cardiorespiratory Flashcards
why is an ECG clinically relevant?
identify and evaluate conduction abnormalities
identify structural abnormalities
identify perfusion abnormalities
how may conduction abnormalities affect heart function?
usually the conduction system produces a cascade of electrical activity that can orchestrate/stimulate mechanical events to result in cardiac output
disruption in conduction system prevents mechanical processes from taking place
how may structural abnormalities affect heart function?
size of myocardium - if enlarged, available volume for the ventricles to take in blood for ejection reduces
how may perfusion abnormalities affect heart function?
interruption of blood flow may cause abnormal behaviour of deprived tissue
what are the practical advantages of an ECG?
relatively cheap and easy to undertake
reproducible results between people and centres
quick turnaround on results/report
is the pain retrosternal?
brought on by exertion?
relieved by rest or GTN?
all yes - typical
2 yes, 1 no - atypical
1 yes, 2 no - non-cardiac
what is a vector?
quantity that has both magnitude and direction
how is a vector represented?
arrow in net direction of movement
size reflects magnitude
what does the isoelectric line on an ECG represent?
no net change in voltage
i.e. vectors are perpendicular to the lead.
what does the width of a deflection on an ECG represent?
‘duration’ of the event
what does an upward deflection on an ECG represent?
towards cathode (+)
wave of excitation travelling towards positive electrode
what does an downward deflection on an ECG represent?
towards anode (-)
wave of excitation travelling towards negative electrode
what is a ‘wave’ on an ECG?
upwards and downwards deflection until return to isoelectric line
what does the steepness of line on an ECG represent?
velocity of action potential (steeper = faster)
what does the P wave show?
atrial excitation phase
what does the P wave stimulate?
atrial systole
what does the QRS complex show?
ventricular excitation phase
what does the QRS complex stimulate?
ventricular systole
what does the T wave show?
relaxation of ventricles
how do the P wave and QRS complex correspond to pressure in the aorta?
slight decrease (85mmHg to 75mmHg)
how does the T wave correspond to pressure in the aorta?
pressure increases between end of S and beginning of T (75mmHg to 115mmHg)
slight decrease over course of T wave (115mmHg to 100mmHg)
how does the relaxation phase (after repolarisation of ventricles, i.e. T wave) correspond to pressure in the aorta?
slight increase (~5mmHg)
steady decrease back to baseline (85mmHg)
how do the P wave and QRS complex correspond to pressure in the atrium?
slight increase from baseline (10mmHg to 15mmHg), decreases to baseline at R/S - a wave
slight increase from S (10mmHg to 15mmHg), decreases to baseline before T - c wave
how does the T wave correspond to pressure in the atrium?
slight increase from start of T to after end of T (10mmHg to 15mmHg) - v wave
how does the relaxation phase (after repolarisation of ventricles, i.e. T wave) correspond to pressure in the atrium?
decrease from 15mmHg back to baseline
how do the P wave and QRS complex correspond to pressure in the ventricle?
slight increase from baseline (5mmHg to 10mmHg), decreases slightly at R/S
pressure increases to 120mmHg between S and T
how does the T wave correspond to pressure in the ventricle?
pressure stays at 120mmHg during T
how does the relaxation phase (after repolarisation of ventricles, i.e. T wave) correspond to pressure in the ventricle?
drops rapidly back to baseline
how do the P wave and QRS complex correspond to ventricular volume?
baseline at 110mL at beginning of P
reaches 120mL at Q
stays at 120mL until T
how does the T wave correspond to ventricular volume?
drops from 120mL to 40mL over course of T wave
how does the relaxation phase (after repolarisation of ventricles, i.e. T wave) correspond to ventricular volume?
increases from 40mL back to baseline 110mL
which cells cause spontaneous depolarisation at the sinoatrial node (SAN)?
autorhythmic myocytes
what kind of deflection is produced by the depolarisation of the sinoatrial node (SAN)?
upwards, positive vector (wave of excitation moves ‘downwards’ towards cathode)
wide deflection
why is the deflection produced by the depolarisation of the sinoatrial node (SAN) (P wave) reasonably small and wide?
thin muscle of atria walls
slow depolarisation = wide deflection
which part of an ECG trace is depolarisation of the SAN responsible for?
P wave
which part of an ECG trace is depolarisation of the atrioventricular node (AVN) responsible for?
