Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2664_Библиотеки_им_академика_М_И_Перельмана
.pdf
USMLE Step 2 CK
l Internal Medicine
and hepatomegaly (manifestations of right-side failure). Jugular venous distension that increases
with inspiration (Kussmaul sign). Heart sounds are distant, and an early diastolic apical sound,
or “pericardial knock,” is often present and can be confused with an S3 gallop.
Diagnosis
• EKG: Findings include low-voltage and nonspecific T-wave changes.
• Chest x-ray: The heart usually is normal in size.
• Chest CT or MRI: Shows thickened pericardium; pericardial calcifications may be seen
in tuberculous constriction.
• Cardiac catheterization: A marked “y” descent is present in the right atrial pressure
tracing. Left and right ventricular pressure tracings demonstrate a characteristic “dip
and plateau” or “square root” sign. There is equalization of end-diastolic pressures in all
4 chambers and the pulmonary artery.
Differential Diagnosis. It is sometimes difficult to distinguish constrictive pericarditis from
restrictive cardiomyopathy. Left ventricular ejection fraction is more likely to be decreased in
patients with restrictive cardiomyopathy. Computed tomography is the procedure of choice to
demonstrate the thickened pericardium.
Treatment. Patients may be treated conservatively at first with mild sodium restriction and
diuretics. Pericardiectomy may be needed.
Disorders of Sinus Node Function
Ventricular complexes are normal width, evenly spaced, rate <60/min.
Etiology
• Excessive vagal tone causes:
– Acute MI, particularly diaphragmatic
– Carotid sinus pressure
– Vomiting
– Valsalva maneuver
– Phenothiazines
– Digitalis glycosides
• Depression of the sinus node automaticity:
– Beta-adrenergic blocking agents
– Calcium blocking drugs
• Marathon running and swimming
• Hypothyroidism
• Normal variant
160
Treatment
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
• None necessary in the absence of symptoms
• Atropine acutely if symptoms are present
• Pacemaker if symptoms and bradycardia persist despite atropine
May be classified in two ways:
• Anatomical, based on the site of block as determined by His bundle electrocardiography.
• Clinical, based on the routine ECG. The 3 classic clinical types are first-, second-, and
third-degree (or complete) AV block.
First-Degree AV Block
Definition. Pulse rate (PR) interval >0.20 s at a heart rate of 70 beats/min.
Etiology
• Degenerative changes in the AV conduction system caused by:
– Aging
– Digitalis
– Exaggerated vagal tone
– Ischemia (diaphragmatic infarction)
– Inflammation (myocarditis, acute rheumatic fever)
• Cardiomyopathies
Chapter 5
l Cardiology
Second-Degree AV Block
See Table 5-13.
161
USMLE Step 2 CK
Beat
Mobitz Type II
l Internal Medicine
Table 5-13. Type I versus Type II Second-Degree AV Block
Type I (Mobitz I, Wenckebach) Type II (Mobitz II)
Mobitz Type I
R R R R
P
P P P
RR R
P
PP
P
Dropped
Beat
Progressive prolongation of the PR interval until
a P wave is completely blocked and a ventricular
beat is dropped. PR interval of the next conducted
beat is shorter than preceding PR interval.
Blocked beat occurs suddenly and is not preceded
by a change in duration of the PR interval. Patient
is equipped with a pacemaker, which cuts in to
sustain a regular ventricular rhythm.
Dropped
Site of block Usually AV nodal (supra-Hisian) Infranodal (intra- or infra-Hisian)
QRS complex Usually normal in width Usually wide (bundle branch block) with infra-
Hisian block; narrow with intra-Hisian block
Causes Degenerative changes in AV node; diaphragmatic
myocardial infarct; digitalis toxicity; myocarditis;
rheumatic fever; increased vagal tone
EKG PR interval lengthens progressively until ven-
tricular beat is dropped
PR interval shortens after dropped beat
Extensive anterior myocardial infarct; degenerative changes in His-Purkinje system; massive calcification of mitral or aortic valve anulus
PR interval is usually normal in duration and
constant in length
if PR interval is prolonged, the duration of prolongation is fixed
RR interval lengthens progressively up to the
dropped beat
Blocked beats occur suddenly without progressive lengthening of the PR interval
RR interval of conducted beats is constant or a
multiple of a basic RR interval cycle length
Effect of carotid
sinus pressure
Effect of atropine
Consequences of
progression to
complete heart
block
162
May increase degree of block No effect
Frequently shortens PR interval and increases AV
No effect
conduction
Escape focus usually junctional; narrow QRS
complex; rate >45 beats/min; Adams-Stoke
attacks uncommon
Escape focus infrajunctional (usually ventricular) wide QRS complex; rate <45 beats/min;
Adams-Stoke attacks common
Junctional escape may be present with intraHisian block
Third-Degree (Complete) AV Block
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
In third-degree, or complete, heart block, all atrial beats are blocked, and the ventricles are
driven by an escape focus distal to the site of block.
