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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
Clopidogrel should be continued for at least a month after fibrinolytic therapy, or for up to
9–12 months after stent implantation, depending on the type of stent used.
Antithrombin Therapy
With PCI: Antithrombin therapy should be used in conjunction with PCI. The dose of
unfractionated heparin therapy will depend on concomitant use of glycoprotein (GP) IIb/IIIa
inhibitors. It may be advisable to give a bolus of heparin while the patient is in transit to the
catheterization laboratory.
The role of enoxaparin in acute STEMI in conjunction with PCI remains to be fully determined, but it appears to be safe and effective.
With fibrinolysis: Antithrombin therapy should be used with fibrin-specific fibrinolytic agents.
IV unfractionated heparin should be given as an initial bolus, adjusted to attain the activated
partial thromboplastin time (APTT) at 1.5 to 2 times control. IV unfractionated heparin is
used when rapid reversal is needed. The half-life is shorter with unfractionated heparin.
Glycoprotein IIb/IIIa Inhibitors
It is reasonable to use abciximab with primary PCI. Epifibatide and tirofiban are the other
GPIIb/IIIa inhibitors. Full-dose GP IIb/IIIa inhibitors should be avoided with fibrinolytic
therapy as there is evidence of excessive bleeding (including intracranial hemorrhage) with
this combination.
Note
To remember issues that
need to be considered at the
time of discharge, remember
“ABCDE” (aspirin and antianginals, beta blockers and
blood pressure, cholesterol
and cigarettes, diet and
diabetes, education and
exercise).
The combination of GP IIb/IIIa inhibitors with reduced doses of fibrinolytic therapy is not
recommended. There is no significant advantage over full-dose fibrinolytic therapy alone, and
the risk of bleeding is increased, particularly in the elderly.
Emergency bypass surgery should be considered in patients with STEMI and: (1) failed PCI
with persistent pain or hemodynamic instability and coronary anatomy suitable for surgery or
(2) persistent or recurrent ischemia refractory to medical therapy and suitable anatomy.
1. Aspirin: All patients should take daily unless contraindicated.
2. Clopidogrel: There is evidence that clopidogrel or prasugrel should be prescribed for
up to 9–12 months after acute myocardial infarction, particularly after stent placement.
Clopidogrel may also be prescribed as an alternative when aspirin is contraindicated, or
to those intolerant to aspirin, in patients with recurrent cardiac events.
3. B-blocker: These drugs should be prescribed for all patients after an ACS unless contraindicated, and continued indefinitely. Metoprolol and carvedilol particularly should
be used in patients after ACS who have heart failure.
4. ACE inhibitors: Should be given in patients with ACS in CHF, left ventricular dysfunction (ejection fraction <40%). Its use should be reviewed later on the course of the
patient and discontinued if the heart failure resolves.
5. Statins: Statin therapy should be initiated in the hospital in all patients with ACS (the
exception is the rare ACS that is not related to atherosclerosis).
6. Nitrates: Long-acting nitrates (isosorbide) should be reserved for the patients with
persistent chest pain.
7. Warfarin: It is recommended after ACS only for those at high risk of systemic thromboembolism because of atrial fibrillation or mural thrombus.
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Secondary prevention through the control or elimination of known risk factors for coronary
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artery disease (e.g., hyperglycemia in patients with diabetes mellitus, HTN control, tobacco
cessation, physical inactivity) also should be part of discharge planning.
You are asked by your patient, who has a history of ischemic heart disease, about
drug treatments that have been shown to decrease mortality in his case. (It doesn’t
matter if he has stable angina or prior history of acute coronary syndrome.)
Answer: Lipid lowering agents (statins), ASA, B-blocking agents and CABG in patients with
triple vessel disease or left main disease.
Exercise ECG testing: Increasingly, submaximal testing is performed 4–7 days after infarction.
A maximal test can be performed at 3–6 weeks postinfarction. It is used to assess prognosis
and to identify those patients with reversible ischemia who should then have an angiogram (if
one has not been done) to assess the need for coronary artery bypass graft.
Myocardial perfusion imaging can be performed before hospital discharge to assess the
extent of residual ischemia if the patient has not already undergone cardiac catheterization
and angiography.
