Electricity and the heart Flashcards
what are the types of muscle?
cardiac
skeletal
smooth
what are the important features of cardiac muscle?
timing
togetherness
achieved by sophisticated electrical mechanisms
what are the specific needs of the heart?
simultaneous, intermittent contraction of all fibres
prevention of sustained (tetanic) contraction
ability to change rate according to circumstances
ion distribution in cardiac myocyte
Na+/K+ ATPase- powered pump maintains the high sodium ion conc outside the cell and high potassium ion conc inside the cell
to sustain the calcium gradient an antiport system exchanges calcium ions for sodium ions
Action potential of a cardiac myocyte
depolarisation - fast inflow of sodium calcium inflow - T type potassium outflow calcium inflow - L-type, continues to create action potential so causes plateau repolarisation
what is the role of calcium in the cardiac myocyte action potential
extended duration of AP
esnures total ventricular depolarisation
Refractory period of AP in cardiac myocyte
prolonged refractory period
ion channel inactivation
prevents tetany
pacemaker
specialised cells in atria, especially SAN and AVN automatic firing, without stimulus results from continuous slow ionic leak natural rate is highest in SAN other areas become active if SAN fails
pacemaker cell action potential
no resting phase
calcium not sodium inflow responsible for main depolarisation
heart rate
pacemaker cycle length determines HR varies under influence of autonomic NS natural rate - 100-110 bpm parasympathetic normally dominant very sensitive to change - even respiration alters HR - sinus arrhythmia
sympathetic influence on heart
slow sodium ion channel permeability increases
slope of phase 4 becomes steeper
threshold reached sooner, increasing HR
where is phase 4 on a cardiac AP?
the first ascending part
parasympathetic influence on heart
increases resting potassium ion channel permeability
trough potential is lowered and slope of phase 4 becomes flatter
threshold reached later and so decreases HR
intra-cardiac conduction
non-specific conduction in atria
AVN acts as a gate in the firewall between atria and ventricles
Bundle of His-Purkinje system supplies the ventricles
what direction does depolarisation happen?
from in to out
what direction does perfusion happen
from out to in
what does the AVN do?
slows conduction
allows time for atrial emptying
protects ventricles from atrial tachyarrhythmias
also affected by autonomic NS
conduction from the AVN
Left bundle branch has 2 fascicles for conduction
there is 1 right bundle branch
the branching nature of cardiac muscle enables the depolarisation to spread and so the ventricles contract simultaneously
electrocardiogram
surface recording of electrical activity
series of electrodes allows multiple views
magnitude = 1-2mV
polarity of impulses on ECG
positive if the impulse moves towards the recording electrode
negative if the impulse moves away from the recording electrode
what colour are the limb leads?
yellow and green for left
red and black for right
which lead goes on the left wrist?
yellow
which lead goes on the right wrist?
red
how many ECG leads are there?
10
4 limb
6 chest
what are the planes in which an ECG shows the heart?
vertical and horizontal
which electrode provides the best recording?
2
what happens at the 3rd electrode of an ECG?
main electrical flow is at 90 degress to the lead so the signal is minor, no QRS complex and minimal T wave
which leads give a lateral view of the heart?
I,aVL,V5,V6
which leads give a reciprocal view of the heart?
aVR
which leads give an inferior view of the heart?
II,III,aVF
which leads give an antero-septal view of the heart?
V1,V2
which leads given an anterior view of the heart?
V4,V3
what needs to analysed from an ECG?
rate
rhythm
axis
morphology
how to calculate rate from an ECG?
count number of large squares between QRS complexes
divide this number into 300
if using small squares divide into 1500
what should the PR interval be?
<200ms
How long should the QRS complex be?
<120ms
Timing
mechanical contraction lags behind depolarisation
QRS complex starts with Phase 0 of ventricular action potential
T wave ends with phase 3 of ventricular AP
what can cause abnormalities in the morphology of an ECG?
ischaemia/ infarction
hypertrophy
electrolyte disturbance
metabolic disturbance
ischaemia/ infarction on ECG
typically produce ST segment changes acutely
damaged cells repolarise early so ST segment is out of step with normal areas
division between ischaemia and infarction is now less clear
acute coronary syndrome
can be reversible
full thickness damage
ST elevation
subendocardial damage
ST depression
coronary artery for inferior heart
right coronary
coronary artery for antero-septal heart
left anterior descending
coronary artery for antero-apical
left anterior descending
coronary artery for antero-lateral
circumflex
coronary artery for posterior
right coronary
why are there abnormal Q waves in infarcts?
act as an electrical window, where there is no electrical activity
electrode records depolarisation of opposite wall, which goes from inside to out and causes a negative deflection - Q wave
what are other causes of ST changes?
trauma
pericarditis
hyperkalaemia
digoxin
what happens to ECG trace during hyperkalaemia?
high peaked T waves and QRS widening
hypertrophy on ECG
negative deflection in V1 and positive deflection in V5
large amplitude QRS complexes
fibrillation
rapid uncoordinated contraction
atrial or ventricular
atrial fibrillation
AV node prevents ventricular fibrillation
cardiac output decreased
thrombo-embolism risk
ventricular fibrillation
no cardiac output
rapidly fatal if not treated
AF on ECG
No P waves
QRS normal
irregularly irregular
how is AF managed?
anti-thrombotic - warfarin or aspirin
cardioversion - synchronised shock to prevent VF
rate control - beta blocker, calcium antagonist
amiodarone
digoxin
deal with underlying cause
What does digoxin do?
slows conduction through AVN
reduces ventricular rete in AF
how does digoxin work?
increases myocardial contractility
sodium/ potassium pump is inhibited, increasing conc of Na+ inside cell
the sodium/ calcium pump becomes less efficient so intracellular calcium increases and is stored in sarcoplasmic reticulum
force of subsequent contractions are enhanced
VF on ECG
continuous bizarre irregular trace no baseline no P ot T waves can cause sudden death if not treated
how to manage VF?
defibrillation - unsychronised, 150-200J
AED
external and internal
External AED
used by paramedics and in public
internal AID
implanted
for high risk patients
more long-term
where do conduction defects occur?
SAN
AVN
Intra-ventricular
SAN conduction defects
pacemaker failure
lower site normally takes over
AVN conduction defects
heart block
Intra-ventricular conduction defects
bundle branch block
what is heart block?
problem with conduction through AVN
3 degrees
1st degree heart block
delayed transmission but it is all transmitted.
1st degree heart block ECG
long P-R interval
Normal QRS complexes
2nd degree heart block
partial AVN transmission
2nd degree heart block ECG
some P waves without associated QRS complex
Some P waves not conducted
regular or variable
3rd degree heart block
no AVN transmission
3rd degree heart block ECG
no link between P waves and QRS complexes
Wide QRS complexes
What is bundle branch block?
a problem with conduction through the R or L bundle branch
This means 1 ventricle depolarises slightly after the other
How does bundle branch block appear on an ECG?
Wide QRS complex after normal P wave
Right bundle branch block
M pattern in V1 and W pattern in V6
Left bundle branch block
M pattern in V6
How does asystole appear on an ECG?
no waves
How does ventricular ectopic appear on an ECG?
No P wave
Wide, bizarre QRS complex
Pacing impulse - artefact on ECG
very brief impulse, external impulse stimulates ventricle and sometimes atrium
cause abnormal, wide QRS complexes
