The Heart (L8-12, 14)

Question 1

Explain the electrical spread of the heart.

Answer 1

Electrical impulses travel through nodal cells, conducting cella nd muscle cells. There are electrical synapses in the gap junctions between cardiac muscle cells. A pulse is initiated at the sinoatrial node (the main pacemaker) - regulation of this changes the heart rate. If there are problems with the SA node it can mean that other tissues like the AV node can become the dominant pacemaker). The pulses from the SA node are conducted to the atria and atrioventricular node, then the fibrous atrioventricular ring (has a structural function). It then passes through the bundle of His and down Purkinje fibres (which go round the bottom of the heart) to the ventricle muscles. (so it goes down the septum and round the bottom of the heart and then up the sides)

Question 2

What are the features of the SA node?

Answer 2

15mm x 15mm x 2mm
It is in the posterior aspect of the heart between the superior vena cava and the right atrium. Its conduction is about 0.05 m/s (not very fast). Conduction if 1m/s via the atrial myocardium or the Bachmann’s bundle (the interatrial tract to the left atrium)

Question 3

What are the features of the AV node?

Answer 3

22mm x 10mmx 3mm (so is a bit bigger than the SA)
It is posterior, on the right side of the interatrial septum
it has 3 subzones
- the atrial nodal (AN), the nodal (N) and the nodal-ventral (NV)
Slow conduction through the AN-N (0.5m/s). Then there’s an AV delay, which allows atrial contraction to finish. AV refractiveness prevents excess ventricular contraction, increases at a high heart rate (because when the heart is going fats, its more likely to over contract and so more blood can be pumped into the ventricles from the atria before it contracts, so more blood is pumped around the body (lets the ventricles fully relax before contracting again) - basically makes the heart work more efficiently

Question 4

What are the sub-nodal conduction speeds?

Answer 4

Fast conduction via the Bundle of His (1 m/s). Septal activation leads tot he activation of the bundle of His and Purkinje fibres - conduction through the Purkinje fibres is about 4 m/s, through the ventricle muscle its 1m/s so conduction goes slow, fast, slow, fast. The ventricular muscle runs in a direction that causes a spiral contraction which evokes a torsion. The timing and spread of contraction also cause a twisting effect.

Question 5

What are the types of cardiac action potentials? Explain the differences

Answer 5

There are 2 main types - the APs from nodal cells, and the APs from contractile cells (so the node Vs muscle)
However, these 2 types of APs are not the same as a nerve cell (the APs are longer)
Nodal cells don’t need external signals to fire action potentials, they just keep sending signals automatically
Muscles will not fire without a pacemaker cell telling it to. The basic mechanism is pretty much the same for nodes and muscles. Nodal APs are a smoother curve and smaller, contractile APs spike and then make a sort of rectangle after

Question 6

How do pacemaker cells produce an automatic rhythm?

Answer 6

Pacemaker cells show automaticity and rhythmicity. They don’t have a constant resting potential like nerve cells. At -60mV, they begin to slowly depolarise (the prepotential stage) and then when a threshold is reached, they fire and AP - this is how the automatic rhythm is made because the potential rises in the same time, then the cell fires then it raises again.

Question 7

Explain the look of the nodal AP

Answer 7

Pre-potential is due to a decrease in potassium efflux and an increase in cation influx (aka If current (the funny current)). The If current is hyperpolarisation-induced and its inactive when positive.
The threshold is between -40 and -50 mV. When this is reached, there is an increase in Ca2+ influx and a potassium efflux causes repolarisation. This is regulated by innervation, temperature and other pacemakers. The 0 current shows there is no movement, so the If current (cation influx) is 0 during repolarization

Question 8

What controls pacemaker cells?

Answer 8

Parasympathetic vagal fibres (M2 ACh) causes hyperpolarization and a decrease prepotential slope - so basically, stimulation of these fibres causes a hyperpolarized membrane potential, so it makes it more negative and therefore harder to depolarise - so heart rate is slowed because it takes longer to build up the potential to the threshold. Sympathetic stimulation (NA fibres) increases the predisposition slope and therefore increases firing rate and heart rate. ACh and NAdr action is regulated by cAMP - by increasing Beta1, Beta2 or decreasing M2 and/or by calcium clock oscillations (rhythmic alterations of sarcoplasmic calcium release)

Question 9

Explain cardiac muscle action potentials

Answer 9

There is no automaticity - their contraction is controlled by pacemaker cell stimulation. There is a long plateau phase. a PRopagated and prolonged action potential. Fast depolarisation and overshoot. During the effective refractory period, it is not possible to start another AP. During the relative refractory period, it is possible to start another AP, but the threshold is a lot higher.

