cardiac arrhythmias Flashcards
what is cardiac arrhythmia?
refers to any variation in the normal heartbeat, includes disturbances in rhythm, rate, or the conduction pattern of the heart.
what happens electrically to the beating heart?
The normal pattern of sequential depolarization involves the structures of the heart in the following order: (1) sinoatrial (SA) node, (2) atrioven- tricular (AV) node, (3) bundle of His, (4) right and left bundle branches, and nally (5) subendocardial Purkinje network.13 The electrocardiogram (ECG) is a recording of this electrical activity. The primary anatomic pace- maker for the heart is the SA node, a crescent-shaped structure 9 to 15 mm long that is located at the junction of the superior vena cava and the right atrium. The SA node regulates the functions of the atria and is respon- sible for production of the P wave (atrial depolarization) on the ECG (Figure 5-2). The ends of the sinus nodal bers connect with atrial muscle bers. The generated action potential travels along the muscle bers (inter- nodal pathways) and eventually arrives at and excites the AV node, which serves as a gate that regulates the entry of atrial impulses into the ventricles. It also slows the conduction rate of impulses generated within the SA node. From the AV node, impulses travel along the AV bundle (His bundle) within the ventricular septum, which divides into right and left bundle branches. The bundle branches then terminate in the small Purkinje bers, which course throughout the ventricles and become con- tinuous with cardiac muscle bers. Simultaneous depo- larization of the ventricles produces the QRS complex on ECG. The T wave is formed by repolarization of the ventricles. Repolarization of the atria occurs at about the same time as depolarization of the ventricles and thus is usually obscured by the QRS wave.13
what are disorders of the conductivity?
Disorders of conductivity (block or delay) paradoxi- cally may lead to rapid cardiac rhythm through the mech- anisms of reentry. Reentry arrhythmias occur when accessory or ectopic pacemakers reexcite previously depolarized bers before they would become depolarized in the normal sequential impulse pathway, typically pro- ducing tachyarrhythmias. The type of arrhythmia may suggest the nature of its cause. For example, paroxysmal atrial tachycardia with block suggests digitalis toxicity.14
How are arrhythmias classified?
Arrhythmias are classi ed by site of origin (Box 5-1). Any arrhythmia that arises above the bifurcation of the His bundle into right and left bundle branches is classi- ed as supraventricular.19 Supraventricular cardiac arrhythmias may be broadly categorized into tachyar- rhythmias and bradyarrhythmias.
what is sinus arrhythmia? sinus tachycardia? sinus bradycardia?
Sinus arrhythmia. Sinus arrhythmia is characterized by phasic variation in sinus cycle length.14 In the respiratory type, heart rate increases with inhalation and decreases with exhalation. It is seen predomi- nantly in the young and re ects variations in para- sympathetic and sympathetic signals to the heart and is considered a normal event. Nonrespiratory sinus arrhythmia is unrelated to respiratory effort and is seen in digitalis intoxication.
Sinus tachycardia. Tachycardia in an adult is de ned as a heart rate greater than 100 beats per minute, with otherwise normal ndings on the ECG.14 The rate usually is between 100 and 180 beats per minute. This condition most often is a physiologic response to exercise, anxiety, stress, or emotion. Pathophysi- ologic causes include fever, hypotension, hypoxia, infection, anemia, hyperthyroidism, and heart failure. Drugs that may cause sinus tachycardia include atro- pine, epinephrine, alcohol, nicotine, and caffeine. Sinus bradycardia. Bradycardia is de ned as a heart rate less than 60 beats per minute, with an otherwise normal ECG tracing.14 It often coexists with a sinus arrhythmia. It is relatively common among well- conditioned athletes and healthy young adults and decreases in prevalence with advancing age. Patho- physiologic causes of bradycardia include intracra- nialtumor,increasedintracranialpressure,myxedema, hypothermia, and gram-negative sepsis. Bradycardia may occur during vomiting and vasovagal syncope and as the result of carotid sinus stimulation. Drugs that may cause bradycardia include lithium, amioda- rone, beta blockers, clonidine, and calcium channel blockers.
disturbances of atrial rhythm?
Premature atrial complexes. Impulses arising from ectopic foci anywhere in the atrium may result in premature atrial beats. Premature atrial complexes, or contractions, occur frequently in otherwise healthy people but often occur during infection, in amma- tion, or myocardial ischemia.14 They may be pro- voked by smoking, lack of sleep, excessive caffeine, or alcohol.13 They are common in conditions associ- ated with dysfunction of the atria such as congestive heart failure.
