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Anesthesia
for Patients with Aortic Stenosis Undergoing Non-Cardiac Surgery
Dr. Irena Vaitkeviciute
Department of
Anesthesiology, Yale
University School
of Medicine.
Causes
of Aortic Stenosis Aortic stenosis is the most common cardiac valve lesion in the United States. The primary etiology of aortic stenosis has become senile degeneration and calcification. About 1-2% of population is born with a bicuspid aortic valve, which is more prone to become stenotic. Pathophysiology The obstruction of left ventricular outflow produces a systolic pressure gradient between the left ventricle and aorta. A peak pressure gradient which exceeds 50 mmHg or an effective aortic orifice of less than 0.5 cm2/m2 of body surface area is considered to be a critical obstruction of left ventricular outflow. As the disease progresses and the pressure gradient gradually increases, cardiac output is maintained by the development of left ventricular hypertrophy. The compliance of the heart muscle will decrease and left ventricular end diastolic pressure will be elevated. Loss of appropriately timed atrial contraction and the so-called "atrial kick", which occurs in conditions such as atrial fibrillation, may result in rapid worsening of patient's condition. As a result of increased left ventricular muscle mass, myocardial oxygen demand is elevated. In addition there may be interference with coronary artery blood flow, since the extramural pressure on coronaries may exceed the perfusion pressure. So even if the cardiac output at rest is normal, it may fail to rise adequately during stress and the patient may develop cardiac ischemia without significant coronary artery disease. Symptoms Patients with gradually developing aortic stenosis usually become symptomatic during the fifth to seventh decades of their life. The main symptoms are angina, syncope and dyspnea. Angina develops as an imbalance occurs between increased myocardial oxygen demand and decreased myocardial blood supply, secondary to compression of vessels by the hypertrophied muscle, impaired relaxation, and increased LVEDP. Syncope develops with peripheral vasodilation in the presence of a relatively fixed cardiac output or as a result of arrhythmias that causes sudden decreases in cardiac output. Dyspnea develops when reduced compliance of left ventricle increases LVEDP, rise in left atrium pressure and elevation in pulmonary capillary pressure. The onset of angina, syncope and dyspnea correlates with an average time to death of 5, 3 and 2 years respectively. In asymptomatic patients with aortic stenosis the risk of sudden death was reported to be between 3-5%. So the consensus is that asymptomatic patients are at low risk for complications or mortality, but that the onset of symptoms signals a dramatic worsening in prognosis. Anesthetic Considerations As the populations of patients presenting for surgery and anesthesia continues to become older, anesthesiologists are seeing more patients with aortic stenosis. These patients are at increased risk for cardiac complications, including supraventricular tachyarrhythmias, congestive heart failure or myocardial infarction. It follows that patients with severe or symptomatic aortic stenosis are at an increased risk for peri-operative cardiac morbidity. The recommendation for this group of patients is elective aortic valve replacement before non-cardiac surgery. A common clinical problem is the elderly patient with aortic stenosis that is asymptomatic. In these patients, a preoperative two-dimensional echocardiogram is recommended to give insight into the severity of stenosis and myocardial contractile function. This testing may identify a small group of patients with severe aortic stenosis and these patients should be referred for aortic valve replacement surgery prior to elective non-cardiac surgery. Anesthetic management should consider the following pathophysiologic principles:
Arrhythmias should be treated aggressively, since atrial "kick" may account for 30-40% percent of left ventricular filling in the presence of a stiff ventricular wall. Intraoperative hypotension should be immediately treated with alpha-agonists, such as phenylephrine, regardless of the primary cause of hypotension. Appropriate and aggressive treatment of the primary cause (for example, rapid fluid infusion for sudden hypovolemia or cardioversion for atrial fibrillation) should follow immediately. Keeping up with intravascular volume losses is important, but the need for invasive hemodynamic monitoring is controversial. Central venous pressure (CVP) poorly estimates left ventricular filling pressures in the presence of decreased left ventricular compliance. Accepting low or normal CVP pressures may lead to under filling of the left ventricle and be a cause of low cardiac output. The placement of a pulmonary artery catheter (PAC) may cause arrhythmias and pulmonary capillary wedge pressure (PCWP) still can underestimate the LVEDP. However, the use of the PAC does allow the measuring of cardiac output, derived hemodynamic parameters and transvenous pacing if needed. Choice of anesthetic technique, medications and methods of monitoring should be done after assessment of the severity of aortic stenosis, existing symptoms and overall risk of surgery. Anesthetic management should be based on the avoidance of systemic hypotension, maintenance of sinus rhythm, monitoring closely for ischemia and maintenance of adequate intravascular volume. REFERENCES 1. J.A.Kaplan, D.L.Reich, S.N.Konstadt; Cardiac anesthesia, 4th edition 2. Harrisson's Principles of internal medicine, 14th edition 3. S.J.Lester, B. Heilbron, K.Gin, A.Dodek, J.Jue; The natural history and rate of progression of aortic stenosis; CHEST 1998; Vol.113(4):1109-1114 4. B.A.Carabello, Aortic stenosis, The New England Journal of Medicine 2002, Vol.346(9):677-682 |
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The Pregnant Patient
With Heart Disease
- part 1 of 2 -
Philip J. Balestrieri, M.D.
