Cardiac Arrhythmias/disturbances
If external pacing is not available, two possible beta-adenergic agonists can be used called ________ (dosing too)
(1) Epinephrine, 2 to 10 μg/min IV, or (2)Dopamine, 3 to 10 μg/kg/min IV
If needed for pain control during transcutaneous pacing, administer a sedative, such as...
(1) Lorazepam, 1 to 2 mg IV (2) Morphine, 2 to 4 mg IV
Emergency treatment for bradyarrhythmia is indicated when...
(1) the heart rate is slower than 50 beats/min accompanied by hypotension or hypoperfusion and/or (2) the bradydysrhythmia is due to structural disease of the infranodal conduction system (This first group requires resuscitative treatment while evaluating the cause. The second group of patients does not require immediate treatment but should be closely monitored, with pacing readily available while arranging definitive care.)
Sinus tachycardia is in response to one of three categories of stimuli:
(a) physiologic (pain or exertion), (b) pharmacologic (sympathomimetics, caffeine, or bronchodilators), or (c) pathologic (fever, hypoxia, anemia, hypovolemia, pulmonary embolism, or hyperthyroidism). In many of these conditions, the increased heart rate is an effort to increase cardiac output to match increased circulatory needs. 3 P's
Sinus bradycardia represents a suppression of the sinus node discharge rate, usually in response to three categories of stimuli:
(a) physiologic (vagal tone), (b) pharmacologic (calcium channel blockers, β-blockers, or digoxin), and (c) pathologic (acute inferior myocardial infarction (MI), increased intracranial pressure, carotid sinus hypersensitivity, hypothyroidism, or sick sinus syndrome). 3 P's
A supraventricular rhythm can present with a widened QRS complex due to...
- Aberrant ventricular conduction - The widened QRS complex resulting from a fixed (i.e., preexisting) bundle-branch block - Rate-related conduction block - Ventricular preexcitation syndrome (i.e., Wolff-Parkinson-White [WPW] syndrome) - Toxic-metabolic condition
Two or more different P wave morphologies suggests...(3 options)
- Atrial ectopy - Wandering atrial pacemaker - Other non-sinus focus.
Pacemakers, AICDs (automated internal cardiac defibrillators), or combination units may be used in patients with a history of sudden death, heart failure, or cardiomyopathy. Malfunction can occur at any level of the device and due to:
- Infection or hematoma in the pocket housing the device - Lead infection/displacement - Failure to pace - Failure to sense - Over-pacing - Inappropriate defibrillation. Most pacemakers will have a magnetic switch which, when triggered by magnet application to the unit, will cause the pacemaker to function in a fixed asynchronous mode.
Common narrow-complex tachycardias include....
- Sinus tachycardia - atrial fibrillation - atrial flutter - paroxysmal supraventricular tachycardia less common narrow-complex tachycardias include multifocal atrial tachycardia, atrial tachycardias, and preexcited tachycardias seen in accessory pathway syndromes including WPW syndrome
In the stable patient, pharmacologic agents used to terminate a wide-complex tachycardia include:
- procainamide, - amiodarone, - lidocaine - magnesium
Wide-complex tachycardias include...
- ventricular tachycardia - supraventricular tachycardia with aberrant conduction. Ventricular tachycardia further is subdivided into: - monomorphic and polymorphic forms; the polymorphic category includes the subtype called torsade de pointes.
Treatment for Second-Degree Mobitz II AV Block is...
1. Atropine 0.5 to 1 mg IV bolus repeated every 5 minutes as needed up to 3 mg total dose is first-line treatment for symptomatic patients but may be ineffective. All patients should have transcutaneous pacing pads positioned and ready for use in the case of further deterioration into complete heart block. 2. Initiate transcutaneous cardiac pacing (see section on sinus bradycardia) in patients unresponsive to atropine. 3. If transcutaneous pacing is unsuccessful, initiate transvenous pacing (0.2 to 20 mA at 40 to 140 beats/min via a semi-floating or balloon tipped pacing catheter). Almost always require permanent cardiac pacemaker placement.
Treatment for hyperkalemia potassium level >6.5 mEq/L or cardiotoxicity....
1. Calcium gluconate 2. Insulin + glucose 3. Sodium bicarb - in acidemic patient 4. Beta-2-adrenergic agonists 5. Forced diuresis (loop diuretics with normal saline solution) If renal failure or ineffective initial treatment --> hemodialysis
The treatment for pulseless VT is...
1. Defibrillate pulseless VT with unsynchronized cardioversion starting at 150 to 200 J.
Emergency department treatment and disposition for pt with premature atrial contractions includes.... (2)
1. Discontinue precipitating drugs (alcohol, tobacco, or coffee) or toxins. 2. Treat underlying disorders (stress or fatigue).
In pacemaker, AICD (automated internal cardiac defibrillators), or combination unit malfunction the management is the following... (4 considerations)
1. Evaluation should include an ECG, electrolytes, and chest x-ray to assess lead position and integrity. 2. Arrangements should be made for electrical interrogation of the unit. 3. Patients with pacing failure may require treatment based on their underlying rhythm and associated symptoms. 4. Patients with over-pacing may require magnet application to convert the pacemaker to asynchronous mode pacing at a lower rate.
Treatment for patients with torsades de pointes
1. For patients with torsades de pointes: Try overdrive pacing set at 90 to 120 beats/min to terminate torsades de pointes. 2. Magnesium sulfate 1 to 2 g IV over 60 to 90 seconds followed by an infusion of 1 to 2 g/h can be effective. 3. Isoproterenol, 2 to 10 μg/min IV infusion, is also used in refractory torsades but carries a risk of increased myocardial oxygen demand.
The treatment for junctional escape beats is...
1. Isolated, infrequent junctional escape beats usually do not require specific treatment. 2. If sustained junctional escape rhythms are producing symptoms, treat the underlying cause. 3. In unstable patients, give atropine 0.5 mg IV every 5 minutes to a total of 3 mg. This will accelerate the SA node discharge rate and enhance AV nodal conduction. 4. Use transcutaneous or transvenous pacing in unstable patients not responsive to atropine. 5. Manage patients with digoxin toxicity as discussed for SVT.