PR segment (isoelectric ECG)
what role does the depolarisation of the atrioventricular node (AVN) play that is important mechanically?
slows conduction, slow signal transduction
adds delay (protective)
which part of an ECG trace is depolarisation of the bundle of His responsible for?
last part of PR segment just before Q
which part of an ECG trace is depolarisation of the 2 septal branches of the bundle of His responsible for?
Q (downwards and upwards back to isoelectric line)
how is depolarisation of the 2 septal branches of the bundle of His responsible for the Q wave?
insulation allowing fast conduction from AVN to bottom of heart does not reach the apex
excitation ‘escapes’ into septum
causes negative vector (wave of excitation travelling ‘upwards’ through septum towards anode)
why is the deflection produced by the depolarisation of the 2 septal branches of the bundle of His (Q wave) small?
thin wall of muscle
why is the deflection produced by the depolarisation of the 2 septal branches of the bundle of His (Q wave) sharp?
conduction in myocardium is very fast
which part of an ECG trace is initial depolarisation of the Purkinje fibres responsible for?
R (from isoelectric line to peak to isoelectric line)
why is the deflection produced by the depolarisation of the Purkinje fibres (R wave) large?
thick wall of muscle at the apex
which part of an ECG trace is the later stage of depolarisation of the Purkinje fibres responsible for?
S (downwards and upwards back to isoelectric line)
how is the later stage of depolarisation of the Purkinje fibres responsible for the S wave?
wave of excitation moves from apex up either side of the ventricles (towards anode, causes negative deflection)
why is the deflection produced by the later stage of depolarisation of the Purkinje fibres (S wave) small?
thin wall of muscle
which part of an ECG trace is full ventricular depolarisation responsible for?
ST segment
which part of an ECG trace is repolarisation responsible for?
T wave
why is the deflection produced by the later stage of depolarisation of the Purkinje fibres (T wave) domed?
repolarisation happens in same direction
instead of depolarising and moving membrane potential upwards, repolarisation occurs to bring wave down (creates dome shape)
what does lead I of an ECG connect? (one L)
right arm to Left arm
what does lead II of an ECG connect? (two Ls)
right arm to Left Leg
what does lead III of an ECG connect? (three Ls)
Left arm to Left Leg
how can you tell which electrode in a lead is the anode and which is the cathode?
drawn as a triangle (right arm, left arm, left leg)
read left to right and top to bottom
first electrode of each pair you reach is the anode (-ve)
where is the V1 electrode placed for an ECG?
right sternal border
4th intercostal space
where is the V2 electrode placed for an ECG?
left sternal border
4th intercostal space
where is the V3 electrode placed for an ECG?
halfway between V2 and V4
where is the V4 electrode placed for an ECG?
mid-clavicular line
5th intercostal space
where is the V5 electrode placed for an ECG?
anterior axillary line
at the level of V4
where is the V6 electrode placed for an ECG?
mid-axillary line
at the level of V4
which artery is associated with lead I in an ECG?
left circumflex artery
which artery is associated with lead II in an ECG?
right coronary artery
which artery is associated with lead III in an ECG?
right coronary artery
which artery is associated with aVL in an ECG?
left circumflex artery
which artery is associated with aVR in an ECG?
n/a
which artery is associated with aVF in an ECG?
right coronary artery
which artery is associated with V1 in an ECG?
left anterior descending artery
which artery is associated with V2 in an ECG?
left anterior descending artery
which artery is associated with V3 in an ECG?
right coronary artery
which artery is associated with V4 in an ECG?
right coronary artery
which artery is associated with V5 in an ECG?
left circumflex artery
which artery is associated with V6 in an ECG?
left circumflex artery
what view of the heart is provided by lead I in an ECG?
lateral
what view of the heart is provided by lead II in an ECG?
inferior
what view of the heart is provided by lead III in an ECG?
inferior
what view of the heart is provided by aVL in an ECG?
lateral
what view of the heart is provided by aVR in an ECG?
n/a
what view of the heart is provided by aVF in an ECG?
inferior
what view of the heart is provided by V1 in an ECG?
septal
what view of the heart is provided by V2 in an ECG?
septal
what view of the heart is provided by V3 in an ECG?
anterior
what view of the heart is provided by V4 in an ECG?
anterior
what view of the heart is provided by V5 in an ECG?
lateral
what view of the heart is provided by V6 in an ECG?
lateral
what is the duration of 1 small square on an ECG?
0.04s (40ms)
how can heart rate be determined using the R-R interval?
