what is the SA NODE?
what is the SA NODE?
– sinus or sinuatrial node
– heart’s pacemaker due to spontaneous depolarizations
– located in the right atrium
– pacing activity known as sinus rhythm
– depolarization of SA node spreads through atria producing P wave
what is the rate of the various pacemakers in the heart?
– SA node is the usual pacemaker, normal rate 60-100 bpm
;60 bradycardia ;100 tachycardia- if SA node fails, other potential pacemakers are:
— atrial pacemakers w/inherent rates of 60-80
— AV node rate 40-60 bpm
— ventricular pacer rate 20-40 bpm

– In certain pathologic conditions ectopic pacemakers can go much faster at rates 150-250 bpm

what is AUTOMATICITY?
– generation of pacemaking stimuli
– focal areas of the heart that have automaticity are called AUTOMATICITY FOCI
what does the P wave represent?
– SA node stimulated atrial depolarization ? contraction
what does the flat EKG pause that follows the P wave represent?
– slow depolarization w/i AV node by Ca?²
– allows blood to flow from atria to ventricles
what comprises the ventricular conduction system?
– His Bundle ? R ; L Bundle Branches ? terminal fibers (made of Purkinje fibers) ? ventricular myocytes
– Purkinje fibers use fast Na? for conduction of depolarization
– produces QRS complex on EKG
what does the QRS complex represent?
– depolarization of the ventricular myocytes ? beginning of ventricular contraction
on EKG what is any downward wave preceded by an upward wave?
– an S wave
what is a downward wave with no preceding upward wave?
– a QS wave
what is the ST segment on EKG?
– flat segment that follows the QRS complex
– plateau/initial phase of ventricular repolarization
– horizontal, flat, level with other areas of baseline
*if ? or ? from normal baseline usually sign of serious pathology
what is the T wave on EKG?
– final rapid phase of ventricular repolarization
what is ventricular repolarization?
– begins immediately after QRS and persists until the end of T wave
– ventricular myocytes recover their interior, resting negative charge ? accomplished by K? leaving myocytes
– part of ventricular systole
what is the QT interval?
– represents the duration of ventricular systole from beginning of QRS ? end of T wave
– indicator of repolarization
*hereditary Long QT interval (LQT) syndromes ………………????
draw and label each wave, segment, and interval from an ECG rhythm strip
draw and label each wave, segment, and interval from an ECG rhythm strip
what does a normal 12-lead ECG strip look like?
what does a normal 12-lead ECG strip look like?
Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of 0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75°.
how can you calculate heart rate from an ECG rhythm strip?
how can you calculate heart rate from an ECG rhythm strip?
– 2.5 small squares = 0.1 sec ? length of each: P wave, PR segment, QRS complex;
– 10-11 small squares = 2-2.2 big sq. = 0.4-0.44 sec ? length of QT interval
– 5 small squares = 1 large sq. = 0.2 sec ? ventricular diastole
– 1 complete waveform should be ? 4 big squares = 0.8 sec
how are the limb leads applied for a 12-lead ECG?
how are the limb leads applied for a 12-lead ECG?
how do the limb leads relate to each other in frontal plane orientation?
how do the limb leads relate to each other in frontal plane orientation?
how are the chest leads applied for a 12-lead ECG?
how are the chest leads applied for a 12-lead ECG?
how all 12 ECG leads related to each other in space?
how all 12 ECG leads related to each other in space?
how do the events from the cardiac cycle relate to ECG tracing?
how do the events from the cardiac cycle relate to ECG tracing?
what are the four basic criteria for a normal cardiac rhythm? i.e. if any one of these four things is abnormal, it is an arrhythmia
1. HR 60-100
2. originates in the SA node (sinus rhythm)
3. normal conduction pathway
4. normal conduction velocity
what is the heart rate values for the various forms of tachyarrhythmias and bradyarrhythmias?
;350: fibrillation
250-350: flutter
150-250: paroxysmal tachyarrhythmia
100-150: simple tachyarrhythmia
60-100: normal
40-60: mild bradyarrhythmias
20-40: moderate bradyarrhythmias
;20: severe bradyarrhythmias
list five types of tachyarrhythmias based on location in the heart
– Supra Ventricular Tachyarrhythmias:
? sinus arrhythmia
? atrial arrhythmia
? junctional (nodal) arryhthmia
– ventricular arrhythmia
what are 3 mechanisms of cardiac arrhythmias?
– ?automaticity
– triggered automaticity
– re-entry (circus movement)
how does epinephrine or NE affect the automaticity of the SA node?
how does epinephrine or NE affect the automaticity of the SA node?
– Epi or NE binds to ?? adrenergic receptors coupled with Gs proteins ? phosphorylates Ca²? channels ? ???Ca²? influx ? more rapid reaching threshold ? tachyarrhythmia
what is the normal action potential of cardiac tissue (myocytes), and what ions are moving in each of the 4 phases?
what is the normal action potential of cardiac tissue (myocytes), and what ions are moving in each of the 4 phases?
- how do the two forms of triggered automaticity induced tachyarrhythmias compare in the shape of their action potentials? ? early after depolarization (EAD) ? delayed after depolarization (DAD) - what are the causes of these tachyarrhythmias?
– how do the two forms of triggered automaticity induced tachyarrhythmias compare in the shape of their action potentials?
? early after depolarization (EAD)
? delayed after depolarization (DAD)
– what are the causes of these tachyarrhythmias?
– if myocardial cells are ischemic,or injured, or exposed to catecholamines ? loading of cations ? cannot stay at resting membrane potential ? fluctuations in REM ? hit threshold ? triggers unwanted events ? tachyarrhythmia
what is anatomic reentry?
what is anatomic reentry?
Anatomic reentry: the central obstacle (damaged tissue) creates 2 paths; when the impulse arrives, unidirectional
what is circus movement?
what is circus movement?
an anatomic obstacle (e.g. scar) blocks impulse which travels around obstacle and when it arrives full circle and area is excitable, it keeps going in rapid circular pattern while throwing off impulses to surrounding tissue ? tachyarrhythmia in people w/ ischemic heart disease
– what is the normal pattern of parasympathetic control of HR?
– how is this affected by phases w/i respiratory cycle? i.e. physiological sinus arrhythmia
? what happens in transplanted hearts?
– Vagus/CN X parasympathetic outflow from medulla ? controls automaticity/activity of SA ; AV nodes ? releases ACh on nodal tissue ? inhibitory ? ?HR
– during inspiration Vagus N. inhibited ? ?ACh, ?inhibition ? mild ?HR
– during expiration Vagus N. stimulated ? ?ACh, ?inhibition ? mild ?HR
? in transplanted heart, not connected to vagus n., does not undergo physiological sinus arrhythmia
how is the ECG tracing affected during physiological sinus arrhythmia?
– R – to – R interval gets shorter
– list at least 3 situations when you would expect sinus tachycardia
– why?
– exercise, fever, hyperthyroidism (thyroid toxicosis)
– because these situations ?parasympathetic/vagus outflow
how is the ECG tracing affected during sinus tachycardia?
how is the ECG tracing affected during sinus tachycardia?
– ?freq. of P waves ? ?HR
– Electrocardiogram (ECG) showing sinus tachycardia at a rate of 150 beats/min: Note the difficulty in separating the P waves from the T waves in the standard leads. The P waves are most evident in lead V1 (arrow) where the terminal negativity suggests left atrial enlargement.
– list at least 4 situations when you would expect sinus bradycardia
– why?
– athletes: have ?vagal tone
– hypothyroidism
– hypothermia
– cholestasis jaundice
how is the ECG tracing affected during sinus bradycardia?
how is the ECG tracing affected during sinus bradycardia?
– ?freq. of P waves ? ?HR
– Sinus bradycardia is defined as a sinus rhythm with a rate less than 60 beats per minute. This rhythm strip shows a sinus rate of 50 beats per minute.
how is the ECG tracing affected when the SA node tissue is injured?
how is the ECG tracing affected when the SA node tissue is injured?
– sinus tachy brady syndrome = sick sinus syndrome
– Tracing of sick sinus syndrome (tachycardia-bradycardia syndrome). The initial three beats show atrial fibrillation (AF) which terminates abruptly and is followed after a long offset pause by a junctional escape beat (J) and then a sinus beat (S).
what are 3 examples of atrial tachyarrhythmias?
– atrial tachycardia: 125-250
– atrial flutter: 250-350 bpm
– atrial fibrillation: ;350
– reentry phenomenon:
how is the ECG tracing affected by atrial tachycardias?
– multiple P waves followed by 1 QRS complex
– 125-250
how is the ECG tracing affected by atrial flutter?
– not well recognized P waves, kind of peaky, like sawtooth = Flutter = F waves
– many P waves/ F waves for each QRS complex
– 250-350
how is the ECG tracing affected by atrial fibrillation?
– lots of v. small electrical activity in many areas and many directions within atria ? cancel each other out ? wave form is v. small = fibrillation = f waves
why is it critical to correct atrial tachyarrhythmias?