Treatment for ventricular fibrillation is... (4 steps)
1. Perform immediate electrical defibrillation (unsynchronized) at 200 J (biphasic) and 360 J (monophasic) along with immediate vigorous chest compressions to augment coronary perfusion. Keep defibrillation pads on the patient and in the same location because, with successive countershocks, transthoracic impedance decreases. 2. If the initial two cycles of cardiopulmonary resuscitation (CPR) and defibrillation are unsuccessful, administer antiarrhythmic treatment using amiodarone 300 mg IV push. Lidocaine is second-line and is dosed at 1.5 mg/kg IV followed by 0.75 mg/kg IV for two more doses. Repeat the CPR-defibrillation cycle. 3. If no pulse is present after the third CPR-defibrillation cycle, give epinephrine 1 mg IV push, or vasopressin 40 units IV push (one time only), followed by a 20-mL normal saline flush and immediate resumption of the CPR-defibrillation cycle. 4. In refractory VF, administer magnesium sulfate 1 to 2 g IV over 60 to 90 seconds followed by an infusion of 1 to 2 g/h.
Treatment for PSVT/SVT (AVNRT or AVRT) in an unstable patient...
1. Perform synchronized cardioversion in any unstable patient (e.g., hypotension, pulmonary edema, or severe chest pain).
The treatment for Third-Degree (Complete) AV Block is....
1. Perform transcutaneous cardiac pacing in unstable patients until a transvenous pacemaker can be placed. 2. In stable patients, apply transcutaneous pacing pads. Treat the same as second-degree Mobitz II AV block. Type II... 1. Atropine 0.5 to 1 mg IV bolus repeated every 5 minutes as needed up to 3 mg total dose is first-line treatment for symptomatic patients but may be ineffective. All patients should have transcutaneous pacing pads positioned and ready for use in the case of further deterioration into complete heart block. 2. Initiate transcutaneous cardiac pacing (see section on sinus bradycardia) in patients unresponsive to atropine. 3. If transcutaneous pacing is unsuccessful, initiate transvenous pacing (0.2 to 20 mA at 40 to 140 beats/min via a semi-floating or balloon tipped pacing catheter).
The treatment for Second-Degree Mobitz I (Wenckebach) AV Block is...
1. Specific treatment is not necessary unless slow ventricular rates produce signs of hypoperfusion. 2. In cases associated with acute inferior MI, provide adequate volume resuscitation before initiating further interventions. 3. Administer atropine 0.5 mg IV repeated every 5 minutes. Titrate to the desired heart rate or until the total dose reaches 3 mg. 4. Although rarely needed, transcutaneous pacing may be used.
Treatment and disposition for PVCs...(3)
1. Stable patients require no treatment. 2. Patients with three or more sequential PVCs should be managed as nonsustained VT. 3. Potential causes such as hypoxia, drug effect, or electrolyte disturbances should be treated.
Management for stable patients with Afib for longer than 48 hours...
1. Stable patients with Afib for longer than 48 hours should be anticoagulated before cardioversion. Consider a transesophageal echocardiogram to rule out atrial thrombus before cardioversion. 2.. Control rate with diltiazem. Administer 15 to 20 mg (or 0.25 mg/kg) IV over 2 minutes followed by a continuous IV infusion, 5 to 10 mg/h, to maintain rate control. Give a second dose of 25 mg (0.35 mg/kg) in 15 minutes if the first dose fails to control the rate. Alternative rate control agents for patients with normal cardiac function include verapamil 2.5 to 5 mg IV or metoprolol 5 to 10 mg IV. 3. In patients with impaired cardiac function (EF <40%), use amiodarone 5 mg/kg IV over 30 minutes, followed by 1200 mg over 24 hours (contraindicated in patients with iodine or shellfish allergy; increased risk of rhabdomyolysis if co-administered with simvastatin). For new-onset atrial fibrillation, consider checking thyroid function. For patients on warfarin, check the prothrombin time. Calculate either the CHADS2 or CHA2DS2-VASc score to risk-stratify the potential for future arterial embolic complications; a CHADS2 score of 0 or a CHA2DS2-VASc score of 0 or 1 identify low-risk patients.
The two ways tachycardias are categorized include...
1. Supraventricular 2. Ventricular
Treatment for multifocal atrial tachycardia is....
1. Treat the underlying disorder. 2. Specific antiarrhythmic treatment is not indicated. 3. Magnesium sulfate 2 g IV over 60 seconds followed by a constant infusion of 1 to 2 g/h may decrease ectopy and convert MAT to sinus rhythm in some patients. 4. Replete potassium levels to greater than 4 mEq/L to increase myocardial membrane stability. With decompensated lung disease (COPD), oxygen and bronchodilators improve pulmonary function and arterial oxygenation and decrease atrial ectopy. Antidysrhythmic treatment is not indicated, and cardioversion has no effect.
Treatment for pt with unstable Afib is....
1. Treat unstable patients with synchronized cardioversion (150 to 200 J).
Sinus arrhythmia is present when the variation in the SA node discharge rate is greater than ________ milliseconds between the longest and shortest P to P wave intervals
120 miliseconds Sinus arrhythmia is a normal finding in children and young adults but is less common in the middle-aged and elderly. Sinus arrhythmia is most commonly a respiro-phasic phenomenon; the sinus node rate accelerates during inspiration and decelerates during expiration. This variation is thought to be due to changes in vagal tone occurring with respiration, termed the Bainbridge reflex. Any condition or medication that alters vagal tone may exaggerate an underlying sinus arrhythmia. During long intervals of sinus arrhythmia, junctional escape beats may occur. Treatment None is required.
The normal QRS complex duration is less than _____ milliseconds for older children and adults
120; therefore, a wide-complex tachycardia possesses a QRS complex width greater than 120 milliseconds.
Treatment for PSVT/SVT (simple AVNRT or orthodromic WPW-associated SVT) in a stable patient...
