Chronic intermittent hypercapnic hypoxia increases pulmonary arterial pressure and haematocrit in rats.

Sleep-disordered breathing is associated with pulmonary hypertension and raised haematocrit. The multiple episodes of apnoea in this condition cause chronic intermittent hypoxia and hypercapnia but the effects of such blood gas changes on pulmonary pressure or haematocrit are unknown. The present investigation tests the hypothesis that chronic intermittent hypercapnic hypoxia causes increased pulmonary arterial pressure and erythropoiesis. Rats were treated with alternating periods of normoxia and hypercapnic hypoxia every 30 s for 8 h per day for 5 days per week for 5 weeks, as a model of the intermittent blood gas changes which occur in sleep-disordered breathing in humans. Haematocrit, red blood cell count and haemoglobin concentration were measured each week and systemic and pulmonary arterial blood pressure and heart weight were measured after 5 weeks. In relation to control, chronic intermittent hypercapnic hypoxia caused a significant increase in systemic (104.3+/-4.7 mmHg versus 121.0+/-10.4 mmHg) and pulmonary arterial pressure (20.7+/-6.8 mmHg versus 31.3+/-7.2 mmHg), right ventricular weight (expressed as ratios) and haematocrit (45.2+/-1.0% versus 51.5+/-1.5%). It is concluded that the pulmonary hypertension and elevated haematocrit associated with sleep-disordered breathing is caused by chronic intermittent hypercapnic hypoxia.     

A case of acute massive pulmonary embolism successfully treated with transvenous pulmonary embolectomy by catheter

A 78-year-old woman, suffering from acute massive pulmonary embolism, was successfully treated with transvenous pulmonary embolectomy by catheter. This patient had been suffering from oppressive chest sensations during exercise, and diagnosed and treated as angina pectoris at a nearby clinic. She consulted our hospital complaining that her chest pains were increasing in frequency. She was admitted to our hospital on July 7, 1988, for coronary angiography (CAG), which she underwent on July 8 by the right femoral approach. After the CAG, she was ordered to rest in bed overnight, with the right inguinal region compressed. 18 hours later, the compression was removed and she was allowed to walk. Soon after she walked to the toilet, she complained of chest discomfort and fell into shock (systolic blood pressure was 60 mmHg). An ECG examination showed a right bundle branch block and an inverted T wave in lead V1-3. An echocardiography showed normal contraction of the left ventricle, but an enlargement of the right ventricle and a flattened interventricular septum. An analysis of arterial blood gas showed hypoxia (Pao2 52.5 mmHg, Paco2, 30.9 mmHg). Acute pulmonary embolism was suspected. 240,000 units of urokinase were administered intravenously, and pulmonary angiography was performed immediately. It revealed that the bilateral pulmonary arteries were almost completely obstructed. Although 720,000 units of urokinase were infused into the pulmonary artery, the obstruction did not improve. At that time, we performed a transvenous pulmonary embolectomy. We used a Judkins R 4 guiding catheter for PTCA made by USCI. The catheter was inserted into the pulmonary artery and clots were aspirated with a syringe.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of acute respiratory failure on plasma renin activity and plasma angiotensin II level in advanced chronic obstructive pulmonary disease and chronic cor pulmonale

Plasma renin activity (PRA) and plasma angiotensin II (PAT II) level were determined with the method of radioimmunoassay in 55 patients with advanced chronic obstructive pulmonary disease (COPD) and chronic cor pulmonale (41 of them had respiratory failure) and 12 healthy aged persons. The results showed that PRA and PAT II levels were significantly elevated in the presence of such factors as severe hypoxia and hypercapnia (PaO2 less than or equal to 45 mmHg, mean 40 mmHg, PaCO2 greater than or equal to 65 mmHg), right heart failure, acidosis, hyponatremia and hypochloremia. It is shown that the prognosis would be poor when the patient's PRA level is significantly elevated.     

