先天性心脏病术后合并肺动脉高压心导管检查及急性肺血管扩张试验分析

目的:探讨先天性心脏病术后(CHD-PO)合并肺动脉高压(PAH)患者,行心导管检查及急性肺血管反应试验的临床价值。方法:研究选自2008年8月至2015年12月,收住北京安贞医院小儿心脏科,行左、右心导管检查及急性肺血管扩张试验的CHD-PO合并PAH的患者,监测血流动力学指标变化。结果:入选40例患者,男性11例(27.5%),女性29例(72.5%),年龄6.61~45.51岁,平均年龄(23.6±9.3)岁,中位手术年龄13.4岁;平均纽约心功能(NYHA)分级(1.88±0.68)[I~II/III~IV,33例(82.5%)/7例(17.5%)],术后最短行心导管检查的时间为0.5年,最长为25.4年,中位时间为3.0年。术中无肺动脉高压危象发生,无低血压现象,其中1例急性肺血管扩张试验阳性。心导管检查:基础状态下,平均肺动脉压力(MPAP)为(58.30±21.32)mm Hg(1mm Hg=0.133k Pa),肺小动脉阻力指数(PVRI)为(16.67±11.64)Wood U·m2,肺动脉收缩压/主动脉收缩压(PP/PS)为(0.75±0.25),肺循环阻力/体循环阻力(RP/RS)为(0.63±0.28),所有患者均被证实仍残存肺动脉高压。吸入伊洛前列素(Iloprost)后,肺动脉收缩压(SPAP)、MPAP、主动脉收缩压(SAOP)、PVRI、RP/RS降低,心指数(CI)增加,且均有显著临床意义(P0.05);平均主动脉压(MAOP)、体循环阻力指数(SVRI)降低,但无明显临床意义。结论:CHD合并重度PAH丧失最佳手术时机的患者,行心脏矫治术后,术后远期随访证实肺动脉压力仍未降至正常,需要长期随访及靶向药物治疗。CHD-PO合并PAH患者,与IPAH相比,其肺血管反应差,心导管检查过程中肺动脉高压危象发生率低。雾化吸入伊洛前列素(Iloprost),在增加或者维持CI不变的前提下,具有良好降低肺循环阻力及压力的作用。     

吸入伊洛前列素在儿童先天性心脏病肺血管扩张试验中的应用

目的:该研究在心导管检查中通过对先天性心脏病(CHD)合并肺动脉高压(PAH)儿童,吸入伊洛前列素前后的血流动力学参数的测定,评价吸入伊洛前列素在CHD相关性PAH儿童急性肺血管扩张试验的安全性、有效性。方法:研究选择2007年6月至2010年5月,于北京安贞医院小儿心脏科住院的左向右分流型CHD合并重度PAH患儿,所有患儿行左、右心导管检查,并采用雾化吸入伊洛前列素,监测吸药前后血流动力学参数改变及不良反应。结果:该研究入选43例左向右分流型CHD合并重度PAH患儿,年龄(8.52±4.76)岁。吸入伊洛前列素后肺动脉平均压由(77.14±12.14)mmHg(1 mmHg=0.133 kPa)降至(69.35±12.14)mmHg(P<0.05);肺体循环血流量比值(Qp/Qs)由1.80±1.26升至3.06±2.90(P<0.05);肺血管阻力指数(PVRI)下降约5 Wood unit.m2〔吸入前(14.51±8.46)Wood unit.m2,吸入后(9.58±7.43)Wood unit.m2,P<0.05),体循环血压无明显变化〔吸入前(83.16±13.69)mmHg,吸入后(83.09±11.03)mmHg,P>0.05〕。以吸入伊洛前列素后PVRI较基础水平下降至少20%以上作为急性肺血管扩张试验阳性标准。肺血管反应阳性患儿31例,占72%,阴性反应患儿(PVRI下降<20%)12例,占28%。结论:对左向右分流型CHD合并重度PAH儿童在心导管检查中吸入伊洛前列素可明显降低肺血管阻力,体循环血压无明显变化,无明显不良反应发生,可作为安全有效的急性肺血管扩张试验的用药。     