Figure 5-12. Third-Degree AV Block
Etiology
•
Most common cause in adults is simple fibrous degenerative changes in the conduc-
tion system that results from aging (Lenègre disease)
• Inferior or posterior infarction
• Infectious and inflammatory processes, such as abscesses, tubercles, tumors, infiltrative
disease of the myocardium, sarcoid nodules, and gummas, myocarditis, and rheumatic
fever
• Drugs like digitalis
• Ankylosing spondylitis
Chapter 5
l Cardiology
Clinical Manifestations
• Symptoms are associated with Adams-Stoke attacks and occasionally CHF.
• Adams-Stoke attacks are caused by either sudden asystole or the development of
ventricular tachyarrhythmias, such as transient ventricular tachycardia or ventricular
fibrillation, that lead to circulatory arrest.
• The bradycardia associated with complete heart block may lead to congestive heart
block in patients with myocardial disease.
Treatment. Pacing.
Sinus tachycardia is defined as a normal rhythm with a rate of >100 beats/minute. In sinus
tachycardia, the ventricular complexes are of normal width, evenly spaced, and a P-wave precedes a QRS complex. It usually represents a physiologic response to fever, hypotension, volume
depletion, anxiety, and pain. Other causes include thyrotoxicosis, anemia, and some drugs.
Transient sinus tachycardia is occasionally the result of a rebound phenomenon following the
discontinuation of beta-adrenergic blocking drugs.
163
USMLE Step 2 CK
l Internal Medicine
Paroxysmal supraventricular tachycardia is a group of ectopic tachyarrhythmias characterized by sudden onset and abrupt termination. They are usually initiated by a supraventricular
premature beat (includes paroxysmal atrial tachycardia)
• 80% are caused by re-entry, mainly in the AV node.
• Manifests as an absolutely regular rhythm at a rate 130–220 beats/min (average 160).
• Initial therapy consists of maneuvers aimed at increasing vagal tone, particularly right
carotid sinus massage. Carotid sinus massage is followed by adenosine.
• IV adenosine is effective in >90% of cases.
• IV propranolol or esmolol, verapamil
• IV digitalis
• Synchronized external cardioversion if patient is unstable
Multifocal atrial tachycardia is characterized by an irregular supraventricular rhythm, at rates
100–200 beats/min.
• The morphology of the P waves (at least 3 different P wave forms) varies from beat to
beat, as does the PR interval. Each QRS complex, however, is preceded by a
P wave.
• Generally seen in elderly patients or those with chronic lung disease who are experiencing respiratory failure
• Use diltiazem, verapamil, or digoxin; avoid beta blockers because of lung disease
Atrial flutter generally presents as an absolutely regular rhythm with a ventricular rate of
125–150 beats/min and an atrial rate of 250–300 beats/min (i.e., 2:1 block).
It has been associated with:
• Chronic obstructive lung disease
• Pulmonary embolism
• Thyrotoxicosis
• Mitral valve disease
• Alcohol
• Atrial flutter may occur as a paroxysmal arrhythmia in persons with normal heart.
• Therapy is cardioversion if hemodynamically unstable (e.g., hypotension), digitalis,
verapamil, diltiazem, and beta-blockers.
Figure 5-13. Atrial Flutter
164
Atrial Fibrillation
Figure 5-14. Atrial Fibrillation
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Atrial fibrillation (AF) is the most common sustained cardiac rhythm disturbance. AF is associated with heart disease but also occurs with no detectable disease. Thromboembolic events
occur with AF and can cause significant morbidity and mortality.
AF is a supraventricular tachyarrhythmia characterized by uncoordinated
atrial activation
with subsequent decline of atrial function. On the ECG, there is replacement of consistent P
waves by fibrillatory waves that vary in size, shape, and timing, associated with an irregular,
frequently rapid ventricular response (irregularly, irregular). The ventricular response to AF
depends on electrophysiologic properties of the AV node, the level of vagal and sympathetic
tone, and the action of drugs. Extremely rapid rates (>200 bpm) suggest the presence of an
accessory pathway (W-P-W syndrome), which may manifest as AF. The rate of ischemic stroke
among patients with nonrheumatic AF averages 5% per year, which is 2–7 times the rate for
people without AF.
Chapter 5
l Cardiology
• The CHADS score is a clinical prediction rule for estimating the risk of stroke in
patients with atrial fibrillation. It is used to determine whether treatment is required
with anticoagulation or antiplatelet therapy.
