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Cardiac tamponade BY PANKAJ
This document discusses cardiac tamponade, including its anatomy, physiology, causes, clinical presentation, diagnosis and treatment. Cardiac tamponade is caused by an accumulation of fluid in the pericardial space that compresses the heart and impairs diastolic filling. It presents with symptoms like chest pain, dyspnea and pulsus paradoxus. Diagnosis is made through echocardiography, ECG changes and chest x-ray. Treatment involves drainage of pericardial fluid, usually through pericardiocentesis, along with medical management including oxygen, medications and ventilation.
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Introduction to the topic of Cardiac Tamponade by Nurse Practitioner Pankaj Singh Rana from Swami Rama Himalayan University.
Discusses the pericardial anatomy, including the visceral and parietal layers, with fluid volumes in the pericardial space.
Explains the physiological role of the pericardium, its effects on cardiac chambers, and the concept of pericardial reserve volume.
Reviews how chronic pericardial stretching affects cardiac function and outlines its mechanical and immunological functions.
Describes the impact of fluid accumulation on cardiac chamber filling, leading to decreased cardiac output and signs of systemic congestion.
Outlines various causes of cardiac tamponade including idiopathic, infectious, and trauma-related factors.
Lists non-specific and specific symptoms associated with cardiac tamponade, including signs of distress and physical findings.
Defines pulsus paradoxus, its causes beyond cardiac tamponade, and how to measure it clinically.
Details significant physical exam findings and diagnostic methods, including JVP, ECG changes, and imaging techniques.Discusses both medical and surgical management strategies for resolving cardiac tamponade, emphasizing therapeutic interventions.
Concludes on the critical nature of cardiac tamponade, emphasizing diagnosis via echocardiography and pericardiocentesis as treatment.
Thanks the audience for their attention and concludes the presentation.
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Cardiac tamponade BY PANKAJ
- 1. CARDIAC TAMPONADE PANKAJ SINGH RANA NURSEPRACTITIONER IN CRITICAL CARE SWAMI RAMA HIMALAYAN UNIVERSITY
- 2. ANOTOMY OF PERICARDIUM Fibro-seroussac The inner visceral layer-- thin layer of mesothelial cells. Parietal pericardium- collagenous fibrous tissue and elastic fibrils. Between the 2 layers lies the pericardial space- 10-50ml of fluid- ultrafiltrate of plasma. Drainage of pericardial fluid is via right lymphatic duct and thoracic duct.
- 3. PERICARDIAL LAYERS Viscerallayer Parietal layer Fibrous pericardium
- 4. PHYSIOLOGY OF PERICARDIUM • Limitsdistension of the cardiac chambers • Facilitates interaction and coupling of the ventricles and atria. • Changes in pressure and volume on one side of the heart can influence pressure and volume on the other side
- 5. • Magnitude &importance of pericardial restraint of vent filling at physiologic cardiac volumes- controversial • Pericardial reserve volume - diff between unstressed pericardial volume and cardiac volume.
- 7. • Chronic stretchingof the pericardium results in "stress relaxation“ • Large but slowly developing effusions do not produce tamponade. • Pericardium adapts to cardiac growth by "creep" (i.e., an increase in volume with constant stretch) and cellular hypertrophy
- 9. FUNCTIONS 1) Effects onchambers Limits short-term cardiac distention Facilitate chamber coupling and disastrous interaction Maintain P-V relation of chambers and output Maintain geometry of left ventricle 2) Effects on whole heart Lubricates, min friction 3) Mechanical barrier to infection 4) Immunologic 5) Vasomotor 6) Fibrinolytic 7) Modulation of myocardial structure and function and gene expression
- 10. PATHOPHYSIOLOGY Accumulation of fluidunder high pressure: compresses cardiac chambers & impairs diastolic filling of both ventricles Decrease SV increase venous pressure Decrease Cardiac Output systemic pulmonary congestion
- 11. Decrease systematic pulmonary Cardiacoutput congestion congestion Hypotension shock Reflex tachycardia ↑JVP hepatomegaly ascites peripheral edema Rales
- 13. CAUSES Idiopathic Infectious-Viral/Bacterial/Mycobacterial/Fungal/Protozoal Immune-inflammatory Connective tissue disease, Early post–myocardial infarction, Post-cardiotomy/thoracotomy, Late post- trauma. Early post–cardiac surgery and post–orthotopic heart transplantation Hemopericardium - Trauma, Post–myocardial infarction free wall rupture, Device and procedure related (percutaneous coronary procedures, implantable defibrillators, pacemakers, post–arrhythmia ablation, post–atrial septal defect closure, post–valve repair or replacement), Dissecting aortic aneurysm.