102例肺高压临床特点及严重度评估分析

目的 分析2003年4月至2011年12月间复旦大学附属中山医院收治的临床诊断肺高压患者102例的临床特点及评估其严重度.方法 采用回顾性方法分析肺高压的好发年龄,病因分布,临床症状,超声心动图及右心导管检查结果的相关性及其对疾病严重度的评估.结果 肺高压中女性患者占多数为72.5％,其发病的峰值年龄段为中青年.肺高压的主要症状为活动后气促(81.4％),静息或活动时胸闷(51.9％).病因前三位为:特发性肺高压49例(占48.0％),先天性体-肺分流19例(占18.6％),慢性肺血栓栓塞10例(占9.8％).用超声心动图法测定的肺动脉收缩压(sPAP)与“金标准”右心导管法比较,在绝对数值上存在差异:数值之差(绝对值)为1～10 mm Hg的占33.4％,11～20 mmHg占33.3％,≥21 mm Hg占33.3％.两法经直线回归分析,相关系数r=0.634(P＜0.01).9例经右心导管测压证实为轻～中度肺高压中,超声心动图结果均为高估.但超声心动图在判断重度肺高压时准确性高,其与右心导管的一致性高达95.23％.结论 超声心动图与右心导管检测的一致性较好,它是诊断肺高压的重要线索.超声检查阴性预测值高,阴性基本可排除肺高压诊断.超声判断重度肺动脉高压准确性高.超声判断的轻～中度肺高压需结合病史、症状、生化指标等综合分析,必要时推荐行右心导管检查.     

肝肺综合征

肝肺综合征 (ｈｅｐｔａｏｐｕｌｍｏｎａｒｙｓｙｎｄｒｏｍｅ ,ＨＰＳ)指慢性肝功能不全患者因肺内血管扩张而出现的严重低氧血症 ,是各种慢性肝脏疾病终末期的一种严重并发症 ,发病率为 5 %～ 2 9%,预后差 ,呈三联征的特点 ,即基础肝脏疾病 -肺血管扩张 -严重低氧血症 ,其中基础肝脏疾病主要包括各种原因的肝硬化和慢性肝功能不全以及非肝硬化性门脉高压和肝外门静脉阻塞等。Ｒｒｏｗｋａ[1] 指出 ,发生ＨＰＳ的决定因素是门静脉高压而不是广泛性肝细胞坏死。严重低氧血症是由于肺内血管扩张、通气血流比例 (Ｖ/Ｑ)失调所致动脉血氧合功…     

肺高压的诊断和治疗策略

<正>肺高压(pulmonary hypertension,PH)是由不同病因导致的,以肺动脉压力和肺血管阻力升高为特点的一组病理生理综合征,往往导致右心负荷增加、右心衰竭甚至死亡。肺高压包括肺动脉高压(pulmonary arterial hypertension,PAH)、肺静脉高压和混合性肺高压3种,目前肺高压的诊断标准是在海平面、静息状态下,右心导管检查肺动脉平均压     

肺动脉高压患者经左前臂行标准右心导管检查科学性的探讨

目的:探讨经左前臂行右心导管检查的科学性。方法:本研究对所有在我科就诊的疑诊肺血管病患者行右心导管检查,首选经肘前静脉穿刺,穿刺失败改为颈内静脉。需要围手术期监测肺动脉压者直接行右侧颈内静脉穿刺。结果:110例患者经肘前静脉穿刺,穿刺置入鞘管成功者为106例(96.4%),置入鞘管成功后完成右心导管检查者为104例(94.5%);6例患者经颈内静脉穿刺,均成功置入鞘管,顺利完成右心导管检查。结论:右心导管检查操作简便,安全性高,尤其经左侧肘前静脉进行右心导管检查操作简便,并发症发生率低,术后患者痛苦小,可以作为右心导管的检查路径。     

肺动脉高压患者心室重构的超声心动图指标与肺阻力的相关性研究

正中国循环杂志,2017,32(2):161-164.该文研究肺动脉高压患者的双心室重构形态特点与肺小动脉阻力的相关性,探讨心室形态指标对肺小动脉阻力升高8.5 Wood的预测价值。方法:收集2012年10月至2014年1月间接受右心导管检查明确诊断为肺动脉高压的患者61例(肺动脉高压组),正     

射血分数降低的心力衰竭患者高肺血管阻力的临床特征和危险因素分析

目的:分析射血分数降低的心力衰竭(HFrEF)患者高肺血管阻力(PVR)的临床特征和危险因素.方法:连续纳入2017年1月至2019年12月在我中心行右心导管检查的HFrEF患者共164例,收集患者的临床和右心导管检查数据.右心导管检查测得PVR≥5.0 Wood单位(WU)定义为PVR显著升高.采用Lasso-Log...     