2. In stable patients, the first intervention should be vagal maneuvers, including: a. Valsalva maneuver: While in the supine position, ask the patient to strain for at least 10 seconds. The legs may be lifted to increase venous return and augment the reflex. b. Diving reflex: Have the patient immerse the face in cold water or apply a bag of ice water to the face for 6 to 7 seconds. This maneuver is particularly effective in infants. c. Carotid sinus massage: Auscultate to ensure that there is no carotid bruit and massage the carotid sinus against the transverse process of C6 for 10 seconds at a time, first on the side of the non-dominant cerebral hemisphere. This should never be done simultaneously on both sides. 3. Administer adenosine, 6 mg rapid IV bolus, into a large vein followed by a 20-mL normal saline rapid flush. If there is no effect within 2 minutes, give a second dose of 12 mg IV. Most patients experience distressing chest pain, flushing, or anxiety lasting less than 1 minute. Ten percent of patients may experience transient atrial fibrillation or flutter after conversion. This is first-line treatment for WPW-associated SVT with a narrow QRS complex (orthodromic conduction) but is ineffective in cases of anterograde conduction over an accessory pathway. Adenosine may induce bronchospasm in asthmatics requiring treatment with bronchodilators. Medical therapy: if vagal maneuvers have failed AVNRT and orthodromic AVRT: First line: IV adenosine: briefly blocks the AV node (↑ refractoriness) Second-line: IV verapamil, IV diltiazem (calcium channel blockers) IV metoprolol, esmolol (beta blockers)
Type II blocks are more dangerous than type I blocks because they are usually permanent and may progress suddenly to complete heart block (although truth is they both progress to complete block equally), especially in the setting of an acute anterior MI. When second-degree AV block occurs with a fixed conduction ratio of ___:___, it is not possible to differentiate between a Mobitz type I (Wenckebach) and Mobitz type II block.
2:1
Patients with Afib who are not anticoagulated have a yearly embolic event rate as high as 5% and a lifetime risk greater than 25%. Conversion from atrial fibrillation of 12 hours duration or less to sinus rhythm carries a 0.3% risk of arterial embolism compared to a risk of 1% for durations of 12 to 48 hours. Patients with heart failure and diabetes mellitus are particularly at risk with embolic rates as high as 9.8%. Anticoagulation for ___ weeks is required before cardioversion in patients with atrial fibrillation for longer than 48 hours duration and in those patients with an uncertain time of onset who are not on anticoagulation therapy.
3 weeks
What time span is considered new A-fib?
<48 hours
____________________________________ are contraindicated in patients with signs of preexcited tachycardia on ECG (e.g., antidromic AVRT; AF in WPW patient)!
AV nodal blocking agents (i.e., adenosine, verapamil, beta-blockers, digoxin, amiodarone)
When third-degree AV block occurs at the _____________, a junctional escape pacemaker takes over with a ventricular rate of 40 to 60 beats/min, and because the rhythm originates from above the bifurcation of the His bundle, the QRS complexes are narrow.
AV node
Tx for bradycardia after failed vagal maneuvers...
Adenosine - 6 mg, 12 mg, 12 mg Is a very-short-acting agent that blocks conduction through the AV node and can interrupt sustained reentry when the AV node is part of the circuit. The AV nodal blocking effect of adenosine is very transient, although quite profound, so a brief period of AV nodal blockade with near-immediate recurrence of the reentrant supraventricular tachycardia is not a treatment failure but a consequence of the medication's short duration of effect. In such situations, repeat adenosine with a higher dose (12 milligrams). β-Blockers and calcium channel blockers slow conduction through the AV node and can convert some supraventricular tachycardias, such as reentrant supraventricular tachycardias, and slow the ventricular response in others, such as atrial fibrillation or flutter.
The management for PEA is the following...
After intubation and initiating CPR, administer epinephrine 1 mg IV/IO (1:10,000 solution) every 3 to 5 minutes. If giving via endotracheal tube, increase the dose 2 to 2.5 times and follow with several rapid ventilations to disperse the drug.
For rapid treatment, ___________ is the antiarrhythmic of choice, given as an IV bolus.
Amiodarone - Give 150 milligrams IV over 10 min Repeat if necessary to max 2.2 grams/24 h (Prepare for synchronized cardioversion) Procainamide is effective for stable ventricular tachycardia in patients with preserved left ventricular dysfunction, given as an IV infusion. Lidocaine is a less effective alternative. Magnesium is used for tachydysrhythmias associated with QT interval prolongation, such as torsade de pointes.
Treat hemodynamically stable patients with VT with...
Amiodarone 150 mg IV over 10 minutes with repeated boluses every 10 minutes up to a total of 2 g. Alternatively, an infusion of 0.5 mg/min over 18 hours may be given after the initial bolus. Second-line agents include procainamide (in patients without suspected MI or LV dysfunction) and lidocaine.
Do not confuse atrioventricular reentrant (or reciprocating) tachycardia (AVRT) with atrioventricular nodal reentrant tachycardia (AVNRT)! AVRT is caused by ________________________, while in cases of AVNRT, ________________________
An accessory pathway between the atrium and ventricle; there are two functional pathways present within the AV node! Atrioventricular nodal reentrant tachycardia (AVNRT): tachycardia caused by a dysfunctional AV node that contains two electrical pathways Atrioventricular reciprocating tachycardia (AVRT): tachycardia caused by an accessory pathway between the atria and ventricles
First step in evaluating someone with suspected dysrhythmia...
Assess for stability! An unstable patient needs rapid assessment and treatment to prevent cardiovascular collapse. Instability means that the dysrhythmia is (1) impairing cardiac output and threatening vital organ function or (2) has the potential to suddenly deteriorate into cardiac arrest (Table 18-1). Dysrhythmia-induced chest pain results from coronary hypoperfusion, and dyspnea results from pulmonary edema, usually with objective evidence: ST segment abnormalities, rales on examination, or low oxygen saturation. As the ventricular rate exceeds 200 beats/min, severe systemic hypoperfusion often results and the RR interval narrows proportionally, increasing the opportunity for malignant ventricular dysrhythmias.
_______________ is the complete absence of cardiac electrical activity and carries a grim prognosis.
Asystole
______________ occurs when there are multiple, small areas of atrial myocardium continuously discharging in a disorganized fashion. This results in loss of effective atrial contraction and decreases left ventricular end-diastolic volume, which may precipitate CHF in patients with impaired cardiac function. The ECG characteristics are: (a) fibrillatory waves of atrial activity, best seen in leads V1, V2, V3, and aVF; and (b) an irregular ventricular response, usually between 170 and 180 beats/min in patients with a healthy AV node
Atrial fibrillation (Afib)
_________________ is a rhythm that originates from a small area within the atria. ECG characteristics include: (a) a regular atrial rate between 250 and 350 beats/min; (b) "saw tooth" flutter waves directed superiorly and most visible in leads II, III, and aVF; and (c) AV block, usually 2:1, but occasionally greater or irregular.
Atrial flutter One-to-one conduction may occur if a bypass tract is present.