Question 10

What channels are involved in cardiac cell firing?

Answer 10

Kv11.1 and Kv7.1 are involved in depolarisation
TTX is a sodium channel inhibitor from puffer fish
HCN4 is the channel that causes the funny current

Question 11

How many sudden deaths do cardiac problems cause a year?

Answer 11

Sudden cardiac death causes about 70,000 deaths per year in the UK. 60% of that is ischaemic heart disease (to do with blockage of coronary arteries) and 40% have no detectable cause - some of which may be due to unknown inherited syndromes like long and short QT syndrome. They cause death because they lead to changes in the ventricular myocyte action potentials which lead to misfiring and therefore ventricular tachycardia. - usually caused by different ion channel mutations.

Question 12

Explain what a normal electrocardiogram looks like and why.

Answer 12

The P segment is from atrial depolarization. The QRS represents ventricular depolarization (atrial depolarization also happens at the same time but its signal is masked). The T wave shows ventricular repolarization

Question 13

How is the ECG different in long and short QT syndrome?

Answer 13

In long/short QT syndrome, the QT segment is altered in length sie to the ventricular repolarisation happening at the wrong time. Long QT shows an increased QT interval and short QT shows a decreases QT interval. However, the P wave is not altered

Question 14

How do ventricular action potentials differ in patients with QT syndromes?

Answer 14

The membrane potential is controlled by the opening and closing fo specific ion channels. The cardiac AP of a normal person lasts about 0.36 seconds. Long QT patients have cardiac APs of more than 0.45 seconds and short QT patients have an AP of less than 0.34 seconds. The QT interval involves calcium, sodium and potassium channels. Sometimes the change in QT syndrome is only seen under stress e.g. exercise. So if it’s suspected, the patient may be monitored under controlled exercise.

Question 15

What are the implications of long/short QT syndrome?

Answer 15

Triggered activity: When another impulse is triggered quickly after another. This causes an additional ectopic beat. This is only a problem when it happens regularly. It can lead to ventricular tachycardia.
Re-enterant excitation: Only happens in clusters of myocytes, not all cells at once. Therefore impacts different layers of cells. The cells send out random impulses and other cells around it may or may not respond, meaning different groups of cells respond at different times. This causes spatial and temporal dispersion of the refractory period, so all cells fire out of time and in the wrong place. This causes re-entry and AP propagation which can induce ventricular tachycardia. Ventricular tachycardia increases the chance of developing ventricular fibrillation - which is when myocytes contract in an uncontrolled manner. This can cause the heart to stop and can be lethal.

Question 16

What are the symptoms and prevalence of long QT syndrome?

Answer 16

Causes by a long QT interval. Causes syncope (fainting) - can lead to sudden death if left undiagnosed. In an ECG you see torsades de pointes (twisting around the ECG baseline) which can stop after a little while or develop into ventricular fibrillation.
Prevalence of LQT is between 1 in 10k to 1 in 15k
There are 12 forms all caused by different mutations in different ion channels. These mutations can be gain ro loss of function. Doesn’t manifest until teenage years and can be triggered by exercise or cold water.
The main types are LQT1, 3 and 5.

Question 17

What causes LQT1?

Answer 17

A mutation in KCNQ1. It affects the alpha subunit of Kv7.1 which usually transports potassium. this mutation was found through patient studies.
It is the most common form of LQT (30-35%)
Kv7.1 has 6 transmembrane spanning domains. Mutations occur in many places but particularly in the TMSDs. Some mutations are dominant and some are recessive. This channel is important because if it’s mutated, not as much potassium can be removed from the cell, so it can’t be repolarised as quickly.

Question 18

How does a mutation in Kv7.1 also effect the ear?

Answer 18

Caused by mutations in the channel and its regulator. Its found in the ear in the stria vascularis. Its function is to secrete potassium into the endolymph in the cochlea. If this channel isn’t working then the endolymph will not have a high enough potassium conc. so when the hair cells open due to a signal - there isn’t enough potassium influx to produce an AP so you get no auditory signals. In electromicrographs of KO mice, you get a collapse of the Reissner’s membrane due to no endolymph

Question 19

What changes to channels need to happen to cause LQT and why?

