EXPLANATION


Cardiac tamponade is characterized by compression of the cardiac chambers leading to hemodynamic compromise due to excessive pressure from the accumulation of fluid in the pericardial space. As the intrapericardial volume is relatively fixed, the rate of fluid accumulation and the compliance of the pericardial sac determine the pressure change within this space. When fluid accumulates in a short period of time, even small volumes can result in rapid increases in pressure. The elevated pericardial pressure transmits to the cardiac chambers compromising cardiac filling and ultimately decreasing cardiac output. In contrast, chronic pericardial effusions are defined as those that accumulate over a period of time greater than three months, thereby allowing the pericardial cavity to accommodate fluid without serious hemodynamic compromise up until a critical volume is reached at a later time point. The prolonged time course allows for compensatory mechanisms to develop, such as tachycardia, vasoconstriction, and fluid retention. These mechanisms allow for larger volumes to accumulate before tamponade physiology occurs. Common etiologies of pericardial effusions trauma, autoimmune disease, malignancy, connective tissue disorders, and post-pericardiotomy syndrome.


Patients present with dyspnea, orthopnea, and chest discomfort. Signs include jugular venous distension, systemic hypotension, tachycardia and pulsus paradoxus. Pulsus paradoxus is an exaggeration of the normal decrease in systolic blood pressure of greater than 10 mmHg during normal spontaneous inspiration and is a key diagnostic feature of cardiac tamponade. It results from the effect of ventricular interdependence during the respiratory cycle being exaggerated by tamponade physiology. During inspiration, venous return is augmented which increases right ventricular volume. The increased right ventricular volume causes a shift of the ventricular septum to the left, thereby reducing left ventricular preload leading to a decrease in cardiac output and systemic blood pressure. In patients with large effusions, an electrocardiogram may demonstrate lower voltages and “electrical alternans”, which is characterized by beat-to-beat variation in QRS amplitude and axis due to excessive movement of the heart within the pericardial fluid. Echocardiographic findings include diastolic collapse of the right atrium and right ventricle, and dilation of the inferior vena cava. Pulsus paradoxus is not unique to cardiac tamponade. It is also associated with several other clinical conditions, which include acute asthma, chronic obstructive pulmonary disease exacerbation, and severe hypovolemia. Acute asthma leads to pulsus paradoxus by several mechanisms, including the following: (1) Highly negative intrathoracic pressures during inspiration further augments systemic venous return and decreases left ventricular preload via septal shift; (2) excessively negative intrathoracic pressure during inspiration increases left ventricular afterload; and, (3) lung hyperinflation increases right ventricular afterload by compressing the pulmonary arteries, which further reduces left ventricular preload.


Cardiac tamponade requires treatment with prompt decompression of the pericardial sac to prevent further hemodynamic compromise and cardiovascular collapse. Sedation and anesthesia can lead to cardiovascular collapse by myocardial depression, vasodilation, and blunting of the compensatory sympathetic mechanisms. In addition, positive pressure ventilation can further compromise venous return and exacerbate cardiac chamber compression, increasing the risk of circulatory collapse. Maintenance of compensatory mechanisms such as relative tachycardia, adequate preload, preservation of contractility and spontaneous ventilation are important to maintain cardiac output. Excessive tachycardia and hypotension in the presence of high ventricular end diastolic pressures can also compromise coronary artery perfusion.


The key goals of anesthetic management for subxiphoid percardiocentesis are to allow drainage of pericardial fluid while minimizing the risk of cardiovascular collapse. The safest option is usually local infiltration combined with small doses of sedative medications titrated slowly while maintaining spontaneous ventilation. Medications, fluids, and blood products must be immediately available to treat cardiovascular collapse. Depending on the clinical status of the patient, presence of a surgical team with the patient prepped and draped, before induction of anesthesia, may be required in case a subxiphoid incision is necessary emergently. If surgical drainage under general anesthesia is planned, partial drainage of the pericardial fluid under minimal sedation and local anesthesia may improve cardiovascular reserve and improve hemodynamic stability, allowing for safer induction of anesthesia and intubation with positive pressure ventilation.


A single-center, retrospective study in a tertiary care children’s hospital by Herron et al analyzed their experience with 127 pediatric patients who underwent 153 pericardiocentesis procedures over a 20-year period. The most common etiology of effusion was post-cardiotomy syndrome in 44% of patients. Approximately 60% of the procedures were performed in the cardiac catheterization laboratory. The overall procedural success rate was 92%. Of note, procedures performed at the bedside had a significantly higher failure rate at 17% than those performed in the catheterization laboratory at 1% (p < 0.01). The incidence of adverse events was 4.6%, which included hemopericardium needing emergent surgery, hemopericardium with hypotension, seizure during induction of anesthesia, and needle puncture of the right ventricle.


The correct answer is acute asthma, which can result in pulsus paradoxus as explained above. Aortic stenosis characteristically results in a low amplitude and delayed pulse, known as “pulsus parvus et tardus”. This may be better appreciated with an arterial line or spectral Doppler downstream of the aortic valve. Pulsus alternans is an arterial pulse with the pattern of alternating strong and weak beats, which is associated with severe ventricular dysfunction. The most likely mechanism is that the poorly contractile left ventricle has a reduced stroke volume which leads to an increased end-diastolic volume for the subsequent contraction, resulting in alternating weak and strong pulses. Again, this is more easily appreciated if an arterial line is in place.


REFERENCES


Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015;36(42):2921-2964. doi:10.1093/eurheartj/ehv318


Johnson J, Horner J, Cetta F. Pericardial Diseases. In: Shaddy RE, Penny DJ, Feltes TF, Cetta, Mital S, eds. Moss and Adams’ Heart Disease in Infants, Children and Adolescents. 10th ed. Philadelphia, PA: Wolters Kluwer; 2021:1393-1406.


Mckenzie I, Markakis Zestos M, Stayer S, Andropoulos D. Anesthesia for Miscellaneous Diseases. In: Andropoulos D, Mossad E, Gottlieb, eds. Anesthesia for Congenital Heart Disease. 3rd ed. Hoboken, New Jersey: Wiley Blackwell; 2015:615-618.


Sarkar M, Bhardwaj R, Madabhavi I, Gowda S, Dogra K. Pulsus paradoxus. Clin Respir J. 2018; 12:2321-2331.


Herron C, Forbes TJ, Kobayashi D. Pericardiocentesis in children: 20-year experience at a tertiary children’s hospital. Cardiol Young. 2022; 32 (4): 606–611. doi: 10.1017/S104795112100278X