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USMLE Step 2 CK
l Internal Medicine
Note
Management of VT without
hemodynamic instability
1. Amiodarone
2. Lidocaine
3. Cardioversion
Note
For systolic dysfunction, the
only antiarrhythmics that
are safe are amiodarone,
lidocaine, and dofetilide.
Treatment. For those with sustained VT and a pulse who are hemodynamically unstable,
immediate synchronized cardioversion is required. Signs of hemodynamic instability requiring cardioversion include hypotension, chest pain, altered mental status, and CHF. A lower
dose of electricity, starting at 100 J, can be used at first for monomorphic VT. The cardioversion should be synchronized. Conscious patients should be sedated with midazolam, fentanyl,
or morphine before cardioversion.
VT in those patients without a pulse should be managed in the same way as ventricular fibrillation (unsynchronized shock). Stable VT (wide, monomorphic, regular) without serious
hemodynamic compromise can be treated medically with adenosine initially and then with
antiarrhythmics if no response. In stable patients with pulse, procainamide and sotalol are
preferred drugs. If there is no response to procainamide, then amiodarone may be tried, followed by lidocaine and finally electrical cardioversion.
Magnesium may be useful in general but it is most useful for Torsade de pointes. If magnesium fails to treat Torsade, then isoproterenol or lidocaine can be attempted. Overdrive pacing
can be used if pharmacologic treatment fails. Patients undergoing cardioversion should be
sedated first with midazolam, fentanyl, or morphine. Long-term therapy is most effective with
beta-blockers. VT that produces sudden death or VT that is sustained through initial drug
therapy may require the placement of an implantable cardiac defibrillator (ICD). All patients
with ejection fraction <35% should have ICD, due to increased risk of VT and VF.
Pulseless electrical activity
Definition. Hypotension to the point of losing one’s pulse; there is still some type of electrical
activity on the EKG that may even be normal or a simple tachycardia.
Etiology. More than the other dysrhythmias, knowing the etiology of pulseless electrical activity (PEA) is the key to the therapy because the specific therapies are so divergent. Essentially,
the heart may still be beating, but there is no blood in the heart, and therefore there is no cardiac output. Examples of this type of PEA are severe hypovolemia, cardiac tamponade, tension
pneumothorax, massive pulmonary embolism, and a massive myocardial infarction. Other
types of PEA in which there may not be actual muscular contraction are hypoxia, hypothermia,
potassium disorders, acidosis, and drug overdoses with tricyclics, digoxin, beta-blockers, or
calcium-channel blockers.
Clinical Presentation. The patient appears to be dead with no pulse. Other symptoms are
based on the specific nature of what led to the PEA, such as those described above.
Diagnosis. A pulseless patient who has significantly organized, and occasionally normal, activity
on the EKG.
Treatment. The most important action is to maintain CPR while determining the specific origin of the PEA. General therapy includes CPR, IV access, intubation, and epinephrine. Do not
shock PEA arrest. The most important therapy is repair of the cause (possibilities described
above). Bicarbonate is useful if a known acidosis has caused the arrest; it can also be used in
a prolonged resuscitation if severe lactic acidosis develops and causes the refractory state of
arrest. Pericardiocentesis may be attempted if all else fails.
350
Atrial dysrhythmias
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A 24-year-old medical student is brought to the emergency department because
of palpitations. He has been studying vigorously for the USMLE Step 2 exam
and has been up for the last 24 hours. He has had 5 cups of coffee, 4 beers, 3
stimulant tablets, 2 cheeseburgers, and 1 Viagra. An electrocardiogram reveals an
atrial dysrhythmia.
Chapter 10
l Emergency Medicine
Definition. A-fib, atrial flutter, and SVT are all characterized by either an ectopic focus in the
atrium or re-entry at the AV node. All have normal conduction in the ventricular myocardium once the impulse successfully passes the AV node and travels down the normal ventricular conduction system. They all have a normal or narrow QRS complex and the absence of a
normal P-wave.
