Download Supraventricular Causes of Palpitations

PALPITATIONS:
From Benign Symptom
to Ominous Warning Sign
Randy Zarraga, M.D.
Staff Cardiologist / Electrophysiologist
VA Portland Health Care System
Assistant Professor
OHSU Knight Cardiovascular Institute
Disclosures
None
Outline
Definition
Epidemiology
Pathophysiology
Etiologies ––– Prognosis
History and physical exam
Diagnostic tools
Treatment options
Palpitations: Definition
Unpleasant awareness of the forceful, rapid, and/or irregular beating of
the heart
Normally, heart beats:
are not perceived at rest
may be perceived when lying on the left side, especially in a
quiet environment
may be perceived during or immediately after intense physical
activity or emotional stress
(physiologic palpitations)
Epidemiology
Account for ~16% of symptoms that prompt patients to visit their
health provider in clinic
Second only to chest pain as the presenting complaint for
specialized cardiac evaluation
Kroenke K. Arch Intern Med 1990.
Pathophysiology
Sensory receptors
Myocardial mechanoreceptors?
Pericardial mechanoreceptors?
Peripheral mechanoreceptors?
Baroreceptors in aortic arch and carotid sinus?
Afferent parasympathetic and sympathetic pathways?
Brain centers that process the afferent stimuli
Subcortical areas (thalamus, amygdala)?
Base of frontal lobes?
In some individuals, cardiac arrhythmias are completely asymptomatic.
Prognosis
Benign in most individuals
Weber and Kapoor, 1996:
Prospective study of 190 pts presenting with
palpitations to a university medical center
Cardiac etiology: 43%
1-year mortality rate: 1.6%
1-year stroke rate: 1.1%
Occasionally, a manifestation of a serious cardiac disorder
and/or life-threatening arrhythmia
Weber BE, Kapoor WN. Am J Med 1996.
Palpitations: Etiologies
1.
Cardiac arrhythmias
Supraventricular / ventricular extrasystoles
Supraventricular / ventricular tachycardias
Anomalies in the function and/or programming of pacemakers and ICDs
Bradyarrhythmias (severe sinus bradycardia, sinus pauses, paroxysmal
AV block)
* rarely perceived as palpitations
European Heart Rhythm Association Position Paper, 2011.
Palpitations: Etiologies
1.
Cardiac arrhythmias
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2.
Supraventricular / ventricular extrasystoles
Supraventricular / ventricular tachycardias
Anomalies in the function and/or programming of pacemakers and ICDs
Bradyarrhythmias (severe sinus bradycardia, sinus pauses, paroxysmal
AV block)
* rarely perceived as palpitations
Structural heart diseases
Mitral valve prolapse
Severe MR, severe AI, mechanical prosthetic valves
Atrial myxoma
Heart failure / cardiomegaly
Hypertrophic cardiomyopathy
Congenital heart diseases with significant shunt
European Heart Rhythm Association Position Paper, 2011.
Palpitations: Etiologies
3.
Psychosomatic disorders
Depression
Somatization disorders
Anxiety
Panic attack
DSM-IV Diagnostic Criteria for Panic Attack
A discrete period of intense fear or discomfort, in which >4 of the following symptoms
developed abruptly and reached a peak within 10 minutes
Palpitations, pounding heart, or
accelerated heart rate
Sweating
Trembling or shaking
Sensations of shortness of breath or smothering
Feeling of choking
Chest pain or discomfort
Nausea or abdominal distress
Feeling dizzy, unsteady, lightheaded, or faint
Derealization or depersonalization
Fear of losing control or going crazy
Fear of dying
Paresthesias
Chills or hot flushes
European Heart Rhythm Association Position Paper, 2011.
