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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2693_Библиотеки_им_академика_М_И_Перельмана.pdf
13 Bradya rrhythmias
219
• AV block is classied into rst-degree, second-degree (of which there are
two types), and third-degree AV block (also referred to as complete heart
block).
• First-degree AV block is dened as a P-R interval greater than 0.20 sec on
an ECG.This indicates delayed conduction through the AV node, but all
impulses are conducted to the ventricles. It may be a normal variant and
generally portends no increased risk of further conduction disease or heart
disease. It may be associated with increased vagal tone, digoxin toxicity,
acute inferior MI, or myocarditis. When there is an underlying cause, the
block usually is transient.
First-degree AV block [Mendoza A, Belda S, Salguero R, Granados MA.Congenital
complete atrioventricular block associated with QT prolongation: description of a
patient with an unusual outcome. Pediatr Cardiol. 2010 Aug;31(6):887–90.] Caption
from original
• Second-degree AV block is marked by the failure of some sinus impulses to
reach the ventricles. On an ECG, some P waves are seen without an associated
QRS complex. There are two types: type I (also called Mobitz I or Wenckebach)
and type II (Mobitz II).
• Type I second-degree, Mobitz I AV (Wenckebach) block: There is progres-
sive prolongation of AV conduction (noted as progressive lengthening of
the P-R interval) until the atrial impulse is completely blocked and a QRS
complex is dropped. The conduction ratio is the ratio of atrial impulses to
those that are conducted into the ventricles, i.e., a 4:3 conduction ratio
means that three of every four atrial impulses are conducted into the ventricles. In other words, there is a dropped QRS complex after every three
sinus beats, so for four P waves, there are only three QRS complexes. This
ratio usually is stable for any given patient, but some patients can manifest
changing (variable) ratios of block. This block occurs at the level of the AV
node. This type of block does not carry an increased risk of progression to
third-degree heart block. It usually is transient, reversible, and asymptomatic. It may be seen during acute inferior MI, with myocarditis, with
digoxin toxicity, and after cardiothoracic surgery.
220
C. J. Rees et al.
Mobitz type I (Wenckebach) Second-Degree AV block. Notice the classic form of
Wenckebach in a 4:3 pattern. The PP intervals are xed, with lengthening of each
successive PR interval with progressively decreasing increments and shorter RR
intervals prior to the dropped beat. The pause is less than a multiple of the shortest
RR interval, the return-cycle PR interval is shorter than the PR interval prior to the
dropped beat, and there is obvious group beating periodicity. [Almasry
IO. Evidenced-based approach to bradyarrhythmias. In: Stergiopoulos K, Brown
DL, editors. Evidence-based cardiology consult [Internet]. London: Springer; 2014
[cited 2015 May 22]. p. 105–18. Available from: http://link.springer.com/
10.1007/978-1-4471-4441-0_9] Caption from original
• Second-degree, Mobitz II AV block: The P-R interval is constant, and there
are nonconducted impulses. As with Mobitz I block, there usually is a constant conduction ratio, but it may be variable. When the conduction ratio is
2:1, it is impossible to tell the difference between Mobitz I and Mobitz II heart
block, as progressive P-R prolongation cannot be appreciated. This level of
block usually occurs below the AV node (infranodal). If the escape pacemaker
is high enough in the conduction system, the QRS complexes may still be
narrow, but if the pacemaker is lower, the QRS complexes may be wide. This
type of heart block almost always indicates some structural damage to the
conduction system and usually is permanent. It carries a high risk of progression to third-degree heart block, especially if it occurs in the setting of an
acute anterior MI.
Mobitz type II second-degree AV block. Note that there is ongoing sinus rhythm
with a xed PP interval before there is a sudden failure of conduction to the ventricles demonstrated by a dropped QRS.Note that there is no change in the PR interval
preceding and following the dropped QRS, and this recurs later in the strip. The
resultant pause is exactly twice the PP interval. Note the narrow QRS in this example that may suggest a nodal site of conduction block. [Almasry IO.Evidencedbased approach to bradyarrhythmias. In: Stergiopoulos K, Brown DL, editors.
