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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
Table 5-5. Vasodilators Used in Congestive Heart Failure
Note
ACE inhibitor (any) and a
diuretic are considered first
line for all patients with HF.
Once the patient is stable, add
carvedilol or metoprolol. Don’t
substitute b-blockers in HF
since not all b-blockers have
the same efficacy.
Drug Site of Action Route of
Administration
Captopril
Enalapril
Lisinopril
Nitroprusside Arteriolar and
Nitroglycerin Venous (arteriolar
Isosorbide
dinitrate
Hydralazine Arteriolar Oral Positive ANA, SLE-like
Chronic adrenergic activation has been implicated in the pathogenesis of HF and thus
b-adrenergic blocking agents are an important part of HF therapy. Along with ACE inhibi-
tors, beta blockers have been demonstrated to decrease mortality, reduce hospitalizations,
improve functional class, and improve ejection fraction in several large-scale, randomized,
placebo-controlled trials.
Arteriolar and
venous ACE
inhibitor
venous
at high doses IV)
Venous Oral or SL Headache, postural
Oral Rash, nonproductive
IV Thiocyanate toxicity,
SL, IV, cutaneous
ointment, or patch
Complications
cough, proteinuria,
renal failure, taste
disturbance, agranulocytosis, hypotension
methemoglobinemia
Headache, postural
hypotension,
methemoglobinemia
hypotension
syndrome (10–20% if
>400 mg/d) drug fever,
rash
Start patients on beta blockers after stabilization of symptoms with diuretic and ACE inhibitor therapy, irrespective of blood pressure status. Beta blockers such as carvedilol, metoprolol,
and bisoprolol have demonstrated survival benefits in trials.
140
Table 5-6. Commonly Used Diuretics in Heart Failure
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Drug Site of Action Complications
Chapter 5
l Cardiology
Thiazides (inhibits NaCl
cotransport); used mostly for
treatment of hypertension
• Hydrochlorothiazide
• Chlorothiazide
Indapamide Distal tube
Loop diuretics (inhibitors
Na/K, 2Cl cotransport); most
commonly used diuretics in
heart failure
• Furosemide
• Ethacrynic acid
• Bumetanide
Potassium-sparing diuretics
• Spironolactone
(aldosterone antagonist)
Other vasodilators, such as a combination of hydralazine and isosorbide, may be used when
ACE inhibitors and ARBs are not tolerated or contraindicated (renal failure). There is a
reduction in death and a decrease in hospitalization when a combination of hydralazine and
isosorbide is used.
Distal tubule Hyponatremia, hypokalemia,
hypercalcemia, metabolic
alkalosis, hyperuricemia, allergy,
agranulocytosis, leukopenia,
pancreatitis, glucose intolerance
As above, but hypokalemia and
(direct
vasodilator)
Loop of Henle Hyponatremia, hypokalemia,
Distal tubule Hyperkalemia, gynecomastia
lipid abnormalities less common
hypocalcemia, metabolic alkalosis,
hyperuricemia, interstitial nephritis,
ototoxicity, thrombocytopenia,
agranulocytosis, leukopenia
(spironolactone only)
In severe HF and especially if there is no improvement of symptoms while the patient is
on standard therapy (diuretic, ACE inhibitor, and beta blocker), the addition of spirono-
lactone may be of benefit. The addition of spironolactone in patients with severe CHF
significantly reduces (about 30% relative risk) death and hospitalizations among treated
patients. Spironolactone is used in patients with NYHA class III-IV. Once the patient is started
on spironolactone, serum potassium levels have to be monitored closely.
Eplerenone is an alternative to spironolactone that does not cause gynecomastia.
The addition of inotropic agents to patients with severe HF improves symptoms and quality
of life and reduces hospitalizations but does not improve survival. The most commonly used
inotropic agent is digitalis. Digitalis inhibits Na+/K+ - ATPase pump which results in increased
intracellular concentration of Na+ and decreased exchanges of intracellular Ca2+. The end
result is an increase in intracellular concentration of Ca2+ which results in improved cardiac
contractility.