In _____________________________ the AV node contains two electrical pathways: one fast and one slow → the electrical impulse circles around the AV node within both pathways → continuous circuit that conducts impulses to the ventricles → tachycardia Approx. 90% of cases are due to anterograde conduction across the slow-conducting pathway and retrograde in the fast pathway (although the reverse is possible)
Atrioventricular nodal reentrant tachycardia (AVnRT) *can occur in a normal heart or in association with rheumatic heart disease, acute pericarditis, MI, mitral valve prolapse, or preexcitation syndromes.
________ is a Class IIa treatment for symptomatic bradycardia. The dose is ________
Atropine The dose is 0.5 mg IV push, repeated every 3 to 5 minutes as needed up to a total of 3 mg IV. If given via endotracheal tube, increase the dose by 2 to 2.5 times over the IV dose. Slow administration or lower doses may cause paradoxical bradycardia. Atropine may not be effective in cardiac transplant patients since the heart is denervated and has no vagal stimulation.
Atropine, β-Adrenergic agents, and glucagon work in bradycardia by...
Atropine is usually effective for sinus bradycardia and junctional rhythms but is not useful (nor particularly harmful) in idioventricular rhythms and second-degree type II and third-degree AV block. β-Adrenergic agents (epi and dopamine) stimulate both chronotropic and inotropic cardiac activity, as well as enhancing electrical conduction within the AV node and infranodal system, thus their potential to produce ischemia and ectopy. Glucagon stimulates inotropic and chronotropic cardiac activity independent of the β-adrenergic receptors. Glucagon is primarily used for bradycardias due to cardiotoxicity from β-blocker or calcium channel blocker overdose. Effectiveness of drug treatment for bradycardia varies, and in general, these agents are best used as a temporary bridge to cardiac pacing.
________________________ occurs when the QRS axis swings from a positive to a negative direction in a single lead at a rate of 200 to 240 beats/min.
Atypical VT (torsades de pointes, or twisting of the points)
______________ block denotes a combination of any two of these fascicles, the most notable of which is left bundle branch block (LAFB + LPFB).
Bifascicular Trifascicular block denotes the presence of first degree AV block in the presence of a bifascicular block and is indicative of significant conduction system disease that includes the AV node, thus increasing the risk of Mobitz II or third-degree AV block and the potential need for permanent pacemaker placement.
Definition of bradycardia...
Bradydysrhythmia describes rhythms with a ventricular rate slower than 60 beats/min in the adult. Age-appropriate heart rates define pediatric bradydysrhythmia. Bradydysrhythmias can be broadly categorized as bradycardias (atria and ventricles beat at the same slow rate) and atrioventricular (AV) blocks (ventricles beat slower than the atria).
________________ syndrome is a genetic disorder of fast sodium channels causing an RBBB pattern in the early precordial leads (V1-2) with a pathognomonic J-point elevation and saddle-shaped or sloped ST segment.
Brugada
Multifocal atrial tachycardia is found most often in elderly patients with decompensated _____________, but it also may be found in patients with CHF, sepsis, methylxanthine toxicity, or digoxin toxicity.
COPD
Treatment of WPW (tachydysrhythmia) should be based on the QRS duration and regularity of the rhythm. All unstable patient should be _____________________________
Cardioverted (synchronized) at 150 to 200 J.
_________ massage or ___________ maneuvers are useful techniques to slow the ventricular response by increasing the degree of AV block, which can unmask flutter waves in uncertain cases.
Carotid sinus; Valsalva
Patients with Afib with a clear duration less than 48 hours may be considered for _____________ using ___________ (medication)
Chemical or electrical cardioversion in the emergency department. Ibutilide (Corvert) has the highest success rate and is dosed at 0.01 mg/kg IV up to 1 mg, infused over 10 minutes. Median time to conversion is 20 to 30 minutes. Ibutilide should not be administered to patients with known structural heart disease, hypokalemia, prolonged QTc intervals, hypomagnesemia, or CHF because of the possibility of provoking torsades de pointes. Monitor for 4 to 6 hours after giving ibutilide. Patients with impaired cardiac function may be cardioverted with amiodarone or electrically.
_____________, which does not have as much potential to induce hypotension, is the calcium channel blocker recommended for ventricular rate control.
Diltiazem
Brugada syndrome and long-QT syndrome increase the risk of spontaneous VT/VF and require evaluation for ______________________________ placement when diagnosed.
Implantable cardiac defibrillator
_______________ is the preferred treatment for wide-complex tachycardia with hemodynamic instability, myocardial ischemia, or failure of pharmacologic treatment
Electrical cardioversion
First actions when evaluating stability of patient...
Establish an IV line, initiate cardiac rhythm monitoring, obtain an ECG, and be prepared for drug or electrical therapy.
__________________ is characterized by a delay in AV conduction, manifested by a prolonged PR interval (>200 milliseconds). It can be found in normal hearts and in association with increased vagal tone, digoxin toxicity, inferior MI, amyloid, and myocarditis.
First-degree AV block
Second line medical therapy for AVRT is...
Flecainide, propafenone (class Ic antiarrhythmic drugs), Sotalol, Amiodarone For initial management of prolonged tachycardia, the "pill-in-pocket" approach may be useful if vagal maneuvers are unsuccessful
tx for torsades de pointes...
Give magnesium sulfate 2 grams IV Consider expert consultation
Signs of arrhythmia induces instability....
Hypotension: e.g., systolic blood pressure <90 mm Hg (<12 kPa) Systemic hypoperfusion Altered mentation Ischemic chest pain Respiratory distress Extremely rapid ventricular rate: e.g., rate over 200 beats/min in adult
The ECG characteristics of _______________ are: (a) wide and regular QRS complexes; (b) a rate between 40 and 100 beats/min, often close to the preceding sinus rate; (c) mostly runs of short duration (3 to 30 beats/min); and (d) an AIVR often beginning with a fusion beat (Fig. 2-5). This condition is found most commonly with an acute MI or in the setting of reperfusion after successful thrombolysis.
Idioventricular rhythm (IVR) AIVR (Accelerated...)
The most common causes of VT are ______________ and _________________, accounting for approximately 50% of all cases of symptomatic VT.
