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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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Test Results
CCS NOTE
Unsynchronized cardioversion is always the first thing to do if ventricular fibrillation
is found. It’s more important than any specific diagnostic test.
Assessment
Ventricular fibrillation causes loss of cardiac output, and death occurs within a few minutes. It
is not a realistic diagnostic consideration in the conscious patient. There is irregularly irregular
undulation of the baseline at variable rates without any organized QRS activity.
Immediate direct-current defibrillation should be administered to all patients with ventricular
fibrillation. Once the heart is successfully defibrillated, immediate attention must be given to
correct underlying causes and to institute prophylactic antiarrhythmics. The absolute priority in
any attempt to resuscitate from ventricular fibrillation is electrical defibrillation. Without an
electrocardiogram, it is not possible to tell if the cause of a patient’s loss of pulse is asystole,
ventricular fibrillation, ventricular tachycardia, or electrical-mechanical dissociation.
Ventricular arrhythmia is a known complication after anterior-wall myocardial infarction.
Further management plan Results
Electrocardiogram
Ventricular fibrillation
281
Treatment Plan
Discussion
In a case of ventricular fibrillation, immediate defibrillation is the critical intervention.
Defibrillation is an unsynchronized shock; when one delivers a synchronized shock, it is
synchronized to the ventricular contraction. There is no ventricular contraction in ventricular
fibrillation. There are 3 conditions where defibrillation should be delivered: ventricular
fibrillation, pulseless ventricular tachycardia, Torsades de pointes.
CCS NOTE
Patients with ventricular rhythm disturbances should be placed in the ICU.
Arterial blood gases
1.
pH 7.12; pCO
2
42 mm Hg; pO
2
90 mm Hg; bicarbonate 14
mEq/L
1.
Cardiopulmonary resuscitation until the defibrillator arrives
1.
Defibrillate at 360 J, perform several cycles of CPR after defibrillation
2.
Repeat defibrillation at 360 J
3.
IV access
4.
Intubate
5.
Epinephrine intravenously or vasopressin once every 5 minutes
6.
Repeat defibrillation at 360 J
7.
Amiodarone or lidocaine; if both are answer choices, choose amiodarone
8.
Consider bicarbonate
9.
Repeat defibrillation at 360 J
10.
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Precordial thumping is indicated only when the arrest is witnessed and no defibrillator is
available. Cardiopulmonary resuscitation should not be interrupted except while defibrillation
is being administered.
Although medications such as amiodarone, lidocaine, and procainamide are used, their efficacy
is considerably less than that of electrical defibrillation. Hence, the order is shock-drug-shock-
drug-shock, etc.
Ventricular Fibrillation
First, administer 360 J of direct-current countershock with one paddle at the apex and the
other at the aortic position.
Proceed with 5 cycles of CPR immediately after the shock.
Evaluate cardiac rhythm after the 5 cycles of CPR. Failure of ventricular fibrillation to
revert to normal sinus rhythm after direct-current countershock may be due to severe
acidosis, hypoxia, myocardial failure, or a combination of all 3.
Continue CPR, correct abnormalities, and continue advanced cardiac life support protocol
according to treatment guidelines.
Vasopressin has been added as an alternative to epinephrine.
Amiodarone has been added as an alternative to lidocaine.
Bretylium should not be used.
Magnesium can be used in any serious ventricular arrhythmia; its greatest efficacy is in
patients with Torsade de pointes.
283
CCS NOTE
Never order intracardiac administration of medications on the CCS.
Final Diagnosis
Ventricular fibrillation
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Case 10
Chief Complaint
“I’m nauseous and can’t stop vomiting.”
History and Physical Examination
A 44-year-old business executive comes to the emergency department with complaints of
severe nausea and vomiting over the past 12 hours. He has been under a great deal of
pressure recently and has been taking numerous over-the-counter cold preparations and
acetaminophen around the clock for a severe upper respiratory tract infection. He has had
several emergency department visits for alcohol intoxication, including one episode of
alcohol withdrawal. He is a chain smoker and has several glasses of wine with dinner
each evening.
Vital signs are T 37.9 C (100.2 F), BP 110/75 mm Hg, pulse 100/min, and respirations
20/min. Physical examination is unremarkable, except for mild right upper quadrant
tenderness without rebound or guarding.
Differential Diagnosis
Acetaminophen overdose1.
Appendicitis2.
Acute gastroenteritis3.
Acute cholecystitis4.
Acute pancreatitis5.
285
Initial Management
Setting: emergency department or office
Diagnostic/Therapeutic Plan
Test Results
CCS NOTE
Sometimes you cannot identify the diagnosis on the initial history in the CCS. Do not
worry. Order tests around the history, and the specific diagnosis will be revealed later.
