Anaesthetic management of a dog with pericardial effusion for pericardial window surgery

Vigo, 9 years old, male, Labrador, non-castrated, 39 kg at the last presentation in the clinic. After several pericardiocentesis, a total pericardiectomy was decided. On the clinical examination, the dog had rapid breathing, a fast heart rate, and a normal, strong pulse. On the ultrasound examination, there is already ascites, not clinically significant pericardial effusion, and the pericardium is thickened.  There was no need for pericardiocentesis. After the intravenous catheter placement, the patient was premedicated with methadone 0,1mg/ kg, ketamine 1mg/kg, midazolam 0,2 mg/ kg, and propofol 3mg/ kg to effect, intubated, and pre-oxygenated at all times of surgical preparation.  An arterial catheter was placed for invasive blood pressure monitoring and arterial blood sample collection.  At the time of surgery, there was a dopamine infusion of 7mcg/ kg/ min to maintain the blood pressure and heart contractility in normal ranges. Pain management was performed with opioid administration and intercostal block from the 4th to 7th ribs with Ropivacaine 1mg/ kg. There was fluid infusion with RLS all the time from 2- 5ml/ kg/ h, depending on the personal need of the patient due to surgery. A rescue analgesia plan with CRI Lidocaine 1mg/kg/h, Ketamine 1mg/kg/h was ready and used. IPPV was performed immediately before the thoracic opening. The hemodynamic support, fluid resuscitation, and vital parameters were closely monitored during the pre-, surgical, and post-operative periods. maintaining the blood pressure in normal ranges. For the pain, there was performed intercostal block from the 4th to 7th ribs was performed with Ropivacaine 1mg/ kg. There was fluid infusion with RLS all the time from 2- 5ml/ kg/ h, depending on the personal need of the patient. Rescue analgesia plan with CRI Lidocaine 1mg/kg/h, Ketamine 1mg/kg/h, Methadone 0,1 mg/kg/h was ready and used. IPPV was performed immediately before the thoracic opening. The hemodynamic support, fluid resuscitation, and the vital parameters were closely monitored during the postoperative period.

The main hemodynamic goals in the anesthetic management of this patient included preservation of preload due to increased intrapericardial pressure and compromised cardiac chamber filling, control of HR to maintain atrial contribution to ventricular filling and avoid decreased CO. Another important goal was to maintain and improve contractility, which is important in patients with decreased myocardial function.

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Pericardial effusions associated with malignancy usually develop slowly, and when the volume of fluid exceeds the limit of stretch of the pericardial membrane, it results in cardiac tamponade. However cardiac effusion or tamponade may be relieved by pericardiocentesis. Malignant pericardial effusions, being chronic and recurrent, are best managed by pericardial window or total pericardiectomy. In this procedure, a passage is created between the pericardial sac and the adjacent space, usually the pleural cavity, for long-term drainage of pericardial fluid. Standard approaches for pericardial windows include a subxiphoid approach and right or left thoracotomy. In this situation, we approached through the left anterior thorax.

Physiology and pathophysiology

The pericardium is the natural covering of the heart, which consists of two layers. The inner visceral, which is thin and connects the epicardium of the heart, and the outer, which is thicker and fibrous. The thickness of the healthy pericardium is 1-2 mm, and between the two layers, there is pericardial serous fluid, which is produced by the mesothelial cells and is drained through the lymphatic system in the right part of the heart. Normally, there is a very small amount of pericardial fluid in the pericardial sac 0, 25ml/kg in a dog. Anatomically, the pericardium is held by ligaments to the diaphragm and sternum. The heart can function normally even without its pericardial sheath because its main function is to stabilize the heart in its natural position and to limit the excess movements of the heart when the position of the body changes.

The pericardial fluid minimizes the friction exerted on the epicardium from normal heart movements during the cardiac cycle and serves to balance hydrostatic pressures over the surface of the heart. The pressure exerted on the cardiac chambers by the pressure within the intrapericardial space prevents acute distention of the chambers and helps optimize atrial and ventricular coupling and filling. The pericardial sac serves as a physical barrier against the spread of infection or neoplastic disease within the mediastinum.

There are several reasons why the function of the pericardium can be disturbed: birth defects, acute or chronic pericarditis, pericardial effusion, and tamponade. In pericardial effusion, as a consequence of an increase in the amount of fluid, the pericardial pressure also increases, which can lead to cardiac tamponade, decreased CO, and blood pressure. Pericardial effusion can be caused by neoplasia, infectious organisms, congenital abnormalities, or idiopathic disease. Pericardial effusion or tamponade is treated by pericardiocentesis to reduce the pressure created and ease the heart's workload. In case of recurrent effusion, surgical removal of the pericardium is recommended.  When effusion accumulates slowly, the pericardium can enlarge to accommodate this increase in volume and, if intrapericardial pressure is low, clinical signs may not be present, and cardiac function remains relatively normal. When effusion accumulates quickly or intrapericardial pressure rises quickly, surpassing the normal diastolic pressure in the right ventricle, cardiac tamponade occurs. Pericardial effusions of large volumes can also compress the lungs and trachea, causing respiratory difficulties and coughing.

