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RESOLUTION OF HYPOTENSION IN LESS THAN 5 MINUTES?

RESOLUTION OF HYPOTENSION IN LESS THAN 5 MINUTES?. Grand rounds June 10, 2014 By Aruna Cheddi PGY 2 Supported by: Dr. Nallamothu and Dr. White. Objectives:. Recognizing presenting signs and symptoms of cardiac tamponade Etiology Pathophysiology Treatment. Case:.

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RESOLUTION OF HYPOTENSION IN LESS THAN 5 MINUTES?

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  1. RESOLUTION OF HYPOTENSION IN LESS THAN 5 MINUTES? • Grand rounds June 10, 2014 • By Aruna Cheddi PGY 2 • Supported by: Dr. Nallamothu and Dr. White

  2. Objectives: • Recognizing presenting signs and symptoms of cardiac tamponade • Etiology • Pathophysiology • Treatment

  3. Case: 45 y/o M with advanced metastatic poorly differentiated adenocarcinoma of the lung s/p chemotherapy x 2 cycles with last chemotherapy approx. 3 weeks prior to presentation. Presented to PCP’s office 1 week prior with increasing dyspnea, b/l LE swelling, started on furosemide, no previous hx of heart failure Presented to OLH with no improvement in symptoms, his SOB and edema were progressing

  4. In OLH ED he received an albuterol/atrovent neb and symptoms improved, pt was to be discharged when he suddenly became unresponsive, apneic and diaphoretic, he was intubated for airway protection and had what appeared to be seizure like activity. • Ativan was administered with resolution of his seizure like activity • He was started on IVF and norepinephrine for hypotension and transferred to MMC ICU for further management.

  5. Workup at OLH:

  6. CT head: negative for any acute intracranial process • ABG: 7.1/67/242/20/100%FiO2 • LA 6.8, WBC 13.73, Cr. 1.2 (baseline 0.6) , AlkP 270, AST 453, ALT 538

  7. Physical exam: • VS: Temp: 36.3 BP 104/48 HR 102 RR 20 SaO2 100% • General: Intubated, unresponsive • HEENT: Normocephalic, PERRL, normal conjunctiva • Neck: no JVD, bilateral cervical lymphadenopathy, soft tissue swelling R>L • Cardiovascular: tachycardic, distant heart sounds, no murmur, pulsus paradoxus of 15mmHg • Respiratory: coarse breath sounds diffusely • GI: soft, nondistended, normoactive bowel sounds • Neuro: unresponsive • Ext: no clubbing or cyanosis, trace pitting edema b/l LE

  8. MMC Labs: • WBC 20, Hb 9.6 • Na 127, K 6.9, Cl 94, CO2 20, BUN 38, Cr. 1.6 • AST 1084, ALT 1082, AlkP 201, Tbili 1.2 • Lactic acid 5

  9. Differential Dx: • Pulmonary Embolism • Septic shock • Cardiogenic shock • RV infarct • Pulmonary HTN • Cardiac Tamponade

  10. Bedside Echo showed large pericardial effusion with swinging motion of heart observed in fluid • Stat cardiology consult was made for emergent pericardiocentesis • 1.3L of serosanguinous fluid was obtained and sent for analysis • VS improved after fluid removed: • BP 117/69, HR 99, norepinephrine was titrated down

  11. Causes of pericardial effusion: • Idiopathic: no cause identified • Radiation • Infection • Viral: coxsackievirus, echovirus, adenovirus, EBV, CMV, influenza, varicella, rubella, HIV, HepB, parvovirus B19, mumps • Bacterial: staph, strep, pneumococcus, haemophilus, Neisseria (gonorrhea/meningitides), chlamydia (psittaci/trachomatis), legionella, TB, salmonella, lymedz • Fungal: histo, aspergillus, blastomycosis, coccidiodomycosis, actinomycosis, nocardia, candida • Other: parasitic (echinococcus, amebiasis, toxoplasmosis), infective endocarditis with valve ring abscess

  12. Neoplastic: metastatic, primary • Cardiac: dissecting aortic aneurysm, post cardiac surgery, myocardial infarction, myocardial rupture • Trauma: blunt/penetrating, iatrogenic (perforation during percutaneous intervention, CPR, post thoracic surgery) • Autoimmune: RA, SLE, vasculitis, scleroderma, mixed connective disease. Sarcoidosis, PAN, IBD, behcet’s, Whipple’s • Drugs: procainamide, isoniazid, hydralazine – drug induced lupus, cromolyn sodium, dantrolene, methysergide, anticoagulation, thrombolytics, phenytoin, penicillin, phenylbutazone, doxorubicin • Metabolic: hypothyroidism, uremia

