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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
l Internal Medicine
In certain patients, symptoms other than pain may occur. For example, a profound sense of
weakness and breathlessness may be an “angina equivalent.” Atypical symptoms are more
likely to occur in the elderly and in diabetics.
The physical exam is usually normal. A new S4 may be heard, suggesting a stiff ventricle due
to ischemia.
Most patients with angina will have ECG changes during an attack. Most commonly, ST segment depression is seen. ST segment elevation occurs in variant angina (Prinzmetal angina)
where coronary artery spasm is responsible and rarely during ischemia caused by stable angina (where atherosclerotic disease is responsible).
Diagnosis. The exercise treadmill test (exercise stress test) is the most useful test for evaluating the cause of chronic chest pain when there is concern about IHD (stable angina). Exercise
stress testing provides a controlled environment for observing the effects of increases in the
myocardial demand for oxygen. In order to do an appropriate analysis, a target heart rate
must be reached.
• Target heart rate is 85% of predicted maximum heart rate: 85% × (220 – patient’s age)
• Reaching target heart rate makes test more accurate than if lower heart rate is achieved
Significant fixed stenoses of the coronary arteries will result in ECG evidence of ischemia.
Low-grade stenoses (<50%) may not produce sufficient impairment of blood flow to affect
the ECG; in these cases the stress test will be normal.
An exercise stress test is considered positive for myocardial ischemia when large (>2 mm)
ST-segment depressions or hypotension (a drop of >10 mm Hg in systolic pressure) occur
either alone or in combination. In general, the earlier the angina or ECG abnormalities occur,
the more significant they will be. The exercise stress testing can help to do the following:
• Determine the severity of IHD and the need for further intervention, i.e., severe symptoms (hypotension) early in the test usually occur in those with triple-vessel disease
• Assess the effectiveness of treatment, i.e., coronary artery disease patients who have
undergone surgical intervention or are receiving medical therapy have an exercise
stress test when they are medically stable and symptom-free
• Determine functional capacity and identify any ECG changes or symptoms during
(low level) exercise for patients who are post-MI
Exercise stress testing is contraindicated when it may place the patient at increased risk of cardiac instability, as in the following settings:
• Aortic dissection
• Acute myocardial infarction
• Unstable angina
• Severe CHF
• Uncontrolled sustained ventricular arrhythmias
• Symptomatic supraventricular arrhythmia
• Significant aortic stenosis
• Hypertrophic cardiomyopathy
• Severe uncontrolled hypertension
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Patients who are unable to exercise or walk should be considered for chemical stress testing,
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such as dipyridamole (Persantine) or dobutamine stress test. Presence of baseline ECG abnormalities such as bundle branch block, left ventricular hypertrophy, or with a pacemaker, may
make it more difficult to interpret test results. In those cases patients should be evaluated by
nuclear stress imaging instead of the exercise stress test. These tests may also be used in patients
who are taking digoxin.
In most cases, medications should not be withheld in preparation for an exercise stress test.
Certain medications require special consideration:
• Beta blockers may blunt the heart rate during exercise and thus should be held 24
hours prior to the test. While patients receiving beta blockers may perform the exercise
required for the test, the usual age-adjusted target heart rate may not be a realistic end
point for them.
• Also, the antihypertensive effect of beta blockers, alpha blockers, and nitroglycerin
may cause significant hypotension during exercise.
Digoxin may depress the ST segments, so if ST-segment depression of ≥1 mm is present on
baseline ECG, the stress test results will be difficult to interpret.
A number of other situations or conditions may reduce the validity of the exercise stress test.
Exercise testing in asymptomatic, young women yields an increased number of false-positive
results, while exercise testing in patients with known CAD may result in an unacceptably high
false-negative rate (e.g., a negative stress test in a 64-year-old man with diabetes, hyperlipidemia, and typical stable angina is likely to be a false-negative result).
Chapter 5
l Cardiology
A 29-year-old woman has a routine stress test done that shows a 1-mm ST
depression. She has no history of chest pain, and she exercises routinely (runs
2–3 miles per day, 3 times per week). Her physical examination is unremarkable.
The most likely cause of her abnormal stress test? False-positive test.
Other types of stress tests include:
• Nuclear stress test: A radioactive substance is injected into the patient and perfusion
of heart tissue is visualized. The perfusion pictures are done both at rest and after
exercise. An abnormal amount of thallium will be seen in those areas of the heart that
have a decreased blood supply. Compared to regular stress tests, the nuclear stress tests
have higher sensitivity and specificity (92% sensitivity, 95% specificity vs. 67% sensitivity, 70% specificity). These tests are also not affected by baseline changes in the ECG
(LBBB, ST-segment depression at baseline, etc.).
