Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2664_Библиотеки_им_академика_М_И_Перельмана
.pdf
Cardiology
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Chapter Title
Learning Objectives
❏ Outline a differential diagnosis and diagnostic plan for patients with acute chest pain
or chest discomfort
❏ List the causes of and treatment for heart rate and rhythm disturbance
❏ Describe the physiology of valvular disease and CHF, and describe the mechanism of
action of appropriate treatments
❏ Give an overview of presentation, epidemiology, and management of ischemic heart
disease, acute coronary syndrome, myocardial disease, and pericardial disease
❏ Describe the most common medications used to treat cardiovascular disease and
their most serious or common side effects
00
5
Chest pain is one of the most common complaints for which a patient comes to the physician’s office or the emergency department. Patients presenting with chest pain or chest discomfort may have an underlying cause that is benign and requires only moderate analgesic
medication, or they may have a life-threatening condition such as acute myocardial ischemia
or aortic dissection that mandates prompt diagnosis and treatment. In the evaluation of chest
pain, the focus should be on excluding the more serious conditions.
History
Assessing the setting in which the chest pain occurs is one of the most important aspects of
the evaluation. The 26-year-old medical resident with chest pain that occurred after on-call
and who is otherwise healthy is unlikely to have cardiovascular disease, no matter the quality
or duration of chest pain. Consider the 58-year-old man with type 2 diabetes and dyslipidemia with chest discomfort of any type; now the probability for cardiac-related chest pain
increases dramatically.
Overall, the chest pain history is more useful than the physical examination. Important
aspects of the history include duration, quality, location, radiation, frequency, alleviating or
precipitating factors (especially exercise), and associated symptoms.
111
USMLE Step 2 CK
l Internal Medicine
• For both stable angina and acute coronary syndromes, the quality of chest pain is
described by the patient as “tightness,” “heaviness,” or “pressure,” but symptoms which
resemble acute abdomen (pain in the upper abdomen, nausea) are not uncommon.
Nausea and vomiting are sometimes the main symptoms in inferoposterior wall ischemia (also, vagal reflexes may cause bradycardia and hypotension, presenting as dizziness or fainting).
• “Sharp” or “knife-like” chest pain and pain which the patient can pinpoint to an “exact
area” are less likely to be related to ischemia or infarction, especially if the chest pain is
reproduced by changes in position or palpation.
• Myocardial infarction is associated with pain that lasts >20–30 minutes in duration.
• Response of chest pain to nitroglycerin (within a few minutes) is most consistent with
transient ischemia or esophageal spasm. Chest pain that worsens with nitroglycerin
sometimes occurs with gastroesophageal reflux disease. The response to nitroglycerin
is not enough to confirm coronary disease as the cause of chest pain.
• Acute coronary syndromes in women present with atypical symptoms: dyspnea, shortness of breath, fatigue. This may be due to the older age group in which myocardial
ischemia and infarction occur in women.
Physical Examination
One of the most important parts of the examination of the chest pain patient is the “initial
impression.” Diaphoresis, tachypnea, and anxious expression should alert the clinician to a
potentially life-threatening process. Tachycardia and tachypnea are both nonspecific but occur
in almost all cases of pulmonary embolism.
• Blood pressure should be checked in both arms: a difference of >20 mm Hg systolic
suggests aortic dissection and is present in ~70% of cases.
• Hypotension may suggest massive pulmonary embolism or cardiac shock.
• Fever may suggest pneumonia or mediastinitis (esophageal rupture) as the cause of
chest pain.
• Evidence of atherosclerosis (corneal lipid rings, narrowed retinal arteries, and pigment
and hair changes in the legs) is commonly seen in patients with coronary syndromes.
112
The chest wall should be inspected for tender areas, respiratory motion, respiratory retractions, or accessory muscle use. If the tender area corresponds to the location of the patient’s
pain and palpation exactly reproduces the pain, consider musculoskeletal chest pain as the
cause of chest pain.
Abnormal heart sounds and new murmurs are commonly found in certain chest pain syndromes. Wide physiologic splitting of the second heart sound (splitting wider with inspiration) can be found in right bundle branch block or in right ventricular infarction. New paradoxical splitting is most often due to left bundle branch block (LBBB), or anterior or lateral
infarction. A new fourth heart sound can occur with angina or infarction. An S3 is more likely
due to underlying heart failure. A new murmur may be significant: aortic regurgitation occurs
in over half of patients with aortic dissection, while mitral regurgitation can occur in patients
with angina or infarction and is due to papillary muscle dysfunction.