Etiology. A-fib is most commonly caused by chronic hypertension, but it can be caused as
well by valvular heart disease (most often mitral valve pathology), left ventricular hypertrophy, cardiomyopathy, atrial fibrosis, atrial dilation, CAD, and CHF. Another cause is toxicity
causing overstimulation of the heart, i.e., hyperthyroidism, pheochromocytoma, caffeine,
theophylline, alcohol, and cocaine. Drug toxicity (such as digoxin), pericarditis, pulmonary
embolism, surgery, chest wall trauma, or ischemia can also cause atrial dysrhythmias.
SVT is caused by a re-entrant mechanism around or within the AV node.
Clinical Presentation. Symptoms vary on the basis of the duration of the disorder, the ventricular rate, and the underlying health of the heart. With a normal heart, only 10-20% of
cardiac output is directly derived from the contribution of atrial systole. With a dilated or
postinfarction heart, or with significant valvular disease, this contribution may rise to 30-40%,
in which case more severe symptoms arise. Symptoms range from complete absence to palpitations to lightheadedness, hypotension, disorientation, CHF, and syncope. Rate-related
symptoms are unlikely in those with heart rate <150 per minute in atrial dysrhythmias.
Narrow complex tachycardia is always atrial in origin (QRS <0.12). Wide complex tachycardia
can be atrial or ventricular. For example, it is very difficult to distinguish A-fib in the presence
of LBBB and VT. The key is that in A-fib with LBBB, the rate is irregular on EKG, whereas in
VT it is regular. If in doubt, treat as VT.
Note
For the exam, you will need
to know atrial fibrillation
(A-fib), atrial flutter, and
supraventricular tachycardia
(SVT). They are discussed as
a group because the initial
management has considerable
overlap.
Diagnosis. Initially, the diagnosis is based entirely on the EKG. Other patients may need a
24-72 hour Holter monitor to detect brief paroxysms of the dysrhythmia not seen on the initial
brief EKG.
Figure 10-7. Normal Sinus Rhythm
351
USMLE Step 2 CK
Figure 10-8. Atrial Tachycardia
Figure 10-9. Atrial Flutter
Figure 10-10. Atrial Fibrillation
Note
• Narrow complex
tachycardia is always atrial
in origin (QRS <0.12).
• Wide complex tachycardia
can be atrial or ventricular
in origin.
l Internal Medicine
352
Treatment. Initial therapy is based on whether there are signs or symptoms of severe hemodynamic compromise, such as hypotension, confusion, CHF, or chest pain. If these are present, then
immediate synchronized cardioversion is performed. Palpitations and lightheadedness are not
signs of hemodynamic compromise. If the patient is hemodynamically stable, then the first step
is to control the ventricular rate. Vagal maneuvers such as carotid sinus massage, Valsalva, or ice
water immersion are most effective in SVT. Do not do carotid sinus massage bilaterally. Avoid
carotid massage in those with carotid bruits. If vagal maneuvers do not work, SVT is initially
treated with several rapid IV infusions of adenosine. For atrial fibrillation, atrial flutter, and in
SVT after the failure of adenosine, several therapies are available to slow the heart rate. These
include calcium-channel blockers (such as diltiazem or verapamil), beta-blockers, or digoxin. Do
not use verapamil in those with severe left ventricular dysfunction and low ejection fractions and
beware of using beta-blockers in those with a history of reactive airway disease.
After the rate has been lowered to <110 beats/min, conversion of the rhythm to normal sinus
does not need to be routinely done. Chronic rate control with anticoagulation with warfarin to
an INR of 2–3 is superior to converting the patient into sinus rhythm. Returning the patient to a
normal sinus rhythm is preferable because chronic atrial fibrillation can result in embolic stroke
in 5-7% of patients per year.
Chapter 10
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l Emergency Medicine
Amiodarone, ibutilide, propafenone, and dofetilide can all convert a minority of patients to
sinus rhythm. At the level of Step 2, you will not need to know much about the specific indications for each. You do, however, need to know that elective cardioversions should be preceded
and followed by several weeks of anticoagulation with coumadin.
Rate Control vs. Rhythm Control. When patients present in A-fib with rapid ventricular
response, hemodynamic stability must first be determined. If they are hemodynamically
stable, they should be rate-controlled with AV nodal blocking agents. If they are unstable,
immediate synchronized cardioversion is required. With long-term management, rate control
and anticoagulation are preferred over rhythm control. Rhythm control should be considered
in the following situations:
• Symptomatic patients on rate control (poor exercise tolerance)
• Younger patients with normal heart structure and function
• Patients that are unable to be rate controlled with AV nodal blocking agents
It is very difficult to keep patients with structural heart disease in normal sinus rhythm.