• Dobutamine or adenosine stress test: Used in people who are unable to exercise. A
drug is given to induce tachycardia, as if the person were exercising.
• Stress echocardiogram: Combines a treadmill stress test and an echocardiogram
(ECHO). The latter can recognize abnormal movement of the walls of the left ventricle
(wall motion abnormalities) that are induced by exercise.
Invasive techniques: Cardiac catheterization is also used in patients with stable angina for (1)
diagnosis and (2) prognosis/risk stratification. Angiography is an appropriate diagnostic test when
noninvasive tests are contraindicated or inadequate due to the patient’s illness or physical characteristics (e.g., morbid obesity, COPD). Cardiac angiography is also used after conventional stress
tests are positive to identify patients that will benefit from stent placement or bypass surgery.
121
USMLE Step 2 CK
l Internal Medicine
Treatment. For individual episodes of angina, nitroglycerin (NTG) sublingual tablets typically alleviate the pain within 3 minutes. Long-term management is with long-acting nitrates
and/or beta blockers. Other medications patients with stable angina should be taking, unless
contraindicated, include aspirin and statins (for lipid lowering). Also, modify the risk factors
(tobacco cessation, exercise, control of hypertension, etc.).
All patients with stable angina need evaluation of the severity of IHD (cardiac angiography or
stress testing, see above), and those who will benefit from revascularization (stent or bypass
surgery) need to be identified.
Lipid lowering treatment for secondary prevention is important in IHD patients who
should be treated aggressively. Most patients will require both pharmacologic and nonpharmacologic interventions to reach target goals. Target goals for hyperlipidemic patients with
coronary artery disease include:
• LDL <100 mg/dL
• HDL ≥40 mg/dL
• Triglycerides <150 mg/dL
The optimal LDL-cholesterol goal is considered to be <70 mg/dL for patients considered to
be very high risk. These are patients with established cardiovascular disease plus diabetes and
patients with acute coronary syndromes. Bottom line: almost all patients with chronic stable
coronary artery disease will likely need to be on statin therapy, unless contraindicated.
Every effort should be made to ensure that patients with coronary artery disease receive optimal lipid therapy. Statin medications are strongly supported as first-line medications due to
compelling evidence of mortality reduction from multiple clinical trials. If patients are intolerant to a statin, consider other statins in reduced doses.
Better medical therapy with aspirin, beta blockers, ACE inhibitors, and statins are decreasing
the need for all revascularization procedures.
Coronary artery bypass graft surgery (CABG) is recommended for patients with obstructive
coronary artery disease whose survival will be improved compared to medical therapy or
percutaneous coronary intervention. Typically, this means patients with left main disease or
triple-vessel disease and low ejection fraction. In addition, patients with angina refractory to
medical therapy qualify for CABG.
CABG is more efficacious in diabetics and in those who have a low ejection fraction. The
procedure involves the construction of 1 or more grafts between the arterial and coronary
circulations. (Many patients receive both arterial and venous grafts.) Long-term graft patency
is significantly better with the arterial graph (e.g., internal mammary artery). Potential consequences of graft failure (loss of patency) include the development of angina, myocardial
infarction, or cardiac death.
122
• Stent placement now standard
• Most cases of stable angina do not need PCI
• PCI is most useful in acute coronary syndrome (ACS)
Acute coronary syndrome (ACS) is used to describe a range of thrombotic coronary diseases,
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including unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI), and
ST-elevation myocardial infarction (STEMI). Collectively, they represent one of the most
common causes of acute medical admission to U.S. hospitals.
The term ACS is clinically useful because the initial presentation and early management of
unstable angina, STEMI, and NSTEMI are frequently similar. ACS should be distinguished
from stable angina, which develops during exertion and resolves at rest.
ACS is due to coronary vessel atherosclerotic obstruction with superimposed thrombotic occlusion.
The natural course of coronary atherosclerotic plaque development and subsequent occlusion does
not proceed in a step-wise, uniform manner, gradually progressing to luminal obstruction (and
symptoms) over many years. This process is characterized by plaque disruption and mural thrombosis. Angiographic data support the concept that noncritical lesions account for the majority of the
ACS. Thus, the pathogenic rate-limiting mechanism of the ACS appears to be acute thrombosis and
the resultant obstruction of the coronary lumen.
