Premature Complexes
A. Premature atrial complexes
- This early beat arises within the atria, firing on its own.
- Causes include adrenergic excess, drugs, alcohol, tobacco, electrolyte imbalances,
ischemia, and infection. - On ECG, look for early P waves that differ in morphology from the normal sinus
P wave (because these P waves originate within the atria and not the sinus node). - QRS complex is normal because conduction below the atria is normal. There is
usually a pause before the next sinus P wave. - Premature atrial complexes (PACs) are found in more than 50% of normal adults
who undergo Holter monitoring and are of no significance in a normal heart, but
may be a precursor of ischemia in a diseased heart. - May cause palpitations or give rise to PSVTs.
7. Usually asymptomatic and do not require treatment. Monitor for increased fre
quency. If symptomatic (e.g., palpitations),
β-blockers may be helpful.
Premature ventricular complexes
- This early beat fires on its own from a focus in the ventricle and then spreads to
the other ventricle (Figure 1-9). - PVCs can occur in patients with or without structural heart disease. Causes
include hypoxia, electrolyte abnormalities, stimulants, caffeine, medications, and
structural heart disease. - Since conduction is not through normal conduction pathways, but rather through
ventricular muscle, it is slower than normal, causing a wide QRS. - Wide, bizarre QRS complexes followed by a compensatory pause are seen; a
P wave is not usually seen because it is “buried” within the wide QRS complex. - PVCs appear in more than 50% of men who undergo 24-hour Holter monitoring.
- Most patients are asymptomatic. Some patients may have palpitations and dizziness related to PVCs. If symptomatic, β-blockers may be used.
- Presence of PVCs in patients with normal hearts is associated with increased
mortality. - If a patient is found to have frequent PVCs, workup for underlying structural
heart disease should be initiated which may require specific treatment. - Patients with frequent, repetitive PVCs and underlying heart disease are at
increased risk for sudden death due to cardiac arrhythmia (especially VFib). Order
an electrophysiologic study because patients may benefit from an ICD.
Tachyarrhythmias
Atrial Fibrillation
A. General characteristics - Multiple foci in the atria fire continuously in a chaotic pattern, causing a totally
irregular, rapid ventricular rate. Instead of intermittently contracting, the atria
quiver continuously. - Atrial rate is over 400 bpm, but most impulses are blocked at the AV node so ventricular rate ranges between 75 and 175.
- Patients with AFib and underlying heart disease are at a markedly increased risk
for adverse events, such as thromboembolism and hemodynamic compromise.
B. Causes - Heart disease: CAD, MI, HTN, mitral valve disease
- Pericarditis and pericardial trauma (e.g., surgery)
- Pulmonary disease, including PE
- Hyperthyroidism or hypothyroidism
- Systemic illness (e.g., sepsis, malignancy, DM
- Stress (e.g., postoperative)
- Excessive alcohol intake (“holiday heart syndrome”)
- Sick sinus syndrome
- Pheochromocytoma
C. Clinical features - Fatigue and exertional dyspnea
- Palpitations, dizziness, angina, or syncope may be seen
- An irregularly irregular pulse
- Blood stasis (secondary to ineffective contraction) leads to formation of intramural
thrombi, which can embolize to the brain.
D. Diagnosis - ECG findings: Irregularly irregular rhythm (irregular RR intervals and excessively
rapid series of tiny, erratic spikes on ECG with a wavy baseline and no identifiable
P waves)
E. Treatment - Acute AFib in a hemodynamically unstable patient: Immediate electrical cardioversion to sinus rhythm (Figure 1-10; see Clinical Pearl 1-11)
- Acute AFib in a hemodynamically stable patient
a. Rate control
• Determine the pulse in a patient with AFib. If it is too rapid, it must be treated. Target rate is 60 to 100 bpm.
• β-Blockers are preferred. Calcium channel blockers are an alternative
• If left ventricular systolic dysfunction is present, consider digoxin or amiodarone (useful for rhythm control).
b. Cardioversion to sinus rhythm (after rate control is achieved)
• Candidates for cardioversion include those who are hemodynamically unstable, those with worsening symptoms, and those who are having their first
ever case of AFib.
• Electrical cardioversion is preferred over pharmacologic cardioversion.
Attempts should be made to control ventricular rate before attempting DC
cardioversion.
• Use pharmacologic cardioversion only if electrical cardioversion fails or is not
feasible: Parenteral ibutilide, procainamide, flecainide, sotalol, or amiodarone
are choices.
c. Anticoagulation to prevent embolic cerebrovascular accident (CVA)
• If AFib present >48 hours (or unknown period of time), risk of embolization
during cardioversion is significant (2% to 5%). Anticoagulate patients for
3 weeks before and 4 weeks after cardioversion.
• An INR of 2 to 3 is the anticoagulation goal range.
• To avoid waiting 3 weeks for anticoagulation, obtain a transesophageal echocardiogram (TEE) to image the left atrium (LA). If no thrombus is present,
start IV heparin and perform cardioversion within 24 hours. Patients still
require 4 weeks of anticoagulation after cardioversion.
- Chronic AFib
a. Rate control with a β-blocker or calcium channel blocker
b. Anticoagulation
• Patients with “lone” AFib (i.e., AFib in the absence of underlying heart disease
or other cardiovascular risk factors) under age 60 do not require anticoagulation because they are at low risk for embolization (aspirin may be appropriate).
• Treat all other patients with chronic anticoagulation (warfarin).
Cardioversion Versus Defibrillation
Cardioversion
• Delivery of a shock that is in synchrony with the QRS complex: Purpose is to terminate certain dysrhythmias such as PSVT or VT; an electric shock during T wave can cause Vfib, so the shock is timed not to hit the
T wave.
• Indications: AFib, atrial flutter, VT with a pulse, SVT
Defibrillation
• Delivery of a shock that is not in synchrony with the QRS complex: Purpose is to convert a dysrhythmia to
normal sinus rhythm.
• Indications: VFib, VT without a pulse.
Automatic Implantable Defibrillator
• Device that is surgically placed: When it detects a lethal dysrhythmia, it delivers an electric shock to defibrillate. It delivers a set number of shocks until the dysrhythmia is terminated.
• Indications: VFib and/or VT that is not controlled by medical therapy