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Transcript
68 y/o female undergoing RFA for paroxysmal ventricular tachycarida PMH: DM, HTN, COPD All: erythromycin – nausea Soc: quit smoking 20 yrs ago, no EtOH or drugs 5 hours into RFA, decreased responsiveness, hypotensive Patient in SVT, paced out by cardiologists Remained hypotensive, pressors started, intubated Marked JVD noted TTE emergently preformed 1.1-1.3cm effusion over right heart RV collaspe Tamponade physiology Effusion drained under ultrasound 35cc frank bloody fluid removed Patient immediately stabilized Extubated at end of case, taken to CICU Discharged 2 days later Continues medical management of SVT A condition where fluid accumulates around the great vessels or chambers of the heart and decreases stroke volume to clinically significant levels 2 layers Parietal pericardium Fibrous ~2mm Visceral pericardium Thin mesothelial layer Typically contains 25 – 50cc serous fluid. Pericardial space can be considered a potential space Slowly accumulating effusion Allows for pericardial distension May have effusion up to 1500cc before symptoms arise Typically ‘medical’ causes’ Uremia Malignancy Hypothyroidism Rapidly accumulating effusion Usually see in perioperative setting As little as 200cc fluid for symptoms Beck’s Triad Hypotension Jugular venous distension (Kussmal’s sign) Distant heart sounds Commonly sited changes: Low voltage QRS T wave inversions PR depression ST changes Not supported by data Combination of low voltage QRS and PR depression has weak association with effusion Alteration in configuration of electrocardiographic complexes arising from the same pacemaker and independent of periodic extracardiac phenomenon Caused by swinging of the heart in pericardial fluid Rare phenomenon Resolves with drainage of effusion Decline in arterial pulse with negative pressure inspiration Not a paradox, but exaggeration of normal respiratory decrease in arterial BP assoc. with effusion Not an all-or none phenomonon Systolic pressure change greater than 10 accepted as significant Respiratory variation switched with positive pressure ventilation Curtiss et al: SBP change greater than 12mm HG or 9% 92% and 97% accurate respectively May be found in other conditions: Tracheal compression Tension pneumothorax Pleural effusion RV infarct PE Hemorrhageic shock May be absent in: Extreme hypotension Aortic regurgitation Atrial septal defect Increased LVEDP Cardiac adhesions All CVP values elevated Obliteration of Y descent PCWP and CVP equalize PA systolic pressure Decreases with inspiration with mild or moderate tamponade May increase with severe tamponade Very sensitive (64-100%) Very specific (80-100%) Free wall diastolic inversion that persists 1/3 into systole Affected by: Tricuspid regurgitation Plerual effusion Ventricular rhythm Pulmonary HTN RVH Not as well described May be tethered to pulmonary veins Found more often with loculated and smaller effusions Seen after CT surgery Optimal views with TEE Decreased chamber size rather than collapse Early to mid-diastolic inward motion of the right ventricle Sensitivity 60 to 81% Specificity 90 to 94% Increased sensitivity and specificity with concurrent RA collapse Affected by same confounding factors as RA collapse Tethering to anterior chest wall may affect sensitivity after open heart surgery Most resistant to circumferential tamponade Most often seen with regional tamponade May be associated with SAM Smaller effusion for tamponade with LV dysfunction Normal VTI ~10% First inspiratory beat: Increase in Tricuspid VTI 80% Increase in Pulmonic VTI 90% Decrease in Mitral VTI 35% Decrease in Aortic VTI 30% May identify subclinical tamponade Useful in identifying low=pressure tamponade Seen in hypovolemia JVD, pulsus paradoxus absent May be resistant to volume loading Effect of transmural pressure Low CVP and modestly elevated intrapericardial pressure result in tamponade physiology May not have typical 2D echo findings Doppler may be diagnostic Evidence indicates rate of tamponade increasing Tamponade associated with ~0.1 – 0.2% of interventional procedures Minimal risk with diagnostic procedures Analysis of 14,972 diagnostic caths showed no tamponade Risk factors include Elderly Female sex Multi-vessel disease Complex coronary lesions Immediate presentation Associated with direct coronary perforation Hypotension, chest pain, shortness of breath 94% patients require ventilatory support 82% of patients require CPR Delayed presentation 45-60% of all cases Usually 2 to 36 hours Mortality Unclear but may be up to 42% Probably related to site of perforation and rate of fluid accumulation Increasing frequency as rate of implanted devices increases Several methods of extraction Manual Constant tension Excitimer laser Wires may fibrose over time ICD wires more likely