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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2664_Библиотеки_им_академика_М_И_Перельмана
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USMLE Step 2 CK
Figure 5-17. Management of VT
l Internal Medicine
Table 5-14. QRS Complex
Wide (>0.12 s) Narrow (<0.12 s)
Regular Irregular Regular Irregular
Ventricular
tachycardia
Supraventricular
tachycardia
(aberration)
Wolff-ParkinsonWhite syndrome
Stable Pulse
Atrial fibrillation
Sinus tachycardia Atrial fibrillation
(rarely)
Paroxysmal
supraventricular
tachycardia
Atrial flutter
Ventricular Tachycardia
O
2
Multifocal atrial
tachycardia
No pulse Treat as VF
Unstable
O
2
IV access
Amiodarone or
lidocaine
Lidocaine until
VT resolves
Procainamide until
VT resolves
Cardiovert if patient
becomes unstable
IV access
Consider sedation
Cardiovert 100 J
Cardiovert 200 J
Cardiovert 300 J
Cardiovert 360 J
170
Torsade de Pointes
Figure 5-18. Torsade de Pointes
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Definition. Characterized by undulating rotations of the QRS complexes around the electrocardiographic baseline.
Arrhythmias initiated by a ventricular premature beat in the setting of abnormal ventricular
repolarization characterized by prolongation of the QT interval.
Etiology. Antiarrhythmic drugs that prolong ventricular repolarization include:
• Quinidine
• Procainamide
• Disopyramide
• Psychotropic drugs, such as:
– Phenothiazines
– Thioridazine
– Tricyclics
– Lithium
– Electrolyte imbalances, especially hypokalemia and hypomagnesemia
– Central nervous system lesions, such as subarachnoid or intracerebral hemorrhage
Chapter 5
l Cardiology
Clinical manifestations. Patients with long QT interval are prone to recurrent dizziness or
syncope from the ventricular tachycardia.
Sudden auditory stimuli, such as the ringing of the telephone at night, may initiate Torsade de
Pointes in a vulnerable individual with a long QT interval syndrome.
Treatment. Treat the underlying disorder. In the case of the antiarrhythmics, use a drug such
as lidocaine.
With electrolyte imbalance disorders, repletion with potassium and magnesium is
•
needed.
• Cardiac pacing or an isoproterenol infusion may suppress episodes of tachycardia and
may be useful for emergency treatments.
• If hemodynamically unstable (e.g., hypotension), consider cardioversion, but this dysrhythmia often reoccurs.
171
USMLE Step 2 CK
l Internal Medicine
Ventricular Fibrillation
See the Emergency Medicine section.
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
Shockable rhythm?
Check 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.
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
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
172
Figure 5-19. ACLS Pulseless Arrest Algorithm
Amiodarone
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Amiodarone is a very effective antiarrhythmic drug, and can be used in ventricular tachycardia, AF, and atrial flutter. Because it has a very long half-life (>50 days), drug interactions are
possible for weeks after discontinuation.
The most severe side effects of amiodarone therapy are related to the lungs and present as
cough, fever, or painful breathing. These reactions can be fatal. About 20% of patients who
receive amiodarone experience some form of nerve toxicity. Symptoms may include imbalance or changes in gait, tremor, numbness in the fingers or toes, dizziness, muscle weakness,
or loss of coordination. Thyroid dysfunction is also common, since the drug molecule is
chemically related to thyroxine. Hypothyroidism seems to be more common, but hyperthyroidism can also occur. Since many patients experience an exaggerated response to the harmful effects of sunlight, avoidance of extensive sun exposure and the use of protective clothing
should be used to help prevent this.
Long-term administration of amiodarone may occasionally result in a blue-gray discoloration
of the skin. This effect seems to be more common in patients with fair skin. Patients also may
experience visual impairment or other disturbances such as “halo lights” and blurred vision.
Corneal deposits (microdeposits) occur in virtually all patients who receive amiodarone for at
least 6 months.
Chapter 5
l Cardiology
Nitrates
• In low doses, nitrates increase venous dilation and subsequently reduce preload.
• In medium doses, nitrates increase arteriolar dilatation and subsequently decrease
afterload and preload.
• In high doses, nitrates increase coronary artery dilatation and subsequently increase
oxygen supply.
Side effects: Vasodilation can lead to orthostatic hypotension, reflex tachycardia, throbbing
headache, and blushing. Nitrates are contraindicated if systolic blood pressure <90 mm Hg. You
must have a window-free period of >8 hours with nitrate therapy to reduce the incidence of
tachyphylaxis.