Palpitations: Psychiatric Etiologies
No optimal screening tool for psychiatric causes of palpitations
Some features might be suggestive
Begin and end gradually
Numerous associated nonspecific symptoms
Tingling in the hands and face
Lump in the throat
Mental confusion
Agitation
Atypical chest pain
Pts may not always be able to discern whether the palpitations preceded
the feeling of anxiety or panic, or followed it
Pts can have both – psychosomatic disorder and arrhythmia
Palpitations: Psychiatric Etiologies
Lessmeier et al., 1997:
Retrospective study of 107 consecutive patients with reentrant PSVT
In 54% of pts, symptoms were attributed to panic, anxiety, or stress
Median of 3.3 years to diagnose PSVT
67% of patients fulfilled DSM-IV criteria for panic disorder
Psychiatric disorders should not be accepted as the sole etiology of palpitations
without performing some tests to work up a cardiac etiology.
Lessmeier TJ et al. Arch Intern Med 1997.
Palpitations: Etiologies
4.
Systemic causes
Hyperthyroidism
Pheochromocytoma
Fever
Anemia
Hypovolemia
Orthostasis
Hpoglycemia
AV fistula
Mastocytosis
Postmenopause
Pregnancy
Heart rate
Cardiac contractility
Stroke volume
European Heart Rhythm Association Position Paper, 2011.
Palpitations: Etiologies
5.
Medical and recreational drugs
Sympathomimetic agents in inhalers
Vasodilators (e.g., hydralazine)
Anticholinergic drugs
Recent discontinuation of beta-blockers (“rebound effect”)
Alcohol, nicotine, caffeine
Amphetamines, heroin, LSD, cannabis
European Heart Rhythm Association Position Paper, 2011.
Cardiac Arrhythmias
Single ectopic beats or couplets
PAC
Thump
Skipped
beat
Interpolated PVC
Cardiac Arrhythmias
Single ectopic beats or couplets
Ventricular
bigeminy
Ventricular
trigeminy
Ventricular
couplet
Cardiac Arrhythmias
Ventricular tachyarrhythmias
VT
Sustained VT – lasts at least 30 seconds,
or <30 seconds but causes
hemodynamic collapse
Cardiac Arrhythmias
Ventricular tachyarrhythmias
VT
Torsades
de pointes
VF
Ventricular Ectopy
PVCs
Seen in up to 80% of people who wear a 24-h Holter but are otherwise
apparently healthy
Frequently asymptomatic or minimally symptomatic
Questions when faced with a patient with frequent PVCs
1. Overtly symptomatic?
2. Underlying structural heart disease?
3. Malignant PVCs that tend to trigger
polymorphic VT or VF?
Prognosis?
Should the PVCs
be suppressed /
eliminated?
Ventricular Ectopy
Bothersome symptoms clearly attributable to frequent PVCs
Suppress or eliminate PVCs
by medical therapy or catheter ablation
Ventricular Ectopy
Frequent PVCs in normal hearts
Conflicting data on whether or not PVCs are associated with increased mortality
Asymptomatic PVCs
No specific tx
No convincing data that PVC suppression in this population leads to
longer survival
Idiopathic PVCs / VT
Frequent monomorphic PVCs or VT in a structurally normal heart
Normal RV and LV dimensions, wall thickness, and systolic function
No prior MI
Excellent prognosis
RV outflow tract (RVOT) PVCs
III
aVF
II
Idiopathic PVCs / VT
Frequent monomorphic PVCs or VT in a structurally normal heart
Normal RV and LV dimensions, wall thickness, and systolic function
No prior MI
Excellent prognosis
Nonsustained RVOT VT
III
aVF
II
Idiopathic PVCs / VT
Other sites in the ventricles that have a
predilection for focal firing like the RVOT
LV outflow tract, including aortic cusps
Mitral and tricuspid annuli
Papillary muscles
Moderator band in the RV
Ventricular Ectopy
Frequent PVCs in normal hearts
Ventricular Ectopy
Frequent PVCs in abnormal hearts
Ventricular Ectopy
PVCs after a myocardial infarction
If persistent beyond 2–3 days after MI, frequent, multifocal:
associated with increased risk of mortality
Beta-blockers to reduce risk of reinfarction and sudden cardiac death:
also help to suppress PVCs
Outside of beta-blockers, be careful about using drugs to suppress these PVCs
Class I antiarrhythmic drugs (Na+ channel blockers):
increase mortality when used after an MI
Ventricular Ectopy
Frequent PVCs in patients with a cardiomyopathy
Which came first – PVCs or cardiomyopathy?
