Haemodynamics in leptospirosis: effects of plasmapheresis and continuous venovenous haemofiltration

BACKGROUND: Haemodynamics in leptospirosis may differ from that of sepsis because of frequently obeserved myocarditis and severe cholestatic jaundice. A haemodynamic study was therefore made in 10 patients with severe leptospirosis. METHODS AND RESULTS: All patients had pulmonary complications with a chest X-ray showing either pulmonary oedema or infiltration. Renal failure was present in nine patients. Three patterns of haemodynamics were revealed. The first pattern was observed in six patients who showed increased cardiac index, decreased systemic vascular resistance, normal pulmonary capillary wedge pressure, normal pulmonary vascular resistance and hypotension. The pattern resembled that of sepsis. The second pattern shown in two patients with haemoptysis consisted of a normal cardiac index, normal systemic vascular resistance, normal blood pressure, normal pulmonary capillary wedge pressure and increased pulmonary vascular resistance. The third pattern was observed in two patients with severe jaundice who had hypotension, a relatively low cardiac index, increased systemic vascular resistance and normal pulmonary capillary wedge pressure, and pulmonary vascular resistance. Plasmapheresis performed in two patients and continuous venovenous haemofiltration performed in two patients improved systemic haemodynamics and normalized blood pressure with a resolution of lung signs.     

Physiology of the normal heart

The mechanical events of the cardiac cycle provide the circulation with normal cardiac output and blood pressure. This requires an appropriate venous return, regulation of outflow resistance, a normal myocardial contractile state and heart rate control, together with an adequate supply of oxygenated blood via the coronary circulation. Other neural influences contribute to cardiac regulation, including natriuretic peptides and the renin–angiotensin system. The atria and ventricles are richly supplied with adrenergic nerves that may augment cardiac function, particularly with increased cardiac output during exercise. Inhibitory vagal fibres are largely confined to the sinus and atrioventricular nodes. Exercise causes increased sympathetic outflow, with a decrease in peripheral vascular resistance and increased cardiac output, heart rate, systolic blood pressure and venous return. Regular rhythmic exercise has a training effect, which enhances cardiac performance. This is important for the maintenance of many aspects of cardiovascular health.     

The use of vasodilator agents in the treatment of heart failure.

In cardiac failure unresponsive to digoxin and diuretics, afterload reduction brings about a dramatic increase in cardiac output, renal perfusion and responsiveness to diuretics; furthermore, the decrease in venous pressure relieves the dyspnoea. Intravenous vasodilators should only be used when sophisticated haemodynamic monitoring equipment and experienced physicians are at hand. Indications for the use of these agents are severe cardiac failure, acute myocardial infarction complicated by left ventricular failure, persistent ischaemic pain and limitation of infarct size. A wide variety of oral vasodilator agents is available, all having different sites of action; the choice of vasodilator agents should be tailored to the needs of the patient. Treatment with these agents is indicated in patients in whom cardiac failure becomes refractory to conventional therapy with digoxin and diuretics. The utmost care must be taken to avoid further impairment of cardiac output by excessive reduction of the left ventricular end-diastolic pressure (LVEDP) and hypotension, which will jeopardize myocardial, renal and cerebral perfusion.     

Physiology of the normal heart

The mechanical events of the cardiac cycle provide the circulation with normal cardiac output and blood pressure. This requires an appropriate venous return, regulation of outflow resistance, a normal myocardial contractile state, and heart rate control, together with an adequate supply of oxygenated blood via the coronary circulation. Other neural influences contribute to cardiac regulation, including natriuretic peptides, and the renin–angiotensin system. The atria and ventricles are richly supplied with adrenergic nerves that may augment cardiac function, particularly with increased cardiac output during exercise. Inhibitory vagal fibres are largely confined to the sinus and atrioventricular nodes. Exercise causes increased sympathetic outflow, with a decrease in peripheral vascular resistance, and increased cardiac output, heart rate, systolic blood pressure and venous return. Regular rhythmic exercise has a training effect, which enhances cardiac performance. This is important for the maintenance of many aspects of cardiovascular health.     

