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USMLE Step 2 CK
l Internal Medicine
usually after a latent period of 30 years. Adenocarcinoma is usually associated with
pleural effusions that have high hyaluronidase levels. Diagnosis often requires thoracotomy with pleural biopsy.
• Squamous Cell Carcinoma. Squamous cell carcinoma is a centrally located lesion. It
is associated with cavitary lesions. Squamous cell carcinoma usually metastasizes by
direct extension into the hilar node and mediastinum. These lesions are associated
with hypercalcemia from the secretion of a parathyroid hormone–like substance.
• Small-Cell Carcinoma. Small-cell carcinomas are centrally located lesions. These
tumors are rapidly growing with early distant metastasis to extrathoracic sites such as
liver, adrenal glands, brain, and bone. Prognosis does not improve with early diagnosis. Small-cell carcinoma is associated with Eaton-Lambert syndrome, syndrome of
inappropriate antidiuretic hormone, and other paraneoplastic syndromes. Small-cell
carcinoma is also the most common cause of venocaval obstruction syndrome.
• Large-Cell Carcinoma. Large-cell carcinoma is a peripherally located lesion. This
carcinoma can metastasize to distant locations late in the course of disease. Large-cell
carcinoma in early stages is associated with cavitation.
Symptoms. The most common symptom at the time of diagnosis is cough (74%). Weight loss
is seen in 68% of patients. Dyspnea is seen in 58% of patients. Other associated symptoms of
bronchogenic carcinoma include hemoptysis, chest wall pain, and repeated pneumonic processes (caused by postobstructive pneumonia).
Hoarseness when seen indicates a nonresectable bronchogenic carcinoma.
Diagnosis. The diagnosis of bronchogenic carcinoma can be made by sputum cytology, with
the highest yield in patients with squamous cell carcinoma (>80%) because it is intraluminal
and centrally located. Bronchoscopy is best for centrally located lesions (yield of 90%) and is
helpful in staging. For the 10% of centrally located lesions not detected by bronchoscopy, a
needle aspiration biopsy should be performed if carcinoma is highly suspect. In other words,
if there is a high degree of suspicion for carcinoma and the bronchoscopy results are nonspecific, a biopsy must be requested. Needle aspiration biopsy is also good for peripheral nodules
with pleural fluid aspirate (positive in 40–50% of cases). Mediastinoscopy is useful in diagnosing and staging mediastinal tumors.
• Workup of a chest x-ray with an effusion and a lung mass. 90% of tumors with
malignant effusions are unresectable. These tumors are usually adenocarcinomas.
Atelectasis on chest x-ray suggests central airway obstruction. Next step in such a
patient is to do thoracocentesis and cytologic evaluation of the pleural fluid.
Treatment. Symptoms that suggest an unresectable lesion include weight loss >10%, bone
pain or other extrathoracic metastases, CNS symptoms (treated by radiation or chemotherapy), superior vena cava syndrome, hoarseness, mediastinal adenopathy on the contralateral
side, split-lung test tidal volume <800 ml, tumor classification of M1 within 3 months, and
tumor involving the trachea, esophagus, pericardium, or chest wall.
Resectable lesions of small-cell carcinoma are treated with chemotherapy; VP16 (etoposide
and platinum) is the treatment of choice. Surgery is not indicated for these lesions. Nonsmall- cell lesions that are resectable are treated with chemotherapy and radiation therapy or
CAP (cyclophosphamide, adriamycin, and platinum). Effusions can be sclerosed with tetracycline. Complications are treated with radiation therapy, which in most cases is palliative.
340
Prognosis. Prognosis is best after surgical resection of squamous-cell carcinoma (30–35%).
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Large-cell carcinoma and adenocarcinoma have a prognosis of 25%. Prognosis is poorest for
small-cell carcinoma.
Recommendation for lung cancer screening are as follows (see also Preventive Medicine section):
• In cases where >30 pack-years of smoking, patients age 55-80 should receive lung
cancer screening with low dose CT (non-contrast). The patient has to be a current
smoker or has quit >15 years.
