by the QRS complex
ST segment
occurs after ventricular depolarization has ended and before repolarization has begun
tme for ECG silence
initial part is termed the J point
T wave
represents ventricular repolarization
Prolonged QTc interval can lead to…
Ventricular arrhythmia that can lead to sudden cardiac death
** occurs at > 0.5 sec = 500msec ***
2 main mechanism of Arrhythmias
- Abnormal impulse generation
- Abnormal impulse propagation
Alterations in Sinus node automaticity
inc SA automaticity = sympatheitc
dec SA automaticity = parasympathetic
Spontaneous Automaticity
Generated in latent pacemakers which generate electrical impulses at a rate that exceeds that of the SA nodes
Ectopic Focus
Some stimulus that stimulates cardiac cells and cranks them up, passing SA node rate
What influences spontaneous Automaticity?
increased slope of phase 4 depolarization that causes a heightened automaticity of tissues and competition with the SA node for dominance of cardiac rhythm
Causes of increased slope in phase 4 depolarization
Autonomic control = catecholamines Digoxin Metabolic Ischemia (leading cause) Hypokalemia Hypercalcemia Fiber stretch
Two types of Triggered Automaticity
Two types
- Early after-depolarization
- Delayed after-depolarization
Early after-depolarization = EAD
transient membrane depolarization that occurs during repolarization (phase 3)
maybe precipitated by hypokalemia, antiarrhythmics, or slow stimulation rates
** implicated as cause of Torsades de pointes **
Cause of Torsades de pointess
EAD
Delayed after-depolarization = DAD
transient membrane depolarization that occurs after repolarization but prior to phase 4 of action potential
maybe precipitated by digoxin** toxicity or excess catecholamine release
Most common influence of automaticity
Altered impulse conduction
Conduction block
occurs when a propagating impulse passes a region of the heart that is unexcitable
Reentry
concept that involves indefinite propagation of the cardiac impulse and continued activation of previously refractory tissue
3 requirements for reentry
- 2 pathways for impulse conduction
- area of unidirectional block in 1 of the pathways
- slow conduction in other pathway
3 things that affect reentry
- Timing (conduction velocity)
- Refractorines (abs refract period)
- Changes in autonomic control
Most common bypass pathway/tract
Bundle of Kent
Shorter PR interval and wide QRS complex
Common causes of Arrhythmias
- Normal physiology
- Cardiac disorders (biggest category)
- Pulmonary disorders
- Disturbances of the autonomic system
- Electrolyte Abnormalities
- Medications
two most common classifications for Arrhythmias
Origin & Rate
Supraventricular Arrhythmias
Originate above bundle of His
characterized by abnormal P waves but normal QRS and QTc intervals
Ventricular Arrhythmias
Originate below the bundle of His
characterized by abnormal QRS and QTc interval but normal P waves
** Most serious arrhythmias **
V-fib = incompatible with life
Nodal and Junctional Arrhythmias
originate in AV nodal or junctional area typically as a result of less rate of impulse formation from SA node
Heart block
characterized by a disruption of impulses through the AV node
1st, 2nd, 3rd degree block
Bradyarrhythmias are
<60 bpm
Sinus Bradycardia
Heart block 1st-3rd degree
Tachyarrhythmias are
> 100bpm
all the ones that aren’t < 60bpm
Wenckebach
2nd degree AV block type I
Biggest cause = inferior wall MI
Wolff-Parkinson-White Syndrome
Preexcitation syndrome
AV conduction occurs through the bypass tract known as “the bundle of Kent”, resulting in earlier activation “pre excitation” of the ventricles than if the impulse had traveled through the AV node
A-fib in WPW is deadly because it may go into….
V-fib
WPW treatment
- slow conduction through the accessory pathway, NOT the AV node (usually req ablation or cardioversion)
- if AV node is blocked unopposed in pts with WPW, rate of transmission through accessory pathway is increased potentially leading to V-fib
Which drugs do you avoid in WPW
- Beta-blockers
- non-DHP CCBs
- digoxin
they block AV node, can lead to deadly arrhythmia
Ventricular Tachycardia
V-tach
Most common in HA, leads to V-fib and death
Torsades de Pointes
Twisting of the points
Proceeded by QT prolongation
QTc interval is usually > 500 msec
Torsades de Pointes causes (drugs)
- Antiarrhythmics (Class IA,IC, III - amiodarone OK)
- Typical antipsychotic (Haloperidol)
- Atypical antipsychotics (ziprasidone)
- Azole antifungals
- Macrolide antibiotics
- Methadone
- Quinolones (moxifloxacin)
- TCA
- Chloroquine
- Pentamidine
- Ranolazine
Clinical Manifestations of Arrhythmias
- Asymptomatic
- Palpitations = heart pounding
- SOB
- Fatigue
- Lightheadedness
- Anxiety
- Chest pain
- Fainting
Complications of Arrythmias
- Tachycardia-induced cardiomyopathy and HF
- Valvular Heart disease
- Cardioembolic embolism
- cardiac arrest n death
