Arrhythmias final

  • 755 views
Uploaded on

cardiac arrhythmias and anaesthesia

cardiac arrhythmias and anaesthesia

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
    Be the first to like this
No Downloads

Views

Total Views
755
On Slideshare
0
From Embeds
0
Number of Embeds
0

Actions

Shares
Downloads
80
Comments
0
Likes
0

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide
  • No signal from the pacemaker site Development of an ectopic pacemaker May arise from conduction cells (most are capable of spontaneous activity) Usually under control of SA node  if it slows down too much conduction cells could become dominant Often a result of other injury (ischemia, hypoxia) Development of oscillatory afterdepolariztions Can initiate spontaneous activity in nonpacemaker tissue May be result of drugs (digitalis, norepinephrine) used to treat other cardiopathologies
  • Antiarrhythmic therapy has progressed over the past years from a concept of empiric arrhythmia diagnosis; that is, diagnosis solely of the appearance of the electrograms on the surface ECG with interventions aimed at making the ECG and the patient appear more “normal”, to a more scientific approach to current electrophysiology. In current pediatric and adult cardiology practices, an attempt is made at understanding the pathophysiologic diagnosis ( the what and how) of the arrhythmia. This allows the cardiologist to evaluate mechanisms and components of the arrhythmia in order to evaluate vulnerable parameters and target the arrhythmia on a subcellular level. Ultimately this intervention leads to, for the most part, making the ECG and the patient appear more “normal”!
  • A simple example of this would be the diagnosis and treatment of AV node reentry tachycardia. The diagnosis of this arrhythmia can be made on a surface electrocardiogram. However, when a Pediatric Cardiologist evaluates this more closely, the AV node reentry circuit that is responsible for this tachycardia is secondary to an anatomic fast and slow pathway within the AV node. The AV node slow conduction pathway provides a retrograde circuit making this much like other types of reentry tachycardia. The vulnerable perimeter in this case would be the AV nodal action potential. On a subcellular level, the L-type calcium channel is prominent within the AV node. Therefore, interventions could be aimed at interfering with this channel either directly with a calcium channel blocker or indirectly with a beta-blocker. In either case, the clinical outcome would be the same and that is returning the patient to sinus rhythm.  
  • The Vaughn-Williams classification of antiarrhythmic therapy takes into account some of this approach. It is a somewhat confusing mechanism of memorizing antiarrhythmics and we will spend little time discussing the classification system itself. It is based on the cellular properties of the normal his-Purkinje cells. Classification of drugs is dependent upon the ion currents responsible for depolarization and repolarization as well as the beta-adrenergic receptors. Its advantages are that it is a physiologically based system and highlights the beneficial and deleterious effects of the specific drugs. Unfortunately, its disadvantages are that all cells are not normal. Therefore in addition to this, all cells in the heart are not his-purkinje in origin and therefore have different dysrhythmia profiles.
  • Therefore, we will focus more on the original approach to antiarrhythmic therapy where you are expected to make an arrhythmia diagnosis based on the surface electrocardiogram and be familiar with some more common antiarrhythmics (including their Vaughn-Williams classification). Your goal would be to identify the dysrhythmia they have in mind certain interventions, which would provide for clinical outcomes.
  • The Vaughn-Williams classification as I stated before divides antiarrhythmics based on certain ion channels they affect. Class I antiarrhythmics are sodium channel blockers and have direct membrane action upon the sodium channel. Class II antiarrhythmics are the beta-blockers and affect the heart by sympatholysis (beta blocking). Class III antiarrhythmics prolong repolarization by affecting the potassium channels and Class IV antiarrhythmics are calcium channel blockers. In addition to these classes other antiarrhythmics would include purinergic agonists and the digitalis glycosides, which do not fall in any of the above classifications.
  • The sodium channel blockers affect Phase 0 of depolarization-the rapid inflow of sodium through the sodium channels. They are divided into 3 subclasses. 1A includes quinidine, procainamide, and disopyramide. Class 1B includes lidocaine, mexiletine, and phenytoin. Finally, Class IC would include flecainide as well as the others listed on the slide.