Metabolic acidosis in dextran-induced anaphylactic reactions

Results of arterial blood gas and acid-base balance analyses were analyzed in 50 patients suffering from dextran-induced anaphylactic reactions. Metabolic acidosis was always present in severe cases, leading to cardiac arrest, and also frequently found in those with less severe reactions with only slightly impaired circulation. Bronchospastic respiratory signs were frequently encountered but acidosis was noted to develop even without these symptoms. The severity of the acidosis was generally underestimated during treatment. Arterial PO2 and PCO2 were not significantly affected during these reactions.     

Sepsis syndrome

A clinical syndrome including fever, leukocytosis, elevated cardiac output, and reduced systemic vascular resistance has been associated with severe infection (i.e., sepsis). However, during the last 15 years, many patients have demonstrated all of the findings that have traditionally been associated with "sepsis" but have not had demonstrated sources of infection. This led to the term "sepsis syndrome" to refer to that population of patients who appeared to have a physiologic and metabolic response associated with, but who did not have, severe infection. More commonly called the systemic inflammatory response syndrome (SIRS), the sepsis syndrome is now associated with the nonspecific systemic activation of the human inflammatory cascade by any of a number of clinical events. The management of the SIRS patient has been ineffective because of incomplete definition of the mechanisms responsible for the syndrome. It is argued that all of the biological mechanisms that are operative in a simple wound and are beneficial are negative for the host when activated systemically. Thus, SIRS is seen in three separate scenarios at present: (1) invasive infection; (2) dissemination of microbes secondary to failure of host defense mechanisms; and (3) severe activation of inflammation by injury, shock, severe soft tissue inflammation, and other noninfectious but proinflammatory events. Newer treatment strategies will need to focus not on the inciting event itself but on better control of the complex responses of the host.     

Acute respiratory failure due to hypokalaemic muscular paralysis from renal tubular acidosis

We report a case of hypokalaemic quadriplegia with acute respiratory failure and life-threatening cardiac arrhythmias in a 26-year-old woman who was diagnosed to have distal renal tubular acidosis. She had persistent metabolic acidosis with severe hypokalaemia and required mechanical ventilation and potassium replacement. The anaesthetic implications of renal tubular acidosis are also discussed.     

Assessment of cardiac output,intravascular volume status,and extravascular lung water by transpulmonary indicator dilution in critically ill neonates and infants

OBJECTIVE: To assess cardiac output, intrathoracic blood volume, global end-diastolic volume, and extravascular lung water in critically ill neonates and small infants using transpulmonary indicator dilution. DESIGN: Prospective, observational, clinical study. SETTING: Pediatric intensive care unit in a university hospital. PARTICIPANTS: Critically ill neonates and small infants suffering from severe heart failure, respiratory failure, or sepsis (n = 10). INTERVENTIONS: A total of 194 transpulmonary indicator dilution measurements were done. Global end-diastolic volume, intrathoracic blood volume, and stroke volume were measured and compared with standard hemodynamic parameters during the clinical course and before and after volume loading (16 +/- 3.7 mL/kg of 10% albumin solution) in 8 of 10 patients. MEASUREMENTS AND MAIN RESULTS: A positive correlation was found for stroke volume index versus global end-diastolic volume (r = 0.76, p < 0.001) and intrathoracic blood volume (r = 0.56, p < 0.001). In contrast, no correlation was observed for stroke volume index versus central venous pressure. Volume loading resulted in significant increases in stroke volume index (p < 0.01), global end-diastolic volume (p < 0.01), and intrathoracic blood volume (p < 0.01); whereas central venous pressure, heart rate, mean arterial pressure, and extravascular lung water remained unchanged. CONCLUSION: Transpulmonary indicator dilution enables measurement of cardiac output and intravascular volume status in critically ill neonates and infants at the bedside. The effects of volume loading on cardiac preload and effective change in stroke volume can be monitored by this technique, whereas central venous pressure was not indicative of changes in intravascular volume status.     

Blood pressure is maintained despite profound myocardial depression during acute bupivacaine overdose in pigs.

