Adult-Gerontology Acute Care Practice Guidelines
Definition
A.Any change from the normal electrical cardiac conduction: Can result in impulses that occur too quickly, too slowly or erratically.
B.Divided into two categories: Ventricular and supraventricular.
1.Ventricular abnormalities begin in the ventricles.
2.Supraventricular disorders originate above the ventricles (in the atria).
C.Can result in tachycardias or bradycardias.
1.With respect to bradycardia: Typically defined as a pulse less than 60 beats/minute and clinically significant when pulse is less than 45 beats/minute.
2.Possible causes of bradycardia: Sick sinus syndrome (SSS) or heart block (first-degree atrioventricular [AV] block, second-degree AV block types 1 and 2, and third-degree AV block).
Incidence
A.Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia where prevalence increases with age. It affects 2.7 to 6.1 million U.S. adults.
1.Median age of AF presentation is 75 years; 84% of patients are older than 65 years of age at time of diagnosis.
2.AF affects 4% of patients younger than 60 years of age and 8% of patients younger than 80 years of age.
3.The incidence of AF is greater in males than in females and more common in Caucasians than in African Americans.
B.Approximately 50% of patients experience sudden cardiac death as an initial clinical presentation of a cardiac arrhythmia.
1.The arrhythmias most likely to cause sudden cardiac death are ventricular fibrillation (VF) or ventricular tachycardia (VT), with approximately 300,000 deaths per year.
2.VT is more commonly seen in males secondary to underlying CAD.
C.Supraventricular tachycardias: Specifically, paroxysmal supraventricular tachycardia (PSVT) maintains a prevalence of approximately 0.2% of U.S. population; noted to also increase with age.
Pathogenesis
A.The pathophysiology of arrhythmias can be complex and vary based on type of abnormality.
B.Overall, there is an abnormality in the normal activation sequence of the cardiac fibers within the myocardium. There are three primary mechanisms.
1.Increased or decreased automaticity: Increased automaticity can result in atrial or ventricular arrhythmia.
2.Triggered activity.
3.Dysfunction in circulatory pathways: Specifically notable for reentry conduction pathways.
C.The pathogenesis of AF occurs because of three underlying factors: Electrical, structural, and contractile dysfunction.
1.In the simplest terms, AF’s irregularly irregular tachycardic rhythm arises because of multiple foci within the atria (principally around orifices of the pulmonary arteries) that send chaotic impulses through the heart’s electrical system.
2.This causes the atria to quiver or fibrillate
instead of contract normally.
3.Typically, the atrial rate is greater than 400 beats/minute, but some impulses are successfully blocked by the AV node. Thus, a ventricular (or calculated pulse) rate of 75 to 175 beats/minutes is appreciated.
D.Atrial flutter is a variation of AF where there is one primary automatic focus in the atria that fires between 250 and 350 beats/minute. The ventricular rate is typically one-half to one-third the atrial rate due to a refractory period of the AV node.
E.PSVT occurs because of AV nodal reentry tachycardia.
1.Two pathways within the AV node: Fast and slow.
2.Reentrant circuit revolving around the AV node.
F.Ventricular arrhythmias.
1.VT originates below the bundle of His and occurs because of quick and constant firing of three or more premature ventricular contractions (PVCs) at a rate of 100 to 250 beats/minute.
2.PVCs are defined as a heartbeat that fires on its own accord from a specific focus in one ventricle and proceeds to simulate the other ventricle.
3.VF occurs when there are multiple foci within the ventricles that are functioning on overdrive. This leads to irregular quivering of the ventricles and results in no cardiac output.
G.Bradycardias.
1.SSS: Typically occurs because of spontaneous persistent bradycardia.
2.First-degree AV block: Noted to have a conduction delay at the AV node that results in decreased pulse.
3.Second-degree AV block.
a.Type 1: Occurs because of a block within the AV node to cause bradycardia.
b.Type 2: Occurs because of a block within the bundle of His-Purkinje fibers to cause bradycardia (this can also progress to third-degree AV block).