  • Lidocaine, mexiletine and phenytoin all fall into the Class IB antiarrhythmics. This is a nice group of medications to use as antiarrhythmics. They have little effect on normal tissues but decrease the effective refractory period and the purkinje cells. This decreases automoticity. Resultantly there is an increase in ventricular fibrillation threshold. Phenytoin in particular is useful in suppressing Digoxin-induced dysrhythmias and mexiletine is useful in depressing conduction times especially at higher heart rates. There is actually a slight decrease in the corrected QT interval with both Lidocaine and phenytoin, and mexiletine is quite useful in the treatment of patients with prolonged QT syndrome secondary to sodium channel abnormalities.
  • 8 Lidocaine is one of the Class 1B antiarrhythmics that you should feel very comfortable using. As you know, its main use is in the acute treatment of ventricular tachycardia. It acts rapidly and there is no depression of contractility or AV conduction. Its half-life is extremely short-5-10 minutes in its first phase, then 80-110 minutes during its second phase. Therefore, a bolus must be followed relatively closely with a maintenance infusion. You must remember that there is decreased metabolism with congestive heart failure and hepatic failure as well as the certain medications including beta-blockers like propranolol and H2 blockers like cimetidine. There is increased metabolism with medications like Dilantin, Phenobarbital, isuprel.
  • 8 The dose is well described in your Harriet Lane manual but basically includes a 1mg/kg bolus followed by a 20-50 microgram/kp/min. infusion.
  • 9 Mexiletine, a second 1B antiarrhythmic has good use in postoperative ventricular tachycardia (on the long-term, not acute basis). Its main side affects are gastrointestinal intolerance with a few patients developing some central nervous system complaints.
  • 10 Phenytoin or Dilantin is also a useful medicine in postoperative ventricular tachycardia however, its use to remember primarily is that in Digoxin-induced arrhythmias. There are many medications which it affects including coumadin and verapamil. Remember the intravenous form of phenytoin can cause hypotension (secondary to the carrier, fos phenytoin is as effective as an antiarrhythmic without the hypotensive effects).
  • 13 These medications are used in a variety of supraventricular as well as ventricular dysrhythmias. All of these medications can interfere with the levels of Digoxin and as well as other antiarrhythmics including amiodarone.
  • 13 I have outlined the dose of flecainide, one of the more common antiarrhythmics that you may see, solely for your reference. Again, I would stress hesitancy in using these medications without the guidance of a Pediatric Cardiologist. The Class 1C antiarrhythmics have very little use in adults currently after a particular 1C-encainide was actually shown to have an increased mortality rate in a large adult study of antiarrhythmias. Based on this study, these medications have absolutely no utility in the postoperative patient.
  • 14 The Class II agents are commonly referred to as the beta- blockers. The first 5 listed here are the primarily beta-blocker medications you will be exposed to. Sotalol is an interesting beta-blocker designer drug with properties both related to its beta-blocker roots as well as properties of potassium channel blocker like the Class III antiarrhythmics.
  • 20 Adenosine’s main treatment use is in the termination of reentry tachycardias. It also can be used in other atrial tachycardias to provide atrio-ventricular block for diagnosis. It is metabolized rapidly by red blood cells and vascular endothelial cells and therefore is a short-acting medication. Its half-life is less than 10 seconds.
  • 22

Transcript

  • 1.  
  • 2.
    • Heart condition where disturbances in
      • Pacemaker impulse formation
      • Impulse conduction
      • Combination of the two
      • Results in rate and/or timing of contraction of heart muscle that is insufficient to maintain normal cardiac output (CO).
      • To understand how anti-arrhythmic drugs work, need to understand electrophysiology of normal contraction of heart.
  • 3.
    • Arrhythmias are common in most people and are usually not a problem but…
    • Arrhythmias esp VA’s are most common cause of sudden death
    • Majority of sudden death occurs in people with neither a previously known heart disease nor history of VA’s
    • Medications which decrease incidence of A’s do not decrease (and may increase) the risk of sudden death  treatment may be worse then the disease!
  • 4.
    • Sinoatrial node
    • Atrioventricular node
    • Bundle of His
    • Bundle Branches
      • Fascicles
    • Purkinje Network
  • 5.