Influence of acute respiratory failure on renal function in advanced chronic obstructive pulmonary disease and chronic cor pulmonale

Renal function was assessed in 89 patients with advanced chronic obstructive pulmonary disease and chronic cor pulmonale, 62 of them had respiratory failure, 18 health aged served as control. The results showed that the creatinine clearance and the free water clearance were decreased in 82.3% and 69.5% of patients with respiratory failure respectively. The renal function was impaired in case of hypoxia, PaO2 less than or equal to 6.0 kPa (45 mmHg), mean 5.33 kPa (40 mmHg). Hypercapnia was one of the most important factors that effected the renal function. There was a clinical threshold which effected the renal function, i.e. PaCO2 equals more than 8.67 kPa (65 mmHg). Renal function was greatly impaired if hypercapnia and hypoxia exist at the same time. The impairment of renal function was further marked when right heart failure and acidosis developed. The causes and effects of the abnormality of renal function were preliminarily discussed.     

Influence of phasic volume feedback on abdominal expiratory nerve activity

Our purpose was to examine the influence of phasic lung volume feedback on the activities of motor nerves innervating the diaphragm and transversus abdominis muscles during hypercapnia and hypoxia. We studied seventeen decerebrate cats that were paralyzed and ventilated with a servo-respirator controlled by the integrated phrenic neurogram. The effects of phasic lung volume feedback were assessed by withholding pulmonary inflation during the central inspiratory period. Withholding lung inflation for a single respiratory cycle under hyperoxic, normocapnic conditions consistently prolonged the durations of the inspiratory and expiratory periods, and caused marked increases in the peak electrical activities of both phrenic and abdominal nerves. Hyperoxic hypercapnia (PaCO2 50-80 mmHg) and isocapnic hypoxia (PaO2 60-35 mmHg) increased peak phrenic and abdominal neural activities, and withholding pulmonary inflation under these conditions caused even greater augmentations of inspiratory and expiratory motor output. The augmentation of expiratory activity by withholding lung inflation was proportionately greater than the concomitant prolongation of the central expiratory period. All responses to non-inflation maneuvers were abolished following bilateral cervical vagotomy. The results indicate that vagally mediated volume feedback during inspiration can attenuate the output of abdominal motoneurons in the subsequent expiratory period. Moreover, hypoxia, which attenuates abdominal motor activity in vagotomized animals, enhances this activity when the vagi are intact.     

Respiratory patterns in anesthetised rats before and after anemic decerebration.

Experiments were undertaken to test the comparability of changes in respiratory frequency and tidal volume during hypoxia and hypercapnia in rats with and without intact peripheral chemoreceptors and with intact vagi. Neural organisation of respiratory control was perturbed by anemic decerebration, achieved by ligation of the common carotid and basilar arteries. Ischemia of the brain was produced as far candal as the rostral pontine nuclei involved in respiratory control but left the medulla well perfused. The dominant respiratory effect in animals breathing air or oxygen was polypnea with hypocapnia (mean PaCO2 when breathing air 24.7 mmHg, when breathing oxygen 29.6 mmHg). After decerebration the increase of ventilation produced by breathing 10% O2 in N2 was reduced compared with responses in the intact state but levels of ventilation (V1) in hypoxia were similar to those before decerebration. After decerebration, the increase of ventilation produced by breathing 5% CO2 was greatly reduced and the level of V1 in animals breathing CO2 was significantly less than in the intact state. Intermediate changes were seen in animals breathing 2-3% CO2 which converted the hypocapnia (PaCO2 30.9 mmHg) to eucapnia (PaCO2 46.4 mmHg). In the intact state, hypoxia dominantly caused increased frequency (f) and hypercapnia caused increased tidal volume (VT); after decerebration, hypoxia produced reduction of VT while hypercapnia produced reduction of f. Bilateral carotid sinus nerve section in decerebrate animals eliminated the ventilatory response to hypoxia but left the responses to hypercapnia unaltered. The results point to differences in the mechanisms by which hypoxia and hypercapnia influence respiration in both intact and decerebrate animals with carotid sinus and vagus nerves functional. The differences can now be interpreted in terms of specific neural features of respiratory control.     

