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    Cardiac Tamponade

    Shahriar Lahouti
    January 9, 2022
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    30 min read

    July 12, 2020 by Shahriar Lahouti. Last update September 10, 2023.

    CONTENTS

    Preface

    Cardiac tamponade is a potentially life-threatening disease process with myriad clinical presentations, frequently resulting in misdiagnosis and mismanagement.

    In clinical practice, cardiac tamponade is not an “all-or-none” phenomenon, but rather a continuum of hemodynamic impairment. Several misconceptions regarding subacute tamponade can make it a challenging diagnosis *. Prompt diagnosis and appropriate management of tamponade is possible only when a clinician grasps the pathophysiology of the disease and the diagnostic value of related findings.

    Anatomy

    Pericardial space is contained by parietal and visceral layers. Arterial supply to the whole pericardium is via branches of the thoracic aorta, and venous flow drains into the superior vena cava. Drainage of pericardial fluid occurs through parietal pericardial lymphatic.

    The parietal pericardium covers the proximal parts of all the great vessels, which is why the rupture of the ascending aorta leads to cardiac tamponade. 

    • Understanding the circulatory dynamic of pericardial fluid helps to grasp the development of pericardial effusion in specific conditions e.g. pulmonary arterial hypertension (discussed later) 

    Physiology of tamponade

    Normally, there’s roughly 50cc of pericardial fluid. The normal intrapericardial pressure is -4 to 1 mm Hg. The unique physical properties of the pericardium are conferred by the parietal pericardium, the majority of which is composed of collagen fiber which is stiff, and only a modest amount of elastin, imparting a small amount of potential stretch, so called the ‘pericardial reserve volume” *. The nature of the pericardial pressure-to-volume relationship is shown below *.

    When pericardial fluid accumulation happens beyond the critical point of exhaustion of elastic reserve and remodeling capacity, the intrapericardial pressure (IPP) rapidly rises and impairs the diastolic filling of the heart.

    • Acute tamponade occurs at a much lesser volume than chronic tamponade, as the pericardium has no time for remodeling the matrix of the pericardium.
    • In chronic tamponade, the pericardium has undergone remodeling, augmenting its stretching capacity, however, a definite amount of elastin will only allow a fixed reserve volume.

    In a healthy physiologic state, the preload of all four chambers changes by inspiration and expiration,  provided that the chambers are operating normally {not on a flat portion of the starling curve}. As shown below, SBP rises during expiration in a physiologic state:

    During tamponade physiology, there is a progressive increase in the IPP, and subsequently cardiac chambers shrink, resulting in reduced diastolic compliance. The following changes happen in a progressive fashion:

    • Progressive decline in SBP during inspiration (ventricular interdependence)
      • Since the RV diastolic filling is jeopardized by the impact of pericardial effusion, the right heart fills during inspiration at the expense of the left heart; therefore the interatrial and interventricular septum bow to the left (picture on the left below). This diminishes LV diastolic filling during inspiration, and therefore LV cardiac output and SBP drop during inspiration (a component of pulsus paradoxus in tamponade).
    • Progressive reducing cardiac output
      • The ongoing shrinkage of cardiac chambers (right-sided chambers collapse earlier than the left side as the right heart filling pressure is lower) during diastole, and reduction in venous inflow to the right atrium, lead to a progressive decline in cardiac output and a narrower pulse pressure.
    physiology of tamponade

    Spectrum of Tamponade severity

    Cardiac tamponade is Not an “all-or-none” phenomenon, rather it has a hemodynamic spectrum ranging from what is called “hemodynamic tamponade” on one extreme to the obstructive shock at the other end *, *. If the latter is not recognized and managed promptly, it can end up with a bradycardic response and eventually cardiac arrest (PEA). 