    • Permits rapid organized depolarization of ventricular myocytes
    • Necessary for the efficient generation of pressure during systole
    • Atrial activation complete 0.09s after SAN firing
    • Delay at AVN
    • Septum activated 0.16s
    • Whole ventricle activated by 0.23s
  • 6. ECG (EKG) showing wave segments Contraction of atria Contraction of ventricles Repolarization of ventricles
  • 7.
    • A transmembrane electrical gradient (potential) is maintained, with the interior of the cell negative with respect to outside the cell
    • Caused by unequal distribution of ions inside vs. outside cell
      • Na + higher outside than inside cell
      • Ca + much higher “ “ “ “
      • K + higher inside cell than outside
    • Maintenance by ion selective channels, active pumps and exchangers
  • 8.  
  • 9.
    • Divided into five phases (0,1,2,3,4)
      • Phase 4 - resting phase (resting membrane potential)
        • Phase cardiac cells remain in until stimulated
        • Associated with diastole portion of heart cycle
    • Addition of current into cardiac muscle (stimulation) causes
      • Phase 0 – opening of fast Na channels and rapid depolarization
        • Drives Na + into cell (inward current), changing membrane potential
        • Transient outward current due to movement of Cl - and K +
      • Phase 1 – initial rapid repolarization
        • Closure of the fast Na + channels
        • Phase 0 and 1 together correspond to the R and S waves of the ECG
  • 10.  
  • 11.
    • Phase 2 - plateau phase
      • sustained by the balance between the inward movement of Ca + and outward movement of K +
      • Has a long duration compared to other nerve and muscle tissue
      • Normally blocks any premature stimulator signals (other muscle tissue can accept additional stimulation and increase contractility in a summation effect)
      • Corresponds to ST segment of the ECG.
    • Phase 3 – repolarization
      • K + channels remain open,
      • Allows K + to build up outside the cell, causing the cell to repolarize
      • K + channels finally close when membrane potential reaches certain level
      • Corresponds to T wave on the ECG
  • 12.
    • PCs - Slow, continuous depolarization during rest
    • Continuously moves potential towards threshold for a new action potential (called a phase 4 depolarization)
  • 13.
    • SNS - Increased with concurrent inhibition vagal tone: 
    • NA binds to B1 Rec
    • Increases cAMP
    • Increases Ca and Na in
    • Decreases K out
    • Increases slope phase 0
    • Non-Nodal tissue:
    • More rapid depolarisation
    • More forceful contraction
    • Pacemaker current (If) enhanced 
    • Increase slope phase 4
    • Pacemaker potential more rapidly reaches threshold
    • Rate increased
  • 14.
    • PSNS (Vagal N)
    • Ach binds M2 rec
    • Increases gK+
    • Decreases inward Ca & Na
    • Non-Nodal tissue:
    • Less rapid depolarisation
    • Less forceful contraction
    • Pacemaker current (If) suppressed
    • Decreases pacemaker rate
    • Decrease slope of Phase 4
    • Hyperpolarizes in Phase 4
    • Longer time to reach threshold voltage
  • 15.
    • Changes in automaticity of the PM
    • Ectopic foci causing abnormal APs
    • Reentry tachycardias
    • Block of conduction pathways
    • Abnormal conduction pathways (WPW)
    • Electrolyte disturbances and DRUGS
    • Hypoxic/Ischaemic tissue can undergo spontaneous depolarisation and become an ectopic pacemaker
  • 16.
    • Branch 2 has a unidirectional block
    • Impulses can travel retrograde (3 to 2) but not orthograde. 
    • An AP will travel down the branch 1, into the common distal path (br 3), then travel retrograde through the unidirectional block in branch 2.
    • When the AP exits the block, if it finds the tissue excitable, it will continue by traveling down (reenter) the branch 1.
    • If it finds the tissue unexcitable (ERP) the AP will die.
    • Tming is critical –AP exiting the block must find excitable tissue to propagate.
    • If it can re-excite the tissue, a circular pathway of high frequency impulses (tachyarrhythmia) will become the source of APs that spread throughout a region of the heart (ventricle) or the entire heart.