Associate Professor
and Director of Obstetric Anesthesia, University of Virginia
Health System.
Effects of Pregnancy on the Normal Cardiovascular System Before discussing the normal cardiovascular changes associated with pregnancy it is necessary to state three caveats, viz. these changes are average values obtained from many different healthy patients and thus may not accurately apply to the particular patient being treated, these normal changes may be significantly modified in the patient with serious heart disease and these changes develop over time. Plasma volume increases early in pregnancy but, because of a transient decrease in red cell mass which is maximal at around eight weeks gestation, the major early increase in total blood volume is not seen until the end of the first trimester when it reaches a value of about 15% above baseline. Thereafter it increases more rapidly, reaching 40% by the end of the second trimester and then slowing to produce at term a plasma volume increase of 55%, red cell volume increase of 30% and a total blood volume increase of 45%. Both systolic and diastolic blood pressures mildly decrease during the first trimester, remain stable during the second trimester and then increase towards their pre-pregnancy values at term. Cardiac output increases by about 20% by the end of the first trimester, mainly due to an increase in heart rate although there is a small increase in stroke volume. Heart rate peaks at about a 20% increase towards the end of the second trimester while cardiac output continues to increase as a function of increasing stroke volume until it reaches a maximum of about 45% above pre-pregnancy values near the end of the third trimester. Several factors account for the improved left ventricular pump function that is seen during pregnancy. These include increased preload, left ventricular compliance and ventricular wall thickness together with a decrease in systemic vascular resistance and no change in end diastolic or left atrial pressures. (1)
Risk Stratification
Maternal and fetal outcome are best correlated with New York Heart Association class. Class I and class II patients have a maternal mortality rate of less than 1% while class III and IV patients have a rate of 5-15% and a perinatal mortality rate of 20-30%. Patients with severe obstructive valvular lesions, pulmonary hypertension, significant pathology of the thoracic aorta and uncontrolled hypertension are considered high risk regardless of functional class.
New York Heart Association Classification of Cardiovascular Disease
Class I: Patients who are not limited by cardiac disease in their physical activity. Ordinary physical activity does not precipitate the occurrence of symptoms such as fatigue, palpitations, dyspnea, and angina.
Class II: Patients in whom the cardiac disease causes a slight limitation in physical activity. These patients are comfortable at rest, but ordinary physical activity will precipitate symptoms.
Class III: Patients in whom the cardiac disease results in a marked limitation of physical activity. They are comfortable at rest, but less than ordinary physical activity will precipitate symptoms.
Class IV: Patients in whom the cardiac disease results in the inability to carry on physical activity without discomfort. Symptoms may be present even at rest, and discomfort is increased by any physical activity.
Obstetric Management
Current obstetric practice generally limits cesarean delivery to patients with obstetric indications. Thus spontaneous or assisted vaginal delivery is the preferred mode in patients with congenital or ischemic heart disease unless the mother is hemodynamically unstable. Exceptions to this are patients who have a dilated aortic root (> 5.5 cm), or uncorrected severe aortic coarctation with poorly controlled hypertension and who are thus at risk for aortic rupture without strict blood pressure control.