Evidence-based cardiology consult [Internet]. London: Springer; 2014 [cited 2015
May 22]. p.105–18. Available from: http://link.springer.com/10.1007/978-1-4471-
4441-0_9] Caption adapted from original
13 Bradya rrhythmias
• Third-degree heart block (complete heart block): All conduction between the
atria and ventricles is blocked. This block is seen on an ECG as the absence
of a relationship between the P waves and the QRS complexes; therefore, it
also is called AV dissociation. The atrial rate must be greater than the escape
pacemaker rate for this lack of a relationship to be appreciated. If the rates are
similar, it may be difcult to determine that there is no relationship between
the P waves and QRS complexes (isorhythmic dissociation). A ventricular
rate greater than the atrial rate precludes the diagnosis of third-degree heart
block. AV dissociation with a ventricular rate greater than the atrial rate may
be seen in some accelerated junctional rhythms, as well as in ventricular
tachycardia. If the escape pacemaker is within the AV node (nodal), the escape
rate is usually 40 to 60 bpm, with narrow QRS complexes. If the escape pacemaker is infranodal, the escape rate may be less than 40 bpm, in which case
the QRS complex usually is widened. Nodal complete heart block may be
transient, especially in the setting of an acute inferior MI.Infranodal complete
heart block usually is permanent and the result of intrinsic conduction system
disease, acute ischemia, drugs, or, rarely, Lyme disease.
221
Third-degree AV block (Complete heart block). Top panel: Ongoing sinus rhythm at
a rate of 75 bpm with complete heart block and a narrow junctional escape at just
over 40 bpm. Bottom panel: Sinus tachycardia at a rate of 125 bpm with a wide
ventricular escape focus at 24 bpm. The sinus tachycardia indicates that this patient
may be in distress and is far more likely to be symptomatic upon presentation.
[Almasry IO.Evidenced-based approach to bradyarrhythmias. In: Stergiopoulos K,
Brown DL, editors. Evidence-based cardiology consult [Internet]. London: Springer;
2014 [cited 2015 May 22]. p. 105–18. Available from: http://link.springer.
com/10.1007/978-1-4471-4441-0_9] Caption adapted from original
Presentation
Typical/“Classic”
• Bradyarrhythmias often are asymptomatic and sometimes are found on routine evaluation or for evaluation of other complaints. This is especially true
for sinus bradycardia, sinus arrhythmia, sinus block, rst-degree AV block,
222
and type I second-degree AV (Wenckebach) block. Sinus bradycardia, sinus
arrhythmia, and rst-degree AV block may be normal variants. It is a common
situation to nd one of these abnormalities on an ECG performed for other
reasons, such as preoperative clearance in an otherwise healthy person.
• These dysrhythmias also may be associated with other, more serious concerns
(e.g., an acute MI or drug overdose or intoxication), and the symptoms of
these disorders may predominate in the clinical presentation. In these situations, it often is difcult to discern whether the symptoms are being caused by
the primary event or the dysrhythmia. However, these dysrhythmias often
are transient and resolve spontaneously or with appropriate treatment of the
primary event.
• Patients who have symptoms from their bradyarrhythmias often have vague
and nonspecic complaints, such as fatigue, exercise intolerance, shortness of
breath (especially on exertion), and feeling generally unwell.
• Most signicantly, these dysrhythmias may present acutely with syncope,
near- syncope, chest pain, acute dyspnea, and other signs of systemic hypoperfusion (change in mental status, hypotension, cyanosis, i.e., shock state).
These presentations are much more likely with heart rates of 40 bpm or less,
as well as with greater levels of block.
• Sick sinus syndrome often presents as syncope or near-syncope in elderly
patients. Sometimes, however, symptoms from the tachycardia predominate,
and the patient will present with palpitations and chest heaviness/pain,
followed by syncope, presyncope, or generalized fatigue.