4.Third-degree AV block: Complete dissociation between the atria and ventricles. There is no continuation of cardiac impulses between the two structures; results in significant bradycardia, typically 25 to 40 beats/minutes.
Predisposing Factors
A.AF.
1.Underlying CAD/previous MI.
2.HTN.
3.Mitral valve dysfunction.
4.History of pulmonary embolus.
5.Endocrine and adrenal disorders: Hypothyroidism or hyperthyroidism, pheochromocytoma.
6.Postoperative physiologic stress.
7.SSS.
8.Systemic illnesses such as sepsis or cancers.
9.Excess alcohol consumption (known as holiday heart syndrome
).
10.Age.
B.Atrial flutter.
1.Chronic obstructive pulmonary disease (most common cause).
2.Comorbid CAD.
3.Congestive heart failure (CHF).
4.Atrial septal defects or rheumatic heart disease.
C.PSVT.
1.Acute cardiac ischemia.
2.Medications: Most common is digoxin toxicity (causes paroxysmal atrial tachycardia with 2:1 block).
3.Atrial flutter with rapid ventricular response.
4.Excess caffeine, stimulant, or alcohol consumption.
D.VT.
1.Comorbid MI and CAD (most common causes).
2.Acute cardiac ischemia or hypotension.
3.Cardiomyopathy.
4.Congenital heart defects.
5.History of prolonged QT syndrome.
E.VF.
1.Ischemic cardiac damage (most common cause).
2.Medications: Antiarrhythmic drugs that prolong the QT interval and combination of drugs, particularly antidepressive agents (SSRIs and Tricyclics).
Subjective Data
A.Common complaints/symptoms.
1.Fatigue.
2.Dyspnea on exertion (or at rest).
3.Chest discomfort.
4.Palpitations or heart fluttering.
5.Dizziness, lightheadedness, syncope, or near-syncope.
6.Diaphoresis.
B.History of the present illness.
1.Recognize that patient presentation varies based on type and degree of arrhythmia.
a.For example, SSS can present with dizziness, fatigue, and change in mental status while VT can present asymptomatically as sudden cardiac death (if rate is slow enough).
2.Understand onset, provoking/palliative factors, quality, severity, and timing of symptoms.
3.Obtain information regarding a patient’s past medical history, specifically regarding the aforementioned conditions, that can predispose patients for abnormal heart rhythms.
C.Family and social history.
1.Determine any family history of CAD, HTN, hyperlipidemia, valvular heart disease (VHD), congenital heart defects, or arrhythmias.
2.Obtain information on tobacco use, alcohol/caffeine consumption, and illegal substance use (especially stimulants).
D.Review of systems.
1.General: Fatigue, malaise, fevers, and chills.
2.Cardiac: Angina, racing heartbeat, palpitations, decreased exercise tolerance, and peripheral edema.
3.Pulmonary: Shortness of breath and dyspnea on exertion.
4.Neurological: Lightheadedness, dizziness, syncope, and near-syncope.
Physical Examination
A.Vital signs: Assess heart rate, blood pressure, respiration, temperature, and oxygen saturation.
1.Important to note temperature, as an underlying febrile illness can exacerbate underlying AF.
2.In VF, it is likely that the patient will be unconscious with no pulse and unmeasurable BP.
B.Neck: Jugular venous distention (JVD; concern for CHF).
C.Pulmonary: Possible rales or crackles (sign of increased fluid accumulation as related to underlying CHF).
D.Cardiac: Inspection and palpation for thrills and auscultation.
1.Auscultation.
a.Assess rate (tachycardic or bradycardic).
b.Rhythm (regular, irregularly irregular, or irregularly regular).
c.Extra heart sounds (S3 and S4).
d.Murmurs consistent with underlying VHD.
E.Peripheral vascular: Assess peripheral pulses, possible peripheral edema (sign of fluid overload and concomitant CHF).
