...Too fast, too slow, or too irregular...
What are the patient's VS?
Any CP or SOB?
Order a stat ECG.
Pt. needs to be seen immediately.
What is cardiology on call pager?
Major Causes of Rapid HR
Regular: Sinus tachy, SVT, AFL, V.tach
Irregular: AFL, AF, MAT
Rates:
PAT/SVT: >150 (151-250)
AFL: atrial rate (250-350); ventricular rate: (60-100)
AFL with SVR (<60)
AFL with RVR (101-150)
AFL with variable ventricular response - irregular R-R
AF: (atrial rate: 350-500)
AF controlled: 60-100
AF with SVR: <60
AF with RVR: (101-150)
AF uncontrolled: >150
Major Causes of Slow HR
Drugs: BB, CCB, digoxin
SSS
MI - inf. MI ?
AV block
History:
Dyspnea, angina, light-headedness or syncope and decreased level of consciousness.
History of baseline sx suggestive of LVS dsyfx, such as DOE, orthopnea, PND, bilateral LE swelling.
Palpitations. Ask regarding nature of onset. Do they start and terminate abruptly?
Sudden onset and termination is highly suggestive of a tachyarrhythmia.
Symptoms get better on holding breath and bearing down (Valsalva maneuver) suggestive of SVT. AV node is critical in maintenance of this arrhythmia.
History of organic heart disease (ischemic CM, nonischemic, VHD) or thyroid disease, or pheochromocytoma.
History of familial or congenital causes of arrhythmias such as HOCM, congenital long QT syndrome, or other congenital heart disease.
Medications: prescription, OTC, herbal medications.
Physical Examination:
Check LOC, BP, pulse, RR, O2 sats, and temp
Quickly look at the patient and the chart.
Check can ECG. Get a cardiac monitor, if one is around.
How distressed does the patient look?
Repeat VS
Check mentation. Is there obvious hemiparesis?
Signs of CHF: JVD, lung crackles, peripheral edema, S3 gallop.
Mitral valve prolapse is associated with SVT, often midsystolic click is heard.
HOCM produces a harsh systolic crescendo-decrescendo ejection murmur heard best along the LSB. Murmur increases with Valvalva maneuver, standing, and decreases with squatting and raising legs. Sustained PMI. S4 gallop, and pardoxically split S2. HOCM is associated with AF, as well as other malignant arrhythmias
Check pulse, assess rate and regularity
Pulse about 150 bpm, suspect AFL with 2:1 block.
Pulse is >150 bpm, suspect AVNRT or AVRT
Pulse is irregularly irregular: AF
Pulse is regularly irregular: second degree HB
"Cannon" A waves: on JVP reflect atrial contraction against a closed tricuspid valve.
If seen with an irregular pattern: AV dissociation and a clue for VT
If regular in 1:1 ratio with pulse: AVNRT or AVRT, or a junctional tachycardia, all leading to retrograde atrial activation occurring simultaneously with ventricular contraction.
Lab/dxtic: Troponin, ECG, ABG, CBC, electrolytes, TSH, serum concentration of digoxin, toxicology screen, and CXR. TEE. 24-hours ambulatory ECG monitoring (Holter), inhospital telemetry monitoring, event recorder (loop recorder), implantable loop recorder (ILR), exercise ECG, EPS.
Management:
Transfer to CCU, or telemetry floor
Get a cardiology consult
If patient is hypotensive and has AF with RVR, SVT, or V.tach, emergency cardioversion (synch) may be required.
In general, if the patient is unstable with serious signs or symptoms, a ventricular rate of greater than 150, or both, you should prepare for immediate cardioversion. The patient may require sedation. Serious signs and symptoms per ACLS protocol include CP, SOB, decreased LOC, hypotension, and shock, CHF, and acute MI. Refer to proper ACLS algorithm.
Always check ABC first, ensure O2, IV access, cardiac monitor.
AF with RVR but hemodynamically stable patient can be rate controlled with dilitazem or digoxin, or amiodarone.
