Cardiac Arrhythmias PDF

DISEASES OF CARDIAC CONDUCTION THE NORMAL BEFORE WE DELVE INTO THE ABNORMAL Depolarisation Atrioventricular Sinoatrial no...

DISEASES OF CARDIAC CONDUCTION THE NORMAL BEFORE WE DELVE INTO THE ABNORMAL Depolarisation Atrioventricular Sinoatrial node spreads through Bundle of His node (delay) atria Depolarisation Right and left spreads through Purkinje fibres bundle branches ventricles THE SPECTRUM OF THE ABNORMAL Arrrhytmias Tachyarrhythmias Bradyarrhythmias Sinus Supraventricular Ventricular Heart block bradycardia AV junctional Ventricular SA node Atrial Extrisic causes Intrinsic causes Av block tahycardia tachycardia Sinus Ventricular 3rd degree Atrial fibrillation Hypothyroidism Sa node infarct 1st degree 2nd degree (complete) tachycardia fibrillation heart block Sick sinus Mobitz 1 Atrial flutter Hyponatraemia Narrow syndrome (wenkenbach) complex escape rhythm Raised ICP (see Mobitz 2 cushing's triad) Broad complex escape rhythm Drugs Advanced block TACHYARRHYTHMIAS  Pathogenesis  Arrhythmias either stem from an abnormality of automaticity/ of conduction o Accelerated automaticity  N spontaneous rhythmicity occurs w slow depolarisation of cells until threshold is reached followed by initiation of AP (BLUE)  This mechanism can be accelerated by ↑ rate of depolarisation (RED)/ ↓ threshold (ORANGE)  Such changes cause sinus tachycardia, escape rhythms, & accelerated AV nodal (jxal) rhythms o Triggered activity  Myocardial damage → oscillators of transmembrane potential @ end of AP   These oscillators, called “after depolarisations” may reach threshold potential & cause arrhythmias  If occur before transmembrane potential reach threshold, termed “early after depolarisation” (E)  If occurs after transmembrane potential is complete, termed “delayed after depolarisations”  Abnormal oscillators may be triggered by pacing, catecholamines, electrolyte disturbances, hypoxia, acidosis & some drugs  Arrhythmias caused by triggered activity  Atrial fib d/t digoxin toxicity  Initiation of ventricular arrhythmias in long QT sd o Re-entry/ circuit movements  Occurs when ring of cardiac tissue surrounds unexcitable core (eg a region of scarred myocardium)  Tachycardia is initiated if one limb of the ring is refractory, resulting in unidirectional block (α)  Provided movement through excitable limb (β) is slow enough, the refractory limb will have recovered, & will allow retrograde activation to complete the re-entry loop  If time to complete loop is longer than refractory period, circus movements will be maintained, producing a run of tachycardia  MAJORITY OF PAROXYSMAL TACHYCARDIAS ARE PRODUCED BY THIS MECHANISM 1. Impulse passes down both limbs of potential tachycardia circuit 2. Impulse blocked in one pw (α) but proceeds slowly down o pw (β) Running along pw α until colliding w refractory tissue 3. Impulse travels so slowly along pw β that it can return along pw α & complete the re-entry circuit, producing a circus movement tachycardia SINUS TACHY o Rate >100; p wave before each QRS o Physiological tachycardia usually accepted as 220-age o Identify & treat the cause (usually infection; may be hypovolaemia, anaemia, cardiac failure, etc) ATRIAL FIBRILLATION o Caused by anything resulting in:  ↑ Atrial pressure  ↑ Atrial volume  Atrial fibrosis  Infiltration / inflammation of atrium  “lone”/ idiopathic atrial fibrillation o A fib is maintained by continuous, rapid (300 – 600/min) activation of atria by multiple meandering re- entry wavelets, often driven by multiple rapidly depolarising automatic foci, predominantly located @ the bases of the pulmonary vv o Only a proportion of these impulses conduct to ventricles o Ventricular response depends on  Rate & regularity of atrial activity (particularly entry to AV node)  Refractory properties of AV node  Balance btw Σ & PΣ tone o Clinical features  Signs  Irregularly irregular pulse  Irregular nature maintained during exercise (differentiates from ventricular ectopic beats)  Pulse alters in amplitude d/t variable diastolic filling times  Pulse deficit may be evident o Auscultated HR @ praecordium higher than radial pulse counted o Every beat is heard, but each contraction