Patients with a cardiomyopathy can develop frequent PVCs
Reverse situation: frequent PVCs can sometimes cause a cardiomyopathy
Normal LV function Æ frequent PVCs Æ LV systolic dysfunction
Elimination of PVCs by ablation Æ LV systolic function normalizes in some
PVCs often arise from the same regions of the ventricles that have
a predilection for causing idiopathic PVCs or VT
Ventricular Ectopy
Frequent PVCs in patients with a cardiomyopathy
Frequent PVCs that cause a cardiomyopathy
How and why?
What burden of PVCs is required to cause a cardiomyopathy?
10,000 – 20,000 PVCs / day (10 – 20% of total heart beats / day)
? Some can have 20,000 / day and maintain normal LV function
? Some can have 5,000 / day and develop LV systolic dysfunction
RVOT PVCs / VT
Often associated with normal hearts and benign
Can also be seen in arrhythmogenic RV cardiomyopathy or dysplasia (ARVC / D),
a rare genetic disorder in which cardiac muscle gets replaced with fibrofatty
tissue and that predisposes to VT / VF
RV
LV
“Malignant” PVCs
Monomorphic PVCs that trigger polymorphic VT or VF
Can happen in normal and abnormal hearts
Tightly coupled PVC
Inheritable Arrhythmia Syndromes
Long QT syndrome
Short QT syndrome
Structurally normal heart
Brugada syndrome
Catecholaminergic polymorphic VT (CPVT)
Hypertrophic cardiomyopathy
Atrial fibrillation
Affected individuals: generally children, adolescents, or young adults
Predispose to polymorphic VT or VF
Manifestation: presyncope, syncope, or sudden cardiac arrest
Supraventricular Causes of Palpitations
Paroxysmal supraventricular tachycardia (PSVT)
Paroxysmal: onset and termination are sudden
(gradual in sinus tachycardia)
Regular
(distinct from paroxysmal atrial fibrillation)
Supraventricular Causes of Palpitations
PSVT
1. AV nodal reentrant tachycardia
Atrial
tachycardia
(AVNRT)
Accessory
pathway
(AVNRT)
2. AV reciprocating tachycardia
(AVRT)
3. Atrial tachycardia
* Atrial flutter with 2:1 AV block *
AVRT
Supraventricular Causes of Palpitations
Atrial flutter
Typical atrial flutter
Supraventricular Causes of Palpitations
Atrial fibrillation
Most common sustained cardiac rhythm disorder in clinical practice
Supraventricular Causes of Palpitations
AF
AFL
Diseased
atria
Supraventricular Causes of Palpitations
Generally not life-threatening
A nuisance – come on unpredictably, accompanied by dyspnea, fatigue, lightheadedness, etc.
Syncope – uncommon, but can occur with very fast heart rates, severe structural heart
disease, or acute vasodilation (vagal response)
AF and AFL
Can persist for a long time and cause persistent symptoms
Frequent / prolonged periods of tachycardia Æ cardiomyopathy
Associated with increased risk of ischemic stroke (CHA2DS2-VASc score)
Supraventricular Causes of Palpitations
WPW
AF
Pre-excited AF
Accessory pathway with a short refractory period
Rare cause of
syncope and
sudden cardiac
arrest in children
and adolescents
with WPW
syndrome
Supraventricular Causes of Palpitations
Postural Orthostatic
Tachycardia Syndrome (POTS)
Frequent symptoms while standing –
lightheadedness, palpitations, weakness, fatigue
Increase in HR by >30, from recumbent to standing
No orthostatic hypotension
Manifestation of dysautonomia, deconditioning,
hypovolemia, hyperadrenergic stimulation,
anxiety, or somatic hypervigilance
Inappropriate Sinus
Tachycardia (IST)
Sinus rate >100 bpm at rest
(mean 24-h HR >90)
No identifiable primary or reversible
cause of tachycardia
Distressing palpitations
Increased sinus node automaticity or
sinus node beta-receptor sensitivity
Affected individuals are often young females
Not associated with increased mortality or tachycardia-mediated cardiomyopathy
Finding a therapy that works can be challenging
Regular exercise?