173
USMLE Step 2 CK
l Internal Medicine
Antiarrhythmic Drugs
Table 5-15. Antiarrhythmic Drugs
Drug Adverse Effects
Disopyramide Anticholinergic effects; hypotension; heart failure; heart block; tachyarrhythmia
Lidocaine CNS (drowsiness, agitation, seizures); heart block
Phenytoin CNS (ataxia, nystagmus, drowsiness); hypotension and heart block with rapid IV injection
Procainamide Lupus-like syndrome; GI; rash; hypotension; aggravation of arrhythmia; blood dyscrasias
Quinidine Aggravation of arrhythmias (“quinidine syncope”); thrombocytopenia; fever, rash;
cinchonism; GI symptoms; digoxin-quinidine interaction (elevation of digoxin levels)
b-adrenergic
blocking agents
Verapamil CHF, asystole, constipation
Adenosine Transient dyspnea, noncardiac chest pain, rarely hypotension
Mexiletine Lidocaine-like drug; local anesthetic
Tocainide Lidocaine-like drug
Amiodarone Very long half-life (20–40 d); may increase digoxin level; may worsen existing cardiac
Encainide Negative inotropism; QRS and PR prolongation
Flecainide Negative inotropism; QRS and PR prolongation
Propafenone Negative inotropism; QRS and PR prolongation
Heart block; hypotension; asthma; hypoglycemia; lethargy; impotence
conduction disturbances; may prolong Coumadin effect
Beta Blockers
• Decrease heart rate, blood pressure, and contractility, which decrease myocardial
oxygen requirement
• Contraindicated in presence of severe asthma in about one-third of patients
• Nonselective beta blockers may mask hypoglycemic symptoms in insulin-dependent
diabetics
• Shown to improve survival after an acute MI and in CHF
174
Adverse effects of beta blockade therapy are as follows:
• Fatigue, insomnia
• Mental depression
• Adverse effects on lipid panel
• Hallucinations
• Raynaud phenomenon
• Bronchoconstriction
• Mask signs and symptoms of insulin-induced hypoglycemia
• Sexual dysfunction
Table 5-16. Pharmacologic Properties of Select
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b-Blocking Agents
Generic Name (Trade Name) Cardio-Selective
Metoprolol (Lopressor) Yes
Atenolol (Tenormin) Yes
Propranolol (Inderal) No
Nadolol (Corgard) No
Timolol (Blocadren) No
Pindolol (Visken) No
Acebutolol (Sectral) Yes
Chapter 5
l Cardiology
Labetalol (Normodyne or
Trandate)
Esmolol (IV) Yes
Nebivolol is a unique beta blocker; it is a beta-1 specific blocker that increases nitric oxide and
thus does not cause erectile dysfunction.
No
Calcium Channel Blockers
Calcium channel blockers work by producing decreases in preload and afterload. They may be
harmful in the postinfarction period, especially if the patient has left ventricular failure. Their
efficacy in angina is very limited—there is no mortality benefit.
Adverse effects of calcium channel blockers are as follows:
Cardiac
• CHF
• Reflex tachycardia
• Hypotension
• Lightheadedness
•
AV block
Noncardiac
• Flushing
• Headache
• Weakness
• Constipation
• Nasal congestion
• Wheezing
• Peripheral edema
• Gingival hyperplasia
175
USMLE Step 2 CK
l Internal Medicine
Shock is a broad term that describes a state where oxygen delivery to the tissues is inadequate
to meet the demands. Shock can be described as the imbalance between tissue oxygen supply
and demand.
Four general types of shock syndromes are recognized: distributive, cardiogenic, hypovolemic,
and obstructive. There are many etiologies within each class.
• Distributive shock: caused by pathologic peripheral blood vessel vasodilation
– Examples are sepsis (especially gram-negative), anaphylaxis, neurogenic
– Septic shock is the most common form of shock among patients admitted to the
ICU (followed by cardiogenic and hypovolemic shock)
• Cardiogenic shock: related to impaired heart pump function
– Typical causes include acute coronary syndromes, valve failure (especially acute)
and dysrhythmias
• Hypovolemic shock: caused by decreased circulatory volume
– Examples are hemorrhage (GI bleed) and fluid loss
• Obstructive shock: non-cardiac obstruction to blood flow
– Examples are pulmonary embolus, tension pneumothorax, and cardiac tamponade
The diagnosis of shock is a clinical diagnosis.
Table 5-17. Physiologic Characteristics of Various Forms of Shock
Type of Shock
Cardiogenic
Hypovolemic
Distributive (sepsis)
Obstructive
In all of the forms above, cardiac output decreases; the only exceptions are the hyperdynamic
state of septic shock and rarely traumatic shock, both of which may have elevated cardiac output.
Treatment should begin emergently since early therapy has been shown to improve outcomes.
• Always start with the ABCs and strongly consider intubation in most cases of shock
for airway protection.
• Arterial oxygen saturation should be maximized.
• Circulatory support with IV fluids is paramount in most cases; use caution with rapid
fluid administration to the patient with cardiogenic shock and pulmonary edema.
• Transfusion of blood products may be necessary in certain types of shock.
• If volume resuscitation does not improve hemodynamic status, consider epinephrine,
dopamine, or vasopressin.
Heart
Rate
↑ ↑ ↓↓ ↑
↑ ↓↓
↑ ↓↓
↑
Central Venous
Pressure
±↑ ±
Contractility
±↑
±
Systemic Vascular
Resistance
↑
↓
↑ (tamponade, PE)
↓ (tension PTX)
176
Furthermore, aggressive treatment of the underlying cause of the shock is warranted, e.g., sepsis syndromes should be treated with broad-spectrum antibiotics, while obstructive shock due
to PE may need thrombolysis and anticoagulation.