Bupivacaine-induced cardiovascular collapse is a feared complication because of the difficulty in restoring stable circulation (1). Early recognition is important so that the injection of bupivacaine can be discontinued. We used an animal model of near-cardiac arrest from bupivacaine infusion to identify the sequence of hemodynamic events that precedes bupivacaine-induced cardiovascular collapse. Twelve pigs (23-25 kg) were sedated with ketamine and anesthetized with halothane. Arterial blood pressure and cardiac output were measured. Bupivacaine (3.75 mg/mL) was administered at a rate of 5.73 mL/min (approximately 1 mg x kg(-1) x min(-1)) through a central venous catheter until severe ventricular arrhythmia occurred. Blood pressure and heart rate were unchanged, but cardiac output decreased by 40% with increasing doses of bupivacaine. Calculated peripheral resistance increased by 54%. The QRS complex of the surface electrocardiogram widened, and the R-wave amplitude decreased 80%, together with the decrease in cardiac output. T-wave amplitude increased initially but returned toward baseline at the largest bupivacaine doses. The plasma concentration of bupivacaine after the infusion was 16+/-6.8 microg/mL. IMPLICATIONS: The increase in vascular resistance that accompanies acute bupivacaine overdose maintains blood pressure but masks severe myocardial depression.     

Acute systemic hypotension after arteriovenous fistula construction in a patient with severe aortic stenosis

We report the case of a 53-year-old hemodialysis patient with severe aortic stenosis, who developed acute systemic hypoperfusion after arteriovenous fistula (AVF) construction. He presented with hypotension and repeated syncope soon after distal radiocephalic AVF construction, and finally developed a respiratory arrest. His blood pressure and hemodynamics recovered promptly by sub-emergent aortic valve replacement surgery. In the present case, the heart with severe aortic stenosis could not increase cardiac output in response to the reduction in peripheral vascular resistance caused by the AVF. High-output heart failure, a relatively rare AVF-associated disorder, occurs with an excessive AVF flow, usually more than 3 L/min or 30% of cardiac output. However, heart failure may develop soon after construction of an AVF with a moderate blood flow if a patient’s cardiac function is severely impaired. In addition, heart failure may improve with AVF preservation if the underlying heart disease is treatable.     

单纯钾停跳氧合血持续灌注不降温心脏直视手术(附160例报告)

应用钾停跳、氧合血持续灌注心肌保护、不降温体外循环行心脏直视手术１６０例，手术均顺利，术后无低心排综合征、无严重心律失常发生。全组死亡２例（１．２５％）。部分病例进行了ＬＤＨ１／ＬＤＨ２、ＣＫ－ＭＢ及血清乳酸测定，与低温体外循环组比较无统计学明显差异（Ｐ＞０．０５）。作者认为，此方法临床效果满意，值得进一步研究、推广应用。     

Isolated left ventricular assist as bridge to cardiac transplantation

The electrically driven Novacor implantable left ventricular assist device has been implanted in six patients (four men and two women) since Sept. 7, 1984. In four of the six patients (67%) the device was a successful bridge to cardiac transplantation. One patient died of multiple organ failure and Candida sepsis after 16 days of support with the device. One patient died in the operating room of uncontrollable hemorrhage and biventricular failure caused by severe cardiac rejection. Three patients are alive with cardiac transplants 38, 17, and 10 months after transplantation. One patient died after cardiac transplantation of presumed sepsis. The Novacor left ventricular assist device performed in all cases without mechanical or electrical failure. Excluding the intraoperative death, assist duration ranged from 2 to 16 days. The cardiac index (synonymous with device output) ranged from 2.4 to 3.4 L/min/m2. No embolic events (cerebrovascular or systemic) occurred during assistance with the device. Minimal red cell hemolysis was documented during the period of support. The Novacor left ventricular assist device is a safe and effective bridge to cardiac transplantation in patients with refractory cardiogenic shock.     

Hemodynamic effects of dopamine in critically ill septic patients.