Chapter 5
l Cardiology
Complications of ACS
• Bradycardia: sinus, atrioventricular junctional, idioventricular. These are treated acutely
with atropine and temporary pacing if severe.
• Premature beats: atrial, ventricular. No treatment is needed for ectopy such as these.
• Tachyarrhythmias (supraventricular): atrial tachycardia, atrial fibrillation, atrial flutter,
AV junctional; are seldom caused by ischemia
• Tachyarrhythmias (ventricular): ventricular tachycardia, accelerated idioventricular
rhythm, ventricular fibrillation
Conduction Abnormalities
•
Atrioventricular nodal: first-, second-, and third-degree block
• Intraventricular: hemiblocks (left anterior, left posterior), bundle branch block, thirddegree atrioventricular block
• Contractile dysfunction: left ventricular, right ventricular, and biventricular failure;
true ventricular aneurysm; infarct expansion
• Mechanical disruption: acute mitral regurgitation (papillary muscle dysfunction or
rupture), ventricular septal rupture, free wall rupture, pseudoaneurysm; treated with
emergency surgical repair
• Electromechanical dissociation
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l Internal Medicine
• Postinfarction ischemia: ischemia in the infarct and ischemia distant to the infarct
• Early recurrent infarction or infarct extension
• Postinfarction angina after thrombolytics or PCI should be treated with bypass surgery
Treated with aspirin, NSAIDs, and later steroids if there is no response.
• Mural thrombus with systemic embolism
• Deep vein thrombosis with prolonged immobilization
Most often due to arrhythmia.
• Ventricular fibrillation (most commonly)
• Ventricular tachycardia
Accompanies 30% of inferior MIs. It is diagnosed with RV leads and treated with fluids.
Non-Cardiac Complications of ACS
Depression is 3x more common in those who have had a heart attack than in the general
population, with 20% of heart attack victims qualifying for a diagnosis of major depressive
disorder, and a far greater proportion experiencing increased levels of depressive symptoms.
Beyond the accompanying emotional distress and suffering, depression also increases one’s
risk of having another heart attack or dying over the ensuing months and years.
There is reliable evidence that both antidepressant medications and certain forms of psychotherapy are effective in reducing depression in the post-MI state. Selective serotonin reuptake
inhibitors (SSRIs) such as sertraline and citalopram have been found to be both effective
in reducing depression and relatively safe for use in patients with coronary heart disease.
Cognitive behavior therapy has also been found to be effective in treating depression.
Erectile dysfunction (ED) is prevalent among patients with CAD and post-MI (in some
series ~ 40%).
• ED complicates the recovery of those post-MI.
• Treatment of post-MI patients includes management of depression, reassurance, and
modification of medications that may cause ED.
• Sildenafil should be used cautiously in men post-MI who are taking nitrates of up to
55 mm Hg, because it can cause a drop in BP. Due to this synergistic effect, it is therefore contraindicated in patients taking nitrates.
• ED is a complication of the conditions that are primary risk factors for developing
CAD, in particular, diabetes, hypertension, dyslipidemias, and arteriosclerosis.
• Smoking and stress are implicated in the development of ED.
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In evaluating risk of MI associated with intercourse in patients with cardiac disease, it has
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been estimated that <1% of MIs occur during sexual activity. Although sexual activity can
trigger MI, the relative risk is low with a slight increase in risk within 2 hours of sexual activity. However, even in high-risk individuals with previous MI the annual risk is 1.10% vs. 1.0%
in the population at large. This risk appears to apply equally to men and women.