Hematology
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Learning Objectives
❏ List the types of anemia and describe their pathophysiology, diagnosis, and treatment
❏ Describe the presentation and diagnosis of hematologic neoplasias including acute
leukemia, chronic leukemias, plasma cell disorders, and lymphomas
❏ Describe common platelet disorders
❏ List defects that can occur in the coagulation cascade and their associated disorders
ANEMIA
Definition. Anemia is a condition marked by the following:
• Hematocrit <41% in men or <36% in women, or
• Hemoglobin <13.5 gm/dL in men or <12 gm/dL in women
6
Etiology. Anemias are most easily classified according to their cell size.
• Microcytic anemia means a low mean corpuscular volume (MCV) <80. These are
most commonly a result of iron deficiency, anemia of chronic disease, thalassemia,
sideroblastosis, and lead poisoning. Anemia of chronic disease can be either microcytic
or normocytic.
• Macrocytic anemia is characterized by an elevated MCV >100. This is most commonly from vitamin B12 or folic acid deficiency but can also result from the toxic effects of
alcohol, liver disease, or chemotherapeutic agents such as methotrexate or medications
such as zidovudine (AZT) or phenytoin.
•
Normocytic anemia is characterized by a normal MCV. This can be from an early
form of the conditions described above, as well as most forms of hemolysis and
aplastic anemia.
Clinical Presentation. The predominant symptoms of anemia are based on the severity of the
anemia rather than the specific etiology. Early symptoms include fatigue, tiredness, and poor
exercise tolerance. As the anemia worsens, the patient develops dyspnea on exertion and lightheadedness. Eventually, confusion and altered mental status may develop as oxygen delivery to
the brain decreases. Death from anemia is most often from decreased oxygen delivery to the
heart, resulting in the development of myocardial ischemia.
177
USMLE Step 2 CK
l Internal Medicine
The severity of symptoms is related to the underlying condition of the patient. A healthy young
patient may have no symptoms at all with hematocrit 27–29%, whereas an older patient with
heart disease may develop dyspnea or anginal symptoms with the same hematocrit.
Diagnosis. Once a diagnosis of anemia is determined based on a low hematocrit or hemoglobin, the first step is to determine the MCV. Iron studies, reticulocyte count, peripheral smear,
red cell distribution width (RDW), Coombs test, vitamin B12, folate levels, and even occasionally a bone marrow biopsy may be necessary to determine a specific etiology. The tests
ordered depend on the specifics of the case presented.
Treatment. Besides blood transfusion, treatment cannot be generalized. Packed RBCs are
used to maintain a hematocrit >25–30%. This is based on the underlying condition of the
patient. A healthy young patient can have transfusion withheld until the hematocrit is in the
low 20%s. An older patient with coronary artery disease will need to be maintained when
hematocrit >30%. The hematocrit should rise approximately 3 points for every unit of packed
RBCs given. Whole blood is rarely, if ever, used.
178
Chapter 6
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l Hematology
MCV <80
Microcytic Anemia
• Iron deficiency anemia
• Anemia of chronic disease
• Sideroblastic anemia
• Thalassemia trait
Reticulocyte Count <3%
(bad bone marrow response)
Normocytic Anemia
• Early stages iron deficiency anemia
• Early stages anemia of chronic disease
• Aplastic anemia
• Chronic renal failure
Anemia
Hct <41% ♂ <36% ♀
Hb <13.5 gm/dL ♂ <12 gm/dL ♀
Check MCV
MCV 80−100
Check Reticulocyte Count
Intravascular Hemolysis
• Hemoglobinuria
• Decreased haptoglobin
MCV >100
Macrocytic Anemia
• Reticulocytosis
(acute hemolysis)
• Alcoholism
• Drugs (AZT, phenytoin)
Megaloblastic Anemia
• Macrocytosis + hypersegmented
neutrophils
• Folic acid deficiency
• Vitamin B12 deficiency
Reticulocyte Count >3%
(good bone marrow response)
Extravascular Hemolysis
• Jaundice
• Increased unconjugated
bilirubin
• Pigment stones
• Autoimmune: Cold
Agglutinin Disease
(IgM Ab)
– Mycoplasma pnemoniae
– EBV
– Cryoglobulinemia
(hepatitis)
• Microvascular
– TTP
– HUS
– DIC
• Macrovascular
– Aortic stenosis
– Prosthetic valves
• Infection
– Malaria
– Babesia
• Complement
– Paroxysmal nocturnal
hemoglobinuria
• Enzyme
– G6PD (severe type B)
Figure 6-1. Evaluation of Patients with Anemia
• Autoimmune: Warm
Agglutinin Disease (IgG Ab)
– SLE
– CLL
– HIV
• Membrane defect
– Hereditary spherocytosis
• Abnormal Hb
– Sickle cell anemia
– HbS and HbC
• Enzyme
– G6PD deficiency
– Pyruvate kinase
deficiency
179
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