Atrial Fibrilation Flashcards
Define the myocardial pacemaker cells and describe the ionic basis of this action potential
the sino-atrial node is the pacemaker of the heart.
- the resting membrane potential is -60mV.
- there is an Na+ and Ca2+ influx and a K+ efflux. 3. once the threshold potential has been reached, there is a Ca2+ influx and the membrane potential reaches are 0mV.
- membrane repolarizes due to a K+ efflux.
Describe the sequence of events by which excitation spreads from the sinoatrial node through the heart and relate this to the sequence of contraction of the cardiac chambers
- order of excitation: SA node, then rapidly through the atria, through the AV node, rapidly through the bundle of His and down the bundle branches and purkinje fibres, and finally through the ventricular muscle cells.
- rapid spread of excitation through the heart is facilitated by the presence of intercalated discs between fibres.
- coordination of the spread of excitation means that atrial excitation and contraction are complete before ventricular contraction due to AV delay. This enables efficient emptying of blood from the atria to the ventricles.
- ventricular excitation occurs synchronously due to the rapid spread down the septum and through purkinje fibres. This enables ventricles to contract as coordinated units and expel blood effectively.
Describe the innervation of the sinoatrial node by identifying the components of the nerve supply, naming the transmitters and describing the effects of the latter on heart rate
- sympathetic nerves: increases the heart rate by activation of beta-1 adrenoceptors in the sino-atrial node. It increases the Na+ and Ca2+ influx per unit time.
- parasympathetic nerves decreases heart rate by activation of M2 muscarinic receptors in the sino-atrial node. This increases K+ permeability to hyperpolarize membrane potential and decrease the slope of the pacemaker potential by decreasing Na+ and Ca2+ influx.
State the effects of alterations in plasma potassium ion concentrations on myocardial excitation
he plateau phase of the action potential provides a long refractory period and therefore protects the heart from tetanus.
State the relationship between the position of a positive recording electrode, a defined vector of depolarisation or repolarisation, and the direction and amplitude of the resultant deflection on an electrocardiogram recording
With unipolar leads, there is one focally positioned limb lead at the positive electrode, and the others are indifferent. There are 3 and are positioned on the right and left arms and the left leg.with the chest leads, there is one focally positioned positive electrode in 6 specific positions. These are called V1 to V6.
With bipolar leads, there are two focally positioned electrodes (both positive and negative) and the potential difference between them is recorded.
Use appropriate nomenclature to label an ECG recording
The first wave, irrespective of its polarity, is always called a P wave, the final wave is called a T wave (unless U waves (rare)) are present. The first positive wave after a P wave is called an R wave. Any negative wave after a P wave but before an R wave is called a Q wave, any negative wave after an R wave is called an S wave, and any positive wave after an S wave is called R’.
Understand the basis for antiarrythmic drug treatment
Class I - blocks sodium channels and reduces the maximum rate of depolarisation. This is used to treat ventricular dysrhythmias.
Class II - beta-adrenoceptor antagonists. These are used to treat tachyarrhythmias and decrease mortality post myocardial infarction.
Class III - blocks potassium channels. This means there is slow repolarisation and prolongs cardiac action potential, thereby increasing refractory period.
Class IV - calcium channel antagonists. These block L-type calcium channels, slow conduction in SA node and AV node. They are used to treat supraventricular tachycardias.
Describe the mechanism of action of an oral anticoagulant (e.g. warfarin) and an injectable agent (e.g. heparin)
warfarin - vitamin K antagonist, stops production of correct anticoagulation factors, takes several days to work
heparin - subcutaneous injection, which activates antithrombin III, a serine protease inhibitor
Describe the therapeutic uses of anticoagulants
prevent formation of and treat existing blood clots.
Describe the effects of prostacyclin and nitric oxide on platelet aggregation
prostacyclin - prevents platelet aggregation by increasing platelet cAMP.
nitric oxide - prevents both platelet adhesion and aggregation by increasing platelet cGMP.
Describe the antiplatelet effects of aspirin and clopidogrel
Low dose aspirin (75mg) is an antiplatelet drug and is used to prevent myocardial infarction in patients who have previously had a myocardial infarction. It is recommended for secondary, but not primary, prevention. It reduces the incidence of stroke and irreversibly inhibits cyclo-oxygenase (the COX pathway).
Clopidogrel inhibits ADP-induced expression for GP. This is used in patients who can’t take aspirin.
Define the process of fibrinolysis and state the major components in the process
Plasminogen is converted to plasmin by the thrombolytic, which will then dissolve the fibrin in the clot.
State how drugs may influence fibrinolysis and list the conditions where these drugs may be used
alteplase in thromboembolic strokes.
Identify the major components of the coagulation cascade
either intrinsic or extrinsic activation, factor X activated, which breaks up prothrombin. This produces thrombin, which produces XIII.
Thrombin can also break down fibrinogen into fibrin, which forms stable fibrin and then a clot.
Describe the role of platelets in clotting and define ‘platelet aggregation’, ‘platelet adhesion’ and the ‘release reaction’
They adhere to the subendothelial surface of the damage or disease due to binding to Von Willebrand’s factor. Adhesion causes a release reaction of ADP and thromboxane, which promote platelet aggregation.
This leads to a platelet mass to plug the area of endothelial damage. This promotes a coagulation reaction where negatively charged phospholipids on activated platelets which have adhered to the site of damage localize fibrin formation. Coagulation is involved in haemostasis, which stops blood loss through damaged vessels.
Describe the differences between haemostasis and thrombosis
hemostasis - coagulation of blood in response to injury
thrombosis - unwanted formation of a blood clot
List the different vascular sites of thrombosis and the associated diseases
Venous clots form in veins due to the stasis of blood, and may travel to the lungs, causing a pulmonary embolism. Atrial fibrillation comes with a risk of transient ischaemic attack or stroke.
Arterial thrombosis forms at atherosclerotic sites, and leads to arterial blockage. It can cause myocardial infarctions and cerebral vessels.
Describe the haematological defects in haemophilia. State the treatment of this disease
Haemophilia A - genetic and carried on the X chromosome, low or lacking factor VIII of the clotting cascade. It can lead to haemorrhage and prolonged bleeding. Treatment with factor VIII from blood donors or analogue of vasopressin (ADH), which increases the patient’s factor VIII release.
Emicizumab is used in treatment for haemophilia A and involves monthly subcutaneous injections. It is very effective at reducing bleeds.
Hemophilia B is a deficiency of factor IX and treated with prophylactic factor IX.