• In cases where patients age >80, quit >15 years, has other medical problems such as
severe COPD which significantly limits life expectancy or ability to undergo surgery,
no screening is recommended.
ATELECTASIS
A 62-year-old man is dyspneic 24 h after cholecystectomy. His respiratory rate is
22/min and pulse 112/min. He has a mild fever, and decreased breath sounds are
3
noted in the left lower lobe. Complete blood count shows leukocytosis 27,000/mm
.
Chapter 9
l Pulmonology
Definition. A collapse of part or the entire lung. It is seen most commonly in the immediate
postoperative period. It occurs secondary to poor inspiration or lack of coughing during this
time. A mucous plug, tumor, or foreign body can also lead to atelectasis.
Signs and Symptoms. Acute symptoms include tachycardia, dyspnea, fever, and hypoxemia.
In the chronic phase patients may be asymptomatic with only x-ray abnormalities. On x-ray,
upper lobe atelectasis can appear as tracheal deviation to the affected side. This phenomenon
occurs secondary to volume loss from atelectasis. Lower lobe atelectasis may cause an elevation of the corresponding part of the diaphragm. In massive atelectasis, a mediastinal shift to
the involved side can be seen. The atelectatic lobe will appear to be densely consolidated and
smaller than the normal lobe on x-ray.
Treatment. In the postoperative phase, it is important to induce deep breathing and stimulate
coughing. Incentive spirometry and pulmonary toilet are effective. Bronchoscopy with subsequent removal of mucous plugs is highly effective for spontaneous atelectasis.
341
USMLE Step 2 CK
l Internal Medicine
ANSWERS TO QUESTIONS THROUGHOUT CHAPTER
Pg. 307 Patient 1a—chronic bronchitis or asthma
Patient 1b—emphysema
Patient 2a—extrapulmonary restriction (e.g., kyphoscoliosis, morbid obesity)
Patient 2b—interstitial lung disease
Pg. 309 Clinical problem—overdose from opiates (any scenario in which the respiratory
rate is decreased)
Pg. 319–
320 What is the treatment of choice in this patient? bronchodilator: albuterol; systemic
corticosteroids (usually start IV) and oxygen. Remember, long-acting bronchodilators are contraindicated in the acute setting.
What are bad prognostic indicators in this patient? cyanosis, silent lung, increase in
CO
2
Which one of the ABGs below…? The first ABG with CO2 of 45 is the worst.
Three days after hospitalization…What is her drug regimen...? oral prednisone
taper, albuterol inhaler, steroid inhaler
What will you do now? What medications is she likely to be taking now? She should
have a PFT to document asthma, and her basic asthma regimen should be inhaled
steroids daily and albuterol inhaler as needed.
Pg. 322 After a bronchodilator is given, you would expect the FEV1/FVC to remain the
same or improve minimally.
Pg. 325 What are you likely to find…? decreased DLco
How will you treat…? systemic steroids, antibiotics, and bronchodilators; O2 as
needed
What are your treatment options…? ipratropium inhaler, home O
She asks you to…what will you consider now? measure FEV1
Pg. 326 How would you treat this patient? antipseudomonal antibiotics (ciprofloxacin,
ceftazidime)
What investigations will you consider…? chloride test to diagnose cystic fibrosis
2
342
Emergency Medicine
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Learning Objectives
❏ List the steps to follow in basic life support (cardiopulmonary resuscitation)
❏ Interpret ECG strips to diagnose cardiac dysrhythmias and present the appropriate
emergency management
❏ Answer questions about principles of toxicology and initial management with spe-
cific management for poisoning or overdose with acetaminophen, various alcohols,
carbon monoxide, caustics, corrosives, digoxin, heavy metals, salicylates, tricyclic
antidepressants, anticholinergic agents, organophosphates, and drugs of abuse
❏ Describe direct and indirect complications and emergency management of acute/
chronic alcohol use
❏ Describe the emergency management of head trauma, anaphylaxis, subarachnoid
hemorrhage, burns, radiation injuries, electrical injuries, drowning, and venomous
bites/stings
10
BASIC LIFE SUPPORT (CARDIOPULMONARY RESUSCITATION)
A 54-year-old man is at the opera when he suddenly jumps up and clutches his
chest. He falls to his side into the lap of the woman sitting next to him.