Cardiovascular Drugs and Pregnancy
The only currently available cardiac drugs clearly proven to be tetratogenic are the angiotensin converting enzyme (ACE)inhibitors and warfarin. ACE inhibitors have been linked to fetal loss and neonatal renal failure while warfarin has been associated with embryopathy with skeletal abnormalities and central nervous system defects when used in the first trimester as well as with increased risk of fetal intracerebral bleeding. Although not clearly associated with teratogenesis, amiodarone has been associated with a 9% incidence of fetal hypothyroidism and a 21% incidence of intrauterine growth retardation and should be reserved for cases of refractory ventricular arrhythmias. Among cardiac drugs thought to be relatively safe to use during pregnancy are heparin(does not cross the placenta), propanolol and other beta blockers, verapamil, digoxin as well as antihypertensives including labetolol, methyldopa, hydralazine, nifedipine, prazosin and others.
Antibiotic Prophylaxis
Currently routine prophylaxis is not recommended in normal vaginal or cesarean delivery. However, there are a variety of conditions that require antibiotic prophylaxis during complicated vaginal delivery or in the presence of infection. These include unrepaired ventricular septal defect or patent ductus arteriosus, residual ventricular septal defect or patent ductus arteriosus after repair, valvular stenosis, repaired or unrepaired aortic coarctation, prosthetic heart valves, patients with previous history of bacterial endocarditis, complex cyanotic congenital heart disease, surgically constructed systemic pulmonary shunts, bicuspid aortic valves, acquired valvular dysfunction such as rheumatic heart disease, obstructive hypertrophic cardiomyopathy and mitral valve prolapse with valvular regurgitation or thickened leaflets. (2)
Anticoagulation
Indications for anticoagulation during pregnancy are not different from the usual indications. They include history of deep venous thrombosis or pulmonary embolism, left atrial thrombus or atrial fibrillation in a patient with valvular heart disease or prosthetic valves and rheumatic mitral stenosis. Heparin and low-molecular-weight heparin (LMWH)are the anticoagulants of choice in pregnancy as warfarin crosses the placenta and is associated with serious fetal adverse effects.
References
(1) Crawford MH and DeMarco JP. Cardiology. 2001 Mosby, London. pp 8-11.2-4.
(2) Ibid. pp. 8-11.5.
The Pregnant Patient
With Heart Disease
- part 2 of 2 -
Philip J. Balestrieri, M.D.
Associate Professor
and Director of Obstetric Anesthesia, University of Virginia
Health System.
Types of Heart Disease CONGENITAL HEART DISEASE: Left-to-right shunts, Tetralogy of Fallot, Eisenmenger syndrome, coartation of the aorta
VALVULAR DISORDERS: Aortic Stenosis, aortic insufficiency, mitral stenosis, mitral regurgitation
OTHER: Primary Pulmonary Hypertension, Peripartum Cardiomyopathy, Hypertrophic Obstructive Cardiomyopathy, Heart Transplant
Anesthetic Management of Particular Cardiovascular Disorders during Labor and Delivery
LEFT TO RIGHT SHUNTS: Although modest left-to-right shunting is usually well tolerated during pregnancy, these patients are at risk for paradoxical air emboli which may be worsened by accidental intravenous administration of air bubbles or use of air rather than saline for loss of resistance during epidural placement. The goal should be avoidance of extreme changes in systemic vascular resistance. Early epidural administration with incremental dosing may avoid both increases in SVR due to maternal catecholamine release from labor pain that may increase the severity of left-to-right shunt and rapid decreases in SVR after sympathectomy that may cause cyanosis with flow reversal. Such flow reversal is usually of clinical significance only in patients with significant preexisting pulmonary hypertension associated with some degree of right ventricular failure. Patients with normal pulmonary vascular resistence may actually benefit from decreases in SVR as this may decrease right ventricular overload. If cor pulmonale is dramatic, inotropic support is indicated. Patients should receive supplemental oxygen with continuous oxygen saturation monitoring as even mild hypoxemia, hypercarbia and or acidosis may cause increased pulmonary vascular resistance and flow reversal. (1, 2)
TETRALOGY OF FALLOT: This lesion includes ventricular septal defect, right ventricular hypertrophy, pulmonic stenosis with right ventricular outflow tract obstruction and overriding aorta and is associated with a cyanotic shunt. Although patients with corrected lesions may not differ from normal patients in most respects, they are at risk for post-repair atrial and ventricular arrhythmias. In patients with uncorrected or partially corrected lesions symptom severity correlates with size of VSD, severity of pulmonic stenosis and functional status of the right ventricle. Anesthetic management should be directed towards avoiding decreases in SVR and in preload. Regional anesthesia with careful titration of agents and attention to hemodynamic stability is acceptable. The use of combined spinal-epidural with intrathecal narcotic alone followed by dilute local anesthetic/narcotic infusion for labor may allow for good analgesia with minimal hemodynamic effects.