– if these arrhythmias travel to ventricals, it could be life threatening
– Tx: terminate atrial tachyarrhythmias, if not, at least slow down AV node
– Rx: Ca²? channel blockers; ? blockers (propranolol); digitalis (positive inotropic drug used in cardiac failure + ?vagal activity (vagaltonic) ? slows AV node w/ ?ACh; …
list ## causes and pathophysiology for junctional (nodal) tachyarrhythmias
– caffeine ? enters cell, inhibits phosphodiesterase (PDE) ? no breakdown of cAMP ? ?[cAMP] ? ?phosphorylation of Ca²? ? ?conduction
how is the ECG tracing affected by junctional/nodal tachyarrhythmias?
– ?length of PR segment due to ?AV conduction
list ## causes and pathophysiology for junctional (nodal) bradyarrhythmias = junctional blocks = nodal blocks = heart blocks
– first degree heart block = ?length of PR interval
– second degree heart block = P wave: QRS complex not 1:1, missing QRS complexes b/c AV node not conduction all impulses
– third degree heart block = complete heart block ? ? new pace established by new pacemaker at v. slow rate (e.g. 40 bpm); atria and ventricles paced independent of each other
how is the ECG tracing affected by junctional blocks = nodal blocks = heart blocks?
– first degree block: ?length of PR interval due to slowed AV conduction
– second degree heart block: missing QRS complexes following P waves; not 1:1
– third degree heart block: P waves and QRS complexes not equally spaced;
what is Atrioventricular (AV) heart block?
– AV block is defined as a delay or interruption in transmission of an impulse, either transient or permanent, from atria to ventricles due to anatomic or functional impairment in conduction system; conduction can be delayed, intermittent, or absent
– commonly used terminology includes first degree AV block (slowed conduction without missed beats), second degree AV block (missed beats, often in a regular pattern, eg, 2:1, 3:2, or higher degrees of block), and third degree or complete AV block.
– PR interval includes atrial depolarization (P wave) and subsequent conduction through AV node, His bundle, bundle branches and fascicles, and terminal Purkinje fibers; normal PR interval is between 120 to 200 msec (0.12 to 0.20 sec) and tends to shorten w/ ?HR due in part to rate-related shortening of action potentials; Children under age 14 tend to have a PR interval of about 140 msec
– what are the three types of second degree heart block?
– how does each type appear on ECG tracing?
– Mobitz I (Wenckebach): progressive elongation of PR interval until 1 P wave not followed by QRS complex ? cycle repeats
– Mobitz II: no variation in PR interval, it is stable; however at some point P wave not followed by QRS complex
– 2:1 second degree heart block: 2 P waves for every QRS complex; QRS is regularly dropped;
how does the ECG tracing reflect third degree heart block?
– no relationship between P wave and QRS complex b/c paced by two separate pacemakers due to complete AV block
– what is the pathophysiology of two junctional tachycardia?
– how does the ECG appear w/ each junctional tachycardia
– Wolff-Parkinson-White Syndrome: extra/alternate conduction pathway connection between atria ; ventricles = bundle of Kent ? if stressed, consume caffeine, or other ?rate of SA node firing (?sympathomimetic activity) ? doubles HR = dangerous tachyarrhythmia HR 140+
? ECG: no Q wave, instead gradual upsweep of PR interval =
– intranodal reentry phenomenon: two types of pathway in AV node, fast one shoots down and may reenter up slow path ? HR 180-200
? ECG:
– Tx: cartoid sinus massage (on one side only) to ?vagal tone;
– Rx: ??
– what are the 3 causes of ventricular tachyarrhythmias?
? what is the pathophysiology of each?
? how are ECG tracings affected?
– ectopic pattern = irritable foci in ventricles after ischemia b/c:
1. ?O? ? ?ATP production ? ?Na?/K?-ATPase fxn ? less negative RMP, hits threshold more easily
2. ? membranes leaky ? more Na? ; Ca²? in and less negative
3. ?adrenaline/Epi in post-ischemic myocardial cells ? epi ? Gs ? ?AC ? ?cAMP ? ?PKa ? ?intracellular Ca²?
? ECG: many pathologic vectors in ventricular myocardial tissue ? widened QRS complex ; ? ventricular premature beats (VPBs) or ventricular systole; dangerous if happening more often
?? ventricular tachycardia when a series of abnormal firings from same focus at rate ;125
?? ventricular flutter from 1-2 centers firing at 250-350 electrical activity but no mechanical activity for longer time
?? ventricular fibrillation ;350 when many areas of irritable foci firing simultaneously ? leads to flat line death if not converted
1. evaluate this ECG pattern
1. evaluate this ECG pattern
Normal sinus rhythm at a rate of 71 beats/min, a P wave axis of 45°, and a PR interval of 0.15 sec.
2. evaluate this ECG pattern
2. evaluate this ECG pattern
The two main electrocardiographic features of Wolff-Parkinson-White (WPW) pattern include a short PR interval (;0.12 seconds) and a delta wave (red arrows). The QRS complex is wide (;0.12 seconds) and represents a fusion beat; the initial portion (delta wave) results from rapid ventricular activation via the accessory pathway (pre-excitation), while the termination of ventricular activation is via the normal conduction system leading to a fairly normal terminal portion of the QRS.
3. evaluate this ECG pattern
3. evaluate this ECG pattern
First degree AV block is caused by a prolongation or delay in impulse conduction through the AV node. It is defined as a PR interval ;0.20 seconds. In this case the PR interval (blue lines) is approximately 0.22 seconds.
4. evaluate this ECG pattern
4. evaluate this ECG pattern
The normal P wave in sinus rhythm is slightly notched since activation of the right atrium precedes that of the left atrium. The P wave is upright in a positive direction in leads I and II. A P wave with a uniform morphology precedes each QRS complex. The rate is between 60 and 100 beats per minute and the cycle length is uniform between sequential P waves and QRS complexes. In addition, the P wave morphology and PR intervals are identical from beat to beat.
5. evaluate this ECG pattern
5. evaluate this ECG pattern
Normal electrocardiogram showing normal sinus rhythm at a rate of 75 beats/min, a PR interval of 0.14 sec, a QRS interval of 0.10 sec, and a QRS axis of approximately 75°.
6. evaluate this ECG pattern
6. evaluate this ECG pattern
– Single lead electrocardiogram (ECG) showing ventricular fibrillation: There is a complete absence of properly formed QRS complexes and no obvious P waves. A recent onset (eg, within minutes) of the arrhythmia is suggested by the coarse morphology of the fibrillatory waves.
7. evaluate this ECG pattern
7. evaluate this ECG pattern
Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS duration is 0.08 sec. Both the P and T waves are upright.
8. evaluate this ECG pattern
8. evaluate this ECG pattern
Nearly full preexcitation is manifest in normal sinus rhythm on the 12 lead ECG in this patient with a short accessory pathway refractory period. The ventricular complex in preexcitation is a fusion of the impulse that preexcites the ventricles due to rapid conduction through an accessory pathway and of the impulse that takes the usual route through the AV node; this fusion creates the delta wave that is characteristic of Wolff-Parkinson-White ECG pattern.
9. evaluate this ECG pattern
9. evaluate this ECG pattern
At the onset of ventricular fibrillation (VF), the QRS complexes are regular, widened, and of tall amplitude, suggesting a more organized ventricular tachyarrhythmia. Over a brief period of time, the rhythm becomes more disorganized with high amplitude fibrillatory waves; this is coarse VF. After a longer period of time, the fibrillatory waves become fine, culminating in asystole.
10. evaluate this ECG pattern
10. evaluate this ECG pattern
Extremely rapid, erratic ventricular activity due to ventricular fibrillation during cardiac arrest.
11. evaluate this ECG pattern
11. evaluate this ECG pattern
Atrial tachycardia with 2:1 atrioventricular (AV) block. The atrial rate is about 160 beats/min while the ventricular rate is about 80 beats/min. The nonconducted P waves (arrows) are superimposed on the ST-T segments. The P waves have a similar morphology to normal P waves suggesting that the ectopic site is near or even in the sinoatrial node. This arrhythmia may be an important sign of digoxin toxicity, but can also occur in other settings.
12. evaluate this ECG pattern
12. evaluate this ECG pattern
ECG of counterclockwise typical atrial flutter: Sawtooth-like oscillations of baseline between flutter waves, best seen in the inferior leads.
13. evaluate this ECG pattern
13. evaluate this ECG pattern
ECG of clockwise typical atrial flutter: Sawtooth-like oscillations of baseline between flutter waves, best seen in inferior leads.
*Positive flutter waves in II, III, aVF, V6. Negative flutter waves in V1
14. evaluate this ECG pattern
14. evaluate this ECG pattern
Lead V1 showing coarse atrial fibrillation with moderate ventricular response. The two characteristic findings in AF are present: the very rapid atrial fibrillatory waves (f waves) which are variable in appearance; and the irregularly irregular ventricular response as the R-R interval between beats is unpredictable. Coarse atrial fibrillation may appear similar to atrial flutter. However, the variable height and duration of the f waves differentiate them from atrial flutter (F) waves which are identical in appearance and occur at a constant rate of about 250 to 350 beats/min.
15. evaluate this ECG pattern
15. evaluate this ECG pattern
Atrial fibrillation is an irregularly irregular rhythm without regular or organized atrial activity. Atrial activation is rapid (generally greater than 320 beats per minute) and of various amplitudes. No discrete P waves are seen on this tracing. Instead, rapid, irregular, variable and low amplitude oscillating fibrillatory waves are observed between the QRS complexes. When the arrhythmia is of long duration, the fibrillatory waves may be inapparent.