The lungs should be auscultated for crackles and asymmetrical breath sounds. Asymmetry
of breath sounds may be found in patients with spontaneous pneumothorax. Absent lung
sounds also may occur in pneumothorax and pleural effusions.
The extremities should be examined for pulses, edema, calf tenderness, and signs of atheroscle-
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
rotic vessel disease. Absence of pedal pulses may occur in aortic dissection. Any swelling of the
legs, especially if unilateral, raises the odds of pulmonary embolism as the cause of chest pain.
Testing
All patients with chest pain should have a 12-lead electrocardiogram (ECG) since the ECG
is the single most important test for the evaluation of the cause of chest pain. The ECG
should be done immediately after initial stabilization and taking of vital signs. Most patients
with myocardial infarction will have an abnormal initial ECG: 50% with acute MI will have
diagnostic findings (ST elevation or Q waves), while 35% will have findings consistent with
ischemia (ST depression and/or T wave inversion). In patients presenting with acute chest
pain who have normal ECG, the chance of acute MI is much less than 10% (in some studies
1–2.6%). An abnormal ECG can be seen in many non-cardiac conditions (pulmonary embolism, electrolyte abnormalities, aortic dissection).
In interpreting the ECG, every effort must be made to obtain previous ECGs, so that the
abnormalities can be compared with those on the old tracing. Any ECG finding is assumed
to be new unless proven otherwise by an old ECG (if one is available). Also, in patients with
acute coronary syndromes, the ECG is the sole test required to select patients for emergency
reperfusion.
Chapter 5
l Cardiology
Serum cardiac biomarker determinations play a vital role in the evaluation of patients who
present with acute chest pain and in the diagnosis of acute myocardial infarction. Serum
markers such as aspartate transaminase, lactate dehydrogenase, and lactate dehydrogenase
subforms no longer are used because they lack cardiac specificity and their delayed elevation
precludes early diagnosis. Creatine kinase (CK) is found in striated muscle and tissues of the
brain, kidney, lung, and GI tract. This widely available marker has low sensitivity and specificity for cardiac damage. Furthermore, CK levels may be elevated in a number of noncardiac
conditions, including trauma, seizures, renal insufficiency, hyperthermia, and hyperthyroidism. Currently, the CK marker largely has been replaced by cardiac troponins and CK-MB.
CK-MB isoenzyme: CK-MB is cardiac specific and is useful for the early diagnosis of acute
myocardial infarction. CK-MB typically is detectable in the serum 4–6 hours after the onset of
ischemia, peaks in 12–24 hours, and normalizes in 2–3 days (see Figure 5-1).
Like the CK level, the peak CK-MB level does not predict infarct size; however, it can be used
to detect early reinfarction. Serial CK-MB levels commonly are obtained at admission to the
emergency department and are repeated in 6–12 hours.
CK-MB subforms: CK-MB may be further characterized into subforms (or isoforms). CK-MB2
is found in myocardial tissue, and CK-MB1 is found in plasma. The CK-MB subform is not routinely used.
Cardiac troponins: Troponins (T, I, C) are found in striated and cardiac muscle. Because the
cardiac and skeletal muscle isoforms of troponin T and I differ, they are known as the “cardiac
troponins.” They are the preferred markers for the diagnosis of myocardial injury. Troponin T
and I generally have similar sensitivity and specificity for the detection of myocardial injury.
Unlike troponin I levels, troponin T levels may be elevated in patients with renal disease,
polymyositis, or dermatomyositis.
The cardiac troponins typically are measured at emergency department admission and
repeated in 6–12 hours. Patients with a normal CK-MB level but elevated troponin levels are
113
USMLE Step 2 CK
Figure 5-1. Progression of Cardiac Enzyme Serum Levels
CK-MB Troponin
l Internal Medicine
considered to have sustained minor myocardial damage, or microinfarction, whereas patients
with elevations of both CK-MB and troponins are considered to have had acute myocardial
infarction. The cardiac troponins may remain elevated up to two weeks after symptom onset,
which makes them useful as late markers of recent acute myocardial infarction.