  • 17.
    • Anaesthetic technique (general>regional>local)
    • Anaesthetic agents
    • Vasopressors
    • Parasympatholytics
    • Muscle relaxants
    • Intubation and
    • ventillation
    • Surgical procedures.
    • Electrolyte imbalance.
  • 18.
    • Wandering pacemaker.
    • AV Dissociation.
    • Nodal rhythm.
    • PVC’ s.
    • Sinus bradycardia.
    • SVT.
    • VT.
  • 19.
    • HR< 60 bpm; every QRS narrow, preceded by p wave
    • Can be normal in well-conditioned athletes
    • HR can be<30 bpm in children, young adults during sleep, with up to 2 sec pauses
  • 20.
    • HR > 100 bpm, regular
    • Often difficult to distinguish p and t waves
  • 21.
    • Variations in the cycle lengths between p waves/ QRS complexes
    • Will often sound irregular on exam
    • Normal p waves, PR interval, normal, narrow QRS
  • 22.
    • All result in bradycardia
    • Sinus bradycardia (rate of ~43 bpm) with a sinus pause
    • Often result of tachy-brady syndrome: where a burst of atrial tachycardia (such as afib) is then followed by a long, symptomatic sinus pause/arrest, with no breakthrough junctional rhythm.
  • 23.
    • Refers to supra-ventricular tachycardia other than afib, aflutter and MAT
    • Usually due to reentry—AVNRT or AVRT
  • 24.  
  • 25.
    • Irregular rhythm
    • Absence of definite p waves
    • Narrow QRS
    • Can be accompanied by rapid ventricular response
  • 26.  
  • 27.
    • P wave from another atrial focus
    • Occurs earlier in cycle
    • Different morphology of p wave
  • 28.
    • PR interval >200ms
    • If accompanied by wide QRS, refer to cardiology, high risk of progression to 2 nd and 3 rd deg block
    • Otherwise, benign if asymptomatic
  • 29.
    • Progressive PR longation, with eventual non-conduction of a p wave
    • May be in 2:1 or 3:1
  • 30.
    • Usually asymptomatic, but with accompanying bradycardia can cause angina, syncope esp in elderly—will need pacing if sxs
    • Also can be caused by drugs that slow conduction (BB, CCB, dig)
    • 2-10% long distance runners
    • Correct if reversible cause, avoid meds that block conduction
  • 31.
    • Normal PR intervals with sudden failure of a p wave to conduct
    • Usually below AV node and accompanied by BBB or fascicular block
    • Often causes pre/syncope; exercise worsens sxs
    • Generally need pacing, possibly urgently if symptomatic
  • 32.
    • Complete AV disassociation, HR is a ventricular rate
    • Will often cause dizziness, syncope, angina, heart failure
    • Can degenerate to Vtach and Vfib
    • Will need pacing, urgent referral
  • 33.
    • Extremely common throughout the population, both with and without heart disease
    • Usually asymptomatic, except rarely dizziness or fatigue in patients that have frequent PVCs and significant LV dysfunction
  • 34.
    • Defined as 3 or more consecutive ventricular beats
    • Rate of >120 bpm, lasting less than 30 seconds
    • May be discovered on Holter, or other exercise testing
  • 35.
    • Defibrillation
  • 36.
    • Pharmacological agents
    • Non Pharmacological agents
  • 37.
    • “ The ideal antiarrhythmic agent does not yet exist, and it is unlikely that it will in the foreseeable future. All the available agents have side effects, and therapy should be regarded as each patient’s dysrhythmia remain an individuals pharmacologic experiment, determined empirically by clinical judgment. Although in some patients one drug may suppress a ventricular tachycardia that is refractory to all other agents, other patients require several combination of drugs. (D.P. Zipes, new eng. J. Med. 304:475, 1981)”
  • 38.