Atrial utter. Atrial utter is characterized by a rapid, regular atrial rate of 250 to 350 beats per minute. It is rare in healthy persons and most often occurs in association with septal defects, pulmonary emboli, mitral or tricuspid valve stenosis or regurgitation, or chronic ventricular failure.14 It ialso may be noted in patients with hyperthyroidism, alcoholism, or pericarditis.
Atrial brillation. AF is the most common sustained arrhythmia in adults.19 It is characterized by rapid, disorganized, and ineffective atrial contractions that occur at a rate of 350 to 600 beats per minute. The ventricular response is highly irregular. The atria do not contract effectively, thereby promoting the for- mation of intraarterial clots, along with consequent embolism and stroke. Thus, patients with AF who are at risk for stroke (e.g., history of previous stroke, systemic emboli, valvular heart disease, hypertension, diabetes, coronary heart disease, heart failure) should be placed on a regimen of warfarin for antithrom- botic therapy, with a target international normalized ratio (INR)20 of 2.0 to 3.0.14,21 Patients who cannot take warfarin, as well as those who do not have risk factors for stroke, may be managed with dabigatran or aspirin therapy. AF is associated with a history of congestive heart failure, valvular heart disease and stroke, left atrial enlargement, abnormal mitral or aortic valve function, or treated systemic hyperten- sion, as well as with advanced age.12,22 It may occur intermittently or may be chronic. Symptoms are vari- able and depend on underlying cardiac status, ven- tricular rate, and loss of atrial contraction. Treatment consists of medication or cardioversion.
Atrial tachycardias. Any tachycardia arising above the AV junction for which the ECG shows a P wave con- guration different from that for sinus rhythm is called atrial tachycardia.19 Atrial tachycardia is character- ized by an atrial rate between 150 and 200 beats per minute14 and may result from enhanced normal auto- maticity, abnormal automaticity, triggered activity, or reentry. It commonly is seen in patients with coronary artery disease, myocardial infarction (MI), cor pulmo- nale (right ventricular hypertrophy and pulmonary hypertension), or digitalis intoxication.
What are tachycardias involving the AV junction?
Preexcitation syndrome (e.g., Wolff-Parkinson-White syndrome). The atria and ventricles are electrically insulated from each other by brous tissue that forms the anatomic AV junction. Normally, impulses are transmitted from atria to ventricles across this electri- cal bridge; however, in some persons, additional elec- trical bridges connect the atria and ventricles, bypassing the normal pathways and forming the basis for preexcitation syndromes such as Wolff- Parkinson-White syndrome.19 The basic defect in this disorder involves premature activation (preexcita- tion) of the ventricles by way of an accessory AV pathway that allows the normal SA-AV pathway to be bypassed. This accessory pathway allows rapid conduction and short refractoriness, with impulses passed rapidly between atria and ventricles, and it provides a route for reentrant (back ow) tachyar- rhythmias. Resultant paroxysmal tachycardia is characterized by a normal QRS complex, a regular rhythm, and ventricular rates of 150 to 250 beats per minute, along with sudden onset and termination.14 Wolff-Parkinson-White syndrome is found in all age groups but is more prevalent among men and decreases with age. For most patients with recurrent tachycardia, the prognosis is good, but sudden death occurs rarely, at a frequency of 0.1%.14 Heart Block • AV block. Heart block is a disturbance of impulse conduction that may be permanent or transient, depending on the underlying anatomic or functional impairment. Conduction impairment in heart block is classi ed by severity, with the various forms divided into three categories.14 During rst-degree heart block, conduction time is prolonged, but all impulses are conducted. Second-degree heart block occurs in two forms: Mobitz type I (Wenckebach) and type II. Type I heart block is characterized by progressive lengthening of conduction time until an impulse is not conducted. Type II heart block denotes occa- sional or repetitive sudden block of conduction of an impulse without previous lengthening of conduction time. When no impulses are conducted, complete or third-degree block is present. AV block occurs when the atrial impulse is conducted with delay or is not conducted at all to the ventricles at a time when the AV junction is not physiologically refractory.14 Con- duction delay may occur at the AV node, within the His-Purkinje system (bundle branches), or at both sites. AV block may be rst-degree or second-degree block, or it may be complete. AV block may be caused by a multitude of conditions such as surgery, electrolyte disturbance, myoendocarditis, tumor, myxedema, rheumatoid nodules, Chagas’ disease,* calci c aortic stenosis, polymyositis, and amyloido- sis. In children, the most common cause is congenital. Drugs (e.g., digitalis, propranolol, potassium, quini- dine) also may cause AV heart block. Symptoms increase in severity with increasing degree of block.
ventricular arrhythmias?
