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91 Cards in this Set
- Front
- Back
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Dysrhythmias are?
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collectively defined as abnormalities in the initiation and/or conduction of the cardiac impulse
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Why are dysrhythmias a reason for concern?
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1. Possible interference with cardiac pumping, leading to decreased cardiac output
2. Life-threatening |
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Normal pacemaker hierarchy
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1. SA node (NSR 60-100bpm)
2. AV node (junctional rhythm) 3. Purkinje system (idioventricular rhythm) |
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Bradydyrhythmias
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heart rate less than 60 bpm
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Sinus bradycardia what is the pacemaker?
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SA node, but rate of discharge is low
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What are possible causes of sinus bradycardia?
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acute inferior MI, high sympathetic blockade, strong vagal input to the SA node, eg, from hypersensitive baroreceptors (carotid sinus syndrome)
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During sinus brady is impulse conduction normal?
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yes
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Junctional (nodal) rhythm
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HR 40-60bpm
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What may the P wave look like on a ECG in a junctional rhythm?
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P wave with shortened PR interval, no P wave, or P wave after QRS
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Idioventricular rhythm
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HR 20-40bpm
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What will an ECG show with an idioventricular rhythm?
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increased QRS duration; amplitude and direction of R and T waves may be abnormal
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Tachydysrhythmias
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heart rate greater than 100 bpm
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Tachydysrhythmias are potentially?
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lethal
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What may be the cause of tachy rythms?
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ectopic focus may be the cause
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What type of ectopic focus?
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enhanced automaticity of some focus (AV node, Purkinje system, myocardium) due to inflammation, chemical agents (catecholamines, nicotine, caffeine), mechanical irritation of the endocardium (cardiac catherization)
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What else may enhance automaticity?
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ischemia may enhance automaticity of some focus or may give rise to reentry, including circus movements through a loop of conducting tissue
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reentry usually involves a?
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unidirectional conduction block
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Where may the ectopic focus lie?
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above the ventricles (supraventricular) or within the ventricles
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With tachycardia due to an ectopic focus, what can the HR exceed?
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150 bpm
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Narrow-complex tachycardia
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QRS duration < 120 ms
usually of supraventricular origin |
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In supraventricular tachycardia (SVT), where is the origin of dysrhythmias? What is PSVT?
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above the bundle of HIS; if the SVT begins/ends suddenly, it is paroxysmal (PSVT)
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Sinus tachycardia
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HR = 100-150 bpm
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What is the pacemaker during sinus tachycardia?
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SA node, but rate of discharge is high
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What is the most common dysrhythmia in the perioperative period?
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sinus tachycardia
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Sinus tachycardia is frequently due to?
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increased sympathetic discharge to the heart, eg, due to pain (light anesthesia), anxiety, hypovolemia (hemorrhage, shock), exercise
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What are some other cause of sinus tachycardia?
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fever, MH, thyrotoxicosis
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Atrial tachycardia has?
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ectopic (automatic) -- enhanced automaticity (phase 4 depolarization) of some focus in the atrium
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Atrial tachycardia is multifocal, meaning?
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involves 2 or more atrial ectopic foci
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Atrioventricular nodal reentrant tachycardia (AVNRT)
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1. Most common type of SVT
2. Two conducting pathways near the AV node: fast pathway (fast conduction, slow recovery) and slow pathway (slow conduction, fast recovery) |
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With atrioventricular nodal reentrant tachycardia (AVNRT) what will see on the ECG?
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no P wave
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Certain conditions (eg, a PAC) may precipitate a reentrant loop (circus movement) through the two pathways; in most cases...?
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anterograde conduction is via the slow pathway and retrograde conduction via the fast pathway
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Atrioventricular reentrant tachycardia (AVRT)
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second most common type of SVT; accessory conduction pathway causes ventricular pre-excitation
-WPW syndrome -Lown-Ganong-Levine (LGL) syndrome |
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Atrial flutter
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atrial rate is very fast (250-350 bpm)
-usually some degree of AV block (2:1 or 3:1) is typically present |
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With atrial flutter what type of waves will you see on the ECG?
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sawtooth P waves (flutter waves)
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What does atrial flutter probably most often result from?
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reentry secondary to CAD, pulmonary embolism, valvular disease
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Atrial fibrillation
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disorder of impulse conduction, ventricular tachycardia
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Junctional tachycardia, what is the pacemaker?
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the bundle of HIS
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Wide-complex tachycardia
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QRS > 120 ms
-usually of ventricular origin |
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monomorphic VT
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QRS complexes are of uniform shape and amplitude
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polymorphic VT
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QRS complexes vary in shape and amplitude
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With polymorphic VT, the QT interval can be?
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normal before dysrhythmia or prolonged QT interval before dysrhythmia (torsades de pointes)
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Wide-complex tachycardia origin?
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is of uncertain origin
eg, SVT with aberrant conduction |
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VT is serious and may cause?
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compromised cardiac output and potential for ventricular fibrillation
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Extrasystole (premature beats)
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may arise from ectopic foci
-could either be an atrial premature beat (APB) or a premature atrial contraction (PAC) |
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Are extrasystole (premature beats) common in healthy adults?
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yes, causes include stimulants, anxiety, ischemia
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What generates the premature beat?