An elevated troponin T or I level is helpful in identifying patients at increased risk for death
or the development of acute myocardial infarction. Increased risk is related to the high serum
troponin levels. The troponins also can help identify low-risk patients who may be sent home
with close follow-up. Those with a normal or nearly normal ECG and a normal troponin I
test 6 hours after admission had a very low risk of major cardiac events (0.3%) during the
next 30 days.
Myoglobin: Myoglobin levels begin to rise as early as 1–4 hours after the onset of pain.
Normal myoglobin at 4 hours has a very high negative predictive value.
Serum enzyme level
Normal
5 10 15
Days after infarction
A chest x-ray should be obtained on patients with chest pain. The x-ray may show pneumothorax, pneumomediastinum (such as from esophageal rupture), pleural effusion, or infiltrates. Aortic dissection can cause widening of the mediastinum. Subtle findings such as loss
of lung volume or unilateral decrease in vascular markings may suggest pulmonary embolism.
Especially if the clinician suspects a noncardiac diagnosis, other tests may be helpful in the
evaluation of patients presenting with acute chest pain. Some of the most common ones used
are: arterial blood gases, BNP (see pulmonary and heart failure section), CT angiogram.
114
Causes of Chest Pain
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Aortic Dissection. Pain is sharp, tearing, and extremely severe; typically radiates to back; loss
of pulses or aortic insufficiency often develop; mediastinum is widened on chest x-ray; MI
may occur if dissection extends into coronary artery; diagnosis confirmed by MRI, CT scan,
or transesophageal echocardiogram.
Pulmonary Embolism. Dyspnea, tachycardia, and hypoxemia are prominent; pain is usually
pleuritic, especially when pulmonary infarction develops; EKG is usually nonspecific but may
show S wave in lead I, Q wave in lead III, or inverted T wave in lead III; diagnosis confirmed by
CT angiogram.
Pericarditis. May be preceded by viral illness; pain is sharp, positional, pleuritic, and relieved by
leaning forward; pericardial rub often present; diffuse ST elevation occurs without evolution of
Q waves; CK level usually normal; responds to anti-inflammatory agents.
Table 5-1. Differential Diagnosis of Conditions Causing Chest Pain
Noncardiovascular Disorders Differentiating Features
Costochondritis Pain exacerbated with inspiration; reproduced with
chest wall palpitation
Chapter 5
l Cardiology
Hiatal hernia Reflux of food; relief with antacids
GERD Acid reflux; relief with antacids
Peptic ulcer Epigastric pain worse 3 h after eating
Gallbladder disease Right upper quadrant abdominal pain and
tenderness
Cardiovascular Disorders Differentiating Features
Myocardial infarction Pain more severe, usually >20 min in duration
Aortic stenosis Typical systolic ejection murmur
Myocarditis Pain is usually vague and mild if present
Pericarditis Pain is sharper, pain worse with lying down and
relieved by sitting up
Dissecting aortic aneurysm Pain is sharp, tearing, often occurs in back
Mitral valve prolapse Transient pain, midsystolic click murmur, and young
female with no risk factors
Pulmonary Disorders Differentiating Features
Pulmonary embolus-infarction Tachypnea, dyspnea, cough, pleuritic pain, hemoptysis
Pulmonary hypertension Signs of right ventricle (RV) failure
Pneumothorax Sudden onset of pain and dyspnea
115
USMLE Step 2 CK
l Internal Medicine
Myocarditis. May be preceded by viral illness; pain is generally vague and mild if present; total
CK and MB fraction of CK (CK-MB) are often elevated; conduction abnormalities and Q
waves may occur.
Musculoskeletal Disorders. Most common cause of chest pain. Includes costochondritis, cervical
osteoarthritis, radiculitis; pain is atypical, stabbing, localized, may be pleuritic; reproduced by
motion or palpation; EKG changes absent.
GI Disorders. Esophageal reflux is often made worse with recumbency or after meals, may be
associated with regurgitation and relieved by antacids; episodes of spasm may be brought on by
cold liquids, relieved by nitroglycerin, and may closely resemble angina or infarction; diagnosis
may be confirmed by upper endoscopy or esophageal manometry. Peptic ulcer disease, pancreatitis, and cholecystitis may occasionally mimic infarction; abdominal tenderness is present, with
radiation to back and elevated amylase in pancreatitis; sonography can confirm cholecystitis.