Volume repletion?
Multidisciplinary team approach
E-blocker?
Ivabradine: blocks an ion channel
responsible for sinus node automaticity
Anomalies in the Function and/or Programming of Pacemakers or ICDs
Pacemaker-mediated tachycardia
Device with 2 leads (A and V)
Rapid pacing, typically at 110-130 bpm
Pacemaker syndrome
Often due to loss of physiologic timing of
atrial and ventricular contractions
Dyspnea, fatigue, palpitations, etc.
Inappropriate positioning or migration of a lead
Stimulation of pectoral muscle or diaphragm
History
History
Age
Prevalence of certain arrhythmias tends to vary with age
Patients with PSVT
AT
AVNRT
AVRT
Porter MJ et al. Heart Rhythm 2004.
AF and reentrant VT are typically rhythms of older people with structural heart
disease.
History
Description
Implication
“Flip-flopping in chest”
“Feeling the heart stop and then start again, as
though there was a skipped beat”
PACs or PVCs
Sustained rapid fluttering
SVT or VT
Have pt tap out rhythm with fingers:
Irregular?
AF, AFL with variable AV block
History
Description
Implication
Pounding in the neck
Arrhythmia where RA contracts
against a closed tricuspid valve
Intermittent
AV dissociation:
Frequent PVCs
VT
Complete heart block
Physical exam:
Cannon a waves
Continuous
AV dyssynchrony
(simultaneous A and V):
AVNRT
AVRT
Physical exam:
“Frog sign”
History
Polyuria during or after a bout of palpitations
Atrial tachyarrhythmias like AF
Secretion of atrial natriuretic peptide (ANP)
Occurrence during states of catecholamine excess (exercise, stress, emotional
excitement)
SVTs and VT
Inheritable arrhythmia syndromes
Inheritable arrhythmia syndrome
Trigger of VT / VF
Long QT syndrome type 1
Exercise
Catecholaminergic polymorphic VT
Exercise
Long QT syndrome type 2
Emotionally startling experiences
History
Termination of sustained palpitations by vagal maneuvers (Valsalva)
Strongly suggests an SVT that relies on the AV node for its mechanism:
AVNRT or AVRT
Also seen with certain types of atrial tachycardia and idiopathic VT
Presyncope or syncope
Not a definitive way of differentiating SVT from VT
Should nonetheless prompt a search for VT / VF / structural heart disease
Family hx of recurrent syncope or premature sudden cardiac arrest –
relevant when looking for an inheritable arrhythmia syndrome of VT / VF
Diagnostic Tests
12-Lead ECG
Diagnostic Tests
12-Lead ECG
Delta wave, short PR interval,
+ abnormal-looking ST/T wave --- accessory pathway
Diagnostic Tests
12-Lead ECG
Large voltages in precordial leads, dagger-like Q waves in inferolateral leads --hypertrophic cardiomyopathy?
Diagnostic Tests
12-Lead ECG
Large voltages and T-wave inversions in precordial leads --apical hypertrophic cardiomyopathy?
Diagnostic Tests
12-Lead ECG
Right or left atrial abnormality --atrial disease that can predispose to AF/AFL or AT
Diagnostic Tests
12-Lead ECG
Pathologic Q waves --old myocardial infarction, substrate for reentrant VT
Diagnostic Tests
12-Lead ECG
Prolonged QTc (>450 ms in males, >470 ms in females)?
QT 540 ms, QTc 675 ms
Diagnostic Tests
Exercise stress test
For patients whose palpitations are
reproducibly triggered by physical
exertion
Echocardiogram
To look for structural heart disease
Diagnostic Tests
Ambulatory ECG Monitoring
Holter monitor (24, 48, or 72 hours)
Continuously records and saves the pt’s rhythm
throughout the monitoring period
Diary for pt to record symptoms
Most useful in pts who feel palpitations everyday or
every other day
Assess adequacy of rate control during AF
Assess burden of PVCs
Diagnostic Tests
Persistent AF:
adequate rate control?