Definition. The initial management algorithm of any patient who seems to have become
unresponsive.
Etiology. A cardiac, neurologic, or toxicologic event leading to markedly diminished responsiveness or loss of pulse. Most causes of cardiac arrest are related to ventricular rhythm
disturbance. The most common etiology of serious cardiac dysrhythmia is ischemia-related,
particularly with coronary artery disease or another cardiac anatomic abnormality (especially
cardiomyopathy).
Clinical Presentation. Any patient with diminished responsiveness that is usually sudden in
onset.
343
USMLE Step 2 CK
l Internal Medicine
Diagnosis. This is a clinically determined diagnosis at first. The initial step is, in fact, to assess
the responsiveness of the patient to make sure that he is truly unresponsive and not just
asleep. This is accomplished by calling to or gently shaking the patient. Be careful about shaking a patient who might have serious traumatic injury, particularly of the cervical spine.
Treatment. After determining that the patient is truly unresponsive, the next step is to call for
help (dial 911). Although it is natural to reach down to check a pulse, this is not the action that
the USMLE or the American Heart Association (AHA) wants you to build as a reflex. Without
the EKG, defibrillator, and cardiac medications you need, there is very little that one or even
two rescuers can do for a patient with a serious dysrhythmia beyond chest compressions and
opening the airway.
If a patient has a serious dysrhythmia such as asystole or ventricular fibrillation, there is virtually no survival if the heart has not been restarted within 10 minutes. Chest compressions just
perfuse vital organs; they will not convert the arrhythmia back to normal sinus.
AHA guidelines emphasize the following:
• High-quality CPR with uninterrupted chest compressions of adequate depth (5 cm,
2 in.) at a rate of 100/min
• Decreased intervals between stopping the chest compression and shock delivery
Avoid excessive ventilation because it can be detrimental. ABC, according to new guidelines, is
now CAB (excluding newborns). Removing the 2 rescue breaths allows chest compressions to
be delivered sooner. Earlier chest compressions and defibrillation are critical elements of CPR.
• Do look, listen, feel for breathing.
• Do check for pulse (for 10 seconds); if you establish that there is no pulse, start chest
compressions (after calling 911).
• Do not give rescue breaths first, as that has been shown to delay vital chest compressions, which leads to an increase in mortality.
• Do not perform jaw thrust, which just delays chest compression.
After calling for help, position the patient on a firm, flat surface, and roll the patient so that he
or she is face up. Check to see if there is a pulse by feeling for at least 5-10 seconds at the carotid
artery. If there is no pulse, perform chest compressions at a rate of 100 per minute, “push hard
and push fast.” In adults, provide 30 compressions and then 2 ventilations, regardless of whether
one or two rescuers is present. In children, perform 30 compressions and 2 ventilations if one
rescuer is present, and give 15 compressions and 2 ventilations if two rescuers are present. Depth
of chest compression is 2 in. or 5 cm.
344
Advanced Cardiac Life Support Algorithms
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1
• BLS Algorithm: call for help, give CPR
• Give oxygen when available
• Attach monitor/defibrillator when available
VF/VT
4
Give 1 shock
• Manual biphasic: device specific (typically 120–200 J)
• AED: device specific
• Monophasic: 360 J
Resume CPR
• Manual biphasic: immediately
Give 5 cycles of CPR*
5
Check rhythm
Shockable rhythm?
6
Continue CPR while defibrillator is charging
Give 1 shock
• Manual biphasic: device specific (same as first
shock or higher dose; if unknown, use 200 J)
• AED: device specific
• Monophase: 360 J
Resume CPR immediately after the shock
When IV/IO available, give vasopressor during CPR
(before or after the shock)
• Epinephrine 1 mg IV/IO
Repeat every 3 to 5 min
or
• May give 1 dose of vasopressin 40 U to replace
first or second dose of epinephrine
7
Check rhythm
Shockable rhythm?