    Hemodynamic tamponade *

    • IPP is increased but remains to less than 10mmHg
    • IPP equilibrates with right atrial pressure (RAP) but is lower than left atrial pressure(LAP).
    • Chamber collapse does not occur. There’s a minimal decrease in cardiac output and SBP during inspiration, but still lying within the normal range

    Echocardiographic tamponade, aka Impending tamponade

    • 10mmHg< IPP <20mmHg
    • IPP equilibrates with LAP.
    • Collapsing right-sided chambers happen (RA collapses earlier than the RV)
    • Further decrease in SBP during inspiration meets the definition of pulsus paradoxicus.
    • Cardiac output decreases further, but there’s no clinical s/s of shock

    Clinical tamponade (obstructive shock)

    • IPP>20mmHg
    • Severe Cardiac output reduction causes s/s of frank shock

    Debunking a common myth: This pericardial effusion is not hemodynamically significant!

    • Tamponade walks through a spectrum of hemodynamic impairment *. Almost all pericardial effusions impair hemodynamics to some extent. Some patients remain clinically asymptomatic through their course and often effusion fades away following the resolution of possibly benign associated conditions e.g. pericardial inflammation; while others may progress to clinical tamponade manifested as frank shock.
    • Studies have shown that drainage of pericardial fluid even in asymptomatic patients will decrease RAP, and PCWP, debunking the myth that asymptomatic pericardial effusion is not hemodynamically significant *.
      • This does not imply that all pericardial effusion should be drained. A large pericardial effusion ‘may be’ conservatively managed. (Indications for urgent pericardial drainage will be discussed below) 

    Causes

    Pericardial effusion can be associated with virtually all causes of pericarditis, but those etiologies with a higher risk for progression to tamponade are *:

    1. Infectious: bacterial, fungal, HIV-associated infections
    2. Neoplastic disease
    3. Hemopericardium:
      1. Chest trauma
      2. Post-MI LV wall rupture
      3. Complications of cardiac procedure
      4. Aortic dissection

    Other causes of pericardial effusion that are less likely to progress to tamponade

    • Systemic autoimmune disease
    • Early and late pericarditis in the setting of acute myocardial infarction

    Finally, some conditions almost never progress to tamponade

    • Pericardial transudate due to heart failure, or pulmonary hypertension
    • Pericardial transudate in the last trimester of pregnancy

    Clinical presentation

    Tamponade is not a clinical diagnosis *. In fact, clinical diagnosis of tamponade is tricky since none of the suggested symptoms and signs are sensitive or specific. Moreover, clinical presentation varies based on severity and subtypes of tamponade.

    Tempo

    The onset of the disease could be classified into:

    • Acute: Acute cardiac tamponade occurs within minutes, due to trauma, rupture of the heart or aorta, or as a complication of an invasive cardiac procedure. This results in a picture resembling cardiogenic shock that if not timely managed leads to cardiac arrest and death. 
    • Subacute: occurs over days to weeks and is associated with neoplastic, uremic, or idiopathic pericarditis. Symptoms include fatigability, chest tightness, shortness of breath, and peripheral edema. 

    Clinical symptoms of tamponade

    • Shortness of the breath (despite normal oxygen saturation): The most sensitive sign, occurs in ~90% of patients.
    • Exertional fatigue
    • Chest tightness
    • Syncope or presyncope upon standing or walking
    • Orthopnea
    • Peripheral edema (in subacute tamponade)
    • Severe tamponade can present with signs and symptoms of shock, e.g. altered mental status, and multiorgan failure.
    • Untreated tamponade ends up with a bradycardic response (impending to crash) and ultimately cardiac arrest (PEA).

    Physical findings

    • Tachycardia
      • It is part of a compensatory response to diminished cardiac output and in contrast to hypotension, it is almost invariably present in all patients with impending to tamponade, except for patients taking medications that alter the HR, as well as when tamponade is associated with hypothyroidism. 
    • Bradycardia
      • In terminal tamponade (impending to crash), the paradoxical bradycardic response may supervene.
    • Tachypnea
      • By and large, it’s not a specific sign but highly sensitive to the presence of occult critical illness.
    • Bradypnea
      • Crashing patient impending to arrest develop bradypnea and agonal breathing.
    • Hypotension (e.g. MAP< 65 mmHg)
      • It is a late finding in subacute cardiac tamponade. On the other hand, not all patients with subacute tamponade are hypotensive.
      • Studies show that 27% to 43% of patients presenting with subacute tamponade are hypertensive *.
    • Shock index (HR/SBP)
      • SI is a more reliable index than tachycardia or BP alone to reveal underlying occult instability. Shock index > 1 suggests possible shock.
    • Narrow Pulse Pressure
      • It could be an early sign of dropping cardiac output.
    • Elevated JVP
    • Diaphoresis, cool clammy skin, mottling
      • Suggest poor tissue perfusion and shock state.