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USMLE Step 2 CK
l Internal Medicine
Note
Agents which lower mortality
in systolic dysfunction
• ACE (ARB)
• Beta blockers
• Spironolactone
(or eplerenone)
Note
Agents which improve heart
failure symptoms but do not
reduce mortality
• Digoxin
• Diuretics
Cardiac glycosides work by inhibition of Na+/K+-ATPase pump, which results in:
• Increased intracellular concentration of Na
• Decreased exchange of intracellular Ca2+ for extracellular Na
+
+
• The end result is an increase in the intracellular concentration of Ca2+, which gives the
(+) inotropic effect characteristic of glycosides
Remember that K+ and digitalis compete for myocardium binding sites. Hyperkalemia will
decrease digitalis activity, whereas hypokalemia results in toxicity.
Digitalis will increase both the force and the velocity of the myocardial contraction. It will
also promote a more complete emptying of the ventricles.
It is used for the treatment of:
• CHF
• Atrial fibrillation/flutter
• Paroxysmal atrial tachycardia/SVT
Conditions which predispose to digitalis toxicity are:
• Renal insufficiency
• Electrolyte disturbances (hypokalemia, hypercalcemia, hypomagnesemia)
• Advanced age
• Sinoatrial and atrioventricular block
• Thyroid disease, especially hypothyroidism
Table 5-7. Drug Interactions Associated with Digoxin
Drug Effect* Mechanism
Quinidine Increase Decreases renal clearance of digoxin
Verapamil, diltiazem Increase Decreases renal clearance of digoxin
Cholestyramine, colestipol Decrease Binds digoxin in GI tract; interferes with
enterohepatic circulation
Spironolactone Increase Inhibits tubular secretion of digoxin
Thiazides, furosemide Increase Diuretic-induced hypokalemia and/or
bumetanide hypomagnesemia potentiates
digitalis action
*Increase enhances digitalis effect; decrease diminishes digitalis effect.
Toxic Effects of Digitalis
• Nausea and vomiting
• Gynecomastia
• Blurred vision
• Yellow halo around objects
• Arrhythmias—commonly paroxysmal atrial tachycardia (PAT) with block, PVCs (premature ventricular contractions), and bradycardia
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Treatment for Intoxication
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• Stop drug
• Lidocaine and phenytoin (for arrhythmia)
• Digibind only for acute overdose
Sympathomimetic amines (dopamine, doputamine) and phosphodiesterase inhibitors (amrinone, milrinone) are sometimes used in the management of severe acute HF (hospitalized
patients). They must be administered by IV infusion and need continuous monitoring of the
blood pressure and cardiac rhythm.
Monitoring of patients with HF includes calculation of fluid intake and excretion (in the hospital) as well as monitoring body weight (in the out-patient setting).
Chapter 5
l Cardiology
In refractory HF (defined as progression of HF despite standard treatment), the patient may
be considered for: biventricular pacing, implantable defibrillator, and heart transplantation.
Medical Devices for Systolic Dysfunction
The automatic implantable cardioverter/defibrillator (AICD) is a standard therapy for ischemic dilated cardiomyopathy. Since the most common cause of death in CHF is an arrhythmia, it is logical that a device which interrupts arrhythmia will lower mortality. A biventricular pacemaker will “resynchronize” the heart when there is dilated cardiomyopathy and
a QRS >120 mSec. When there is a wide QRS, the 2 ventricles do not beat or depolarize in
synchrony. When you put a biventricular pacemaker into the heart, this will “resynchronize”
the 2 ventricles, resulting in an immediate decrease in symptoms.
When do I answer AICD?
• Dilated cardiomyopathy with a persistent ejection fraction <35%
When do I answer biventricular pacemaker?
