RECAPEM

Cardiac Tamponade

Cardiac Tamponade 

July 12, 2020 via Shahriar.Lahouti

CONTENTS

 

Preface

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Cardiac tamponade is a potentially life-threatening disease process with myriad of 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.1 Prompt diagnosis and appropriate management of tamponade is possible only when a clinician grasps pathophysiology of the disease and diagnostic value of related findings.

Anatomy

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

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

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

Physiology of tamponade

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Normally, there’s roughly 50cc of pericardial fluid. The normal intrapericardial pressure is -4 to 1 mmHg. The unique physical properties of pericardium is conferred by parietal pericardium, the majority of which is composed of collagen fiber which is stiff, and only modest amount of elastin, imparting a small amount of potential stretch, so called the ‘pericardial reserve volume’1. The nature of pericardial pressure to volume relationship is shown below2.

When pericardial fluid accumulation happens beyond the critical point of exhaustion of elastic reserve and remodeling capacity, the intrapericardial pressure (IPP) rapidly rises, and will impair 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 pericardium. In chronic tamponade, pericardium has undergone remodeling, augmenting its stretching capacity, however again a definite amount of elastin will allow only a fixed reserve volume.

In healthy physiologic state, preload of all four chambers change 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 physiologic state:

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

  • Progressive decline in SBP during inspiration (ventricular interdependence): since the RV diastolic filling is impaired 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).
  • 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 return, lead to progressive decline in cardiac output and a narrower pulse pressure.

Spectrum of Tamponade severity

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Cardiac tamponade is Not an “all-or-none” phenomenon, but rather it includes a hemodynamic spectrum

ranging from what is termed ‘hemodynamic tamponade’ on one extreme to the obstructive shock34 at the

other. If the latter was not recognized and managed promptly, it can end up with bradycardic response

and eventually cardiac arrest (PEA).

Hemodynamic tamponade5:

  • 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 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!

  • Pericardial tamponade walks through a spectrum of hemodynamic impairment6. Almost all pericardial effusions impair hemodynamic to some extent. Some patients remain clinically asymptomatic through their course and often effusion fade 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, PCWP, debunking the myth that asymptomatic pericardial effusion is not hemodynamically significant7. This does not imply that all pericardial effusion should be drained, rather a large pericardial effusion ‘may be’ conservatively managed. (Indications for urgent pericardial drainage discussed later)

Causes

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Pericardial effusion can be associated with virtually all causes of pericarditis, but those etiologies with higher

risk for progression to tamponade are8:

  1. Infectious: bacterial, fungal, HIV-associated infections
  2. Neoplastic disease
  3. Hemopericardium:
    1. Chest trauma
    2. Post-MI LV wall rupture
    3. Complication 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 setting of acute myocardial infarction

And finally some conditions almost never progress to tamponade

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

Clinical Presentation

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Tamponade is not a clinical diagnosis6. 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

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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, peripheral edema.

Classic symptoms of tamponade

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  • Exertional Fatigue
  • Syncope or presyncope upon standing or walking
  • Shortness of the breath (despite normal oxygen saturation)
  • Orthopnea
  • Chest tightness
  • Cough, dysphagia
  • Peripheral Edema (in subacute tamponade)
  • Severe tamponade can present with symptoms / signs of shock, e.g. altered mental status.
  • Untreated tamponade ends up with bradycardic response (impending to crash) and ultimately cardiac arrest (PEA)

Physical findings

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  • Tachycardia: is part of 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.
  • Bradicardia: In terminal tamponade (impending to crash), paradoxical bradycardic response may supervene.
  • Tachypnea: by enlarge it’s not a specific sign but highly sensitive for the presence of occult critical illness.
  • Bradypnea: crashing patient impending to arrest develop bradypnea and agonal breathing.
  • Hypotension (e.g. MAP< 65 mmHg): 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.9
  • Shock index (HR/SBP): is a more reliable index than tachycardia or BP alone to reveal underlying occult instability. Shock index > 1 suggests possible shock.
  • Elevated JVP
  • Pulsus paradoxus: Pulsus paradoxus is not a ‘paradoxical’ phenomenon6, rather it is an exaggeration of physiological decrease in SBP with inspiration. Under normal conditions, the decrease in SBP is < 10 mm Hg. The inspiratory drop in SBP is always more than physiologic normal range during all spectrum of tamponade, but may not meet the definition of Pulsus paradoxus ( it’s defined as ↓SBP >10 during inspiration). Even a systolic drop in blood pressure of 8 mmHg may be enough to call ‘impending tamponade’.
    • Condition in which pulsus paradoxus is present despite absence of tamponade10:
      • Obesity
      • Asthma, COPD
      • RVMI
      • PE
      • CHF
      • Tension pneumothorax
      • Bilateral pleural effusion
      • Hypovolemic shock
    • Condition in which pulsus paradoxus is absent despite presence of tamponade:
      • Low pressure tamponade
      • Aortic regurgitation
      • ASD
      • RVH without Pulmonary arterial hypertension
      • Cardiogenic shock due to severe Pericardial tamponade
      • Decreased LV Compliance i.e. Diastolic dysfunction
      • Local pericardial adhesion
      • Positive pressure ventilation
  • Diaphoresis, cool clammy skin, mottling, cyanosis: suggest poor tissue perfusion and possibly shock state.
  • Muffled heart sounds

Subtypes of tamponade11

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

Hypertensive hyperadrenergic tamponade 12, 13

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

Low pressure tamponade14:

  • 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 in improvement of their hemodynamic indices is not well-established.