R-R interval = time between two R peaks
60 divided by R-R interval = heart rate
what electrodes are used for the augmented leads (aVL, aVR, aVF)?
fixed cathode (+ve)
virtual anode (-ve)
what does aVR connect?
anode halfway down lead III (between left arm and left leg) to right arm
what does aVL connect?
anode halfway down lead II (between right arm and left leg) to left arm
what does aVF connect?
anode halfway across lead I (between right arm and left arm) to left leg
what are the 3 pairs of perpendicular leads?
lead I - aVF
lead II - aVL
lead III - aVR
how is cardiac axis calculated?
use 1 pair of perpendicular leads (lead II, aVL)
work out net amplitude of QRS complex for both leads using ECG (positive deflection from isoelectric line minus negative deflection; 1 square = 1mm)
create a triangle, SOHCAHTOA to find missing angle
60 degrees minus angle = axis
what 4 things should be considered when reporting an ECG?
correct recording?
review signal
quality and leads
verify voltage
and paper speed
review patient background if
available
what is step 1 of the ECG reporting procedure?
rate (R-R) and rhythm
- regularity of spacing between beats
- frequency of beats
what is step 2 of the ECG reporting procedure?
P wave and PR interval
- duration
- how many of the P waves result in R waves - i.e. does a signal for atrial contraction always result in ventricular contraction (ratio between both)
what is step 3 of the ECG reporting procedure?
QRS duration
- time taken for signal to get through ventricular myocardium
what is step 4 of the ECG reporting procedure?
QRS (cardiac) axis
- standard between -30 and 90 degrees
what is step 5 of the ECG reporting procedure?
ST segment
- should be flat, no elevation or depression
what is step 6 of the ECG reporting procedure?
QT interval
- duration
what is step 7 of the ECG reporting procedure?
T wave
- shape
what is a ‘normal’ variant of the cardiac axis for a shorter, wider individual?
0 to -10 degrees (left axis deviation)
what is a ‘normal’ variant of the cardiac axis for a taller, thinner individual?
90 to 100 degrees (right axis deviation)
what does ‘sinus’ refer to in context of ECG rhythms?
generated by sinoatrial node (SAN)
what does a normal sinus rhythm look like?
each P wave followed by a QRS wave (1:1)
rate is regular (even R-R intervals) and normal (i.e. normal bpm)
what are the features of sinus bradycardia on an ECG?
each P wave followed by a QRS wave (1:1)
rate is regular (even R-R intervals) but slow (i.e. low bpm)
what are some normal, healthy causes of sinus bradycardia?
medication
vagal stimulation
being very athletic
how does being athletic cause sinus bradycardia?
muscular heart ejects greater proportion of its blood (i.e. stroke volume is higher)
since stroke volume is higher, heart rate can be lower to maintain the same cardiac output
what are the features of sinus tachycardia on an ECG?
each P wave followed by a QRS wave (1:1)
rate is regular (even R-R intervals) but fast (i.e. high bpm)
what can cause sinus tachycardia?
physiological response - e.g. to medication, excitation of sympathetic nervous system
what are the features of sinus arrhythmia on an ECG?
each P wave followed by a QRS wave (1:1)
rate is irregular (variable R-R intervals) and relatively normal (65-100 bpm)
R-R interval varies with breathing cycle
how does the breathing cycle affect the R-R interval to cause sinus arrhythmia?
parasympathetic nervous system (vagus) modulates on breathing depending on phase - sometimes increased activity, sometime decreased
variable nerve activity causes irregular heart rate
what is a quick method to estimate heart rate using an ECG?
300 over number of large squares between R peaks
what are the features of atrial fibrillation on an ECG?
oscillating baseline, no clear P waves
rhythm can be irregular, rate may be slow
what is the risk caused by atrial fibrillation?
turbulent flow pattern increases clot risk
therefore increased risk of infarct or stroke if clot enters arterial system
why is atrial fibrillation not as severe as ventricular fibrillation?
manageable condition with oral anticoagulant - atria not essential for cardiac cycle
what causes the oscillating baseline on an ECG in atrial fibrillation?
atria contract asynchronously
even during QRS complex and T wave (not visible as fluctuations are overshadowed by ventricular contraction and repolarisation)
what are the features of atrial flutter on an ECG?
