Brief history Situs inversus with dextrocardia, Complex congenital heart disease status post correction (critical PS status post percutaneous transcatheter pulmonary valvuloplasty with residual PS (22mmHg), left atrial isomerism, PDA status post coil embolization, interruption of IVC) Sick sinus syndrome with bradycardia
Brief history Bradycardia persisted with cardiomegaly and hepatomegaly noted in recent few years. She was quite well except felt fatigue easily without history of syncope or cyanosis. Therefore, this time she was admitted for EPS study and pacemaker implant.
Brief history On 92/09/09, EPS - sick sinus syndrome, extremely long sinus pause followed by junctional escape rhythm - mild to moderate pulmonary hypertension, - moderate to severe PR - subnormal AV conduction She underwent DDD pacemaker implantation on 92/09/10.
DDD pacemaker implantation ETGA Midline sternotomy with pericardium opening Implantation of pacemaker wire over epicardium of RV and LAA Creation of RLQ pocket for generator Pacing current threshold - LAA 1.3 volts, - RV 1.2 volts Set two pericardial tube
Brief history After pericardial tube removal, F/U CXR on 9/17 revealed suspected pericardial effusion.
Brief history Heart echo confirmed pericardial effusion. She underwent peri-cardiocentesis under echo guide on 9/18. The drain amount was 373.5ml, clear. Lasix and Ibuprofen were prescribed under the impression of post-pericardiotomy syndrome.
F/U echocardiography 92/09/22 Increased pericardial effusion amount with paradoxial septal motion but no significant chamber compression.
Brief history Prednisolone was prescribed for post- pericardiotomy syndrome since 9/22. Surgical drainage with chest tube insertion was indicated.
Physical examination Consciousness: clear HEENT: Conjunctiva: not pale, Neck: Supple, JVE(+), LAP (-) Chest: Symmetric expansion, clear breathing sound Heart: Dextrocardia, systolic murmur over LUSB Gr III /VI Abdomen: soft and flat, normoactive bowel sound; Liver/spleen:3 f b below LCM / impalpable Extremities: freely movable, polydactyly
Pre-anesthetic evaluation BW 17.6 kg ASA classification: 4E No adequate NPO Sick sinus syndrome post DDD pacemaker implantation Large amount pericardial effusion No dyspnea, orthopnea BP 112/82mmHg, HR 80 /min
Anesthetic management O2 IVF bolus 200ml Phenylephrine 0.2mg Atropine 0.2mg Induction with Ketamine 40mg and SCC Rapid sequence intubation with 5.5# ET tube fix 15cm Maintenance with Desflurane A-line and CVP were inserted thereafter.
During anesthesia Initial BP 112/82mmHg, HR 80 /min, CVP 40mmHg During anesthesia, pulse pressure decreased with HR increased progressively. At the time before pericardial incision, BP was 82/71 and HR was 133/min.
During anesthesia After low midline pericardiotomy BP was increased to 125/95 mmHg and CVP was reduced to 16mmHg. Massive amount of pericardial effusion about 500ml with straw color was drained.
Post-op After pericardiotomy, her hemodynamic status became stable. She was then sent to ICU for post –op observation. She was discharged on 10/4.
Cardiac tamponade Cardiac tamponade results when enough fluid accumulates between the heart and the pericardium to impair ventricular diastolic filling, especially thin-walled atria and RV. Fluid volume acute tamponade: 150 ml chronic tamponade: 1000 ml
Acute cardiac tamponade Incidence: % Significant chest tube output in the immediate post-op period. Chest tube clogged by blood clots.
Delayed cardiac tamponade Incidence: % Occurs greater than 5 to 7 days after operation Delayed diagnosis because of low index of suspicion - congestive heart failure - pulmonary embolism - generalized fatigue
Pathophysiology Ventricular end-diastolic volume, stroke volume, CO and BP usually decrease. Increased diastolic ventricular pressure will decrease the coronary perfusion pressure predisposing those with CAD to ischemia, particularly if tachycardia is present and O2 requirement is increased.
Pathophysiology Compensatory increased sympathetic activity leading to increase HR and contractility, which help maintain CO and vasoconstriction to maintain BP. Because of increased SVR, some patient exhibit an elevated arterial BP. When the compensatory tachycardia is unable to maintain CO in the face of declining stroke volume, cardiogenic shock results.
Pathophysiology CVP elevation is caused by vasoconstriction and elevated RV end-diastolic pressure. Pericardial stretching may produce disastrous vagally mediated depressor reflex.