    Pulsus paradoxus

    Physiologic background: Normally, during inspiration, increased venous inflow to the right ventricle causes an increase in right ventricle size that stimulates a reciprocal compression of the left ventricle (secondary to pericardial restraint), leading to reduced cardiac output. This will cause a drop in systolic blood pressure by ~10 mmHg.

    • Definition: Pulsus paradoxus is present when the decrease in systolic arterial pressure is >10 mmHg during inspiration (shown below).
    • Nomenclature: Pulsus paradoxus is not a ‘paradoxical’ phenomenon *, rather it is an exaggeration of physiological decrease in SBP with inspiration
    • Measurement: It can be measured most accurately by examining the arterial line tracing over several respiratory cycles.

    • Pulsus paradoxus correlates with  👉 variation in echocardiographic flow velocities. see below

       

    Cutoff: In tamponade, the inspiratory drop in SBP is generally >10 mm. However, there is some disagreement about the optimal cutoff value. For patients with severe hypotension, a lower cutoff value will have superior sensitivity. Even a systolic drop in blood pressure of 8 mmHg may be enough to call it ‘impending tamponade’. 

    Specificity: An elevated pulsus is not entirely specific for tamponade. Other causes include *:

    • Obesity
    • Asthma, COPD
    • RVMI
    • PE
    • CHF
    • Tension pneumothorax
    • Bilateral pleural effusion
    • Hypovolemic shock

    Sensitivity: An elevated pulsus is reasonably sensitive, with sources quoting sensitivity rates of 75-98%. However, there are several causes of a falsely normal pulsus despite the presence of tamponade

    • Low-pressure tamponade
    • Aortic regurgitation
    • ASD
    • RVH without pulmonary arterial hypertension
    • Cardiogenic shock due to severe tamponade 
    • Decreased LV Compliance i.e. diastolic dysfunction
    • Local pericardial adhesion
    • Positive pressure ventilation
    •  

    Kussmaul’s sign

    Physiologic background: Normally during inspiration, jugular venous pressure decreases due to negative intrathoracic pressure.

    Definition: Kussmaul’s sign refers to a paradoxical increase in JVP during inspiration 

    Pathophysiologic basis: During inspiration, downward diaphragmatic excursion compresses the abdominal contents. This increases venous return from the abdomen into the thorax. If the RV is unable to accommodate this influx of blood, then increased blood entry into the chest will cause intrathoracic venous congestion which, in turn, increases the jugular vein pressure. 

    Etiology: 

    • Right ventricular failure (either acute or chronic), for example:
      • Right ventricular myocardial infarction.
      • Pulmonary embolism.
    • Constrictive pericarditis or restrictive cardiomyopathy.

    Clinical values

    • Diagnostic value: The presence of Kussmaul’s sign indicates RV dysfunction and requires appropriate investigations for possible causes.
    • Therapeutic value: Kussmaul’s sign reflects an inability of the RV to handle additional preload *. This might theoretically imply that additional volume administration will not be beneficial.

    Subtypes of tamponade

    • Hypertensive hyperadrenergic tamponade *
    • Low-pressure tamponade 
    • Tamponade with atypical regional pericardial effusion
    • Tamponade with atypical chamber collapse 

    Hypertensive hyperadrenergic tamponade * , *

    • Most commonly seen in patients with a history of hypertension, and advanced CKD.
    • Mechanism: Excessive sympathetic-adrenergic response to distress
    • Systolic blood pressure may reach 200 mm Hg; exemplifying the poor correlation of SBP with cardiac output and tissue perfusion
    • ⚠️The most serious treatment error is to treat the hypertension without draining the pericardial fluid since antihypertensive medications will blunt physiologic compensatory response, and cause worsening hemodynamic status. 