EISENMENGER SYNDROME: This syndrome involves irreversible pulmonary hypertension following pulmonary vascular occlusive disease of varying etiologies. Normal physiologic changes of pregnancy tend to worsen maternal hypoxemia with increasing oxygen demand and decreased SVR and functional residual capacity in the setting of fixed pulmonary vascular resistance. Maternal mortality approaches 50% with frequent thromboembolic events (3). Anesthetic management is directed towards maintenance of SVR, intravascular volume and venous return and the prevention of pain, hypoxemia, hypercarbia, acidosis and myocardial depression. Monitoring should include pulse oximetry and intraarterial catheter. The advisability of central venous and pulmonary artery catheter placement is controversial. Regional anesthesia for labor, using either a continuous spinal catheter or combined spinal-epidural (CSE) technique primarily with narcotics (fentanyl/sufentanyl or morphine) is a good choice, as it will decrease pain without extensive sympathectomy. Cesarean section may be performed either under epidural or general anesthesia. If epidural anesthesia is selected, the block should be established slowly and preload and SVR maintained with intravenous crystalloid and neosynephrine infusion as needed. General anesthesia should include systemic narcotics and minimal cardiac depressants. Whether rapid sequence or slow induction of general anesthesia should be performed remains controversial as the former may be associated with myocardial depression and decreased SVR and the latter is associated with aspiration risk.
COARCTATION OF THE AORTA: Uncorrected coarctation is rare in pregnancy but when present tends to be exacerbated by normal physiologic changes with fixed aortic outflow obstruction and distal hypoperfusion. These patients are at increased risk of left ventricular failure, aortic dissection and rupture, endocarditis and cerebrovascular accident. Anesthetic goals should center on maintaining normal to slightly elevated SVR and heart rate and adequate preload. Regional anesthesia is relatively contraindicated. General anesthesia is the preferred technique for cesarean section with invasive hemodynamic monitoring with postductal intraaterial catheter, CVP or PA catheters to guide fluid administration and to assess left ventricular function and use of ephedrine and dopamine as vasopressors of choice.
AORTIC STENOSIS: This lesion becomes hemodynamically significant when valve area decreases to one third of normal (normal valve area 2.6-3.5 cm) and gradients of 50 mm Hg or greater are associated with severe disease and increased risk of myocardial ischemia (4). Anesthetic goals include maintenance of normal heart rate and rhythm, adequate SVR and venous return and avoidance of myocardial depression. Patients with severe disease should be invasively monitored with intraarterial catheter and either CVP or PA catheters. Single shot spinal anesthesia for cesarean section is relatively contraindicated in patients with moderate-to-severe disease. CSE or incrementally dosed epidural infusions without epinephrine provide good labor analgesia. General anesthesia with a combination of etomidate and narcotic for induction at cesarean section should avoid both maternal tachycardia and decreased SVR and is the anesthetic of choice.
AORTIC INSUFFICIENCY: Acute aortic insufficiency is a life-threatening condition requiring emergent surgical repair. Chronic aortic insufficiency is more common and is often well tolerated during pregnancy as normal physiologic changes of pregnancy tend to lessen the regurgitant flow (increased heart rate, decreased SVR and increased blood volume). Goals in anesthetic management include maintenance of normal-slightly elevated heart rate, prevention of increases in SVR and avoidance of myocardial depressants. Regional anesthesia is the anesthetic of choice for both labor analgesia and cesarean section.
MITRAL STENOSIS: Mitral stenosis produces increased pulmonary arterial pressure which may result in pulmonary edema and right heart failure. Goals of anesthetic management include maintenance of slow heart rate, sinus rhythm with aggressive treatment of atrial fibrillation, maintenance of venous return and pulmonary capillary wedge pressure to maximize left ventricular end diastolic volume without producing pulmonary edema, maintenance of adequate SVR and prevention of increased pulmonary vascular resistance. Regional anesthesia can be employed for labor or cesarean section. Phenylephrine is the vasopressor of choice to treat hypotension as it is not associated with maternal tachycardia. Should general anesthesia be required, drugs which increase heart rate should be avoided and beta-blockers together with a modest dose of narcotic should be given prior to induction with etomidate. Invasive hemodynamic monitors including a PA catheter should be placed in patients with severe disease regardless of mode of delivery.
