Arrow AutoCAT 2 Series Operating Manual page 18

1 . C l i n i c a l U s e s
1 . 1 : C l i n i c a l U s e s o f I A B P
Valvular Insufficiency (Mitral) including Papillary Muscle Rupture
The two types of valvular insufficiency are aortic insufficiency (see Section 1.2) and
mitral insufficiency. In mitral insufficiency, the leaflets of the valve become unable to
seal off the left atrium from the left ventricle during systole. As a result, a portion of the
left ventricle's contents is ejected backward into the left atrium. The left ventricle works
under a condition of chronic volume overload and ejects its contents into a relatively
low-resistance left atrium. In spite of severe myocardial dysfunction, the heart is able to
maintain CO because of the low impedance to ejection. Most of the energy expended is
used in fiber shortening instead of tension development. Therefore, the Isovolumetric
Contraction (IVC) phase is shortened and myocardial oxygen demand is reduced.
Mitral insufficiency causes fatigue and chronic pulmonary vascular congestion. The left
atrium becomes dilated and the left ventricle hypertrophies. If mitral insufficiency is
sudden, such as in the case of papillary muscle rupture, the heart cannot compensate
completely and the patient presents with florid pulmonary edema and cardiogenic
shock. It is important to reduce afterload because decreased aortic pressure enhances
forward CO and minimizes regurgitation into the left atrium. The IABP may be
necessary if pharmacologic agents do not reduce afterload adequately. Reduction of
afterload by IABP may be the key to survival following valve replacement. When the
incompetent valve is replaced, the left ventricle is forced to eject its full SV into the high
pressure aorta. Myocardial workload increases dramatically with the increase in the
IVC phase. If the myocardium is dysfunctional (which may not be apparent preoperatively),
mortality will be high if myocardial workload is not reduced adequately.
Ventricular Septal Defect (VSD)
In VSD, blood is shunted from the left ventricle to the right ventricle with each
ventricular contraction (The pressure on the left side of the heart is greater than that on
the right.). As blood is shunted to the right side, the SV ejected into the aorta is
decreased and right ventricular pressures rise. Blood begins to pool in the systemic
venous circuit because the right ventricle is unable to contain the extra volume it
receives from the left ventricle.
Systemic venous congestion is the main symptom of VSD. The patient may not show
signs of congestive heart failure until the end stages of the disease because there is no
obstruction from the pulmonary artery to systemic circulation. IABP increases SV by
providing a favorable pressure gradient (with balloon deflation). The left ventricle
empties more completely at a lower aortic pressure because less blood is shunted across
the septum into the right ventricle. The right ventricle, in turn, is able to empty more
completely because the end-diastolic volume is less, relieving wall tension. Right
ventricular function is improved and the symptoms of venous congestion lessen.
Mechanical Defects
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