Ischemic heart disease and acute MI Other etiologies include hypertrophic cardiomyopathy, mitral valve prolapse, drug toxicity (digoxin, antiarrhythmics, or sympathomimetics), hypoxia, hypokalemia, and hyperkalemia. In general, all wide complex tachycardia should be treated as VT regardless of clinical symptoms or initial vital signs. Adenosine appears to cause little harm in patients with VT; therefore, stable patients with wide complex tachycardia due to suspected SVT with aberrancy (see previous section) may be treated safely with adenosine when the diagnosis is in doubt.
_________________ syndrome is characterized by a QT interval greater than 470 milliseconds in men and greater than 480 milliseconds in women and may be congenital or acquired, leading to an increased risk of torsades de pointes.
Long-QT The risk of arrhythmia increases significantly with QTc durations greater than 500 milliseconds.
Treatment options for bradycardia include...
Medications used to increase heart rate in symptomatic bradycardias include: - Atropine - 0.5-milligram IV push, may repeat every 3-5 min until desired heart rate is achieved or to total dose of 3 milligrams (0.04 milligram/kg) - β-adrenergic agonists - (dopamine - IV infusion at rate 2-20 micrograms/kg per min, titrate to desired heart rate) (epi - IV infusion at rate 2-10 micrograms/min, titrate to desired heart rate) - Glucagon - 3-10 milligrams IV infused over 1-2 min, followed by an IV continuous infusion of 1-5 milligrams/h
_________ is a longer acting β-blocker used in more stable patients, typically for ventricular rate control in patients with atrial fibrillation.
Metoprolol
_____________________ is defined as at least three different sites of atrial ectopy. The ECG characteristics are: (a) three or more differently shaped P waves; (b) changing PP, PR, and RR intervals; and (c) atrial rhythm usually between 100 and 180 beats/min
Multifocal atrial tachycardia (MAT) Because the rhythm is irregularly irregular, MAT can be confused with atrial flutter or atrial fibrillation (AFib).
Supraventricular tachycardias originate from a focus within or above the AV node and most often present with a _______ (narrow or wide) QRS complex
Narrow; thus, they are termed narrow-complex tachycardias.
Treatment for first-degree AV block is...
No treatment.
What drugs should be avoided in WPW treatment?
Nodal blocking agents such as β-blockers and calcium channel blockers should be avoided due to the risk of enhancing conduction across the bypass tract.
If three or more PVCs occur in a row, patients are considered to have _____________
Non-sustained ventricular tachycardia.
_____________ contractions are associated with stress, fatigue, alcohol use, tobacco, coffee, chronic obstructive pulmonary disease (COPD), digoxin toxicity, and coronary artery disease, and may occur after adenosine-converted paroxysmal supraventricular tachycardia (PSVT). Patients may complain of palpitations or an intermittent "sinking" or "fluttering" feeling in the chest.
PACs (premature atrial contraction) PACs are common in all ages, often in the absence of significant heart disease, but can precipitate sustained atrial tachycardia, flutter, or fibrillation under certain circumstances.
What psychiatric disorders should be considered when evaluating for dysrhythmia?
Panic or anxiety is a diagnosis of exclusion in tachycardic ED patients.
Treatment for WPW with a narrow regular tachycardia is....
Patients with a narrow regular tachycardia should be treated as SVT (orthodromic conduction) using vagal maneuvers followed by adenosine, if ineffective. Refractory cases may require procainamide, 15 to 17 mg/kg IV over 30 minutes up to 50 mg/kg, or until 50% QRS widening is noted.
The following ECG characteristics are representative of ____________: (a) the ectopic P wave appears sooner (premature) than the next expected sinus beat (b) the ectopic P wave has a different shape and direction; (c) the ectopic P wave may or may not be conducted through the AV node
Premature atrial contractions (PACs)
_______________ are due to impulses originating from single or multiple areas in the ventricles. The ECG characteristics are as follows: (a) a premature and wide QRS complex; (b) no preceding P wave; (c) the ST segment and T wave of the this impulse is directed opposite the preceding major QRS deflection; (d) most of these types of impulses do not affect the sinus node, so there is usually a fully compensatory postectopic pause, or the impulse may be interpolated between two sinus beats; (e) many of these impulses have a fixed coupling interval (within 40 milliseconds) from the preceding sinus beat; and (f) many of these impulses are conducted into the atria, thus producing a retrograde P wave
Premature ventricular contractions (PVCs) PVCs are very common, occurring in most patients with ischemic heart disease and acute myocardial infarction (MI). Other common causes of PVCs include digoxin toxicity, congestive heart failure (CHF), hypokalemia, alkalosis, hypoxia, and sympathomimetic drugs. Pooled data and meta-analyses have found no reduction in mortality from suppressive or prophylactic treatment of PVCs. Ventricular parasystole occurs when the ectopic ventricular focus fires frequently enough to compete with the SA node and is associated with cardiac ischemia, electrolyte imbalance, and hypertensive or ischemic heart disease.
Common dysrhythmia symptoms include....
Presenting symptoms may include: - palpitations, - lightheadedness, - fatigue, - weakness. Ischemic symptoms (may be due to dysrhythmia-induced ischemia), such as: - chest pain, - nausea, - dyspnea, or - lightheadedness
Treatment of WPW with wide QRS tachycardias, whether regular (SVT with antidromic conduction) or irregular (atrial fibrillation with antidromic conduction), should be treated with ________________
Procainamide
________________ is the presence of electrical complexes without accompanying mechanical contraction of the heart. Potential mechanical causes should be diagnosed and treated, including severe hypovolemia, cardiac tamponade, tension pneumothorax, massive pulmonary embolus, MI, and toxic ingestions (e.g., tricyclic antidepressants, calcium channel blockers, β-blockers). In addition, profound metabolic abnormalities such as acidosis, hypoxia, hypokalemia, hyperkalemia, and hypothermia also should be considered and treated.
Pulseless electrical activity (PEA)
Treatment for known WPW patients with Afib is
Rate control with procainamide 17 mg/kg IV over 30 mins up to 50 mg/kg or 50% widening of QRS complex OR Synchronized cardioversion 50-100 J (0.5-2 J/kg) (b/c remember if WPW wasn't present, you would just rate control with a beta-blocker) Avoid digoxin, beta blocker, adenosine, and CCB (these meds block the AV node and may lead to unopposed ventricular stimulation through the accessory tract, worsening the tachycardia) ****So when assessing SVT, first make sure its not afib and then secondly make sure its not WPW bc if either present, it will switch into afib and/or VT****
In stable symptomatic patients with Brugada syndrome or Long QT syndrome, the management is...