8
Continue CPR while defibrillator is charging
Give 1 shock
• Manual biphasic: device specific (same as first
shock or higher dose; if unknown, use 200 J)
• AED: device specific
• Monophase: 360 J
Resume CPR immediately after the shock, consider
antiarrhythmics; give during CPR
(before or after the shock)
amiodarone or lidocaine
Consider magnesium for torsades de pointes
After 5 cycles of CPR,* go to Box 5 above
Shockable
Give 5 cycles of CPR*
Shockable
Pulseless Arrest
23
Check rhythm
Shockable rhythm?
No
12
• If asystole, go to Box 10
• If electrical activity,
check pulse
If no pulse, go to Box 10
• If pulse present, begin
No
postresuscitation care
• Push hard and fast (100/min)
• Ensure full chest recoil
• Minimize interruptions in
chest compressions
• One cycle of CPR: 30 compressions
then 2 breaths; 5 cycles = 2 min
• Avoid hyperventilation
• Secure airway and confirm
placement
• After an advanced airway is
placed, rescuers no longer deliver
“cycles” of CPR. Give continuous
chest compressions without
pauses for breaths. Give 8–10
breaths/minute. Check rhythm
every 2 minutes.
Chapter 10
9
Asystole/PEA
10
Resume CPR immediately for 5 cycles
When IV/IO available, give vasopressor
• Epinephrine 1 mg IV/IO
Repeat every 3 to 5 min
or
• May give 1 dose of vasopressin 40 U
IV/IO to replace first or second dose of
epinephrine
Give 5 cycles
of CPR*
11
Check rhythm
Shockable rhythm?
Not
shockable
Shockable
l Emergency Medicine
13
Go to
Box 4
• Rotate compressors every
2 minutes with rhythm checks
• Search for and treat possible
contributing factors:
–Hypovolemia
–Hypoxia
–Hydrogen ion (acidosis)
–Hypo-/hyperkalemia
–Hypoglycemia
–Hypothermia
–Toxins
–Tamponade, cardiac
–Thrombosis (coronary or
pulmonary
–Trauma
Figure 10-1. ACLS Pulseless Arrest Algorithm
345
USMLE Step 2 CK
Figure 10-2. Asystole
l Internal Medicine
CARDIAC DYSRHYTHMIAS
Management of Specific Cardiac Dysrhythmias
Asystole
A 54-year-old man is at the opera when he suddenly jumps up and clutches
his chest. He falls to his side into the lap of the woman sitting next to him. After
confirming that he is unresponsive, a nearby physician performs chest compressions
and ventilations. An EKG is done and reveals no evidence of electrical activity.
Definition. The complete absence of electrical activity in the heart. This does not necessarily mean a completely flat line on an EKG because there may be slight variability on the
rhythm strip.
Etiology. Ischemia and severe underlying cardiac disease most commonly underlie asystole.
Other possible etiologies include metabolic derangements, drug overdose, trauma, and others.
Note
For asystole and other
arrhythmias in this chapter,
remember the “Hs and Ts”:
Hypoxia
Hyper/Hypokalemia
Hypothermia
Hypoglycemia
Hypovolemia
Trauma
Toxins (including overdose)
Tamponade
Tension pneumothorax
Thrombosis (coronary and
pulmonary)
Note
Atropine is no longer indicated
in asystole.
Clinical Presentation. An unresponsive person with asystole on EKG; person has no pulse.
Diagnosis. Asystole should always be confirmed by observing the rhythm in more than one
lead on the EKG.
Treatment. As you continue cardiopulmonary resuscitation (CPR), obtain IV access and prepare the patient for intubation.
1. Transcutaneous pacing should be considered and performed only for very slow bradycardia.
Perform it as early as possible. Pacing is not for asystole.
2. Next, administer 1 mg epinephrine via IV push every 3–5 minutes. (Atropine is no longer
recommended for asystole.)
3. If asystole persists, withhold resuscitative efforts in order to evaluate the presence of atypical
clinical features or cease-effort protocol.