SVT without hemodynamic compromise can sometimes be broken by performing Valsalva's maneuver, carotid sinus massage (one side at a time, and always listen for bruits first. Avoid in elderly). If patient persists in SVT, give adenosine 6 mg IVP, followed by 12 mg in 1 - 2 min if no effect, may repeat 12 mg/dose once more in 1 - 2 min if no effect maximum 30 mg/total dose.
If QRS complex width is narrow with stable BP, diltiazem, 10 mg IV, can be used.
Esmolol, 0.5 mg/kg, IV x 1 min, maintenance dose 0.05 - 0.2 mg/kg/min. Very effective.
Supraventricular Tachyarrhythmias require atrial or AV nodal tissue, or both, for the initiation and maintenance.
QRS in most SVTs is narrow (<120 msec). In SVT with aberrancy or prexcited tachycardia, SVT is wide complex tachycardia (QRS >120 msec).
AF: most common narrow-complex tachycardia seen in the inpatient setting.
AFL: 2nd most common arrhythmia.
May present as regular rhythm or irregularly irregular when associated with variable AV block (2:1, 4:1, 3:1)
Atrial rate is 250 - 350 bpm.
SVT with regular ventricular rate of 150 bpm should raise the suspicion of AFL.
ECG, "saw-tooth" pattern best seen in leads II, III, and aVF, with negative deflection in V1.
Both AF and AFL is commonly associated with post-cardiac surgery period (25%), pulmonary disease, thyrotoxicosis, and atrial enlargement.
MAT: irregular irregular SVT seen generally in elderly hospitalized patients with multiple comorbidities
COPD, CHF, hypokalemia, glucose intolerance, hypomagnesemia, drugs (theophylline), and chronic renal failure.
ECG shows SVT with at least 3 distinct P-wave morphologies, seen best in II, III, V1.
Sinus Tachycardia (ST):
ST with PACs can lead to irregularly irregular rhythm.
Most common mechanism of long RP tachycardia.
Most commonly it is a normal physiological response to hyperadrenergic states (fever, pain, hypovolemia, anemia, hypoxia, etc.), but can also be induced by illicit drugs (cocaine, amphetamines, methamphetamine), and prescription drugs (theophylline, atropine, B-adrenergic agonists).
Ectopic atrial tachycardia (EAT):
EAT with variable block presents as irregularly irregular rhythm and can be distinguished from AFL by an atrial rate of 150 - 200 bpm.
Commonly associated with digoxin toxicity.
ECG is characterized by regular atrial activation pattern with a P-wave morphology originating outside of the sinus node complex resulting in a long RP tachycardia.
AVNRT (AV nodal reentrant tachycardia): When there is functional dissociation of the AV node into two pathways one slower than the other. This occurs due to changes in refractory periods between pathways, allowing impulse to go down one and inappropriately come back up to the atrium through the other pathway. More common than AVRT.
"Typical" AVNRT
More common
Conduction goes antegrade down the slow pathway in the AV node, and goes back up (retrograde) the fast pathway, leading to short RP (<50% of RR interval) tachycardia.
ECG: P wave are hidden in QRS complexes or buried at the end of the QRS complexes creating a pseudo-r seen in V1 or pseudo-s in II.
"Atypical" AVNRT
Less common
Antegrade conduction goes down the fast AV nodal pathway, with retrograde conduction over the slow AV nodal pathway, leading to long RP tachycardia.
The retrograde P wave is seen well after the QRS complex in the second half of the RR interval.
AVRT (AV reentrant tachycardia): An accessory pathway is present. More common in younger patient (age 40).
Orthodromic (O-AVRT): Accessory pathway mediated reentrant rhythm when the antegrade conduction from atria to the ventricles occurs through the AV node and retrograde conduction to the atrium occurs through the accessory or "bypass" tract, leading to short RP tachycardia.