MITRAL REGURGITATION: Mitral regurgitation is usually well tolerated in pregnancy, however, there is an increased risk of atrial fibrillation and embolic events. Goals of anesthetic management include avoidance of increases in SVR, maintenance of normal-slightly elevated heart rate and sinus rhythm and avoidance of myocardial depressants and increases in pulmonary vascular resistance. Maternal monitoring during labor and delivery should include continuous ECG and arterial line with PA catheters in patients with severe disease. Regional anesthesia is the anesthetic of choice for labor and vaginal or cesarean delivery.
PRIMARY PULMONARY HYPERTENSION: Unlike patients with Eisenmenger syndrome, these patients may have a reactive pulmonary vasculature that may respond to pulmonary vasodilators such as sodium nitroprusside, nitroglycerin, prostaglandin E and isoproterenol (5). It should be remembered that all of these vasodilators will also affect peripheral vessels and may result in significant decreases in SVR. The only pure pulmonary vasodilators are oxygen, which should be used liberally, and nitric oxide. The maternal mortality rate in primary pulmonary hypertension is greater than 50% and correlates with the severity of the pulmonary hypertension (6). Anesthetic management should be directed to avoidance of increases in pulmonary vascular resistance (pain/hypoxia/hypercarbia/acidosis), maintenance of adequate SVR, intravascular volume and venous return and avoidance of myocardial depressants. Regional anesthesia as well as systemic narcotics have been used successfully for labor and both regional and general anesthesia for cesarean section. Invasive monitoring including systemic and pulmonary artery catheters and continuous pulse oximetry are essential. Drugs which can increase pulmonary vascular resistance such as ergot alkaloids, oxytocin, prostaglandin F2alpha, ketamine and nitrous oxide should be avoided. Should general anesthesia be selected, induction may be accomplished using a combination of etomidate and narcotics.
PERIPARTUM CARDIOMYOPATHY: This is a rare disorder of unknown etiology defined as onset of left ventricular dilatation and congestive cardiac failure during the third trimester of pregnancy or in the first six months postpartum without prior evidence of cardiac disease. Regional anesthesia for labor and delivery has several advantages including decreased SVR which improves cardiac output. Patients who are symptomatic or demonstrate severe LV dysfunction should be monitored with systemic and pulmonary artery catheters. Should general anesthesia be necessary, agents that increase afterload or have a negative inotropic effect should be avoided. Positive ionotropic support is often indicated.
HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY: Also known as asymmetric septal hypertrophy this rare condition affects the interventricular septum in the left ventricular outflow tract and ultimately results in ventricular hypertrophy and dysfunction. Goals in anesthetic management include maintenance of intravascular volume, venous return, SVR, a slow heart rate with sinus rhythm and prevention of increases in cardiac contractility. Regional anesthesia for labor and delivery may be used safely with proper monitoring of intravascular volume and SVR. Single-shot spinal anesthesia for cesarean section is relatively contraindicated. General anesthesia is usually well tolerated for operative delivery provided that positive inotropic agents are avoided. Should hypotension occur, phenylephrine is the preferred vasopressor. As outflow obstruction may worsen acutely, these patients should be monitored with systemic and pulmonary artery catheters.
HEART TRANSPLANT: Denervation (autonomic and somatic) gives rise to several effects: lack of vagal innervation results in increased baseline heart rate, no reflex slowing, absent heart rate variation with respiration and no effects of drugs such as atropine which exert their cardiac effects through vagal stimulation. Denervation also results in upregulation of cardiac beta adrenegic receptors with increased sensitivity to agonists, resistance to all but direct-acting sympathomimetic agents and delayed chronotropic response to stress. Both regional and general anesthesia have been used successfully for cesarean section in these patients. Ketamine has the advantage over thiopental as an induction agent because of its ability to maintain sympathetic tone. Hypotension and bradycardia are best treated with phenylephrine and isoproterenol respectively.
References
(1) For a more detailed discussion of this topic, see Chestnut, D.H., Obstetric Anesthesia: Principles and Practice, Chapter 40. Mosby Inc. 1999.
(2) Ibid. pp.777-8.
(3) Gleicher R, Midwall J, Hochberger D. Eisenmenger syndrome and pregnancy. Obstet Gynecol Surv 1979; 34:721-41.