Patients can therefore be risk-stratified and counseled about safely returning to or continuing
sexual activity:
• Low risk: asymptomatic patients with fewer than 3 risk factors for CAD, stable angina,
recent uncomplicated MI, mild valvular heart disease, mild CHF, controlled hypertension, or post successful revascularization; patients can generally be managed medically
and followed at regular intervals
• Intermediate risk: those with recent MI (but beyond 2 weeks), moderate CHF (New
York Heart Association class II) and those with >3 risk factors for CAD; patients may
benefit from functional testing, i.e., exercise treadmill tests (ETT), echocardiography,
or nuclear imaging study with re-stratification based on results of testing
– ETT can assist in gauging cardiac risk of sexual activity, both for induction of isch-
emia or arrhythmia. In general, if a patient can achieve 5 METs on ETT without
demonstrable ischemia or significant arrhythmia, he is not at high risk to resume
normal sexual activities
– Similarly, if echocardiography does not yield evidence of more than moderate left
ventricular dysfunction, resumption of sexual activity is probably safe
Chapter 5
l Cardiology
High-risk: those with unstable angina, MI within 2 weeks, poorly controlled hypertension,
severe CHF (New York Heart Association class III/IV), significant arrhythmias, severe cardiomyopathies; patients should be referred for cardiovascular evaluation and stabilization prior
to recommending resumption of sexual activity.
Nonatherosclerotic Acute Coronary Syndromes
Although thrombotic complications of the atherosclerotic process account for most cases of acute
coronary syndromes, there are a few rare etiologic factors that have been proposed as causes of or
contributors to acute coronary occlusion. These causes include coronary artery spasm, spontaneous coronary dissection, coronary artery embolization, coronary arteritis, and hypercoagulability
states such as factor V gene mutation, deficiencies of proteins C and S, antithrombin III deficiency, antiphospholipid antibody syndrome, and prothrombin gene mutation. Cocaine use has been
documented to induce coronary vasoconstriction in nondiseased coronary segments but is more
pronounced in atherosclerotic segments.
Prinzmetal angina, or variant angina, is a very uncommon condition in which episodes
of severe angina are triggered when one of the major coronary arteries suddenly goes into
spasm. These episodes are accompanied by ST-segment elevation on the ECG. Although the
spasm almost always terminates spontaneously, Prinzmetal angina may be associated with
acute MI, serious ventricular arrhythmias, and sudden death.
As opposed to typical angina, Prinzmetal angina usually occurs during periods of rest, most
often at night and in the early morning hours. Frequently, episodes appear in clusters. In men,
Prinzmetal angina is often associated with atherosclerosis; in women it is not. Women with
Prinzmetal tend to have few risk factors for CAD, though many have a history of migraine
headaches (another condition associated with arterial spasm).
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l Internal Medicine
Exercise testing and routine coronary angiography usually give normal results. Ergonovine
has been used to trigger coronary artery spasm in susceptible patients, confirming the diagnosis. Treatment with calcium channel blockers or nitrates eliminates spasm in most of these
patients. Once adequately treated, their prognosis is good.
During an acute episode of pain and ST segment elevation, you cannot tell who has
Prinzmetal variant angina and who has an acute ST elevation MI. Therefore, you must initially treat everyone with chest pain and ST elevation as if they were having an acute MI.
Prinzmetal angina can be confirmed only after coronary angiography.
Causes of MI without Coronary Atherosclerosis
• Vasculitis
– Systemic lupus erythematosus
– Polyarteritis nodosa
– Takayasu arteritis
– Mucocutaneous lymph node syndrome (Kawasaki)
• Anomalous origin of coronary artery
• Coronary spasm
– Variant angina
– Cocaine abuse
• Coronary artery embolus
– Atrial myxoma
– Atrial or ventricular thrombus
• Hypercoagulable states
– Polycythemia vera
– Thrombocytosis
– Factor V Leiden
– Protein C deficiency
– Antiphospholipid antibodies
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Heart failure (HF) arises from the inability of the ventricle to efficiently pump blood
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throughout the circulation. Clinically HF presents with symptoms of breathlessness, exercise
intolerance, and fatigue.
A 62-year-old man with hypertension and dyslipidemia presents with dyspnea
and lower-extremity edema for 2 months. On exam there is jugular venous
distention (about 9 cm.), an S3 gallop, and the apical impulse is displaced to the
left of the mid-clavicular line at the 6th intercostal space. The chest x-ray shows
enlarged cardiac silhouette. The echocardiogram shows a dilated left ventricle
with an ejection fraction of 35%.