Premature ventricular complexes. Premature ventric- ular complexes (PVCs) (or contractions) are very common arrhythmias that are characterized by the premature occurrence of an abnormally shaped QRS complex (ventricular contraction), followed by a pause. PVCs may occur alone, as bigeminy (every other beat is a PVC), as trigeminy (every third beat is a PVC), or with higher periodicity. The combina- tion of two consecutive PVCs is called a couplet; three or more in a row at a rate of 100 beats per minute are referred to as ventricular tachycardia.23 PVCs may be provoked by a variety of medications, by electrolyte imbalance, by tension states, and by excessive use of tobacco, caffeine, and alcohol. In patients without structural heart disease, PVCs have no prognostic signi cance and no impact on longev- ity or limitation of activity.18 The prevalence of PVCs increases with age; they are associated with male gender and are related to low serum potassium concentration. Among patients with previous MI or valvular heart disease, however, frequent PVCs are associated with an increased risk of death.12 Ventricular tachycardia. The occurrence of three or more ectopic ventricular beats (PVCs) at a rate of 100 or more per minute is de ned as ventricular tachycar- dia (VT). VT may be sustained or episodic. Sustained VT that persists for 30 seconds or longer may require termination because of hemodynamic instability. VT can quickly degenerate into ventricular brillation. A variant of VT called torsades de pointes is character- ized by QRS complexes of changing amplitude that appear to twist around the isoelectrical line; this rhythm occurs at rates of 200 to 250 beats per minute.24 VT almost always occurs in patients with heart disease, most commonly ischemic heart disease and cardiomyopathy.14 Certain drugs such as digi- talis, sympathetic amines (epinephrine), potassium, quinidine, and procainamide may induce VT.25 Ventricular utter and brillation. Ventricular utter and ventricular brillation (VF) are lethal arrhyth- mias characterized by chaotic, disorganized electrical activity that results in failure of sequential cardiac contraction and inability to maintain cardiac output.23 The distinction between utter and brillation can be dif cult and is of academic interest only; therefore, the two can be discussed together. If these disorders are not rapidly treated within 3 to 5 minutes, death will ensue. VF occurs most commonly as a sequela of ischemic heart disease.
disorders of repolarization?
Long QT syndrome. Long QT syndrome is a disorder of the conduction system in which the recharging of the heart during repolarization (i.e., the QT interval) is delayed. It is caused by a genetic mutation in myo- cardial ion channels and by certain drugs, or may be the result of a stroke. The condition can lead to fast, chaotic heartbeats, which can trigger unexplained syncope, a seizure, or sudden death.24,26
what are signs and symptoms of cardiac arrhythmias?
signs
- slow heart rate (100 beats/min)
- irregular rhythm
symptoms
- palpitations, fatigue
- dizziness, syncope, angina
- congestive heart failure:
- shortness of breath
- orthopnea
- peripheral edema
what about warfarin (coumadin)?
Patients with atrial brillation often are given anticoagulant therapy (warfarin) to prevent thrombus formation, embolism, and stroke; thus, they are at risk for increased bleeding. The target range for anticoagulation in patients with atrial brilla- tion usually is an INR between 2 and 3 times the normal value.54 Studies have shown that minor oral surgery, such as simple extractions, can be performed without altering or stopping the warfarin regimen, provided that the INR is within the therapeutic range. (Depending upon the reason for the anticoagulant, the therapeutic range of the INR is between 2.0 and 3.5.)55-58 Management recom- mendations also include the use of local measures such as placing of gelatin sponges, oxidized cellulose or
chitosan hemostatic products in the sockets, suturing, gauze sponges for pressure pack, or stents during the surgery; and the topical use of tranexamic acid or ε-aminocaproic acid as a mouthrinse and/or to soak sponges postoperatively (see Box 5-7). For more signi cant surgery, consultation with the physician should be obtained.