Diagnosis The diagnosis of tamponade depends on a high index of suspicion and knowledge of associated clinical findings. Symptoms of cardiac tamponade are usually rapid in onset but depend on the rate and volume of pericardial fluid accumulation
Diagnosis PE: JVE, distant heart sound CVP: elevation with monophasic morphology owing to loss of y descent PA catheter: equalization of right- and left- sided diastolic pressure and low cardiac output. CXR: enlarged cardiac silhiuette, may be normal in acute tamponade
Diagnosis EKG - decreased QRS voltage in all leads - signs of pericarditis ( generalized ST change in two or three limb leads as well as V2 to V6) - electrical alternans in large pericardial effusion ( cyclic alteration in magnitude of the P, QRS, T waves)
Diagnosis Echocardiography -invaluable in diagnosis and pericardiocentesis -estimate effusion size -signs of tamponade: 1. diastolic compression or collapse of RA 2. Leftward displacement of the ventricular septum 3. Increased RV size with a reciprocal decrease in LV size during inspiration
Management Find the etiology Maintenance of compensatory changes - tachycardia, vasoconstriction… - Inotropes and vasopressors, such as dopamine, bosmine, isoproterenol, that increase CO without lowering diastolic BP improve organ perfusion and coronary perfusion pressure.
Management Percutaneous pericardiocentesis with or without a drainage catheter under local anesthesia with ultrasound guidance is treatment of choice.
Management Surgical relief of tamponade is accomplished by pericardiotomy through subxiphoid incision, using local anesthesia with the patient breathing spontaneously. Premedication with atropine is often recommended to prevent reflex bradycardia.
Anesthetic management Induction of general anesthesia in patients with cardiac tamponade is extremely hazardous and may precipitate cardiac arrest. Pericardiocentesis or subxiphoid drainage under local anesthesia prior to induction is often advisable.
Anesthetic management After removal of pericardial fluid and lowering of intrapericardial pressure, CO is improved greatly and general anesthesia is induced more safely.
Anesthetic management If induction of anesthesia before peri- cardiotomy is chosen, the abdomen and chest are prepared and draped before induction. If cardiac arrest does not respond to CPCR, emergency thoracotomy and open-chest massage are indicated.
Anesthetic management Routine monitors Intraarterial, CVP or PA catheters before induction of anesthesia.
Anesthetic management The anesthetic aims are therefore to maintain adequate filling pressures, adequate heart rate and maintain contractility. Unconsciousness will withdraw systemic outflow, and bolus epinephrine should be available.
Anesthetic management Omit drugs and minimize manipulations that decrease venous return, reduce HR, produce hypotension, result in hypoxemia, or impair ventricular contractility. Ketamine may be the best induction drug. Narcotics cause undesirable slowing of HR. BZD lower systemic vascular resistance.
Anesthetic management Positive pressure ventilation further embarrasses venous return and CO. High-frequency jet ventilation (HFJV) may be better tolerated. Spontaneous ventilation should be maintained until the tamponade is relieved.
Anesthetic management Pulmonary edema has occurred after relief of pericardial tamponade because of sudden enhancement of venous return.
Anesthetic management Positive measures such as expansion of the circulating blood volume, infusion of an inotrope, and maintenance of a high oxygen content of arterial blood are often beneficial. Antidysrhythmic drugs and extracorporeal circulation may be needed during pericardiectomy when surgical manipulation of the heart leads to dysrhythmias and impairs cardiac output.
Low CO Complicating pericardiectomy for Pericardial tamponade Fatal or near-fatal systolic dysfunction occurring soon after decompression of pericardial tamponade accomplished by either pericardiocentesis or subxiphoid pericardiectomy. Ann Thorac Surg 1999;67:228 –31
Low CO Complicating pericardiectomy for Pericardial tamponade The cause of this relatively sudden heart failure - myocardial damage from antineoplastic drugs - direct myocardial involvement by tumor - decreased coronary blood flow during tamponade with resultant myocardial ischemia - stunning - reversible myocardial hibernation
Low CO Complicating pericardiectomy for Pericardial tamponade Another possibility is that occult systolic dysfunction may already be present during tamponade but it may be masked by reduced chamber sizes and the tachycardia. High levels of sympathetic tone and endogenous catecholamines during tamponade may mask preexisting myocardial dysfunction.
Low CO Complicating pericardiectomy for Pericardial tamponade The chronic external support of the heart by the tight pericardium and fluid when released may allow the heart to overdilate rapidly, leading to systolic dysfunction and heart failure.
Low CO Complicating pericardiectomy for Pericardial tamponade Neelakandan and associates for gradual decompression of the pericardial effusion with gradual removal of pericardial fluid with an indwelling catheter might be a feasible approach. However, this syndrome, no matter how lethal, is relatively rare.
Low CO Complicating pericardiectomy for Pericardial tamponade Be aware of the possibility that patients might develop transient or even fatal heart failure after relief of a benign or malignant pericardial tamponade. Treatment for this problem should be supportive with appropriate invasive monitoring and inotropic support, which will result in recovery in some patients. Ann Thorac Surg 1999;67:228 –31
In our patient Pericardiotomy through subxiphoid incision, using local anesthesia. Percutaneous pericardiocentesis under local anesthesia with ultrasound guidance before induction.
In our patient Expansion of the circulating blood volume, increase SVR, and maintenance of a high O2 content of arterial blood before induction. Intraarterial, CVP or PA catheters before induction of anesthesia The abdomen and chest should be prepared and draped before induction.
In our patient Spontaneous ventilation - no adequate NPO - gas induction Induction with Ketamine rapid sequence intubation Hemodynamic improve after decompression, no s/s of heart failure.