16. evaluate this ECG pattern
16. evaluate this ECG pattern
Electrocardiogram of lead II showing normal sinus rhythm, first degree atrioventricular block with a prolonged PR interval of 0.30 sec, and a QRS complex of normal duration. The tall P waves and P wave duration of approximately 0.12 sec suggest concurrent right atrial enlargement.
17. evaluate this ECG pattern
17. evaluate this ECG pattern
Several characteristic features of Wenckebach second degree AV block are noted on this ECG (P waves are marked by arrows):
1) The PR interval after the second P wave is longer than the preceeding PR interval; the third P wave is not conducted at all.
2) The PP intervals are constant; however, the RR interval surrounding the completely blocked P wave is longer than the preceeding normal RR interval.
3) The fourth P wave (after the blocked beat) is conducted normally; this PR interval is shorter than the PR interval that immediately preceeded the pause.
– Mobitz I second degree AV block (Wenckebach)
18. evaluate this ECG pattern
18. evaluate this ECG pattern
The third and sixth P waves are not conducted through the AV node (there is no associated QRS complex). The PR interval is constant prior to and after the non-conducted beats.
– Mobitz II second degree AV block
19. evaluate this ECG pattern
19. evaluate this ECG pattern
Single lead electrocardiogram (ECG) showing Mobitz type I (Wenckebach) second degree AV block with 5:4 conduction. The characteristics of this arrhythmia include: a progressively increasing PR interval until a P wave is not conducted (arrow); a progressive decrease in the increment in the PR interval; a progressive decrease in the RR interval; and the RR interval that includes the dropped beat (0.96 sec) is less than twice the RR interval between conducted beats (0.53 to 0.57 sec).
20. evaluate this ECG pattern
20. evaluate this ECG pattern
Third degree (complete) atrioventricular block with narrow QRS escape rhythm: The P waves are completely dissociated from the QRS complexes. The QRS complexes are narrow, indicating a junctional escape rhythm. The atrial and ventricular rates are stable; the former is faster than the latter.
21. evaluate this ECG pattern
21. evaluate this ECG pattern
Electrocardiogram (ECG) showing complete heart block in a patient with syncopal episodes who previously had shown mobitz II type AV block: The first two beats are paced. After the pacemaker is turned off, a normally conducted beat followed with a PR interval of 0.19 sec and a LBBB morphology. The next eight P waves fail to conduct and no lower pacemaker appears to assume control of the ventricles. Restarting the artificial pacemaker led to the QRS complex at the end of the rhythm strip.
22. evaluate this ECG pattern
22. evaluate this ECG pattern
A rapid ventricular tachycardia, with rates usually over 240 beats per minute, is characteristic of ventricular flutter, with predominantly monomorphic QRS complexes, and an absence of atrial activity (P waves).
23. evaluate this ECG pattern
23. evaluate this ECG pattern
Single lead electrocardiogram (ECG) showing monomorphic ventricular tachycardia: Three or more successive ventricular beats are defined as ventricular tachycardia (VT). This VT is monomorphic since all of the QRS complexes have an identical appearance. Although the P waves are not distinct, they can be seen altering the QRS complex and ST-T waves in an irregular fashion, indicating the absence of a relationship between the P waves and the QRS complexes, ie, AV dissociation is present.
24. evaluate this ECG pattern
24. evaluate this ECG pattern
Single lead electrocardiogram (ECG) showing polymorphic ventricular tachycardia (VT): The QRS complexes in polymorphic VT have markedly differing morphologies due to changes in the direction (vector) of myocardial activation.
- what is asystole? - how does it look on an ECG tracing?
– what is asystole?
– how does it look on an ECG tracing?
– Asystole/ agonal rhythm is defined as a complete absence of demonstrable electrical and mechanical cardiac activity. By definition, asystole is a non-perfusing rhythm requiring the initiation of excellent CPR immediately when present
- what is pulseless electrical activity? - how does it look on an ECG tracing?
– what is pulseless electrical activity?
– how does it look on an ECG tracing?
– Pulseless electrical activity (PEA) is defined as any one of a heterogeneous group of organized electrocardiographic rhythms without sufficient mechanical contraction of the heart to produce a palpable pulse or measurable blood pressure. By definition, PEA is a non-perfusing rhythm requiring the initiation of excellent CPR immediately when present
– Like the clinical events that can cause PEA, the rhythms associated with this entity are numerous. The dysrhythmias most frequently seen in PEA include idioventricular, junctional, and sinus bradycardias
25. evaluate this ECG tracing
25. evaluate this ECG tracing
asystole/agonal rhythm
26. evaluate this ECG tracing
26. evaluate this ECG tracing
Rhythm strip of sinus rhythm recorded from ECG lead AVR
27. evaluate this ECG tracing
27. evaluate this ECG tracing
– fine ventricular fibrillation (FVF)
– Ventricular fibrillation is identified by the complete absence of properly formed QRS complexes and no obvious P waves. There is no uniform activation of the ventricular myocardium and the QRS complexes have markedly different morphology, axis, and amplitude. The rate is irregular and usually greater than 300 beats per minute. When the fibrillation is recent onset, the amplitude is usually high, but as time passes, the fibrillatory waves become finer and may resemble asystole. Ventricular fibrillation leads promptly to cardiac arrest.
how does second-degree AV block (Mobitz I Wenckebach) appear in lead V1?
how does second-degree AV block (Mobitz I Wenckebach) appear in lead V1?
28. evaluate this ECG tracing
28. evaluate this ECG tracing
Single lead electrocardiogram (ECG) strip showing an atypical Mobitz type I (Wenckebach) AV block with 18:17 ratio. The last three cycles of the group, the skipped beat (with the P wave lost in the T wave; arrow), and the first three cycles of the next group are shown. The last three cycles had a PR interval of 0.36 sec while the first three cycles showed PR intervals of 0.23, 0.32 and 0.34 sec with a decreasing R-R interval. This demonstrates the importance of comparing the PR interval of the last beat before the dropped QRS to the PR interval of the first and second beats of the new cycle. The PR interval is the longest in the beat before the dropped beat, shortest in the first beat of the cycle, and increases in the second beat.
29. evaluate this ECG tracing
29. evaluate this ECG tracing
Electrocardiogram (ECG) showing concurrent Mobitz type I (Wenckebach) atrioventricular (AV) block and inferior myocardial infarction (MI): This rhythm strip shows a Mobitz type I (Wenckebach) atrioventricular block with 4:3 and 3:2 conduction and progressive prolongation of the PR intervals of conducted beats. The marked ST segment elevation suggests acute inferior wall ischemia or infarction that may be responsible for the arrhythmia
30. evaluate this ECG tracing
30. evaluate this ECG tracing
A 12-lead ECG showing narrow complex tachycardia with P waves (arrow) inscribed well after the QRS, taken from a patient who had paroxysmal supraventricular tachycardia supported by an accessory pathway.
what is the pathophysiology of Atrioventricular Nodal Reentry Tachycardia?
what is the pathophysiology of Atrioventricular Nodal Reentry Tachycardia?
– Normally, sinus impulses are discharged into the surrounding atria and directed to the region of the node that resides in the atrial septum. The AV nodal impulses then propagate through the ventricles over the His-Purkinje system. The normal AV node has a single transmission pathway. **In two to three persons per 1,000 population, however, the AV node has both a normal (fast) pathway and a second, slow pathway. ? In such persons, the sinus impulse is ordinarily transmitted over the fast pathway to the ventricle, and slow pathway conduction is preempted. However, if an atrial premature complex (APC) occurs at a critical point in the conduction cycle, the impulse can block in the fast pathway, thus allowing for anterograde (forward) conduction over the slow pathway and retrograde (backward) conduction over the fast pathway. The latter situation may produce a single echo beat (a beat that returns to the chamber of origin) or stabilize into a circus-movement tachycardia.
– SVT is often paroxysmal (PSVT). Clinically, PSVT is marked by palpitations, occurring in episodes that start and end abruptly. During these episodes, the 12-lead ECG shows a heart rate greater than 100 beats/min and, typically, narrow QRS complexes. For almost all patients with PSVT, the underlying mechanism of the tachycardia is atrioventricular node reentry (AVNRT), reentry involving an accessory pathway (AVRT), or atrial tachycardia. AVNRT and AVRT are the most common and the second most common causes of PSVT, respectively. Atrial flutter also presents as a rapid regular tachycardia, but this arrhythmia usually does not begin and end abruptly.
31. evaluate this ECG tracing
31. evaluate this ECG tracing
A 12-lead ECG shows paroxysmal supraventricular tachycardia from AV nodal reentry (AVNRT). The arrows point to a pseudo r1 in lead V1 and S waves in the inferior leads (II, III, and aVF), which disappeared with conversion to sinus rhythm.
32. evaluate this ECG tracing
32. evaluate this ECG tracing
A 12-lead ECG shows tachycardia with P waves (arrows) just preceding the QRS complex. The patient in this case had a focal atrial tachycardia emanating from the lateral tricuspid annulus.
what are the acute management strategies for SVT?