O-AVRT is the most common mechanism of SVT in patients with preexcitation syndromes, like WPW syndrome (defined by short PR interval, shorter than 0.12 sec, delta wave a.k.a slurred wave on upstroke of QRS complex) present on sinus rhythm ECG
Antidromic AVRT: Renterant form of SVT, when conduction to the ventricles occur through the accessory or "bypass" tract with retrograde conduction through the AV node.
Short PR interval because the impulse bypasses the inbuilt delay of the AV node. As the ventricle is activated early through the accessory pathway, the QRS is widened as the impulse travels in a retrograde manner. The upstroke of the QRS reflects this in what is know as a delta wave. A delta wave is a gradual beginning to the QRS, as opposed to the normal sharp upstroke that occurs with normal conducted electrical activity.
If a patient with an accessory pathway, were to develop AF, the rapid rate can be conducted to the ventricles via the accessory pathways, which has none of the built-in delays of the normal system. This can lead to extremely rapid ventricular rates, which can be deadly.
Junctional tachycardia
Arises from enhanced automaticity within AV junction as the electrical impulses conduct to the ventricle and atrium simultaneously, similar to typical AVNRT, so that retrograde P wave are often buried in QRS complex.
Common in young children after cardiac surgery.
Sinoatrial nodal reentrant tachycardia (SANRT)
Rentrant circuit is localized at least partially within the sinoatrial node itself.
Abrupt onset and termination, triggered by a PAC.
P-wave morphology and axis are identical to the native sinus P wave during normal sinus rhythm.
Ventricular Tachyarrhythmias
Malignant course until proven otherwise
Ventricular arrhythmias are the major cause of sudden cardiac death (SCD).
SCD is defined as death that occurs within 1 hour of the onset of symptoms.
Non-sustained VT is defined as three or more consecutive ventricular complexes >100 bpm that terminates spontaneously within 30 sec without significant hemodynamic consequences or need for intervention.
Sustained monomorphic VT is defined as tachycardia composed of ventricular complexes of a single QRS morphology that lasts longer than 30 sec or requires cardioversion due to hemodynamic compromise.
Polymorphic VT is characterized by everchanging QRS morphology. TdP is a variant of polymorphic VT which is typically preceded by prolonged QT interval in sinus rhythm. Polymorphic VT is usually associated with hemodynamic collapse or instability.
VF is associated with disorganized mechanical contraction, hemodynamic collapse and sudden death.
Etiology:
VT associated with structural heart disease
Ischemia, infarct
Nonischemic CM involving dilatation and fibrosis of myocardium
Inflitrative CM (sarcoidosis, hemochromatosis, amyloid)
Congenital heart disease
Bundle branch reentry VT
VT in the absence of structural heart disease
Inherited channelopathies, such as Brugada syndromeand long QT syndrome
Catechoaminergic polymorphic VT (CPVT)
Idipopathic VT
Most idiopathic VT originate form RVOT
Patients with structural heart disease are much more likely to have VT rather than SVT as the etiology of Wide complex tachycardia (WCT).
If the patients has a PPM, AICD, or wide QRS at baseline (i.e. RBBB, LBBB, IVCD), then suspect for a device mediated WCT.
The tachycardia rate is typically equal to the programmed upper rate limit (URL) of the device. A commonly programmed URL is 120 paces per minute (ppm).
Tachycardia above the URL effectively excludes device-mediated WCT.
Medications: proarrhythmic agents that can prolong QT interval and increase the risk of polymorphic VT or TdP. Class I, III antiarrhythmics, certain ABx, antipsychotics, etc. Check here
Medications that lead to electrolyte abnormalities include loop diruretics, potassium sparing diuretics, ACEIs, ARBs, digoxin toxicity.
Wide QRS induced by the right ventricular pacing leads has an LBBB pattern and is preceded by a short pacing spike seen on ECG. Modern devices don't show this, so do not exclude presence of device mediated WCT by the absence of visible pacing spikes during the tachycardia.
WCT may be due to either SVT with aberrant conduction (presence of BBB) or VT. Differentiation between these two is critical, since medications in the management of SVT (i.e. adenorsine, BB, CCB) can cause severe hemodynamic instability if used in the setting of VT. Therefore, all WCT are considered ventricular in origin until clearly proven otherwise. Other, less common causes of WCT include antidromic AVRT, hyperkalemia-induced arrhythmia, or pacemaker-induced tachycardia.
