Cardiac Arrhythmia How to approach นพ.พ น จ แกวส วรรณะ หน วยโรคห วใจและหลอดเล อด

Transcription

1 Cardiac Arrhythmia How to approach นพ.พ น จ แกวส วรรณะ หน วยโรคห วใจและหลอดเล อด

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3 EKG paper is a grid where time is measured along the horizontal axis. Each small square is 1 mm in length and represents 0.04 seconds. Each larger square is 5 mm in length and represents 0.2 seconds. Voltage is measured along the vertical axis

4 Voltage is measured along the vertical axis. 10 mm is equal to 1mV in voltage. The diagram below illustrates the configuration of EKG graph paper and where to measure the components of the EKG wave form

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6 P wave Indicates atrial depolarization, or contraction of the atrium. Normal duration is not longer than 0.11 seconds (less than 3 small squares) Amplitude (height) is no more than 3 mm No notching or peaking

7 QRS complex Indicates ventricular depolarization, or contraction of the ventricles. Normally not longer than.10 seconds in duration Amplitude is not less than 5 mm in lead II or 9 mm in V3 and V4 R waves are deflected positively and the Q and S waves are negative

8 T wave Indicates ventricular repolarization Not more that 5 mm in amplitude in standard leads and 10 mm in precordial leads Rounded and asymmetrical

9 ST segment Indicates early ventricular repolarization Normally not depressed more than 0.5 mm May be elevated slightly in some leads (no more than 1 mm)

10 PR interval Indicates AV conduction time Duration time is 0.12 to 0.20 seconds QT interval Indicates repolarization time General rule: duration is less than half the preceding R-R interval

11 Sinus Bradycardia

12 Rate40-59 bpm P wavesinus QRSnormal ( ) ConductionP-R normal or slightly prolonged at slower rates Rhythmregular or slightly irregular

13 This rhythm is often seen as a normal variation in athletes, during sleep, or in response to a vagal maneuver. If the bradycardia becomes slower than the SA node pacemaker, a junctional rhythm may occur

14 Treatment includes: treat the underlying cause, atropine, isuprel, or artificial pacing if patient is hemodynamically compromised

15 Sinus Tachycardia

16 Rate P wave QRS Conduction Rhythm /min sinus normal normal regular or slightly irregular

17 Underlying causes include The clinical significance of this dysrhythmia depends on the underlying cause. It may be normal. increased circulating catecholamines CHF hypoxia PE increased temperature stress response to pain

18 Sinus Arrhythmia

19 Rate P wave QRS Conduction Rhythm /bpm sinus normal normal regularly irregular

20 The rate usually increases with inspiration and decreases with expiration. This rhythm is most commonly seen with breathing due to fluctuations in parasympathetic vagal tone. During inspiration stretch receptors in the lungs stimulate the cardioinhibitory centers in the medulla via fibers in the vagus nerve.

21 The non respiratory form is present in diseased hearts and sometimes confused with sinus arrest (also known as "sinus pause"). Treatment is not usually required unless symptomatic bradycardia is present.

22 Wandering Atrial Pacemaker

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24 This dysrhythmia may occur in normal hearts as a result of fluctuations in vagal tone. It may also be seen in patients with heart disease or COPD. Wandering atrial pacemaker may also be a precursor to multifocal atrial tachycardia. There is usually no treatment required

25 Premature Atrial Contractions

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27 PAC's occur normally in a non diseased heart. However, if they occur frequently, they may lead to a more serious atrial dysrhythmias. They can also result from CHF, ischemia and COPD.

28 Sinus Arrest

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30 This may occur in individuals with healthy hearts. It may also occur with increased vagal tone, myocarditis, MI, and digitalis toxicity. If the pause is prolonged, escape beats may occur. The treatment of this dysrhythmia depends on the underlying cause. If the cause is due to increased vagal tone and the patient is symptomatic, atropine may be indicated.

31 Sinoatrial Block

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33 In a type I SA block, the P-P interval shortens until one P wave is dropped. *In a type II SA block, the P-P intervals are an exact multiple of the sinus cycle, and are regular before and after the dropped P wave. This usually occurs transiently and produces no symptoms. It may occur in healthy patients with increased vagal tone. It may also be found with CAD, inferior MI, and digitalis toxicity.

34 Multifocal Atrial Tachycardia

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36 Multifocal atrial tachycardia (MAT) may resemble atrial fibrillation or flutter. It almost always occurs in seriously ill, elderly individuals. COPD is the most common underlying cause. Treatment depends upon the underlying cause

37 Paroxysmal Atrial Tachycardia

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39 PAT may occur in the normal as well as diseased heart. It is a common complication of Wolfe-Parkinson- White syndrome. For more on WPW, click here. This rhythm is often transient and doesn't require treatment. However, it can be terminated with vagal maneuvers. Digoxin, antiarrhythmics, and cardioversion may be used

40 Atrial Flutter

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42 Atrial flutter almost always occurs in diseased hearts. It frequently precipitates CHF. The treatment depends on the level of hemodynamic compromise. Cardioversion, vagal maneuvers and verapamil are used when prompt rate reduction is needed. Otherwise, digoxin and other antiarrhythmic drugs can be used.

