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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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reveal ischemic heart disease. Remember, up to 25% of patients who have sudden death from
an acute MI have no history of chest pain.
The major risk factors for coronary artery disease are diabetes, hypertension, tobacco smoking,
hyperlipidemia, HDL <40 mg/dL, and a family history of premature coronary disease in a first-
degree relative. In fact, even in the absence of these traditional risk factors, the peripheral
vascular disease itself could be considered evidence of probable coronary disease until
proven otherwise.
The other clear problem here is that our patient has elevated LDL with cardiovascular disease.
The most recent cholesterol guidelines recommend an approach which focuses primarily on
risk level and intensity of statin therapy. In essence, there was a switch from treating ‘lab tests’
to treating ‘patients.’
Based on extensive research, there are 4 groups of people for whom statin therapy seems to
reduce cardiovascular events with a good margin of safety:
The guidelines are the same for women as for men. The panel found no evidence that use of
non-statin therapies for prevention would provide acceptable risk reduction compared to their
potential for adverse events. They provided a risk calculator to identify those with a risk
≥7.5% for having a cardiovascular event in the next 10 years. It quantifies risk based on age,
Those with clinical cardiovascular disease
Those with primary elevation of LDL ≥190 mg/dL
Those age 40–75 with diabetes and LDL 70–189 mg/dL without clinical cardiovascular
disease
Those age 40–75 without clinical cardiovascular disease or diabetes with LDL 70–189
mg/dL and with an estimated 10-year cardiovascular disease risk ≥7.5% (risk is identified
using a calculator, see below)
141
sex, race, cholesterol, BP, diabetes, and smoking. The data are inadequate to quantify risk for
some racial, sex, and age groups, i.e., those age >75.
The guidelines stress that lifestyle modification (adherence to a heart healthy diet, regular
exercise, avoidance of tobacco, and maintenance of a healthy weight) is critically important for
everyone, both before and during treatment.
Hence, target LDL in our patient should be <70 mg/dL given that he has a positive stress test,
peripheral vascular disease, and diabetes.
Further Management Plan
Discussion
This patient has an LDL >130 mg/dL in the presence of coronary artery disease. In addition, the
diabetes and the peripheral vascular disease should be considered the equivalent of coronary
artery disease. Although dietary modification and exercise should be implemented, drug
therapy should be started.
In addition to the statins, other drugs which will lower the LDL are bile-acid sequestrants (e.g.,
cholestyramine, nicotinic acid) and fibric-acid derivatives (e.g., gemfibrozil). All of these
drugs will raise HDL and lower both the total cholesterol and triglycerides. Ezetimibe is useful
to add to statins; it is not known if ezetimibe will lower mortality, but it will lower lipid level.
Nor do we know what to do with the other non-statin agents such as cholestyramine, fibric acid
derivatives, or niacin. Their role in therapy remains uncertain.
Dietary modification to limit the intake of saturated fats
1.
HMG CoA reductase inhibitors (rosuvastatin, pravastatin, lovastatin, simvastatin,
atorvastatin)
2.
Exercise
3.
Liver function tests (AST, ALT, bilirubin)
4.
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The statins are generally the initial drug of choice because they have the greatest demonstrated
effect upon mortality and the incidence of serious cardiac events such as myocardial
infarctions. The most common adverse effects of statins are an elevation in liver function tests
and myositis, leading to an elevation in creatinine phosphokinase (CPK) levels. There is no
routine recommendation to monitor CPK levels.
Follow-up Management and Prevention
Final Diagnosis
Hyperlipidemia
Repeat LDL, triglyceride, and cholesterol levels in 6 wks
LFTs if there were any baseline abnormalities
Don’t forget to “counsel” your patients about lifestyle modification. The CCS also accepts
the terms “educate” and “advise.”
Check lipid levels no more than every 6–12 mos
143
Case 6
Chief Complaint
“I can’t breathe!”
History and Physical Examination
A 68-year-old woman is brought to the emergency department by ambulance because of
acute shortness of breath. She has a history of multiple myocardial infarctions and is
normally on a diuretic, metoprolol, digoxin, and enalapril. She is normally somewhat
edematous but not dyspneic. Over the past several days she has become more short of
breath, and this has considerably worsened over the past several hours. Vital signs are T
36.8 C (98.2 F), BP 140/90 mm Hg, pulse 120/min, and respirations 32/min. Physical
examination shows marked jugular venous distention and bilateral rales to the apices. Her
abdomen is soft and nontender. Cardiovascular examination shows tachycardia with a 3/6
systolic murmur at the apex and S3 gallop. There is also evidence of a bilateral lower
extremity edema to the midthigh.
Differential Diagnosis
Acute pulmonary edema
1.
Noncompliance with medications
2.
Arrhythmia
3.
Ischemia
4.
Acute myocardial infarction
5.
Valvular rupture
6.
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Initial Management
Setting: emergency department
Diagnostic/Therapeutic Plan
CCS NOTE
Pulmonary edema is a perfect CCS case. Order everything together—oxygen,
furosemide, morphine, nitrates, electrocardiogram, chest x-ray, oximeter, and CK-MB
—all on the same screen.
Test Results
Papillary muscle rupture7.