Pneumothorax. Onset abrupt with sharp pleuritic chest pain and dyspnea; breath sounds
absent; chest x-ray confirms.
Pleuritis. Pain is sharp and increases on inspiration; friction rub or dullness may be present;
other respiratory symptoms and underlying pulmonary infection usually present.
Ischemic heart disease (IHD), also known as coronary heart disease, refers to an imbalance
in coronary oxygen demand and supply resulting from insufficient blood flow. In nearly all
cases, the reduction in blood flow is caused by coronary atherosclerotic disease. When the atherosclerotic plaque ruptures, there is superimposed thrombus formation that acutely occludes
the artery; this is the most common cause of life-threatening acute coronary syndromes.
Rarely, other abnormalities may occur, including coronary artery embolism, coronary artery
spasm, coronary arteritis, and coronary artery dissection (see section on nonatherosclerotic
acute coronary syndromes) that may cause ischemic heart disease in the absence of atheroma
formation.
IHD is one of the most prevalent diseases in society, and those affected are likely to die from
their disease (though age-specific deaths have declined over the past 30 years). IHD, as part of
a systemic process that involves all arteries in the body, is an insidious process that begins in
early adulthood with fatty streaks; these lesions progress into plaques and thrombus formation in middle age.
116
Ischemic Heart Disease
Figure 5-2. Ischemic Heart Disease
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Chapter 5
l Cardiology
Clinically Silent
(asymptomatic)
Stable angina
(symptoms with
exertion)
Intima
Media
Atherosclerotic
plaque
Progression of
atherosclerotic plaque
The more risk factors a person has, the greater the chance that he will develop heart disease.
Also, the greater the level of each risk factor, the greater the risk. For example, a person with
total cholesterol 260 mg/dL has a greater risk than someone with total cholesterol 220 mg/dL,
even though all people with total cholesterol ≥220 are considered high risk.
Symptomatic
Acute coronary syndromes:
• Unstable angina
• Non ST-segment elevation MI
• ST-segment elevation MI
Atherosclerotic
plaque
Ruptured
plaque
Thrombosis
formation
Major Modifiable Risk Factors
Elevated cholesterol levels: The risk of IHD rises as blood cholesterol levels increase. The
concentrations of lipid fractions, especially low-density lipoprotein (LDL) and high-density
lipoprotein (HDL), are also important. LDL cholesterol is the single most important sub-
group that carries risk for IHD, although there are several other abnormalities that increase
coronary risk: low HDL cholesterol, hypertriglyceridemia, increased total-to-HDL-cholesterol
ratio and increased lipoprotein A. When other risk factors (such as high blood pressure and
tobacco smoke) are present, this risk increases even more.
Proof of the importance of serum cholesterol has come from randomized trials, which
showed that reductions in total LDL levels reduce coronary events and mortality.
Tobacco: Cigarette smoking is an important factor for IHD because a smoker’s risk of heart
attack is >2x that of a nonsmoker. Cigarette smoking also acts with other risk factors (hypertension, dyslipidemia) to greatly increase the risk for IHD.
117
USMLE Step 2 CK
l Internal Medicine
• Cigar or pipe smokers have a higher risk of death from IHD, though less than cigarette
smokers.
• Secondhand smoke or passive smoking increases the risk of heart disease, even for
nonsmokers.
• The risk for myocardial infarction in those who quit smoking was reduced to that of
nonsmokers within 2 years of cessation; the benefits were seen regardless of how long
or how much the patient smoked.
Hypertension (HTN): HTN is a well-established risk factor for increase in risk of myocardial ischemia, stroke, kidney failure, and heart failure. Studies in the general population have
shown that the risk for cardiovascular events increases at BP >110/75 mm Hg. Systolic BP is
as important as diastolic BP in terms of risk for IHD, especially in older patients.
Treatment of HTN to optimal levels reduces the risk of IHD and all cardiovascular events. In
fact, data from recent randomized trials suggest that reducing BP below previously recommended levels is beneficial in high-risk patients.
Physical inactivity and exercise: Inactivity and sedentary lifestyle are risk factors for IHD.