Answer 19

To cause LQT you either need to have a gain of function mutation in a sodium or calcium channel, or a loss of function in a potassium mutation. this means that the membrane is too positive, so it takes longer to repolarise, or it is unable to remove potassium which also increases the length of repolarisation.

Question 20

What are the treatments of long QT syndrome?

Answer 20

Beta-blockers (class 2 anti-dysrhythmic drugs) eg. Atenolol which is a beta -1 selective antagonist. Its a cAMP linked receptor and have a negative chronotropic effect (reduces heart rate) and positive ionotropic action. However, it also causes bronchoconstriction, so you can’t take it if you have asthma or another COPD.

Question 21

What are the symptoms and prevalence of short QT syndrome?

Answer 21

Caused by a reduced QT interval. Symptoms include arrhythmias, palpitations, syncope, ventricular tachycardia and fibrillation - which may lead to sudden death.
There are 5 forms of short QT. Again, the mutations can be gain or loss of function. Males account for 75% of cases - possibly due to X-linking. Usually becomes prevalence in late adolescence.
On an ECG you can see a short or absent ST segment, a taller T wave and a shorter QT interval. The QT interval also stays fixed regardless of a change in heart rate. Usually, during exercise, the QT segment will shorten to allow for increased heart rate through stimulation by symp. NS, but in patients with SQT, this isn’t possible because it’s already short.
SQT is not as common as LQT.

Question 22

What mutations cause SQT syndrome?

Answer 22

Short QT is a mirror for LQT in some mutations. E.g. a gain of function mutation in potassium channels and a loss of function mutation in sodium and calcium channels. In a loss of calcium channel mutation, its thought that either the channels do’t open normally so the membrane is not depolarised fully, making it easier to repolarise. Or, they close early but are able to open normally. In a gain of function potassium channel mutation, its though that there are either more channels in the membrane, so transport is increased, or they open earlier than they should.

Question 23

What are the treatments of short QT syndrome?

Answer 23

Implantation of a defibrillator which kicks in if the heart suddenly stops. Research suggests quinidine (a potassium channel blocker) might be effective as it stops early repolarization. However, it blocks other types of potassium channels too, so the side-effects are unknown and might be serious.

Question 24

What is the cardiac cycle and what are the 4 main stages?

Answer 24

The mechanical and electrical events that repeats with every heat beat.

1. Diastole - inflow of blood to the atria
2. Isovolumetric contraction (systole) - no blood is ejected from the heart due to valves being closed - so the volume doesn’t change
3. Otflow of blood phase (systole)
4. Isovolumetric relaxation (diastole) - volume remains unchanged because valves are closed

Question 25

What first initiates the cycle? What does the cycle begin with?

Answer 25

• The cycle is initiated with the P wave, this causes both atria to contract simultaneously thanks to a faster conduction velocity in Bachmann’s branch
• The atria contract which leads to blood pressure in each atrium increasing. Blood is squeezed into the ventricles. The duration of this is 0.1 seconds
• 80% of the blood flows into the ventricles passively. – contribution of the atria is small – The left atria only contribute 10% of the flow into the ventricles
• Additional atrial contribution is known as an atrial kick.
• Atrial fibrillation etc. can reduce or extinguish atrial kick
• After atrial contraction is complete, the atrial pressure begins to fall, causing a pressure gradient reversal across the AV values.
• This causes the valves to float upwards (pre-position) before closure

Question 26

What is Phase 1 of the cycle?

Answer 26

At phase 1 - ventricular volumes are maximal, which is termed the end- diastolic volume (EDV). The left ventricle EDV which is typically about 120ml, represents the ventricular preload. End diastolic pressures are 8-12 mmHg for the left ventricle and 3-6mmHg for the right ventricle

Question 27

What is phase 2 of the cycle?

Answer 27

All Valves are closed. This phase of the cardiac cycle begins with the appearance of the QRS complex on the ECG (ventricular depolarisation). This triggers excitation- contraction coupling, myocytes contraction and a rapid increase in intraventricular pressure. Early in this phase, the rate of pressure development becomes maximal (dP/dT). The AV valves close when intraventricular pressure exceeds atrial pressure
Ventricular contraction also triggers contraction of the papillary muscles with the chordae tendineae that are attached to the valve leaflets. This tension of the AV valve leaflets prevents them from bulging back too far into the atria and becoming incompetent (i.e. leaky)
• Closure of the V valves result in the first heart sound (S1). This sound is normally split (approx. 0.04 sec) because the mitral valve closure is slightly before tricuspid closure

Question 28

What is phase 3 of the cardiac cycle?

