Session 6- When things go wrong Flashcards
(28 cards)
QT interval
QT interval time taken for depolarisation and repolarisation ventricle
- varies with heart rate
- calculation to correct for heart rate
- start of the Q wave and the end of the T wave
0.44-0.45 seconds 11 small boxes
what does a prolonged QT interval indicate
indicates prolonged ventricular repolarisation
associated risk for dangerous arrythmias
characteristics of normal sinus rhythm
- regular rhythm at a rate of 60-100 bpm
- each QRS complex id preceded by a p wave
- normal p wave axis: p waves should be upright in leads I and II inverted aVR
- the PR interval remains constant
- QRS complexed are < 100ms wide
what causes heart block
degeneration electrical conducting system with age- sclerosis and fibrosis
acute myocaridal ischaemia
medications
valvular heart disease
first degree AV/heart block
1st-degree AV block: conduction is slowed without skipped beats. All normal P waves are followed QRS complexes, but PR interval is longer than normal
second degree heart block
mobitz type 1
also called wenkebach
successively longer PR interval until one QRS is dropped- is electrical signal not conducted through to ventricles- then cycle starts again
second degree AV block- Mobitz type 2
PR intervals do not lengthen- sudden dropped QRS complex without prior PR changes
atrial rhythm is regular
ventricular rhythm is irregular
HIGH RISK PROGRESSION TO COMPLETE HEART BLOCK
third degree AV block
atria and ventricles are depolarising independently- complete failure of AV conduction
- ventricular pacemaker takes over- slow 20-4- bpm
- typically too slow to maintain blood pressure
- usually wide QRS complex
bundle branch block
delayed conduction within the BB
- can be RBBB and LBBB
- p wave and PR intervals are normal
- wide QRS complex because ventricular depolarisation takes longer
supraventricular arrhythmia
sinus node
atrium itself
AV node
normal (narrow) QRS complex-when conducted ventricles depolarise normally
arises from multiple atrial folci rapid chaotic impulses no p waves- wavy baselines irregular R-R intervals impulses AV node at rapid irregular rate not all conducted
ventricular arrhythmia
wide and bizarre QRS complex
Afib
slow- ventricular response- <60 bpm
fast- ventricular response >100 bpm
normal- 61-99 bpm
Afib with coarse fibrillation- amplitude >0.5mm
fine fibrillation amplitude <0.5mm
haemodynamic effects of atrial fibrillation
• Loss of atrial contraction leads to increased blood stasis c/w normally
contracting atria - stasis most evident in left atrium - flow velocity
markedly reduced concomitantly with impaired contractility of left
atrial appendage; leads to small clots in LA – therefore atrial
fibrillation well-established risk factor for ischaemic stroke
secondary to emboli
premature ventricular ectopic beats
- Ectopic focus in ventricle muscles
- Impulse does not spread via fast
His-Purkinje system - - Therefore much slower
depolarization ventricular muscle
Therefore Wide QRS - Premature because occurs earlier
than would be expected for the next
sinus impulse - May be ASx or cause palpitations
without haemodynamic
consequences
VTACH
Run of ≥ 3 Consecutive PVC -VTACH is broad complex tachycardia -Persistent VTACH is a dangerous rhythm requiring urgent treatment -High risk progression to Ventricular fibrillation
venricular fibrillation
-Abnormal, chaotic, fast ventricular depolarisation - Impulses from numerous ectopic sites in ventricle - No coordinated contraction - Ventricles quiver - No cardiac output - If sustained – cardiac arrest
myocardial infarction
muscle necrosis present- therefore blood tests will be positive
STEMI
ST segment elevation myocardial infarction
Due to complete occlusion of coronary artery
• “Full thickness” of myocardium involved
• Sub-epicardial injury causing ST Segment elevation in leads facing
affected area is the earliest sign
Non- STEMI
non ST elevation MI
in anterior cardiac wall necrosis. Which artery?
which leads?
left anterior descending artery- also known as Anterior Interventricular branch of left coronary artery
widow maker
major ECG changes will be seen precordial/chest leads- V3 and V4. If septum involved also V2 and sometimes in limb leads
unstable angina
•
“Unstable angina (UA) is an acute coronary syndrome that is defined
by the absence of biochemical evidence of myocardial damage…
characterised by specific clinical findings of prolonged (>20
minutes) angina at rest; new onset of severe angina; angina that
is increasing in frequency, longer in duration, or lower in threshold;
or angina that occurs after a recent episode of myocardial
infarction.”
ECG Changes in Non-STEMI and
Ischaemia: ST segment
• ECG changes due to subendocardial injury
• ST segment DEPRESSION and T wave inversion
• On ECG tracing behaves as if abnormal current traversing
damaged tissue is moving AWAY from recording electrode
ECG Changes in Non-STEMI and Ischaemia: T waves
Acutely, there is either a depressed ST segment or there is an inverted T wave.
Within hours there is raised troponin I and T on a blood test (indicating myocyte death).
After a few weeks the ST segment and T wave return to normal.
No pathological Q wave develops because the infarction is not the entire thickness of the myocardium.
ECG changes- stable angina
• ST depression during exercise because of coronary disease – but
“stable” atherosclerotic plaque causing fixed narrowing
• ECG changes will REVERSE at rest
• ECG: down sloping of ST-segment depression or elevation