– AVNRT may respond to carotid sinus massage but is highly responsive to intravenous adenosine, beta blockers, or calcium channel blockers
– Adenosine: If carotid massage fails to convert SVT, the drug of choice is intravenous adenosine, which is effective in 95% of cases.
? initial dose is given as a rapid bolus infusion of 6 mg, followed by 12 mg and finally 18 mg if necessary. The bolus must be given rapidly and then followed by a saline flush. If administration is too slow, the adenosine may be metabolized before it reaches the AV node.
? Possible adverse effects include headache, wheezing, and flushing. These effects disappear within 45 to 60 seconds. It is important to note that atrial, ventricular, and junctional premature beats are commonly observed after adenosine. In 3% to 5% of cases, the APCs trigger atrial fibrilla-tion, which may result in serious problems for patients with accessory pathways. If possible, an external defibrillator should be readily available when adenosine is administered.
? The most common reason for failure to respond to adenosine is that multiple premature beats are retriggering the tachycardia. In this setting, a longer-acting intravenous preparation (i.e., 5 mg of metoprolol or 0.1 mg/kg of verapamil) is indicated. Agents that more selectively block purogenic receptors have been shown to be very effective and associated with fewer side effects than older agents.
what is on the DDx for a widened QRS?
what is on the DDx for a widened QRS?
DDx for wide (; 120 ms) QRS complex tachycardia. If the tachycardia is regular and comparison with a baseline electrocardiogram shows that the QRS complex is identical to that during sinus rhythm, the patient may have supraventricular tachycardia (SVT) with bundle branch block (BBB) or antidromic atrioventricular reentrant tachycardia (AVRT). If the patient has a history of myocardial infarction or has structural heart disease, ventricular tachycardia (VT) is likely. Vagal maneuvers or adenosine may convert regular tachycardia, although adenosine should be used with caution when the diagnosis is unclear, because this drug may produce ventricular fibrillation (VF) in patients with coronary artery disease and patients with alternative pathways who have atrial fibrillation with a rapid ventricular rate. Precordial leads are concordant when all show either positive or negative deflections. Fusion complexes are diagnostic of VT. In preexcited tachycardias, the QRS is generally wider (i.e., more preexcited) than during sinus rhythm. (AT—atrial tachycardia; AV—atrioventricular; LBBB—left bundle branch block; RBBB—right bundle branch block)
what are the common causes of pulseless electrical activity?
what are the common causes of pulseless electrical activity?
33. evaluate this ECG tracing
33. evaluate this ECG tracing
Electrocardiogram (ECG) showing sinus tachycardia at a rate of 150 beats/min: Note the difficulty in separating the P waves from the T waves in the standard leads. The P waves are most evident in lead V1 (arrow) where the terminal negativity suggests left atrial enlargement.
34. evaluate this ECG tracing
34. evaluate this ECG tracing
The normal P wave in sinus rhythm is slightly notched since activation of the right atrium precedes that of the left atrium. The P wave is upright in a positive direction in leads I and II. A P wave with a uniform morphology precedes each QRS complex. The rate is between 60 and 100 beats per minute and the cycle length is uniform between sequential P waves and QRS complexes. In addition, the P wave morphology and PR intervals are identical from beat to beat.
35. evaluate this ECG tracing
35. evaluate this ECG tracing
Sinus tachycardia is defined as a sinus rhythm with a rate of greater than 100 beats per minute and less than approximately 160 to 180 beats per minute. In this tracing, the rate is about 130 beats per minute.
36. evaluate this ECG tracing
36. evaluate this ECG tracing
Single lead electrocardiogram (ECG) showing marked sinus bradycardia at a rate of 25 to 30 beats/min. The normal P waves (upright in lead II) and PR interval and consistent with a sinus mechanism with normal atrioventricular (AV) conduction.
37. evaluate this ECG tracing
37. evaluate this ECG tracing
Electrocardiogram showing multifocal atrial tachycardia in a woman with severe pulmonary disease. The diagnostic criteria include an average atrial rate above 100 beats/min and at least three different non-sinus P waves in the same lead. Note the multiple P wave morphologies – inverted (I), upright (U), and biphasic (B).
38. evaluate this ECG tracing
38. evaluate this ECG tracing
Supraventricular tachycardia commonly presents in two forms – AV reentry and AV nodal reentry. In AV reentry, the SVT presents as a regular tachycardia originating outside the ventricular myocardium. In this type of SVT, the AV node is used for impulse conduction to the ventricles, while an accessory pathway is used to return electrical conduction back to the atria. The heart rate is usually regular, at a rate of 170 to 250 bpm (below = 188 bpm). In this type of SVT, P waves are always present outside of the QRS complex, while their polarity depends on the atrial insertion of the accessory pathway. The QRS complex is narrow with a duration less that 0.2 seconds and an atrioventricular conduction ratio of 1:1. In 25% – 30% of patients demonstrating AV reentry, QRS alternans is present (varying amplitudes of the QRS complex in all leads except V4). AV reentry is not usually associated with structural heart disease and commonly presents as a variety of symptoms including palpitations, nervousness, anxiety, syncope or heart failure.
what sorts of conditions are covered by the term supraventricular tachycardia (SVT)?
what sorts of conditions are covered by the term supraventricular tachycardia (SVT)?
– The term supraventricular tachycardia (SVT), whilst often used synonymously with AV nodal re-entry tachycardia (AVNRT), can be used to refer to any tachydysrhythmia arising from above the level of the Bundle of His.
– Different types of SVT arise from or are propagated by the atria or AV node, typically producing a narrow-complex tachycardia (unless aberrant conduction is present).
– Paroxysmal SVT (pSVT) describes an SVT with abrupt onset and offset — characteristically seen with re-entrant tachycardias involving the AV node such as AVNRT or atrioventricular re-entry tachycardia (AVRT).
how are SVTs classified?
– SVTs can be classified based on site of origin (atria or AV node) or regularity (regular or irregular).
– Classification based on QRS width is unhelpful as this is also influenced by the presence of pre-existing bundle branch block, rate-related aberrant conduction or presence of accessory pathways.
– Atrial Regular: Sinus tachycardia; Atrial tachycardia; Atrial flutter; Inappropriate sinus tachycardia; Sinus node re-entrant tachycardia
– Atrial Irregular: Atrial fibrillation; Atrial flutter with variable block; Multifocal atrial tachycardia;
– Atrioventricular Regular: Atrioventricular re-entry tachycardia (AVRT); AV nodal re-entry tachycardia (AVNRT); Automatic junctional tachycardia;
what is AV Nodal Re-entry Tachycardia (AVNRT)?
– commonest cause of palpitations in patients with structurally normal hearts.
– AVNRT is typically paroxysmal and may occur spontaneously or upon provocation with exertion, caffeine, alcohol, beta-agonists (salbutamol) or sympathomimetics (amphetamines).
– It is more common in women than men (~ 75% of cases occurring in women) and may occur in young and healthy patients as well as those suffering chronic heart disease.
– Patients will typically complain of the sudden onset of rapid, regular palpitations. The patient may experience a brief fall in blood pressure causing presyncope or occasionally syncope.
– If the patient has underlying coronary artery disease the patient may experience chest pain similar to angina (tight band around the chest radiating to left arm or left jaw).
– The patient may complain of shortness of breath, anxiety and occasionally polyuria due to elevated atrial pressure releasing atrial natriuretic peptide.
– The tachycardia typically ranges between 140-280 bpm and is regular in nature. It may cease spontaneously (and abruptly) or continue indefinitely until medical treatment is sought.
– The condition is generally well tolerated and is rarely life threatening in patients with pre-existing heart disease.
what is the pathophysiology of AVNRT?
what is the pathophysiology of AVNRT?
– In comparison to AVRT, which involves an anatomical re-entry circuit (Bundle of Kent), in AVNRT there is a functional re-entry circuit within the AV node.
– Different types of re-entry loops: Functional circuit in AVNRT (left), anatomical circuit in AVRT (right)
- what are the Functional pathways within the AV node? - how is re-entry initiated?
– what are the Functional pathways within the AV node?
– how is re-entry initiated?
– In AVNRT, there are two pathways within the AV node:
? The slow pathway (alpha): a slowly-conducting pathway with a short refractory period.
? The fast pathway (beta): a rapidly-conducting pathway with a long refractory period.
– Initiation of re-entry: During sinus rhythm, electrical impulses travel down both pathways simultaneously. The impulse transmitted down the fast pathway enters the distal end of the slow pathway and the two impulses cancel each other out.
? However, if a premature atrial contraction (PAC) arrives while the fast pathway is still refractory, the electrical impulse will be directed solely down the slow pathway (1).
? By the time the premature impulse reaches the end of the slow pathway, the fast pathway is no longer refractory (2) — hence the impulse is permitted to recycle retrogradely up the fast pathway.
? This creates a circus movement whereby the impulse continually cycles around the two pathways, activating the Bundle of His anterogradely and the atria retrogradely (3). The short cycle length is responsible for the rapid heart rate.
? This is the most common type of re-entrant circuit and is termed Slow-Fast AVNRT.
? Similar mechanisms exist for the other types of AVNRT.
