Heart 1 Flashcards
What are the most common cardiovascular diseases?
Coronary heart disease and stroke.
How can most cardiovascular diseases be prevented?
Addressing behavioural risk factors such as tobacco use, unhealthy diet/obesity, physical inactivity and harmful use of alcohol.
What are some of the risk factors for cardiovascular disease?
Hypertension, diabetes, hyperlipidaemia.
What are the main conduction pathways of the heart?
Atrial excitation and contraction (rapid - 1m/s) and ventricular excitation and contraction (rapid - 0.3-1m/s).
What is involved in atrial excitation and contraction?
SA node excitation, AV node excitation.
What is involved in ventricular excitation and contraction?
His bundle and branches, purkinje fibres.
What is sinus rhythm?
A regular heart beat driven by the SAN with rate 60-100 bpm.
What is a normal heart rate?
60-100bpm.
What is dysrhythmia?
An abnormal heart rhythm.
What is arrthymia?
No rhythm of the heart.
What is the difference between dysrhythmia and arrhythmia?
The terms are used interchangably and mean the same thing.
What is the P wave?
Depolarisation of the atria.
What is the QRS complex?
Depolarisation of the ventricles.
What is the T wave?
Repolarisation of the ventricles.
What does the PR segment represent?
The AV delay.
What does the ST segment represent?
Ventricular plateau.
What does the PR interval represent?
Atrial depolarisation and AV delay.
What does the QT interval represent?
Ventricular depolarisation and repolarisation.
What are the two principle types of action potentials of the heart?
The pacemaker action potential and the cardiac action potential.
Where does the pacemaker action potential occur?
The SAN and AVN.
Where does the cardiac action potential occur?
In atrial and ventricular myocytes and in Purkinje fibres.
What are the features of the pacemaker action potential?
Starts with slow depolarisation, repolarisation and there is no true baseline - there is spontaenous depolarisation.
What are the features of the cardiac action potential?
There is rapid depolarisation, rapid repolarisation, a pleateau, further depolarisation and then a stable baseline.
What causes the depolarisation in the cardiac action potential?
Rapid Na+ influx via voltage activated sodium channels.
What causes the rapid repolarisation in the cardiac action potential?
Transient K+ efflux.
What causes the plateau in depolarisation in the cardiac action potential?
K+ efflux is slow, and there is rapid delayed rectifier potassium channels.
What causes the stable baseline in the cardiac action potential?
K+ efflux via an inwardly rectifying potassium channel.
What does the duration of the cardiac action potential determine?
The refractoriness of the heart.
What is the absolute/effective refractory period?
Generation of the 2nd action potential is not possible even at the strongest consecutive stimulus.
What is the relative refractory period?
When generation of the 2nd action potential is possible, but requires a stronger stimulus.
Why are there refractory periods after the cardiac action potential?
There is rapid inactivation of the fast voltage-activated sodium channels by maintained depolarisation.
What relevance does phase 0 in cardiac action potential?
Class I Anti-arrthythmic drugs target this phase.
What relevance does phase 2 of cardiac action potential have in terms of drugs?
This phase is inhibited by class IV anti-arrythmic drugs.
What relevance does phase 2 of cardiac action potential have in terms of drugs?
A target for class III anti-arrhythmic drugs.
How is the HCN channel activated?
Hyperolarisartion-activated. It is a cyclic nucleotide-gated channel.
What structure do HCN channels have?
They are tetramers. Each subunit is composed of 6 transmembrane helixes.
What is the channel type of the funny current?
It is a hyperpolarised activated cyclic nucleotide-gated channel.
What is the selectivity of the funny current?
Non-selective cation current, permeable to both Na+ and K+ but at physiological potentials it is mainly sodium influx.
What is the activation of the funny current?
By membrane repolarisation and directly by increased intracellular cAMP.
What is the modulation of the funny current?
Sympathetic positive via beta1 and beta2 adrenoceptors (beta2 are mainly at the SAN and atria) and parasympathetic negative modulation by muscarinic M2 receptors.
What is the role in the funny current in the heart?
Cardiac automaticity and the heart rate is controlled by the autonomic NS and by circulating adrenaline.
What is the pharmacology of the funny current?
Direct inhibition - selectivity of ivabradine and indirect effects via a decrease in sympathetic or an increase in parasympathetic input.
How can the pacemaker potential be modified by sympathetic stimulation?
An increase in sympathetic stimulation increases the magnitude of the inward directed funny current, hence speeding up depolarisation as a consequence of its activation.
What does an increased action potential frequency result in?
An increased heart rate.
How is the pacemaker potential modified by parasympathetic stimulation?
The smaller the funny current, the more time is required to reach the threshold and the frequency of the action potential is reduced.
What are arrhythmias that affect heart rate?
Bradycardia and tachycardia.
What are arrthythmias that are classified by heart rhythm?
Regular and irregular.
What are arrhythmias that classified by the site of origin in the heart?
Supraventricular (SAN, atria and AVN) and ventricular (bundles of His, Purkinje fibres and ventricles).
What are arrhythmias that are classified by the type of QRS complex?
Narrow and broad.
What are the signs of arrhythmias?
Feeling heartbeats/palpitations, shortness of breath and fatigue, chest pain, dizziness and feeling faint, blackouts/syncope and cardiac arrest.
What are the physiological causes of sinus bradycardia?
Increased vagal tone (activity of the vagus nerve) which is common in trained athletes.
What are some non-cardiac causes of bradycardia?
Endocrine disorders such as hypothyroidism, an electrolyte imbalance such as severe hyperkalemia, hypo/hyper calcaemia, anti-arrhythmic drugs (beta blockers, CCBs, digoxin), antihypertensives and hypothermia.
What are some intrinsic causes of bradycardia?
Sick sinus syndrome - ischaemia and infarction of the SAN, atrioventricular blockade or heart block (ischaemia; fibrosis, congenital heart defects, infections and inflamamtons such as myocarditis, diptheria and rhematic fever)
In the case of hypothermia induced bradycardia, why are drugs such as atropine not useful?
The cause is due to reduced metabolism rather than parasympathetic activities, so would not be responsive.
What is sick sinus syndrome?
A group of heart rhythm disorders due to the malfunction of the SA node that may be present on the ECG as: sinus pause, sinus arrest, bradycardia-tachycardia syndrome.
What are the different degrees of atrioventricular block in bradycardia?
First degree (slower AV conduction), second degree (missed beats to the ventricles), third degree (no
What are drugs that may cause bradycardia?
Drugs that block the funny current directly, heart rate control drugs that act on the SAN and AVN and drugs that are used in the treatment of bradycardias.
What is a drug that directly blocks the funny current?
Ivabradine.
What are heart rate control drugs that act on the SAN & AVN?
Beta blockers (as anti-arrhythmic agents) and digoxin.
What are some drugs that are used in the treatment of bradycardias?
Atropine and isoprenaline.