Hypercapnic acidosis and compensated hypercapnia in control and pulmonary hypertensive piglets

Low tidal volume/inspiratory pressure ventilator strategies result in hypercapnia, which has been shown to increase pulmonary vasomotor tone. This may be particularly detrimental in infants and children with preexistent pulmonary hypertension. In this study, a piglet model of chronic hypoxia-induced pulmonary hypertension was used to test the hypotheses that: 1) the effects of hypercapnic acidosis are exaggerated by preexistent pulmonary hypertension; and 2) the pulmonary hemodynamic effects of hypercapnic acidosis are attenuated by normalizing pH. Pulmonary hypertension was induced by 2 weeks of hypoxia. Hemodynamic responses were measured in control and pulmonary hypertensive piglets during both normoxia and hypoxia under normocapnic, hypercapnic acidotic, and compensated hypercapnic conditions. We found that: 1) hypercapnic acidosis increased both normoxic and hypoxic pulmonary vascular resistance index (PVRI) in control piglets; 2) the pressor effects of hypercapnia were not attenuated by infusing bicarbonate to normalize the pH; and 3) piglets with chronic hypoxia-induced pulmonary hypertension had elevated baseline normoxic and hypoxic PVRI, but responded to hypercapnic acidosis and compensated hypercapnia in a similar way to control piglets. These data suggest that acute hypercapnic acidosis may have deleterious effects on the pulmonary hemodynamics of normal and pulmonary hypertensive subjects which may not be acutely reversed by buffering the pH.     

Role of the Autonomic Nervous System in the Acute Blood Pressure Elevation during Repetitive Hypoxic and Hypercapnic Breathing in Rats

Acute intermittent repetitive hypoxia simulating sleep apnoea syndrome is responsible for acute rises in blood pressure (BP). In the rat, the BP rises are enhanced by added hypercapnia. To investigate the role of the autonomic nervous system (ANS) in acute hypertension during repetitive hypoxia alone, FiCO₂ (inspiratory fractional concentration of oxygen) 2 to 5%, or combined with hypercapnia FiCO₂ (inspiratory fractional concentration of carbon dioxide) 2 to 5%, we used autonomic blockade by atropine (1 mg kg¹) + propranolol (1 mgkg¹) + phentolamine (1 mgkg^-1). Seven Wistar male rats were chronically instrumented with two aortic and venous catheters. Repetitive administration of N₂ and N₂ + C0₂ for 10s followed by 20 s compressed air was repeated for 4-5 min before (control) and after autonomic blockade. After autonomic blockade there was no significant difference in mean blood pressure (MBP) during severe hypoxia (SHO) (14.9 ± 0.5 mmHg) compared to control (10.5 ± 0.9 mmHg), while MBP was significantly decreased in severe hypoxia + hypercapnia (SHOHC) (14.1 ± 0.4 mmHg) compared to control (26.8 ± 0.3 mmHg) (p 0.001). We conclude that the acute BP rise observed during hypoxic breathing is not due to the activation of ANS, but when hypercapnia is added to the hypoxic stimulus about half of pressor response is caused by ANS.     

AaDO2 as a predictor of pulmonary hypertension resulting from pulmonary emboli

The authors examined the records of all patients referred for right heart catheterization between 1963-84 because of persistent dyspnoea after one or more episodes of pulmonary emboli. Patients with a history of congestive heart failure, angina, restrictive or obstructive pulmonary disease that could explain their symptoms were excluded. Catheterization was performed 15.8 +/- 24 months after the first suspected episode of pulmonary embolism. Seven of the 29 patients included had resting pulmonary hypertension (PH). All of these had an alveolo-arterial oxygen difference (AaDO2) greater than 25 mmHg. Twenty patients of the group, taken as a whole, had an AaDO2 greater than 25 mmHg. Information was available from 1 month to 5 years later in 6/9 patients with an AaDO2 less than 25 mmHg. In all of them dyspnoea improved or resolved. Information was available in 15/20 patients with AaDO2 greater than 25 mmHg. Three of 8 patients without PH but with an increased AaDO2 on the initial catheterization developed PH within 2 years. Dyspnoea increased in 1 of the remaining five. Four patients who initially had PH developed right heart failure 6 months-3 years later. In the remaining 3, dyspnoea was stable in 1, increased in 1 and one patient died with autopsy evidence of multiple pulmonary emboli. Abnormal oxygenation predicts the presence or subsequent development of PH in patients who are chronically dyspnoeic after pulmonary embolism.     

