Download SVT

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Management of acute coronary syndrome wikipedia , lookup

Antihypertensive drug wikipedia , lookup

Cardiac surgery wikipedia , lookup

Coronary artery disease wikipedia , lookup

Mitral insufficiency wikipedia , lookup

Cardiac contractility modulation wikipedia , lookup

Myocardial infarction wikipedia , lookup

Lutembacher's syndrome wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Arrhythmogenic right ventricular dysplasia wikipedia , lookup

Ventricular fibrillation wikipedia , lookup

Electrocardiography wikipedia , lookup

Heart arrhythmia wikipedia , lookup

Atrial fibrillation wikipedia , lookup

Transcript
Supraventricular
Tachycardia
Teresa Menendez Hood, MD FACC
Presbyterian Hospital of Dallas
Supraventricular Tachycardias
• AV nodal reentry tachycardia
• AV reentry tachycardia - the WPW(WolffParkinson White) Syndrome
• Atrial flutter
• Atrial Fibrillation
• Atrial Tachycardia
• Sinus Tachycardia and Sinus Node Reentry
Atrial Fibrillation
• Unorganized, very rapid electrical foci in the atria
• No contraction of the atria as a whole
• In order to protect the ventricles, the AV node
blocks most of the atrial impulses from conducting
through to the ventricles, thus protecting the
ventricles
• Controlled rate = ventricular rate < 100 beats/min
• Uncontrolled rate = ventricular rate > 100
beats/min
Atrial Fibrillation
• Characteristics of atrial fibrillation:
–
–
–
–
–
Ventricular rhythm is usually irregularly irregular
Average ventricular rate is 160 – 180 beats/min on no drugs
No P waves seen
QRS interval is usually normal (narrow)
If see discrete P waves…think of MAT
• This clinical scenario is a cardiac or pulmonary patient in the ICU.
Thought to be due to a hyperadrenergic state and CCB and helpful.
Atrial Fibrillation
– Control the rate using IV calcium channel blockers or
beta-blockers…IV dig does not work
– If the A-fib is chronic (> 48 hours)
• Chemical cardioversion after a period of anticoagulation
• Electrical cardioversion only after anticoagulation
Atrial fibrillation
accounts for 1/3 of all
patient discharges
with arrhythmia as
principal diagnosis.
6%
PSVT
6%
PVCs
18%
Unspecified
4%
Atrial
Flutter
9%
SSS
34%
Atrial
Fibrillation
8%
Conduction
Disease
10% VT
3% SCD
Data source: Baily D. J Am Coll Cardiol. 1992;19(3):41A.
2% VF
Classification of Atrial Fibrillation
The 3 Ps
• Permanent - Conversion to sinus rhythm not
possible
• Persistent - Capable of being converted to
sinus rhythm
• Paroxysmal - Converts spontaneously to
sinus rhythm
Gallagher MM and Camm AJ Clin Cardiol 1997;20:381
AF: Anticoagulation - General Points
• AF most common significant rhythm disorder
– Prevalence: 1.5%-3% of patients in their 60s
5%-7% of patients in their 70s
15% of patients in their 80s
• AF most potent common risk factor for stroke
– Relative risk = 5
• Patients with AF can be stratified according to
risk of stroke
Feinberg WM e al. Arch Intern Med 1995;155:469 Wolf PA et al. Stroke1991;22:983
AF: Anticoagulation - General Points
• Anticoagulation (INR 2.0 - 3.0) can reduce
risk of stroke by 2/3 1,2
• Aspirin has little effect on risk of stroke due
to AF 3
1 Hylek EM and Singer DE. Arch Intern Med 1994;120:897
2 Hylek EM et al. New Engl J Med 1966;335:540
3 The Atrial Fibrillation Investigators. Arch Intern Med 1997;157:1237
1/98
medslides.com
9
Risk Factors for Stroke in AF
Risk Factor
Prior stroke
Age
Hypertension
Diabetes
Relative Risk (multivariate)
2.5
1.4 (per decade)
1.6
1.7
Absolute Risk
Age < 65 years and no risk factors, “lone AF”: 1%/yr.
All others: 3.5%-8+%/yr lowered to ~1.5%/yr by warfarin
The Atrial Fibrillation Investigators Arch Intern Med 1994;154:1449
1/98
medslides.com
10
Elective Cardioversion of AF
Anticoagulation