    Low-pressure tamponade *

    • In one study, 20% of patients who met catheterization criteria for tamponade were identified to have a lower IPP (< 7mmHg) before pericardiocentesis. 
    • This can happen when ‘severe hypovolemia’ is superimposed on tamponade.
      • Volume loss can be caused by severe traumatic hemorrhage in patients with acute tamponade, or by long-term diuretic use, excessive dialysis, and dehydration in patients with subacute tamponade. 
    • Clinically; their most common presenting finding is dyspnea on exertion.
      • Other classic finding of tamponade e.g. venous distension is less prominent (intravascular volume depletion masks classic finding of tamponade).
    • They fulfill catheterization criteria for diagnosis of tamponade, however, their IPP has modest elevation.
    • Echo: Findings do not differ from classic tamponade, except that IVC is not plumped.
    • Their hemodynamic response, e.g. cardiac output improvement, to therapeutic pericardial fluid drainage is excellent. However, the effect of volume resuscitation on the improvement of their hemodynamic indices is not well-established.
    • Oftentimes the initial step in management involves volume resuscitation e.g. crystalloid or blood depending on the clinical context. This may have one of two general consequences: 
      • The patient stabilizes, and no longer has any significant tamponade. Such patients remain at risk for subsequently developing tamponade, but they don’t represent an immediate emergency.
      • The central filling pressures increase, but this doesn’t cause clinical improvement.  At this point, the patient has transitioned to a typical state of tamponade (aka, “high-pressure tamponade”).

    Tamponade with atypical regional effusion*

    • Etiology: after cardiac surgery, pericardiotomy
    • Localized effusion, if limited around the left heart, may not show up in some typical clinical and echocardiographic findings of classic tamponade, such that the jugular vein distension and right-sided chamber collapse on echo are absent.

    Tamponade with atypical chamber collapse *, *, *, *, *

    • The likelihood of cardiac chamber collapse is influenced by:
      • Net balance between the two opposing forces, the IPP which puts restraints on cardiac chambers distensibility during diastole, and the intracardiac end-diastolic pressure within each chamber. 
      • The wall thickness of cardiac chambers
    • Right-sided chamber collapse may be absent in conditions where either right ventricle end-diastolic pressure is very high, or the RV wall has been thickened, including:
      • Right ventricular hypertrophy (RVH)
      • Tricuspid regurgitation (TR)
      • Right-sided paced chamber
      • Coexisting severe LV dysfunction
      • Pulmonary arterial hypertension (PAH)

    Tamponade in Pulmonary Arterial Hypertension

    Pathogenesis of pericardial effusion in PAH relates to the elevated pulmonary arterial pressure which leads to increased right ventricular and subsequently right atrial filling pressure. Elevated RAP, will impair venous and lymphatic drainage of the parietal pericardium resulting in pericardial fluid accumulation.

    Development of pericardial effusion in PAH is a compensatory response, restraining distensibility of the high-pressured right ventricle and therefore preventing intraventricular and interatrial septal bowing to the left. Thereby it preserves left-sided filling pressure and cardiac output to some degree (Picture on the right below).

    ⚠️It is extremely dangerous to remove pericardial fluid in the context of PAH, as following drainage, restraint to the RV is eliminated, and septal bowing to the left occurs; leading to rapid hemodynamic decompensation of the patient (picture on the left below).

    General management strategies:

    • By and large, drainage of hemodynamically stable pericardial effusion in PAH is not warranted and is risky.
    • If the patient’s hemodynamic is stable; a gentle trial of diuretic may be tried. 
    • In unstable patients: 
      • Measures to ↓RV afterload in order to optimize the RV pressure-volume curve should be attempted prior to disturbing the integrity of the protective pericardial restraint mechanism. This may include the administration of pulmonary artery vasodilators such as nitric oxide, nitroglycerin *, or milrinone * via inhalation, and optimizing oxygenation and ventilation (as hypoxia, and acidosis cause pulmonary artery vasoconstriction).
    • As a last resort, removing a minimal amount of fluid is enough. Gradual drainage is advised. 
    • Development of pericardial effusion in patients with PAH is a poor prognostic sign *.