43 Atrial Fibrillation

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45 Atrial fibrillation may occur paroxysmally, but it often becomes chronic. It is usually associated with COPD, CHF or other heart disease. Treatment includes: Digoxin to slow the AV conduction rate. Cardioversion may also be necessary to terminate this rhythm

46 Premature Junctional Contractions

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48 PJCs may occur in both healthy and diseased hearts. If they are occasional, they are insignificant. If they are frequent, junctional tachycardia may result. Treatment is usually not required

49 Junctional Tachycardia

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51 The clinical significance of this rhythm depends upon the basic rhythm disturbance. If the ventricular rate is rapid, cardiac output may decrease. Treatment includes: finding and correcting the underlying cause, vagal maneuvers, verapamil, and cardioversion.

52 Junctional Escape Beats and Rhythm

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54 The most common cause of this rhythm in healthy individuals is sinus bradycardia. It may also be seen in the presence of a high degree or complete AV block. If the ventricular rate is slow, hemodynamic compromise may occur. Treatment depends upon the underlying cause and the baseline dysrhythmias. Atropine or a pacemaker may be used to increase the ventricular rate

55 First Degree AV Block

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57 This is the most common conduction disturbance. It occurs in both healthy and diseased hearts. First degree AV block can be due to: inferior MI, digitalis toxicity hyperkalemia increased vagal tone acute rheumatic fever myocarditis. Interventions include treating the underlying cause and observing for progression to a more advanced AV block.

58 Second Degree AV Block (Mobitz type I, Wenkebach

59 Rate P wave QRS variable normal morphology with constant P-P interval normal Conduction the P-R interval is progressively longer until one P wave is blocked; the cycle begins again following the blocked P wave. Rhythm irregular

60 Second degree AV block type I occurs in the AV node above the Bundle of His. It is often transient and may be due to acute inferior MI or digitalis toxicity. Treatment is usually not indicated as this rhythm usually produces no symptoms

61 Third Degree AV Block or Complete AV Block

62 Rate P wave QRS Conduction Rhythm atrial rate is usually normal; ventricular rate is usually less than 70/bpm. The atrial rate is always faster than the ventricular rate. normal with constant P-P intervals, but not "married" to the QRS complexes. may be normal or widened depending on where the escape pacemaker is located in the conduction system atrial and ventricular activities are unrelated due to the complete blocking of the atrial impulses to the ventricles. irregular

63 Complete block of the atrial impulses occurs at the A-V junction, common bundle or bilateral bundle branches. Another pacemaker distal to the block takes over in order to activate the ventricles or ventricular standstill will occur. May be caused by: digitalis toxicity acute infection MI and degeneration of the conductive tissue.

64 Treatment modalities include: external pacing and atropine for acute, symptomatic episodes and permanent pacing for chronic complete heart block

65 Bundle Branch Block

66 Rate P wave QRS variable normal if the underlying rhythm is sinus wide; > 0.12 seconds Conduction This block occurs in the right or left bundle branches or in both. The ventricle that is supplied by the blocked bundle is depolarized abnormally. Rhythm regular or irregular depending on the underlying rhythm

67 Left bundle branch block is more ominous than right bundle branch block because it usually is present in diseased hearts. Both may be caused by hypertension, MI, or cardiomyopathy. A bifasicular block may progress to third degree heart block. Treatment is artificial pacing for a bifasicular block that is associated with an acute MI.

68 Premature Ventricular Contractions

69 Rate P wave QRS Conduction Rhythm variable usually obscured by the QRS, PST or T wave of the PVC wide > 0.12 seconds; morphology is bizarre with the ST segment and the T wave opposite in polarity. May be multifocal and exhibit different morphologies. the impulse originates below the branching portion of the Bundle of His; full compensatory pause is characteristic. irregular. PVC's may occur in singles, couplets or triplets; or in bigeminy, trigeminy or quadrigeminy

70 PVCs can occur in healthy hearts. For example, an increase in circulating catecholamines can cause PVCs. They also occur in diseased hearts and from drug (such as digitalis) toxicities. Treatment is required if they are: associated with an acute MI, occur as couplets, bigeminy or trigeminy, are multifocal, or are frequent (>6/min).