Note
Transcutaneous pacemaker is
not useful for asystole.
346
When you see asystole on the monitor, make sure of the following:
• There are no loose or disconnected leads
• The power to ECG machine and monitor is on
• There is not a low signal gain on the monitor
Chapter 10
Figure 10-3. Ventricular Fibrillation
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Note: Bicarbonate is useful if the cause of asystole is attributed to a preexisting acidosis
(except hypercarbic acidosis), tricyclic antidepressant overdose, aspirin overdose, hyperkalemia, or diabetic ketoacidosis.
Ventricular fibrillation
A 54-year-old man is at the opera when he suddenly jumps up and clutches his
chest. He falls to his side into the lap of the woman sitting next to him. He is not
breathing. After confirming that he is unresponsive, a nearby physician performs
chest compressions and ventilations. An EKG is done and reveals ventricular
fibrillation. He has no spontaneous respirations.
Definition. Significant electrical activity on EKG with no signs of an organized pattern.
Etiology. Ischemia, myocardial infarction, cardiomyopathy, and severe underlying cardiac dis-
ease most commonly underlie ventricular fibrillation. Remember the “Hs and Ts.”
Clinical Presentation. A dead person with ventricular fibrillation on EKG.
l Emergency Medicine
Diagnosis. Entirely based on the EKG.
Treatment. The differences between defibrillation and cardioversion are very important.
• Defibrillation is a nonsynchronized delivery of shock at any phase of cardiac cycle.
It is used in VF and pulseless VT. During defibrillation you depolarize all of the myocytes simultaneously, hoping that the SA node will start up normal sinus rhythm.
• Cardioversion means that the shock is synchronized with the QRS complex. When
performing cardioversion, the defibrillator will not shock until the QRS complex
appears. You will be able to see spikes over the QRS complexes on the monitor. If you
shock on the T wave, when ventricular repolarization is taking place, you may induce
VF.
Make sure that the SYN button is pushed when performing cardioversion. Use
UNsynchronized shock (defibrillation) for VF or pulseless VT only.
Post-Resuscitation Care. Most patients who survive resuscitation have anoxic brain injury.
Hypothermia protocol reduces the risk of this type of severe neurologic injury. If a patient
is not following commands or showing purposeful movements, the hypothermia protocol
should be used. The goal of protocol is to reach core temperature 32–34° C (90–93° F) within
6 hours and maintain for 12–24 hours. Absolute contraindications for induced hypothermia
are active bleeding and do-not-resuscitate order.
347
USMLE Step 2 CK
1
61
l Internal Medicine
TACHYCARDIA
with Pulses
2
• Access and support ABCs as needed
• Give oxygen
• Monitor ECG (identify rhythm) blood pressure, oximetry
5
• Establish IV access
• Obtain 12-lead ECG
(when available) or rhythm
strip
Is QRS narrow (<0.12 sec)?
• Identify and treat reversible causes
3
Stable Unstable
Unstable signs include altered
mental status, ongoing chest pain,
hypotension, or other signs of shock
Note: rate-related symptoms
uncommon if heart rate <150/min
Is patient stable?
Symptoms Persist
4
Perform immediate
synchronized cardioversion
• Establish IV access and give
sedation if patient is conscious;
do not delay cardioversion
• Consider expert consultation
• If pulseless arrest develops, see
Pulseless Arrest Algorithm
Wide (20.12 sec)
Narrow
NARROW QRS*:
Is rhythm regular?
Regular
7
• Attempt vagal maneuvers
• Give adenosine
8
Does rhythm
convert?
