ECG and heart disorders Flashcards
what is ECG
measure of hearts electrical activity recorded on the skin surface
heart sounds
lubb: closing of AV valve
dubb: cemilunar valves closing
two other songs if listened to closely: blood rushing into the ventricles and atrial systole
Abnormal sounds
if entrance of the valves are narrowed: stenosis -> causes turbulance
if valves fail to seal during fibrosis -> turbulance
-> hear a 3rd sound = murmur
pacemaker cells triggering electrical activity
cardiac rhythm is generated by pacemaker cells in SA node :
wave of excitement spreads from the atria from teh DA node to the AV node - AV delays wave of excitation -> conducting to the ventricles via bundle of His
- Purkinje fibres in ventricles ensure synchronous depolarization of ventricular muscle
ECG is made up uf different components (PQRST)
- amplitude and duration of the waves are caused by electrical activity in different parts of the heart
P wave: depolarization of atria
QRS complex: depolarization of vventricles
T wave: repolarization of the ventricles
waveforms in relation to electrical activity during cardiac cycle
P wave (upward)- SA node triggers depolarization in the atria
Q wave (downward)- AV node triggers depolarization of septum (moves left to right)
R wave (upward)- Depolarization of ventricular wall
S wave (downward)- depolarization in ventricles spreads upwards to atria
T wave (upward)- Repolarization of ventricles (charge moves left to right)
Resting heart at the end of the cardiac cycle
why does the T wave (repolarizing) cause an upward deflection(same as R)
The wave of depolarization (R wave) moves from cells inside the heart to the outside (right to left)
The wave of repolarization (T wave) moves from the outermost cells to the inside (left to right)
clinical signs detected by the ECK
- Electrical rhythm of the heart (waveform and frequency)
- Size of the muscle mass of the chamber of the heart (amplitude)
- Dysfunction in heart excitation/conduction
- Abnormal pacemaker activity
- Abnormal cardiac excitability due to altered plasma electrolyte levels
- Metabolic state and viability of the myocardium
Heart block
conduction between the atrium and ventricles is very slow / blocked
ectopic beats or extrasystoles originating in atria or ventricle
supraventricular extrasystoles: inverted P wave followed by extrasystoles -> slows heart beat
ventricular extrasystoles: wider QRS complex -> speed of conduction is slowed
cardiac rythms caused by premature excitation
a. Atrial tachycardia: resting heart rate= 100-200 bpm
b. atrial flutter: atrial contract > 290 times /min
c. ventricular tachycardia: wide and slow QRS complex
cardiac fibrillation
non pacemaker cells sponatneously generate a rythm out of phase from SA node -> ectopic discharges generate fibrillation and parts of the heart contract out of phase with SA node
a. atrial fillibration: atria contract> 350 times/ min -> disappearance of P waves
b. ventricular fillibration: ventricles fail to contract in concerted way
Electrocyte imbalance and ECG - potassium
High plasma K+ levels increase the amplitude of teh T wave
Low plasma K+ levels decrease teh amplitude of T wave
Electrocyte imbalance and ECG - calcium
high plasma Ca2+= shorter QT interval
low plasma Ca2+= prolonged cardoac AP
ECG changes following ischaemia and infraction
-> damages cells repolarize early
Ischaemia: STsegment is negative
Injury: ST segment doesnt return to baseline
Treatment of arrhythmias
-> drugs slow down heart rate and decrease cardiac contractility
- Class I-sodium channel blockers
- Class II-beta- adrenoreceptor antagonists
- Class III- slow heart rate by prolonging the refractory period
- Class IV calcium channel blockers
- In severe arrhythmia artificial pacemakers are used to maintain a normal regular rhythm