Diagnostic Tests
Ambulatory ECG Monitoring
External cardiac ambulatory telemetry (ECAT)
Up to 30 days of continuous rhythm recording (extended Holter)
Burden of AF over an extended period of time
Diagnostic Tests
Ambulatory ECG Monitoring
30-Day event monitor
Only records the rhythm a few minutes before and after a trigger
Patient trigger
Activate monitor during symptoms
Transmit recording by landline or cel phone
Automatic trigger
Device programmed to automatically record certain abnormalities –
e.g., pause >3 sec, tachyarrhythmia >150 bpm, irregular rhythm
Most useful for symptoms that occur infrequently (e.g., a few times a month)
Diagnostic Tests
Ambulatory ECG Monitoring
Patch
No wires or box
Convenient, especially for pts who are very active
and get their arrhythmias during exertion
Data cannot be transmitted over the phone
Needs to be mailed for data review
Not advisable when looking for a potentially
dangerous arrhythmia (long pauses, VT)
Diagnostic Tests
Ambulatory ECG Monitoring
Implantable loop recorder (ILR)
For patients whose symptoms occur rarely –
e.g., once or twice a year
Up to 3 years of rhythm monitoring
Data can be transmitted wirelessly
More high-yield than conventional monitoring in
screening for AF in patients with cryptogenic
stroke
Diagnostic Tests
Ambulatory ECG Monitoring
Pacemakers and ICDs
Record tachyarrhythmias with rates beyond a programmed value
Interrogation can help with symptom-rhythm correlation
Diagnostic Tests
Ambulatory ECG Monitoring
In general, goal is to check if pt’s symptoms correlate with any
brady- or tachyarrhythmia
Definitive situations:
+ arrhythmia --- correlates with symptoms
+ symptoms --- no arrhythmia
Otherwise equivocal
Therapies
Discussion with
cardiologist /
electrophysiologist
Reassurance
Watchful waiting
Conservative
Valsalva
maneuver
as needed
Aggressive
Drug
therapy
Catheter
ablation
Device
therapy
Therapies
Discussion with
cardiologist /
electrophysiologist
Conservative
Reassurance
Watchful waiting
Aggressive
Valsalva
maneuver
as needed
Drug
therapy
Catheter
ablation
Device
therapy
Occasional PVCs
Therapies
Discussion with
cardiologist /
electrophysiologist
Reassurance
Watchful waiting
Conservative
Valsalva
maneuver
as needed
Infrequent,
mildly
symptomatic
PSVT
Aggressive
Drug
therapy
Catheter
ablation
Device
therapy
Therapies
Discussion with
cardiologist /
electrophysiologist
Reassurance
Watchful waiting
Conservative
Aggressive
Valsalva
maneuver
as needed
Drug
therapy
Rate-slowing drugs /
AV nodal blockers
Catheter
ablation
Device
therapy
Membrane-active
antiarrhythmic drugs
Therapies
Discussion with
cardiologist /
electrophysiologist
Reassurance
Watchful waiting
Conservative
Valsalva
maneuver
as needed
Aggressive
Drug
therapy
Catheter
ablation
Device
therapy
Therapies
Discussion with
cardiologist /
electrophysiologist
Reassurance
Watchful waiting
Conservative
Aggressive
Valsalva
maneuver
as needed
Drug
therapy
Catheter
ablation
Device
therapy
ICD
Pacemaker
Therapies
Discussion with
cardiologist /
electrophysiologist
Reassurance
Watchful waiting
Conservative
Valsalva
maneuver
as needed
Aggressive
Drug
therapy
How serious or life-threatening is the arrhythmia?
How much is it affecting the pt’s quality of life?
What are the relative efficacies of the various therapies for that
particular arrhythmia?
What are the side effects of the drug or potential complications from
the procedure, what are the chances of these happening, and
how does the pt perceive these problems?
Catheter
ablation
Device
therapy
Questions ?