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)