1、Prof. of Internal Medicine SANAVNImpulse conductionImpulses originate regularly at a frequency of 60-100 beat/ min-100-80-60-40-20020Phase 0Phase 1Phase 2Phase 3 Phase 4Na+ca+ATPase mvCardiac Action PotentialResting membrane PotentialNa+mNa+Na+Na+Na+Na+hK+ca+K+K+K+ca+ca+(Plateau Phase)K+K+K+Na+K+Dep
2、olarization-100-80-60-40-20020Phase 0Phase 1Phase 2Phase 3 Phase 4Na+ca+ATPase mvCardiac Action PotentialR.M.PNa+mNa+Na+Na+Na+Na+hK+ca+K+K+K+ca+ca+(Plateau Phase)K+K+K+Na+K+DepolarizationPhase 4 (only in pacemaker cellsCardiac ArrhythmiasAn abnormality of the cardiac rhythm is called a cardiac arrhy
3、thmia. Arrhythmias may cause sudden death, syncope, heart failure, dizziness, palpitations or no symptoms at all. There are two main types of arrhythmia:bradycardia: the heart rate is slow ( 100 b.p.m).Mechanisms of Cardiac ArrhythmiasMechanisms of bradicardias:Sinus bradycardia is a result of abnor
4、mally slow automaticity while bradycardia due to AV block is caused by abnormal conduction within the AV node or the distal AV conduction system.Mechanisms generating tachycardias include:- Accelerated automaticity. - Triggered activity- Re-entry (or circus movements)ACCELERATED AUYOMATICITY It occu
5、rs due to increasing the rate of diastolic depolarization or changing the threshold potential. Abnormal automaticity can occur in virtually all cardiac tissues and may initiate arrhythmias. Such changes are thought to produce sinus tachycardia, escape rhythms and accelerated AV nodal (junctional) rh
6、ythms. TRIGGERED ACTIVITY Myocardial damage can result in oscillations of the transmembrane potential at the end of the action potential. These oscillations, which are called after depolarizations, may reach threshold potential and produce an arrhythmia. The abnormal oscillations can be exaggerated
7、by pacing, catecholamines, electrolyte disturbances, and some medications. Examples as atrial tachycardias produced by digoxin toxicity and the initiation of ventricular arrhythmia in the long QT syndrome.Re-entry (or circus movement) The mechanism of re-entry occurs when a ring of cardiac tissue su
8、rrounds an inexcitable core (e.g. in a region of scarred myocardium). Tachycardia is initiated if an ectopic beat finds one limb refractory () resulting in unidirectional block and the other limb excitable. Provided conduction through the excitable limb () is slow enough, the other limb () will have
9、 recovered and will allow retrograde activation to complete the re-entry loop. If the time to conduct around the ring is longer than the recovery times (refractory periods) of the tissue within the ring, circus movement will be maintained, producing a run of tachycardia. The majority of regular paro
10、xysmal tachycardias are produced by this mechanism. Reentry ArrhythmiasNormalRe-enterantTachycardiaAtrial Arrhythmias Sinus arrhythmia: A condition in which the heart rate varies with breathing. This is usually a benign conditionSUPRAVENTRICULAR TACHYCARDIAS Supraventricular tachycardias (SVTs) aris
11、e from the atrium or the atrioventricular junction. Conduction is via the His-Purkinje system; therefore the QRS shape during tachycardia is usually similar to that seen in the same patient during baseline rhythm.Causes of SVTTachycardiaECG featuresCommentSinus tachycardiaP wave morphology similar t
12、o sinus rhythmNeed to determine underlying causeAV nodal re-entry tachycardia (AVNRT)No visible P wave, or inverted P wave immediately before or after QRS complexCommonest cause of palpitations in patients with normal heartsAV reciprocating tachycardia (AVRT)P wave visible between QRS and T wave com
13、plexesDue to an accessory pathway. If pathway conducts in both directions, ECG during sinus rhythm may be pre-excitedAtrial fibrillationIrregularly irregular RR intervals and absence of organized atrial activityCommonest tachycardia in patients over 65 yearsAtrial flutterVisible flutter waves at 300
14、/min (saw-tooth appearance) usually with 2 : 1 AV conductionSuspect in any patient with regular SVT at 150/minAtrial tachycardiaOrganized atrial activity with P wave morphology different from sinus rhythmUsually occurs in patients with structural heart diseaseMultifocal atrial tachycardiaMultiple P
15、wave morphologies (3) and irregular RR intervalsRare arrhythmia; most commonly associated with significant chronic lung diseaseAccelerated junctional tachycardiaECG similar to AVNRTRare in adultsSVT Sinus tachycardia A condition in which the heart rate is 100-160/min Symptoms may occur with rapid he
16、art rates including; weakness, fatigue, dizziness, or palpitations. Sinus tachycardia is often temporary, occurring under stresses from exercise, strong emotions, fever, dehydration, thyrotoxicosis, anemia and heart failure. If necessary, beta-blockers may be used to slow the sinus rate, e.g. in hyp
17、erthyroidism SINUS TACHYCARDIASinus tachycardia converted to NSRAtrial Arrhythmias Premature supraventricular contractions or premature atrial contractions (PAC) A condition in which an atrial pacemaker site above the ventricles sends out an electrical signal early. The ventricles are usually able t