Mechanical properties of the rabbit upper airway during hypoxia and hypercapnia

It has been suggested that the response of upper airway muscles to hypoxia may be different from the response of these muscles to hypercapnia. We therefore measured pulmonary ventilation and the mechanical properties of the isolated upper airway in 9 anesthetised rabbits during respiration of hypoxic and hypercapnic gas mixtures. Each animal was exposed to several levels of elevated inspiratory CO2 fraction, FICO2 (0.03 to 0.17) and depressed inspiratory O2 fraction, FIO2 (0.19 to 0.09). The steady-state ventilatory response, the tidal pressure in the upper airway (PTUA) and the upper airway elastance were measured under each condition. Straight lines were calculated by least squares regression relating pulmonary VT to FICO2 and FIO2 and PTUA to FICO2 and FIO2. The PTUA was estimated graphically at two levels of hypoxia and hypercapnia producing equal augmentation of VT. The ratio of PTUA during hypoxia to PTUA during hypercapnia was 1.06 +/- 0.21 (mean +/- 95% C.I.) at low VT and 1.15 +/- 0.25 at high VT. Elastance of the upper airway rose from 6.25 +/- 1.13 cmH2O/ml under control conditions to a maximum of 7.95 +/- 1.24 cmH2O/ml (P less than 0.05) during hypercapnia and to a maximum of 8.02 +/- 1.17 cmH2O/ml (P less than 0.05) during hypoxia. There was no difference between the mean (+/- 95% C.I.) change associated with hypercapnia (1.64 +/- 1.08 cmH2O/ml) and the mean change associated with hypoxia (1.77 +/- 1.26 cmH2O/ml). We concluded that hypoxia did not result in a greater change in upper airway mechanical properties than hypercapnia.     

Diagnosis and treatment of acute pulmonary embolism in 2010

Diagnostic approaches in acute pulmonary embolism include evaluation of clinical likelihood, D-dimers, echocardiography and spiral CT angiography and pulmonary scintigraphy. Determination of D-dimers is only meaningful in patients with low or intermediate clinical likelihood. It is safe not to initiate anticoagulation treatment (or to discontinue such treatment) in patients with low clinical likelihood of acute pulmonary embolism and negative D-dimer test (only if methods with 99-100% sensitivity are used). Duplex sonography and pulmonary scintigraphy are only necessary at the centres with a first generation spiral CT and not those with multidetector devices. Investigations in normotensive patients should include echocardiography that should also include assessment of the right ventricular function using echocardiography and determination of biomarkers of pulmonary embolism. Right ventricular dysfunction together with elevated troponins identifies a normotensive group at an increases risk. Highly sensitive troponin T (hsTnT) appears to be particularly valuable. Echocardiography reading might the decisive factor for treatment initiation in patients with massive acute pulmonary embolism. Negative or unclear echocardiography finding warrants spiral CT angiography (CTA). Ventilation/perfusion scan or pulmonary arteriography are recommendable in patients with unclear CTA finding and patients with high clinical likelihood of pulmonary embolism and negative CTA finding. A combination of CTA and CTV also appears useful as it increases the overall sensitivity of the investigation and enables imaging of pelvic veins. Thrombolytic treatment is indicated in haemodynamically unstable patients, patients with a high risk of a massive pulmonary embolism associated with cardiogenic shock or hypotension (systolic pressure below 90 mmHg or a decrease in systolic pressure by > 40 mmHg) or symptoms of acute right-sided heart failure. Thrombolytic treatment is also indicated in pulmonary embolism not receding following heparin treatment, in recurring or expanding pulmonary embolism, in the presence of thrombi in the right heart and in patients with right-to-left shunting through patent foramen ovale. This treatment should also be considered in patients with submassive pulmonary embolism associated with a dysfunction of the right ventricle and increased troponins, and particularly in patients lacking even a relative contraindication of thrombolytic treatment. A thrombolytic of choice is alteplase. Embolectomy or catheterization should be used if thrombolytic treatment is contraindicated or ineffective. Long-term monitoring of massive and submassive acute pulmonary embolism is highly recommended. Low molecular weight heparins or unfractioned heparin or fondaparinux are used in haemodynamically stable patients.     