- 14. Trauma -Blunt and penetrating, Post–cardiopulmonary resuscitation Congenital - Cysts, congenital absence Miscellaneous - Chronic renal failure, dialysis related, Chylopericardium, Hypothyroidism and hyperthyroidism, Amyloidosis, Neoplastic, Radiation Idiopathic pericarditis and any infection, neoplasm, and autoimmune or inflammatory process that can cause pericarditis can cause an effusion
- 15. Bacterial / Mycobacterial / Fungal Hemopericardium Traumatic Iatrogenic Aortic Dissection HIV Uremia / Dialysis associated Malignancy Common Viral Post-MI pericarditis Post cardiotomy, Post cardiac transplant Autoimmune Drug-induced MOST COMMON CAUSE UNCOMMON CAUSE
- 16. CLINICAL SYMPTOMS NOT SPECIFIC Apprehension Chest pain Oppressive precordial Positional Dyspnea Dry Cough Hoarseness Dysphasia
- 17. SPECIFIC General Anxious Apprehensive Ashen gray facies Cool perspiration Tachypnea Tachycardia - Exceptions include patients with bradycardia during uremia and patients with hypothyroidism Tachypnea Jugular venous distension Quiet precordium with both inspection and palpation, Impure muffled heart sounds Rub Peripheral Cyanosis
- 19. PULSUS PARADOXUS Pulsusparadoxus, also paradoxic pulse or paradoxical pulse, is an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is less than 10 mmHg. When the drop is more than 10 mmHg, it is referred to as pulsus paradoxus.
- 20. OTHER CAUSES OFPULSE PARADOXUS Large pulmonary embolus Severe COPD exacerbation Labored respiration Constrictive pericarditis Restrictive cardiomyopathy Right ventricular infarction Circulatory shock Large pleural effusions Tense ascites Extreme obesity
- 21. How to CheckPulsus Paradoxus Place the patient in a position of comfort and conduct manometric studies during baseline respiration. Raise sphygmomanometer pressure until Korotkoff sounds disappear. Lower pressure slowly (2 mmHg per sec) until first Korotkoff sounds are heard during early expiration with their disappearance during inspiration. Record this pressure. Lower pressure until Korotkoff sounds are heard throughout the respiratory cycle with even intensity. Record this pressure. The difference between the two recorded pressures is the Pulsus Paradoxus. Conventionally difference >10 mmHg considered significant. Other definition: Pulsus paradox is greater than or equal to 10% of the pressure at which all Korotkoff sounds are heard with even intensity.
- 22. PHYSICAL EXAMINATION PHYSICAL FINDINGPERCENTAGE PRESENT ELEVATED JVP 100 PULSE PARADOX 98 TACHYPNEA 80 TACHYCARDIA 77 SBP< 100 36 DECREASE HEART SOUND 34 RUB 29 RAPID FALLING BP 25 Physical findings in 56 patients diagnosed with Cardiac Tamponade at the bedside.Circulation. 1981: 64, 633-9
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- 30. MEDICAL MANAGEMENT Oxygenation Increasing the volume may help only in patients with Hypovolemic, since in patients with normovolemia and hypervolemia, volume infusion may increase intracardiac pressures as well as heart size, which in turn increases pericardial pressure, further reducing or eliminating the low transmural myocardial pressures supporting the circulation Bed rest and leg elevation Inotropic drugs ( Dobutamine) Mechanical ventilation with positive airway pressure should be avoided in patients with tamponade, because this further decreases cardiac output
- 31. SURGICAL MANAGMENT Thetreatment of cardiac tamponade is drainage of the pericardial contents, preferably by needle paracentesis, with the use of echocardiography or another type of imaging, such as fluoroscopy or CT.
- 34. CONCLUSION Acute cardiactamponade is a life-threatening, slow or rapid compression of the heart due to the pericardial accumulation of fluid, pus, blood, clots, or gas, as a result of effusion, trauma, or rupture of the heart. The gold standard for the diagnosis of pericardial effusion is echocardiography. The diagnosis of Cardiac Tamponade is based solely on physical exam. In most circumstances, closed pericardiocentesis is the treatment of choice, and is life-saving when performed with adequate precautions.
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