Ventricular tachycardia. ECG below showing AV dissociation (arrows mark P waves), wide QRS > 200 ms, superior frontal plane axis, slurring of the initial portion of the QRS, and large S wave in V6—all clues to the diagnosis of ventricular tachycardia.
Approach to unstable tachycardia (ACLS)
Suprventricular tachycradia - Esomolol.
Dosage needs to be titrated, using ventricular rate as the guide.
An initial loading dose of 0.5 mg/kg (500 mcg/kg) infused x 1 min duration followed by a maintenance infusion of 0.05 mg/kg/min (50 mcg/kg/min) for the next 4 minutes is recommended. This should give a rough guide with respect to the responsiveness of ventricular rate
After the 4 minutes of initial maintenance infusion (total treatment duration being 5 minutes), depending on the desired ventricular response, the maintenance infusion may be continued at 0.05 mg/kg/min or increased in a step-wise fashion (0.1 mg/kg/min, 0.15 mg/kg/min to a maximum of 0.2 mg/kg/min) with each step being maintained for 4 or more minutes.
If more rapid slowing of ventricular is imperative, the 0.5 mg/kg loading dose infused over a minute may be repeated, followed by a maintenance infusion of 0.1 mg/kg/min x 4 min. Then, depending upon ventricular rate, another (and final) loading dose of 0.5 mg/kg/min infused x 1 min period may be administered followed by a maintenance infusion of 0.15 mg/kg/min. If needed, after 4 min of the 0.15 mg/kg/min maintenance infusion, the maintenance infusion may be increased to a maximum of 0.2 mg/kg/min.
If wide complex, manage as stable VT.
For VT, if pulseless and without BP, manage as VF.
If VT with serious signs and symptoms, consider immediate synch. cardioversion. If stable, start lidocaine, 1 mg/kg IV push, and follow ACLS protocol.
TACHYARRHYTHMIAS
Definition
Cardiac rhythms whose ventricular rate exceeds 100 bpm
Classification: Tachyarrhythmia are broadly classified based on the width of the QRS complex on the ECG:
Narrow-Complex Tachyarrhythmia (QRS <120 ms): Arrhythmia is SVT, originates within or above the AV node and rapidly activates ventricles via the normal His-Purkinje system.
Wide-Complex Tachyarrhythmia (QRS >120 ms): Arrhythmia is VT, originates outside the normal conduction system or travels via an abnormal His-Purkinje system (SVT with aberrancy) activating the ventricles in an abnormally slow manner.
Etiology: Divided into
Disorders of impulse conduction: Reentry responsible for the majority of arrhythmias. Refers to conduction of electrical impulse retrograde into a region in the heart that was initially refractory to antegrade conduction of the electrical impulse, in a normal fashion. This occurs because of differences in the refractory periods of myocardial tissue. Consequently, reentry results in propagation of the electrical impulses around a myocardial circuit sustaining the arrhythmia (e.g. VT).
Disorders of impulse formation: Enhanced automaticity (e.g. acclerated junctional and accelerated idioventricular rhythm) and triggered activity (e.g., long QT syndrome and digitalis toxicity) are other less common mechanisms of tachyarrhythmias.
SINUS ARRHYTHMIA — Not uncommonly, the rate of the SA node varies, and these variations are called sinus arrhythmia. The formal definition of sinus arrhythmia is a variation in the P-P interval by 0.12 sec (120 msec) or more in the presence of normal P waves and the usual PR interval. There are two types of sinus arrhythmia: respiratory or phasic; and nonrespiratory or nonphasic.
Respiratory type — Respiratory sinus arrhythmia is common, usually normal, and decreases with age. In one study, for example, respiratory sinus arrhythmia in older subjects (age 59 to 71 years) was less than 20 percent of that in younger subjects (<31 years of age). A possible reason for this observation is an age-related decrease in carotid distensibility and baroreflex sensitivity, without a change in resting vagal tone.