Tamponade with atypical regional efusion15

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

Tamponade with atypical chamber collapse 16 17 18 19 20

  • The likelihood of cardiac chambers collapse is influenced by:
    • Net balance between the two opposing forces, the IPP which put restraints on cardiac chambers distensibility during diastole, and the intracardiac end-diastolic pressure within each chamber.
    • 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 RV wall has been thickened, including:
    • Right ventricular hypertrophy
    • Tricuspid valve regurgitation
    • Right-sided paced chamber
    • Coexisting severe LV dysfunction
    • Pulmonary arterial hypertension (PAH)

Tamponade in Pulmonary Arterial Hypertension

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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 parietal pericardium resulting in pericardial fluid accumulation.

Development of pericardial effusion in PAH is a compensatory response, so that 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 enlarge, drainage of hemodynamically stable pericardial effusion in PAH is not warranted and is risky.
  • If patient hemodynamic is stable; a gentle trial of diuretic may be tried
  • In unstable patients:
  • Measures to ↓RV afterload in order to optimize RV pressure-volume curve should be attempted prior to disturbing the integrity of the protective pericardial restraint mechanism. This may include administration of pulmonary artery vasodilators such as nitric oxide, or nitroglycerin21 or milrinone22 via Inhalation, and optimizing oxygenation and ventilation (as hypoxia, and acidosis cause pulmonary artery vasoconstriction).
  • As the 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.23

Parasternal short-axis view showing a large pericardial effusion, systolic and diastolic flattening of theinterventricular septum, and severely enlarged right ventricle16

Differential Diagnosis

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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 effusion24

Echocardiography

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Although Bedsideecho is by far the most useful diagnostic tool in recognizing tamponade and plays a crucial life-saving role in diagnostic approach to crashing patients, echocardiographic signs of tamponade are not virtually diagnostic for tamponade in some cases25.

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 size and location of pericardial fluid. 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 includes26:

  • RA diastolic collapse on 2D echo
    • RA collapse during atrial diastole (when tricuspid and mitral valve 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), 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, presence of RA collapse has a PPV of 8%.
    • Pitfalls:
      • False positive finding in large pleural effusion, 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
  • 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)27
    • Normal physiologic respiratory variation in RV inflow and LV inflow velocity is < 25% and < 10% respectively.
    • Different cutoffs have been suggested for diagnosis of tamponade. Variation in RV inflow velocity of ( >50%) and LV inflow velocity (>25%)2829 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 diagnostic value of echocardiographic signs for tamponade

ECG

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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, no features of acute myocardial ischemia30

Labs

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

Objectives

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  • 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 tamponade31 by constellation of findings from history, presenting clinical picture, and specific echocardiographic signs of tamponade.
  • Determine the safest, and most logical methods for drainage of TP, if ever needed

Diagnostic approach

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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, myocardial rupture, are 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, development of septic shock in a patient with underlying chronic pericardial effusion can precipitate 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 intervention32.

Evidence of Cardiac Tamponade

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Pericardial drainage

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Definitive diagnosis of tamponade is only made by improvement of 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 in the experienced hand. There are no absolute contraindications for pericardiocentesis when the patient is in cardiac arrest or when hemodynamic is worsening33.

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).

Resuscitation

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Follow 5 crucial steps to keep your patient alive!

  1. Avoid inotropic medications as possible; since endogenous inotropic stimulation is often maximal in such patients
  2. Avoid Intubation and mechanical ventilation as possible, since positive pressure ventilation can further impair cardiac filling. Employ hemodynamically neutral intubation34, Use minimal PEEP, low inspiratory pressure
  3. Avoid vasodilators, e.g. Nitrates, since this will compromise vasoconstrictor compensatory response
  4. 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 critical role in determining LV cardiac output than does RV preload.35 Several studies show that fluid is not always beneficial in tamponade.36
  5. Avoid diuretics except in certain conditions such as hemodynamically stable patients with PAH, wherein gentle diuretic may be considered

Patients with tamponade and atrial fibrillation with rapid ventricular response

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AF with rapid ventricular response (RVR) 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 heart rate is more than 130-150 bpm.

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

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

Although such patients are poor 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: presence of AF does not distort interpretation of Mitral and Tricuspid valve inflow variation on doppler

Recap

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  • No single finding is sensitive or specific enough to make you think about tamponade.
  • Do not be fooled by BP! Hypotension is a late finding in shock state. Moreover, Hypertensive taponade 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 outcome.
  • 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 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.
  • Prediction tools are not a substitute for clinical judgement of an expert physician.
  • 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. Ultrasound is always your friend!
  • 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.
  • 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.
  • Human body is designed such that low volume states and dehydration are better tolerated than congestion. Volume is not a ‘permanent’ solution for almost any conditions. There is a shifting paradigm to start vasoconstrictor medications sooner for patients in shock states.
  • 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:

The Pericardium (FOAMcast)

Acute Myopericardial Syndromes (EM:RAP)

The Hemodynamically Neutral Intubation (EMcrit RACC)

Pericardial Tamponade (Core Ultrasound)

Top Photo from, Hutchison, Stuart J.Pericardial disease: Clinical diagnostic imaging atlas, Philadelphia, Saunders, Elsevier, 2009

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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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