Answer 28

During the time period between the closure of the AV valves and the opening of the aortic and pulmonic valves, ventricular pressure rises rapidly without a change in ventricular volume (i.e. no ejection occurs). This is isovolumetric
The rate of pressure increases as the ventricles is determined by the rate of contraction of the muscle fibres, which is determined by mechanisms governing excitation-contraction coupling
The C- wave noted in the LAP (big graph above) may be due to the bulging of the mitral valve leaflets back into the atrium

Question 29

What happens phase 4 of the cardiac cycle?

Answer 29

Ejection
Aortic and pulmonic valves open – AV valves remain closed
Ejection begins when the intraventricular pressures exceed the pressures within the aorta and pulmonary artery, which causes the aortic and pulmonic valves to open.
Maximal outflow velocity is reached early in the ejection phase and maximal (systolic) aortic and pulmonary artery pressures are achieved
No heart sounds are ordinarily noted during ejection because the opening of healthy valves is silent.
Left atrial pressure initially decreases as the atrial base is pulled downward, expanding the atrial chamber. Blood continues to flow into the atria from their respective venous inflow tracts and the atrial pressures begin to rise. This rise in pressure continues until the AV valves open at the end of phase 5.

Question 30

What happens in stage 5 of the cardiac cycle?

Answer 30

Isovolumetric relaxation:
When the intraventricular pressures fall sufficiently at the end of phase 4, the aortic and pulmonic valves abruptly close (aortic then pulmonic) causing the second heart sound (S2).
Valve closure is associated with a small backflow of blood into the ventricles and a characteristic notch (dicrotic notch) in the aortic and pulmonary artery pressure tracings.
After valve closure, the aortic and pulmonary artery pressures rise slightly (dicrotic wave) followed by a slow decline in pressure.
The rate of pressure decline in the ventricles in determined by the rate of relaxation of the muscle fibres, which is termed lusitropy. This relaxation is regulated largely by the sarcoplasmic reticulum that are responsible for rapidly re-sequestering calcium following contraction.
Although ventricular pressures decrease, during this phase volumes do not change because all the valves are closed. The volume of blood that remains in a ventricle is called the end-systolic volume and is approx. 50ml in the left ventricle. The difference between the end-diastolic volume and end-systolic volume is about 70 ml and represents the stroke volume.
Left atrial pressure (LAP) continues to rise because of the venous return from the lungs. The peak LAP at the end of this phase is known as the V wave.

Question 31

What happens during stage 6 of the cardiac cycle?

Answer 31

• Rapid filling
• As the ventricles continue to relax at the end of phase 5, the intraventricular pressures will at some point fall below their respective atrial pressures. When this occurs, the AV valves rapidly open and passive ventricular filling begins.
• Despite the inflow of blood from the atria, intraventricular pressure continues to briefly fall because the ventricles are still undergoing relaxation. Once completely relaxed, their pressures will slowly rise as they fill with blood from the atria
• The opening of the mitral valve causes a rapid fall in the LAP. The peak of the LAP just before the valve opens is the V-wave. This is followed by the y-descent of the LAP. A similar wave and descent are found in the right atrium and in the jugular vein.
• Ventricular filling is normally silent. When a third heart sound (S3) is audible during rapid ventricular filling, it may represent tensing of the chordae tendineae and the AV ring during ventricular relaxation and filling
• As the ventricles continue to fill with blood and expand, they become less compliant and the intraventricular pressures rise. The increase in intraventricular pressure reduces the pressure gradient across the AV valves so that the rate of filling falls late in diastole.
• In normal resting hearts, the ventricle is about 90% filled by the end of this phase. In other words, about 90% of ventricular filling occurs before atrial contraction (phase 1) and therefore is passive.
• Aortic and pulmonary arterial pressures continue to fall during this period

Question 32

Explain the heart sounds

Answer 32

• The first heart sound (S1) is produced by vibrations generated by closure of the mitral and tricuspid valves. It corresponds to the end of diastole and beginning of ventricular systole.
• The second one (S2) is produced by the closure of the aortic and pulmonary valves at the end of systole
• S3 is a low-pitched, early diastolic sound audible during the rapid entry of blood from the atrium to the ventricle. These are best heart with the bell of the stethoscope.