Lack of positive interaction between CO2 and hypoxic stimulation for P(CO2)-VAS response slope in humans

To compare the effect of hypoxia on ventilatory responses and respiratory sensation to carbon dioxide, 29 young adults were examined using a modified Read's rebreathing method with four experimental conditions. We used varying gas mixtures and kept PET(O2) constant at >300, 100, 80 and 60 mmHg for each four rebreathing tests. Respiratory sensation was measured by visual analog scale (VAS). The slope of the CO2-ventilation response curve increased significantly with hypoxia, confirming a positive ventilatory interaction between hypoxia and hypercapnia. However, the slope of the CO2-VAS response curve remained unchanged. The V(E)-VAS relation slope tended to become depressed with advancing hypoxia, i.e. the magnitude of VAS elicited by a given ventilation decreased with hypoxia, signifying that dyspneic sensation was effectively mitigated during hypoxic hyperventilation. We suggest that this relief of dyspneic sensation might be due to the inhibitory respiratory effect from augmented pulmonary stretch receptor (PSR) activity.     

Nitrendipine attenuates the pulmonary vascular remodeling and right ventricular hypertrophy caused by intermittent hypoxia in rats

We designed experiments to determine whether intermittent hypoxia would produce significant pathologic and physiologic changes in rats and whether pretreatment with a calcium channel blocker, nitrendipine, would reduce the pulmonary vascular remodeling and right ventricular hypertrophy caused by intermittent hypoxia. Intermittent exposure to hypobaric hypoxia (0.5 atmospheres) 10 h a day for 30 days increased the hematocrit (65 +/- 1 versus 42 +/- 1%, mean +/- SEM), right ventricular systolic pressure (33 +/- 1 versus 20 +/- 1 mmHg), and right ventricular weight adjusted for body weight (RV/BW) (126 +/- 6 versus 60 +/- 2 mg/100 g) in male Sprague-Dawley rats. Intermittent hypoxia also increased the percentage of small pulmonary vessels with muscle (76 +/- 3 versus 19 +/- 5%) and the thickness of the vessel wall as a percentage of the total vessel diameter (34 +/- 1 versus 22 +/- 1%). Nitrendipine (10 mg/kg) prevented the acute increase in right ventricular systolic pressure caused by hypoxia. Chronic treatment with nitrendipine (10 mg/kg given twice a day by gavage for 30 days) significantly reduced the increase in hematocrit (61 +/- 1 versus 65 +/- 1%), right ventricular systolic pressure (29 +/- 1 versus 33 +/- 1 mmHg), and RV/BW (108 +/- 4 versus 126 +/- 6 mg/100 g) caused by hypoxia. Chronic treatment with nitrendipine also reduced the percentage of small pulmonary vessels with muscle (38 +/- 8 versus 76 +/- 3%) and prevented the increase in vessel wall thickness (20 +/- 2 versus 34 +/- 1%). Thus, nitrendipine treatment significantly reduces the right ventricular hypertrophy and pulmonary vascular changes caused by intermittent hypoxia.     

Abnormal troponin I levels in acute pulmonary embolism without abnormal concentrations of D-dimer at admission

Serum troponin I is a sensitive indicator of myocardial damage but abnormal troponin I levels have been reported without acute coronary syndrome and without cardiac damage. It has been reported that right ventricular overload and hypoxia in acute pulmonary embolism may lead to right ventricular myocardium injury reflected by elevated cardiac troponin levels and that in patients with acute central sub-massive or non-massive pulmonary embolism, even mild increase in troponin I >0.03 mug/L may provide relevant short-term prognostic information independent to clinical, laboratory and echocardiographic data. It has also been reported that patients with acute small pulmonary embolism might present with relatively low concentrations of D-dimer and it might have implications regarding the diagnostic yield of D-dimer in patients who are suspected of having an acute pulmonary embolism. We present a case of abnormal troponin I levels without abnormal concentrations of D-dimer at admission in a 26-year-old Italian man with acute pulmonary embolism. Also this case focuses attention on the importance of a correct evaluation of abnormal troponin I levels and not elevated D-dimer levels in acute pulmonary embolism.     