Just don’t count on consultants to help you.
Hepatitis
6.
CBC
Electrolytes
LFTs
Prothrombin time
Amylase level
Abdominal U/S
WBC count 12,800/mm
3
, hemoglobin 13.0 g/dL, platelets 210,000/mm3
Electrolytes: normal
AST (SGOT) 74 U/L, ALT (SGPT) 92 U/L, total bilirubin 1.6 mg/dL
Prothrombin time: 12.2 sec
Amylase: normal
U/S: normal
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Assessment
The differential diagnosis in a 44-year-old patient presenting with nausea and vomiting is quite
broad. It is important to recognize that many over-the-counter cold preparations contain
acetaminophen. In addition, the patient has been taking large doses of supplemental
acetaminophen.
Patients with significant alcohol ingestion are at increased risk for developing clinical
acetaminophen toxicity, as they may have some level of baseline hepatic injury. The absence of
significant associated fever and a normal WBC count speak against appendicitis, pancreatitis,
and cholecystitis, though those are all considerations here.
Further Diagnostic Plan/Results
CCS NOTE
Normal values are routinely provided with the test results on the CCS. Do not worry
about memorizing uncommon test results, such as acetaminophen levels.
Treatment Plan
Serum acetaminophen level: 150 μg/mL
Aspirin level: 0 mg/dL
Gastric lavage or induced emesis with ipecac if patient not already vomiting; most
useful within 1 hour of ingestion. There is a non-significant effect after 2 hrs.
1.
Acetylcysteine (Mucomyst) which is beneficial up to 24 hours after ingestion2.
287
Discussion
Early clinical manifestations of acetaminophen overdose include anorexia, nausea, vomiting,
diaphoresis, and malaise. Hepatotoxicity is the major concern, with peak injury occurring 72–
96 hrs after ingestion.
To determine if the patient is at risk for the sequelae of acetaminophen overdose, the serum
acetaminophen level is plotted against time after ingestion. The level is more accurate after 4
hrs; prior to that, absorption is still occurring and the level may still be rising.
CLINICAL PEARL
Ipecac is rarely used in the ED, as it delays the administration of antidotes orally. It is
most useful for those with an accidental ingestion at home.
Further Management:
The initial management of acetaminophen overdose focuses on minimizing absorption of the
drug with gastric lavage or induced emesis.
Charcoal administration in between the doses of acetylcysteine (administer 1 hr apart)
3.
Ipecac is rarely, if ever, used in the ED; it is primarily for home management of overdose in
those who have not yet arrived at the hospital.
Charcoal may interfere with absorption of acetylcysteine (the antidote) if given at the exact
same time, so the doses should be interspersed.
Acetylcysteine should be administered as quickly as possible for up to 24 hrs after ingestion
of acetaminophen.
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CCS NOTE
Order acetaminophen and aspirin levels with any overdose case on the CCS. Co-
ingestion is frequent. You won’t lose points, even if the aspirin level is normal (as seen
here). On the CCS, missing an occult aspirin or acetaminophen overdose is more
dangerous than finding an additional normal level.
Patients with hepatic injury due to acetaminophen toxicity may require liver transplant. One
very important value to monitor is prothrombin time. If this rapidly increases along with signs
of hepatic encephalopathy, the patient has fulminant hepatic failure and needs a liver transplant.
A single dose of 10–15 grams is sufficient to result in evidence of hepatic injury. Fatalities can
occur with >15-gram ingestion; however, in chronic alcoholics, toxicity may begin with as
little as 4 grams. In the first 4–12 hrs, the early symptoms are nausea, vomiting, diarrhea, and
abdominal pain, which often resolve; 24–48 hrs later, evidence of hepatic injury begins. The
injury is not directly caused by the acetaminophen but rather by a toxic metabolite formed by
the hepatic cytochrome p450 system.
A common question seen on the USMLE is acetaminophen overdose in alcoholics. Chronic
alcohol depletes the glutathione stores and can predispose to acetaminophen toxicity at lower
levels than in non-alcoholics. One important point is that alcoholic hepatitis can never lead to
AST > 500. Thus, if a patient has AST and ALT in the thousands, it is very likely the patient
has acetaminophen toxicity and needs to be treated with acetylcysteine.
Acetylcysteine repletes glutathione stores.
289
CLINICAL PEARL
Acetaminophen toxicity causes hepatic injury, which elevates transaminase (ALT, AST)
levels >1,000. When hepatic injury occurs in acetaminophen toxicity, acetylcysteine is
not effective since this occurs typically 2 days after the ingestion.
Final Diagnosis
Acetaminophen overdose
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