    Parasternal short-axis view showing a large pericardial effusion, systolic and diastolic flattening of the interventricular septum, and severely enlarged right ventricle 16

    Differential diagnosis

    DDx of acute right heart failure:

    • Pulmonary embolism
    • Right ventricular myocardial infarction
    • Tension pneumothorax

    DDx of chronic right heart failure

    • Constrictive pericarditis
    • Restrictive cardiomyopathy
    • Dilated cardiomyopathy
    • Corpulmonale
    • Tricuspid valve regurgitation, stenosis
    • Cirrhosis
    • Large pleural effusion *

    Echocardiography

    Although Bedside echo is by far the most useful diagnostic tool in recognizing tamponade and plays a crucial life-saving role in diagnostic approaches to crashing patients, echocardiographic signs of tamponade are not virtually diagnostic for tamponade in some cases *. 

    It is important to interpret echocardiographic signs, in the context of a patient’s clinical picture and comorbidities.   

    Echocardiography identifies pericardial effusion, though it should be differentiated from a Large pleural effusion and pericardial fat.

    Echo delineates the size and location of pericardial fluid. The effusion may be loculated or circumferential. The latter is graded into:

    • Small: echo-free space in diastole < 10mm
    • Moderate: 10-20mm
    • Large: > 20mm

    Classic findings for tamponade on echo includes *

    • RA diastolic collapse on 2D echo
      • RA collapse during atrial diastole (when tricuspid and mitral valves are closed) may be considered as an ‘earliest sign’ of tamponade, though it’s not a highly specific finding. The duration of RA collapse (RA Collapse > 1/3 cardiac cycle) is a more accurate sign for tamponade.
      • Although RA collapse is a sensitive sign, the predictive value of the sign is heavily influenced by the clinically derived pretest probability of tamponade. For example, in a patient with aortic dissection and pericardial effusion (High PTP), the presence of RA collapse on echo has a positive predictive value of 89%. On the other hand, in a patient with hypothyroidism and small pericardial effusion, the presence of RA collapse has a PPV of 8%.
      • Pitfalls:
        • False positive finding in large pleural effusion, and severe dehydration.
        • False negative finding in states of ↑ RAP e.g. PAH
    • RV diastolic collapse on 2D echo
      • RV collapse during ventricular diastole is a later finding in tamponade but is a more specific sign than RA collapse.
      • It’s critically important to identify whether RV collapses in diastole (which is pathologic) or in systole (which is normal).
      • Pitfalls:
        • RV diastolic collapse is relatively sensitive (~60%), however, it may be absent if there are other pathologies that increase right-sided pressures (e.g. pulmonary hypertension, right ventricular myocardial infarction, tricuspid regurgitation).
          • In this situation, the collapse of the left atrium may become a useful diagnostic sign.
        • RV diastolic collapse has a high specificity (90%) but it may be seen in low-pressure tamponade or a large left pleural effusion.
    right ventricular collapse in diastole in tamponade
    • IVC Plethora
      • Plethoric IVC (size > 2.1 cm with collapsibility < 50%) is reasonably sensitive but lacks specificity for tamponade.
      • Pitfalls:
        • False negative finding in hypovolemic states.
        • False positive finding in ↑ RAP: Massive PE, PAH, RVMI.
    • Mitral and Tricuspid valve inflow variation on Doppler (echocardiographic sign of pulsus paradoxus in tamponade) *
      • Normal physiologic respiratory variation in RV inflow and LV inflow velocity is < 25% and  < 10% respectively. 
      • Different cutoffs have been suggested for the diagnosis of tamponade. Variation in RV inflow velocity of ( >50%) and  LV inflow velocity (>25%) is seen in cardiac tamponade *, *.
    Hutchison, Stuart J.Pericardial disease: Clinical diagnostic imaging atlas, Philadelphia, Saunders, Elsevier, 2009. LV inflow recording shows the E wave inflow velocity variation of > 25% 

    Summary of echocardiographic signs

    ECG

    Not a sensitive or specific diagnostic tool. Possible findings may include Sinus tachycardia, low voltage (max QRS amplitude < 0.5 mV in the limb leads), electrical alternans, and no features of acute myocardial ischemia *.

