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80 Cards in this Set
- Front
- Back
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what is the normal HR |
70 bpm or less |
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what does myogenic mean |
heart generates its own beat |
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what does electrical syncitium mean |
all cells in heart electrically coupled to each other via gap junctions so activity can spread throughout the whole heart |
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outline phase 4 of the cardiac action potential |
diastolic period -inward K current and Na/K pump current holds potential -ve - Na and Ca channels closed - inwards current in nodal cells gradually depol cells due to If and NCX |
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outline phase 0 of the cardiac action potential |
Na channels open inward current causes rapid depol to > 40mV |
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outline phase 1 of the cardiac action potential |
initial rapid repolarization gives rise to notch not seen in nodal tissue due to Ito and Icl |
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outline phase 2 of the cardiac action potential |
plateau due to outward K currents and inward Na Ca and NCX currents |
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outline phase 3 of the cardiac action potential |
repolarisation increasing K current inactivation of inward Na Ca currents |
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how is tetany achieved |
APs fire fast enough for a sustained contraction |
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what is the benefit of a long AP |
cannot enter tetany and can relax to fill up with blood again |
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outline the electrical activation sequence |
electrical activity fromSA spreads thorugh atria and contracts them so ventricles fill up with blood signal reaches AVN AVN acts as delay so contraction of atria can fill ventricles |
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what is the role of the AVN |
acts as a pacemaker to make sure heart does not fail |
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why cant the AVN produce an Ap |
rate of depol slower than that of SA |
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what is the role of the septum |
fibrous tissue to separate atria and ventricles |
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what is the role of the bundle of His |
specialised muscle cells along whole ventricle (Purkinje fibres) which allow electrical signal to pass from SA to AVN |
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what does the P wave signify |
atrial contraction |
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what does the QRS complex signify |
depol of ventricles |
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what does T wave signify |
repol of ventricles |
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outline the changes in ventricular pressure |
after atrial contraction ventricular pressure increases when depol of ventricles, pressure greatly increases and blood ejection |
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when does S1 occur |
during ventricular pressure rise due to AV valve |
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when does S2 occur |
during the fall in ventricular pressure due to bicuspid valves |
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what are the characteristics of a normal sinus rhythm |
regular narrow complex rate 601-100bpm each QRS wave has P wave with delay T wave normal |
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what does atrial reentry look like |
multiple P waves between each QRS contracions not getting through to ventricle |
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what does atrial fibrillation look like |
irregular baseline QRS fine multiple P waves |
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what does ventricular tachycardia look like |
high rate St segments supressed |
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what does polymorphic VENTRICULAR tachycardia look like |
QRS bizzare high rate and change with time |
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what does ventricular fibrillation look like |
heart not pumping blood chaotic contractions |
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what can cause abnormality in action potential |
genetic channelopathies ischaemia electrolyte disturbances drugs |
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what can cause abnormality in conduction |
anatomy ischaemia , infarct electrolyte disturbances drugs |
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what can cause abnormality in excitability |
increased sympathetic drive surgery drugs |
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what is an EAD |
early after depolarisation |
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what happens during an EAD |
prolonged AP membrane oscillation |
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what is a DAD |
delayed after depol |
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what isDAD caused by |
due to abnormal Ca release in the cells from SR caused by Ca overload due to increase in sympathetic NS depol of cell or ischaemia |
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what happens in DAD |
elevated cystolic Ca causes late inward current by channels and Na/Ca exchange leading oscillatory depol of membrane |
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why are EADs and DADs bad |
possibility of new AP and extensive prolongation of refractory period may impact on next normal AP |
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what happens if a pacemaker is abnormal |
damaged cells may not be able to hold -ve MP may reach depol threshold creating ectopic focus i.e. pacemaker in nonpacemaker region |
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outline re-entry from unidirectional block |
conducting pathway forks with block fewer cells available for next cells to fire and AP stops on fork with block AP spreads from other fork returns to block b/x crowd of cells can depol a few cells in that area running anterograde AP runs in circus =self sustaining resistance current |
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what determines the refractory periiod |