18、o respond to this signal, but the result is an irregular heart rhythm. PACs are common and may occur as the result of stimulants such as coffee, tea, alcohol, cigarettes, or medications. Treatment is rarely necessary.PACSVT Paroxysmal Supraventricular tachycardia HR 160-250/min Atrioventricular noda
19、l re-entry tachycardia (AVNRT) It usually begins and ends rapidly, occurring in repeated periods. This condition can cause symptoms such as weakness, fatigue, dizziness, fainting, or palpitations if the heart rate becomes too fast. In AVNRT, there are two functionally and anatomically different path
20、ways within the AV node: one is characterized by a short effective refractory period and slow conduction, and the other has a longer effective refractory period and conducts faster. In sinus rhythm, the atrial impulse that depolarizes the ventricles usually conducts through the fast pathway. If the
21、atrial impulse (e.g. an atrial premature beat) occurs early when the fast pathway is still refractory, the slow pathway takes over in propagating the atrial impulse to the ventricles. It then travels back through the fast pathway which has already recovered its excitability, thus initiating the most
22、 common slow-fast, or typical, AVNRT.AVNRT (continue)The rhythm is recognized on ECG by normal regular QRS complexes, usually at a rate of 140-240 per minute. Sometimes the QRS complexes will show typical bundle branch block. P waves are either not visible or are seen immediately before or after the
23、 QRS complex because of simultaneous atrial and ventricular activation.SVTAtrioventricular reciprocating tachycardia(AVRT) In AVRT there is a large circuit comprising the AV node, the His bundle, the ventricle and an abnormal connection from the ventricle back to the atrium. This abnormal connection
24、 is called an accessory pathway or bypass tract. Bypass tracts result from incomplete separation of the atria and the ventricles during fetal development. Atrial activation occurs after ventricular activation and the P wave is usually clearly seen between the QRS and T complexes PSVT Acute Managemen
25、t Patients presenting with SVTs and haemodynamic instability require emergency cardioversion. If the patient is haemodynamically stable, vagal manoeuvres, including right carotid massage, Valsalva manoeuvre and facial immersion in cold water can be successfully employed. If not successful, intraveno
26、us adenosine (up to 0.25 mg/kg) , verapamil 5-10 mg i.v. over 5-10 minutes, i.v. diltiazem, or beta-blockers should be tried.Long-term management It includes ablation of an accessory pathway. Also, verapamil, diltiazem & -blockers; are effective in 60-80% of patients. N.B. The Wolf Parkinson White S
27、yndrome (WPW)An abnormal band of atrial tissue connects the atria and ventricles and can electrically bypass the normal pathways of conduction; a re-entry circuit can develop causing paroxysms of tachycardia.ECG shows: - Short PR interval - Delta wave on the upstroke of the QRS complexDrug treatment
28、 includes flecainamide, amiodarone or disopyramide.Digoxin and verapamil are contraindicated.Transvenous catheter radiofrequency ablation is the treatment of choice.WPW syndromeAtrial Arrhythmias Atrial flutter (HR200-350/min) A condition in which the electrical signals come from the atria at a fast
29、 but even rate, often causing the ventricles to contract faster and increase the heart rate. When the signals from the atria are coming at a faster rate than the ventricles can respond to, the ECG pattern develops a signature sawtooth pattern, showing two or more flutter waves between each QRS compl
30、ex.Atrial Arrhythmias Atrial flutter (TREATMENT) Treatment of the symptomatic acute paroxysm is electrical cardioversion. Patients who have been in atrial flutter more than 1-2 days should be treated in a similar manner to patients with atrial fibrillation and anticoagulated for 4 weeks prior to car
31、dioversion. Recurrent paroxysms may be prevented by class Ic and class III agents The treatment of choice for patients with recurrent atrial flutter is radiofrequency catheter ablationATRIAL FLUTTERAtrial Arrhythmias Atrial fibrillation (AF) - A condition in which the electrical signals come from th
32、e atria at a very fast and erratic rate. The ventricles contract in an irregular manner because of the erratic signals coming from the atria. The ECG shows normal but irregular QRS complexes, fine oscillations of the baseline (so-called fibrillation or f waves) and no P waves. Common causes include
33、CAD, valvular heart disease, hypertension, hyperthyroidism and others. In some patients no cause can be found lone atrial fibrillation. ATRIAL FIBRILLATION Atrial Arrhythmias Management When atrial fibrillation is due to an acute precipitating event such as alcohol toxicity, chest infection or hyper
