Our patient population has changed fairly dramatically in the last 10 years as our medical skills have progressed and we have
become capable of supporting patients with advanced disease and advancing age. Now we must hone our anesthesia skills in order
to support patients that largely don't fit into the 'young, healthy' category and it is no longer appropriate to think that
safe anesthesia means recovering as many patients as we anesthetize. Patients with cardiovascular disease often require anesthesia
and it is imperative that we understand the medical implications of the cardiovascular disease as well as the pharmacologic
implications of the anesthetic drugs.
The ultimate goal of the cardiovascular system is to provide adequate cardiac output (Q) and subsequent oxygen delivery (DO2)
to the working cells. Physiologic responses occur in an attempt to maintain adequate Q, even in the face of progressive cardiac
disease. Cardiac output is a product of heart rate (HR) and stroke volume (SV), which is comprised of preload, afterload and
myocardial contractility (inotropy).
Heart rate is affected by sympathetic and parasympathetic nervous system balance and by the anesthetic drugs themselves. Arrhythmias
change HR and can decrease SV if their rate or timing results in inadequate cardiac filling. Obviously, since HR is an integral
determinant of Q, bradycardia can result in inadequate flow. Conversely, tachycardia can be as hazardous as bradycardia, especially
as cardiac disease becomes more severe. During tachycardia, diastolic filling time is decreased, resulting in decreased SV.
In addition, ventricular relaxation time is decreased. Since the myocardium receives most of its blood flow during diastole,
myocardial oxygen delivery is decreased at a time when myocardial oxygen consumption is increased, resulting in inadequate
oxygen delivery to the myocardium. In fact, tachycardia in itself can result in myocardial ischemia and heart failure. Myocardial
oxygen delivery is often inadequate in patients with hypertrophic cardiomyopathy since the large myocardial mass consumes
a significant amount of oxygen and blood supply is limited. Tachycardia in these patients can cause decompensation and overt
Preload, or cardiac filling, is dictated in part by blood flow and blood volume. Afterload, or resistance to ejection, is
dictated primarily by vascular tone. Ideally, an appropriate preload will cause stretch of the myocardium which will improve
contractility and increase SV (due to Starling's Law). Also ideally, the arterial tree should provide minimal resistance to
ejection so that adequate SV is ejected with minimal cardiac work. However, failing hearts may not be able to accommodate
(hypertrophic cardiomyopathy) or eject (dilatative cardiomyopathy) the blood delivered to it, in which case stroke volume
is decreased and cardiac output will decrease unless the heart rate can increase to compensate. Also, afterload may increase
to the point that cardiac output is limited and cardiac work is excessive, often leading to hypertrophic cardiomyopathy. Contractility
is severely impaired in patients with dilatative cardiomyopathy and drugs that improve or support contractility (positive
inotropes) should be administered perioperatively. Conversely, hypertrophic cardiomyopathy produces a hyper-contractile state
and drugs that increase cardiac work in any manner should be avoided.
A thorough physical exam, complete blood count (CBC) and serum chemistry are imperative. Mucous membrane color, capillary
refill time, cardiac sounds, thoracic radiographs and an electrocardiogram (ECG) should be carefully evaluated. Depending
on the severity of the disease, a more thorough cardiac workup including advanced techniques such as cardiac ultrasound may
be necessary. A detailed and exhaustive history with emphasis on evidence of cardiovascular dysfunction such as exercise intolerance,
syncope, recurrent coughing, etc... is important. All current medications should be noted and concurrent diseases evaluated.
Stabilization of patients with cardiovascular disease is crucial and the first goal of the anesthesiologist is to attempt
to return cardiovascular function to as close to normal as possible. Heart rate should be normalized and arrhythmias should
be treated. Myocardial contractility should be supported with positive inotropic drugs (eg, pimobendin). Adequate blood volume
is essential and the judicious use of fluids may be warranted, especially in hypovolemic patients. However, since pump function
is impaired, overhydration should be avoided at all costs. Whole blood should be administered if anemia is present. Oxygen
should be administered for 5-10 minutes prior to administering induction drugs ("preoxygenate"). Patient support should continue
throughout anesthesia and recovery.