An operational classification is clinically helpful since it allows the simple distinction of the
different types of ACS. In this classification, the ECG is the most important clinical tool. The
initial ECG findings, in particular, the presence or absence of ST-segment elevation, will further define the patient’s condition and dictate treatment options.
Chapter 5
l Cardiology
Acute Coronary Syndrome
Electrocardiogram
ST elevation (cardiac markers
commonly negative on initial
testing but eventually positive)
STEMI
No ST elevation
Cardiac
markers
Positive
Myocardial infarction
NSTEMI
Negative
Unstable
angina
Figure 5-3. Acute Coronary Syndromes
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USMLE Step 2 CK
l Internal Medicine
Unstable Angina and NSTEMI
UA and NSTEMI are closely related in terms of clinical presentation and pathogenesis, but
patients with these conditions have widely varying risks. Both are usually caused by atherosclerotic CAD and present an increased risk for death and MI.
• NSTEMI is more severe than UA, and is considered to have occurred if ischemia produces damage detectable by biochemical markers of myocardial injury (troponin I or
CK-MB).
• If there are no detectable serum markers of myocardial injury 12–18 hours after
symptom onset, the patient should be diagnosed with UA.
• At the time of presentation, UA and NSTEMI may be indistinguishable and can be
identically managed.
• Therefore, in establishing the diagnosis of NSTEMI, cardiac troponins (elevated enzymes
show evidence of infarction) should be used to distinguish this entity from UA.
Outcomes in UA/NSTEMI are generally better than in STEMI, but certain UA/NSTEMI
screening because they may require intensive monitoring and management.
Thrombolytic therapy is beneficial in patients with STEMI, but is not effective in UA or
NSTEMI and may be harmful.
Unstable angina is sometimes referred to as “crescendo” or “preinfarction” angina. Typically,
it is defined as angina of increasing severity, frequency, duration; angina showing increasing
resistance to nitrates; or angina occurring at rest. Experts also regard any new-onset angina as
unstable. Sudden change in the pattern of angina usually means a physical change within the
coronary arteries, such as hemorrhage into an atherosclerotic plaque or rupture of a plaque
with intermittent thrombus formation.
About 35% of patients with the clinical syndrome of UA will already have coronary thrombosis on catheterization. In fact, untreated UA progresses to MI in 50% of cases, thus the patient
with new-onset or unstable angina should be hospitalized for intensive medical treatment.
Most patients with NSTEMI have a normal physical examination. An abnormal ECG, particularly dynamic ST-segment deviation (≥0.5 mm), or new T-wave inversion (≥2 mm), will confirm the diagnosis, but the ECG may be normal or show minor changes in up to 50% of cases.
High-risk features for patients with presumed UA/NSTEMI include:
• Repetitive or prolonged chest pain (>10 min)
• Elevated cardiac biomarkers
• Persistent ECG changes of ST depression >0.5 mm or new T-wave inversion
• Hemodynamic instability (SBP <90)
• Sustained ventricular tachycardia
• Syncope
• LV ejection fraction <40%
• Prior angioplasty or prior CABG
• Diabetes
• Chronic kidney disease
124
Aspirin is recommended (unless contraindicated) in all patients. High-risk patients should be
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treated with aggressive medical management and arrangements should be made for coronary
angiography and possible revascularization, except in those with severe comorbidities. Age
alone should not be a barrier to aggressive therapy.
Antiplatelet therapy (beyond aspirin): Early treatment should be initiated with aspirin and
clopidogrel or prasugrel, with the following considerations:
• Avoid clopidogrel in patients likely to require emergency coronary bypass surgery.
Prasugrel and ticagrelor are alternatives to clopidogrel.
• If possible, discontinue clopidogrel 5 days before coronary bypass surgery.
• Use ticagrelor in addition to aspirin for acute coronary syndromes. It is not clearly
better than clopidogrel or prasugrel.
•
Give heparin along with the recommended antiplatelet therapy for
UA/NSTEMI.
Antithrombin therapy: Give unfractionated heparin or subcutaneous enoxaparin until angiography or for 48–72 hours. The enoxaparin dose must be reduced in patients with impaired
renal function.
Chapter 5
l Cardiology
Glycoprotein (GP) IIb/IIIa inhibitors: This class of antithrombotic agents inhibits platelet
function by blocking a key receptor involved in platelet aggregation. The use of these agents
provides a more comprehensive platelet blockade than the combination of aspirin and heparin.
• These drugs take advantage of the fact
that platelets play an important role in the
development of ischemic complications that may occur in patients with UA/NSTEMI.