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ectopic site in atria
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With premature beats what happens to the P wave?
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abnormal P wave; may be inverted
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Ectopic impulse is normally conducted to ?
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the ventricles unless a portion of the ventricular conduction system is refractory, in which case the impulse may follow an abnormal pathway
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If the impulse follows an abnormal pathway, this situation is characterized by?
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an abnormal QRS and is referred to as an APB with aberrant ventricular conduction (may be confused with a ventricular premature beat)
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If retrograde conduction of the impulse resets the SA node, then the interval from the APB to the subsequent sinus beat will be?
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normal, ie, no compensatory pause (distinguishes an APB from a ventricular premature beat, where a compensatory pause usually occurs)
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Ventricular premature beat (VPB); premature ventricular contraction (PVC) conduction follows? ECG tracing shows?
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an abnormal conduction path; therefore:
wide QRS, prominent R wave or S wave, sometimes a large inverted T wave |
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The VPB or PVC beat typically is?
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not conducted back to the SA node, and thus does not reset the node; thus a compensatory pause occurs on the ECG
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What are the causes of PVC's or VPB's?
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myocardial ischemia, MI, digoxin toxicity, excess catecholamine release
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VPBs comprise what percentage of observed dysrhythmia during anesthesia?
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15%
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If a VPB occurs singly and infrequently, and is not closely coupled to the preceding beat, then the hemodynamic consequences are?
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minimal
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When a VPB is closely coupled to the preceding beat (R-on-T phenomenon), the two-beat complex may?
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immediately precipitate a more severe dysrhythmia such as ventricular tachycardia or even ventricular fibrillation
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What are the three areas of the heart where conduction defects are prone to develop?
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1. In and around the SA node, eg, SA ("exit") block
2. Within the AV node 3. Within the conduction system of the ventricles |
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1st degree block
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slowed AV conduction, increased PR interval > 0.20sec; all impulses transmitted to ventricles
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What are possible causes of a 1st degree block?
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CAD, digitalis toxicity
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2nd degree block
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some impulses are conducted to the ventricles and some are not
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Mobitz type I (Wenckebach phenomenon)
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PR interval increases progressively until a dropped beat occurs
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With Mobitz Type I, the conduction defect is usually in the?
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AV node and benign; does not usually progress to complete heart block
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What are some causes of Mobitz type I?
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ischemia, inferior MI, aortic valve disease, digitalis toxicity
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Mobitz Type II
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loss of AV conduction after constant PR interval
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What Mobitz is more serious?
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type II
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Where is the block in Mobitz type II?
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below the AV node, within the His bundle or bundle branches; widened QRS is common
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What is a common cause of Mobitz type II?
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anterior MI
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3rd degree block (complete AV Block)
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no impulses are conducted
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What occurs in a 3rd degree block?
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P waves and QRS waves occur at independent frequencies
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Stokes-Adams syndrome
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INTERMITTENT complete block; fainting usually occurs with onset of block; recovery occurs with junctional or ventricular escape
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Bundle Branch Block
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Prolonged QRS complex- readily detected in right (V1 or V2) or left (V5 or V6) precordial leads, shift of mean electrical axis toward the block
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LBBB manifests significant?
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heart disease; wide-notched R wave ("rabbit ears") is commonly seen in leads I and V6
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RBBB may not reflect clinically significant heart disease, though is sometimes associated with?
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chronic lung disease or atrial septal defects; rSR' pattern is commonly seen in lead V1
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Hemiblocks are what ventricle?
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left
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LAFB what will you see on the ECG?
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Q wave in lead I, S wave in lead III, left axis deviation
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LPFB what will you see on the ECG?
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less common than LAFB; Q wave in lead III, S wave in lead I, right axis deviation
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Is the QRS prolonged with a hemiblock?
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no
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Fibrillation
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asynchronous electrical activity in the myocardium
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Asynchronous mechanical activity
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myocardium is ineffective as a pump; "twitching;" loss of CO
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Fibrillation can be explained by?
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circus movements of multiple impulses
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Atrial fibrillation is one cause of?
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narrow-complex SVT
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Pre-excitation syndrome
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premature activation (pre-excitation) of part or all of the ventricle
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pre-excitation syndrome occurs through an?
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anomalous accessory conduction pathways between atria and ventricles; cardiac impulse can bypass AV node
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Wolff-Parkinson-White (WPW) syndrome
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shortened PR interval
-leading edge of QRS complex is distorted |
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The R wave in WPW syndrome starts?
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early and rises slowly to merge with R wave near its peak; this distortion is termed delta wave
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delta wave results from?
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premature activation of only part of the ventricle, the major portion being activated normally
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Patients with WPW syndrome commonly develop?
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SVT (reciprocating rhythm) when a normally conducted impulse reenter the atria via the anomalous pathway in a retrograde manner and reactivates the atria; delta waves disappear
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What is the anatomic basis of WPW?
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Kent Bundle- anomalous conduction pathway between the atria and ventricular septum
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Lown-Ganong-Levine syndrome
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shortened PR but no delta wave
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In LGL is the conduction pathway normal?
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yes, just premature; bypass fibers probably lead from atria to AV bundle so that ventricular activation is via the normal pathway
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tachydysrhythmias can also develop as in?
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WPW
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