• Dilated cardiomyopathy with a QRS wider than 120 mSec
The following classes of medications lower mortality:
•
ACE inhibitor or ARBs; use one or the other, not both
• Beta blockers
• Spironolactone (or eplerenone)
• AICD
• Biventricular pacemaker (if QRS >120 mSec)
Clinical Pearl
Diastolic HF may worsen when
diuretics and vasodilators are
used excessively. The goal
in diastolic HF is to slow the
heart rate with beta blockers
and calcium channel blockers
(verapamil, diltiazem) in order
to allow adequate diastolic
filling.
ACE inhibitors are a class effect; there is no difference in efficacy between the drugs. There
is no benefit to adding an ARB to an ACE inhibitor. With beta blockers, not all the drugs
are equal; those that benefit mortality in CHF are metoprolol, carvedilol, and bisoprolol.
Biventricular pacemakers and cardiac resynchronization therapy also have implantable defibrillator function.
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l Internal Medicine
Pulmonary Edema
Pulmonary edema is considered a medical emergency and requires hospitalization. It leads to
impaired gas exchange and may cause respiratory failure. There are non-cardiogenic causes
of pulmonary edema but in this section we will discuss only cardiogenic pulmonary edema.
Cardiogenic pulmonary edema is caused by an acute increase in left ventricular pressure due
to ventricular dysfunction which leads to fluid accumulation in the pulmonary interstitium.
Signs and Symptoms
• Increased respiratory rate
• Cough with expectoration (pink frothy sputum)
• Cyanosis
• Nocturnal dyspnea
• Rales, rhonchi, wheezing
Chest X-ray Findings
• Effusions
• Enlarged cardiac silhouette
• Kerley B lines
EKG is used to determine if an arrhythmia is contributing to the development of the pulmonary edema.
Treatment
• Oxygen
• Diuretic therapy (furosemide) reduces preload
• Morphine sulfate; side effects include respiratory depression and rarely hypotension
• Sitting the patient upright
• Nitroglycerin to reduce preload
• Digoxin if in atrial fibrillation
• IV ACE inhibitors
Mitral Stenosis
Definition. Most common lesion caused by rheumatic fever consisting of thickened mitral valve
leaflets, fused commissures, and chordae tendineae. It may result in right ventricular failure. It
often becomes clinically symptomatic during pregnancy.
Etiology. Most cases of mitral stenosis are secondary to rheumatic fever. Rarely, it is caused by
a congenital defect, calcification of the valve, or post-radiation treatment to the chest.
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Pathogenesis
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Mitral valve stenosis impedes left ventricular filling. Increased left atrial pressure is referred to
the lungs, causing pulmonary congestion. Forward cardiac output becomes reduced, secondary pulmonary vasoconstriction occurs, and eventually right ventricular failure results.
Clinical Symptoms. Usually manifest slowly over years.
• Dyspnea
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Fatigue
• Wasting
• Hemoptysis (due to rupture of pulmonary vessels)
• Systemic embolism (due to stagnation of blood in an enlarged left atrium)
• Hoarseness (due to impingement of an enlarged left atrium on the recurrent laryngeal
nerve)
• Right-sided heart failure
– Hepatomegaly
– Ascites
– Peripheral edema
Physical Signs
• Atrial fibrillation (irregular cardiac rhythm)
• Pulmonary rales
• Decreased pulse pressure
• Loud S
• Opening snap following S
1
2
• Diastolic rumble (low-pitched apical murmur)
• Sternal lift (due to right ventricular enlargement)
Chapter 5
l Cardiology
Diagnosis
EKG
• May show signs of right ventricular hypertrophy
• May show left and right atrial abnormalities
• Atrial fibrillation often occurs
Chest X-ray
• Large left atrium (indicated by a double-density right heart border, posterior displacement of esophagus, and elevated left mainstem bronchus), straightening of the left
heart border
• May show signs of pulmonary hypertension, including Kerley B lines and increased
vascular markings
• Large pulmonary artery
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l Internal Medicine
Echocardiography
• Shows thickening of mitral valve leaflets and a reduction in the excursion and area of
the valve leaflets
• May also show left atrial enlargement
Treatment
Medical Therapy
• Diuretics and salt-restricted diet
• Digitalis to control the ventricular rate in patients with AF
• Anticoagulants in patients with AF
• Balloon valvulotomy is the standard of care for MS
Surgical Management
• Indicated when patient remains symptomatic (functional class III) despite medical
therapy
• Mitral commissurotomy or valve replacement, if balloon dilation fails
• Pulmonary hypertension is not a contraindication for surgery
Mitral Regurgitation
Definition. Backflow of blood from the left ventricle into the left atrium, due to inadequate
functioning (insufficiency) of the mitral valve. Most commonly from ischemia.
