Page 478 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

348 PART 3: Cardiovascular Disorders

orifice and regurgitant volume are ≥30 mm and ≥60 mL, respectively. pathophysiology of AR it seems reasonable to choose a vasodilating
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The left ventricle is enlarged, but ejection fraction is preserved for long agent for treatment of hypertension.
time; presence of reduced left ventricular function is an indication for Aortic valve repair or replacement is the solution to AR with acute
surgery even in asymptomatic patients. Of note, parallel with clinical decompensation, and should be performed promptly.
examination, echocardiographic diagnosis in acute severe AR is chal-
lenging. As aortic and left ventricular pressure rapidly equalize, the driv-
ing force for regurgitation (and hence the color Doppler appearance of KEY POINTS—AORTIC REGURGITATION
the jet) decreases. Key in diagnosis is presence of presumably acute val- • Acute AR is most often due to native valve endocarditis, aortic dis-
vular lesion (eg, endocarditis leading to incompetence, flail leaflet after section, or traumatic rupture. It is a medical and surgical emergency.
chest trauma, ascending aortic dissection), typical dagger shape of the
regurgitant jet on continuous wave Doppler, or presence of premature • Chronic AR of any cause may present acutely with heart failure. It
closure of the mitral valve and diastolic mitral regurgitation (due to is characterized by both volume and pressure overload.
increased left ventricular pressure). Transesophageal echocardiography • Acute AR causes reduced ventricular compliance, high filling pres-
should be considered whenever endocarditis or acute aortic dissection is sure, and reduced coronary perfusion pressure.
suspected. TEE has sensitivity comparable to that of magnetic resonance • Acutely, AR has an unimpressive diastolic murmur, while arterial
imaging (MRI) or computed tomography (CT) for detecting an acute hyperpulsatility and large blood pressure differential clue to severe AR.
aortic dissection, and it is more easily performed in an intensive care
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unit on an unstable critically ill patient. However, a small part of the • ECG and chest x-ray: Acutely, pulmonary edema may contrast with
ascending aorta cannot be visualized due to acoustic shadowing by the normal heart size and lack of ventricular hypertrophy. Chronic AR is
characterized by evidence of left ventricular hypertrophy.
left main bronchus.
Cardiac catheterization provides information about the degree of • Echocardiography (particularly TEE) confirms diagnosis of AR
regurgitation, and it can be used to evaluate the aortic root and the and provides clues to etiology. It also provides assessment of left
status of the coronary arteries if surgery is indicated. Similar to all other ventricular size and function. AR may be quantified by calculating
techniques, presence of a rapidly equalizing aortic and left ventricular the effective regurgitant orifice and regurgitant volume (severe if
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pressure can reduce the angiographic appearance in the case of acute AR. ≥30 mm and ≥60 mL, respectively).
Pulmonary artery catheterization is helpful in management of acute • Cardiac catheterization may show AR severity by aortography;
AR. The pulmonary artery wedge pressure is usually elevated, and pul- coronary angiography is usually performed in older patients prior
monary hypertension may be present. Stroke volume may be normal or to surgery.
increased. Diagnostic coronary angiography is commonly performed in • Afterload reduction is central to acute and chronic medical treat-
the elderly prior to surgical intervention. ment of AR.
■ MANAGEMENT • Surgical valve replacement is urgently required with heart failure.

Acute aortic insufficiency is a medical and surgical emergency. Aortic valve repair is sometimes possible. Periannular repair is
necessary for abscesses.
Fulminant pulmonary edema is common. It is important to determine
the cause of the lesion, especially if endocarditis or an acute aortic dis-
section is suspected. Aortic valve replacement is indicated when the
regurgitation is severe. Early aortic valve replacement has been shown to MITRAL STENOSIS
decrease mortality in patients with endocarditis. If heart failure can be
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medically managed, aortic valve replacement may be delayed until after ■ ETIOLOGY
completion of an antibiotic regimen. 24
Medical management is used for stabilizing the patient. Loop diuret- Rheumatic fever is the main cause of mitral stenosis (MS), with a history
ics are used to relieve congestion. Nitroprusside is used for afterload of rheumatic fever being elicited in up to 60% of patients with isolated
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reduction, usually with hemodynamic guidance (Swan Ganz catheter); MS. Calcific degeneration (especially of the mitral annulus) is common
it improves cardiac output, reduces the amount of regurgitation, and among elderly and patients with long-standing renal failure, but is not
lowers left ventricular filling pressures. Newer vasodilating agents usually associated with severe stenosis. Other causes are quite rare, such
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such as nicardipine and fenoldopam have been used in hypertensive as congenital malformations of the mitral valve, mucopolysaccharidoses
emergencies. Their role in treatment of acute AR is unknown. Inotropic (Morquio and Maroteaux-Lamy syndromes), and obstruction of the
agents are of limited use (left ventricle is already hyperdynamic), and mitral valve by a large left atrial myxoma.
vascular resistance worsens regurgitation). IABP or other left ventricular ■ PATHOPHYSIOLOGY
peripheral vasoconstrictors are relatively contraindicated (an increase in
assist devices are of no use, as their function relies on a competent aortic Rheumatic MS is characterized by commissural fusion and progressive
valve. Mechanical ventilation is frequently required given the severity of scarring of the valvular structures, leading to the typical funnel-shaped
dyspnea and pulmonary edema. mitral valve (Fig. 41-5). Many patients remain asymptomatic for
Chronic vasodilator therapy should be considered in patients that decades after the initial episode of carditis. Left atrial pressure increases
can be stabilized. There are three potential circumstances for their in parallel with the progressive reduction in the mitral valve area from
use: (a) long-term treatment of patients with severe symptomatic a normal of 4 to 5 cm down to 1 cm (which defines presence of severe
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AR who are not candidates for surgery, (b) short-term treatment for MS), and leads to development of pulmonary hypertension.
improvement in hemodynamic profile before proceeding with aortic Patients with atrial fibrillation lose the atrial contribution to left
valve replacement, and (c) long-term treatment of asymptomatic ventricular filling (which may account for 20% of total cardiac out-
patients who have severe AR and evidence of hypertension. The lat- put), and can acutely worsen with pulmonary edema and congestive
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ter is more controversial, as the initial promising results of nifedipine heart failure symptoms. Atrial fibrillation dramatically increases the
(delaying surgery and preventing left ventricular remodeling when risk of systemic embolization. Thus, maintenance of sinus rhythm is
compared to digoxin) have not been confirmed in a more contem- important in patients with chronic MS. MS that may be well tolerated
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porary randomized trial. The latter showed that neither nifedipine nor can also suddenly worsen due to anemia, pregnancy, or thyrotoxicosis,
enalapril prevented left ventricular dysfunction or delayed aortic valve conditions that increase cardiac output and thus increase the mitral
replacement when compared to placebo. However, understanding the valve pressure gradient.
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