C. J. Rees et al.
Atypical
• Because there is no “typical” presentation for bradyarrhythmias, almost all
presentations are atypical.
Primary Differential Considerations
• Bradycardia is a self-evident diagnosis based on a heart rate less than 50 bpm.
The differential diagnosis of causes of bradyarrhythmias is broad and includes:
• Heart blocks or slow atrial brillation
• Primary cardiac causes such as MI with cardiogenic shock
• Metabolic causes such as hyperkalemia
• Neurologic causes such as increased intracranial pressure or spinal cord
injury
• Drug toxicity (calcium channel blockers, beta-blockers, digitalis, clonidine)
• Infections such as myocarditis, rheumatic fever, or Lyme disease
• Malfunctioning pacemaker
13 Bradya rrhythmias
History andPhysical Exam
Findings That Conrm Diagnosis
• The diagnosis is considered by nding a slow pulse rate on physical exam,
then conrmed by nding a bradyarrhythmia on a 12-lead ECG and/or
continuous cardiac monitoring.
Factors That Suggest Diagnosis
• The diagnosis may be suggested in patients presenting with the symptoms
reviewed above (syncope, near-syncope, fatigue, exercise intolerance, chest
pain or heaviness, palpitations).
• Patients with any of the aforementioned symptoms should undergo 12-lead
ECG and may need further, more prolonged cardiac monitoring if the ECG
does not secure the diagnosis.
Factors That Exclude Diagnosis
223
• Because many of these arrhythmias may be both transient and intermittent,
they are all difcult to exclude, and the patient may require reassessments
over time for complete exclusion. Patients also may require extended cardiac
monitoring and/or electrophysiologic study for any of these abnormalities to
be completely excluded.
Ancillary Studies
Laboratory
• In general, there are no specic laboratory tests that are diagnostic for any of
these arrhythmias.
• All patients should have their electrolyte levels checked, as hypo- and hyperkalemia may lead to or exacerbate some of these disturbances.
• Thyroid-stimulating hormone levels also should be checked, as hypothyroidism
also may cause bradycardia (most commonly sinus bradycardia).
• Patients on digoxin should have their serum levels checked, as digoxin toxicity
may cause many of these arrhythmias.
224
• Patients who present with more acute symptoms, such as chest pain/heaviness
or dyspnea, should have their cardiac biomarkers checked, as many of these
rhythms may occur in the setting of an acute MI, especially an inferior MI.
• Many times, the laboratory evaluation of these patients is guided by the acuity
of the presentation, not the bradyarrhythmia.
• Lyme disease may cause conduction disturbances; therefore, in the correct
clinical setting, a Lyme titer may need to be analyzed. Chagas disease also
may cause conduction disturbances so in the correct clinical setting, also may
need to be evaluated.
C. J. Rees et al.
Imaging
• Most patients being evaluated for cardiovascular-related complaints will have
a chest x-ray, which may indicate contributing issues or show evidence of
other heart disease (e.g., heart failure and/or cardiomegaly).
• Echocardiogram (either transthoracic or transesophageal) usually is performed in the workup of patients with symptomatic bradycardias. These studies may help reveal any structural heart disease that may be causative or
contributory (e.g., cardiomyopathy, cardiac amyloidosis).
Special Populations
Age
• Most of these arrhythmias increase in incidence as age increases, as they often
are associated with underlying heart disease or medication use.
• Exceptions include sinus bradycardia, sinus arrhythmia, and low-level heart
blocks, which may be normal variants in the young.
• The most common cause of bradycardia in infancy is hypoxia.
• In adolescents and young adults, the pulse rate may drop normally to 35 to
40 bpm during sleep. This also may be associated with sinus pauses of up to
2 seconds. These ndings are normal in this age group and usually do not
require further evaluation.
• Complete heart block may be seen in infants and children and is almost always
associated with congenital heart disease.