Note: Consider
expert consultation
ConvertsDoes Not Convert
Irregular
11
Irregular narrow-complex
tachycardia
Probable atrial fi brillation or pos-
sible atrial fl utter or MAT
(multifocal atrial tachycardia)
• Consider expert consultation
• Control rate (e.g., diltiazem,
β-blockers; use β-blockers with
caution in pulmonary disease or
CHF)
13 14
If ventricular
tachycardia or
uncertain rhythm
• Amiodarone
• Prepare for elective
synchronized
cardioversion
If SVT with aberrancy
• Give adenosine
(go to Box 7)
910
If rhythm converts,
probable reentry SVT
(reentry supraventricular
tachycardia):
• Observe for recurrence
• Treat recurrence with
adenosine or longeracting AV nodal blocking
agents (e.g., diltiazem,
β-blockers)
If rhythm does NOT convert,
probable atrial fl utter, ectopic
atrial tachycardia, or junctional
tachycardia:
• Control rate (e.g., diltiazem,
β-blockers; use β-blockers with
caution in pulmonary disease or
CHF)
• Treat underlying cause
2
WIDE QRS*:
Is rhythm regular?
Expert consultation
advised
Regular
Irregular
If atrial fi brillation with
aberrancy, see irregular
narrow-complex tachycardia (Box 11)
If pre-excited atrial
fi brillation (AF + WPW),
seek expert consultation
• Avoid AV nodal blocking
agents (e.g., adenosine,
digoxin, diltiazem, verapamil)
• Consider antiarrhythmics
If recurrent polymorphic
VT, seek expert consultation
If Torsades des pointes,
give magnesium
*Note: If patient becomes
unstable, go to Box 4.
348
During evaluation:
• Secure, verify airway and
vascular access when
possible
• Consider expert consultation
• Prepare for cardioversion
Figure 10-4. Algorithm for Tachycardia with Pulses
Treat contributing factors:
– Hypovolemia
– Hypoxia
– Hydrogen ion (acidosis)
– Hypo-/hyperkalemia
– Hypoglycemia
– Hypothermia
– Toxins
– Tamponade, cardiac
– Tension pneumothorax
– Thrombosis (coronary or
pulmonary)
– Trauma (hypovolemia)
Chapter 10
Figure 10-5. Torsade
Figure 10-6. Ventricular Tachycardia
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l Emergency Medicine
Ventricular tachycardia
A 54-year-old man is at the opera when he suddenly jumps up and clutches
his chest. He falls to his side into the lap of the woman sitting next to him.
He is awake but disoriented and confused. He is complaining of dyspnea and
lightheadedness. His exam reveals jugulovenous distention and a blood pressure
of 114/80. The EKG shows ventricular tachycardia at a rate of 180.
Definition. A wide complex tachycardia with an organized, uniform pattern on the EKG.
There are no P-waves visible.
Etiology. Ischemia, myocardial infarction, and anatomic cardiac disease most commonly underlie VT. Other possible etiologies include quinidine, tricyclics, and phenothiazines. Long QT syndromes also cause VT. The dysrhythmia originates from an ectopic focus in the myocardium or
from the AV node. When the impulse originates from around the AV node, this is from reentry.
The electrical impulses must travel throughout the myocardium from myocyte to myocyte without the benefit of the more rapidly conducting normal pathways, such as the bundle branches
or the His-Purkinje fibers.
The slowness of the conduction produces the slower and therefore wider complexes on the EKG.
The rate most often varies 160–240/min. Torsade de pointes is a form of VT in which the morphology varies with an undulating amplitude, making it seem that it “twists around a point.”
Torsade may be associated with hypomagnesemia and preceded by long QT interval.
Note
Medications that prolong QT
interval
TCAs
Antipsychotics
Erythromicin
Methadone
Fluoroquinolones
Amiodarone
Quinidine
Sotolol
Flecainide
Procainamide
Causes of prolonged QT and
Torsade
Mg
K
Ca
Clinical Presentation. Symptoms are often related to duration of the dysrhythmia. Short
bursts of a few seconds may produce no symptoms at all. VT lasting >30 seconds is referred to
as sustained VT. Symptoms include lightheadedness, hypotension, CHF, syncope, and death.
Diagnosis. The EKG shows the VT. For those patients presenting with syncope suspected to
be of cardiac origin and in whom an arrhythmia is not visible on the initial EKG, an electrophysiologic study can be done to try to elicit the VT.
Note
Amiodarone is superior
to lidocaine for VF/VT.
349
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