Several studies have shown an increase in overall mortality with rhythm control. Catheterdirected ablation of the AV node or accessory pathway may also be used when pharmacological treatment fails to control rate.
The rate control goal is 60–80 bpm at rest and 90–115 bpm with moderate exercise.
Medications that might be used for rate control are diltiazem, beta-blockers, verapamil, or
digoxin. Most patients require combined therapy. B-blockers with digoxin have been shown to
be the best combination. Digoxin should be used for rate control in patients with CHF first;
amiodarone can be used as second-line therapy. B-blockers should be started with caution in
CHF patients once they are euvolemic on exam.
Note
A-fib Plus Flutter
• For patients with A-fib and
flutter, give rate control
treatment along with
anticoagulation (aspirin,
warfarin, etc).
• When warfarin is used,
optimal INR therapeutic
range should be 2.0−3.0.
Agents for chemical cardioversion in A-fib: amiodarone, dofetilide, flecainide, ibutilide,
propafenone. In CHF patients, use amiodarone and dofetelide.
Agents for maintaining sinus rhythm: flecainide, propafenone, sotalol, dofetilide, and amiodarone. To maintain normal sinus rhythm in CHF patients, use only amiodarone or dofetilide.
In patients with coronary artery disease, dofetilide and sotalol are superior to amiodarone.
The CHADS2 score is used to determine if a patient with non-valvular A-fib needs anticoagulation.
CHADS2 Score Treatment
0 Give aspirin
1 Give aspirin or anticoagulation
≥2 Give anticoagulation
Dabigatran is an oral direct thrombin inhibitor that has been shown to reduce the incidence
of ischemic stroke compared to warfarin, with similar rates of bleeding. Rivaroxaban is an
oral factor Xa inhibitor. For anticoagulation, you can use coumadin, dabigatran, or rivaroxaban. Apixaban, another oral factor Xa inhibitor, may be used instead of coumadin for stroke
prophalaxis in patients with atrial fibrillation and a high risk of stroke (CHADS2 score of 2 or
higher). All 3 drugs—dabigatran, rivaroxaban, and apixaban—lead to similar or lower rates
Note
CHADS2 RISKS
CHF
HTN
Age >75
Diabetes mellitus
Stroke (gives 2 points)
353
USMLE Step 2 CK
l Internal Medicine
both of ischemic stroke and major bleeding compared to coumadin; there is no need for monitoring INR.
Important additional advantages of these newer agents include convenience (no requirement
for routine testing of the international normalized ratio), a small reduction in the risk of
intracranial hemorrhage, and less susceptibility to dietary and drug interactions.
Disadvantages include lack of an antidote and the potential that new side effects may be seen
over time.
Note
Patients with A-fib and
thyrotoxicosis always get
anticoagulation until euthyroid
and back in NSR.
For patients undergoing elective cardioversion, first determine if they have been in A-fib for
>48 hours. If they have, there are 2 options:
• Transesophageal echo can be done to exclude a clot; then, cardioversion (electrical or
chemical). Cardioversion should be followed by 6 weeks of coumadin.
• Coumadin can be administered for 3 weeks before electrical or chemical cardioversion. Cardioversion should be followed by another 6 weeks of coumadin.
It is very difficult to maintain patients with structural heart disease in NSR, and most convert
back into atrial fibrillation. Atrial flutter is managed the same way as atrial fibrillation.
For patients in A-fib with Wolff-Parkinson-White syndrome, administration of drugs which
slow AV node conduction (Ca-channel blockers, digoxin) is strongly contraindicated as they
can induce VT. Procainamide, ibutilide, flecanide, or amiodarone can be used in such cases.
If none of the medications described above can successfully convert the patient to a normal sinus rhythm, then elective electrical cardioversion can be attempted. This too must
be preceded and followed by several weeks of anticoagulation if the A-fib has been present
for >48 hours. Transesophageal echo can be done to exclude a clot and allow the cardioversion without preconversion anticoagulation. Neither medical nor electrical cardioversion can permanently maintain the majority of patients on sinus rhythm. Most convert
back into atrial fibrillation.