Pulmonary arterial flow-pressure characteristics in dogs--effects of hypoxia and nitroglycerin.

To investigate the effects of hypoxia and nitroglycerin on pulmonary vascular tone, multipoint mean pulmonary arterial flow-pressure (Q-P relationship) plots were constructed by producing stepwise increments of pulmonary flow with a roller pump installed in a right ventricle-pulmonary artery shunt in 12 mongrel dogs under pentobarbital sodium anesthesia. The normal Q-P relationship was convex to the pressure axis when pulmonary flow was 0-0.2 L/min, but it became linear when pulmonary flow was over 0.2 L/min. The slopes and pressure intercepts extrapolated (RAPI) from linear regression fits to the linear parts of the Q-P relationship were determined to compare the effects of hypoxia and nitroglycerin on pulmonary vascular tone. Hypoxic ventilation (FIO2: 0.1) increased the slope from 8.3 +/- 3.3 to 12.5 +/- 3.6 mmHg/L (p less than 0.01), with no significant effect on PAPI. Nitroglycerin (1 microgram/min/kg as a continuous infusion) decreased the slope from 8.9 +/- 4.4 to 5.8 +/- 2.6 mmHg/L (p less than 0.05), again with no significant effect on PAPI. The results suggest that hypoxia and nitroglycerin, respectively, increased and decreased incremental pulmonary vascular resistance upstream to the site of pulmonary vascular closure.     

Does saddle embolism influence short-term prognosis in patients with acute pulmonary embolism?

BACKGROUND: In some patients with acute pulmonary embolism (APE) thrombi may lodge at the levels of the bifurcation of pulmonary trunk and extend into both main pulmonary arteries, forming so-called saddle embolism (SE). AIM: To assess the incidence of SE and whether it is associated with an increased risk of complicated clinical course. METHODS: We studied 150 consecutive patients (94 females, 56 males) aged 63.6+/-16.7 years with APE confirmed with contrast enhanced spiral computed tomography or transesophageal echocardiography. RESULTS: SE was detected in 22 (14.7%) patients. Mean age (SE vs N-SE) was 64.3+/-17.4 vs 63.5+/-16.6 years, heart rate 100.8+/-14.1 beats/min vs 97.8+/-21.1 beats/min, systolic blood pressure 126.2+/-20.1 vs 127.1+/-23.3 mmHg and blood pulsoximetry 92 (68-98) vs 91 (30-98) % (all differences NS). In patients with SE, echocardiographic signs of the right ventricular overload, defined as right to left ventricular end - diastolic ratio >0.6 with right ventricular hypokinesia and/or maximal tricuspid peak systolic gradient >30 mmHg with shortened acceleration time of pulmonary ejection <80 ms, were more frequent (77.3% vs 51.6%, p=0.04), as was the mid-systolic deceleration of pulmonary ejection velocity (77.3% vs 49.2%, p=0.04). Mortality and complicated clinical course rates were similar in patients with SE or N-SE (mortality: 4.5% vs 13.3%, NS, and complicated clinical course: 34.4% vs 25.0%, NS). CONCLUSIONS: Saddle pulmonary embolism is frequent, especially in patients with echocardiographic signs of impaired pulmonary ejection pattern. Saddle embolism does not indicate unfavourable clinical outcome and probably should not influence treatment selection.     

Dehydroepiandrosterone sulphate reduces chronic hypoxic pulmonary hypertension in rats.