Recognition of the ECG pattern should prompt close outpatient followup with a cardiologist, especially in stable symptomatic patients.
_________________ will prolong the QRS duration (>120 milliseconds) and cause an RSR', or "rabbit ears," in the early precordial leads (V1-2).
Right bundle branch block (RBBB)
__________________ is a nodal block causing a progressive prolongation of conduction through the AV node until the atrial impulse is completely blocked. Usually, only one atrial impulse is blocked at a time. After the dropped beat, the AV conduction returns to normal and the cycle usually repeats itself with the same conduction ratio (fixed ratio) or a different conduction ratio (variable ratio). Although the PR intervals progressively lengthen before the dropped beat, the increments by which they lengthen decrease with successive beats causing a progressive shortening of each successive R-R interval before the dropped beat
Second-Degree Mobitz I (Wenckebach) AV Block This block is often transient and usually associated with an acute inferior MI, digoxin toxicity, or myocarditis or can be seen after cardiac surgery. Because the blockade occurs at the level of the AV node itself rather than at the infranodal conducting system, this is usually a stable rhythm.
_______________________ is typically due to infranodal disease, causing a constant PR interval with intermittent non-conducted atrial beats. One or more beats may be non-conducted at a single time. This block indicates significant damage or dysfunction of the infranodal conduction system; therefore, the QRS complexes are usually wide coming from the low His-Purkinje bundle or the ventricles.
Second-Degree Mobitz II AV Block
___________________ is characterized by intermittent AV nodal conduction: some atrial impulses reach the ventricles, whereas others are blocked, thereby causing "grouped beating." These blocks can be subdivided into nodal blocks which are typically reversible and infranodal blocks which are due to irreversible conduction system disease
Second-degree AV block
_______________ consists of a variety of abnormalities in impulse generation and conduction, leading to various supraventricular tachycardic rhythms as well as bradycardia due to sinus arrest and SA block. It can be seen in myocardial ischemia, myocarditis, rheumatologic disease, cardiomyopathies, or metastatic disease. Conditions that increase vagal tone such acute abdominal pain, thyrotoxicosis, and hypo- or hyperkalemia exacerbate this condition.
Sick sinus syndrome (Otherwise known as tachy-brady syndrome)
Patients with long-QT syndrome should be advised to avoid....
Strenuous exercise (particularly swimming) which can increase the chance of sudden death.
Other disease considerations for new arrhythmia include...
Symptoms of hyperthyroidism should be sought. Patients with a family history of sudden death, syncope, or dysrhythmias and those with organic heart disease have a higher risk of cardiac dysrhythmias and complications.
Treatment for unstable WPW tachycardia is...
Synchronized cardioversion: 50-100 J (0.5-2 J/kg)
_________________ can be used in narrow-complex tachycardias when patients are unstable or do not respond to pharmacologic measures
Synchronized electrical cardioversion
Definition of tachydysrhythmia
Tachydysrhythmia describes rhythms with a ventricular rate greater than 100 beats/min in an adult, with age-appropriate limits in children.
Types of bradyarrhythmias...
The bradycardias include - sinus bradycardia, junctional rhythm, - idioventricular rhythm (ventricle beating and not following atria), - hyperkalemia-related sinoventricular rhythm. - Bradydysrhythmias due to AV blocks include second-degree (usually type II) and third-degree AV block, as well as atrial fibrillation and atrial flutter with a slow ventricular response. The most common bradycardia is sinus bradycardia, followed by junctional rhythm, and less commonly idioventricular rhythm. (About 80% of bradydysrhythmias are caused by factors external to the cardiac electrical system including acute coronary syndrome, drug effects or overdose, and hypoxia with cardiac hypoperfusion.)
Medication hx to be considered with dysrhythmias includes...
The medication history includes: - prescribed medications, herbals, recreational drugs, and caffeine-containing beverages. Especially note recently started new medications or increased medication doses.
The treatment for atrial flutter is...
The treatment is the same as atrial fibrillation and is discussed below.
_____________ is characterized by complete interruption in AV conduction with resulting AV dissociation.
Third degree AV block
In ____________ block, there is no AV conduction. The ventricles are paced by an escape pacemaker from the AV node or the infranodal conduction system at a rate slower than the atrial rate.
Third-Degree (Complete) AV Block Nodal third-degree AV block may develop in up to 8% of acute inferior MIs and it is usually transient, although it may last for several days.
Drugs that further prolong repolarization—quinidine, disopyramide, procainamide, phenothiazines, and tricyclic antidepressants—exacerbate the following arrhythmia ________________
Torsade de pointes
________________________ is the only Class I treatment for unstable patients with bradycardia.
Transcutaneous cardiac pacing a. Attach the patient to the monitor leads of the external pacing device. b. When placing transcutaneous pacing pads, place the anterior pad over the left lateral precordium and the posterior pad at the level of the heart in the right infrascapular area. Do not use multifunction pacing defibrillation pads unless the patient is unconscious as the pads cause a lot of discomfort. c. Slowly increase the pacing output from 0 mA to the lowest point where capture is observed, usually at 50 to 100 mA, but may be up to 200 mA. A widened QRS after each pacing spike denotes electrical capture. d. If needed, administer a sedative, such as lorazepam, 1 to 2 mg IV, or an opiate, such as morphine, 2 to 4 mg IV, for pain control.
Most appropriate pacing method for the acutely symptomatic bradycardic patient patient...
Transcutaneous pacing can be applied quickly and is the most appropriate pacing method for the acutely symptomatic patient (see chapter 33, "Cardiac Pacing and Implanted Defibrillation"). Transvenous pacing requires considerable physician expertise and specialized equipment for insertion and proper placement.
Patients with wide complex SVT (antidromic across accessory pathway) (AVRT) should be treated with ________________ (unless known orthodromic WPW)
Treat stable patients with procainamide, 15 to 17 mg/kg IV over 30 minutes up to 50 mg/kg, or until 50% QRS widening is noted (contraindicated in patients with myasthenia gravis since it may increase weakness). For antidromic AVRT: procainamide - AV nodal blocking agents are contraindicated! For WPW patients with AF: generally rhythm control (e.g., procainamide) - AV nodal blocking agents are contraindicated!
Treatment for idioventricular rhythm is...