– Image: Mechanism of re-entry in “slow-fast” AVNRT (ERP = effective refractory period)
Electrocardiographic Features of AVNRT
Electrocardiographic Features of AVNRT
– Regular tachycardia ~140-280 bpm.
– QRS complexes usually narrow (; 120 ms) unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction.
– ST-segment depression may be seen with or without underlying coronary artery disease.
– QRS alternans – phasic variation in QRS amplitude associated with AVNRT and AVRT, distinguished from electrical alternans by a normal QRS amplitude.
– P waves if visible exhibit retrograde conduction with P-wave inversion in leads II, III, aVF.
– P waves may be buried in the QRS complex, visible after the QRS complex, or very rarely visible before the QRS complex
– Image: Cardiac rhythm strips demonstrating (top) sinus rhythm and (bottom) paroxysmal SVT. The P wave is seen as a pseudo-R wave (circled in bottom strip) in lead V1 during tachycardia. By contrast, the pseudo-R wave is not seen during sinus rhythm (it is absent from circled area in top strip). This very short ventriculo-atrial time is frequently seen in typical Slow-Fast AVNRT.
Management of AVNRT?
– May respond to vagal maneuvers with reversion to sinus rhythm.
– The mainstay of treatment is adenosine.
– Other agents which may be used include calcium-channel blockers, beta-blockers and amiodarone.
– DC cardioversion is rarely required.
– Catheter ablation may be considered in recurrent episodes not amenable to medical treatment.
39. evaluate this ECG tracing
39. evaluate this ECG tracing
Slow-Fast (Typical) AVNRT:
Narrow complex tachycardia at ~ 150 bpm.
No visible P waves.
There are pseudo R’ waves in V1-2.
40. evaluate this ECG tracing
40. evaluate this ECG tracing
Slow-Fast (Typical) AVNRT: Pseudo R’ waves in V1-2
41. evaluate this ECG tracing
41. evaluate this ECG tracing
– Slow-Fast AVNRT:
– Narrow complex tachycardia ~ 220 bpm.
– No visible P waves.
– Subtle notching of the terminal QRS in V1 (= pseudo R’ wave).
– Widespread ST depression — this is a common ECG finding in AVNRT and does not necessarily indicate myocardial ischaemia, provided the changes resolve once the patient is in sinus rhythm.
42. evaluate this ECG tracing
42. evaluate this ECG tracing
– Fast-Slow (Uncommon) AVNRT:
– Narrow complex tachycardia ~ 120 bpm.
– Retrograde P waves are visible after each QRS complex — most evident in V2-3.
43. evaluate this ECG tracing
43. evaluate this ECG tracing
– Fast-Slow (Uncommon) AVNRT: Retrograde P waves
Adult cardiac arrest algorithm: 2010 ACLS guidelines
Adult cardiac arrest algorithm: 2010 ACLS guidelines
CPR: cardiopulmonary resuscitation; ET: endotracheal tube; EtCO2: end tidal carbon dioxide; IO: intraosseous; IV: intravenous; PEA: pulseless electrical activity; VF: ventricular fibrillation; VT: ventricular tachycardia.
Adult bradycardia algorithm (with pulse): 2010 ACLS guidelines
Adult bradycardia algorithm (with pulse): 2010 ACLS guidelines
Adult tachycardia algorithm (with pulse): 2010 ACLS guidelines
Adult tachycardia algorithm (with pulse): 2010 ACLS guidelines
CHF: congestive heart failure; ECG: electrocardiogram; IV: intravenous; J: joules; NS: normal (isotonic) saline; VT: ventricular tachycardia
ACLS cardiac arrest circular figure
ACLS cardiac arrest circular figure
Treatable conditions associated with cardiac arrest
– Condition ? Common associated clinical settings
– Acidosis ? Diabetes, diarrhea, drug overdose, renal dysfunction, sepsis, shock
– Anemia ? Gastrointestinal bleeding, nutritional deficiencies, recent trauma
– Cardiac tamponade ? Post-cardiac surgery, malignancy, post-myocardial infarction, pericarditis, trauma
– Hyperkalemia ? Drug overdose, renal dysfunction, hemolysis, excessive potassium intake, rhabdomyolysis, major soft tissue injury, tumor lysis syndrome
– Hypokalemia* ? Alcohol abuse, diabetes mellitus, diuretics, drug overdose, profound gastrointestinal losses
– Hypothermia ? Alcohol intoxication, significant burns, drowning, drug overdose, elder patient, endocrine disease, environmental exposure, spinal cord disease, trauma
– Hypovolemia ? Significant burns, diabetes, gastrointestinal losses, hemorrhage, malignancy, sepsis, trauma
– Hypoxia ? Upper airway obstruction, hypoventilation (CNS dysfunction, neuromuscular disease), pulmonary disease
– Myocardial infarction ? Cardiac arrest
– Poisoning ? History of alcohol or drug abuse, altered mental status, classic toxidrome (eg, sympathomimetic), occupational exposure, psychiatric disease
– Pulmonary embolism ? Immobilized patient, recent surgical procedure (eg, orthopedic), peripartum, risk factors for thromboembolic disease, recent trauma, presentation consistent with acute pulmonary embolism
– Tension pneumothorax ? Central venous catheter, mechanical ventilation, pulmonary disease (eg, asthma, chronic obstructive pulmonary disease), thoracentesis, thoracic trauma
* Hypomagnesemia should be assumed in the setting of hypokalemia, and both should be treated.
A patient is in cardiac arrest. Ventricular fibrillation has been refractory to a second shock. Of the following, which drug and dose should be administered first by the IV/IO route?
A. vasopressin 20 units
B. sodium bicarbonate 50 mEq
C. epinephrine 1 mg
D. atropine 1 mg
C. epinephrine 1 mg
A patient is in cardiac arrest. High-quality chest compressions are begin given. The patient is intubated, and an IV has been started. The rhythm is asystole. Which is the first drug/dose to administer?
A. atropine 0.5 mg IV or IO
B. dopamine 2-20 mcg/kg per minute IV or IO
C. atropine 1 mg IV or IO
D. epinephrine 3 mg via endotracheal route
E. epinephrine 1 mg or vasopressin 40 units IV or IO
E. epinephrine 1 mg or vasopressin 40 units IV or IO
A patient is in refractory ventricular fibrillation and has received multiple appropriate defibrillation shocks, epinephrine 1 mg IV twic, and an itial dose of 300 mg amiodarone IV. The patient is intubated. A second dose of amiodarone is now called for. The recommended second dose of amiodarone is
A. 150 mg IV push
B. an endotracheal dose of 2-4 mg/kg
C. 1 mg/kg IV push
D. 300 mg IV push
E. an infusion of 1-2 mg/min
A. 150 mg IV push
A patient is in refractory ventricular fibrillation. High-quality CPR is in progress, and shocks have been given. One dose of epinephrine was given after the second shock. An antiarrhythmic drug was given immediately after the third shock. What drug should the team leader request to be prepared for administration next?
A. escalating dose of epinephrine 3 mg
B. second dose of epinephrine 1 mg
C. sodium bicarbonate 50 mEq
D. repeat the antiarrhythmic drug
B. second dose of epinephrine 1 mg
A patient with possible ST-segment elevation MI has ongoing chest discomfort. Which of the following would be a contraindication to the administration of nitrates?
A. left ventricular infarct w/ bilateral rales
B. use of a phosphodiesterase inhibitor w/i 12 hrs
C. HR 90/min
D. BP > 180 mm Hg
B. use of a phosphodiesterase inhibitor
A patient w/ sinus bradycardia and a HR of 42/min has diaphoresis and a BP of 80/60 mmHG. What is the inital dose of atropine?
A. 0.1 mg
B. 0.5 mg
C. 3.0 mg
D. 1.0 mg
B. 0.5 mg
Your patient has been intubated. IV/IO access is not available. Which combination of drugs can be administered by the endotracheal route?
A. vasopressin, amiodarone, lidocaine
B. lidocaine, epinephrine, vasopressin
C. amiodarone, lidocaine, epinephrine
D. epinephrine, vasopressin, amiodarone
B. lidocaine, epinephrine, vasopressin
A patient is in pulseless ventricular tachycardia. Two shocks and 1 dose of epinephrine have been given. Which is the next drug/dose to anticipate to administer?
A. vasopressin 40 units
B. lidocaine 0.5 mg/kg
C. epinehrine 3 mg
D. amiodarone 300 mg
E. amiodarone 150 mg
D. amiodarone 300 mg
Which of the following statements about the use of magnesium in cardiac arrest is most accurate?