心导管检查对小儿不同类型肺动脉高压的诊治价值分析

目的总结不同类型肺动脉高压患者心导管检查结果,分析其特点,为临床诊断及治疗提供参考。方法回顾性分析6例肺动脉高压患者的临床症状,心脏超声检查结果,心导管检查结果[包括肺动脉压力与主动脉压力比值、肺动脉阻力指数(pulmonary vascular resistance index,PVRI)、选择性肺小动脉造影(selective pulmonary arteriography,SPA)、肺循环时间(pulmonary circulation time,PCT)、急性肺血管扩张试验(acute pulmonary vasodilation test,AVT)等]以及治疗效果、随访等资料。结果患者1提示室间隔缺损合并动力型肺动脉高压。患者2为室间隔缺损合并非动力性肺动脉高压。患者3为特发性肺动脉高压。患者4为骨形成蛋白Ⅱ型受体(bone morphogenetic protein type Ⅱ receptor,BMPR2)相关性肺动脉高压。患者5及患者6分别为活化素Ⅰ型受体(activator type Ⅰ receptor,ACVR1)(c.789CA,p.D263E)及ACVR1(c.1450CT,p.R484W)相关性肺高压。结论心导管检查对于肺动脉高压诊断和治疗具有指导意义,特别是SPA对肺动脉高压分型具有一定诊断意义。     

经前臂静脉径路行右心导管检查和肺动脉造影的可行性研究

目的 探讨经前臂静脉径路进行右心导管检查及肺动脉造影的可行性和安全性.方法 本研究为多中心横断面临床研究,连续观察68例符合人选标准的疑诊肺血管病患者,采用前臂静脉径路进行右心导管检查及肺动脉造影.结果 经前臂静脉径路穿刺置入鞘管成功率为97.1%,成功完成右心导管检查和肺动脉造影成功率为91.2%.本组病例中有6例患者经前臂静脉径路未能完成右心导管检查,其中2例前臂静脉细小,3例患者存在左侧锁骨下静脉纤细,1例有前臂注射毒品史导致浅表静脉充盈差.仅有1例患者发生腋静脉分支出血和局部血肿的并发症.结论 经前臂静脉径路进行右心导管检查操作简便,并发症发生率低,术后患者舒适度高,建议作为右心导管和肺动脉造影可选的检查径路.     

The case for treatment of selected patients with primary pulmonary hypertension

The treatment of primary pulmonary hypertension with pulmonary vasodilator agents is controversial. Some patients have benefited, while others have not. To shed light on the mater we reviewed published reports of 117 patients having acute vasodilator challenge and found that 53 reduced their pulmonary vascular resistance by 30% or more. Calcium antagonists (n = 46), hydralazine (n = 23), and diazoxide (n = 18) gave approximately equivalent acute reductions in resistance (30%, 35%, 32%, respectively), but captopril (n = 17) gave a poor response (-7%). The reports indicated that chronic treatment (3 months or longer) benefited only 4 of 64 patients (6%) having acute reduction in resistances of less than 30%. However, when resistance was lowered acutely by more than 30%, 33 of 53 patients (62%) improved with treatment. In 5 patients having multiple catheterization, improvement was sustained for the duration of follow-up (10 to 48 months). Except for captopril, the agents employed gave similar reductions in resistance, and perhaps the choice should be determined by avoidance of side-effects. Long-term benefit is never certain, but selecting patients with brisk acute vasodilator responses may predict the benefit from chronic vasodilator treatment.     

Improvement in pulmonary hemodynamics during intravenous epoprostenol (prostacyclin): A study of 15 patients with moderate to severe portopulmonary hypertension.