• Children presenting with high-grade heart block and no signicant medical
history should be evaluated for drug ingestion (digoxin, beta-blockers,
calcium channel blockers, other antiarrhythmics, and opiates). It also may be
necessary to consider conduction abnormalities from cardiac Lyme disease
and, if appropriate (prolonged travel or immigration from endemic areas),
Chagas disease.
13 Bradya rrhythmias
Co-morbidities
• There are multiple co-morbidities of interest in patients presenting with
bradyarrhythmias.
• Many of these disturbances are seen in patients with underlying structural
heart disease and in those with coexistent coronary artery disease. Many of
these conduction disturbances may be seen with or caused by cardiac
medications.
• Increased vagal tone may precipitate many of these abnormalities, so anything
that increases vagal tone should be considered (e.g., carotid sinus hypersensitivity, intra-abdominal catastrophe, increased intracranial pressure, drugs).
• As noted, conduction disturbances also may be found in association with
many other diseases:
• Inammatory: rheumatic heart disease, myocarditis, pericarditis, and col-
lagen vascular diseases such as rheumatoid arthritis and systemic sclerosis
• Infectious: Lyme disease and Chagas disease
• Systemic/cardiac amyloidosis
• Post open heart surgery
• Post mediastinal radiation therapy
• Chest trauma
• Rare genetic and familial diseases, such as myotonic dystrophy
225
Pitfalls inDiagnosis
Critical Steps Not toMiss
• It is critical to consider the entire clinical picture when confronted with a
patient who is bradycardic.
• It must be determined whether the patient is symptomatic and, if so, whether
the symptoms arise from the bradycardia itself or an underlying/causative
disorder.
• It is critical to look for these underlying disorders and not to stop at the
diagnosis of bradycardia.
• All patients who are bradycardic should have a 12-lead ECG and, if in an
appropriate clinical setting, continuous cardiac and vital sign monitoring.
Mimics
• Because bradycardia usually is dened by an absolute rate, there are no
mimics; however, multiple potential etiologies must be considered in patients
with bradycardia.
226
C. J. Rees et al.
Time-Dependent Interventions
• Time-dependent interventions in bradycardias are necessary only in patients
who have symptoms and show signs of reduced cardiac output, such as hypotension, a change in mental status, cyanosis, and syncope.
• In these situations, treatment must begin before obtaining a complete database.
• When a patient demonstrates any of these signs or symptoms, it is critical to
act quickly to attempt to return cardiac output to more normal levels.
• Support of airway, breathing, and circulation is of paramount importance. All
patients should have supplemental oxygen and adequate intravenous access
for administration of medications and uid. All unstable, or potentially unstable, patients with an arrhythmia should have debrillator pads placed and
attached to the debrillator/monitor.
Overall Principles ofTreatment
• As mentioned earlier, support of airway, breathing, and circulation is the most
important management principle.
• All unstable, or potentially unstable, patients should have supplemental oxygen, adequate intravenous access for administration of medications and uid,
and debrillator pads placed and attached to the debrillator/monitor.
• In general, emergent treatment of bradycardias is not necessary unless the
heart rate is less than 50 bpm and associated with signs of hypoperfusion, or
if there is a risk of progression to complete heart block.
• Several urgent/emergent treatments are common and relevant to all the
bradycardias:
• Atropine. Atropine is a class II medication in the treatment of symptomatic
bradycardias. It is a naturally occurring antimuscarinic drug that competitively antagonizes the effects of acetylcholine and other antimuscarinic
agents. It increases the rate of sinus node ring (automaticity) and enhances
AV nodal conduction. Because it blocks vagal activity, it sometimes is
described as parasympatholytic or vagolytic. It is administered intravenously as 0.5-mg boluses (in situations other than bradycardia, it may be
given as 1-mg boluses). It may be given every 5 minutes until the desired
effect is achieved, or until a total of 3mg (0.04 mg/kg) has been administered (this is the fully vagolytic dosage). If the conduction abnormality is
an SA or AV nodal problem, it likely will respond to atropine. If the problem is infranodal or lower, the response rate decreases. Atropine’s onset of
action is about 2 to 4 minutes, and the effects may last for 5 to 6 hours.