A. magnesium is indicated for VF refractory to shock and amiodarone or lidocaine
B. magnesium is contraindicated for VT associated w/ normal QT interval
C. magnesium is indicated for shock-refractory monomorphic VT
D. magnesium is indicated for VF/pulseless VT associated w/ torsades de pointes
D. magnesium is indicated for VF/pulseless VT associated w/ torsades de pointes
Preferred thrombolytic regimens for acute ST elevation myocardial infarction
Preferred thrombolytic regimens for acute ST elevation myocardial infarction
Absolute and relative contraindications to the use of thrombolytic therapy in patients with acute ST elevation myocardial infarction
Absolute and relative contraindications to the use of thrombolytic therapy in patients with acute ST elevation myocardial infarction
Cooperative cardiovascular project risk model for intracranial hemorrhage with thrombolytic therapy
Cooperative cardiovascular project risk model for intracranial hemorrhage with thrombolytic therapy
A patient w/ ST-segment elevation MI has ongoing chest discomfort. Fibrinolytic therapy has been ordered. Heparin 4000 units IV bolus was administered, and heparin infusion of 1000 units per hour is being administered. Aspirin was not taken by the patient because he had a history of gastritis treated 5 years ago. Your next action is to
A. give 325 mg enteric-coated aspirin rectally
B. give 75 mg enteric-coated aspirin orally
C. give aspirin 160-325 mg chewed immediately
D. substitute clopidogrel 300 mg loading dose
C. give aspirin 160-325 mg chewed immediately
A patient has sinus bradycardia w/ a HR of 36/min. Atropine has been administered to a total dose of 3 mg. A transcutaneous pacemaker has failed to capture. The patient is confused, and her BP is 100/60 mmHg. Which of the following is now indicated?
A. start epinephrine 2-10 mcg/min
B. give normal saline bolus 250-500 mL
C. start dopamine 10-20 mcg/kg per minute
D. give additional 1 mg atropine
A. start epinephrine 2-10 mcg/min
A patient has a rapid irregular wide-complex tachycardia. The ventricular rate is 138/min. He is asymptomatic, with a BP of 110/70 mm Hg. He has a history of angina. Which of the following actions is recommended?
A. seeking expert consultation
B. give lidocaine 1-1.5 mg IV bolus
C. giving adenosine 6 mg IV bolus
D. immediate synchronized cardioversion
A. seeking expert consultation
– no adenosine b/c not regular
A 57-year-old woman has palpitations, chest discomfort, and tachycardia. The monitor shows a regular wide-complex QRS at a rate of 180/min. She becomes diaphoretic, and her blood pressure is 80/60 mm Hg. The next action is to
A. obtain a 12-lead ECG
B. perform immediate electrical cardioversion
C. give amiodarone 300 mg IV push
D. establish IV access
B. perform immediate electrical cardioversion
A 35-year-old woman has palpitations, light-headedness, and a stable tachycardia. The monitor shows a regular narrow-complex QRS at a rate of 180/min. Vagal maneuvers have not been effective in terminating the rhythm. An IV has been established. What drug should be administered IV?
A. epinephrine 2-10 mcg/kg per minute
B. lidocaine 1 mg/kg
C. adenosine 6 mg
D. atropine 0.5 mg
C. adenosine 6 mg
A 62-year-old man suddenly experienced difficulty speaking and left-sided weakness. He was brought to the emergency department. He meets initial criteria for fibrinolytic therapy, and a CT scan of the brain is ordered. What are the guidelines for antiplatelet and fibrinolytic therapy?
A. administer heparin if CT scan is negative for hemorrhage
B. administer aspirin 160-325 mg chewed immediately
C. give aspirin 160 mg and clopidogrel 75 mg orally
D. do not give aspirin for at least 24 hours if rtPA is administered
D. do not give aspirin for at least 24 hours if rtPA is administered
Which of the following statements is most accurate regarding the administration of vasopressin during cardiac arrest?
A. vasopressin is recommended instead of epinephrine for treatment of asystole
B. vasopressin can be administered twice during cardiac arrest
C. vasopressin is indicated for VF and pulseless VT before delivery of the first shock
D. correct dose of vasopressin is 40 units administered IV or IO
D. correct dose of vasopressin is 40 units administered IV or IO
Bradycardia requires treatment when
A. the patient’s 12-lead ECG shows an MI
B. chest pain or shortness of breath is present
C. the BP ; 100 mmH systolic w/ or w/o symptoms
D. HR ; 60/min w/ or w/o symptoms
B. chest pain or shortness of breath is present
You arrive on the scene with the code team. High-quality CPR is in progress. An AED has previously advised “no shock indicated.” A rhythm check now finds asystole. After resuming high-quality compressions, your next action is to
A. gain IV or IO access
B. place an esophageal-tracheal tube or laryngeal mask airway
C. call for a pulse check
D. attempt endotracheal intubation with minimal interruptions in CPR
A. gain IV or IO access
A patient with a possible acute coronary syndrome has ongoing chest discomfort unresponsive to 3 sublinguqal nitroglycerin tablets. There are no contraindications, and 4 mg of morphine sulfate are administered. Shortly afterward, BP falls to 88/60 mmHg, and the patient has increased chest discomfort. You should
A. give an additional 2 mg of morphine sulfate
B. give normal saline 250-500 mL fluid bolus
C. give sublingual nitroglycerin 0.4 mg
D. start dopamine at 2 mcg/kg per minute and titrate to a systolic BP of 100 mm Hg
B. give normal saline 250-500 mL fluid bolus
A patient is in cardiac arrest. Ventricular fibrillation has been refractory to an initial shock. What is the recommended route for drug administration during CPR?
A. central line
B. external jugular vein
C. femoral vein
D. IV or IO
E. endotracheal
D. IV or IO
44. evaluate this ECG rhythm strip
44. evaluate this ECG rhythm strip
In this ECG rhythm strip, arrows point to atrial flutter waves @ 280bpm with ventricular rate @ 140bpm (atrial flutter with 2:1 block)
45. evaluate this ECG pattern
45. evaluate this ECG pattern
Selected leads with multifocal tachycardia. The multifocal ectopic P waves are best seen in leads II and V1. In other leads the rhythm looks like atrial fibrillation.
46. evaluate this ECG pattern
46. evaluate this ECG pattern
asystole
47. evaluate this ECG pattern
47. evaluate this ECG pattern
PEA encompasses a heterogeneous group of pulseless rhythms that includes pseudo-electromechanical dissociation (pseudo-EMD), idioventricular rhythms, ventricular escape rhythms, postdefibrillation idioventricular rhythms, and bradyasystolic rhythms. Research with cardiac ultrasonography and indwelling pressure catheters has confirmed that pulseless patients with electrical activity have associated mechanical contractions, but these contractions are too weak to produce a blood pressure detectable by palpation or noninvasive blood pressure monitoring. PEA is often caused by reversible conditions and can be treated if those conditions are identified and corrected. The possible causes of PEA are presented as the 6 H’s and the 6 T’s. These 6 H’s are hypovolaemia, hypoxia, hydrogen ion-acidosis, hyper-/hypokalaemia, hypothermia, hypoglycaemia and 6 T’s are tablets (drug overdose), tamponade (cardiac tamponade), tension pneumothorax, thrombosis (coronary), thrombosis (pulmonary) and trauma. Information from the ECG, the history, and the physical examination can be used to identify possible diagnoses. If rescuer can identify the specific condition and treat appropriately, cardiac arrest can be reversed
48. evaluate this ECG pattern
48. evaluate this ECG pattern
(coarse) Ventricular Fibrillation: The most critical interventions during the first minutes of VF are immediate bystander CPR with minimal interruption in chest compressions and defibrillation as soon as it can be accomplished.
49. evaluate this ECG pattern
49. evaluate this ECG pattern
Pulseless Ventricular Tachycardia: The most critical interventions during the first minutes of pulseless VT are immediate bystander CPR with minimal interruption in chest compressions and defibrillation as soon as it can be accomplished.
what are three irregularly irregular ECG patterns?
what are three irregularly irregular ECG patterns?
– Atrial fibrillation occurs when action potentials fire very rapidly within the pulmonary veins or atrium in a chaotic manner. The result is a VERY fast atrial rate (about 400-600 beats per minute). Since the atrial rate is so fast and the action potentials produced are of such low amplitude, P waves will NOT be seen on the ECG in patients with atrial fibrillation. At times, the P wave activity can be seen as “coarse fibrillatory waves” and the term “coarse atrial fibrillation” is used, although there is no clinical significance to this finding.
The atrial action potentials all attempt to conduct through the AV node, however the AV node becomes intermittently refractory and will only allow a certain number of atrial action potentials to reach the ventricles. This is why the ventricular rate is NOT also 400-600, but rather around 100-200 beats per minute. The degree to which action potentials can cross the AV node to the ventricles is variable and reduced by AV blocking medications.
Since the AV node is intermittently (not regularly) refractory, the QRS complexes that are produced when an atrial action potential does reach the ventricles will occur in an “irregularly irregular” manner as there is no pattern to their frequency. This is commonly described as varying RR intervals.
– The only two other rhythms that are irregularly irregular are atrial flutter with variable conduction and multifocal atrial tachycardia. Atrial flutter has the typicl “Sawtooth pattern” while multifocal atrial tachycardia (MAT) requires three distinct P wave morphologies in one 12-lead ECG tracing.
50. evaluate this ECG pattern
50. evaluate this ECG pattern
– atrial tachycardia
what are the signs, symptoms and ECG patterns for paroxysmal supraventricular tachycardias?
what are the signs, symptoms and ECG patterns for paroxysmal supraventricular tachycardias?
51. evaluate the ECG pattern
51. evaluate the ECG pattern
52. evaluate this ECG pattern
52. evaluate this ECG pattern
Single lead electrocardiogram (ECG) showing torsades de pointes: This is an atypical, rapid, and bizarre form of ventricular tachycardia that is characterized by a continuously changing axis of polymorphic QRS morphologies.