Pulmonary hypertension associated with increased pulmonary vascular resistance (PVR) and occurring in the setting of portal hypertension is referred to as "portopulmonary hypertension." Intravenous epoprostenol (prostacyclin) is a potent pulmonary and systemic vasodilator with antithrombotic properties. It can decrease PVR and pulmonary artery pressure in patients with primary (idiopathic) pulmonary hypertension. Using right-heart catheterization, we evaluated the acute pulmonary hemodynamic effects of intravenous epoprostenol in patients with moderate to severe pulmonary hypertension (mean pulmonary artery pressure [MPAP] >/=35 mm Hg) associated with clinical manifestations of portal hypertension. Effects of long-term infusion of epoprostenol were also evaluated. We studied 15 consecutive patients with portopulmonary hypertension; 14 underwent acute administration of epoprostenol, and no significant side effects were noted. Ten patients received continuous epoprostenol (range, 8 days-30 months). Acute changes in PVR (-34% +/- 18%), MPAP (-16% +/- 10%), and cardiac output (CO) (+21 +/- 18%), were statistically significant (P <.01). Long-term use of epoprostenol further lowered PVR (-47% +/- 12% from baseline and -31% +/- 22% from the acute change; P <.05) in the 6 patients restudied by right-heart catheterization. Death occurred in 6 of 10 (60%) of those receiving long-term epoprostenol. In moderate to severe portopulmonary hypertension, intravenous epoprostenol resulted in a significant improvement (both acute and long-term) in PVR, MPAP, and CO. Potential adverse effects on portal hypertension and implications for orthotopic liver transplantation (OLT), however, require further study.     

Comparison of the effects of adenosine and nifedipine in pulmonary hypertension.

The hemodynamic effects of intravenously administered adenosine, a potent vasodilator, were examined in 15 patients with pulmonary hypertension. All patients were given adenosine, 50 micrograms/kg per min, increased by 50 micrograms/kg per min at 2 min intervals to a maximum of 500 micrograms/kg per min or until the development of untoward side effects. The patients were then given oral nifedipine, 20 mg every hour, until a greater than or equal to 20% decrease in pulmonary vascular resistance or systemic hypotension occurred. The administration of maximal doses of adenosine, 256 +/- 46 micrograms/kg per min, produced a 2.4% reduction in pulmonary artery pressure (p = NS), a 37% decrease in pulmonary vascular resistance (p less than 0.001) and a 57% increase in cardiac index (p less than 0.001). The administration of maximally effective doses of nifedipine (91 +/- 36 mg) produced a 15% reduction in the mean pulmonary artery pressure (p less than 0.05), a 24% decrease in pulmonary vascular resistance (p less than 0.01) and an 8% increase in cardiac index (p = NS). There was a significant correlation (r = 0.714, p = 0.01) between the reduction in pulmonary vascular resistance that resulted from adenosine administration and that achieved with the administration of nifedipine. Six patients had substantial reductions in pulmonary vascular resistance with adenosine but not with nifedipine. Thus, adenosine is an effective vasodilator in patients with pulmonary hypertension and can be used for safe and rapid assessment of vasodilator reserve in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute effects of the combination of sildenafil and inhaled treprostinil on haemodynamics and gas exchange in pulmonary hypertension

BACKGROUND: Inhaled treprostinil was recently developed for the treatment of pulmonary arterial hypertension (PAH). We investigated the safety and acute haemodynamic effects of the combination oral sildenafil and inhaled treprostinil in an open label study in patients with precapillary pulmonary hypertension. METHODS AND PATIENTS: Inhaled nitric oxide (20ppm; n=50), sildenafil (50mg; n=50) and inhaled treprostinil (15mug; n=25 or 30mug; n=25) were applied in subsequent order during right heart catheter investigation to consecutive patients with pulmonary arterial hypertension (PAH; n=28), non-operable chronic thromboembolic pulmonary hypertension (CTEPH; n=17) and pulmonary fibrosis associated pulmonary hypertension (n=5). RESULTS: Inhaled nitric oxide reduced pulmonary vascular resistance (PVR) to 87.3+/-5.1% of baseline values, reduced mean pulmonary arterial pressure (PAP) to 89.7+/-3.5% and increased cardiac output (CO) to 102.4+/-2.9%. Sildenafil reduced PVR to 80.1+/-5.0%, mPAP to 86.5+/-2.9% and increased CO to 103.8+/-3.2%. Treprostinil, inhaled 1h after sildenafil, reduced PVR to 66.3+/-3.8%, mPAP to 77.8+/-3.3%, and increased CO to 107.1+/-3.3% (mean+/-95% confidence interval). Subgroup analysis showed similar acute haemodynamic effects in PAH and CTEPH patients. Ventilation/perfusion distribution measurement in six patients with pre-existing gas exchange limitations was not changed by sildenafil and treprostinil. Relevant side effects were not observed. CONCLUSION: The combination of sildenafil and inhaled treprostinil was well tolerated and induced additive, pulmonary selective vasodilatation in pulmonary hypertension patients. This could be of relevance also for long-term treatment of PAH and CTEPH patients.     

