Lecture 02 Heart Physiology 1 Flashcards
1. Describe the heart rate and rhythm, and the physiology of myocardial blood flow in detail 2. understand arrhythmias and the use of anti-arrhythmic drugs
What is an echocardiogram?
an ultrasound of the heart
Why are valves important?
they control the directional flow of the blood (in and out flow of the heart)
Can the heart control its own rhythm?
yes, it is made of excitable tissue and will spontaneously on its own without any external influence
What are the three key ions involved in balancing membrane potential?
sodium, potassium and calcium
Why is the heart rate of firing limited?
limited by the refractory period of the ion channels
What are the five phases of the cardiac action potential?
- rapid depolarisation
- partial repolarisation
- plateau phase
- repolarisation
- pacemaker potential
What happens during Phase 0?
rapid depolarisation
when membrane potential reaches -60mV an action potential will occur
voltage-dependent sodium ion channels snap open causing large, rapid influx of sodium
How can you describe the type of action potential seen in the myocardium?
an all-or-nothing depolarisation or degenerative response
What is the resting potential of the myocardium?
-70mV
What happens during Phase 1?
partial repolarisation
sodium channels become refractory
causes a small depolarisation
What happens during Phase 2?
plateau phase
slow, inward calcium current making the cell more positive
initial fall in outward potassium current
Why is Phase 2 important?
allows widening of the action potential and maintaining the depolarised state, preventing another action potential from occurring
What happens during Phase 3?
repolarisation
calcium channels become refractory
outward potassium current increases to achieve a negative membrane potential
What happens during Phase 4?
pacemaker potential
a gradual depolarisation during diastole through sodium and calcium
small inward increase in membrane potential and decreasing outward potassium current
once reach critical point, another action potential will fire
What is the critical point?
the point at which an action potential will occur
-60mV
Where is the pacemaker potential found?
in the nodal and conducting tissue
What is the main pacemaker and where is it found?
sinoatrial (SA) node found in the right atrium
What order does the electric impulse move through the heart?
SA node - atrium - AV node - bundle of His - purkinje fibres - ventricle
Why is the AV node important?
causes a delay between atrial and ventricular contraction, allowing the ventricles to fill with blood from the atria
Which parts of the heart have pacemaker activity?
SA node, AV node and Purkinje Fibres
What is the ion activity in the SA and AV nodes?
absence of fast sodium currents
presence of slow calcium currents - which in nodal tissue cause depolarisation
Which node is dominant?
SA node is dominant but if it fails the AV node can taken over producing a slower, ectopic rhythm
Why are drugs affecting calcium important in the heart?
characteristically long action potentials and refractory periods for nodal/pacemaker tissue due to calcium influx during the plateau phase
What are the two mechanisms of arrhythmias?
- abnormal impulse generation
2. abnormal impulse propagation
Define: Arrhythmia
an abnormal rhythm of the myocardial action potentials
What are the two types of abnormal impulse generation?
- triggered activity
2. increased automaticity
What is triggered activity in an abnormal impulse generation arrhythmia?
delayed after-depolarisation and increase in intracellular calcium
triggers abnormal impulse to occur after depolarisation is completed (phase 4)
elevated intracellular calcium concentrations may occur in disease states/digoxin toxicity
How can triggered activity lead to tachycardia?
overloading of the SR causing spontaneous calcium release after repolarisation
calcium leaves the cell through the 3Na/2Ca exchanger resulting in a net depolarising current
one stimuli provides a small depolarising current
closer the stimuli are together, the larger the after-depolarisation
given enough stimulation, the heart goes over the threshold and produces a train of impulses - tachycardia
What is increased automaticity in an abnormal impulse generation arrhythmia?
ectopic activity, where the beat occurs in the wrong part of the heart
What are the two types of abnormal impulse propagation?
- re-entry
2. heart block/AV block
What is re-entry?
a problem with the refractory tissue
normally impulse can only pass in one direction as the tissue behind it is refractory
can be a uni- or bi-directional block preventing the passing of the current
What is Circus Movement?
a re-entrance circuit in a unidirectional block which can lead to tachycardia
a time delay allows the impulse to depolarise tissue that has already depolarised, propagating the current
How does re-entry commonly caused?
scarring of the heart or through MI
What is the most common cause of arrhythmias?
re-entry through abnormal impulse propagation
What is 1st degree heart block?
delayed P-wave
normally delay between P-wave and QRS complex is 200ms
here the delay is longer that 200ms
What is 2nd degree heart block?
AV node completely refractory
no QRS complex following the P wave resulting in a missing beat
bradycardia
What is 3rd degree heart block?
complete heart block atria and ventricles aren't connecting atria firing in the background AV node takes over ventricular rhythm (more spaced out) P wave and ventricular beats independent
What occurs in a normal sinus rhythm?