    Labs

    Identifying the cause of the pericardial effusion is often suggested by the clinical setting in which it occurs, the size of the effusion, and associated symptoms. 

    If not suggestive, labs may be obtained including CBC, CMP, coagulation studies, thyroid function, inflammatory markers (CRP, ESR), troponin (only if myopericardial syndrome is suspected), ANA.

    • 👉Pearl: The diagnostic yield of pericardial fluid analysis is low.

    Approach to diagnosis and management

    Objectives

    • Recognize critically ill patients
    • Prompt mindful resuscitative efforts.
    • Immediately perform POCUS in unstable patients to identify the possible causes that could explain patient hemodynamic instability 
    • In the presence of pericardial effusion on bedside echo, determine the likelihood probability of tamponade by a constellation of findings from history, presenting a clinical picture, and specific echocardiographic signs of tamponade *.
    • Determine the safest, and most logical methods for drainage of TP, if ever needed 

    Diagnostic approach

    Rapid recognition of patients with tamponade is critical since the underlying hemodynamic derangement can rapidly progress, leading to patient death. Likewise identifying life-threatening etiologies of tamponade, e.g. aortic dissection, and myocardial rupture, is important as these warrant appropriate intervention.

    It is also crucial to search for other disease processes that could otherwise explain the hemodynamic instability (innocent pericardial effusion).

    Not uncommon in practice, patients presenting with shock may have multifactorial hemodynamic insults, i.e. mixed shock. For example, the development of septic shock in a patient with underlying chronic pericardial effusion can precipitate the development of obstructive tamponade physiology in addition to the distributive nature of septic shock. 

    Integrative information obtained from patients’ history, physical exam, ECG, and most importantly bedside echocardiography are critical in diagnostic and therapeutic decision-making, 

    A tree-step scoring system has been proposed and can be employed for triage and appropriate therapeutic decision-making for patients with pericardial effusion who are not in cardiac arrest or impending to arrest. 

    In the presence of indications for surgical drainage e.g. type A aortic dissection, there’s no need to use this scoring system, as patients obviously need urgent intervention *.

    Pericardial drainage

    Definitive diagnosis of tamponade is only made by improvement of the clinical picture and hemodynamic indices following pericardial drainage, however, not all pericardial effusion (even a large one) warrants drainage, and conservative management may be a suitable option in some cases.

    Pericardial drainage is the only definitive treatment of tamponade if indicated. Both catheter pericardiocentesis under echo guidance and surgical drainage with or without pericardiectomy are effective in removing pericardial fluid, however under certain conditions surgical method is preferred (listed below). Pericardiocentesis under echo guidance is a relatively safe procedure for the experienced hand. There are no absolute contraindications for pericardiocentesis when the patient is in cardiac arrest or when hemodynamic is worsening *.

    In general therapeutic pericardiocentesis is not performed for traumatic hemopericardium, rather resuscitative thoracotomy may be considered. 

    Relative contraindications for pericardiocentesis include:

    • Type A aortic dissection
    • Ventricular free wall rupture following AMI
    • Iatrogenic hemopericardium  
    • Recurrent malignant effusion
    • Suspicion of Purulent pericarditis 
    • Bleeding diathesis
    • Severe pulmonary arterial hypertension (PAP >70 mmHg).