53. evaluate this ECG pattern
53. evaluate this ECG pattern
third-degree AV block
54. evaluate this ECG pattern
54. evaluate this ECG pattern
third degree AV block / complete heart block
55. evaluate this ECG pattern
55. evaluate this ECG pattern
atrial fibrillation
56. evaluate this ECG pattern
56. evaluate this ECG pattern
(coarse) Ventricular Fibrillation: The most critical interventions during the first minutes of VF are immediate bystander CPR with minimal interruption in chest compressions and defibrillation as soon as it can be accomplished.
57. evaluate this ECG pattern
57. evaluate this ECG pattern
polymorphic v. tach
58. evaluate this ECG pattern
58. evaluate this ECG pattern
Electrocardiogram of lead II showing normal sinus rhythm, first degree atrioventricular block with a prolonged PR interval of 0.30 sec, and a QRS complex of normal duration. The tall P waves and P wave duration of approximately 0.12 sec suggest concurrent right atrial enlargement.
59. evalute this ECG pattern
59. evalute this ECG pattern
Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS duration is 0.08 sec. Both the P and T waves are upright.
60. evaluate this ECG pattern
60. evaluate this ECG pattern
Single lead electrocardiogram (ECG) showing Mobitz type I (Wenckebach) second degree AV block with 5:4 conduction. The characteristics of this arrhythmia include: a progressively increasing PR interval until a P wave is not conducted (arrow); a progressive decrease in the increment in the PR interval; a progressive decrease in the RR interval; and the RR interval that includes the dropped beat (0.96 sec) is less than twice the RR interval between conducted beats (0.53 to 0.57 sec).
61. evaluate this ECG pattern
61. evaluate this ECG pattern
The lead II rhythm strip shows four sinus beats with P wave followed by a QRS complex; the fifth P wave is not followed by a QRS complex and represents second degree heart block. There is no change in the PR interval prior to or after the blocked P wave and thus this is Mobitz II second degree heart block. A second episode of second degree heart block can be seen after the seventh QRS complex.
62. evaluate this ECG pattern
62. evaluate this ECG pattern
Third degree (complete) atrioventricular block with narrow QRS escape rhythm: The P waves are completely dissociated from the QRS complexes. The QRS complexes are narrow, indicating a junctional escape rhythm. The atrial and ventricular rates are stable; the former is faster than the latter.
63. evaluate this ECG pattern
63. evaluate this ECG pattern
AV reentrant tachycardia breaking to sinus rhythm with Wolff-Parkinson-White syndrome.
64. Evaluate this ECG pattern
64. Evaluate this ECG pattern
Single lead electrocardiogram (ECG) showing monomorphic ventricular tachycardia: Three or more successive ventricular beats are defined as ventricular tachycardia (VT). This VT is monomorphic since all of the QRS complexes have an identical appearance. Although the P waves are not distinct, they can be seen altering the QRS complex and ST-T waves in an irregular fashion, indicating the absence of a relationship between the P waves and the QRS complexes, ie, AV dissociation is present.
65. evaluate this ECG pattern
65. evaluate this ECG pattern
– At the onset of ventricular fibrillation (VF), the QRS complexes are regular, widened, and of tall amplitude, suggesting a more organized ventricular tachyarrhythmia.
–> Over a brief period of time, the rhythm becomes more disorganized with high amplitude fibrillatory waves; this is coarse VF.
–> After a longer period of time, the fibrillatory waves become fine VF
–> culminating in asystole.
66. evaluate this ECG pattern
66. evaluate this ECG pattern
Single lead electrocardiogram (ECG) showing torsades de pointes: This is an atypical, rapid, and bizarre form of ventricular tachycardia that is characterized by a continuously changing axis of polymorphic QRS morphologies.
67. evaluate this ECG pattern
67. evaluate this ECG pattern
PEA –> asystole
68. evaluate this ECG pattern
68. evaluate this ECG pattern
There is a regular, wide complex tachycardia at rate of 170 bpm, with QRS duration of 124 ms. There are no p-waves, no AV dissociation, no concordance (QRS in precordial leads are not all in the same direction). There is inferior axis (all positive in II, III, aVF, and all negative in lead aVR. There is an initial wide septal r-wave in V1 and V2 (greater than 40 ms). There is a left bundle branch block morphology, except that the initial r-wave is wider than 40 ms.
69. evaluate this ECG pattern
69. evaluate this ECG pattern
Wide Complex Tachycardia Rhythm Strip
70. evaluate this ECG pattern
70. evaluate this ECG pattern
Wide Complex Tachycardia Rhythm Strip
71. evaluate this ECG pattern
71. evaluate this ECG pattern
Electrocardiogram during conversion of supraventricular tachycardia to sinus rhythm with administration of adenosine. During tachycardia at a rate of 230 beats/min, there is a normal-appearing QRS complex without a delta wave (no ventricular preexcitation), and there is no distinct P wave. After conversion to sinus rhythm, there is a short PR interval (80 milliseconds) and wide up-sloping QRS complex (90 milliseconds) representing ventricular preexcitation, indicative of the Wolff-Parkinson-White syndrome.
72. evaluate the ECG patterns
72. evaluate the ECG patterns
ECG recordings from people with SANDD syndrome and normal controls.
(a-d) ECG recordings from an unaffected person (a) and three individuals who are homozygous for the CACNA1D mutation (b-d). In b and c, asterisks mark P waves that precede QRS complexes; arrows indicate waveforms that suggest P waves c…
d: vasovagal bradycardia???
73. evaluate this ECG pattern
73. evaluate this ECG pattern
Torsades de Pointes ( a unique subtype of polymorphic VT) QT interval is abnormally long. Leads to increase in relative refractory period of cardiac cycle.
1.
– What does the X axis refer to?
– What does the Y axis refer to?
– X axis: time
– Y axis: mm; voltage mV
2.
Each small X axis box represents _____ seconds
Each large X axis box represents _____ seconds
Each small Y axis box represents _______ mm
Each large Y axis box represents _____ mm
– Each small X axis box represents 0.04 seconds
– Each large X axis box represents 0.2 seconds
– Each small Y axis box represents 1 mm; 0.1 mV
– Each large Y axis box represents 5 mm; 0.5 mV
3. Identify normal interval lengths for the:
– P wave
– QRS complex
– PR intervals
– QT interval
– QTc interval
– P wave: 0.1 sec
– QRS complex: 0.1 sec; ;0.12
– PR intervals: 0.12-0.2 sec
– QT interval: ;1/2 RR interval; ~0.2 sec
– QTc interval: QT/?RR = 0.38-0.42 sec
4. Know how to do a ballpark calculation of rate
4. Know how to do a ballpark calculation of rate
300 – 150 – 100 – 75 – 60 – 50 – 43
– “300 rule”: HR = 300/number of big boxes between RR
5. - Be able to determine approximate axis (normal, LAD, RAD) - Where does the normal axis lie? (-30 to 90 degrees)
5.
– Be able to determine approximate axis (normal, LAD, RAD)
– Where does the normal axis lie? (-30 to 90 degrees)

6. Know what each part of the EKG wave means:
– P wave
– QRS wave
– T wave
– P wave: atrial depol
– QRS wave: ventricular depol
– T wave: vent. repol
7. Be able to place the chest leads of an EKG on a patient
7. Be able to place the chest leads of an EKG on a patient
8. Know the direction of travel of the vector in each of the leads:
Lead I
Lead II
Lead III
AvL
AvR
AvF
– Lead I: 0
– Lead II: +60
– Lead III: +120
– aVL: -30
– aVR: -210
– aVF: -90
9. Know anatomic location of injury based on EKG changes in STEMI and its associated coronary artery:
Septal
Anterior
Inferior
Lateral
– Septal: V1, V2
– Anterior: V3, V4
– Inferior: II, aVF, III
– Lateral: I, aVL, V5, V6
10. Identify the progression of EKG changes in MI and what they mean:
– Ischemia:
– Injury:
– Infarct/ Necrosis:
– Ischemia – flipped Ts – reversible
– Injury – ST Elevation
– Infarct/ Necrosis – q waves/ tissue death – irreversible
11. Pattern recognition – spend some time on the internet looking at examples of each of these
A. Distinguish between LBBB and RBBB (rabbit ears or turn signal method)
– LBBB:
– RBBB:
LBBB
LBBB
Electrocardiogram in typical complete LBBB. The asynchronous activation of the two ventricles increases the QRS duration (0.16 second in this example). The abnormal initial vector results in loss of “normal” septal forces as manifested by absence of q waves in leads I, aVL, and V6. The late activation of the left ventricle prolongs the dominant leftward progression of the middle and terminal forces, leading to a positive and widened R wave in the lateral leads. Both the ST segment and T wave vectors are opposite in direction from the QRS, a “secondary” repolarization abnormality.
RBBB:
RBBB:
Electrocardiogram showing characteristic changes in the precordial leads in common RBBB. The asynchronous activation of the two ventricles increases the QRS duration (0.13 sec). The terminal forces are rightward and anterior due the delayed activation of the right ventricle, resulting in an rsR’ pattern in the anterior-posterior lead V1 and a wide negative S wave in the left-right lead V6 (and, not shown, in lead I).
