Dept Of Anesthesiology & Critical Care, University Of Pennsylvania School Of Medicine

Bainbridge reflex and hypovolemia

Daniel Weil, M.D. discusses the role of the Bainbridge reflex in hypovolemia.  Cardiac reflexes are reflex loops between cardiovascular structures and the CNS that regulate and modulate cardiac function and vascular tone. In 1915, Francis Arthur Bainbridge published an observation, which bears his name that intravenous volume administration produces tachycardia in anesthetized dogs.  The increase in venous return detected by stretch receptors in either atrium sends signals along vagal afferents to the cardiovascular center in the medulla. These afferent signals inhibit parasympathetic activity, i.e. vagus efferents, thus increasing the heart rate. The response is absent following bilateral vagotomy or heart transplant. This reflex caused by increased preload increases cardiac output by increasing the heart rate. The magnitude of the change in heart rate is dependent on the underlying heart rate before stimulation and baseline vagal tone. This reflex competes with the baroreceptor-mediated decrease in heart rate produced by volume expansion and is diminished or absent when the initial heart rate is high. Its physiologic role and clinical significance remains unsettled.

            The baroreceptor reflex is the dominant cardiovascular mechanism responsible for control of blood pressure.  Stretch receptors located in the carotid sinus and aortic arch send afferent impulses via the glossopharyngeal and the vagus nerves to the nucleus solitarius located in the cardiovascular center of the medulla. The baroreceptor reflex plays a dominant role during acute blood loss and shock. It is unlikely that one would observe a further increase in heart rate with volume administration during acute hemorrhage.  References: Bainbridge FA, The influence of venous filling upon the rate of the heart, J Physiol 1915;50:65-84; Secher NH, Jacobsen J, Friedman DB, Matzen S: Bradycardia during reversible hypovolaemic shock:   Associated neural reflex mechanisms and clinical implications. Clin Exp Pharmacol Physiol 1992;19, 733-743

Dr. Weil has completed his anesthesia residency and is now a fellow in Cardiac Anesthesia.

Coronary Artery Embolism

            It is very uncommon, but possible for air to be introduced into the left atrium during cardiac conduction pathway ablation procedures.  If that air embolus should transit into a coronary artery the signs and symptoms of acute coronary artery occlusion may occur.          

            Dr. Mandel notes that coronary air embolus is a rare complication outside of the cardiac ORs. Patients in the heart room are generally intubated and ventilated with 100% oxygen, but patients experiencing this complication in out-of-OR locations are frequently breathing room air. While certainly not the only measure to be taken during such an event, prompt denitrogenation is an important intervention. Use of a Mapleson system with high fresh gas flow and a good seal should be considered as an important first step in responding to this event.  Treatment review paper attached.

            Dr. Eckmann provides further detail: 1) if the gas bubble is accessible to an interventional catheter already in situ, attempts should be made to aspirate the bubbles.  2) Once they have lodged, it is very difficult to dislodge bubbles to push them distally. 3) Once bubbles are in and stuck, there is very little that can be done to alter the adhesion that has developed between the bubble and endothelial cell surface. So nothing injectable is helpful at this point, though there may be some rationale to try to dilate the coronary vasculature locally to dislodge bubbles and permit them to flow distally. 4) It is therefore necessary to alter gas adsorption to enhance the rate at which gas exits the bubble and becomes solubilized in surrounding tissue. My experimental and computational/theoretical work has shown that microvascular bubbles as small as a few nanoliters in volume can survive for 20-30 min, and larger bubbles may last for hours! So changing the partial pressure gradients (essentially, the concentration gradients) in surrounding tissues enhances the driving force for gas to exit the bubbles. This can only be accomplished by two methods: change the breathing gas admixture (decrease nitrogen, especially if the bubble is at all composed of nitrogen) and increase the ambient pressure. Placing the patient on 100% oxygen or initiating hyperbaric therapy are both appropriate steps.  Clearly placing the patient on 100% oxygen can be quickly started while other therapy is arranged.