AP duration average membrane potential recovery time of Na channel from inactivation in nodal tissue with less Na current, recovery of Ca current |
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what are the pre requisites for re entry |
unidirectional block and / or inhomogenous conduction in circuit refractory period shorter than time taken for conduction of reentering `AP reentered beat must pass confuction defect before next normal AP arrives |
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how does a defibrillator work |
causes heart to depol so no possibility of abnormal re entry and conduction because all tissue refractory and abnormal APs die bc they hit refractory tissue |
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how do drugs stop automaticity |
increase mem threshold hyperpol mem block sym activity inhibit Na and Ca entry |
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how do drugs stop re entry |
convert uni directional block to bi direction so AP cannot propogate in either direction abolish unidirectional block |
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what is the singh vaughan - williams classification |
I Na channel blockade Ia moderate Ib weak Ic strong II B blockers III K channel blockade IV Ca channel blockers |
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example of class Ia |
quinidine |
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what does quinidine do |
prolongs AP duration reduces upstroke decreases Na entry into cell |
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what is the mechanism of quinidine |
binds to inactivated Na channel in use dependent manner slow binding and unbinding slows phase 4 depol and suppresses propagation of automaticity |
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what is quinidine useful for |
ventricular arrhythmias prevention of paroxysmal recurrent atrial fibrillation |
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name class Ib |
lignocaine |
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what does lignocaine do |
decreases AP duration and reduces upstroke supresses automaticity by -prolonging refractory period binding to inactiva state -decreasing conduction -decreasing Na influx |
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what is lignocaine useful for |
treatment and prevention during and after MI ventricular tachycardias |
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why is lignocaine not really used for MI anymore |
increased risk of asystole |
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describe Na influx |
resting Ca in cardiac cell controlled by NCX ability of NCX to keep low Ca depends on Na levels if you decrease Na you decrease Ca so much less likely for spontaneous Ca release to occur - spontaneous Ca release leads to delayed refractory period |
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name class Ic |
flecainide |
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what does flecainide do |
minimal change in AP duration blocks Na entry and inhibits SR release channels suppresses automaticity increases refractory period |
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when is flecainide useful |
in WPW syndrome CPVT recurrent tachyarrhythmias arising in abnormal conduction system |
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why can flecainide not be use after MI |
can decrease cardiac contractility |
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name class II |
atenolol |
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what does atenolol do |
lengthen K channel effect -AP duration prolong refractory period decrease conduction in SA and AVN hemodynamic depression esp. if heart failure present |
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when is atenolol used |
supraventricular tachycardias and improves survival post MI |
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what is class III |
amiodarone |
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what does amiodarone do |
prolongs AP duration prolongs refractory period lesser hemodynamic depressent |
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side effects of class III |
satalol is B blocker bretylium adrenergic neuron blocker |
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class III uses |
WPW syndrome ventricular tachycardias and atrial fibrillation |
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class Iv agent |
diltiazem |
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what does diltiazem/verapamil do |
block AV node may reduce O2 demand and CO |
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what is diltiazem used for |
can prevent recurrrence of paroxysmal supraventricular tachycardia reduce ventricular rate in patients with atrial fibrillation |
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class V drugs |
digoxin |
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what does digoxin do |
supresses AV conduction decreeases Ventricular rate |
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what is digoxin used for |
supraventricular tachyarrhytmias can be used to convert atrial flutter to fibrillation |
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what drugs act at the SA node |
b blockers atropine digitalis |
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what drugs act at the atrial muscle |
quinidine amiodarone digitalis disopyramide procainamide flecainide |
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what drugs act at the AVN |
B blockers verapamil digitalis |
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what drugs act at the bypass tract |
quinidine disopyramide amiodorane flecainide procainamide digitalis |
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what drugs act at the ventricle |
lignocaine quinidine B blockers amiodarone disopyramide amidarone mexiletine bretylium sotalol tocainine |
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what does Mg do |
Ca channel blocker reduces Ca entry through sarcolemma binds ATP involved in regulating metabolic processes |
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when is Mg used |
ventricular arrhytmias in ischaemic cells esp. if there is hypomagnesemia |
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what is adenosine used for |
SVT |
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what does adenosine do |
enhances K in atrial tissue |
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side effects of adenosine |
transient flusing breathlessness |
