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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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Initial Management
Setting: emergency department
Diagnostic/Therapeutic Plan
Test Results
Assessment
This case is meant to illustrate all the main complications of myocardial infarction (MI). All
the disorders listed in the differential can result in sudden hypotension in a patient with an
acute MI. Inferior wall MI usually carries the lowest mortality, at about 5% after 1 year.
However, extension to the other walls or the valves is always possible. Jarisch-Bezold reflex
is a vagally mediated reflex, resulting in bradycardia, hypotension, nausea, and vomiting. This
is particular to inferior wall MI because of the inferior wall’s proximity to the diaphragm. All
of the arrhythmias could be excluded first because an electrocardiogram is generally much
Complete heart block6.
Ventricular tachycardia7.
Sinus bradycardia8.
Ventricular rupture9.
Ventricular septal defect10.
Electrocardiogram
Atropine
IV fluids (normal saline or Ringer’s lactate)
Discontinue beta blockers, nitrates, and calcium channel blockers while hypotensive
Complete heart block with ventricular rate 40/min
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easier to obtain than an echocardiogram. In addition, all of the valvular abnormalities severe
enough to give this presentation would certainly result in an audible murmur.
Anatomic defects such as ventricular septal defect, valve rupture, and free wall rupture usually
occur several days after an infarction. They usually need several days for sufficient necrosis to
occur.
CCS NOTE
Always bolus the patient with normal saline or the initial set of orders in a hypotensive
patient.
The most essential feature of this case is the bradycardia. All the complications of MI
described here—besides AV block—should cause tachycardia. Valve rupture and ventricular
septal defect should give rales on lung examination. The most common cause of third-degree
AV block is idiopathic fibrosis.
The “cannon” a-waves visible on the physical exam are exaggerated pulsations from the atria
contracting out of sync with the ventricles and, hence, against a closed AV valve. This produces
a backflow of blood into the neck veins, resulting in the cannon a-waves. The cannon a-waves
are the main way to clinically distinguish this case from simple sinus bradycardia. Complete
heart block is a well-known complication of MI. It is particularly associated with inferior wall
infarction because in most people the right coronary artery supplies the blood to both the
inferior wall and the AV node.
Further Management Plan
Pacemaker placement, transcutaneous
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CCS NOTE
In an unstable patient with bradycardia, atropine can be ordered at the same time as the
electrocardiogram and bolus of saline. All symptomatic bradycardias should be treated
with atropine, so the specific etiology is not as important as stabilization.
Discussion
Although large volumes of IV fluid is generally the initial treatment for hypotension, atropine
should be the primary, specific treatment for complete heart block. Atropine can accelerate the
heart rate instantly and restore BP that way. If it does not work, fluids should be given. On the
exam when you see isoproterenol in the answer choice, it is always wrong.
Pacemaker placement is central to the treatment because it is the only modality that can
continually keep the heart rate adequate. Complete heart block can also occur as a form of
toxicity with any medication that is negatively dromotropic, such as beta-blockers or calcium-
channel blockers or digoxin. Myocarditis from viruses or Lyme disease can also cause
complete heart block, although this is rare. Besides the acute MI described in this case, the
most common cause of an AV block is aging and fibrosis of the conduction system. The
treatment of third-degree AV block from digoxin overdose is with digoxin-binding antibodies,
or Digibind.
If ineffective, possible use of dopamine to support BP—
Trans-venous pacemaker
Cardiology consult
Keep in ICU
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Simple hypovolemia is treated with fluids and dopamine. Wall and valve rupture and
ventricular septal defects would need an emergent operative repair. Ventricular tachycardia
with the hypotension described in this case would need immediate electrical cardioversion.
Right ventricular infarction could cause hypotension and is often associated with an inferior
wall myocardial infarction. This is because the right ventricle has the same arterial supply as
the inferior wall. Right ventricular infarction should give tachycardia and would not give the
cannon a-waves. Right ventricular infarction is treated with fluid administration.
CCS NOTE
Consultants will see the patient in 20 min. They will never give specific advice or
direction.
Follow-up Management and Prevention
CLINICAL PEARL
Prasugrel or ticagrelor are used as second anti-platelet agents in conjunction with
stenting.
