An Exploration of Issues Associated with Pericardial Dysfunction in Postoperative Cardiac Patients

Glenda Pack, RN, NP, MN, CCCN(C), CCN(C) Dynamics 2013 Nurse Practitioner, CV Surgery September 23/13 Eastern Health, St. John’s, Newfoundland  Review the anatomy and pathophysiology associated with conditions involving the  Explore the trajectory of pericardial dysfunction  Assist the nurse to hone assessment skills to detect pericardial dysfunction  Review historical and current treatment methodologies

 Approach to Excising  Approach to Closing  Open  Improved hemodynamics in the early phase  Decreased incidence of graft failure  ? Reduced incidence of cardiac tamponade  Closed  Protective from sternal adhesions in redo-operations

 Might not have control over how the pericardium is handled, but knowing how it was handled is important for patient management Pericardial Effusion  Excess accumulation of fluid in the pericardium  May or may not be clinically significant Pericarditis  Inflammation of the  Cardiac Tamponade pericardium Pericardial Effusion that causes significant compression of the  Acute  Latent

PPtost-PPiericar ditdiotomy Synd rome  70 yo male  POD #1 CABG x3  Chest tubes removed 3 hours ago  Complaining of vague chest discomfort  Unable to take a deep breath  Pericardial friction rub LSB POD #! Inflammation of the pericardium

CV patient Idiopathic Direct and/or indirect trauma Benign and self limiting Diagnosis Treatment ECG Relieve Symptoms Symptoms Analgesics Friction rub NSAIDs Corticosteriods

Colchicine  Symptomatic treatment  Monitor for development of pericardial effusions  Monitor for development of Post- Pericardiotomyyy Syndrome  Prior to transfer from CVICU was started on Ibuprofen 400mg tid x 24 hours

 POD # 2 creatine had increased from 90 to 140

 Ibuprofen D/C

 EKG POD#3: POD #3  Incidence as high as 85% in post-operative CV patients  Insult to pericardium  Manifestations dependant on the rate of fluid accumulation  Many undetected /Transient / Benign  Maximum size POD #10 – regress after  30% are quantified are “large”  ~ 1% of larggppe effusions develop tamponade

Diagnosis Treatment  ECG  None  CXR  NSAIDs  TTE*  Corticosteriods  TEE  Colchicine  CT   MRI  Oppgen Surgical Draina ge  Supportive (usually self limiting)  Monitoring for signs of decreasing cardiac output malaise, orthopnea, fatigue, dyspnea, unexplained tachycardia, hypotension, Hemodynamically pulses paradoxus, jugular venous Significant? distension, distant heart sounds, ascites, peripheral edema, progressive azotemia, gradual equalization of R atrial, PAD and wedge pressures, mediastinal widening on CXR Worsening Effusion  Possibly prepare for pericardiocentesis  Monitoring for decompensation post pericardiocentesis  Possibly prepare for re-sternotomy Mr. S  70 year old male elective admission for Bentall Procedure  Normal  GdGrade 2 LVF on cat h  Bicuspid AV  3+ AI  Dilated aortic root and ascending  Chronic Atrial Fib – On coumadin, stopped x 7/7 bridged with Lovenox  ppgytt slightly elevated / remained of coa gs OK  HT N  Exsmoker (x 20yrs)  Single presyncopal episode 8 yrs ago  Experiencing increasing dyspnea OR • Bentall procedure with #27 Carbomedics Mechanical Prosthesis / #30 Valsava graft • Pericardium was closed with 2.0 silk • Total operating time 4.25 hours • Transported to CVICU in critical condition

POST-OP • Uncomplicated • Transf erred to Car diac Spec ia l Care uni t POD #1 A pericardial effusion that causes significant compression of the heart