Sit patient upright
Electrocardiogram
Oxygen
Furosemide IV (or bumetanide)
Nitroglycerin IV or paste to chest wall
Morphine IV
Chest x-ray
Arterial blood gases
Electrocardiogram: sinus tachycardia, Q-waves in V2–V4
Chest x-ray: cardiomegaly, bilateral pleural effusions, and pulmonary vascular
redistribution with cephalization of flow; Kerley B lines are present
145
Assessment
This patient has multiple signs of fluid overload and CHF; most importantly, dyspnea, rales,
hypoxia, and an S3 gallop. The electrocardiogram shows signs of an old anterior wall
myocardial infarction, and the chest x-ray is consistent with a dilated cardiomyopathy and poor
left ventricular function. Pulmonary edema is most commonly due to acute systolic or diastolic
left ventricular dysfunction or to arrhythmia. Ischemia, arrhythmia, infarction, noncompliance
with medications or diet, insufficient medications, or infection can all precipitate acute left
ventricular dysfunction in this patient. Less common causes are the “high-output” types of
failure, such as with anemia, thyrotoxicosis, and pregnancy. Fluid overload from renal failure
could also be a cause.
Brain natriuretic peptide (BNP) is a blood test that is elevated when there is acute congestive
failure. BNP is most useful to exclude a diagnosis of dyspnea caused by CHF when the
diagnosis is not clear. When a patient is short of breath and you can’t tell if it’s from CHF,
COPD, or pneumonia, use a BNP. BNP is not useful with renal failure because it is renally
excreted.
CCS NOTE
There are several ways to move the clock forward on the CCS: “on,” “in,” or “next
available result.” They are all equivalent as long as the clock moves forward the same
amount of time.
Remember, 100% of patients with decompensated heart failure have elevated BNP.
Arterial blood gases: pH 7.42, pCO
2
34 mm Hg, pO
2
72, saturation 93%
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Basic Science Correlate
Aside from just ‘not taking medications,’ why would a person with CHF suddenly
go into acute pulmonary edema?
Mechanism of S3 gallop: rapid ventricular filling in diastole
Mechanism of furosemide: inhibition of 2Cl-/K+/Na+ pumps in the thick ascending
limb of the loop of Henle; loop diuretics do not work at the tip of the loop of Henle, but
rather at the thick ascending limb.
Mechanism of nitroglycerin: nitrates are venous dilators, i.e., they increase the size of
the capacitance vessels and decrease the amount of blood in the lungs; preload
reducers like nitrates, morphine, and diuretics all decrease hydrostatic pressure in
pulmonary veins and lessen transudation of fluid across pulmonary vessels.
Further Management Plan
Ischemia
Oxygen is needed to detach actin and myosin filaments from each other. Hypoxic
myocardium does not relax or contract normally. Hypoxia induces wall motion
abnormalities.
Arrhythmia
The usually small atrial contribution of 10–15% to cardiac output can become as
large as 40–50% in a diseased heart. This is why normally benign rhythms like
atrial fibrillation can result in pulmonary edema.
Repeat doses of furosemide
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Discussion
Pulmonary edema results from fluid overload, causing death by hypoxia. Because the problem
comes from too much fluid in the lungs, the treatment is based on reducing this by:
Continue oxygen
Transfer patient to intensive care
Consult critical care team
CK-MB
Brain natriuretic peptide when diagnosis not clear (used only as a rule-out test)
Diuresis, as rapidly as possible to decrease preload; furosemide is given in double doses
every 20 min until sufficient urine is produced
Morphine, which dilates pulmonary vasculature and also decreases preload
Nitrates, which dilate the venous system and reduce blood return to the lungs
Positive inotropes, which are useful only for impaired left ventricular function. (The entire
class has not shown mortality benefit.) Dobutamine is an IV positive inotrope that will
increase contractility and empty the lungs by causing the heart to pump better. Milrinone is a
phosphodiesterase (PDE) inhibitor that works in a similar fashion to dobutamine, but is
rarely indicated. Digoxin is of no use in the acute setting as a positive inotrope.
Afterload reduction: Enalaprilat or nitroprusside can only be given intravenously in an ICU
and will rapidly reduce afterload and allow more blood to be squeezed out of the heart with
each beat. This has the same effect as an ACE inhibitor such as captopril and enalapril.
Reducing the afterload will allow for an increase in stroke volume. Always continue the
ACE inhibitor later.
Spironolactone, a drug which helps inhibit the renin-angiotensin system and lowers
mortality in systolic dysfunction; used when ejection fraction <30%
Nesiritide, a synthetic atrial natriuretic peptide (rarely given by infusion with acute CHF not
responding to maximum medical therapy, such as diuretics, nitrates, and morphine).
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Basic Science Correlate
Why do beta blockers help CHF?
If beta blockers are negative inotropes, why do they increase cardiac output?
Follow-up Management and Prevention
Most common cause of death in CHF is sudden death
Ischemia leads to arrhythmia
Arrhythmia leads to sudden death
Beta blockers are anti-arrhythmic and anti-ischemic
Beta blockers slow the heart rate
Slow heart rate increases preload and ventricular filling
More preload and filling of the heart increase stroke volume
Beta blockers decrease aldosterone by inhibiting renin production
ICU monitoring for 24-48 hrs
Transfer to floor when MI excluded and hypoxia improved
Echocardiography
Dobutamine or milrinone if still symptomatic after use of repeated does of preload reduction
(nitrates, furosemide, morphine)
Swan-Ganz catheter placement, if still critical after initial treatment and the diagnosis is not
clear
Add beta-blockers and spironolactone only after stabilization
Digoxin after stabilization if still symptomatic on beta blockers, diuretics, ACE inhibitors
and spironolactone
ACE inhibitor or ARB for all patients with heart failure unless contraindicated
149
Final Diagnosis
Pulmonary edema
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