Etiology. Due to abnormalities of the mitral leaflets, annulus, and chordae tendineae.
• Common causes are hypertension, CHF, ischemic heart disease, rheumatic fever, and
any cause of dilation of the left ventricle
• Occurs more commonly in men
Table 5-8. Acute versus Chronic Etiologies of Mitral Valve Regurgitation
Acute Chronic
• Rupture chordae tendineae (permits
prolapse of a portion of a mitral valve
leaflet into the left atrium)
• Papillary muscle rupture
• Endocarditis (may lead to valvular
destruction)
• Trauma
• Rheumatic heart disease (causing
scarring and retraction of valve and
leaflets)
• Papillary muscle dysfunction
• Mitral valve prolapse (click-murmur
syndrome, Barlow syndrome, floppy
mitral valve)
• Endocarditis
• Calcification of the mitral valve annulus
• Accompanying hypertrophic obstructive
cardiomyopathy
• Congenital endocardial cushion defect,
corrected transposition
• Endocardial fibroelastosis
• Severe left ventricular dilatation
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Pathogenesis
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• A portion of the left ventricular stroke volume is pumped backward into the left
atrium instead of forward into the aorta, resulting in increased left atrial pressure and
decreased forward cardiac output.
• Volume overload occurs, increasing preload.
• Afterload is decreased as the left ventricle empties part of its contents into the relatively low-pressure left atrium.
• This helps to compensate for the regurgitation by augmenting ejection fraction.
• Left ventricular dysfunction occurs after prolonged compensation.
Clinical Manifestations
Left ventricular failure is manifested by:
• Dyspnea
• Orthopnea
• Paroxysmal nocturnal dyspnea
Severe and chronic mitral regurgitation lead to right-sided failure presenting with:
• Edema
• Ascites
• Anorexia
• Fatigue
Chapter 5
l Cardiology
May also have pulmonary hypertension as a late finding.
Physical Signs
• Hyperdynamic and displaced (downward and to the left) left ventricular impulse
• Carotid upstroke diminished in volume but brisk
• Holosystolic apical murmur radiating to the axilla and often accompanied by a thrill
• S3 heard with a soft S1 and widely split S
2
• Distended neck veins when severe or acute
Diagnosis
• EKG shows signs of left ventricular hypertrophy and left atrial enlargement.
• Chest x-ray shows cardiac enlargement, with vascular congestion when the regurgitation has led to heart failure.
• Echocardiography: The mitral valve can prolapse into the left atrium during systole in
cases of a ruptured chordae or mitral valve prolapse. Regardless of the cause, left atrial
and left ventricular enlargement occurs if the condition is chronic.
• Catheterization is the single most accurate test.
Treatment. With medical therapy, the goal is to relieve symptoms by increasing forward cardiac output and reducing pulmonary venous hypertension.