does not produce an adequate stroke volume to be palpated @ wrist  Varying intensity of S1 o Patients vary from asymptomatic (incidental finding) to dyspnoeic & distressed w palpitations, hypotension, angina & CCF  Clinical classification 1. First detected (irrespective of duration/ severity) 2. Paroxysmal: stops spontaneously w/in 7d 3. Persistent: continuous >7d 4. Longstanding persistent: continuously for >1y 5. Acute: 48h 7. Permanent: continuous w joint decision btw physician & pt to stop attempts at regaining sinus rhythm o ECG features  Fine oscillations @ baseline (fibrillatin/ f waves)  No clear P waves  Rapid QRS rate (120-180bpm) w irregularly irregular rhythm o Management  Mx depends on the pt’s stability (whether he/ she is hypotensive/ has angina/ in acute CCF) & whether it is acute or chronic  Mx of A fib Acute (48h) Haemodynamically stable Revert to sinus rhythm Unstable patient patient Aim to control ventricular rate & anticoagulate Synchronised DC cardioversion If no organic cardiac dz Give IV bolus of 60U/kg heparin, then, if chronic, follow w antoagulation for If organic cardiac >=4w post cardioversion. Then dz cardiovert w 200J, w a monophasic/ biphasic defibrillator Digoxin, 0,125mg, PO, dly Adjust dose according to After 3 attemps @ unsuccessful B-blocker/ CCB rate response & plasma synchronised cardioversion, Atenolol, 50-100mg, PO, dly levels, aiming for a attempt pharmacological (CI in CCF/ asthma) plasma level of 0,6- cardioversion w Amiodarone, 1nmol/L 300mg, IV, over 10-20min Carvedilol in compensated CCF Digoxin has positive if cannot use B blocker, inotrpoic effects, making consider: it an appropriate chose in Verapamil, 40-120mg, PO, those w systolic dysfx Repeat attempt at synchronised 8hrly Digoxin is relatively cardioversion (verapamil has negative ineffective at controlling inotropism, so avoid in systolic ventricular rate, esp dysfunction) during exercise when Σ If the above is ineffective, tone is increased. useful consider adding Digoxin in elederly & those who Follow w infusion of are relatively inactive. amiodarone: 900mg over 24h Counsel on, & monitor for digoxin toxicity. Pts at risk of toxicity: in pts uncontrolled on the above, consider (under specialist Elderly supervision)... renal dysfx hypokalaemia Pts w lean body mass Amiodarone Ablate & pace  Rate control (AV nodal slowing PLUS oral anticoag)  Appropriate as 1⁰ strategy in pts who o Have permanent form or arrhythmia w symptoms that may improve w rate control o Persistent tachyarrhythmias w failed cardioversions & high risk: benefit ratio for antiarrhythmic drug  Usually achieved by digoxin, β-blockers/ CCBs (verapamil/ diltiazem)  Digoxin monotherapy may be sufficient for elderly, non-ambulant pts o Cardiac glycoside o 2 major actions  Increased inotropism  Increases intracellular availability of ca, by inhibiting mg dependent na/k pump, improving contractility  Enhancement of PΣ activity & red in Σ tone = inc refractive period of AV nodal cells = dec in hr  Also increases the excitability of the myocardium (NB to remember in toxicity) o Indication generally limited to rate control in pts w CCF AND A fib  Extremely compromised efficacy in pts who are young & active – the vagotonic effect is easily dwarfed by Σtone o Caution: narrow therapeutic window  Signs of dig toxicity  GI – anorexia, n&v  CNS – headache, drowsiness, confusion, disturbed colour vision  CVS – arrhythmias – almost all brady & tachyarrhythmias may occur  Mx: activated charcoal if presenting w/in 3hrs of ingestion. Measure plasma digoxin (only of value if w/in 6-8hrs of ingestion). Perform ECG. Obtain K & Mg concentrations. Correct hypokalaemia/ hypomagnesaemia, but do not attempt to correct mild to moderate hyperkalaemia. K/ Mg replacement may exacerbate AV block. If marked sinus bradycardia/ 2nd/ 3rd degree heart block, use atropine (iv, 1mg, rpt as necessary). Use digitalis antitoxin if available (not readily available in SA) o Dosing  “Digitalisation” (loading) is not always safe, & it is rather recommended to use maintenance dose, which usually reaches steady state w/in 7-10d  Maintenance dose: 0,0625-0,5mg, po, dly o Resting ventricular rate of 150bpm o Narrow (