34、thyroidism, the provoking cause should be treated. Strategies for the acute management of AF are ventricular rate control or cardioversion ( anticoagulation). Ventricular rate control is achieved by drugs which block the AV node Cardioversion is achieved electrically by DC shock or medically either
35、by IV infusion of an anti-arrhythmic drug such as a class Ic or a class III agentThe choice depends upon: How well the arrhythmia is tolerated (is cardioversion urgent?) Whether anticoagulation is required before considering elective cardioversion Whether spontaneous cardioversion is likely (previou
36、s history? reversible cause?). Atrial Arrhythmias Management (continue) Patients are anticoagulated with warfarin for 4 weeks before cardioversion. Anticoagulants are used to minimize the risk of thromboembolism associated with cardioversion unless atrial fibrillation is of less than 1-2 days durati
37、on. Transoesophageal echocardiography is being used to document the presence or absence of atrial thrombus as a guide to the necessity for long-term anticoagulation. Atrial Arrhythmias Management Long-term management of atrial fibrillation include two strategies: Rhythm control: antiarrhythmic drugs
38、 plus DC cardioversion plus warfarin Rate control: AV nodal slowing agents plus warfarin Recurrent paroxysms may be prevented by oral medication; class Ic agents are employed in patients with no significant heart disease and class III agents are preferred in patients with structural heart disease. R
39、ate control is usually achieved by a combination of digoxin beta-blockers or calcium channel blockers (diltiazem or verapamil). Anticoagulation (target INR 2.0-3.0) This is indicated in patients with atrial fibrillation and one of the following major or two of the moderate risk factors: Major risk f
40、actors: Prosthetic heart valve, Rheumatic mitral valve disease, Prior history of CVA/TIA, Age 75 years, Hypertension, Coronary artery disease with poor LV functionModerate risk factors: Age 65-75 years, Coronary artery disease but normal LV function, Diabetes mellitus. Ventricular Tachyarrhythmias V
41、entricular tachyarrhythmias can beconsidered under the following headings: life-threatening ventricular tachyarrhythmias (Sustained ventricular tachycardia and ventricular fibrillation) torsades de pointes normal heart ventricular tachycardia non-sustained ventricular tachycardia ventricular prematu
42、re beats Ventricular Arrhythmias Ventricular tachycardia (VT) A condition in which an electrical signal is sent from the ventricles at a very fast but often regular rate. The ECG shows a rapid ventricular rhythm with broad (often 0.14 s or more), abnormal QRS complexes. AV dissociation may result in
43、 visible P waves Treatment: in haemodynamically compromised patients, emergency DC cardioversion may be required. If the blood pressure and cardiac output are well maintained, intravenous therapy with class I drugs or amiodarone is usually used. First-line drug treatment consists of lidocaine (50-10
44、0 mg i.v. over 5 minutes) followed by a lidocaine infusion (2-4 mg i.v. per minute). DC cardioversion is necessary if medical therapy is unsuccessful. Ventricular TachycardiaVentricular Arrhythmias Ventricular fibrillation (VF) A condition in which many electrical signals are sent from the ventricle
45、s at a very fast and erratic rate. As a result, the ventricles are unable to fill with blood and pump. This rhythm is life-threatening because there is no pulse and complete loss of consciousness.The ECG shows shapeless, rapid oscillations and there is no hint of organized complexes A person in VF r
46、equires prompt defibrillation to restore the normal rhythm and function of the heart. It may cause sudden cardiac death. Basic and advanced cardiac life support is needed Survivors of these ventricular tachyarrhythmias are, in the absence of an identifiable reversible cause (e.g. acute myocardial in
47、farction, severe metabolic disturbance), at high risk of sudden death. Implantable cardioverter-defibrillators (ICDs) are first-line therapy in the management of these patients Ventricular FibrillationVentricular Arrhythmias Torsades de pointes - This is a type of short duration tachycardia that rev
48、erts to sinus rhythm spontaneously.It may be due to: - Congenital - Electrolyte disorders e.g. hypokalemia, hypomagnesemia, hypocalcemia. - Drugs e.g. tricyclic antidepressant, class IA and III antiarrhythmics.It may present with syncopal attacks and occasionally ventricular fibrillation.QRS complex
49、es are irregular and rapid that twist around the baseline. In between the spells of tachycardia the ECG show prolonged QT interval.Treatment includes; correction of any electrolyte disturbances, stopping of causative drug, atrial or ventricular pacing, Magnesium sulphate 8 mmol (mg2+) over 10-15 min
50、 for acquired long QT, IV isoprenaline in acquired cases and B blockers in congenital types Long-term management of acquired long QT syndrome involves avoidance of all drugs known to prolong the QT interval. Congenital long QT syndrome is generally treated by beta-blockade, left cardiac sympathetic