    Methods

    Ideally, drainage will typically be performed by cardiology (usually with the placement of a pericardial drain) or cardiothoracic surgery (with the creation of a pericardial window in some patients). However, patients in shock who cannot immediately receive these procedures will require emergent drainage. This section discusses emergent pericardiocentesis, with the caveat that this isn’t the ideal procedure for most patients. Different patients may accumulate the deepest pockets of fluid in variable locations.

    • The subxiphoid approach may generally be less desirable, for the following reasons:
      • The needle needs to traverse a longer distance (especially in obese patients). This may make it impossible to reach the effusion using the finder needle from a central line or pigtail catheter kit. A lumbar puncture (LP) needle may be needed to remove fluid from the subxiphoid position (but this generally doesn’t allow passage of a guidewire through it).
      • A subxiphoid approach introduces a risk of liver laceration causing hemoperitoneum.
    • Parasternal or apical approaches (through the chest wall) may allow fluid to be reached more easily.
      • If a parasternal approach is taken, avoid the internal mammary artery, which often runs vertically a few centimeters lateral to the sternum. Ideally, the internal mammary artery may be identified using Doppler ultrasonography with a linear probe and specifically avoided.
      • Elevating the head of the bed may cause fluid to shift into a more anterior distribution, facilitating pericardiocentesis from a parasternal or apical approach.
      • The needle should be inserted just above a rib in order to avoid the neurovascular bundle (similar to a thoracentesis).
      • Needle insertion should ideally be performed with direct visualization (using an in-plane approach). Continuous negative pressure should be used to aspirate fluid as soon as the needle punctures the pericardium.  The tip of the needle should ideally be seen entering the pericardial space.
      • If amber fluid returns, then fluid may be therapeutically aspirated (or a wire & catheter may be inserted).
      • If bloody fluid returns, there may be some confusion regarding whether the needle is in the pericardium or the ventricle. This can be rapidly sorted out by injecting agitated saline with ultrasound guidance.  Ideally, the bubbles will show up within the pericardium, confirming intrapericardial location.

    Resuscitation

    In some situations, it’s not possible to immediately drain the pericardium. The following measures may provide a bridge to definitive treatment (pericardial drainage). Follow 7 crucial principles to keep your patient alive!

    1. Do not over-resuscitate your patients with fluid in the absence of clinically overt volume loss.
      • The teaching that tamponade is a preload-dependent condition; requiring volume loading is overly simplistic. Ventricular interdependence plays a much more critical role in determining LV cardiac output than does RV preload *.  Several studies show that fluid is not always beneficial in tamponade *.
      • Volume resuscitation should be performed under extreme caution.
        • Patients who are volume-depleted are particularly susceptible to tamponade (low-pressure tamponade). Such patients can be stabilized by fluid administration. In other situations be extremely cautious and administer fluid (if ever required) under careful monitoring.
        • The appearance of Kussmaul’s sign may be an indicator that the limit of pericardial constraint has been exceeded and additional fluid is not beneficial *.
    2. Avoid diuretics except in certain conditions such as hemodynamically stable patients with PAH, wherein gentle diuretics may be considered.
    3. Vasopressor support (e.g. norepinephrine) may be used as a transient bridge to pericardiocentesis.
    4. Avoid inotropic medications as possible; since endogenous inotropic stimulation is often maximal in such patients.
      • Patients with tamponade have a limitation on diastolic filling and stroke volume. Therefore their cardiac output is strongly dependent on heart rate. 
      • Most patients will develop compensatory tachycardia, except those who are taking medications that alter the HR, as well as when tamponade is associated with hypothyroidism.
      • If the patient’s heart rate is inappropriately normal or bradycardic, the use of an inotrope (e.g. epinephrine) to accelerate the heart rate may be beneficial *.
    5. Avoid Intubation and mechanical ventilation as possible, since positive pressure ventilation can further impair cardiac filling.
      • If the patient requires intubation for some other reason, it is generally preferable to drain the pericardium before intubation.
      • Employ hemodynamically neutral intubation *, Use minimal PEEP and low inspiratory pressure.
    6. Avoid vasodilators, e.g. nitrates, since this will compromise vasoconstrictor compensatory response.
    7. Reduce intrapericardial pressure. It is essential to identify and rapidly reverse other contributing factors leading to elevated external pressure compressing diastolic cardiac chambers. Some adjunctive interventions may indirectly reduce the pericardial pressure:
      • Drainage of a large pleural effusion.
      • Reduction of intra-abdominal pressure.
      • Avoiding excessively high PEEP (among intubated patients).