Question 33

What happens during left and right asynchrony

Answer 33

• Left and right asynchrony =

• Right atrial before left atrial
• But left ventricular before right
• But right ventricular ejection before left

Question 34

How do heart rates differ between different groups of people?

Answer 34

• Heart rates vary between ages.
• Newborns less than 30 days old = 70-190 bpm
• Infants (1-11mnths) = 80-120 bpm
• Children 1 – 10 = 70-130 bpm
• Children over 10 and adults – 60-100 bpm
• Well-trained athletes 40-60 bpm

Question 35

What is meant by excitation-contraction coupling?

Answer 35

Electrical excitation leads to muscle contraction.T-tubules and intercalated discs rapidly transmit APs in the myocardium

Question 36

What is the sarcolemma?

Answer 36

The myocyte plasma membrane. It has thousands of invaginations - inward foldings of sarcolemma, forming transverse tubules (t-tubules) The allows the AP to stimulate all parts, deep into the myocyte simultaneously, therefore you get a faster rate of contraction.
Smaller animals don’t need as many T-tubules because its muscles are small so you can have fact conduction without them.

Question 37

Explain the structure of the myocytes in relaxed muscle.

Answer 37

Sarcoplasmic calcium is low (about 0.1microM)
Calcium pumps ‘mop up’ the calcium from the surrounding sarcoplasm and stored it in the sarcoplasmic reticulum so the conc of calcium is about 10nM. Calsequestrin in the SR binds to free calcium thus lowering the SR Ca conc. and allowing the pump to work more effectively and quickly, and allowing more calcium to be stored in the SR. Thus, the tropomyosin strand obscures the myosin/actin binding site, preventing the myosin head from sticking to the actin molecule. So, the muscle is relaxed, extendable and soft.

Question 38

Explain what happens in the myocytes during contraction.

Answer 38

An action potential propagates along the transverse tubules activating the voltage gated calcium channels.
Calcium rapidly diffuses out of the SR, down its concentration gradient into the sarcoplasm (10 fold) where it binds to troponin
This produces a conformational change in the troponin/tropomyosin complex which exposes the myosin/actin binding site. The myosin head sticks to the binding site
If ATP/ADP-Pi is available, cross bridge cycling occurs and the muscle shortens. Calcium binds to troponin, which changes the shape of the troponin-tropomyosin complex and uncovers the myosin-binding sites on actin

Question 39

What are the consequences of sliding filaments?

Answer 39

Muscle tension should be proportional to the number of cross bridges. The muber of cross bridges is proportional to sarcomere length. This is the optimum resting length for maximum tension generation. Short sarcomeres have overlapping thin filaments, so generate less tension. Long sarcomeres have reduced areas for cross-bridge formation so less tension generation. Therefore, there is a length/tension relationship which can be measured. You do this by using a clamp to hold the muscle in place, an electrode stimulates the muscle to produce a brief twitch. There is a thread tethering the muscle tendon to a force transducer which measures the force of the twitch. Repeat this over a range of muscle lengths to determine the optimum resting length.

Question 40

What is the relationship between length and tension in filaments?

Answer 40

Maximum active tension leads to the maximal length and therefore the max number of cross bridges. There is greater regulation at the cellular level in cardiac muscles. In skeletal muscles you get fibre recruitment

Question 41

Explain the relationship between force and velocity and how it is measured.

Answer 41

• Linked to papillary muscle and isotonic contraction
• Muscle is stretched by pre-load, and stimulated to lift afterload
• Preload= initial stretching, sarcomere length, indicated by ventricular EDV
• Afterload = force against which the ventricles act to eject blood – essentially arterial blood pressure and vascular tone
• In isotonic contraction, the heavier the load, the slower the contraction
• Therefore, there is an inverse relationship between shortening velocity ad afterload
• You can measure velocity of shortening with varied pre- and afterloads
• Key results: an increase preload gives and increased maximal force (PO). the length-tension again
• For any given afterload, increased preload = increased velocity
• Vmax is constant, which indicates the cardiac muscle contractility

Question 42

What is contractility and how does it vary?