Effects of nebulised iloprost on pulmonary function and gas exchange in severe pulmonary hypertension

Nebulised iloprost is established therapy of severe pulmonary hypertension; however, the effects on the bronchoalveolar compartment have not been investigated so far. We studied the short- and long-term effects of nebulised iloprost on pulmonary function tests and gas exchange in 63 patients with severe pulmonary hypertension (idiopathic n=17, chronic thromboembolism n=15, connective tissue disease n=12, congenital heart disease n=11, respiratory diseases n=8). Patients received iloprost in increasing dose up to 140 micro g iloprost/24h via an ultrasonic nebuliser. Short-term effects were assessed before and after every nebulisation: peak expiration flow decreased in mean by 1.9% (423+/-98 to 415+/-98) and percutaneous oxygen saturation increased in mean by 0.7% (90+/-6 to 91+/-5) post-nebulisation. There were no significant differences concerning underlying diagnosis or dose of nebulised iloprost. Within 3 months, 9 patients stopped treatment due to non-compliance with frequent nebulisations (n=3), or severe side effects (n=4); 2 patients with additional obstructive lung disease developed bronchoconstriction. Long-term effects were assessed by pulmonary function tests and gas exchange parameters at baseline and after 3 months treatment. There were no significant differences after 3 months therapy neither in FEV(1), FVC, TLC, residual volume nor in diffusions capacity, SO(2) at rest and during 6 min walking test, also in respect of the underlying diseases. However, there was a significant increase in 6 min walking distance (6 MWD) after 3 months (246+/-113 to 294+/-115 m, P<0.05). In conclusion, treatment with nebulised iloprost leads to functional improvement in severe pulmonary hypertension without systematic adverse short- and long-term effects on pulmonary function test or gas exchange. Patients with additional obstructive lung disease might develop bronchoconstriction. Severe side effects leading to discontinuation of treatment occurred in 9% of patients.     

Complications of stress-echocardiography used for diagnosis of ischemic heart disease

Prevalence of minor and major complications, side effects of stress echocardiography (stress-echoCG) was studied in a group of 1359 patients with suspected ischemic heart disease (IHD). Dipyridamole/atropine test was carried out in 184, dobutamine/atropine test - in 231, transesophageal atrial pacing (TEAP) - in 154, veloergometry (VEM) in half sitting position - in 122, and combination stress-echoCG - in 668 patients (dipyridamole/TEAP, n=151; dipyridamole/dobutamine, n=162; dipyridamole/paired TAP, n=112). We classified ventricular and supraventricular extrasystoles, head ache, nausea, muscular tremor as side effects, short paroxysms (less than 2 min) of hemodynamically insignificant supraventricular and ventricular tachycardia - as minor complications, and development of acute coronary syndrome, ventricular fibrillation - as major complications. Most frequent side effects during stress-echoCG were rare ventricular extrasystoles (26.0% during dobutamine, 18.9% during VEM test), and head ache (16,7% in dipyridamole tests). Major complications occurred in 2 cases (0,147%). One patient during standard dipyridamole test developed acute coronary syndrome requiring urgent coronary angiography and angioplasty of the right coronary artery. Another patient after administration of 0.25 ml of 0.1% atropine solution at the background of dobutamine infusion (40 mcg/kg/min) had ventricular fibrillation requiring resuscitative measures. Although stress-echoCG in general is a safe and highly informative method of diagnosis of IHD it can be accompanied with side effects during action of stress-agents, minor and major complications during conduction of tests. This dictates necessity of obtainment of compulsory informed consent from patients.     

