L2 - Physiology of the Heart I Flashcards
What do valves determine?
The direction of blood flow
When heart contracts – mitral valves closes so blood goes up the aorta
What is the heart driven by?
Its own intrinsic pace maker
What kind of tissue is the heart?
Excitable tissue
Voltage gated channels in the membrane
Transmit Na, Ca and K predominantly
Resting membrane potential -70mV
How long does a whole heart beat take?
150ms
What are the 4 phases of the cardiac cycle?
Phase 0 - rapid depolarisation Phase 1 - partial repolarisation Phase 2 - plateau Phase 3 - repolarisation Phase 4 - pacemaker potential
What is phase 0 of the cardiac cycle?
Critical membrane potential - 60mV
All or nothing depolarisation
Rapid Na influx
What is phase 1 of the cardiac cycle?
If membrane stays depolarised for more than a few ms
Rapid Na influx deactivation
What is phase 2 of the cardiac cycle?
Slow inward Ca current
Initial fall in outward K
Heart is refractors –> stops further action potentials occurring too quickly
What is phase 3 of the cardiac cycle?
Deactivation of inward Ca current
Increasing outward K current
Cells reset themselves back to baseline
What is phase 4 of the cardiac cycle?
Gradual depolarisation in diastole
Found in nodal and conducting tissue
Decreasing outward K
Increasing inward Na and Ca
What 3 things does depolarisation trigger in the heart?
Rapid Na influx
Slow Ca influx
Reduced K outflux
Where is the sinoatrial node?
Right atrium
What is the role of the SAN?
Intrinsic pacemaker
Fires action potential which get transmitted down conduction tissue
Some go across atria
What is the role of the AVN?
Delays conduction - by 200ms
If ventricles instantaneously activated after atria – they would contract at same time inefficient
Fires action potential which gets transmitted down His bundle and Purkinje fibres
Where is pacemaker activity found?
In nodal and conducting tissue - AV node - SA node - Purkinje fibres It is slow depolarisation - No fast Na current
What electrical activity is found in Purkinje fibres and ventricles?
Long action potential due to plateau –> causes refractory period
This plateau is mediated by Ca
What does each wave in the ECG trace mean?
P wave – atrial activity
QRS – rapid ventricular depolarisation
T wave – repolarisation
What two arrhythmias can cause abnormal impulse generation?
Triggered activity
Increased automaticity
What is triggered activity?
Delayed after-depolarisation
If you narrow timing between stimulations the after polarisation is so big it triggers another action potential
What is increased automaticity?
Ectopic activity
Lower level pace maker takes over
What happens if the heart pacemaker breaks down?
Other part of the heart with pacemaker potentials can fire to keep you alive
- Tend to fire at a slower rate
- E.g. Purkinje fibres
Get abnormal pulse if they do not do this correctly
What two arrhythmias can cause abnormal impulse propagation?
Re-entry
Heart block
What is re-rentry?
Circular movement of impulses
If impulse has to go around an obstruction - waveforms form normally
As waveforms rushes over heart it leaves behind a trail of refractiveness
- Stops the impulse going backwards
However, if damage to the heart you can get circus movement and re-entrant excitation
What is an heart/atrioventricular block?
Block between atria and ventricles at the AV node
- AV node normally causes a delay
Disease states can lead to complete blockages
- Can lead to a non-conducting P wave –> transient –> 2nd degree
- If AV node blocked completely –> 3rd degree
How can you measure an AV block?
Can be measured on an ECG
Gap between P wave and QRS – time delay at the AV node – PR interval
PR interval prolonged in a heart block –> 1st degree
What happens in a third degree heart block?
Atria contract independently of the ventricles
Ventricles contract much slower but it keeps you alive
Most require pacemakers
What are the two ways arrhythmias can be classified?