(similar to atrial fibrillation but atria are just contracting very regularly)
atrial to ventricular beats at a 2:1 ratio, 3:1 ratio or higher
regular saw-tooth pattern in baseline (II, III, aVF) - more reproducible than in atrial fibrillation
saw-tooth not always visible in all leads
what are the features of first degree heart block on an ECG?
inappropriately prolonged PR segment/interval (caused by slower AVN conduction)
regular rhythm (1:1 ratio of P waves to QRS complexes)
what causes the prolonged PR segment in first degree heart block?
slower than normal conduction through the atrioventricular node (AVN)
what is the most probable cause of first degree heart block?
probably a result of of progressive disorders associated with ageing
how severe is first degree heart block?
most benign heart block
what are the 2 types of second degree heart block?
Mobitz type I (also called Wenckebach)
Mobitz type II
what are the features of Mobitz type I heart block on an ECG?
gradual prolongation of PR segment (and therefore PR interval) until lengthened to the point that it doesn’t conduct through atrioventricular node (AVN) and beat skipped
most P waves followed by QRS (some are not)
regularly irregular rate (i.e. pattern formed)
what is the cause of the regularly irregular rate in Mobitz type I?
diseased atrioventricular node (AVN)
what are the features of Mobitz type II heart block on an ECG?
regular P waves, but only some are followed by QRS
regularly irregular rate - successes (e.g. 2:1) or random (e.g. 6 beats followed by no beat, then 2 beats, then no beat)
how do the ECG traces of Mobitz type I and II differ?
no PR segment prolongation in Mobitz II
why is Mobitz type II dangerous?
can rapidly deteriorate into third degree heart block
what is the cause of the regularly irregular rate in Mobitz type II?
beats usually dropped in bundle of His or in bundle branches
(different to Mobitz type I - signal is conducted through AVN)
what are the features of third degree heart block on an ECG?
complete dissociation between P waves and R waves
P waves are regular, QRS waves are regular, but spaced at different rates
P waves may be hidden within bigger vectors
non-sinus rhythm
if the sinoatrial node fails, how does the heart regulate contraction?
usual pacemaker = sinoatrial node (SAN)
failure of SAN means atrioventricular node (AVN) will act as a pacemaker
how does the atrioventricular node (AVN) differ from the sinoatrial node (SAN) as a pacemaker?
AVN as pacemaker - slower rate
why is the rhythm of a third degree heart block considered non-sinus?
failure of atrioventricular node (AVN) as pacemaker
ventricles themselves create electrical signals required for mechanical contraction - sinoatrial node (SAN) not involved
what are the features of ventricular tachycardia on an ECG?
P waves obscured (dissociated atrial rhythm)
rate is regular and fast (100-200bpm)
why is ventricular tachycardia dangerous?
high risk of deteriorating into fibrillation (cardiac arrest)
how can you intervene in ventricular tachycardia?
defibrillator (shockable rhythm)
what are the features of ventricular fibrillation on an ECG?
heart rate irregular - asynchronous ventricular contraction
heart rate 250 bpm and above
why is ventricular fibrillation dangerous?
no coordinated muscular contraction or electrical activity - no generation of cardiac output
risk of cardiac arrest
how can you intervene in ventricular fibrillation?
defibrillator (shockable rhythm)
what are the features of ST elevation on an ECG?
P waves visible, always followed by QRS (1:1)
regular rhythm, normal rate
ST segment elevated >2mm above isoelectric line
what causes ST elevation?
infarction (tissue death caused by hypoperfusion
what are the features of ST depression on an ECG?
P waves visible, always followed by QRS (1:1)
regular rhythm, normal rate
ST segment depressed >2mm below isoelectric line
what causes ST depression?
myocardial ischaemia (coronary insufficiency)
what causes valves to open and close?
passive process
depends on pressure of chambers separated by valve
what is the atrial kick?
atrial depolarisation of heart causes atria to contract
what effect does the atrial kick have on pressure in the aorta?
increases
how does the action of the valves increase ventricular pressure?
contraction of ventricles causes change in pressure to close atrioventricular valves (mitral or tricuspid)
semilunar valves (aortic or pulmonary) are also shut
therefore chamber volume stays constant while pressure increases
allows large pressure increase to happen as quickly as possible
how does the action of the valves allow passive filling of the ventricles?
repolarisation occurs
ventricles relax - pressure in ventricles is lower than pressure than aorta, causes blood to flow into ventricles
semilunar valves (aortic or pulmonary) close
volume of chamber stays constant while pressure in chamber decreases
eventually ventricular pressure falls below atrial pressure, allows opening of atrioventricular valves (mitral or tricuspid)
passive filling of ventricles can occur
in pathological states such as heart failure which phase of the cardiac cycle is impaired first?
isovolumetric relaxation
how can impairment of isovolumetric relaxation in states such as myocardial infarction be prevented?
treatments such as beta blockers
minimises damage to the heart, promotes remodelling
why is it necessary to prevent impairment of isovolumetric relaxation in states such as myocardial infarction?
diastole - coronary arteries supply myocardium
what are the determinants of cardiac stroke volume?
preload and afterload
how can preload be defined?
stress applied to myocardium when in diastole
what 2 factors determine preload?