• A high CHADS score corresponds to a greater risk of stroke (C for CHF; H for
hypertension; A for age over 75; D for diabetes; S for prior stroke or TIA).
• Each condition receives 1 point except prior stroke, which gets 2.
CHADS Score Treatment
0 • Give aspirin
1 • Give aspirin or warfarin
≥2 • Give warfarin
When AF is compared with atrial flutter, atrial flutter is found to be more organized than AF,
with a sawtooth pattern of regular atrial activation called flutter (f) waves on the ECG, particularly visible in leads II, III, and aVF.
The diagnosis of atrial fibrillation should be considered in elderly patients who present with
complaints of shortness of breath, dizziness, or palpitations. The arrhythmia should also be
suspected in patients with acute fatigue or exacerbation of CHF. In some patients, atrial fibrillation may be identified on the basis of an irregularly irregular pulse or an ECG obtained for
the evaluation of another condition.
165
● Internal Medicine
New onset AF
Hemodynamically stable
(no hypotension, no acute heart failure, etc.)
Yes No
Control rate (<110 beats/min) with
diltiazem, verapamil, b-blocker,
or digoxin
Spontaneous conversion to SR
Yes
Assess cause
and follow-up
AF recurs
AF persists
Consider cardioversion
(electrical or pharmacologic)
Yes
Cardioversion: sedate before
(100J, 200J, 300J
until sinus rhythm returns)
Consider anticoagulation
after patient is stable
No
AF >48 hours
No or
questionable
Observe off
anticoagulation
166
• Long-term anticoagulation
and rate control
• May consider rhythm control:
ablation, cardioversion
Figure 5-15. Management of Atrial Fibrillation (AF)
Cardiac conditions commonly associated with the development of AF include rheumatic
mitral valve disease, coronary artery disease, CHF, and hypertension (cause atrial structures to
dilate). Noncardiac conditions that can predispose patients to develop atrial fibrillation include
hyperthyroidism, hypoxemia, and alcohol intoxication.
Evaluation of Patients with AF (Minimum Workup):
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
•
H and P: identifies the severity of symptoms associated with AF as well as the clinical
type (paroxysmal, persistent, first episode); also allows the assessment of frequency
and duration of AF, as well as identification of precipitating factors and presence of
underlying heart or lung disease.
ECG: verifies the rhythm as well as identifies LVH, pre-excitation, prior MI.
•
•
Chest x-ray: allows evaluation of the lung parenchyma and identifies coexisting lung
disease.
Echocardiogram: identifies LVH, valvular disease, atrial size, and possible left atrial
•
thrombus.
Thyroid function tests: excludes hyperthyroidism as a cause of AF.
•
Management. Two general approaches are used for managing AF: (1) ventricular rate control,
and (2) rhythm control (attempts to convert to and maintain sinus rhythm). There is little difference in mortality between rate control and pharmacologic rhythm control. Studies confirm
the importance of anticoagulation to reduce the risk of stroke in patients with AF. Interestingly,
<25% of patients on an antiarrhythmic regimen remained in sinus rhythm at the end of 1 year.
The standard of care is to slow the rate and anticoagulate if the CHADS score is >1.
As a general concept, rate control alone is considered for the patient who notices very little
of the symptoms of the arrhythmia, while rhythm control is more likely to be applied to the
patient who immediately notices the arrhythmia and is experiencing consequences of the
arrhythmia, such as shortness of breath, or development of heart failure.
Chapter 5
l Cardiology
Cardioversion (rhythm control)—mechanical cardioversion: Involves an electrical shock
synchronized with the intrinsic activity of the heart. The synchronization ensures that electrical stimulation does not occur during the vulnerable phase of the cardiac cycle. Mechanical
cardioversion may be performed electively to restore sinus rhythm in patients with persistent
AF. On the other hand, the need for mechanical cardioversion can be immediate, when the
arrhythmia is the main factor responsible for hemodynamic instability (acute heart failure,
hypotension, or angina). Since mechanical cardioversion carries a risk of thromboembolism,
in cases of elective cardioversion, anticoagulation should be initiated before the procedure.
Cardioversion (rhythm control)—pharmacologic cardioversion: Cardioversion can be
achieved by drugs. Pharmacologic cardioversion is less effective than electrical cardioversion,
but the latter requires conscious sedation or anesthesia, whereas the former does not. The risk
of thromboembolism or stroke does not differ between pharmacologic and electrical cardioversion. Thus, recommendations for anticoagulation are the same for both methods. Drugs
proven effective for pharmacologic cardioversion of atrial fibrillation include: amiodarone,
dofetilide, flecainide, ibutilide, propafenone, and quinidine. Drugs used to maintain sinus
rhythm in patients with atrial fibrillation include amiodarone, disopyramide, dofetilide, flecainide, propafenone, and sotalol. Rate control is the standard of care for most patients.