F.Neurology: Mental status examination (if mental status changes) or complete neurological examination if concern for associated syncope/near-syncope.
Diagnostic Tests
A.ECG.
1.AF: Tachycardia rate (110–180 beats/minute), irregularly irregular rhythm (irregularly spaced R-R intervals) with no discernable P-waves.
2.Atrial flutter: Tachycardic rate with a saw-tooth
(F-wave) baseline pattern; best seen in leads VI, II, III and aVF where the QRS complex appears after several saw-tooth
P-waves (number of F waves can vary depending on atrioventricular node [AVN] blockade).
3.VF: Irregular rhythm, no identifiable P-waves, or QRS complexes.
4.VT: Tachycardic rate (150–250 beats/minute) and wide QRS complexes (can have identical morphologies in monomorphic VT or different ones in polymorphic VT).
5.PSVT (most common etiology of reentry conduction): Tachycardic rate, narrow QRS complexes with no discernable P-waves (P-waves are buried within the QRS complexes secondary to simultaneous rapid firing of the atria and ventricles).
6.First-degree heart block: Hallmark is a PR interval greater than 0.20 seconds where a QRS complex follows each P-wave.
7.Second-degree heart block.
a.Type 1 (Mobitz Type I or Wenckebach): Hallmark is progressive prolongation of the PR interval with a nonconducted P-wave. The longest PR interval preceding the dropped QRS and the shortest immediately after.
b.Type 2 (Mobitz Type II): Hallmark is an intermittent nonconducted P-wave without progressive prolongation, but immediate PR interval to dropped QRS is prolonged.
8.Third-degree heart block: Bradycardic rate, with no discernable pattern or connection between P-waves and QRS complexes.
B.Laboratory tests.
1.Complete blood count with differential: Determine if an anemia is contributing to the arrhythmia.
2.Complete metabolic panel: Determine if an electrolyte disturbance or renal dysfunction is contributing to the arrhythmia.
3.Thyroid panel: Hypothyroidism or hyperthyroidism can be an underlying etiology for arrhythmias (i.e., thyrotoxicosis can trigger AF).
4.Cardiac biomarkers: These should be obtained in any patient with chest discomfort or evidence of an arrhythmia; they evaluate for the possibility of underlying myocardial infarction.
5.Digitalis level (if clinically indicated): Supratherapeutic levels can lead to various arrhythmias, including PSVT and AF with rapid ventricular response.
6.Toxicology screening (if clinically indicated): Illegal substances, especially stimulants, can precipitate arrhythmias.
7.D-dimer: This can help rule out a pulmonary embolus, which can occur in the setting of AF.
C.Chest x-ray: Checks for underlying cardiomegaly, pulmonary edema, or pulmonary infections such as pneumonia, or pneumothorax, which can exacerbate or precipitate arrhythmias.
D.Exercise stress testing: Helps provide an overall understanding of one’s cardiovascular health and evaluate for underlying ischemia.
E.Holter monitor or loop recorder: Can be helpful for monitoring patients on a continuous basis when an arrhythmia is suspected but unable to be captured via ECG; can also be helpful for patients with vague or nonspecific cardiac symptoms.
F.Transesophageal echocardiogram (TEE): Especially important for new-onset arrhythmias to evaluate overall cardiac function (ejection fraction [EF]), identify VHD, and measure atria and ventricle sizes.
7.If considering a device for geriatric patients, it is important to address comorbidities, life span, impact on quality of life, maintenance of device, and occurrence of unnecessary shocks during end-of-life care.
8.The use of anticoagulants in the geriatric population should be carefully reviewed with patients (and family members, if necessary) to ensure that risks versus benefits of these medications are evaluated.
a.Cognitive status (important for medication compliance).
b.Comorbidities (e.g., is patient already utilizing other antiplatelet or anticoagulant agents, thus increasing the risk of bleeding events?).
c.Overall functional status—important to address risk of falls and bleeding complications.
Bibliography
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