Keep patient in ICU until pacemaker placed and hemodynamically stable
Continue ACE inhibitor, statin, aspirin, and second anti-platelet agent (clopidogrel)
Consider angiography and angioplasty/stenting (relieving ischemia improves many
arrhythmias)
Administer GP IIb/IIIa agent if patient gets stented (e.g., eptifibatide, tirofiban)
Educate patient on smoking cessation and exercise when he is stable
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Final Diagnosis
Complete heart block
CLINICAL PEARL
Other causes of rapid drop in BP in the setting of an MI include:
Valvular Rupture and Septal Rupture
Ventricular Rupture/Tamponade
Cardiogenic Shock
Occurs 5–10 days after an MI with sudden dyspnea, rales, and tachycardia
Prominent new murmur confirmed with echocardiography
Afterload reduction with ACE inhibitors and immediate surgery
Sudden hypotension, tachycardia, and clear lungs
Jugulovenous distension and pulsus paradoxus
Confirm with echocardiogram and treat with an emergent pericardiocentesis and
surgical correction
Tachycardia, hypotension, and prominent rales on examination
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Case 3
Chief Complaint
“I have a funny sensation in my chest.”
History and Physical Examination
A 72-year-old man comes to the emergency department suffering from chest discomfort for
less than 1 hour. He states that he has a history of arrhythmia but is taking no medications.
He has had similar episodes in the past. The chest discomfort does not radiate and does
not cause dyspnea but is associated with diaphoresis.
Vital signs are BP 80/60 mm Hg, pulse 180/min, and respirations 24/min. Physical
examination shows jugular venous distention. Breath sounds are diminished at the bases,
and heart sounds are distant. The remainder of the examination is unremarkable.
Differential Diagnosis
Ventricular tachycardia1.
Supraventricular tachycardia2.
Atrial fibrillation3.
Atrial flutter4.
Myocardial infarction5.
Myocardial ischemia6.
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CLINICAL PEARL
Although you cannot determine a specific etiology from the physical examination, the
heart rate means that there has to be a rhythm disturbance in this patient. Sinus rates
maximize at 220/min minus the age. Thus, in this patient, any rate >150/min would
indicate an arrhythmia.
Initial Management
Setting: emergency department
Diagnostic/Therapeutic Plan
Test Results
PATIENT SAFETY NOTE
Check oximeter and give oxygen to anyone who is dyspneic or hyperventilating.
Electrocardiogram
Oxygen, normal saline bolus
Oximeter
Oxygen: ventricular tachycardia at rate 180/min
Oximeter: 98% saturation on room air
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Assessment
Ventricular tachycardia is characterized electrocardiographically by a rapid rhythm with a
widened QRS complex and evidence of atrial-ventricular dissociation.
Electrolyte abnormalities such as hypomagnesemia, hypocalcemia, hyperkalemia, and
hypokalemia can also lead to ventricular tachycardia. Tricyclic antidepressant overdose can
lead to ventricular tachycardia as well.
Torsades de Pointes is a particular type of ventricular tachycardia with an undulating baseline.
Torsades is particularly associated with hypomagnesemia, drugs that widen the QT interval,
and a congenital prolonged QT syndrome. Drugs that prolong the QT are quinidine,
procainamide, and tricyclic overdose.
Further Management Plan
CCS NOTE
Often associated with underlying heart disease, which is often ischemic.
Often deteriorates into ventricular fibrillation; stroke volume will be markedly decreased
because of loss of filling time for the ventricles, resulting in cardiovascular collapse
Arises from a focus of irritability in the ventricle due to ischemia or scar; heart rate is
usually 100–180/min
DC cardioversion
Lidocaine or amiodarone
Check and treat underlying potassium, calcium or magnesium abnormalities
Electrolytes : Normal
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Any patient with a ventricular rhythm disturbance should be placed in the ICU at the
end of the case.
Discussion
Ventricular tachycardia can be confused with supraventricular tachycardia with a bundle
branch block; SVT with aberrant conduction or Wolff-Parkinson-White. Because of the risk of
deterioration into ventricular fibrillation, ventricular tachycardia is a serious arrhythmia, even
in the asymptomatic patient with adequate cardiac output.
CLINICAL PEARL
Any wide-complex tachycardia in a patient with ischemic heart disease is ventricular
tachycardia until proven otherwise.
Treatment of ventricular tachycardia, in the presence of significant hemodynamic compromise,
is cardioversion, and the decision has to be made at bedside. Cardioversion should be done
with systolic BP <90 mm Hg, mental status changes, CHF, and/or chest pain.
Amiodarone should be used first in an acute episode of ventricular tachycardia.
Lidocaine is the agent of choice for ventricular tachycardia when the myocardium is
ischemic and the patient is hemodynamically stable to prevent recurrence after
cardioversion.
Procainamide and amiodarone can be used instead of lidocaine to convert the rhythm in a
hemodynamically stable patient.
Amiodarone is the better agent when there is an abnormal left ventricle.
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