    Tamponade in cardiac arrest

    • Chest compressions alone are unlikely to be beneficial in this situation.
    • The only viable options include:
      • Immediate pericardiocentesis.
      • Immediate thoracotomy.
    • Drainage of the pericardium should probably be prioritized ahead of chest compressions.

    Tamponade and atrial fibrillation with rapid ventricular response

    AF with rapid ventricular response (RVR) is defined as a ventricular rate of more than 100 bpm. Patients with underlying AF rhythm can have RVR during high catecholamine states, fever, etc. however AF is seldom the cause for instability (innocent bystander) unless the heart rate is more than 130-150 bpm. 

    Patients with tamponade are poorly tolerant to atrial fibrillation. Why?

    • Tamponade causes RV early diastolic collapse → ↓RV diastolic filling during the passive phase. 
    • Therefore RV filling is more tightly dependent on atrial kick. This atrial contraction is lost in AF.

    Although such patients are poorly tolerant to AF, trial of rate control medications is not safe as almost all of these drugs have vasodilator properties which can blunt the compensatory response to tamponade, resulting in patient deterioration.

    Rhythm control often is not helpful in chronic AF since even if the rhythm is converted to sinus rhythm, the cardiac output will not significantly improve (atrial stunting). 

    AF with RVR will slow down often when the acute physiologic insult is resolved.

    👉Pearl: the presence of AF does not distort the interpretation of mitral and tricuspid inflow variation on the Doppler study.

    RECAP

    • Do not be fooled by BP! Hypotension is a late finding in a shock state. Moreover, Hypertensive tamponade presents with high BP. Shock Index is a better marker to identify ↑HR in relation to SBP.
    • Not all pericardial effusions are enemies. Pericardial effusion in PAH is a compensatory response of our body to preserve LV cardiac output. Often, draining effusion results in poor outcomes.
    • Do not mistake pleural effusion and pericardial fat for pericardial effusion.
    • Remember that a plumped IVC is not specific for tamponade and is also seen in the state of RV strain (e.g. PAH, RVMI, MPE, biventricular heart failure)
    • If you notice any chamber collapse on echo, Pause there and identify whether it is collapsing during systole or diastole. Systolic collapse per se can happen during a hypovolemic state.
    • During tamponade ‘ventricular interdependence’ is more tightened. This explains the development of the pulsus paradoxus.
    • Mitral and tricuspid valve inflow variation on Doppler is the echocardiographic sign of pulsus paradoxus in tamponade. 
    • Always think about the etiology that has caused tamponade. It might be more life-threatening than tamponade by itself.
    • When tamponade is highly suspected based on a constellation of findings, the job is not done yet! Mixed shock is not uncommon in practice. Perform echocardiography on every shock patient.
    • The most critically ill patients deserve the most aggressive management. Pericardiocentesis is not contraindicated for crashing patients or those in cardiac arrest. In traumatic tamponade, resuscitative thoracotomy is warranted for such patients.
    • The benefit of performing chest compression for patients in cardiac arrest with tamponade is under question.
    • Always calibrate your management to patient physiology. Patients who are on the end-rope of their physiologic reserve are extremely susceptible to even a minor fault. Rate-controlling patients with RVR AF may be counterproductive in such situations.
    • Do not over-resuscitate your patients with fluid. It may be counterproductive as it worsens interventricular septum bulging to the left, further insulting LV cardiac output.

    Going further

    References

    Expand to view the reference list

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    Shahriar Lahouti

    Founder, Chief Editor
    I am Shahriar Lahouti and RECAP EM is my primary FOAMed project. The philosophy of RECAP EM is to promote critical thinking and enlightening the mindsets with most rational, current evidence towards a safer practice.

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