Bradycardia
354
A 48-year-old manager comes for advice about vaccinations and travel medicine
before traveling to a far-off land. He feels well and has no symptoms. He takes no
medications. On examination you find a blood pressure 118/76 mm Hg and pulse
40/min.
Definition. A slow heart with a rate <60 beats/min.
Etiology. Sinus bradycardia can be a normal phenomenon, particularly in trained athletes.
Medications such as beta-blockers can also give a sinus bradycardia without serious sequelae.
Symptomatic sinus bradycardia from sinus node disease can be from degeneration of the
node or from ischemia. More serious types of bradycardia can be from Mobitz type II seconddegree heart block and third-degree (complete) heart block. These can occur secondary to
ischemic damage of the AV node. Other causes are myocarditis, infiltrative disease, such as
amyloidosis or sarcoidosis, or neoplasms.
Chapter 10
Figure 10-11. First-Degree Heart Block
Figure 10-12. Second-Degree Heart Block
Figure 10-13. Complete Heart Block
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Clinical Presentation. This can range from the lifelong absence of symptoms to severe symptoms of hypotension and decreased cardiac output.
Diagnosis. EKG
l Emergency Medicine
Note
Mobitz type I second-degree
block is characterized by
progressive P-R lengthening,
whereas in Mobitz-type II, the
P-R interval remains constant.
Note
Transcutaneous pacing
is always preferred over
transvenous pacing in the
acute setting.
Treatment. Asymptomatic sinus bradycardia, first-degree AV block, and Mobitz type I
(Wenckebach) second-degree AV block often need no specific therapy. Any form of severe
symptomatic bradycardia is treated initially with atropine and then a pacemaker, if there is no
improvement in symptoms.
Mobitz type II second-degree block and third-degree block require the placement of a pacemaker, even in the absence of symptoms. Dopamine or epinephrine is used to improve blood
pressure if there is still hypotension after the use of atropine.
For symptomatic sinus bradycardia, treatment is atropine. If atropine fails, then use transcutaneous pacing.
Note
If the patient is on a
beta blocker, give glucagon.
If the patient is on a calcium
channel blocker, give calcium.
355
USMLE Step 2 CK
3
l Internal Medicine
1
BRADYCARDIA
Heart rate <60 bpm and
inadequate for clinical condition
2
• Maintain patent airway; assist breathing as needed
• Give oxygen
• Monitor ECG (identify rhythm), blood pressure, oximetry
• Establish IV access
Signs or symptoms of poor perfusion caused by the bradycardia?
(e.g., acute altered mental status, ongoing chest pain, hypotension, or other signs of shock)
4A
Observe/Monitor
Reminders
• If pulseless arrest develops, go to pulseless arrest algorith m
• Search for and treat possible contributing factors:
– Hypovolemia – Toxins
– Hypoxia – Tamponade, cardiac
– Hydrogen ion (acidosis) – Tension pneumothorax
– Hypo-/hyperkalemia – Thrombosis (coronary or pulmonary)
– Hypoglycemia – Trauma (hypovolemia, increased ICP)
– Hypothermia
Adequate
Perfusion
Poor
Perfusion
Figure 10-14. Algorithm for Bradycardia
4
• Perfect for transcutaneous pacing;
use without delay for high-degree block
(type II second-degree block or
third-degree AV block)
• Consider atropine while awaiting pacer;
if ineffective, begin pacing
• Consider dopamine infusion while
awaiting pacer or if pacing ineffective
and blood pressure is low
5
• Prepare for transvenous pacing
• Treat contributing causes
• Consider expert consultation
356
Chapter 10
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TOXICOLOGY: GENERAL PRINCIPLES/INITIAL EVALUATION
A 25-year-old medical student goes home after class and finds no messages
on the answering machine from his girlfriend. In a fit of despair he takes a full
bottle of pills in an attempt to commit suicide. He takes the label off the bottle
to prevent any attempt to reverse the poisoning through the identification of the
specific agent. Immediately after doing this, his girlfriend calls, after which he runs
to the nearest emergency department and states that he has changed his mind
and wants to live after all. He walks into the emergency department 30 minutes
after the ingestion. He won’t tell you the specific name of what he took and wants
to know what is the next best thing to do.