Catheter ablation of AF foci is sometimes used as one of the nonpharmacologic therapies for
eradicating AF. The techniques evolved with the demonstration that most AF is initiated by
ectopic beats from focal areas that may be targeted for ablation. These foci arise more commonly from the 4 pulmonary veins. Thus, techniques have focused on the identification and
elimination of these foci.
Note
Routine rhythm control
for atrial fibrillation is not
indicated. It is an exception.
167
USMLE Step 2 CK
l Internal Medicine
Ventricular rate control to achieve a rate of <100–110 beats/min is one of the first steps in
managing AF. Beta blockers, calcium channel blockers, and digoxin are the drugs most commonly used for rate control. These agents do not convert atrial fibrillation to sinus rhythm
and should not be used for that purpose. Beta blockers and calcium channel blockers are
effective in reducing the heart rate at rest and during exercise in patients with AF. Digoxin,
because of the inotropic effects, is the drug of choice in patients with coexisting systolic heart
failure. Factors that should guide drug selection include the patient’s medical condition and
the presence of concomitant heart failure. The following drugs are recommended for their
demonstrated efficacy in rate control at rest and during exercise: diltiazem, atenolol, metoprolol, and verapamil.
Other key points: Rate control with chronic anticoagulation is the recommended strategy for
the majority of patients with chronic AF. Rhythm control has not been shown to be superior
to rate control (with chronic anticoagulation) in reducing morbidity and mortality.
Control the heart rate, then anticoagulate. Use aspirin for those with CHADS 0 or 1, and
dabigatran, rivaroxaban, or warfarin for CHADS 2 or more. Heparin is not necessary prior to
starting oral anticoagulants.
Patients with AF should receive chronic anticoagulation with dabigatran, rivaroxaban, or
adjusted-dose warfarin, unless they have a specific contraindication.
Initial management: The goals are hemodynamic stabilization, ventricular rate control, and
prevention of embolic complications. When AF does not terminate spontaneously, the ventricular rate should be treated to slow ventricular response and anticoagulation started.
Wolff-Parkinson-White Syndrome (WPW)
• Pre-excitation has been defined as a condition in which all or some portion of the
ventricle is activated by atrial impulses earlier than if the impulses were to reach the
ventricles by way of the normal cardiac conduction pathways. This is achieved by the
use of accessory pathways (Kent bundle).
• Classically, the EKG shows a short PR interval followed by a wide QRS complex with a
slurred initial deflection, or delta wave, that represents early ventricular activation.
• WPW is associated with:
– Paroxysmal supraventricular arrhythmias alternating with ventricular arrhythmias
– Atrial fibrillation and flutter
Treatment
If the patient is hemodynamically unstable, then immediate electrical cardioversion is indicated
(synchronized cardioversion). If the patient is hemodynamically stable, then procainamide is
the best medication. Avoid digoxin, beta blockers and calcium-channel blockers, as they can
inhibit conduction in the normal conduction pathway. This will potentially increase the likelihood of developing ventricular or supraventricular tachycardia. If conduction is inhibited in the
normal pathway, this will increase conduction in the aberrant conduction pathway. Ablation is
used as definitive treatment.
168
Chapter 5
Figure 5-16. Wolff-Parkinson-White Syndrome
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
l Cardiology
I
II
III V3 V6
II
Ventricular tachycardia (VT) is defined as 3 or more consecutive beats of ventricular origin at
a rate >120 beats/min. QRS complexes are wide and often bizarre.
Etiology
• Particularly after an acute MI
• Cardiomyopathies and rarely seen in patients with mitral valve prolapse
• Metabolic derangements, such as hypokalemia, hypercalcemia, hypomagnesemia, and
hypoxia
• Digitalis toxicity and thioridazine drugs
aVR V1 V4
aVL V2 V5
aVF
Clinical Manifestations
• Patients with VT often present with concomitant hypotension, CHF, syncope, or cardiac
arrest.
• Independent and asynchronous atrial and ventricular contractions produce the following signs. These signs are absent when atrial fibrillation is present.
– Variation in systolic blood pressure, as measured peripherally
– Variation in the intensity of the heart sounds
– Intermittent cannon A waves in the jugular venous pulses caused by the simultane-
ous contraction of the atrium and the ventricles
– Extra heart sounds
• Because of asynchronous activation of the right and left ventricles, the first and second
sounds are widely split.
Diagnosis and differential diagnosis: See Table 5-14.
169
Соседние файлы в папке Библиотека им академика М.И. Перельмана