ECG Problems Flashcards
Sinus Arrhythmia
Inspriation: Increases the heart rate
Expiration: Decreases the heart rate
Postulated Mechanism:
Circulatory mechanisms that alter the strengths of the
sympathetic and parasympathetic nerve signals to the sinus node e.g. respiratory type
Cyclic cariation of the vagal tone increasing near the end of expiration and decreasing near the end of inspiration, this is a physilogical phenomenon seen in young people and athletes which normally disappears with physical exertion
What is a Cardiotachometer
A cardiotachometer is is an instrument that records by the height of successive spikes the duration of the interval between the successive QRS complexes in the ECG
Extrasystole/Ectopic beat/ Premature Beat
Causes:
A premature contraction that happens in the heart before the time that the normal contraction would have been expected
Most extrasystoles/premature beats or
contractions/ectopic beats are caused by ectopic foci.
Common causes of ectopic foci:
- Local areas of ischaemia
- Small calcified plaques at different points in the heart pressing against the adjacent cardiac muscle so that some of the fibres are irritated’
- Toxic irritation of the AV node, Purkinjee system or myocardium caused by infection,drugs, nicotine or coffee.
- Mechanical irritation during cardiac cathetirization, when catheter enters right ventricle and presses against the endocardium
Ventricular Escape beat Or Rhythm
Pathophysiology: Upon sinus nodal slowing of ecitation, a more appropriate discharge rate of an ectopic atrial, av junctional/ventricular pacemaker takes control of the cardiac rhythm.
Ventricular Escape
Response of an atrial, junctional (AV junction) or
ventricular automaticity focus to a pause in normal SA
nodal pacemaker activity.
The automaticity focus escapes the SA nodes overdrive suppression temporarily to pace at its own intrinsic rate
® causes one beat or (with long periods) causes an escape
rhythm.
Current of Injury
Part of the heart remains partially or totally
depolarized all the time, because the potassium ion
channels (that are normally responsible for repolarization)
are most susceptible to ischaemic injury.
Current flows between the pathologically depolarized
and the adjacent normally polarized areas, even
between heart beats.
The injured part of the heart is negative
Common causes:
- Mechanical trauma
- Infectious processes that damage the muscle membranes
- Ischaemia
Common cardiac arrhythmias and their
underlying mechanisms.
- Disorders of impulse formation:
abnormal automaticity due to an ectopic pacemaker) - Abnormal impulse conduction:
- AV and Intraventricular conduction blocks:Delayed conduction or total block
- Re-entry phenomenon
- Accessory conduction pathways: Wolf-Parkinsion white Syndrome
ECG patterns which are associated with abnormal impulse conduction:
AV Conduction blocks Paraxysomal Supraventricular Tachycardia(PST) Wolff-Parkinson White Syndrome Atrial Flutter Atrial Fibrillation Ventricular Fibrillation Ventricular Tachycardia Ventricular Flutter Idiopathic Long QT syndrome
Sino-Atrial Node
Highest frequency (60/70 -80 beats/min) →
overdrive suppression of pacemaking by the AV node (40/50-60
beats/min) or Purkinje fibres (20/30 to 40 beats/min).
Causes of increased automaticity in the Mlatent
pacemakers:
ischaemia, hypokalaemia, fibre stretching or local catecholamine
release (e.g. due to psychological stress).
If their membrane potential is sufficiently hypopolarized (e.g. due to ischaemia), the atrial and ventricular muscle cells can also initiate impulses.
Triggered Automaticity
Caused by afterdepolarizations which occur during repolarization
(“early afterdepolarizations”) or after repolarization (“delayed
afterdepolarizations”).
Potentials that reach threshold initiate premature action potentials and
therefore premature heart beats.
The afterdepolarization magnitude is influenced by the cardiac rate,
catecholamines and a decrease in parasympathetic input.
Early afterdepolarizations
•Occur during the terminal plateau or repolarization phase
•The Purkinje fibres are most susceptible
Predisposing factors:
1. Agents that prolong the action potential and increase the
sodium ion influx or block potassium ion efflux.
2. Hypokalaemia
3. Bradycardia
Delayed afterdepolarizations
• Occur after complete repolarization.
Caused by an excessive increase in [Ca++] in the myocytes,
e.g.
digitalis toxicity or ↑ catecholamines that
increase Ca++ influx through the L-type (slow) Ca++
channels.
The atrial or junctional foci (especially) become
irritable due to:
•Hypoxia (= also the most common cause of ventricular ectopic foci)
•Stretching
•Hyperthyroidism
•Adrenaline released by adrenal medullae
•Increased sympathetic nervous stimulation
•Caffeine, amphetamines, cocaine or other beta 1 adrenergic receptor
stimulants
•Excess concentrations of digitalis, some toxins, and occasionally ethanol
Abnormal impulse conduction
- Slowed conduction (i.e. more gradual phase 0
depolarization slope/gradient) - Re-entry (cf. previous slide)
Slowed Conduction
amplitude and slope of phase 0 depolarization depressed
• Depressed fast responses occur when impulses arise while
many Na+ channels are inactivated.
• Can occur due to a premature impulse during the relative
refractory period and RMP is low (-60 to -70 mV), so that
many channels remain inactivated for a long time following
action potentials.