    • Restore normal rhythm, rate and conduction or prevent more dangerous arrhythmias
    • Alter conduction velocity (SAN or AVN)
    • Alter slope 0 depolarisation or refractoriness
    • Alter excitability of cardiac cells by changing duration of ERP (usually via changing APD)
    • ERPinc – Interrupts tachy caused by reentry
    • APDinc – Can precipitate torsades
    • 3. Suppress abnormal automaticity
  • 39. Empiric Arrhythmia Diagnosis Interventions Clinical Outcomes Pathophysiologic Arrhythmia Diagnosis Known or suspected mechanisms Critical components Vulnerable parameters Targeted subcellular units BLACK BOX Interventions Clinical Outcomes
  • 40. Pathophysiologic Arrhythmia Diagnosis Interventions Clinical Outcomes Known or suspected mechanisms Critical components Vulnerable parameters Targeted subcellular units AV node reentrant tachycardia AV node reentry Anatomical fast/slow pathway AV node (slow conduction ) AV nodal action potential L-type Ca ++ channel Ca ++ channel blocker  -blocker Sinus rhythm
  • 41.
    • Based on cellular properties of normal His-Purkinje cells
    • Classified on drug’s ability to block specific ionic currents (i.e. Na + , K + , Ca ++ ) and beta-adrenergic receptors
    • Advantages:
      • Physiologically based
      • Highlights beneficial/deleterious effects of specific drugs
  • 42. Empiric Arrhythmia Diagnosis BLACK BOX
    • Goals
    • Identify the type of dysrhythmia
    • Be familiar with more common antiarrhythmics and their Vaughn-Williams Classification
    Interventions Clinical Outcomes
  • 43.
    • Class I - Na + - channel blockers (direct membrane action)
    • Class II - Sympatholytic agents
    • Class III - Prolong repolarization
    • Class IV- Ca ++ - channel blockers
    • Purinergic agonists
    • Digitalis glycosides
  • 44.
    • IA - Quinidine/Procainamide/Disopyramide
    • IB - Lidocaine/Mexiletine/Phenytoin
    • IC - Flecainide/Propafenone/Ethmozine
    Affects Phase 0 1 0 2 3 4 ERP RRP
  • 45.
    • Block open ACTIVATED Na channels
    • Slow phase 0 depolarisation - upstroke of AP
        • Lengthen APD and ERP. ( Atrial, His-Purkinje, ventricular tissue)
    • Prolong PR and QRS duration on ECG
    • Anticholinergic S/E. Also blocks K Ch.
    • Greater affinity for rapidly firing channels
      • Toxicity: QTc increases by 30% or QT > 0.5 sec
    • Disopyramide : Prevent rec VT. - Inotrope
    • Quinidine : SVT and VT. Torsades
    • Procainamide
  • 46.
    • Procainamide has been a long-used intravenous
    • infusion for a wide range of dysrhythmias:
      • Narrow complex tachycardia:
        • Atrial tachycardia, resistant re-entrant tachycardia
      • Wide-complex tachycardia:
        • Ventricular tachycardia
    • Downside:
    • Side effects, negative inotrope, pro-arrhythmic
  • 47.
    • Block INACTIVATED Na channels
    • Slow phase 0 depolarisation- Slows upstroke of AP
    • Shorten APD and ERP in purkinge fibres and increase VF threshold
    • Ratio ERP/APD is increased
    • Greater affinity for ischaemic tissue that has more inactivated channels, little effect on normal cells – dissociates quickly (0.5sec)
    • ECG Changes decrease QT interval.
    • Lignocaine : VT in heart with normal EF
    • Phenytoin
  • 48.
    • Use: VT (acute)
      • Acts rapidly; no depression of contractility/AV conduction
    • Kinetics
      • t 1/2 : 5-10 min (1st phase); 80-110 min (2nd phase)
    • Drug interactions
      • Decreased metabolism w/ CHF/hepatic failure, propranolol, cimetidine
      • Increased metabolism w/ isuprel, phenobarbital, phenytoin
  • 49.
    • Dose
      • 1 mg/kg, then 20-50 g/kg/min (level: 2-5 g/ml)
    • Side effects
      • CNS toxicity w/ levels > 5 g/ml
  • 50.
