Cardiac Tamponade

Cardiac Tamponade: 
  • Cardiac tamponade – Characterized by the accumulation of pericardial fluid under pressure.  
  • Constrictive pericarditis – Scarring of pericardium with resultant loss of elasticity of the pericardial sac.  
  • An important pathophysiologic feature of both cardiac tamponade and constrictive pericarditis is greatly enhanced ventricular interaction or 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. 
Mechanism:  In cardiac tamponade, there is compression of all cardiac chambers due to increased pericardial pressure.  As cardiac tamponade progresses, the cardiac chambers become obliterated, and chamber diastolic compliance is reduced.  Eventually, venous return drops. When the pericardium can no longer stretch, very little fluid is needed to cause tamponade. 
  1. Infections like coxsackie, EBV, CMV, influenza, HIV, Hep.B, TB, Bacterial Sepsis 
  2. Malignancy 
  3. Iatrogenic/ Traumatic/ Blunt trauma 
  4. Dissecting aortic aneurysm
  5. Post-MI 
  6. Collagen vascular disease 
  7. Hypothyroidism / Myxedema 
  8. Uremia 
  9. Systemic inflammatory diseases like RA, SLE, vasculitis and mixed connective tissue disorders. 
  10. Drugs 
  11. Radiation 
  12. Dissecting aortic aneurysm 
  13. Idiopathic 
Clinical findings:  Physical findings such as sinus tachycardia, elevated JVP and pulsus paradoxus may be seen. In contrast, Kussmaul's sign (the absence of an inspiratory decline in jugular venous pressure) is not usually seen in cardiac tamponade. 
Pulsus paradoxus  – Pulsus paradoxus, defined as a decrease in systolic blood pressure (>10 mmHg) on inspiration, is a common finding in cardiac tamponade and is due to ventricular interdependence.  
Electrocardiography –  The electrocardiogram (ECG) in cardiac tamponade typically shows sinus tachycardia with low voltage and may also show pulsus alterans.  
  • Chamber collapse – Collapse of any cardiac chamber, but usually the right sided chambers, occurs when intrapericardial pressure exceeds intracardiac pressure within a particular chamber.  
  •  Diastolic collapse of the right atrium:  At end-diastole (during atrial contraction), the RA volume is minimal, but pericardial pressure is maximal, causing the RA to buckle. RA collapse, especially when it persists for more 30% of the cardiac cycle, is highly sensitive and specific for cardiac tamponade. In contrast, brief RA collapse can occur in the absence of cardiac tamponade. 
  •  Diastolic collapse of the right ventricle :  RV diastolic collapse occurs in early diastole when the RV volume is still low. RV diastolic collapse is less sensitive for the presence of cardiac tamponade than RA diastolic collapse, but is very specific for cardiac tamponade.  
  • Left sided chamber collapse:  Left atrial collapse is seen in about 25 percent of patients with hemodynamic compromise and is very specific for cardiac tamponade. Left ventricular collapse is less common since the wall of the left ventricle is more muscular. 
IVC Collapsibility :  Dilatation and less than a 50% IVC collapsibility during inspiration reflects a marked elevation in central venous pressure and is frequently seen in patients with cardiac tamponade. 
Cardiac catheterization :  Two major findings in patients with cardiac tamponade are equalization of diastolic pressures across all cardiac chambers (usually between 10 and 30 mmHg) and characteristic respiratory reciprocation of cardiac pressures – an inspiratory increase in right-sided pressures with reduction in left-sided pressures that are responsible for pulsus paradoxus. 
Differential Diagnosis: 

Acute cardiac tamponade, in which patients typically present with elevated JVP and hypotension, must be distinguished from an acute myocardial infarction (especially with right ventricular involvement), Acute on chronic heart failure, massive PE, constrictive pericarditis and an aortic dissection.  

The former is associated with characteristic electrocardiographic changes of infarction and the latter, in the absence of cardiac tamponade, should not cause an increase in JVP. Pulmonary embolus can cause shortness of breath, hypotension, and even elevated jugular venous pressures, but not pulsus paradoxus.  
In cardiac tamponade, the pericardial space is open and transmits respiratory variation in intrathoracic pressure to the heart. In contrast, patients with constrictive pericarditis have a thickened, rigid pericardium which prevents the normal inspiratory decrease in intrathoracic pressure from being transmitted to the heart. In cardiac tamponade, systemic venous return increases with inspiration, enlarging the right heart and encroaching on the left, while in constrictive pericarditis, systemic venous return does not increase with inspiration under resting conditions. In cardiac tamponade, there is equalization of the right atrial pressure, right and left ventricular diastolic pressures, and pulmonary arterial diastolic pressures. This is different from constrictive pericarditis, where the right atrial pressure is constant during inspiration, while the pulmonary arterial diastolic pressure decreases. 
Treatment :
Pericardiocentesis: Definitive treatment of cardiac tamponade is achieved by removal of the pericardial fluid. Acute removal of as little as 50 mL of fluid is often sufficient to correct the acute hypotension. 
Pericardiocentesis is relatively contraindicated in severe pulmonary hypertension. In severe PH, tamponade may be preventing the RV dilation and thereby its failure. 
Volume repletion – Patients with cardiac tamponade may require volume expansion with agents such as blood, plasma, dextran, or saline, but only as a temporizing measure under therapeutic pericardicentesis can be performed. Increasing the volume may help only in patients with hypovolemia, 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. Moreover, intravenous administration of resuscitative fluid can precipitate tamponade. J Trauma. 2002 Dec;53(6):1183-4 Korean J Anesthesiol. 2013 Jul; 65(1): 71–76
Vasopressors – In patients with cardiac tamponade, vasopressors might be needed to maintain perfusion pressure.  
Avoid Positive pressure ventilation – In patients with cardiac tamponade, positive pressure mechanical ventilation increases the intrathoracic pressures and hence, should be avoided. 
In patients with a normal pericardium, intrathoracic pressure decreases during inspiration, leading to an increase in venous return to the right heart and transient increase in right ventricular chamber size. Because the normal pericardium accommodates the increased venous return by expanding, this increase in venous return does not impair left ventricular filling. 
In constrictive pericarditis the upper limit of cardiac volume is constrained by the inelastic pericardium. The thickened, rigid pericardium prevents the normal inspiratory decrease in intrathoracic pressure from being transmitted to the heart chambers. The abnormal pericardium also does not expand to accommodate increased venous return to the right heart during inspiration. Thus, pulmonary venous pressure, but not left ventricular pressure, declines during inspiration, leading to a reduction in left ventricular volume because of a decrease in the transpulmonary gradient. Because of ventricular interaction, the right heart volume expands via shifting of the interventricular septum. This interaction between the left and right ventricles is termed ventricular interdependence. 
With constrictive pericarditis, early diastolic filling is even more rapid than normal. Compression does not occur until the cardiac volume approximates that of the pericardium, which begins in mid-diastole. As a result, virtually all ventricular filling occurs in early diastole with little or no filling subsequently. As constrictive pericarditis becomes more severe, ventricular volumes and stroke volumes are reduced 
  • An acute accumulation of pericardial fluid of greater than 100 mL will produce haemodynamic effects of tamponade whereas a chronic pericardial collection of fluid up to 2000 mL may occur without imposing any effect upon cardiac output. 

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