Rare, but life- Rare, but life-threatening threatening

SCHIAVONE W A Cleveland Clinic Journal of Medicine 2013;80:109-116 Within 5-7 dayyps post cardiac sur ger y  0.1% - 6%  As a r esul t of post-oper ati ve bleed in g  Limited expansion of the pericardium  Low pressure tamponade / regional tamponade because of loculated effusions & localized pericardial adhesions  Fluid accumulation (and therefore pressure) in the pericar dium compresses the myocardildial tissue and bldblood is not able to propel forward  Cardiogenic shock  Know who is at risk  Bleeding  Pre-oppg(g) risk of bleeding (medications, bleeding hx)  Hemodilution (excessive I/V fluids, prolonged pump run)  HhiHypothermia  Serum lab values (platelets, hgb, azotemia)  Heparin rebound  Post epicardial pacing wire removal Greater than 7 dayyggys following surgery –up to 1 year (30-45 days)  Higher mortality rate than Early Tamponade  Almost exclusively patients who have had valve surgery  IdIncreased iiidncidence excessi ve INR values  As a result of  Fluid (blood /exudate)  Air (pneumopericardium)  Lyyp(mph (chyyplopericardium) Later that day..... (POD#1) When ambulating pre-syncopal, hypotensive eppgisode.... Recovered.....vital signs and labs stable . Over the next few days Mr. S was slow to ambulate, vital signs were stable, developed increasing peripheral edema, rhythm atrial fib wit h v. rate 100-110/ min POD#6 – still not right.. Stable.. Echo • Normal functioning Bentall with functioning • LVH • Dildlated LV with hbdl borderline impairment of systol ic function • Small to moderate ppjyericardial effusion with the majority of fluid located posteriorly without hemodynamic effect POD #8 – decreasing B/P , Temp increased, WBC increase to 17, lower sternum uns tbltable, stlternal drainage, CXR- bilateral pleural effusions  Monitoring  Vital signs (HR, B/P)  EKG changg(es (tachy / low voltagg)e)  Mental status  Leftward deviation of PA catheter on CXR  Chest tube losses Sudden large volume – bleeding  Sudden slowing – clotting Classic Signs  Monitoring  ? Pulses Paradox Decreased systolic upstoke on arterial pressure monitor  SBP drop greater than 10mmHg between expiration and inspiration ElitiEqualization of the R artilterial pressure an d PCWP

Pulses Paradoxus Suppressed: •LV dysfunction •Regional tamponade •PPV •COPD with cor pul monal e •Severe AI •Intracardiac shunt  Quiet heart sounds Beck’s triad  High JVP

 Low arterial pressure

 Distended neck veins Dx – Cardiac Tamponade - Late … ? Early too and mechanical sternal dehiscence

Returned to OR for medistinal Re-exploration with the evacuation of a large pericardial effusion – relief of tamponade, drainage of bilateral pleural effusions, and sternal rewiring.

Mr. S was discharged 12days later Intra op cultures were negative Follow up echo Valve fn N/ no pericardial effusion noted / CXR N EARLY  Re-sternotomy to determine and alleviate the source of bleeding  Support hemodynamics  Correct coagulopathies  Correct hypothermia  Decrease metabolic demands LATE  Periocardiocentesis (when possible)  Re-sternotomy  unable to tolerate echo  failure of percutaneous drainage  presence of intrapericardial hematoma  Mr. B. 62 yo male with bicuspid aortic valve with critical aortic stenosis  Elective admission for AVR  Aortic with #27 St. Jude Mechanical Prosthesis  Uncomplicated post-operative course  Discharge home on POD#5  On coumadin with therapeutic INR 2.5  Common complication of  Occurs a few days–weeks (even months) after cardiac surggyery  Incidence 10-40%  Prolonging and disabling  Immune-mediated inflammatory process  Mild(isolated pleural/pericardial involvement) to severe (hemodynamic consequences) Presentation  Post cardiac surgery  Pericarditis  Pericardial rub  Fever  Leukocytosis  Increased sed rate  Pulmonary infiltrates +/- pleural effusion  2 weeks followinggg() discharge (POD#19)  Mr. B presented to his community hospital with increasing shortness of breath, low grade fever and signifi can t L pl eural eff us ion  Transferred to tertiary hospital:  CXR – Large L pleural effusion  TTE – Mod sized pericardial effusion without comprise - N functioning mechanical aortic valve prosthesis No vegetation  INR erratic control noted by his family physician  L chest tube – drained 2 liters sero-sang drainage  Placed on prednisone  Discharged home 3 days after CT discontinued  Diagnosis  Fever without alternative causes  Pleuritic chest pain  Friction rub  Evidence of pleural effusion  Evidence of a new or worsening pericardial effusion

Imazio et al. propose the presence of at least 2 of these criteria for diagnosis of PPS International Journal of Cardiology 159(2012) 1-4 Management

Diagnostics Treatment  Echo Anti-inflammatory agents Corticosteriods  CT  Thoracentesis

Prevention – Colchicine shown to be safe and effective Decreased occurrence of chest pppain and pleural effusions (COPPS &COPPS2 trials)  3 weeks later Mr. B ppyresented to his community hospital with  increasing dyspnea  Increased JVP  Increased WBC  Transferred to tertiary facility again - CCU  CXR - Mod L pleural effusion  Echo - Large pericardial effusion  CT – drained L pleural effusion  PiPeriocardi ocentesi s – large effiffusion diddrained

Discharggpe home on prednisone –no further readmissions  CV patients do not follow classic pictures of disease symptomatology

 There can be a significant delay in post- oppperative complications

 Manyyg signs of pericardial d ysfunction are masked by post-operative pain and “expected” recovery symptoms (fatigue / dyspnea)  Low threshold for performing an echo in CV patient with atypical symptoms

 Pericardial dysfunction is often benign and transient, but an index of suspicion needs to be maintained when patients are not progressing just as expected

 ? Role of colchcine