P wave - atrial depolarisation
QRS complex - ventricular depolarisation
T wave - ventricular repolarisation
When are the atria contracted/relaxed?
contracted following P wave and atrial depolarisation
relaxed following the beginning of ventricular depolarisation
When are the ventricles contracted/relaxed?
contracted following completion of ventricular depolarisation / after S wave
relaxed following ventricular depolarisation / after T wave
What are the four classification of arrhythmia origins?
- sinus node
- atrial
- nodal
- ventricular
What is atrial tachycardia?
atrial contract very rapidly with multiple atrial waves
due to delay at AV node not all impulses get through to the ventricles
offers some protection to the heart - can beat faster than 220bpm
What is ventricular tachycardia
more serious that atrial tachycardia
produces a complex ventricular rhythm with a fast heart rate
improper electrical activity in the ventricles
What is seen on an ECG showing atrial fibrillation? What does this result in?
no true P waves or atrial rhythm
fibrillation waves
irregular ventricular response
no proper atrial output or atria contraction
What can occur as a result of atrial fibrillation?
atrial thrombosis
blood clot collects in the atria due to standstill of blood
passing of the clot around the body can lead to a stroke and travels to cerebral circulation
treat with anti-coagulants
What is seen on an ECG showing ventricular fibrillation? What does this result in?
no defined rhythm or output wide and complex ventricular waves irregular ventricular response variable morphology if not stabilised can result in patient death
How do you treat ventricular fibrillation?
defibrillator
electric shock to stabilise the heart rate
How does sympathetic stimulation affect heart rate?
increased heart rate with stimulation positive chronotropic effect release of NA activate flight-or-fight response increased slope of pacemaker potential increased automaticity
What is sympathetic stimulation mediated by?
beat-1 adrenoceptors
How does parasympathetic stimulation affect heart rate?
reduces heart rate with stimulation negative chronotropic effect AV conduction inhibited PR interval prolonged decreased slope of pacemaker potential decreased automaticity
What can prolongation of the PR interval lead to?
heart block
What is parasympathetic stimulation affect heart rate?
muscarinic (M2) acetylcholine receptors
Where are M2 receptors most commonly found?
nodal and atrial tissue
What are the four classes of Vaughan-Williams Antiarrhythmic drugs?
- sodium channel blockers
- beta-adrenoceptor antagonists
- prolongation of action potential
- calcium channel blockers
What are the three classes of sodium channel blockers and what do they treat?
1a. AF, atrial flutter, ventricular tachycardia
1b. ventricular tachycardia
1c. ventricular tachycardia
Give examples of 1a sodium channel blockers (x3)
disopyramide
quinidine
procainamide
Give examples of 1b sodium channel blockers (x2)
lidocaine
mexilitene
Give examples of 1c sodium channel blockers (x2)
flecainide
propafenone
What can lidocaine be used for?
a local anaesthetic
intravenous control of heart rhythm
What are the two types of beta-adrenoceptor antagonists?
- non-selective
2. beta1-selective
Give examples of non-selective beta-adrenoceptor antagonists (x3)
propranolol
nadolol
carvedilol
Give examples of beat1-selective beta-adrenoceptor antagonists (x2)
bisprolol
metaprolol
Give examples of drugs that prolong the cardiac action potential (x2)
amidarone
sotalol
What are calcium channel blockers used to treat?
hypertension and ventricular tachycardia
Give examples of calcium channel blockers (x2)
verapamil
diltiazem
What are the three states of ion channels?
resting, open and refractory
What state do drugs bind to ion channels in?
open
How does Digoxin work?
inhibition of sodium-potassium pump disrupting the resting membrane potential
decreases sodium gradient across the cell
decreases action of sodium-calcium pump
What effect does Digoxin have on the heart?
increased vagal tone - bradycardia and slowing AV conduction
increased ectopic activity - pro-arrhythmia
increased force of contraction - increased IC calcium
positive inotropic effect
reduced ventricular rate
What is Digoxin used to treat?
atrial fibrillation
severe heart failure
What are the adverse effects of Digoxin?
narrow therapeutic window
nausea and vomiting
diarrhoea
confusion
What are QT prolongation drugs used to prevent?
polymorphic ventricular tachycardia
Name two drugs that act to prolong the QT interval
amiodarone
sotalol
What are the adverse effects of Amiodarone?
large drug distribution interstitial pneumonitis abnormal liver function hyper/hypo-thyroidism increased sun sensitivity slate grey skin discolouration corneal micro deposits optic neuropathy multiple drug interactions