(4) American College of Obstetrics and Gynecology. Cardiac Disease in Pregnancy. ACOG Technical Bulletin No. 168, 1992.
(5) Chestnut, op.cit. p.780
(6) Datta S. Anesthetic and Obstetric Management of High-Risk Pregnancy. Mosby-Year Book, Inc. St. Louis, 1991; p.237.
Sevoflurane, but Not
Propofol, Significantly Prolongs the Q-T Interval
- Survey of Anesthesiology: December
2000 -
AXEL KLEINSASSER, ELISABETH
KUENSZBERG, ALEXANDER LOECKINGER, CHRISTIAN KELLER, CHRISTOPH HOERMANN, KARL H.
LINDNER and FRIEDRICH PUEHRINGER
Department of
Anesthesiology and Critical Care Medicine, The Leopold-Franzens-University of Innsbruck, Innsbruck, Austria
Anesth.
Analg., 90: 25-27, 2000 It is thought that prolongation of the Q-T interval may be associated with polymorphic ventricular tachycardia, known as torsade de pointes, as well as syncope and sudden death. Data show that isoflurane prolongs the Q-T interval, whereas halothane shortens it. Whether sevoflurane or propofol affects the Q-T interval was determined in a study of 30 female patients undergoing gynecologic surgery. The patients were randomly assigned to one of two groups, one of which received inhaled induction with sevoflurane and the other total intravenous anesthesia with propofol. Before and 20 min after the induction, a six-lead electrocardiogram was recorded, and blood pressure was measured. the Q-T interval and the heart rate-adjusted Q-T interval (Q-Tc interval) were markedly prolonged during the administration of sevoflurane anesthesia, whereas the Q-T interval was markedly shortened and the Q-Tc interval was statistically unaffected during administration of propofol anesthesia. It was concluded that in otherwise healthy female patients, sevoflurane prolongs the Q-T interval.
Comment
Sevoflurane is now immensely popular in the United Kingdom and elsewhere for the induction of general anesthesia in children, and sometimes for adults who fear the needle. This study shows that, in healthy female patients, sevoflurane prolongs Q-Tc (i.e., Q-T interval adjusted for heart rate). Does this matter? We know that Q-Tc is prolonged with isoflurane anesthesia but shortened with halothane anesthesia. Furthermore, acquired forms of the long Q-T syndrome can result from the administration of some drugs (e.g., droperidol, class la and III antiarrhythmics, antidepressants) or metabolic disorders. The message of this paper is that sevoflurane may not be a sensible choice for patients who are known to have a long Q-Tc. It also raises the question of excluding a prolonged Q-Tc before inducing any patient with sevoflurane; this can only be done by obtaining an ECG. We are likely to see more papers on this topic.
Anthony P. Adams, M.B., B.S., Ph.D., F.R.C.A., F.A.N.Z.C.A.
Survey of Anesthesiology: December 2000 Contents
http://www.gasnet.org/sa/1997/01/06.php
Myocardial Ischemia
and Reperfusion Are Associated with an Increased Stiffness of Remote
Nonischemic Myocardium
- Survey of Anesthesiology: February
1997 -
S. C. U. MARSCH, S. DALMAS, D. M.
PHILBIN, W. A. RYDER and P. FOËX
Nuffield Department
of Anesthetics, University
of Oxford, The Radcliffe
Infirmary, Oxford, United Kingdom
Anesth.
Analg., 82: 695-701, 1996 In a previous report, the authors noted that graded myocardial ischemia was associated with increased stiffness of remote nonischemic myocardium, but no data about reperfusion were included. To determine if this phenomenon persists during the reperfusion period, the authors studied a series of anesthetized beagles whose hearts were isolated via left thoracotomy. Instrumentation was designed to permit measurement or calculation of left ventricular pressure and dimensions in ischemic and nonischemic myocardium. Data were recorded at baseline in this absence of myocardial ischemia, during severe ischemia produced by occlusion of the left anterior descending coronary artery for 45 min, and then for 60 min after reperfusion. At each study period, 200 mL of arterial blood were infused and withdrawn with determination of hemodynamic variables. At the end of studies, the animals were sacrificed, and Evans blue dye was injected into the left anterior descending coronary artery to permit determination of the size of the ischemic area in terms of total ventricular weight.