A 57-year-old man with history of multiple myeloma presents with dyspnea
and lower-extremity edema for 2 months. On exam there is jugular venous
distention (about 8 cm.), an audible S4, and the apical impulse is non-displaced
at the 5th intercostal space. The chest x-ray shows normal cardiac silhouette. The
echocardiogram shows a thickened left ventricle with an ejection fraction of 65%.
Chapter 5
l Cardiology
As HF evolves, changes in vascular function, blood volume, and neurohumoral status occur
throughout the body. These changes serve as compensatory mechanisms to help maintain cardiac output (primarily by the Frank-Starling mechanism) and arterial blood pressure (by systemic vasoconstriction). However, these compensatory changes over time can worsen cardiac
function. Cardiac changes during HF include increased end-diastolic volume; ventricular dilatation or hypertrophy; decreased stroke volume and cardiac output; reduced ejection fraction
(systolic dysfunction) or impaired filling (diastolic dysfunction). Compensatory mechanisms
during HF include:
• Cardiac: Frank-Starling mechanism, tachycardia, ventricular dilatation
•
Neuronal: increased sympathetic adrenergic activity, reduced cardiac vagal activity
• Hormonal: activation of angiotensin-aldosterone system, vasopressin, catecholamines,
and natriuretic peptides
In clinical practice, HF is commonly categorized by whether the abnormality is due to contraction or relaxation of the heart. Systolic HF (systolic dysfunction) is due to a loss of contractile strength of the myocardium accompanied by ventricular dilatation. This type of HF
is also accompanied by a decrease in normal ventricular emptying (usually ejection fraction
<45%). Examples of systolic HF include ischemic cardiomyopathy and dilated cardiomyopathy (Case 1 in this section).
Heart failure with preserved ejection fraction (diastolic dysfunction) occurs when the filling
of one or both ventricles is impaired while the emptying capacity is normal (echocardiogram
confirms that the ejection fraction is normal). The infiltrative cardiomyopathies (amyloidosis)
are typical examples (Case 2 in this section).
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USMLE Step 2 CK
Figure 5-7. Inter-related Cycles in Congestive Heart Failure
l Internal Medicine
↑ afterload
(LV impedance)
↑ systemic vascular
resistance
Impaired
LV function
Reflex arteriolar
vasoconstriction
↓ cardiac output
↓ stroke volume
↓ renal perfusion
↑ LV filling pressure
↑ renin
↑ angiotensin II
↑ aldosterone
↑ vasopressin
Peripheral
edema
↑ blood
volume
NaCl and H
retention
0
2
Congestive HF indicates a clinical syndrome of dyspnea and fatigue as well as evidence of
features of circulatory congestion (peripheral edema, elevated jugular venous pressure [JVP]).
In heart failure, intravascular congestion occurs with elevation of left ventricular diastolic and
pulmonary venous pressures that eventually causes transudation of fluid from the pulmonary capillaries into the interstitial space. Pulmonary edema develops when the rate of fluid
accumulation goes above the rate of lymphatic absorption. Pulmonary edema is detected by
audible crackles, increased JVP and edema on exam, and chest x-ray findings.
136
Wikipedia, James Heilman, MD
Figure 5-8. Elevated JVP
Decompensated HF or exacerbation of HF denotes worsening of symptoms and clinical find-
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ings in pre-existing HF. This can be due to precipitating factors such as non-adherance to
medication, increase in dietary salt, acute ischemia, tachycardia, or pulmonary infection.
In evaluating patients with HF or worsening of pre-existing HF, it is also important to exclude
precipitating factors. Commonly, HF manifests for the first time when a precipitating factor
places additional burden on the heart. Such factors include:
• Cardiac ischemia and myocardial infarction
• Infections (especially pulmonary infections)
• Arrhythmias (especially atrial fibrillation)
• Excessive dietary salt (commonly after holiday meals)
• Uncontrolled hypertension (especially after abrupt cessation of anti-hypertensive
medication)
• Thyrotoxicosis
• Anemia
Chapter 5
l Cardiology
HF may occur as a consequence of most causes of heart disease, but ischemic heart disease
is responsible for over 70% of all cases in the western world. Other common causes include:
hypertensive heart disease, the cardiomyopathies (idiopathic, alcohol related, etc.), and valvular
and congenital heart diseases.