• ARBs or hydralazine
• Arteriolar vasodilators (ACE inhibitors)
• Digitalis
• Diuretics
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With surgery, mitral valve replacement is used. Guidelines for selecting patients with mitral
regurgitation for operation:
• With significantly limiting symptoms and severe mitral regurgitation, surgery is usually indicated. The risk of surgery rises in chronic heart failure.
• In patients with regurgitation who have few or no symptoms, surgery should be
deferred. Their condition may remain stable for years.
• Surgery is indicated when symptoms persist despite optimal medical management.
• Criterion is an ejection fraction <60% or left ventricular end systolic diameter >40 mm.
• Repair is preferable to replacement.
Mitral Valve Prolapse
Definition. The most common congenital valvular abnormality (2–3% population) typically
seen in young women. Mitral valve prolapse may occur with greater frequency in those with
Ehler-Danlos syndrome, polycystic kidney disease, and Marfan syndrome.
Presentation. Most patients are asymptomatic. Lightheadedness, palpitations, syncope, and
chest pain may occur. These symptoms are often due to arrhythmias, which may occur.
Auscultation
• Mid-to-late systolic click and a late systolic murmur at the cardiac apex
• Worsens with Valsalva or standing
• Improves with squatting or leg raise
Complications (all very rare)
• Serious arrhythmias
• Sudden death
• CHF
• Bacterial endocarditis (but does not mean routine dental prophylaxis is indicated)
• Calcifications of valve
• Transient cerebral ischemic attacks
Laboratory
Two-Dimensional/Doppler Echocardiography: Marked systolic displacement of mitral leaflets
with coaptation point at or on the left atrial side of the annulus; moderate systolic displacement
of the leaflets with at least moderate mitral regurgitation.
Treatment. No specific treatment is needed in the majority of cases.
Medical Management: Beta blocker for chest pain and palpitations
Surgical Management: Mitral valve replacement, rarely
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Aortic Stenosis
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Etiology
• Calcification and degeneration of a congenitally normal valve; more common in the
elderly population. This is the most common cause.
• Calcification and fibrosis of a congenitally bicuspid aortic valve.
• Rheumatic valvular disease: If the aortic valve is affected by the rheumatic fever, the
mitral valve is also invariably affected.
Pathophysiology
Aortic stenosis results in elevation of left ventricular systolic pressure, and the resultant left
ventricular hypertrophy maintains cardiac output without dilation of the ventricular cavity.
Therefore, the stroke volume is normal until the late stages of the disease.
Forceful atrial contraction augments filling at the thick, noncompliant ventricle and generates
a prominent S4 gallop that elevates the left ventricular end-diastolic pressure.
Left ventricular hypertrophy and high intramyocardial wall tension account for the increased
oxygen demands and, along with decreased diastolic coronary blood flow, account for the
occurrence of angina pectoris.
Chapter 5
l Cardiology
As the myocardium fails, mean left ventricular diastolic pressure increases, and symptoms of
pulmonary congestion ensue.
Clinical Manifestations
• Classic symptoms are angina, syncope, and dyspnea from CHF
• Pulsus tardus et parvus
• Carotid thrill
• Systolic ejection murmur in aortic area, usually with thrill, harsh quality, radiates to
carotids
• S4 gallop
• A2 decreased, S2 single or paradoxically split
• Aortic ejection click
Diagnosis
• EKG will often show left ventricular hypertrophy.
• Chest x-ray may present with calcification, cardiomegaly, and pulmonary congestion.
Echocardiography shows thick aortic valve leaflets with decreased excursion and LVH.
•
Treatment
• Endocarditis prophylaxis is no longer recommended.
• Surgery (valve replacement) is advised when symptoms develop, which is when the
valve area is reduced below 0.8 cm2 (normal aortic orifice, 2.5–3 cm2). Generally, if
patient has symptoms from stenosis, surgery is the treatment of choice.
• Balloon valvuloplasty may be useful in those too ill to tolerate surgery.
Clinical Pearl
Look for AS in older patients
presenting with syncope
related to exertion.
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