Answer 42

• Varying definitions
• A change in contractility is shown when an intact heard changes its output per beat when the end diastolic volume is constant
• Contractility increases can occur when more cross bridges form (increase in calcium per stimulus)
• Contractility may also reflect the qualitative state of the actin/myosin cross bridges
• Changes in contractility are called positive or negative ionotropic effects
• Changes in rate are called chronotropic effects
• Noradrenaline increases both PO (maximal force) and Vmax
• Therefore, has positive ionotropic and chronotropic

Question 43

Explain the relationship between frequency and force.

Answer 43

• Inter-beat duration influences the force of contraction
• Increased frequency (reduced time between beats)
• Increased contractility (treppe or bowditch staircase)
• An increase in frequency or an extra beat increases tension
• Due to changes in calcium availability
• Accumulation of calcium with each beat, so if is going faster there’s less time for removal

Question 44

What are some diseases that cause abnormal ECGs? what is abnormal about them?

Answer 44

Atrial hypertrophy causes a high P wave
Ventricular hypertrophy causes a high QRS complex.
Ventricular hypoxia causes a lower t amplitude and ST interval
A longer ST interval is seen in acute myocardial ischemia/infarctions - due to tissue damage

Question 45

What are arrhythmias?

Answer 45

A lack of rhythmic heartbeats
Heart rate naturally varies between brachycardia and tachycardia e.g. when exersicing heart rate varies between 65-108 bpm)
In sinus arrhythmia, you can see a 15% increase on inspiration and a 15% decrease on expiration - changes pace when you breath (i.e. heart cycles with your breathing)
Non-exercise induced tachycardia is when a heart varies between 150-200bpm for no reason.
Flutters are when the heart goes at 200-300 bpm for a short period of time.
Fibrillation is when the heart goes at 300+bpm and is irregular - if it does this for too long it’ll just cut out and you’ll die.
Arrhythmias are usually caused by interruption/breaks in the heart’s conduction pathway - these are called heart blocks

Question 46

What are heart blocks?

Answer 46

impairment of heart conduction pathways e.g. an infarct clot or artery disease
They can be seen as an abnormality of the ECG e.g. an increased time period between the P-wave and QRS complex

Question 47

Explain first-degree heart block.

Answer 47

An interruption somewhere between the sinoatrial node and the AV node - this causes a slowing down of SA -AV conduction which causes an increased P-R interval. - Usually asymptomatic

Question 48

Explain second-degree heart block.

Answer 48

Split into 2 subtypes - 1. Mobitz type I (aka Wenckebach) and Mobitz type II

• Mobitz I shows progressive prolongation of the PR interval, which eventually leads to a dropped beat (non-conducted p wave) - progressive fatigue of AV cells
• Mobitz II - failure of conduction at the level of the His-Purkinje fibres below the AV node - all or nothing phenomenon when either a signal is conducted properly or not at all. - maybe no pattern or more often is in a fixed relationship e.g. 2:1, 3:1. You see no QRS complex on an ECG in some beats. Symptoms include syncope, chest pain, and fatigue - this type of heart block is likely to cause damage to the heart cells (fibrosis, necrosis etc) which can lead to type 3 heart block

Question 49

Explain third-degree heart block.

Answer 49

A complete absence of AV conduction - no supraventricular impulses are conducted to the ventricles a perfusing rhythm is maintained by a junctional or ventricular escape rhythm. Alternatively, the patient may suffer ventricular standstill which may lead to syncope (if it stops by itself) or sudden death (if leads to cardiac arrest). Typically patients will have severe brachycardia with independent atrial and ventricular rates (atrioventricular dissociation) It can also cause atrial contraction against a closed tricuspid valve which can cause a cannon wave in the jugular vein - happens when the right atrium contracts at the same time as the right ventricle and the pressure causes a wave to be sent back up the external jugular, which can be seen pulsing. This leads to reduced perfusion and syncope.

Question 50

What are bundle branch blocks?

Answer 50

A prolonged QRS, delayed contraction

Question 51

What is Sick sinus syndrome?

Answer 51

Impaired SA node causes switching between brachycardia and tachycardia.

Question 52

Explain atrial fibrillation

Answer 52

A very common type of arrhythmia
Causes an abnormal heartbeat, irregular rapid beating of the atria.
It starts with brief episodes of abnormal rhythm which becomes longer and more constant
Usually asymptomatic but atrial fibrillation is usually accompanied by symptoms related to a rapid heartbeat, palpitations or angina, shortness of breath or oedema of ankles due to fluid build up.