Feasibility and safety of transeophageal atrial pacing stress echocardiography in patients with known or suspected coronary artery disease

To investigate the feasibility and safety of the transesophageal atrial pacing stress test combined with echocardiography (TAPSE) 1,727 TAPSE tests were performed on 1,641 patients consecutively referred to our echocardiographic laboratory for nonexercise stress testing (1,319 men; mean age 60 ± 9 years; 34% of whom were outpatients). Wall motion abnormalities were present at baseline echocardiography in 975 cases (56%). TAPSE was feasible in 1,648 cases (95.4%). It was not feasible in 79 patients due to failure of positioning the transnasal catheter (n = 11), the patient's intolerance of esophageal stimulation (n = 24), failure to obtain any or stable atrial capture (n = 36), or because the echocardiogram could not be evaluated at the peak of the test (n = 8). TAPSE was diagnostic in 1,584 cases (96% of the feasible tests, 92% of all attempts). TAPSE was nondiagnostic in 64 cases (4% of the feasible tests) due to second-degree atrioventricular type I block resistance to atropine administration with failure to achieve 85% of the age-predicted maximum heart rate (n = 59) or due to side effects, such as arrhythmias (n = 3) or hypertension (n = 2), which required premature interruption of the test. There were no major complications (death, myocardial infarction, or life-threatening arrhythmias). There were 28 instances of minor complications that comprised transient arrhythmias, including atrial fibrillation (n = 8), paroxysmal supraventricular tachycardia (n = 6), automatic atrial tachycardia (n = 1), sinus arrest (n = 1), atrioventricular junctional rhythm (n = 2), ectopic atrial rhythm (n = 2), nonsustained ventricular tachycardia (maximum 6 beats, N = 3), hypotension (n = 1), and hypertension (n = 4) leading to interruption of the test. Only 5 complications hampered a diagnostic result, whereas 18 occurred during or after a positive test and 5 during a negative, but diagnostic, test. Thus, TAPSE is a highly feasible and very safe stress test. It gives high percentage of diagnostic tests and may represent a valid alternative to pharmacologic stressors.     

Adenosine as a vasodilator in primary pulmonary hypertension

BACKGROUND. The acute administration of vasodilator drugs to patients with primary pulmonary hypertension has been advocated to identify those with reversible pulmonary vasoconstriction. Unfortunately, the usefulness of the drugs currently available is limited by accompanying systemic hypotension. A vasodilator with effects confined to the pulmonary circulation would therefore be advantageous in such patients. METHODS AND RESULTS. The purine nucleoside adenosine was infused into the pulmonary artery in seven patients with primary pulmonary hypertension (baseline pulmonary vascular resistance [PVR], 442-1,295 dyne/cm/sec-5) to determine its effect on PVR. In all patients, there was a dose-dependent and significant reduction (mean maximal percent decrease from baseline, 38.9%; p less than 0.001) in PVR mediated through a decrease in pulmonary artery pressure and an increase in cardiac output. Systemic vascular resistance (SVR) also decreased, but the ratio of PVR to SVR decreased (maximal mean percent decrease from baseline) by 10.5% (p less than 0.025), indicating that adenosine has a preferential vasodilator effect on the pulmonary circulation when administered in this manner. CONCLUSIONS. Because of its pharmacokinetic and vasodilator properties, adenosine may have a specific role in the investigation of primary pulmonary hypertension.     

Portopulmonary hypertension in liver transplant candidates

Pulmonary vascular disorders including portopulmonary hypertension(PoPHT) are among the common complications of liver disease and are prognostically significant. Survival is very low without medical treatment and liver transplantation. With advances in medical therapy for elevated pulmonary artery pressure(PAP) and liver transplant surgery, survival of patients with Po PHT and advanced liver disease is significantly improved. Because of the prognostic significance of Po PHT and the limited donor pool, a comprehensive preoperative cardio-pulmonary assessment is of great importance in cirrhotic patients prior to transplant surgery. Therefore, a detailed transthoracic Doppler echocardiographic examination must be an essential component of this evaluation. Patients with mild Po PHT can safely undergo liver transplant surgery. In cases of moderate to severe Po PHT, right heart catheterization(RHC) should be performed. In patients with moderate to severe Po PHT on RHC(mean PAP 35-45 mm Hg), vasodilator therapy should be attempted. Liver transplantation should be encouraged in cases that demonstrate a positive response. Bridging therapy with specific pulmonary arterial hypertension treatment agents should be considered until the transplant surgery and should be continued during the peri- and post-operative periods as needed.