71 Ventricular Tachycardia

72 Rate usually between 100 to 220/bpm, but can be as rapid as 250/bpm P wave QRS Conduction Rhythm obscured if present and are unrelated to the QRS complexes. wide and bizarre morphology as with PVCs three or more ventricular beats in a row; may be regular or irregular

73 Ventricular tachycardia almost always occurs in diseased hearts. Some common causes are: CAD acute MI digitalis toxicity CHF ventricular aneurysms. Patients are often symptomatic with this dysrhythmia

74 Ventricular tachycardia can quickly deteriorate into ventricular fibrillation. Electrical countershock is the intervention of choice if the patient is symptomatic and rapidly deteriorating. Some pharmacological interventions include lidocaine, pronestyl, and bretylium

75 Torsade de Pointes

76 Rate usually between 150 to 220/bpm, P wave obscured if present QRS wide and bizarre morphology Conduction Rhythm as with PVCs Irregular

77 Paroxysmal starting and stopping suddenly Hallmark of this rhythm is the upward and downward deflection of the QRS complexes around the baseline. The term Torsade de Pointes means "twisting about the points." Consider it V-tach if it doesn t respond to antiarrythmic therapy or treatments Caused by: drugs which lengthen the QT interval such as quinidine electrolyte imbalances, particularly hypokalemia myocardial ischemia

78 Treatment: Synchronized cardioversion is indicated when the patient is unstable. IV magnesium IV Potassium to correct an electrolyte imbalance Overdrive pacing

79 Ventricular Fibrillation

80 Rate P wave QRS Conduction unattainable may be present, but obscured by ventricular waves not apparent chaotic electrical activity Rhythm chaotic electrical activity

81 This dysrhythmia results in the absence of cardiac output. Almost always occurs with serious heart disease, especially acute MI. The course of treatment for ventricular fibrillation includes: immediate defibrillation and ACLS protocols. Identification and treatment of the underlying cause is also needed

82 Idioventricular Rhythm

83 Rate 20 to 40 beats per minute P wave QRS Absent Widened Conduction Failure of primary pacemaker Rhythm Regular

84 Absent P wave Widened QRS > 0.12 sec. Also called " dying heart" rhythm Pacemaker will most likely be needed to re-establish a normal heart rate.

85 Causes: Myocardial Infarction Pacemaker Failure Metabolic imbalance Myoardial Ischemia Treatment goals include measures to improve cardiac output and establish a normal rhythm and rate. Options include: Atropine Pacing Caution: Supressing the ventricular rhythm is contraindicated because that rhythm protects the heart from complete standstill.

86 Asystole/Ventricular Standstill

87 Rate none P wave may be seen, but there is no ventricular response QRS Conduction Rhythm none none none

88 Asystole occurs most commonly following the termination of atrial, AV junctional or ventricular tachycardias. This pause is usually insignificant. Asystole of longer duration in the presence of acute MI and CAD is frequently fatal. Interventions include: CPR, artificial pacing, and atropine.

89 Artifact

90 Artifact occurs when something causes a disruption in monitoring. Some common causes are: AC interference -causes 60 cycle artifact Muscle tremors Respiratory artifact-wandering baseline Loose electrode Broken lead wire

91 WCT: Wide Complex Tachycardia How to differentiated between VT vs SVT, basic features Rate The rate of the WCT is of limited use in distinguishing VT from SVT Regularity - Slight irregularity suggests VT as opposed to most SVTs Axis - A right superior axis (axis from -90 to ±180º), sometimes called an indeterminate or "northwest" axis, is strongly suggests VT In a patient with a RBBB-like WCT, a QRS axis to the left of -30º suggests VT In a patient with an LBBB-like WCT, a QRS axis to the right of +90º suggests VT QRS duration >140 msec suggests VT; while in a LBBB-like WCT, a QRS duration >160 msec suggests VT Concordance is present when the QRS complexes in all six precordial leads (V1 through V6) are monophasic with the same polarity

92 AV Dissociation Dissociated P waves PP and RR intervals are different PR intervals are variable There is no association between P and QRS complexes The presence of a P wave with one, but not all, QRS complexes Fusion beats Capture beats

93 ALGORITHMS FOR WCT DIAGNOSIS

94 QRS morphology V1 positive (RBBB) pattern Findings in V1 A monophasic R or biphasic qr complex in V1 favors VT. A triphasic RSR' or RsR' complex (the so-called "rabbit-ear" sign) with left peak of the RsR' complex is taller than the right peak, VT is more likely Findings in lead V6 An rs complex (R wave smaller than S wave) in lead V6 favors VT. In contrast, an Rs complex (R wave larger than S wave) in lead V6 favors SVT.

95 V1 negative (LBBB) pattern Findings in lead V1 or V2 A broad initial R wave of 40 msec duration or longer in lead V1 or V2 favors VT Slurred or notched downstroke of the S wave in lead V1 or V2, Duration from the onset of the QRS complex to the nadir of the QS or S wave of 60 msec in lead V1 or V2. Findings in lead V6 The presence of any Q or QS wave in lead V6 favors VT

96 AVR Criteria

97 NCT: Narrow Complex Tachycardia Regularity Regular sinus tachycardia, A.flutter, AT, AVNRT, AVRT Irregular AF, MAT P wave Regular with P ST, AT, A.Flutter, AVRT, AVNRT Regular without P AVNRT Irregular with P MAT Irregular without P - AF