The hemodynamic effects of various doses of dopamine were studied in 20 severely septic hypotensive patients, 18 of whom also had moderate or severe acute respiratory failure. Dopamine raised the mean arterial blood pressure in virtually all instances by an average of 21 mm Hg (+28%). This increase in blood pressure was brought about primarily by an increase in cardiac index (average +19%) with only a minimal average increase (3%) in the systemic vascular resistance index. There was little or no change in pulse rate, central venous pressure, pulmonary artery pressure, or pulmonary wedge pressure. Left heart function, as reflected by stroke work index increased significantly (+55%), but right ventricular stroke work index increased by only 17%, and the pulmonary vascular resistance index fell by an average of 3%.Dopamine appears to be a very useful agent for improving systemic blood pressure in hypotension complicating sepsis with little or no adverse effects on the lungs or pulmonary hemodynamics.     

Cardiac Depression in Bacteremia

Hemodynamic and respiratory effects of a 5-hr IV infusion of Ps. aeruginosa at a dose of 10(8) organisms per ml per minute were studied in 6 dogs. Four dogs served as controls. Gramnegative bacteremia, with 70,000 +/- 1,800 organisms per ml of blood, caused a 50% reduction of cardiac output at three hrs. Peripheral vascular resistance increased significantly, but mean heart rate fell below control levels. Decline in mean systemic blood pressure from 150 +/- 5 mm Hg to 88 +/- 6 mm Hg was accompanied by a significant increase in pulmonary arterial wedge pressure with normal right atrial and pulmonary arterial pressures. Pulmonary vascular resistance also remained unchanged. With progression of the low output state and development of hypothermia, arteriovenous oxygen difference (A-V DO(2)) fell significantly. Despite a decline in functional residual capacity, venoarterial admixture diminished in the face of reduced pulmonary capillary perfusion, normal arterial Po(2) values, decline in body temperature and finally very narrow A-V DO(2). Histologically, ventricular myocardium revealed severe interstitial edema. It is concluded that myocardial dysfunction may occur early during gramnegative bacteremia, and formation of myocardial edema appears to be a significant contributing factor in myocardial failure.     

Anaphylaxis in the Monkey: Pulmonary Oedema after Pre-treatment with β-Receptor Stimulants

Aggregate anaphylaxis was induced in seven ovalbumin-sensitized monkeys, with high tires of ovalbumin specific haemagglutinating antibodies. After pretreatment with an intravenous (i.v.) injection of 0.25 mg/kg terbutaline (n = 6) or an infusion of isoprenaline (n = 1), anaphylactic shock was induced by i.v. challenge with specific antigen. Haemodynamics, regional blood flows, respiratory mechanics, blood gases and haematological changes were studied during the following 30 min. Severe shock developed following ovalbumin challenge and the cardiac output was reduced by a mean of 74%. Pulmonary vascular resistance increased 11-fold. Pulmonary dynamic compliance decreased, but there was only a minor increase in pulmonary resistance. Hypoxaemia and severe metabolic acidosis developed. Circulating platelets and leucocytes decreased markedly. Three animals died with fulminant pulmonary oedema. In conclusion, the reaction pattern was similar to that found in studies of monkeys that received no prior treatment. However, the occurrence of pulmonary oedema suggests that the effects of large doses of terbutaline on the heart, combined with the high pulmonary vascular resistance, resulted in more severe pulmonary changes than took place in untreated animals.     

Hemodynamic mechanisms in the development of pulmonary venous admixture (shunting)

Hemodynamics, oxygen transport and pulmonary venous admixture (shunting) were measured sequentially in 34 critically ill patients at times remote from therapy. Increased PVR occurred early, often before development of maximal hypotension and low cardiac output. The magnitude of the PVR increase was roughly related to the extent of the trauma and hemorrhage, the increase being greater in those who died. The increased PVR response was associated with acidosis during hypovolemia, increased central blood volume after volume deficits were restored, and the subsequent appearance of pulmonary shunting. We interpreted this pattern of events as follows: hemorrhage produced pulmonary vasoconstriction, acidosis and backup of blood behind the lesser circulation. The persistence of a high PVR resulted in redistribution of pulmonary blood flow, uneven flow in the microcirculation and subsequent ventilation-perfusion abnormalities, which is the major pathophysiologic problem underlying acute pulmonary insufficiency.     