At membrane potentials less negative than -60 mV,
Na+ channels are completely inactivated, but slow Ltype Ca++ channels can still open, resulting in a slowly
propagated action potential (i.e. a slow response)
“Re-entry phenomenon” and predisposing
conditions
The most common pathophysiological mechanism that undrlies premature beats and tachyarrhytmias
Re-entry often causes tachycardia due to the circus movement that occurs
Conditons which must be present for a re-entry arrythmia to occur:
- Two adjacent pathways-over which the cardiac impusle is conducted,The second pathway can be a true anatomical oneor can result from pathological changes in which certains areas of the myocardium that alteer the its electrical activiuty
- Differences in the conduction velocities of the two pathways
- Recovery of excitability proximal and distal to the re-entry sites rapid enough
Accesory Conduction Pathways
WPW Syndrome-A syndrome in which an extra electrical pathway in the heart causes a heart beat
Important abnormal ECG patterns that you
must recognize
- Sinus bradycardia
2.Four main types of “atrial/supraventricular tachycardia”:
sinus tachycardia, PAT/PSVT, atrial flutter, atrial fibrillation
3.Premature cardiac beats - atrial, junctional (i.e. AV junction)
and ventricular
- Ventricular tachycardia and Ventricular fibrillation
- Sino-atrial block
6.Conduction blocks: Atrioventricula (three degrees, but 4 types)
Intraventricular: LBBB en RBBB
7.Myocardial ischaemia and –infarct, cardiac arrest
Sinus Bradycardia
Two Pathophysiological Mechanisms:
- Reduced sinus node automaticity-due to an increase in the vagal tone-Sleep,carotid sinus massage, increasing age, beta-adrenergic receptor antagonists and calcium ion channel antagonists.
- Bocked AV conduction-Av node and Bundle of his are the only normal physiological connections between the atria and the ventricles.
Tachycardia
It is divided into Supraventricular and ventricular Tachycarcdia
4 main types of atrial tachycardia and cause:
- Sinus tachycardia (due to sympathetic nervous stimulation)
- Paroxysmal atrial tachycardia
– (Cause: an ectopic atrial pacemaker due to, inter alia, caffeine, nicotine, excessive
alcohol) - Atrial flutter
– Cause: single re-entry/ectopic focus in the atrium (usually R.A): usually regular
pulse rate - Atrial fibrillation (fast or slow)
– Cause: multiple atrial re-entry circuits/ectopic foci – usually in L.A.). Often
triggered by mitral stenosis, hyperthyroidism or IHD.
– Irregular pulse rate, -rhythm or force
– Prolonged atrial fibrillation → CF and atrial thrombosis with pulmonary/systemic
emboli
Sinus Tachycardia
A specific form of sinus rhythm and fulfills all the criterai for a sinus rhythm,except for the cardiac contraction rate.
Underlying pathophysiology mechanism: Accelerated SA node activation-due to sympathomimetic drugs or physilogical stress.
- Accelerated phase 4 depolarization
- Delayed repolarization
- Re-entry phenomenon
Cardiac causes: Myocarditis, multiple ectopic pacemakerss-due to ischaemia
Extracardiac: Excessive SNS stimulation due to physiological/physical stress, drugs, fever , acute hemorrhage or hyperthyrodism
Atrial Paroxysomal Supraventricular Tachycardia
P wave is seen during the rapid heartbeat before each QRS-T complex, and this P-wave is partially superimposed onto the normal T wave pf preceeding beat
AV Nodal Paroxysomal Tachycardia
There is almost normal QRS complexes but totally missing or obscured p waves
Atrial Flutter
Electrical signal travels as a single large wave always in one direction around and around the atrial muscle mass.
Rapid rate of contraction of the atria with a heart beat usually around 200-350 bpm
Signal reaches AV node to rapidly for all of them to be passed out into the ventricles becasue the refractory periods of the av-node and bundle are toolong to pass more than a fraction of the atrial signals therefore there are usually two to three beats of the atria for every single beat of the ventricles
Mechanisms: single atrial re-entry (usually) / ectopic focus (usually in
right atrium): usually regular pulse rate
Atrial Fibrilation
Cause:
- Atrial Enlargement- which can result from heart valve lesion that prevents the atria from emptying adequatley into the ventricles
- Ventricular Failure with excessibve damming of blood in the atria
The dilated atrial walls provide ideal conditions of a long conductive pathway, as well as slow conduction, both of which predispose to atrial fib.
Mechanisms: multiple atrial re-entry circuits (usually)/ectopic foci
(usually in left atrium). Often triggered by mitral stenosis,
hyperthyroidism or IHD.
Irregular irregular pulse rate, -rhythm and force
Prolonged atrial fibrillation → cardiac failure and atrial
thrombosis with pulmonary/systemic emboli
Premature Cardiac Beats/Contractions
Mechanism: an ectopic site temporarily becomes the dominant pacemaker
Supraventricular Arrhythmias
Occur due to discharges of a focus of automatic cells from the atria,but outside the SA node or AV node.
Impulse does not originate in the sa node thus each excitation wave does not spread over the atria in the usual fashion but is refelcted by an abnormal or inverted p wave
Atrial Premature Beat
Atrial: premature P wave
An ectopic atrial pacemaker discharges the SA node, but the SA node usually
repolarizes in time with a normal impulse on time → extrasystole
Usually disappears with exercise
AV Nodal Premature Beat
ectopic pacemaker is usually in the AV node)
Normal QRS complex, preceded by or followed by an inverted P wave.
Common in cardiac tissue
Loss of atrial function becomes clinically significant:
- Strenuous physical activity
- Decreased ventricular function de to cardiac disease-mitrial or tricuspid valve disease
- Drugs-Negatively inotrpic drugs
Premature ventricular Contraction
Pathophysilogical Mechanism: An ectopic pacemaker site-which momenteraly becomes the dominat pacemaker develops in any part of the sub-atrial conducting sytem or ventricular myocardium
Cause: All formsof cardiac disease esp IHD, WHICH INCREASES THE EXCITABILTY OF THE CONDUCTING SYSTEM and myocaridum
ECG:
Bizarre, prolonged QRS complexes.
• No P wave.
• Inverted T wave.