However, it is important to remember that the effect is temporary. Atropine
must be administered with caution in settings of concurrent myocardial
ischemia, as it increases the heart rate, which increases myocardial oxygen
13 Bradya rrhythmias
demand, and may worsen ischemia. Atropine is not indicated in asymptomatic bradycardia. Atropine likely will have no effect on a transplanted
heart, as heart transplants are denervated. Doses below 0.4mg may cause
a paradoxic bradycardia.
• Transcutaneous pacemaker. Transcutaneous pacing is a class I intervention
for unstable patients with symptomatic bradycardia. All unstable patients
should undergo transcutaneous pacing. Although atropine may be given as
a temporizing measure, it should not replace transcutaneous pacing in
unstable patients with high-grade (type II second-degree and complete)
heart block. Self-adhesive pads are placed with the left pad over the left
anterolateral precordial area and the right pad in the right subscapular
region. Most patients have capture (i.e., when the pacing impulse results in
a heartbeat) with 100 mA of output. Sometimes, however, it may require
up to 200 mA of output for capture to occur. Outputs above 200 mA should
not be attempted. Transcutaneous pacing may be uncomfortable and painful; therefore, all patients should receive either pain control or sedation
with anxiolytics. If it is impossible to induce capture, it may be necessary
to move to transvenous pacing.
227
Placement of transcutaneous pacemaker pads. [Healey JS, Merchant R, Simpson C,
Tang T, Beardsall M, Tung S, Fraser JA, Long L, van Vlymen JM, Manninen P,
Ralley F, Venkatraghavan L, Yee R, Prasloski B, Sanatani S, Philippon F.Society
position statement: Canadian Cardiovascular Society/Canadian Anesthesiologists’
Society/Canadian Heart Rhythm Society joint position statement on the perioperative management of patients with implanted pacemakers, debrillators, and neurostimulating devices. Can J Anaesth. 2012 Apr;59(4):394–407.] Caption adapted
from original
228
C. J. Rees et al.
The right pad is placed in the alternative, right upper anterior chest and apex
positions. [Woodcock B. Hemodynamic emergencies. In: Tremper KK, editor.
Principles of anesthetic techniques and anesthetic emergencies. Philadelphia:
Current Medicine; 1998. 195 p. (Miller RD, editor. Atlas of anesthesia; vol. 4).]
https://www.youtube.com/watch?v=qkSGaJkNqvg
Video demonstrating transcutaneous pacing.
• Transvenous pacing. Transvenous pacing has the same indication as transcutaneous pacing. It requires central venous access because the leads are passed
through the central catheter into the heart. This is an invasive procedure, and
although it may be attempted emergently at the bedside, it is best performed
in conjunction with expert consultation and guidance. Currently, this technique is performed most often under uoroscopic guidance in a cardiac catheterization laboratory as a bridge to a permanent pacemaker.
• Epinephrine and dopamine. Epinephrine and dopamine may be considered
for blood pressure support if atropine and emergent pacing have been unsuccessful. Administration of these agents is only temporizing measure until the
patient can be prepared for denitive therapy.
• Specic drug ingestions that lead to symptomatic and/or unstable bradycardias should be treated with specic antidotes if available, but also may be
treated with atropine and pacing as required.
Following is a list of recommendations based on the specic bradycardia:
• Sinus bradycardia: generally requires no treatment unless the rate is less than
50 bpm and associated with symptoms, which may occur with profound vagal
stimulation. If necessary, treatment may start with atropine and, if necessary,
transcutaneous pacing.
• Sinus arrhythmia: requires no treatment.
• Sinus pauses/sinus arrest: treatment should be aimed at the underlying causes.