• Tirofiban or eptifibatide is particularly recommended in high-risk patients in whom
an invasive strategy is planned.
• Concomitant tirofiban is particularly beneficial and recommended in patients with
diabetes.
• Complications include bleeding and thrombocytopenia (occurs with all GP IIb/IIa
agents; incidence ranges 1–5.5% in clinical studies; an immune mechanism is likely
responsible; all patients receiving parenteral GP IIb/IIa antagonsists should be monitored for 24 hours for development of thrombocytopenia).
Other: A beta blocker should be given unless contraindicated. IV nitroglycerin (NTG) can be
given for refractory pain.
In patients with diabetes, good glycemic control should be targeted in the hospital and after
discharge. This may require considering an insulin-based regimen in hospital.
Early coronary angiography (within 48 hours) and revascularization are recommended in
patients with NSTEMI and high-risk features, except in patients with severe comorbidities.
Pain or ischemia refractory to medical therapy and high-risk features on early exercise testing
can also identify patients suitable for early invasive therapy.
125
USMLE Step 2 CK
l Internal Medicine
Note
The strongest indication for
PCI is an acute coronary
syndrome.
ST Elevation MI
The pain of typical MI (STEMI; in the past referred to as Q wave MI) is substernal, diffuse
with a pressure quality. It may radiate to the neck or jaw, shoulders, or arms. Often, the pain is
accompanied by additional symptoms, such as dizziness (lightheadedness), nausea or vomiting, diaphoresis, or shortness of breath (dyspnea).
The symptoms of MI last >20 minutes and do not respond completely to nitroglycerin. The
duration of the pain is variable. Pain may resolve completely after a few hours or may persist
for over a day.
Elderly or diabetic patients are prone to atypical symptoms such as nausea or dyspnea as the
sole symptoms of infarction. As many as 20% of MI are “silent”—that is, whatever symptoms
were present did not impress the patient enough for them to seek medical care or even to
remember the incident.
The exam usually shows the patient to have anxiety and pain. Diaphoresis is often present.
Pulse rate may be normal, but often bradycardia is present in inferior infarction. Tachycardia
is often seen with large infarctions. Blood pressure is often elevated.
Cardiac exam will usually be normal. Large infarctions may cause signs of ventricular failure
or valve dysfunction. A fourth heart sound (S4) is common due to a stiffened ventricle. Mitral
regurgitation may occur if papillary muscles malfunction. The second heart sound may be
paradoxically split as the left ventricular contraction time increases due to LBBB and weakened left ventricle.
Later in the course of MI, other findings may be present: mild fever, pericardial friction rub,
ventral septal defect murmur due to septal rupture, or severe mitral regurgitation due to papillary muscle rupture.
STEMI is defined as clinical symptoms consistent with ACS and ECG features including any
of these:
• Persistent ST-segment elevation of ≥1 mm in two contiguous limb leads
• ST-segment elevation of ≥2 mm in two contiguous chest leads
• New LBBB pattern
Initially, you don’t need increased cardiac biomarkers (troponin, CPK-MB, etc.) to make the
diagnosis of STEMI (although these are usually eventually positive at some point during the
course of the disease).
Initial nonspecific management for all patients with possible MI (anyone with a compatible
chest pain history) is to keep them on a cardiac monitor. Oxygen therapy and an IV line
should be established as quickly as possible. Aspirin should be given unless contraindicated, as
early as possible. Nitroglycerin and pain control (morphine) should be given as required.
Patients with STEMI usually have a completely occluded coronary artery with thrombus at the
site of a ruptured plaque. This eventually leads to myonecrosis. Restoring coronary patency
(emergency reperfusion) as promptly as possible is a key determinant of short-term and longterm outcomes.
Patients with STEMI who present within 12 hours of the onset of ischemic symptoms should
have a reperfusion strategy implemented promptly. Reperfusion may be obtained with fibrinolytic therapy or percutaneous coronary intervention (PCI).
Patients presenting with NSTEMI will not benefit from thrombolytics.