Management. The initial evaluation of a patient who has been poisoned involves attempting
to find out the nature of the toxin ingested. At the same time, history and physical examination can give clues to the nature of the toxin. In this patient, the key issue is the short time
between the ingestion and his arrival in the emergency department. He is awake.
l Emergency Medicine
Toxidromes
Associated physical findings in specific toxidromes
• Miosis: clonidine, barbiturates, opiates, cholinergics, pontine stroke
• Mydriasis: sympathomimetics, anticholinergics
• Dry skin: anticholinergics
• Wet skin: cholinergics, sympathomimetics
• Blisters: barbiturates, carbon monoxide poisoning
Management of Toxic Ingestions or Overdose
Gastric emptying is rarely, if ever, utilized. In ingestions of an unknown type, a urine or blood
toxicology screen should be performed, but this should not delay the administration of antidotes, charcoal, or gastric emptying in the rare circumstances in which emptying is indicated.
• Induced vomiting. Ipecac can only be used within 1-2 hours after ingestion, so it has
no use in the hospital setting. Very few people arrive within the first hour. In addition,
ipecac can delay the use of oral antidotes such as charcoal or N-acetyl cysteine because
of the vomiting it induces. Ipecac is more useful for ingestions in the home, in which
the time period since ingestion is short and there are no other effective modalities
immediately available. Ipecac decreases absorption by 60% at 5 minutes after ingestion, 32% at 30 minutes, and 30% at one hour. Ipecac is never recommended for use
in children.
Lavage. Gastric emptying with a large-bore (37-42 French) oropharyngeal hose (e.g., an
•
Ewald tube) should only be used in those with an altered mental status and in whom
ipecac is dangerous because of possible aspiration. Lavage should therefore be preceded
by endotracheal intubation. Lavage is also only useful within the first hour after ingestion,
and is therefore very rarely, if at all, useful any more. Both ipecac and lavage are contraindicated with the ingestion of caustic substances such as acids or alkalis. Lavage decreases
absorption by 52% at 5 minutes, 26% at 30 minutes, and 16% at 60 minutes. The exact
indications for lavage are not clear, however, the contraindications are very clear.
Note
• Ipecac is never used
by physicians.
• Lavage has almost
no utility.
357
USMLE Step 2 CK
l Internal Medicine
Note
Charcoal does not bind to
some substances (PHAILS):
Pesticides
Heavy metals
Acid/alkali/alcohol
Iron
Lithium
Solvents
Note
Substances/drugs that may
require hemodialysis for
removal include (I STUMBLE):
Isopropanol
Salicylates
Theophylline
Uremia
• Charcoal. After gastric emptying or if, as in most cases, the patient arrives >1-2 hours
after the ingestion, the mainstay of therapy is activated charcoal administration.
Repeated doses every 2-4 hours are recommended to both block further absorption of
the substance and to accelerate the removal of already absorbed toxins from the body.
Charcoal is safe for all patients.
• Whole bowel irrigation. For large-volume pill ingestions in which the pills can be
seen on an x-ray, whole bowel irrigation can be effective. A gastric tube is placed and
high-volume (1-2 liters per hour) GoLYTELY (polyethylene glycol) is administered
until the bowel movements run clear.
• Dialysis. Dialysis is rarely necessary because the time delay to its initiation limits its
efficacy. If it is necessary, hemodialysis is 20x more efficacious at removing drugs from
the body than peritoneal dialysis. Dialysis is your answer when there are profoundly
serious symptoms such as coma, hypotension, or apnea, especially when renal or
hepatic failure limits the usual means of excreting substances from the body.
• Cathartics. Cathartics are useful when used with charcoal administration. Otherwise,
they are almost never helpful. When you see cathartics in the answer, it is generally the
wrong answer.
• Forced diuresis. Alkaline diuresis can help eliminate salicylates and phenobarbital.
Otherwise, simply making patients urinate in high volumes does not help the patient.
Except for salicylates and phenobarbital, forced diuresis is generally the wrong answer.
• Naloxone/dextrose/thiamine. These agents should be given first to any patient who
presents with altered mental status or coma. They are particularly useful in any toxin
ingestion that produces confusion. Naloxone has almost no adverse effects and works
instantly. Because of its rapid response, naloxone is both therapeutic and diagnostic.