Respiratory sinus arrhythmia results from changes in autonomic tone during the respiratory cycle. Inspiration reflexively inhibits vagal tone, thereby increasing the sinus rate. With expiration, vagal tone rises to its previous state, and the rate declines. This type of sinus arrhythmia disappears with breath holding. However, stimulation of the carotid baroreceptors by neck suction during breath holding will restore sinus arrhythmia, suggesting that the autonomic changes responsible for sinus arrhythmia can also be due to baroreflex stimulation. Baroreceptor stimulation may result from cyclic alterations in arterial blood pressure induced by the respiratory effect on venous return .
Other factors may contribute to respiratory sinus arrhythmia. These include sympathetic mechanisms, elevations in arterial PCO2 that increase the magnitude of respiratory sinus arrhythmia, probably via a direct effect on the medulla, and drugs that increase vagal tone, such as morphine or digitalis. In contrast, hypocapnia caused by voluntary hyperventilation reduces sinus arrhythmia. Sinus arrhythmia is also reduced in diabetes mellitus, perhaps reflecting autonomic dysfunction.
In some subjects, autonomic change during respiration causes the pacemaker to change location within the SA node, leading to subtle changes in P wave morphology and the PR interval. If depression of the SA node is sufficient, ectopic atrial pacemakers may occur; in this setting, prominently different P waves may be seen.
Respiratory sinus arrhythmia may improve the efficiency of pulmonary gas exchange by matching ventilation to perfusion within each respiratory cycle. The result would be that respiratory sinus arrhythmia could suppress unnecessary heart beats during expiration and ineffective ventilation during the last phases of perfusion, thereby saving cardiac and respiratory energy.. Respiratory sinus arrhythmia can continue in normocapnia during positive-pressure mechanical ventilation in normal unanesthetized humans.
A number of chronic diseases have been associated with respiratory sinus arrhythmia including obesity, diabetes mellitus and hypertension. Some studies suggest that respiratory sinus arrhythmia is the result of disease, while others have documented a reduced respiratory sinus arrhythmia among individual prior to the onset of disease. This suggests that decreased vagal tone may be involved in the pathogenesis of some chronic diseases.
Nonrespiratory type — Nonrespiratory sinus arrhythmia differs in that the acceleration and deceleration of the SA node is not related to the respiratory cycle. This form of sinus arrhythmia can occur in the normal heart, in the diseased heart, or after digitalis intoxication.
Ventriculophasic type — A ventriculophasic sinus arrhythmia occurs most often in patients with third degree AV block, but can also be seen after a compensatory pause induced by a premature ventricular contraction. This arrhythmia is characterized by intermittent differences in the PP intervals based upon their relationship to the QRS complex. The two P waves surrounding a QRS complex have a shortened interval (ie, they occur at a faster rate) when compared to two P waves that occur sequentially without an intervening QRS complex. The cause is not fully understood, but seems to be related to increased filling during the long cycle; this is followed by a forceful systole and increased stroke volume which, in turn, trigger a baroreceptor response. In orthotopic cardiac transplantation, ventriculophasic arrhythmia is absent despite intact vagal innervation to the atrial remnant, which suggests that the lack of pulsatile blood flow in the SA node may contribute to the absence of the ventriculophasic arrhythmias.
Heart rate turbulence (HRT) is based on the evaluation of ventriculophasic arrhythmia following a premature ventricular beat and describes the short term fluctuation in sinus cycle length that follows such a beat. HRT quantifies these heart rate changes by two parameters. The first is turbulence onset, which approximates the amount of sinus acceleration following the premature ventricular beat. The second is turbulence slope, which is the rate of sinus deceleration that follows the sinus acceleration. A large prospective study suggests that HRT has predictive value for risk stratification in individuals who have had an acute myocardial infarction and can identify individuals at an increase risk for subsequent death. HRT also seems to have predictive value for both heart failure and arrhythmic death in patients with class II and III CHF.