Origin
- Sinus
- Atrial
- Nodal
- Ventricular
Heart rate
- Bradycardia
- Tachycardia
Normal sinus rhythm
Originates in sinus node of right atrium
After P wave short delay before QRS
Rate – 60-80
Sinus bradycardia
Same as normal sinus rhythm except the whole thing is slower
Rate – 30-40
Occurs during sleep
Sinus tachycardia
Same as normal sinus rhythm except the whole thing is faster
Atrial tachycardia
Originates in the atria -multiple P waves
Atria contract quickly
Ventricles contract slightly slower due to delay at AVN node
Ventricular tachycardia
Path it is taken through the ventricles is slower - wide complex
- Takes longer through heart conduction tissue
Ventricles still contracting quickly
Ventricular fibrillation
No clear rhythm
Wide complex
Ventricles in fibrillation Causes cardiac arrest
Require defibrillator
Atrial fibrillation
Atria don’t contract at all
- Just acting as channels to the blood
- Can get blood clots in the atria –> atrial thrombus
Atria fibrillations waves occasionally trigger the AVN and fire off the ventricles
Random ventricular rhythm
Rate – tends to be fast
What are the two types of autonomic control of the heart?
Sympathetic
Parasympathetic
What is sympathetic stimulation of the heart?
Increased heart rate –> positive chronotropic (affect on heart rate) effect
Release adrenaline –> β-1 adrenoceptors –> cAMP
Increased slope of pacemaker potential –> fires action potentials quicker
Increases automaticity –> intrinsic ability of heart to fire its own action potentials
Can trigger arrhythmias in people that are susceptible
What is parasympathetic stimulation of the heart?
Reduces heart rate –> negative chronotropic effect
Release Ach –> Muscarinic (M2) acetylcholine receptors
- M2 mainly in nodal and atrial tissue
Decreased slope of pacemaker potential –> fires action potentials slower
Decreased automaticity
Inhibits atrioventricular conduction
How does parasympathetic stimulation of the heart inhibit atrioventricular conduction?
Through vagal nerve which acts on the nodal tissue
Inhibits AV node
Nervous system superimposing itself on the hearts normal function
E.g. common in athletes with low heart rates
How are anti arrhythmic drugs classified?
Vaughan Williams classification
Class I anti arrhythmic drugs
Sodium channel blockers
If you can influence the depolarisation – can influence tachycardia
Na channels also important for contractility of the heart
Have to be careful not to influence this while stopping the arrythmia
Class I anti arrhythmic drugs examples
Ia - disopyramide, quinidine, procainamide
Ib - lidocaine, mexilitene
Ic - flecainide, propafenone
Class II anti arrhythmic drugs
Beta adrenceptor antagonists
Class II anti arrhythmic drugs examples
Propranolol, nadolol, carvedilol (non-selective)
Bisoprolol, metoprolol (β1-selective)
Class III anti arrhythmic drugs
Prolong the action potential
Class III anti arrhythmic drugs examples
Amiodarone
Sotalol
Class IV anti arrhythmic drugs
Calcium channel blockers
Act on the heart muscle
Class IV anti arrhythmic drugs examples
Verapamil
Diltiazem
What does Digoxin do?
Cardiac glycoside
Inhibit Na/K pump
- Works in combination with the Na/Ca pump
If you block Na/K ATP you get an increase in intracellular Ca
What are digoxin main effects on the heart?
Bradycardia (increased vagal tone)
Slowing of AV node conduction (increased vagal tone)
Increased ectopic activity (due to increased intracellular Ca)
Increased force of contraction (due to increased intracellular Ca)
None of the other drugs increase contraction
What is digoxin used for?
Atrial fibrillation to reduce ventricular rate response
- Blocks AV node enough to slow everything down
Severe heart failure as positively inotropic
What are the issues with digoxin?
Narrow therapeutic range
Can cause nausea, vomiting, diarrhoea, confusion
Why does digoxin increase vagal tone?
Vagal nerve decreases the heart rate
This is accentuated by Digoxin
What are the issues with class III drugs?
Prolong the QT interval
Can trigger arrythmias -polymorphic ventricular tachycardia
What are the adverse effects of amiodarone (class III)?
QT prolongation - polymorphic ventricular tachycardia
- Treat one rhythm problem and you cause another rhythm problem
Spreads everywhere in the body
Multiple drug interactions
Large volume of distribution
Where does amiodarone spread?
Lung - interstitial pneumonitis
Liver - abnormal function
Thyroid - hyperthyroidism / Hypothyroidism
Skin - sun sensitivity, slate grey skin discolouration (only after several years)
Eye - corneal microdeposits and optic neuropathy