Exercise of moderate degree has a protective effect against IHD and cardiovascular events.
More vigorous activities are associated with more benefits. Physical activity can help increase
HDL cholesterol and control diabetes and obesity, as well as help to lower blood pressure.
Obesity: Patients with increased body fat (elevated body mass index), especially if a lot is in
the waist area, are more likely to develop heart IHD and stroke. Excess weight raises blood
pressure, blood cholesterol, and triglyceride levels, and it lowers HDL cholesterol levels. It can
also increase risk for type 2 diabetes by causing insulin resistance.
Studies have shown that loss of as little as 10–20 lb can significantly reduce the risk of cardiovascular disease.
Diabetes mellitus: Elevated blood glucose levels and insulin resistance are associated with IHD
and overall cardiovascular events. All-cause mortality in diabetic patients is comparable to that of
all-cause mortality in patients with prior myocardial ischemia; hence, diabetes is now considered
an “IHD equivalent.” Even when glucose levels are under control, diabetes greatly increases the
risk of IHD. Almost 75% of patients with diabetes die of some form of cardiovascular disease.
There is compelling evidence that aggressive treatment of HTN and cholesterol, as well as
tight glycemic control, reduces the risk of cardiovascular events in these patients significantly.
Major Uncontrollable Risk Factors
Age: Four out of 5 people who die of IHD are age ≥65. Also, women who develop myocardial
ischemia at older ages have a higher mortality than men within the first few weeks of the cardiac event.
Sex: Men have a greater risk of IHD than women, and overall they develop cardiovascular disease earlier in life.
118
Heredity: Family history is a significant independent risk factor if there is a family history of
premature disease (age <55 in male relative and <65 in female relative).
Minor Contributing Factors
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Sex hormones: Men have more heart attacks than women before menopause. Several population studies show that the decrease of natural estrogen as women age may contribute to a
higher risk of heart disease after menopause.
Stress: Various studies have shown relationship between IHD risk and stress in a person’s
life. This may be a true association or just a secondary correlation: for example, people under
stress may overeat, start smoking, or be less active than people who are not under stress.
Myocardial Ischemia As a Manifestation of IHD
During ischemia, an imbalance occurs between myocardial oxygen supply and demand.
Ischemia may manifest in any of the following ways:
• Anginal chest discomfort
• ST-segment deviation on ECG
• Reduced uptake of tracer during myocardial perfusion scanning
• Regional or global impairment of ventricular function
Myocardial ischemia can occur as a result of increased myocardial oxygen demand,
reduced myocardial oxygen supply, or both. In the presence of coronary obstruction, an
increase of myocardial oxygen requirements caused by exercise, tachycardia, or emotion
leads to a transitory imbalance. This condition is frequently termed “demand ischemia”
and is responsible for most episodes of chronic stable angina.
Chapter 5
l Cardiology
In other situations, the imbalance is caused by acute reduction of oxygen supply secondary to marked reduction or cessation of coronary flow as a result of platelet aggregates or
thrombi. This condition, termed “supply ischemia,” is responsible for myocardial infarction (MI) and most episodes of unstable angina (UA). In many circumstances, ischemia
results from both an increase in oxygen demand and a reduction in supply.
Angina (Stable Angina)
A 62-year-old man presents with substernal chest pain that occurs with exertion
and is relieved by rest. He has been having this on and off for 8 months, and the
last episode occurred 3 days ago while he was running to the bus. He has a history
of well-controlled diabetes and dyslipidemia. Vital signs, physical examination, and
ECG are normal. An exercise stress test shows a 2-mm ST depression.
Stable angina occurs when the myocardium becomes ischemic. This occurs during periods of
increased demand for oxygen, such as exercise, or decreased supply, such as hypotension or
anemia (see demand ischemia, above). Stable angina is typically a substernal pressure lasting
5–15 minutes. It may be accompanied by radiation to the jaw, neck, shoulders, or arms. It is
less likely to have the symptoms often associated with MI: sweats, nausea, and shortness of
breath. Anginal pain is not typically affected by respiration or by position. Typically, patients
with stable angina will have pain after a predictable amount of exertion and will have identical symptoms with each attack.
119
Соседние файлы в папке Библиотека им академика М.И. Перельмана