11. Pattern recognition – spend some time on the internet looking at examples of each of these
B. Frequently encountered rhythms
– Normal Sinus Rhythm – one P for every QRS
– normal sinus rhythm:
11. Pattern recognition – spend some time on the internet looking at examples of each of these
B. Frequently encountered rhythms
– Sinus bradycardia –
– sinus bradycardia: rate is < 60
11. Pattern recognition – spend some time on the internet looking at examples of each of these
B. Frequently encountered rhythms
– Sinus tachycardia
– sinus tachycardia: rate is > 100
11. Pattern recognition - spend some time on the internet looking at examples of each of these B. Frequently encountered rhythms - A fib -
11. Pattern recognition – spend some time on the internet looking at examples of each of these
B. Frequently encountered rhythms
– A fib –
– Afib: irregularly irregular; no clear P waveforms
11. Pattern recognition - spend some time on the internet looking at examples of each of these B. Frequently encountered rhythms - A flutter -
11. Pattern recognition – spend some time on the internet looking at examples of each of these
B. Frequently encountered rhythms
– A flutter –
– A flutter: sawtooth pattern
11. Pattern recognition - spend some time on the internet looking at examples of each of these B. Frequently encountered rhythms - 1st degree AV block -
11. Pattern recognition – spend some time on the internet looking at examples of each of these
B. Frequently encountered rhythms
– 1st degree AV block –
– 1st degree AV block: prolonged PR interval > 0.2 sec
11. Pattern recognition - spend some time on the internet looking at examples of each of these B. Frequently encountered rhythms - 2nd degree AV block , Type I (Wenkebach) -
11. Pattern recognition – spend some time on the internet looking at examples of each of these
B. Frequently encountered rhythms
– 2nd degree AV block , Type I (Wenkebach) –
– 2nd degree AV block Mobitz Type I (Wenkebach): PR interval progressively lengthens until a QRS is dropped
11. Pattern recognition - spend some time on the internet looking at examples of each of these B. Frequently encountered rhythms - 2nd degree AV Block, Type 2 -
11. Pattern recognition – spend some time on the internet looking at examples of each of these
B. Frequently encountered rhythms
– 2nd degree AV Block, Type 2 –
– 2nd degree AV block Mobitz Type II: PR intervals don’t change, but a QRS drops intermittently
11. Pattern recognition - spend some time on the internet looking at examples of each of these B. Frequently encountered rhythms - 3rd Degree AV Block -
11. Pattern recognition – spend some time on the internet looking at examples of each of these
B. Frequently encountered rhythms
– 3rd Degree AV Block –
– 3rd degree AV block: complete AV dissociation – needs a pacer
11. Pattern recognition - spend some time on the internet looking at examples of each of these B. Frequently encountered rhythms - VTach -
11. Pattern recognition – spend some time on the internet looking at examples of each of these
B. Frequently encountered rhythms
– VTach –
– V tach: wide, regular QRS, rate usually ; 180
11. Pattern recognition - spend some time on the internet looking at examples of each of these B. Frequently encountered rhythms
11. Pattern recognition – spend some time on the internet looking at examples of each of these
B. Frequently encountered rhythms
– V fib:- VFib – chaotic waveforms
what 3 characteristics are used to describe waveforms?
– duration
– amplitude
– morphology
waveform duration:
– what might an unusually long/wide P wave indicate?
– L. atrial enlargement
waveform duration:
– what might an unusually long/wide QRS complex indicate?
– conduction block in either R. or L. BB
waveform amplitude:
– what might an unusually tall P wave indicate?
– R. atrial enlargement
waveform amplitude:
– what might an unusually tall QRS complex indicate?
– ventricular hypertrophy
waveform morphology:
– what might an inverted P wave indicate?
– origin of heart rhythm other than sinus node
waveform morphology:
– what might an inverted or biphasic T wave indicate?
– ischemia
– what are segments?
– what 1 characteristic is used to describe segments?
– segments connect waveforms
– characteristics used to describe segments include: morphology
segment morphology:
– what might depression of the PR segment (relative to the TP segment) indicate?
– pericarditis
segment morphology:
– what 4 things might depression or elevation of the ST segment (relative to the TP segment) indicate?
– ischemia
– myocardial infarction
– conduction blocks
– ventricular hypertrophy
– what are intervals?
– what 1 characteristic is used to describe intervals?
– intervals include waveforms +/- segments
– duration is used to describe intervals
- what are the normal ranges of each of the ECG intervals? PR, QRS, QT - what do abnormalities of each indicate?
– what are the normal ranges of each of the ECG intervals? PR, QRS, QT
– what do abnormalities of each indicate?
– PR interval normal duration: 0.12-0.2 sec
– PR ;0.12 sec: abnormal connection btw atria ; ventricles – PR ;0.2 sec: delayed conduction through AV node
– QRS interval normal duration: ?0.12 sec
– QRS ;0.12 sec: abnormal seq of vent. depol; or excessive vent. mass
– QT interval normal duration: ?½RR interval
– QT ;½RR interval: delayed ventricular repolarization
what is an EKG lead?
– a view of the voltage between two points (known as poles) as a fxn of time
– positive pole for each lead is marked by a single recording electrode on the body
– negative pole for each lead is marked by either a single recording electrode or a virtual electrode known as a “central terminal” which averages input from multiple other electrodes
– a lead ? electrode
– electrodes are electrically conductive sticker attached to chest or limbs
what are the locations of the 10 conventional EKG electrodes?
what are the locations of the 10 conventional EKG electrodes?
what are arrangements of the 6 limb leads?
what are arrangements of the 6 limb leads?
– standard or bipolar limb leads: I, II, III
– augmented or unipolar limb leads: aVR, aVL, aVF
what are the 6 electrode placements and 6 precordial lead views?
what are the 6 electrode placements and 6 precordial lead views?
– 6 precordial leads examine the heart’s electrical activity in the transverse/ axial plane
– the positive pole for each is at a location on the anterior or L. lat. chest wall
– the negative pole for each is the central terminal
– V1: 4th ICS, just R. of sternum
– V2: 4th ICS, just L. of sternum
– V3: between V2?V4
– V4: 5th ICS, midclavicular line
– V5: between V4?V6
– V6: 5th ICS, mid axillary line
what are the 6 electrode placements for the 6 precordial lead views?
what are the 6 electrode placements for the 6 precordial lead views?
– V1: 4th ICS, just R. of sternum
– V2: 4th ICS, just L. of sternum
– V3: between V2?V4
– V4: 5th ICS, midclavicular line
– V5: between V4?V6
– V6: 5th ICS, mid axillary line
- what are the 12 conventional EKG leads? - what are the angles from which each lead views the heart's electrical activity?
– what are the 12 conventional EKG leads?
– what are the angles from which each lead views the heart’s electrical activity?
– standard or bipolar limb leads: I, II, III
– augmented or unipolar limb leads: aVR, aVL, aVF
– precordial leads: V1-V6
– inferior leads: II, III, aVF
– septal leads: V1-V2
– anterior leads: V3-V4; b/c lie over ant. wall of L. ventricle
– lateral leads: I, aVL, V5, V6; best views of lateral wall of L. ventricle
which 3 leads are frequently used as the rhythm strips and why?
which 3 leads are frequently used as the rhythm strips and why?
– V1 ; II: are leads where atrial activity is most prominently seen
– V5: ?? has an orthogonal direction to V1 ; II
correlate specific groups of leads w/ anatomic regions of the heart
correlate specific groups of leads w/ anatomic regions of the heart
calculate the HR from the ECG of a regular rhythm
calculate the HR from the ECG of a regular rhythm
calculate the HR from an EKG of irregular rhythm
calculate the HR from an EKG of irregular rhythm
– “10 second rule” = length of rhythm strip
– HR (bpm) = (# of beats across EKG)*6
– what is the meaning of the QRS axis?
– what information does QRS deviation provide?
– QRS axis represents the average direction of electrical activity in the heart during ventricular depolarization
–> reporting of the axis uses classic hexaxial reference system as angle on frontal plane
– deviation of QRS axis can provide insight into chamber enlargement, abnormalities of the conduction system, MIs, and origin of some arrhythmias
- what are the normal QRS axis values? - what are the QRS deviations?
– what are the normal QRS axis values?
– what are the QRS deviations?
– normal: no consistent defintion; often -30° –> +90°
– left axis deviation (LAD) = QRS axis ; normal – right axis deviation (RAD) = QRS axis ; normal
what are non-pathologic factors affecting QRS axis?
– age: moves leftward as an individual ages
– body type:
— tall and thing –> vertical axis
— short and obese –> leftward axis
determine the QRS axis qualitatively
determine the QRS axis qualitatively
– quadrant approach: examine QRS complex in Leads I, II and aVF
— normal: ?Lead I; ?aVF
— normal (-30° to 0°): ?Lead I; ?aVF; predominatnly positive Lead II
— LAD (-90° to -30°): ?Lead I; ?aVF; predominantly negative Lead II
— RAD: ?Lead I; ?aVF
— extreme: ?Lead I; ?aVF
what is an indeterminate axis?
– when all limb leads have QRS complex that is equal parts positive and negative
– most common in COPD as manifestation of pulm. dz pattern
lbbb
lbbb
rbbb
rbbb

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