In the case of developed pericarditis or a fibrosed and thickened pericardium, the work of the heart becomes difficult and limited by the harder "shell". Once intrapericardial and intracardiac pressures increase beyond a certain limit, cardiac chamber filling and preload are reduced, which causes a drop in stroke volume and cardiac output. This drop in cardiac output causes a reduction in organ perfusion, which triggers compensatory mechanisms including activation of the sympathetic nervous system and the renin-angiotensin-aldosterone axis. The resultant tachycardia, peripheral vasoconstriction, and fluid retention are an attempt to maintain systemic blood pressure, cardiac output, and organ perfusion.

Anaesthetic management

Management of pericardial effusion can be divided into two groups: the pre-tamponade patients, who are hemodynamically stable, and those with tamponade who are not. Unstable patients demand urgent intervention. Since pressure caused by fluid within the pericardial sac is the underlying problem, drainage of the pericardial fluid is a lifesaving procedure.

In pericardial effusion and cardiac tamponade, impaired ventricular diastolic filling leading to a decrease in stroke volume is compensated by an increase in heart rate, contractility, and systemic vascular resistance. Cardiovascular compromise can be worsened by mechanical ventilation, and when it is required, it should be instituted cautiously with the minimal inspiratory pressure required to provide adequate minute ventilation. The combination of positive pressure ventilation that decreases venous return, as well as vasodilation and direct myocardial depression from the anesthetic agents themselves, can result in significant hemodynamic deterioration. Anesthetic considerations in these patients focus on the increase of preload and maintenance of afterload, contractility, and heart rate, and the use of low positive end-expiratory pressure (PEEP) during positive pressure ventilation.

The optimal anesthetic plan varies with the patient's clinical condition, especially the severity of effusion. Local anesthesia is preferred for pain management, as most of the opioids and general anesthetic agents cause myocardial depression and systemic vasodilation. For intravenous induction, ketamine, midazolam, and etomidate are preferred, as the former supports the heart rate, contractility, and systemic vascular tone, and the latter has minimal effects on blood pressure.

The hemodynamic goals are to maintain adequate cardiac output by increasing chronotropy, to decrease afterload, and to decrease right atrial pressures. Dopamine and dobutamine are all appropriate first-choice inotropes. But they all increase the oxygen and metabolic requirements of the myocardium and decrease its perfusion time, and so close monitoring of the hemodynamic parameters is crucial.

The role of fluid resuscitation may have a big advantage. Successful volume expansion primarily depends on the outcome measures defining it (i.e., cardiac index, end-organ perfusion, or patient symptom relief), the type of tamponade, and the overall fluid status of the patient. The effects of hypovolaemia are very obvious. A single fluid challenge is beneficial, especially in the setting of hypotension. Excess fluid administration risks worsening ventricular function in the patient and decreasing their cardiac output. The use of fluid as a bridging management is important in those with a poor preload, and a single fluid challenge is unlikely to cause harm. Subsequent fluid bolus needed to be carefully assessed with the knowledge that they may not be of benefit.

Anesthesia maintenance can be accomplished with various combinations of volatile inhalational agents; intravenous opioids, propofol, and ketamine have all been used successfully. Short- or intermediate-acting muscle relaxants may be used if necessary, but ideally only when the patient does not tolerate positive pressure ventilation. Continuous intravenous infusions of vasopressor or inotropic agents may be required to maintain hemodynamic stability, but they should be considered with their adverse consequences due to excessive vasoconstriction, which may restrict cardiac output. Opioids can be used for postoperative analgesia. Consideration should be given to loco-regional nerve blocks (i.e., intercostal nerve blocks, serratus plane block), preferably under ultrasound control.

The formulation of a perioperative management plan for patients undergoing pericardial drainage procedures should follow general principles common to all causes of pericardial effusion. The plan should be modified specifically according to the etiology, acuity of presentation, the presence of signs or symptoms of tamponade, and the planned surgical approach.

The general perioperative hemodynamic goals are:

·  Preload: Expand intravascular volume to maintain preload (despite the high central venous pressure observed in tamponade physiology).

· Heart rate and rhythm: Avoid bradycardia and treat any bradyarrhythmias if they occur. Maintain sinus rhythm so that cardiac output remains optimal.

· Afterload: Maintain systemic vascular resistance (SVR), which is high in patients with tamponade because of high sympathetic nervous activity. The compensatory cardiovascular mechanisms (tachycardia and raised SVR) must be maintained during the induction of anesthesia.

· Contractility: Maintain optimal contractility and avoid myocardial depressants.

In patients who are in a decompensated hemodynamic state, pericardiocentesis may be performed under local anesthesia.