to tenaciously fibrose 1.4% experience cardiac tamponade Associated with 20% mortality Tamponade most common major problem Risk Factors Female ICD Multiple leads Leads greater than 8 years old North American Society of Pacing and Electrophyiology Policy Statement Large bore peripheral IV Arterial Line “Adequate” anesthesia MHMC Endotracheal intubation/GA Large bore IV Arterial line No longer have OR and surgeon ready ASA Closed Claims Database Analysis 2004 16 cases of cardiac tamponade in 6449 claims Significantly (p<0.05) higher association with mortality compared to other complications 78-95% rate of mortality Right atrium most common site of perforation, right ventricle second Presentation may be from minutes to days Many reports of finding previously healthy patients expired at bedside Several reports of pericardiocentesis removing TPN Increased incidence of tamponade with left internal jugular placement Tip position important Vessel wall erosion plays a major role in delayed presentations More vessel wall contact increases change of erosion Right atrial placement increases risk of perforation Don’t be the ‘I’ in iatrogenic NOT necessary to ‘bury’ guidewire or elicit dysrhythmia Check line with CXR Don’t place lines too deep Consider contrast injection Observe PA catheter waveforms after transport to the ICU Two main categories: Penetrating Trauma Blunt Trauma Tamponade in 80-90% of all penetrating wounds Wounds of axilla, neck, back, mediastinum, epigastrium, and upper abdomen Typically caused by knives and guns. Reports of embolized bullets, nails, knitting needles, lawn mower projectiles , and ice picks permeate literature Review of 1802 penetrating cardiac injuries found Right ventricle 43% Left ventricle 33% Right atrium 14% Left atrium 5% Intrapericardial vessels 5% Associated with area each structure occupies in the anterior chest Left ventricle often spontaneously seals due to thick myocardium Right ventricle unlikely to spontaneously seal Atria may seal due to low pressure and tethering to pericardium but thin walls make this unlikely *Remember myocardial wall stress inversely related to thickness Smaller wounds (>2.5cm) are associated more commonly with tamponade Larger wounds are associated with exsangiunation into chest Larger wounds less likely to spontaneously seal Only 20% present with tamponade Remainder result in exsanguination into chest Higher velocity associated with exsanguination Lower velocity associated with tamponade Knife wounds more likely to result in tamponade because pericardium will spontaneously close Stab and gunshot wounds usually affect more than one cardiac structure Penetrating injury usually declares itself immediately Can have delayed presentation up to four weeks Re-bleed usually in non- surgically repaired wounds Pericardial effusion seen in 22% of all penetrating injuries but rarely a problem 10% of all blunt chest trauma sustain cardiac or aortic injuries Very few patients require operative treatment Most patients expire before they reach the hospital Chirillo et al TEE study of 83 patients with chest trauma 40 with pericardial effusion One with pericardial tamponade History of airbag deployment associated with tamponade 1st and 2nd rib fractures often associated with tamponade COPD patients at risk of pneumopericardium Effusion found in 50 to 85% of patients Tamponade estimated at 0.75 to 0.8% from two recent large reviews (range Zero to 8.8%) Higher rate in valve replacement vs CABG More common in females Early tamponade Active re-bleed Signs/symptoms of low CO Acute decrease in chest tube output Late tamponade Post-pericardotomy syndrome Presents 15-20 days post-op Very inconsistent presentation Anterior effusion more common with CABG Typical TEE findings Loculated effusion Posterior location Small volume Left atrial collapse common Paradoxical LV motion possible effusions with valves Recognize Condition Medical management “Tight” - increase SVR, minimize chamber collapse “Tachy”– fixed CO, increase HR “Tank full” –volume load Surgical Decompression Open chest Subxiphoid incision Pericardiocentesis w/wo drain w/wo echo guidance Mayo Clinic Study (1999) 97% successful in most cases 96% successful with loculated effusions Major complication 2% Coronary chamber laceration Pneumothorax w/ chest tube Minor complications 1.2% Small pneumothorax Pleural-pericardial fistula Optimize patient pre-op Avoid positive pressure ventilation Anesthetic depends on etiology Consider relief of tamponade under local Consider pre-induction arterial line Central line in EJ if time Consider double set-up Most agents cause hypotension Anesthetic requirements increase after relief of tamponade Have epinephrine and atropine available Consider ketamine May be sympathetically depleted Theoretical concern? Described in several case reports