Dextrose is also very effective at preventing permanent brain damage from hypoglycemia. It does not matter whether the dextrose or thiamine is given first.
Methanol
Barbiturates
Lithium
Ethylene glycol
Remember: Any toxin-related seizure should be treated with benzodiazepines as first-line
therapy. When benzodiazepines are not effective, barbiturates should be used next. Phenytoin
and fosphenytoin are not indicated or even effective for this type of seizure.
Toxicology Screening
Toxicology screen (tox screen) is a testing used to determine the approximate amount and
type of legal and/or illegal drugs. It is used to screen for drug abuse, monitor a substance
abuse problem, and evaluate drug intoxication for overdose.
• The best initial test in toxicology screen is the urine immunoassay (qualitative test).
The drugs typically screened for include alcohol, cocaine, PCP, amphetamines, and
cannabinoids.
• The confirmatory test is considered gas chromatography/mass spectrometry,
which provides qualitative analysis and allows identification of the specific drug or
its metabolites.
Tox screen must be done within a certain amount of time after the drug is taken, or while
metabolites can still be detected in the body. Some examples of the time it takes for drugs to
clear are listed below.
• Alcohol: 3−10 hrs
• Amphetamines: 24−48 hrs
358
• Barbiturates: up to 6 wks
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• Benzodiazepines: up to 6 wks with heavy use
• Cocaine: 2−4 days; up to 10−22 days with high level use
• Codeine: 1−2 days
• Heroin: 1−2 days
• Hydromorphone: 1−2 days
• Methadone: 2−3 days
• Morphine: 1−2 days
• Phencyclidine (PCP): 1−8 days
• Tetrahydrocannabinol (THC): 6−11 wks with heavy use
ACETAMINOPHEN
A 38-year-old man comes to the emergency department 4 days after the
ingestion of a full bottle (60 tablets) of acetaminophen (500 mg each). He
complains of vomiting and right upper quadrant pain. He has an elevated
bilirubin, AST, and prothrombin time.
Chapter 10
l Emergency Medicine
Definition. Acetaminophen is one of the few toxins about which precise toxicity levels are
known; the ingestion of approximately 140 mg per kg is usually sufficient to cause serious
toxicity. In other words, in an average-sized, 70-kg person, about 7–10 grams is enough to
produce toxicity, and fatalities can occur >12–15 grams. In those patients with liver disease
or concomitant alcohol abuse and thus depleted glutathione stores, the hepatotoxic dose is
less (4 grams/day).
Clinical Presentation. As with most large-dose pill ingestions, the initial symptoms are nausea
and vomiting, caused mostly from a gastritis caused by irritation from the pills over the first
12-24 hours (Stage I). Between 24-72 hours (Stage II), there often follows an asymptomatic period as the acetaminophen is metabolized and part of the drug is converted to a toxic metabolite.
Starting at 24-48 hours, subclinical elevation of the transaminases and bilirubin develops. This
is followed at 48-72 hours after ingestion by clinically symptomatic signs of liver damage: more
nausea, jaundice, abdominal pain, and signs of hepatic encephalopathy, renal failure, and death.
Diagnosis. A clear history of a large volume of acetaminophen ingestion is initially sufficient
to establish a diagnosis that warrants therapy with N-acetyl cysteine (NAC). Starting at 4
hours after ingestion, when most of the drug has been absorbed, drug levels are reliable. A
nomogram based on relating the drug level to the time of ingestion is necessary to determine
who will develop toxicity. In other words, a level by itself is not enough to determine who will
develop toxicity. A certain level at 5 or 6 hours may not be toxic; however, the same level at
10–12 hours after ingestion may lead to the development of liver failure.
Elevated AST is more common than elevated ALT. If a patient is known for alcohol abuse
and presents with AST and ALT >500 U/L, the diagnosis is more likely to be acetaminophen
toxicity than alcoholic hepatitis. NAC should be given in such cases. Elevated bilirubin and
prothrombin time indicates severe toxicity and hepatic necrosis. Studies show that NAC
administration within the first 8 hours of severe drug poisoning improves liver microcirculation and prevents the need for liver transplant.
359
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