Clinical case

Clinical history

Vigo, 9 years old labrador for elective pericardiectomy. After two previous pericardiocentesis, the decision for pericardiectomy was made. Previous cytological and culture examinations were negative, and the diagnosis was idiopathic pericarditis. On the day of surgery, he was admitted with minimal pericardial effusion and ascites, which do not require centesis.

Physical examination

On the day of surgery, Vigo was tachypneic, with tachycardia, CRT >2 sec, pink mucous membranes, strong pulse, conscious, and adequate. The only significant abnormality in the preoperative blood tests was mild hypoproteinemia, explained by the patient's condition and effusion. Lateral thoracic access and subtotal pericardiectomy were planned, and a chest tube was placed.

Induction and maintenance of anesthesia

During preoperative preparation, the patient was premedicated with methadone 0.1mg/kg, diazepam 0.2mg/kg, and ketamine 1mg/kg. Induction was done with propofol 3 mg/kg until effect, and intubated with ET 11. Preoxygenation throughout the presurgical preparation for 5-10 min. Two venous and one arterial catheters were placed. The operative field was prepared for left-sided thoracotomy and cleaned with an antiseptic solution. As part of the pain management plan, a local intercostal block was performed under ultrasound guidance from the 3rd to the 7th rib space on the left, using Ropivacaine 1mg/kg. During the surgery, all parameters were normal: HR 115-127bpm, oscillometric blood pressure MAP 60-80mmHg, strong and regular pulse, SpO2 96-98%, T 38.6. LRS infusion 2-5 ml/kg/h. Antibiotic prevention with ampicillin 20mg/ kg intravenously. During the thoracotomy, mechanical ventilation was used with parameters on Pressure Control Mode and SIMV, 10-12 RR, PEEP 3-4mmHg, PIP 7-10 mmHg,a but not exceeding total pressure more than 10- 12 mmHg, and reached the goal for adequate minute volume without compromising the cardiovascular system and saturation above 97%. Unfortunately, arterial blood pressure was not successfully monitored due to technical reasons, but arterial samples were taken for blood gas analysis.  Due to the surgery, it was decided to perform a pericardial window technique instead of subtotal pericardiectomy. A chest tube and nasal catheter were placed for postoperative continuation monitoring and oxygen therapy. The surgery was successful without any anesthetic events.

Test performed and its interpretation

 Because of the open chest surgery and the anesthesia features, it was performed blood gas analysis was repeated after surgery and the next day. The expected acute respiratory acidosis was treated with continual oxygen supplementation via a nasotracheal catheter and FiO2 50%.   Mild hypoproteinemia may be present due to pericardial effusion. ALT may be increased depending on the degree of poor perfusion and chronicity of the condition. After surgery, there is anemia, which was regenerative and monitored closely during the period of recovery.

Postoperative care

The post-operative period went well. After full awakening, Vigo received acepromazine 0.01mg/kg due to his temperament and overexcited behavior. As part of the analgesic plan, meloxicam was included in the pain management regimen. Fluid therapy was continued with maintenance 3ml/kg/h RLS. Oxygen therapy, via nasal catheter and saturation monitoring, oscillometric measurement of blood pressure, and monitoring of physiological parameters were continually performed. The prescribed therapy for the stay in the clinic remained Ampicillin 20mg/kg, Furosemide 2mg/kg, Vetmedin 5mg/kg, rescue analgesia with CRI ketamine 0.8mg/ kg/ h, lidocaine 1mg/ kg/ h, and methadone. 0,05 mg/ kg/ h. The CRI was titrated till the desired effect and stopped the next morning. The chest tube was checked every 2- 4 hours for the first day and replaced on the third day. Because of the elevated liver enzymes hepatoprotection therapy was included. Broad-spectrum antibiotics, diuretics, and Pimobendan were continued at home. The follow-up from Vigo in the next control examinations is that he is feeling good.

Post-surgery X-ray

References:

1. Anesthesia for patients with pericardial disease; M Correia, Department of Anaesthesia and Pain Medicine, Nelson Mandela Children’s Hospital

2. Anesthesia management for pericardiectomy case series study Chunxia Shi , Chao Dong , Lan Yao , Nicole Weiss and Hong Liu, BMC Anesthesiology volume 23, Article number: 191 (2023)

3. Perioperative implications of pericardial effusions and cardiac tamponade, P.R. Madhivathanan, C. Corredor, and A. Smith^,  BJA Educ. 2020 July; 20(7): 226–234., Published online 2020 Jun 12. doi: 10.1016/j.bjae.2020.03.006

4. Clinical approach to etiology, diagnosis, and treatment in dogs with pericardial effusion – a retrospective study;  Meriç KOCATÜRK1 , Hakan SALCI2 , Volkan İPEK3 , Nureddin ÇELİMLİ 2 , Zeki YILMAZ1 Uludağ University, Faculty of Veterinary Medicine, 1Department of Internal Medicine, 2Department of Surgery, 3Department of Pathology, Animal Hospital, Bursa, Turkey

5. Veterinary Emergency and Critical Care Manual, 2nd Edition by Karol A. Mathews