Combined cardiac operation and carotid endarterectomy during aortic cross-clamping.

We present a surgical technique that we believe provides superior cerebral protection for simultaneous correction of carotid and cardiac pathology with low operative mortality and stroke rate. Our study population consists of 23 consecutive patients undergoing cardiac operation between August 1989 and April 1991 who also had associated critical (greater than 85%) carotid artery stenosis. Using 20 degrees C systemic hypothermia for cerebral protection, we performed simultaneous correction of both lesions during the aortic cross-clamp period, using continuous retrograde blood cardioplegia for myocardial protection. Mean patient age was 69.4 years; 83% were 65 years or older. Eighty-seven percent had angina, 35% had recent myocardial infarctions (within 30 days), and 52% had congestive heart failure. Asymptomatic bruit was found in 39%, and 61% had previous strokes, neurologic symptoms, or both. All had 85% or greater luminal narrowing on cerebral angiography, with 65% having severe or critical contralateral disease as well. Sixty-one percent had associated other vascular pathology, including peripheral vascular occlusive disease, renal artery stenosis, or abdominal aortic aneurysm. There were no postoperative strokes or neurologic events. One early vein graft occlusion resulted in postoperative myocardial infarction and subsequent death (4.3%).     

Ventilating the patient with severe asthma: nonconventional therapy

Conventional pharmacotherapy of severe asthma and status asthmaticus includes beta2-sympathomimetics, theophylline, corticosteroids and occasionally topical anticholinergics (ipratropium bromide). Since hypoxemia is the most severe phenomenon in status asthmaticus the administration of oxygen is mandatory. However, if the bronchodilating therapy fails and hypoxemia continues, usually respiratory failure develops due to progressive respiratory muscle failure. An increasing PaCO(2) and respiratory acidosis are indications for mechanical ventilatory support to unload the failing respiratory pump. Nowadays, there is increasing consensus that ventilatory support should be administered primarily as non-invasive ventilation (NIV) via a face mask1. However, in a significant number of patients with severe asthma NIV is either contraindicated or insufficient. In this case usually the patient must be endotracheally intubated and mechanically ventilated "invasively". Intubation and ventilation of patients with severe asthma or status asthmaticus is associated with a high incidence of complications compared to patients ventilated for other causes of respiratory failure2,3. Therefore the risks of invasive mechanical ventilation have to be weighted carefully to ongoing conservative therapy and NIV. Cardiopulmonary arrest and severe hypoxemia in spite of O2 supplement and NIV are absolute criteria for intubation and ventilation. Mostly deterioration in mental status and exhaustion are the clinical findings leading to mechanical ventilation. Decision is guided rather by the course of the deterioration (how fast the patient's condition is worsening) than by pathological values alone. An increased PaCO(2) with moderate respiratory acidosis alone is not per se an indication for mechanical ventilation. However, a continuously rising PaCO(2) or the development of a severe metabolic acidosis after 1 hour of NIV is a strong argument for invasive mechanical ventilation. Other criteria are evidence of cardiac failure with fall in pulse volume and dysrhythmias, pneumomediastinum or pneumothorax (which has to be drained before mechanical ventilation!).     

Troponin in critically ill patients

Assays of cardiac troponin have become a cornerstone in the diagnosis of myocardial infarction across a broad range of clinical settings. In critically ill patients, cardiac troponin is detectable in the plasma in up to 60% of cases, and this incidence may increase further as assays become more sensitive. Troponin rises in critical care are commonly unrelated to pathology in the coronary arteries, but are frequently associated with conditions such as sepsis and respiratory failure. Such non-coronary troponin release is a significant, independent predictor of poor patient outcomes, and can be incorporated into risk scoring systems. Despite adding prognostic value, treatment for non-coronary troponin rises remains limited to management of the underlying cause, and restoration of a favourable balance between myocardial oxygen demand and supply. Conversely, troponin rises secondary to myocardial infarctions are amenable to the same interventions as in any other setting, albeit with additional diagnostic and therapeutic challenges. In this review, we will explore the utility of troponin as a biomarker in critical care, and we will outline a pragmatic management strategy for this patient population.