    • Use: VT (post-op CHD)
    • Kinetics: t 1/2 = 8 - 12 hrs
    • Drug interactions- rare
    • Dose
      • 3-5 mg/kg/dose (adult 200-300mg/dose) po q 8 hrs
    • Side effects
      • Nausea (40%)
      • CNS - dizziness/tremor (25%)
  • 51.
    • Uses
      • VT (post-op CHD), digoxin-induced arrhythmias
    • Drug interactions
      • Coumadin-  PT; Verapamil-  effect (displaces from protein)
    • Dose
      • PO: 4 mg/kg q 6 hrs x 1 day, then 5-6 mg/kg/day ÷ q 12hr
      • IV: bolus 15 mg/kg over 1 hr; level 15-20 g/ml
    • Side effects
      • Hypotension, gingival hyperplasia, rash
  • 52.
    • Class IB antiarrhythmics are very effective and very safe.
    • Little or no effect on “normal” tissues
    • First line for ischemic, automatic arrhythmia's (Ventricular tachycardia)
    • Not a lot of effect on normal conduction tissue – not a good medicine for reentry and atrial tachycardias.
  • 53.
    • Block Na channels.
    • Most potent Na channel block
    • Dissociate very slowly (10-20 sec)
    • Strongly depress conduction in myocardium
    • Slow phase 0 depolarisation - upstroke of AP
    • No effect on APD
    • No effect on QRS
    • ECG Changes prolong QT interval.
    • Flecainide : Prophylaxis in paroxysmal AF
    • Propafenone
  • 54.
    • Uses: PJRT, AET, CAT, SVT, VT, Afib
    • Kinetics
      • t 1/2 = 13 hrs (shorter if between 1-15 mos old)
    • Drug interactions
      • Increases digoxin levels (slight)
      • Amiodarone: increases flecainide levels.
  • 55.
    • Dose
      • 70-225 mg/m 2 /day ÷ q 8-12 hr
      • Level: 0.2-1.0  g/ml
    • Side effects
      • Negative inotrope- use in normal hearts only
        • (NO POST-OPs)
      • PROARRHYTHMIA - 5-12% (CAST)
  • 56.
    • IC’s have a lot of side effects that make them appropriate for use only by experienced providers.
  • 57.
    • Propranolol
    • Atenolol
    • Metoprolol
    • Nadolol
    • Esmolol
    • d,l-Sotalol
  • 58.
    • Beta Blockers - Block B1 receptors in the heart
    • Decrease Sympathetic activity
    • Non-Nodal Tissue:
    • Increase APD and ERP
    • SA and AVN:
    • Decrease SR
    • Decrease conduction velocity (Block re-entry)
    • Inhibit aberrant PM activity
  • 59.
    • Beta-blockers are good for re-entry circuits and automatic dysrhythmias.
    • Their effect of decreasing contractility may be limiting .
  • 60.
    • Non-selective B-Blocker (B1 and B2)
    • Indications: Convert or Slow rate in SVTs
    • 2 nd line after Adenosine/Digoxin/Diltiazem
    • IV atenolol 5 mg over 5 minutes
    • Repeat to maximum 15 mg.
    • 50 mg PO BID if IV works
    • Contraindiactions:
    • Asthma
    • CCF. Poor EF. High degree heart block.
    • Ca channel blockers. Cocaine use.
  • 61.
    • Anti-Fibrillatory agents.
    • Block K channels
    • Prolong repolarisation
    • Prolong APD and ERP
    • Useful in Re-Entry tachycardias
    • AMIODARONE (also Class IA, II BB)
    • SOTALOL (also Class II BB)
  • 62.  
  • 63.
    • Most tachyarrhythmias
    • OK if impaired LV function
    • Rate control and converts rhythm
    • Cardiac arrest: 300 mg IV push (max 2.2g/24hrs)
    • Stable VT: 150 mg IV repeat 10 min or infusion 360 mg IV over 6 hrs (1mg/min)
    • Maintenance infusion: 540 mg over 18 hrs (0.5mg/min)
    • Side Effects:
    • Hypotension. Negative Inotropy. Prolonged QT.
    • Photosensitivity. Thyroid disorders.
    • Pulmonary alveolitis. Neuropathy.
  • 64.