Symptoms of HF include dyspnea (differentiate from pulmonary dyspnea), orthopnea, paroxysmal nocturnal dyspnea, and fatigue/weakness.
Table 5-4. Most Common Causes
of Acute Pulmonary Edema
Ischemia
Arrhythmia
Non-adherence with medication
Dietary indiscretion
Infection
Physical findings in HF:
• Pulmonary rales
• Peripheral edema, ascites
• Hepatomegaly
• Jugular venous distention
• Displaced apical impulse (systolic HF)
Clinical Pearl
In the work-up of patients with
new-onset HF, always try to
identify potentially reversible
causes.
Clinical Pearl
In the work-up of patients with
exacerbation of HF, always:
• Check cardiac enzymes
to exclude myocardial
ischemia or infarction
• Do a chest x-ray to exclude
infection
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l Internal Medicine
Wikipedia, James Heilman, MD
Figure 5-9. Pitting Edema
The severity of heart failure is commonly classified by using a HF staging system. The New
York Heart Association Functional Classification (NYHA staging system) relates symptoms to
everyday activities and the patient’s quality of life:
• Class I: patients have no limitation of activity; they suffer no symptoms from ordinary
activities
• Class II: patients with slight, mild limitation of activity; they are comfortable with rest
or with mild exertion
• Class III: patients with marked limitation of activity; they are comfortable only at rest
• Class IV: patients are confined to bed or chair; any physical activity brings on discom-
fort and symptoms occur at rest
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Copyright 2007 Gold Standard Multimedia Inc.
Figure 5-10. Chest X-ray Demonstrating Acute Exacerbation
of Congestive Heart Failure
Chapter 5
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l Cardiology
Diagnosis. Echocardiography is the test-of-choice to confirm the diagnosis of HF and to
classify the type (systolic vs. diastolic). With the echocardiogram, the clinician is able to determine ejection fraction and identify valvular heart disease as well as other cardiac anomalies
(dilated ventricle, thickened ventricle, etc.).
Chest x-rays are also used to aid in the diagnosis of heart failure. They may show cardiomegaly, vascular redistribution, Kerley B-lines, and interstitial edema.
Electrocardiogram is used to identify ventricular hypertrophy and/or the presence of ischemic
heart disease, arrhythmias, or conduction delays which may cause or precipitate HF.
Brain Natriuretic Peptide (BNP) is a polypeptide secreted by the heart in response to excessive
stretching of the myocytes. It is a valuable tool in the evaluation of patients with presumed HF
or decompensated HF in the acute setting. The BNP is almost always elevated (97% sensitivity)
in patients with decompensated HF. Normal BNP excludes CHF as the cause of dyspnea.
Management. The treatment goals in HF are to improve hemodynamics, relieve symptoms
(improve quality of life), and prolong survival. Remember, always evaluate for reversible
causes at the same time.
Non-pharmacologic treatment includes primarily reduction of salt intake.
For pharmacologic treatment, ACE inhibitors are the basis of therapy and recommended
for all patients with HF (especially systolic HF), irrespective of blood pressure status. They
improve survival and reduce ventricular hypertrophy—and eventually, symptoms. ACE inhibitors through vasodilation reduce preload and afterload, thereby reducing right atrial, pulmonary
arterial, and pulmonary capillary wedge pressures. All ACE inhibitors have been studied and are
considered equal in terms of HF treatment. Angiotensin receptor blockers (ARB) are acceptable
alternatives if the patient is unable to tolerate ACE inhibitors (cough, angioedema).
Clinical Pearl
The single best test for the
evaluation and diagnosis
of heart failure is the
echocardiogram.
Note
BNP is used acutely if the
cause of dyspnea is not clear.
Diuretic therapy, especially loop diuretics, is the treatment of choice for the relief of acute
pulmonary edema symptoms. Several classes are used but the loop diuretics (furosemide)
class is the most commonly used. Thiazide diuretics (hydrochlorothiazide) are useful only in
mild HF. Spironolactone and eplerenone (aldosterone antagonists) have been used as add-on
therapy to ACE inhibitors in severe heart failure to prolong survival by presumed aldosterone inhibition.
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