Data were obtained from 10 animals. The ischemic area comprised 28 plus/minus 2% of the left ventricle. Ischemia and reperfusion were associated with significant decreases in cardiac output and systemic blood pressure. Reperfusion was associated with a recovery of ischemia-induced increased left ventricular end-diastolic pressure. Ischemic myocardium demonstrated decreased contractile function, regional will motion abnormalities, and increased end-diastolic dimensions and stiffness. Contractile function and wall motion abnormalities did not fully recover with reperfusion.
There were no regional wall motion abnormalities in nonischemic myocardium. Neither ischemia nor reperfusion affected coronary blood flow velocity and systolic shortening fraction. Myocardial ischemia and reperfusion were associated with an increase of approximately 50% in chamber stiffness and myocardial stiffness in remote nonischemic myocardium.
The present study is the first to demonstrate that after a severe ischemic injury, stiffness of remote nonischemic myocardium remains increased 1 hr after the onset of reperfusion. Whether and how the increase in stiffness in the nonischemic myocardium depends on extent and reversibility of damage in the ischemic area remain to be determined. The mechanism(s) of the noted changes are not evident, although the authors speculate about potential mechanisms suitable for investigation. The clinical implications of the results are also unclear.
Comment
This study is fascinating because 1) it is an excellent study and 2) it disturbs one of my long held beliefs. This study claims that during the period after reperfusion of myocardial ischemia, the remote nonischemic myocardium stays disturbed. On the other hand, this confirms another hypothesis--that stress or perhaps adrenergic tone or the decreasing stress or decreasing adrenergic tone may be important to recovery of normal function after an ischemic event. Although the mechanisms are not explained in this study, I commend all of us interested in myocardial ischemia to read this study that may have important implications for elucidating the disordered function after muscle injury occurs.
M. F. Roizen, M.D.
Survey of Anesthesiology: February 1997 Contents
Perioperative
Ventricular Dysrhythmias in Patients with Structural Heart Disease Undergoing
Noncardiac Surgery
- Survey of Anesthesiology: December
1998 -
ELISABETH MAHLA, BRIGITTE ROTMAN,
PETER REHAK, JOHN L. ATLEE, HANS GOMBOTZ, JUTTA BERGER, WERNER F. LIST, WERNER
KLEIN and HELFRIED METZLER
Departments of
Anesthesiology, Cardiology, and Surgery, University of Graz, Graz, Austria and
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee,
Wisconsin
Anesth.
Analg., 86: 16-21, 1998 Patients scheduled for noncardiac surgery who have preoperative ventricular dysrhythmias and structural heart disease may be at an increased risk of an adverse cardiac outcome. How anesthesia and surgery affect the course of ventricular dysrhythmias (premature ventricular beats [PVB] and repetitive forms of ventricular beats [RFVB]: couplets and nonsustained ventricular tachycardia) that were noted preoperatively in patients with structural heart disease and whether the frequency of ventricular dysrhythmias affects cardiac outcome were evaluated. Seventy patients who had structural heart disease and RFVB on preoperative Holter electrocardiography and who were scheduled for noncardiac surgery were prospectively studied. The patients were continuously monitored intraoperatively and for 3 days postoperatively. Analysis of Holter tracings was made for rhythm and medians of total PVB and RFVB per hour. Preoperative RFVB recurred intraoperatively in 35% of patients and postoperatively in 87% of patients. A marked intraand postoperative decrease in total PVB per hr and RFVB per hr was observed. The frequency of ventricular dysrhythmias in five patients with adverse outcomes (unstable angina, n = 1; congestive heart failure, n = 4) did not differ markedly from those with a good outcome. It was concluded that, in patients undergoing noncardiac surgery who have structural heart disease and RFVB, the frequency of ventricular dysrhythmias was not associated with an adverse cardiac outcome.
Comment
Surprisingly, there was a decrease in intra- and postoperative ventricular dysrhythmias in this patient population with structural heart disease. This may speak for the safety of currently used anesthetics. It is possible that the reduction in ventricular dysrhythmias is the result of a reduction in pain associated with anesthesia and analgesia. It is also interesting that the incidence of perioperative ventricular dysrhythmias did not differ in patients with good and bad outcomes. It is possible that the study population was too small to demonstrate outcome differences; however, this may also mean that ventricular dysrhythmias are a marker of cardiac disease rather than an indicator of outcome.
George F. Rich, M.D., Ph.D.
Survey of Anesthesiology: December 1998 Contents
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