• Cardioversion appears to raise risk of embolism
– 1%-5% emboli within hours to weeks
– Anticoagulation well before and after greatly
reduces risk
• Standard guideline for electrical or drug
cardioversion
– INR 2 - 3 for 3 weeks before; and
– INR 2 - 3 for 4 weeks after NSR
– IF AF < 2 days’ duration, no anticoagulation
Laupacle A et al. Chest 1995;108
Prystowsky EN et al. Circulation 1996;1262
Adequate Rate Control
• At office visits
– Apical (not radial) heart rate (sitting):  80 /
min
• On 24-hour Holter monitor
– Goal: average hourly heart rate  80 / min
• Exercise testing
– Inadequate:  85% age-predicated maximum
heart rate in stage I (Bruce) or 3 min of exercise
– Digoxin alone will never control the rate unless the
patient has intrinsic AVN conduction system disease
Tachycardia - Induced Cardiomyopathy
• Chronic tachycardia in otherwise structurally
normal heart as the sole cause of developing
ventricular dysfunction
• Can follow any chronic cardiac tachyarrhythmia
Fenelon G et al. Pacing Clinical Electrophysiol 1996;19:95
Preference for Acute
Cardioversion
• DC Cardioversion
• i.v. Ibutilide
• Other:
– Oral Flecainide
– Oral Propafenone
– i.v. Procainamide
Preference for Acute Cardioversion
i.v. Ibutilide
•
•
•
•
•
•
•
QTc  460 msec
Short duration of AF (<30 days)
No clinical CHF. K and Mg levels OK
Anesthesia risk (e.g., COPD)
Patient preference
Acute efficacy - flutter (63%), fib (31%)
Caution: risk of polymorphic VT (8%)
Stambler BS, et al. Circulation 1996; 94:1613-1621
Long term treatment
• Beyond the scope of this talk
• Guided by patient symptoms
• AFFIRM trial did not show any benefit of
NORMAL SINUS RHYTHM versus AFIB
with rate control in patients who had
minimal symptoms
• Ablation for AFIB is guided by patients’
symptoms and drug failures
Atrial Flutter
• Usually a single, irritable foci in the atria (right)
• AV node protects the ventricles by blocking some of the
atrial impulses (decremental conduction)
• P waves take on a “sawtooth” appearance and are called
F waves or flutter waves
– Atrial rhythm and ventricular response are usually regular
– Atrial rate 250-350 beats/min. Ventricular rate varies
depending on the number of impulses the AV node is blocking
– No P waves or PR interval
– QRS normal width or with aberrancy
Atrial Flutter
• Treatment:
– Same as atrial fibrillation but often harder to slow the
ventricular rate
– Long term treatment is ablation and NOT drugs!
RF Ablation of Atrial Flutter
• Atrial flutter involves a macro-reentry circuit within the
right atrium.
• Critical areas of conduction within the right atrium are
necessary to sustain atrial flutter.
• RF ablation of conduction within such critical sites (most
commonly the inferior vena cava-tricuspid valve isthmus)
abolishes atrial flutter in 85% of cases.
Cosio FG. Am J Cardiol. 1993;71:705-709.
Diagram of Atrial Flutter Circuit Within Right
Atrium
Cosio FG. Am J Cardiol. 1993;71:705-709.
Inferior vena cava tricuspid valve isthmus
Differential Diagnosis of
Wide-Complex Tachycardia
• VT
• SVT with aberrancy (atrial fibrillation/flutter)-i.e.
BB Block
• Antidromic AV reentry –i.e. antegrade via WPW
accessory pathway
• Atrial fibrillation, atrial flutter, atrial tachycardia,
or AV nodal reentry in setting of WPW with rapid
conduction down accessory pathway that is
activated as a bystander-I.e. not an integral part of
the circuit.
Narrow QRS
Wide QRS - BBB
(Aberrant conduction)
AVN
A
B
HB
RB
LB
Wide QRS - VT
Wide QRS - Preexcitation
(Conduction via AP)
C
D
Akhtar M. In:Zipes and Jalife. Cardiac Electrophysiology from Cell to Bedside. 1990:636.
Key ECG Signs
•
•
•
•
•
Atrial activity
QRS configuration
R-R cycle length
Aberrant ventricular conduction
Response to vagal maneuvers
An EKG you will see on the
Boards………..
• This has been on every Board exam I have