126
Chapter 5
3
Figure 5-5. Inferior STEMI with Changes in II, III, and aVF
Figure 5-6. NSTEMI Affecting Leads II, III, and aVF
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l Cardiology
I
II
III V2 V6
II
VI
V5
aVR V1 V4
aVL V2 V5
aVF
Figure 5-4. Anteroseptal STEMI with Changes in V1–V
I
II
III V3 V6
aVR V1 V4
aVL V2 V5
aVF
I
II
III
II
V1
V5
VI
aVR V1 V4
aVL V2 V5
aVF
V2 V6
127
USMLE Step 2 CK
l Internal Medicine
Table 5-2. Localization of STEMI
EKG Changes (Q Waves, ST
Area of Infarction
Elevation, T Wave Inversions) Artery Involved
Inferior II, III, aVF Right coronary
Anteroseptal V1–V
Anterior V2–V
3
4
Lateral I, aVL, V4, V5, and V
6
Left anterior descending
Left anterior descending
Left anterior descending
or circumflex
Posterior V1–V2: tall broad initial R wave,
Posterior descending
ST depression, tall upright T wave;
usually occurs in association with
inferior or lateral MI
Table 5-3. Typical Electrocardiographic Evolution of a STEMI
EKG Abnormality Onset Disappearance
Hyperacute T waves (tall,
Immediately 6–24 hours
peaked T waves in leads facing
infarction)
ST-segment elevation Immediately 1–6 weeks
Q waves longer than 0.04 seconds One to several days Years to never
T wave inversion 6–24 hours Months to years
128
The choice of reperfusion therapy is between PCI and thrombolysis therapy. PCI is the best
available treatment if provided promptly. PCI improves short-term and long-term outcomes
(reduction of deaths and MI) in patients with STEMI presenting within 12 hours when compared with thrombolytic therapy. This benefit over thrombolysis may occur only if the additional time delay associated with PCI is <1 hour. In general, a time delay of 90 minutes from
first medical encounter to PCI is the maximum desirable. For patients presenting with STEMI
at a facility without PCI access, transfer to another facility capable of performing PCI usually
takes too long. Where PCI is delayed or not available, reperfusion with thrombolytic therapy
should occur unless contraindicated.
Thrombolytics (Fibrinolytics)
Thrombolytics such as streptokinase or tissue-type plasminogen activator (tPA) restore perfusion to the ischemic area by lysing the clot, thereby reducing infarct size and improving survival.
Thrombolysis benefits patients with all types of ST elevation infarction, but the benefit is
several times greater in those with anterior infarction. The earlier the treatment is given, the
greater the absolute benefit. The greatest benefit is in patients with ST elevation or new left
bundle branch block who have had symptoms for <12 hours.
Streptokinase and alteplase are given by IV infusion. Reteplase and tenecteplase can be given
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by rapid bolus injection. tPA is the most common agent used in the U.S. Prolonged persistence of antibodies to streptokinase may reduce the effectiveness of subsequent treatment;
therefore, streptokinase should not be used if used within the previous 12 months in the same
patient. Complexity of administration differs among the different thrombolytics: tenecteplase
and reteplase are ready in about one minute; for streptokinase or tPA, the typical time from
physician order to administration is 12 to 15 minutes.
Bottom line: consider a thrombolytic agent as an alternative to primary PCI in suitable candidates with:
• ST-elevation MI (>1 mm ST elevation in 2 contiguous leads)
• New LBBB
Contraindications to thrombolytic therapy:
• Absolute contraindications:
• Active bleeding or bleeding diathesis
• Significant closed head or facial trauma within 3 months
• Suspected aortic dissection
• Prior intracranial hemorrhage
• Ischemic stroke within 3 months
Chapter 5
l Cardiology
Relative contraindications:
• Recent major surgery (<3 weeks)
• Traumatic or prolonged cardiopulmonary resuscitation
• Recent (within 4 weeks) internal bleeding
• Active peptic ulcer
• Severe, poorly controlled HTN
• Ischemic stroke (<3 months)
Late presentation (>12 hours after symptom onset): Reperfusion therapy with either PCI or
fibrinolysis is not routinely recommended in patients who are asymptomatic and hemodynamically stable, and who present >12 hours after symptom onset.
Other interventions may include coronary artery bypass grafting (CABG). CABG surgery may
occasionally be more appropriate—particularly in patients who have suitable anatomy and are
not candidates for fibrinolysis or PCI. CABG surgery may also be considered in patients with
cardiogenic shock or in association with mechanical repair.
Antiplatelet Therapy
Aspirin should be given to all patients with presumed STEMI unless contraindicated, and, in
the absence of significant side effects, low-dose therapy should be continued in the long term.
Clopidogrel or prasugrel should be prescribed in addition to aspirin for patients undergoing
PCI with a stent. Ticagrelor is an alternative to clopidogrel or prasugrel.
In patients selected for fibrinolytic therapy, clopidogrel should be given in addition to aspirin,
unless contraindicated. Note, however, that if it is thought that the patient is likely to require
CABG acutely, clopidogrel should be withheld.
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