Starling’s law of the heart
cardiac contractility
what is Starling’s law of the heart?
length-tension relationship
greater myocyte stretch enhances contractile force generated by myocardium (causes more forceful systolic contraction)
stroke volume of the left ventricle will increase as the left ventricular volume increases
all myocardial contraction is supposed to be at maximum rate
what 2 things determine the physiological mechanism of Starling’s law of the heart?
faster, immediate effect - stressing myocardium slightly reduces overlap of myocardial fibres, decreases interference that causes negative effect (in terms of contractile energy)
slower effect (Anrep effect) - subcellular increase in calcium stores increases force of contraction by increasing number of cross bridges in myocardium
what determines cardiac contractility?
sympathetic stimulation
action of adrenaline
(increases with contractile force of myocardium)
what generates afterload?
pressure in the aorta
how may hypovolemia (e.g. hypotension, as a result of blood loss or dehydration etc.) affect contractile energy?
less preload on the heart stretching myocardium to be able to generate ventricular force
therefore less energy of contraction
how may decreased contractile energy as a result of hypovolemia affect blood pressure?
decrease in energy of contraction decreases stroke volume
therefore blood pressure falls
how may hypertension have negative effects on the myocardium with respect to stroke volume?
increased afterload impairs stroke volume
may cause negative remodelling of the heart - heart muscle thickens, therefore pumps dysfunctionally
what does Laplace’s law state?
internal pressure generated inside a chamber is:
- directly proportional to the wall tension
- inversely proportionate to chamber radius
pressure = (2 x tension)/radius
OR
pressure = (2 x wall thickness x wall stress)/radius
how does Laplace’s law relate to states such as heart failure or dilated cardiomyopathy?
chamber radius increases
inverse proportionality means ineffective generation of internal pressure
therefore cardiac contractility fails
how does radius affect pressure using Laplace’s law?
smaller radius means greater pressure
what are the 2 types of valvular lesion?
stenotic
regurgitation
what is aortic stenosis?
aortic valve becomes significantly narrow
when is aortic stenosis classified as severe?
valvular area < 1cm²
transthoracic ECG - blood flow > 4m/s
what are the 3 common causes of aortic stenosis?
bicuspid aortic valve (genetic, seen in young patients)
degeneration of valve itself (elderly patients)
rheumatic heart disease
what are the 2 rarer causes of aortic stenosis?
infective endocarditis
hyperuricaemia
what are some causes of mitral stenosis?
rheumatic fever
rheumatoid arthritis
systemic lupus erythematosus
Whipple’s disease
why is it important to treat aortic stenosis?
can cause increased afterload on left ventricle - has to pump harder, contraction less effective
abnormal remodelling of left ventricle - hypertrophy
why is it important to treat mitral stenosis?
can cause increased pressure in left atrium
left atrium dilates to produce greater force required to pump blood to left ventricle through narrow opening
what kind of irregular rhythms may mitral stenosis cause?
atrial fibrillation
what are the 4 causes of mitral regurgitation?
rheumatic fever
mitral prolapse
infective endocarditis
dilation of left ventricle (functional)
how can mitral regurgitation affect circulation of blood?
leakage of blood during (left) ventricular contraction
less cardiac output pumped into aorta - lower volume of blood reaching body
how is mitral regurgitation addressed?
medication - diuretics to offload
valve replacement if severe
what are some causes of aortic regurgitation?
bicuspid aortic valve (congenital)
tissue diseases (e.g. Marfan’s syndrome)
rheumatic fever
high blood pressure
infection (e.g. acute endocarditis)
how can aortic regurgitation affect circulation of blood?
blood reaching aorta returns to left ventricle (doesn’t enter systemic circulation)
causes volume overload of ventricle, chamber dilates
contraction is more inefficient (Laplace’s law)
what are the symptoms of mitral regurgitation?
systolic murmur
what are the symptoms of aortic regurgitation?
diastolic murmur