  13. Presentation: • Depends upon length of time pericardial fluid accumulates • Acute cardiac tamponade: occurs w/in minutes, usually caused by trauma, aortic or cardiac rupture, complication of invasive procedure. Resembles cardiogenic shock • Subacute cardiac tamponade: may be asymptomatic initially, occurs over days or weeks and can be associated with neoplastic, uremic or idiopathic pericarditis. Symptoms include dyspnea, chest discomfort, peripheral edema, pts may have hypotension or hypertension in pts with preexisting HTN

  14. Low pressure (occult) tamponade: Occurs in pts who are severely hypovolemic, intracardiac and pericardial diastolic pressures are only 6-12mmHg. Seen in pts who have been overdiuresed, traumatic hemorrhage, HD or ultrafiltration • Regional cardiac tamponade: localized hematoma or loculated effusion can produce regional tamponade in which only some chambers are compressed, typical signs of cardiac tamponade are usually absent, most often seen after pericariodotomy, or MI

  15. Physical Exam Findings: • “Beck’s Triad” hypotension, distended neck veins, muffled heart sounds • Sinus tachycardia: attempt to maintain cardiac output, bradycardia seen in effusion due to hypothyroidism, HR may be normal in pts with early cardiac tamponade • Elevated JVP: May be associated with venous distention in the forehead and scalp, x descent is preserved while the y descent is attenuated or absent because of the limited or absent late diastolic filling of the ventricle • Pulsus paradoxus: abnormally large decrease in SBP > 10mmHg on inspiration, found in moderate to severe cardiac tamponade, direct consequence of ventricular interdependence • Pericardial rub: seen in inflammatory process

  16. Imaging Studies: EKG: sinus tachycardia, low voltage, electrical alternans

  17. CXR: enlarged cardiac silhouette with clear lung fields. Not usually seen in acute cardiac tamponade as pericardial fluid usually less than 200mL

  18. Echo: • Moderate to large effusion present • swinging of the heart w/in effusion can be seen • cardiac chamber collapse • Diastolic collapse of the right atrium. • Diastolic collapse of the right ventricle • Chamber collapse occurs when intrapericardial pressure exceeds intracardiac pressures • Left sided chamber collapse – left atrial collapse seen in approx. 25% of pts • IVC plethora: dilatation and <50% reduction in IVC diameter during inspiration

  19. JVP tracing: Tricuspid closed RA contraction Ventricular filling Atrial filling

  20. Pathophysiology • RA pressure becomes negligible • Competition between right atrium and right ventricle • Cardiopulmonary interactions: • Normal: • both pleural and intrapericardial pressure ↓ during inspiration and remain negative during resp. cycle • Pressure depression during inspiration is transmitted to the heart and esp. the right heart leading to an ↑ in filling of R. cavities by increasing SVR • Increase in anterograde tricuspid flow  dilation of RV and expense of LV (ventricular interdependence)  increase in RV ejection • Tamponade: • Phenomenon is amplified: during inspiration expansion of the RV compresses the LV which decreases pulmonary venous return,  ↓LV filling, ↓SV  inspiratory ↓ in SBP

  21. Respiratory variation in volumes and flows: • during inspiration the ventricular and atrial septa move leftward, which is reversed with expiration. • Variation of mitral and tricuspid flow velocities is greatly increased and out of phase, reflecting the increased ventricular interdependence in which the hemodynamics of the left and right heart chambers are directly influenced by each other to a much greater degree than normal. • Normally between 20 – 25% variation in amplitude of inflow and outflow signals across the valves during respiration. • In cardiac tamponade mitral flow variation usually exceeds 30% tricuspid valve flow usually exceeds 60%

  22. Treatment • Temporizing measure: • Fluid resuscitation and/or inotropic support • Avoid intubation and mechanical ventilation if possible • Definitive treatment: • Pericardiocentesis with removal of fluid • Percutaneous preferred over surgical

  23. Back to the Case: • Catheter was left in place after initial removal of fluid • An additional 725cc fluid removed 24 hours after pericardiocentesis was performed • Effusion cytology showed rare poorly preserved atypical cells, cannot exclude malignancy • Pt remained unresponsive • Family elected to make pt comfort care after a discussion with pt’s oncologist, he died 4 days after admission

  24. References • Bodson, L., Bouferrache, K, Vieullard-Baron, A. (2011). Cardiac Tamponade. Current opinion in Critical Care. Vol 17: 416-424 • Funk, D.J., Jacobson, E., Kumar, A. (2013). Role of the venous return in Critical Illness and shock: Part II, Shock and Mechanical Ventilation. Critical Care Medicine. Vol 41: 573 - 579 • Jacob, S., Sebastian, J., Et al. (2008). Pericardial effusion impending tamponade: a look beyond beck’s triad. New England Journal of Medicine. Vol 27: 216 - 219 • Imazio, M. (2014) Volume expansion as a temporizing measure for cardiac tamponade: when and how? European Heart Journal Acute cardiovascular care. Vol3(2): 165-166 • Spodick, D. (2003). Acute Cardiac Tamponade. New England Journal of Medicine. Vol 349: 684-690

  25. Questions?

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