Pathogenesis of pulmonary hypertension includes vascular smooth muscle cell membrane depolarisation and consequent calcium influx. Usually, calcium-gated potassium channels are activated under such conditions and repolarise the membrane. However, in pulmonary hypertension they are downregulated. The authors hypothesised that pharmacological augmentation of these channels would reduce pulmonary hypertension. Dehydroepiandrosterone sulphate (DHEA-S, 0.1 mg x mL(-1)), a recently characterised activator of calcium-gated potassium channels, was given to rats in drinking water. Pulmonary arterial blood pressure, increased by 4 weeks of hypoxia (from 15 +/- 0.2 to 29.4 +/- 2.5 mmHg), was selectively attenuated in rats treated with DHEA-S for the whole duration of the hypoxic exposure (23.9 +/- 0.9 mmHg) and in rats given DHEA-S only after pulmonary hypertension had fully developed (last 2 weeks of hypoxia; 24.4 +/- 1.4 mmHg). Pulmonary vascular remodelling and right ventricular hypertrophy associated with pulmonary hypertension were also reduced by DHEA-S. Cardiac index and systemic arterial blood pressure did not differ among the groups. The authors conclude that treatment with an activator of calcium-gated potassium channels, dehydroepiandrosterone sulphate, known to be well tolerated by humans, reduces hypoxic pulmonary hypertension in rats.     

Treatment of shock in a canine model of pulmonary embolism

Despite the high mortality (greater than 30%) associated with hypotension complicating pulmonary embolism, previous studies have not systematically investigated how best to treat shock resulting from pulmonary embolism. In 24 dogs, we measured relevant hemodynamic parameters before and after shock was produced by intravenously injected autologous blood clots. When systemic blood pressure fell to 70 mmHg, dogs were randomly divided into groups and treated blindly for 1 h. All control dogs and all dogs treated with volume and isoproterenol died. In contrast, all dogs treated with noradrenaline were resuscitated and remained hemodynamically stable for 1 h. This effect of noradrenaline was significant (p less than 0.01, Fisher's exact test). Noradrenaline improved right ventricular performance by increasing blood pressure and improving right ventricular perfusion and/or by a direct increase in contractility. We conclude that in a canine model of pulmonary embolism and shock, noradrenaline may be the drug of choice for acute resuscitation.     

Troponin levels as a guide to treatment of pulmonary embolism

Right ventricular dysfunction in hemodynamically stable patients with acute pulmonary embolism may be a harbinger of adverse outcomes and may potentially result in the early use of thrombolytic therapy. Risk stratification of these patients is an area of recent and intense investigation with a focus on the assessment of right ventricular function after the embolic event. Echocardiography has been used to identify right ventricular dysfunction but is potentially hampered by a number of limitations. With the onset of right ventricular dilation and possible ischemia in acute pulmonary embolism, elevated serum troponins may be an early and reliable marker of right ventricular dysfunction. In acute pulmonary embolism, both right ventricular dysfunction by echocardiogram and elevated troponin levels have been shown to predict an adverse outcome. Therefore, serum troponin levels should help stratify patients with submassive acute pulmonary embolism into a group in which aggressive medical or surgical intervention would be considered.     

溶栓与单纯抗凝治疗急性次大面积肺栓塞的疗效及安全性

目的：探讨溶栓与单纯抗凝治疗急性次大面积肺栓塞患者的疗效与安全性。方法：63例急性次大面积肺血栓栓塞症患者,被随机分为溶栓组（n＝32）与单纯抗凝组（n＝31）。观察两组治疗前与治疗2周后动脉血气指标及右心功能指标变化,进行疗效分析。统计两组出血、血小板减少发生情况。结果：治疗后两组动脉血气指标及右心功能指标较治疗前显著改善（P＜0.05或＜0.01）;与单纯抗凝组比较,溶栓组动脉血氧分压[PaO2,（77.8±7.3）mmHg比（83.4±8.7）mmHg]、右室前壁活动度[RVAWM,（4.9±1.7）mm比（5.8±2.2）mm]显著上升,肺泡-动脉血氧分压差[P （A-a）O2,（23.1±2.8）mmHg比（16.5±2.4）mmHg]、肺动脉收缩压[PASP,（54.6±7.9）mmHg比（34.2±7.5）mmHg]显著下降（P＜0.05或＜0.01）。溶栓组总有效率显著高于单纯抗凝组（100％比80.6％,P＝0.002）。两组出血发生率及血小板减少发生率无统计学差异（P＞0.05）。结论：溶栓治疗可显著降低急性次大面积肺栓塞患者的肺动脉压力,改善氧合及右室功能指标,无禁忌患者可考虑优先推荐。