ever taken. Please do give AVN blockers
for this!When in doubt, treat as if you
thought this was VT.
Atrial Fibrillation with
Preexcitation
Electrocardiographic
Differentiation of VT vs. SVT
with Aberrancy
• Clinical history – if the patient has had an MI
in the past?…it is VT until proven otherwise
• AV dissociation
• QRS morphology
• QRS axis
• Fusion beat
• Capture beat
A-V Dissociation, Fusion, and
Capture Beats in VT
V1
E
ECTOPY
F
C
FUSION
Fisch C. Electrocardiography of Arrhythmias. 1990;134.
CAPTURE
ECG Distinction of VT from SVT with
Aberrancy
Favors VT
Favors SVT
with Aberrancy
Duration
RBBB: QRS > 0.14 sec.
LBBB: QRS > 0.16 sec.
< 0.14 sec.
< 0.16 sec.
Axis
QRS axis -90° to ±180°
Normal
ECG Distinction of VT from SVT with
Aberrancy
Favors VT
Morphology
Precordial concordance
If LBBB:
V1 duration > 30 ms
S wave > 70 ms
S wave notched or slurred
V6: qR or QR
If RBBB:
V1: monophasic R wave
qR
If triphasic, R > R1
V6: R < S
Favors SVT
with Aberrancy
R wave
R < R1
Sinus Tachycardia
• Sinus node is still the pacemaker, but the rate is
accelerated for some physiologic reason:
– Rhythm is regular
– Rate > 100 beats/minute
– P wave, PR interval, and QRS complex are all normal
• Can look like Sinus Node Reentry – paroxysmal
and less than 160 BPM; incidence of ~10% of all
PSVT’s
Sinus Tachycardia
• Treatment:
– Alleviate the underlying cause-anemia, pheo, hyperthyroid…
– Could be inappropriate ST- a type of autonomic dysfunction with HR
consistently above 120
Paroxysmal Supraventricular
Tachycardia
• Repeated episodes of tachycardia with an
abrupt onset and ending (paroxysmal)
• SVT is usually due to a reentry mechanism.
• Could also be to abnormal automaticity or
triggered activity but would have more of a
warm-up and cool-down effect.
Supraventricular Tachycardia
• Characteristics:
– Rhythm is regular
– Rate 140-220 beats/minute
– P waves may be buried in the QRS or the T wave
and may differ in morphology from sinus P waves
– PR and QRS interval may be normal or prolonged.
Supraventricular Tachycardia
– Long term treatment is with ablation in most cases
– Response to vagal maneuvers is helpful
– Acutely: meds used to decrease the rate or convert the
patient to NORMAL SINUS RHYTHM: Adenosine, IV
Verapamil or Esmolol
– If patient is unstable:
• Electrical cardioversion
Pearls
• ST depression is common during SVT and is not a
marker of serious ischemia
• If the first dose of Adenosine does not work? Then
add 6mg to the amount and give again (6-1218)…do not repeat the same dose. (If given via
central line then 3-6-9-12)
• Adenosine may put the patient in AFB…be ready
to cardiovert.
Classification of PSVT
• Short R-P
– AVRT(slow-fast)
– AVNRT
• Long R-P
– Atypical forms of the AVNRT (fast-slow)or
AVRT(usually will have a negative P wave in 2,3,avf)
– Most atrial tachycardias, SNRT
– PJRT
Atrial Tachycardia
• Reentry, Automaticity and Triggered (rare)
Activity have been found as causes
• Rates 120 to 150
• Usually 1:1 AVN conduction and persistence
despite AV block
• Usually from right atria (Ring of Fire)
• Can be seen as an incisional tachycardia from
previous surgery..i.e. ASD repair
• May see remission in children so do not attempt
ablation until adulthood.
AVN reentry
• Most common from of PSVT
• Can occur at any age and more common in women
• Typical form is down the slow and up the fast
pathway in the AVN region.
• Adenosine is the drug on choice for conversion.
Need to be careful about pts with reactive airway
disease and those on persantine. It may not work
in pts with theophylline.
WPW
• Pre-excitation affects 3/1000 patients on
routine screening….not all develop PSVT
• Antegrade (delta wave) and retrograde
conduction
• More common in men
• Most present in young adulthood
• 15% incidence of AFIB
• Multiple pathways in 10%