         Injection of contrast agent directly into the affected vessel may also help solubilize the gasses in the embolus.

         Jeff Mandel M.D. is Clinical Associate Professor of Anesthesiology and Critical Care

         David Eckmann M.D. is Associate Professor of Anesthesiology and Critical Care

Hypertrophic cardiomyopathy

     At the Frank Murphy Memorial Lecture Dr. Kukafka discussed issues related to hypertrophic cardiomyopathy.  He provides the following summary of key points: Given that the prevalence of hypertrophic cardiomyopathy (HCM) is approximately one in 500 (0.2%), it is likely that anesthesiologists care for these patients on a fairly regular basis.  These patients may deteriorate perioperatively through these three main mechanisms:  arrhythmia, dynamic left ventricular outflow tract (LVOT) obstruction, and diastolic dysfunction.  When a patient with a known diagnosis of HCM presents for surgery, preparations can be undertaken in an attempt to prevent or treat these problems.  These include: 1) aggressive maintenance of sinus rhythm with appropriate cardioversion/defibrillation when necessary.  2) Prevention or treatment of LVOT obstruction by maintaining preload through volume administration, maintaining afterload with peripheral vasoconstrictors, administration of negative inotropes (beta blockers, verapamil), and avoidance of sympathetic stimulation or positive inotropic drugs.  3) Treatment of diastolic dysfunction impaired LV relaxation or LV hypertrophy is managed in a similar fashion.  Impaired LV filling can be managed by ensuring adequate diastolic filling time (avoiding tachycardia) and by maintaining sinus rhythm as the atrial contraction can provide up to 50% of the cardiac output.  HCM with diastolic dysfunction is also a significant risk factor for coronary ischemia despite normal coronary arteries, as these patients have a large ventricular mass coupled with an inadequate coronary density.

     When patients with undiagnosed hypertrophic cardiomyopathy present for surgery, these same problems as noted above can arise and they may present a significant diagnostic dilemma.  Preoperative signs and symptoms suggesting this disease may include left ventricular hypertrophy on EKG or echo without concomitant hypertension or aortic stenosis, a history of syncope/presyncope or cardiac arrest, or a family history of HCM.  A preoperative echo with a normal LVOT and mitral valve does not rule out the possibility of dynamic LVOT obstruction.  Intraoperatively the disease may manifest itself via arrhythmia or signs of heart failure despite a normal ejection fraction (diastolic heart failure).  LVOT obstruction may manifest itself as a paradoxical response to positive inotropic drugs or by an exaggerated decrease in blood pressure following vasodilation or hypovolemia.  When this happens volume should be administered in aliquots (250-500 ml depending on patient size) while observing hemodynamics; positive inotropic drugs should be withheld.  With volume administration there is typically a fairly abrupt improvement in hemodynamics which correlates with the cessation of LVOT obstruction.  Peripheral vasoconstrictors may be needed to temporize until LVOT obstruction resolves.  Definitive diagnosis is based on direct imaging with echocardiography.  Intraoperative TEE can be used to make both the diagnosis and to guide fluid and pharmacologic therapy aimed at minimizing LVOT obstruction.  References: Maron BJ, et al.  American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document of Hypertrophic Cardiomyopathy: a report of the American College of Cardiology Foundation Task Force of Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines. JACC 2003; 42:1687-713.  Poliac LC, et al.  Hypertrophic Cardiomyopathy.  Anesthesiology 2006; 104:183-192. Haering J, et al. Cardiac Risk of Noncardiac Surgery in Patients with Asymmetric Septal Hypertrophy.  Anesthesiology 1996; 85:254-259.

     Jeremey Kukafka, M.D. has completed his residency training in Anesthesiolgy and is now a cardiac fellow in the Department of Anesthesiology and Critical Care