Treatment is not necessary unless the patient is unstable or pulseless. On occasion, especially after reperfusion therapy, the IVR may be the only functioning pacemaker, and suppression with lidocaine can lead to cardiac asystole. If the patient is hypotensive or in arrest, treatment includes identifying contributing mechanical factors (e.g., aggressive volume resuscitation) and α-adrenergic agents.
Treatment for Sick Sinus syndrome is...
Treatment should be based on the presenting rhythm depending on the heart rate and patient instability. Temporary pacing may be needed and admission for permanent pacemaker placement is frequently indicated.
First treatment step for SVT is...
Vagal maneuvers (blow into straw (then sit back and legs up), bare down (Hold for as long as practical, ideally >20 s), ice on face, etc.) Only do carotid massage if checked for bruits first. Vagal maneuvers heighten parasympathetic tone and may slow electrical conduction in the heart to a degree that abolishes sustained reentry. If applied early, vagal maneuvers can convert about 20% of patients presenting with reentrant tachycardias, such as paroxysmal supraventricular tachycardia and narrow-complex tachycardia associated with WPW syndrome. Effective vagal maneuvers include carotid sinus massage, the release phase of the Valsalva maneuver, and the diving reflex; the response to these vagal maneuvers is enhanced by placing the patient supine. Basic supportive therapy in most patients involves an IV fluid bolus to expand the circulating intravascular volume and supplemental oxygen
________________ is the totally disorganized depolarization and contraction of small areas of ventricular myocardium during which there is no effective ventricular pumping activity. The ECG shows a fine-to-coarse zigzag pattern without discernible P waves or QRS complexes. It is seen most commonly in patients with severe ischemic heart disease, with or without an acute MI. It also can be caused by digoxin or quinidine toxicity, hypothermia, chest trauma, hypokalemia, hyperkalemia, or mechanical stimulation (e.g., catheter wire).
Ventricular fibrillation Primary VF occurs suddenly, without preceding hemodynamic deterioration, and usually is due to acute ischemia or peri-infarct scar reentry. Secondary VF occurs after a prolonged period of hemodynamic deterioration due to left ventricular failure or circulatory shock.
_________________ is the occurrence of three or more successive beats from a ventricular ectopic pacemaker at a rate faster than 100 beats/min. The ECG characteristics are: (a) a wide QRS complex, (b) a rate faster than 100 beats/min (most commonly 150 to 200 beats/min), (c) a regular rhythm, although there may be some initial beat-to-beat variation, and (d) a constant QRS axis.
Ventricular tachycardia
Patients with wide complex tachycardia should be approached as having ___________ until proven otherwise
Ventricular tachycardia (patients aren't always unstable with VT)
__________ is a calcium channel blocker used for conversion of reentrant supraventricular tachycardias, and although it can be used for ventricular rate control, there is potential for hypotension.
Verapamil
Second line medical therapy for AVNRT is...
Verapamil, diltiazem (non-dihydropyridine calcium channel blockers), β-blockers, Digoxin MUST MAKE SURE THEY DO NOT HAVE antidromic-AVRT (Antidromic WPW)
Before initiating treatment for Afib what underlying heart condition should you ask about? (Similar to SVT)
WPW Treat patients with preexcitation syndromes (e.g., WPW) with procainamide 15 to 17 mg/kg IV over 30 minutes followed by an infusion of at 1 to 4 mg/min up to 50 mg/kg or until 50% QRS widening is noted. Avoid β-adrenergic or calcium channel blockers (i.e., verapamil) due to the risk of causing degeneration to VF.
_________________ is the most common form of ventricular pre-excitation involving an accessory conduction pathway that bypasses the AV node. The ventricles are activated by an impulse from the atria sooner than would be expected if the impulse were transmitted down the normal conducting pathway. This premature activation causes initial fusion beat morphology with slurring of initial QRS complex.
WPW syndrome Causing the pathognomonic delta wave. Among patients with WPW-PSVT, 80% to 90% will conduct in the orthodromic direction and the remaining 10% to 20% will conduct in the antidromic direction. ECG findings of atrial fibrillation or flutter with antidromic conduction down the bypass tract show a wide QRS complex that is irregular with a rate faster than 180 to 200 beats/min (see Atrial Fibrillation).
Ventricular tachycardias, resulting from a focus below the AV node in the ventricular myocardium, usually demonstrate a _______ (narrow or widened) QRS complex.
Widened
Rates of greater than 300 beats/min with a wide QRS complex are concerning for a pre-excitation syndrome such as ______________
Wolff-Parkinson-White (WPW)
Atrial flutter is seen most commonly in patients with ischemic heart disease as well as CHF, acute MI, pulmonary embolus, myocarditis, blunt chest trauma, and digoxin toxicity. Atrial flutter may be a transitional arrhythmia between sinus rhythm and __________________.
atrial fibrillation Consider anticoagulation in patients with an unclear time of onset or duration longer than 48 hours before conversion to sinus rhythm due to increased risk of atrial thrombus and embolization.
________________________ is a congenital condition characterized by intermittent tachycardias and signs of ventricular pre-excitation on ECG, which both arise from an accessory pathway known as the "Bundle of Kent" (an accessory pathway that conducts impulses from the atria to the ventricles). The bundle of Kent connects the atria and ventricles, bypassing the AV node and leading to a pre-excitation of the ventricles. Up to one-third of patients may develop paroxysmal atrial fibrillation. May result in supraventricular tachycardia due to a reentry circuit
Wolff-Parkinson-White syndrome (WPW) Impulses coming early from the ventricle going up to the atria (antidromic), which is why it may actually lead to a SVT
Patients with Brugada or Long QT syndromes presently with unstable rhythms or concerning clinical presentations (e.g., drop attacks) should be
admitted for monitoring and cardiology consultation. Patients should be advised to avoid any medications that may potentially worsen QT prolongation (http://www.brugadadrugs.org).