    • Calcium Channel Blockers
    • Bind to L-type Ca channels
    • Vascular SmM, Cardiac nodal & non-nodal cells
    • Decrease firing rate of aberrant PM sites
    • Decrease conduction velocity
    • Prolong repolarisation
    • Especially active at the AVN
    • VERAPAMIL
    • DILTIAZEM
  • 65.
    • Narrow complex tachycardias
    • Terminates PSVT/SVT
    • Rate control in AFib/Aflutter
    • NOT WPW or VT or high degree block
    • NOT with BBlockers
    • Negative Inotropy
    • Vasodilation – Hypotension
    • Dose: 5mg IV bolus. Rpt 15 min max 30 mg
    • Diltiazem less adverse effects
  • 66.
    • Purine nucleoside
    • Acts on A1 adenosine receptors
    • Opens Ach sensitive K channels
    • Inhibits Ca in current – Suppresses Ca dependent AP (Nodal)
    • Increases K out current – Hyperpolarisation
    • Inhibits AVN > SAN
    • Increases AVN refractory period
    • ECG Changes slows AV Node conduction.
  • 67.
    • Uses
      • SVT- termination of reentry
      • Aflutter- AV block for diagnosis
    • Kinetics
      • t 1/2 = < 10 secs
      • Metabolized by RBCs and vascular endothelial cells
    • Dose
      • IV: 100-300 g/kg IV bolus
  • 68.
    • Interrupts re-entry and aberrant pathways through AVN – Diagnosis and Treament
    • Drug for narrow complex PSVT
    • SVT reliant on AV node pathway
    • NOT atrial flutter or fibrillation or VT
    • Contraindications:
    • VT – Hypotension and deterioration
    • High degree AV block
    • Poison or drug induced tachycardia
    • Bronchospasm but short DOA
  • 69.
    • Cardiac glycoside
    • Blocks Na/K ATPase pump in heart
    • Less ECF Na for Na/Ca pump
    • Increased IC Ca
    • Inotropic: Increases force of contraction
    • AVN increased refractoriness
    • Decreases conduction through AVN and SAN
    • Negative chronotrope: Slows HR
    • Reduces ventricular response to SVTs
  • 70.
    • ECG changes
      • Increases PR interval
      • Depresses ST segment
      • Decreases QT interval
  • 71.
    • Contraindications: WPW. SSS.
    • Elderly or renal failure – reduce dose or TOXICITY
    • 0.25 to 0.5 mg IV; then 0.25 mg IV every 4 to 6 hours to maximum of 1 mg
    • 0.125 to 0.25 mg per day IV or orally
  • 72.
    • Dronedarone-SR33589
    • • Inhibits Ikr , Iks, B1 ,ICa (L-type), Ito
    • • Lacks iodine moiety
    • • No thyroid or pulmonary toxicity
    • • Similar electrophysiology to amiodarone
    • • Half-life = 24 h, dose BID
    • • Food increases levels 2-3 x
    • • Undergoes 1st pass metabolism, ~ 15%
    • Available
    • Tedisamil
    • • Class III antiarrhythmic
    • • Blocks multiple K channels and slows SR
    • • Blocks Ito , IK-ATP, IKr, IKs, Ikur
    • • Prolongs APD atria > ventricles
    • • Excreted by the kidney
    • • T ½ 8-13 hours
    • • Has significant anti-anginal, anti-ischemic
    • properties
  • 73.
    • Wide range from Carotid massage to radiofrequency ablation .
  • 74.
    • Cardioversion success rate in AF
    • Size of RA.
    • Duration of AF
    • Sleep apnoea
    • Anti arrhythmic drugs.
    • Obesity
  • 75. Implantable cardioverter defibrillator (ICD) reduces the chances of dying from a second SCA. An ICD is surgically placed under the skin in the chest or abdomen. The device has wires with electrodes on the ends that connect to the heart's chambers. The ICD monitors the heartbeat. If the ICD detects a dangerous heart rhythm, it gives an electric shock to restore the heart's normal rhythm. The electrodes are inserted into the heart through a vein.
  • 76.
    • Success rate >90% in
    • AVNRT
    • AVRT
    • Atrial tachycardia
  • 77.