In patients with Afib + impaired cardiac function (EF <40%), use ________________ 5 mg/kg IV over 30 minutes, followed by 1200 mg over 24 hours (contraindicated in patients with iodine or shellfish allergy; increased risk of rhabdomyolysis if co-administered with simvastatin).
amiodarone
Patients with Afib with a clear duration less than 48 hours and impaired cardiac function may be cardioverted with _____________________ or electrically
amiodarone
In patients with _____________________, reentry can occur in either direction, usually (80% to 90% of patients) in a direction that goes down the AV node and up the bypass tract producing a narrow QRS complex (orthodromic conduction). In the remaining 10% to 20% of patients, reentry occurs in the reverse direction (antidromic conduction).
atrioventricular bypass tracts (AVRT) Ectopic SVT usually originates in the atria, with an atrial rate of 100 to 250 beats/min and may be seen in patients with acute MI, chronic lung disease, pneumonia, alcohol intoxication, or digoxin toxicity. There is a high incidence of tachyarrhythmias in patients with preexcitation syndromes including PSVT (40% to 80%), atrial fibrillation (10% to 20%), and atrial flutter (about 5%).
There are two types of _____________________ tachycardia. The direction of the reciprocating impulse helps distinguish between the two: - Orthodromic type: most common (90-95%) → narrow QRS complex: Antegrade conduction (atrium → ventricle) through AV node; retrograde conduction (ventricle → atrium) through accessory pathway - Antidromic type: least common (5-10%) → delta wave: Antegrade conduction (atrium → ventricle) through accessory pathway; retrograde conduction (ventricle → atrium) through AV node
atrioventricular reentrant tachycardia (AVRT)
Stable patients with Afib for longer than 48 hours should be anticoagulated _____________ (after or before) cardioversion
before
In treating SVT, __________ should also be at bedside in case of worsening rhythm
defibrillator
Sinus bradycardia usually does not require specific treatment unless the heart rate is slower than 50 beats/min and there is evidence of ______________.
hypoperfusion
Causes of Afib include:
idiopathic (lone Afib) or may be found in association with: - longstanding hypertension - ischemic heart disease - rheumatic heart disease - alcohol use ("holiday heart") - COPD - thyrotoxicosis Patients with LV dysfunction who depend on atrial contraction may suffer acute CHF with Afib onset
When third-degree AV block occurs at the ____________ level, the ventricles are driven by a ventricular escape rhythm at a rate slower than 40 beats/ min.
infranodal Third-degree AV block located in the bundle branch or the Purkinje system invariably has an escape rhythm with a wide QRS complex. Like Mobitz type II block, this indicates structural damage to the infranodal conduction system and can be seen in acute anterior MIs. The ventricular escape pacemaker is usually inadequate to maintain cardiac output and is unstable with periods of ventricular asystole.
The sinus node rate accelerates during _______ (inspiration or expirations)
inspiration
Treatment for symptomatic tachycardia is primarily ___________ for the stable patient and _____________ for the unstable patient. The QRS width, often indicating the portion of the heart where the dysrhythmia originates, guides therapeutic choices
intravenous medications; electrical therapy
A ________________ beat is a delayed heartbeat originating not from the atrium but from an ectopic focus somewhere in the atrioventricular junction. It occurs when the rate of depolarization of the sinoatrial node falls below the rate of the atrioventricular node. This dysrhythmia also may occur when the electrical impulses from the SA node fail to reach the AV node because of SA or AV block.
junctional escape In patients with sinus bradycardia, SA node exit block, or AV block, junctional escape beats may occur, usually at a rate between 40 and 60 beats/ min, depending on the level of the rescue pacemaker within the conduction system. Junctional escape beats may conduct retrogradely into the atria, but the QRS complex usually will mask any retrograde P wave. When alternating rhythmically with the SA node, junctional escape beats may cause bigeminal or trigeminal rhythms. Sustained junctional escape rhythms may be seen with CHF, myocarditis, acute MI (especially inferior MI), hyperkalemia, or digoxin toxicity ("regularized Afib"). If the ventricular rate is too slow, myocardial or cerebral ischemia may develop. In cases of enhanced junctional automaticity, junctional rhythms may be accelerated (60 to 100 beats/min) or tachycardic (≥100 beats/min), thus overriding the SA node rate.
Conduction blocks may arise in one or more of the three infranodal conduction pathways. Blockage of either of the left fascicles does not prolong the QRS duration, but will change the QRS axis. Left anterior fascicular block (LAFB) causes ______ axis deviation with qR complex seen in aVR.
left
The much less common _________ fascicular block causes right axis deviation
left posterior (LPFB)
Patients with stable recurrent episodes may be ______________ after cardioversion and discharged to outpatient follow-up. Instability, loss of consciousness, or other concerning features warrant observation on monitoring for recurrence. Asymptomatic patients with WPW, found incidentally, warrant outpatient referral to a cardiologist for further evaluation.
monitored
Afib may be ________________ (lasting for less than 7 days), persistent (lasting for more than 7 days), or chronic (continuous).
paroxysmal
Supraventricular tachycardia (SVT) is a regular, rapid rhythm that arises from impulse reentry or an ectopic pacemaker above the bifurcation of the His bundle. The reentrant variety is the most common. Patients often present with acute, symptomatic episodes termed _______________________
paroxysmal supraventricular tachycardia (PSVT).
Permanent pacemaker placement is indicated in the patient with symptomatic recurrent or persistent sinus bradycardia due to _______________________.
sick sinus syndrome.
The ECG characteristics of ______________- are: (a) normal sinus P waves and PR intervals and (b) an atrial rate usually between 100 and 160 beats/min.
sinus tachycardia
Treat unstable patients with VT who are not pulseless with...
synchronized cardioversion (biphasic doses) - narrow regular: 50-100 J - narrow irregular: 120-200 J - wide regular: 100 J - wide irregular: defibrillate (not synchronized): 120-200J - if narrow complex, consider adenosine 6 mg rapid IVP, followed by 12 mg prn
Treatment for asystole is....
the same as that for pulseless electrical activity. After intubation and initiating CPR, administer epinephrine 1 mg IV/IO (1:10,000 solution) every 3 to 5 minutes. If giving via endotracheal tube, increase the dose 2 to 2.5 times and follow with several rapid ventilations to disperse the drug.
Patients with wide complex SVT (antidromic across accessory pathway) should be approached as presumed _______________ unless there is a known history of WPW syndrome.
ventricular tachycardia Patients with this type of tachycardia are at risk for rapid ventricular rates and degeneration into VF; therefore, agents that preferentially block the AV node such as β-blockers, calcium channel blockers, and digoxin should not be used.
Glucagon 3 to 10 mg IV over 1 to 2 minutes, followed by an infusion of 1 to 5 mg/h may be used in _____________ or _____________ toxicity.
β-blocker or calcium channel blocker toxicity.
