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

293381704_5664537806890011_4414435878500424694_nDr Denica Djodjeva

Central Vet Clinic

Sofia, Bulgaria

 

 

ari-spada-Cn9XO8qeJpE-unsplashVigo, 9 years old, male, labrador, non castrаted, 39 kg at the last present in the clinic. After several pericardiocentesis was decided for subtotal pericardiectomy. On the clinical examination, the dog had rapid breathing, a fast heart rate, and a normal strong pulse. On the ultrasound examination, there are 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 for maintaining 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 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. 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 hemodynamyc support, fluid resuscitation and the vital parameters was closely monitored during the post operative 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.

Introduction

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 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. Inner visceral, which is thin and connects the epicardium of the heart, and 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 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 intra-pericardial 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 abnormality, 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, surpasses the normal diastolic pressure in the right ventricle and 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 is an attempt to maintain systemic blood pressure, cardiac output, and organ perfusion.

Pericardial-disease-1

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 inspiration 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 correlation 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 be not 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, 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, there was performed local intercostal block under ultrasound guidance from the 3rd to the 7th rib space at 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 intravenous. During the thoracotomy, mechanical ventilation was used with parameters on Pressure Control Mode and SIMV, 10-12 RR, PEEP 3-4mmHg, Pinsp 7-10mmHg but not exceeding total pressure more than 10- 12mmHg 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 anesthetic events.20230913_151317

 

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, 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.Vigo 91075-5_page-0001 20230914_191339

 

Basic anaesthesia of brachycefalic dog

denicaDr Denica Djodjeva

Blue Cross Veterinary Clinic

Sofia, Bulgaria

 

 

 

Quite often in our practice we have to sedate or keep under anaesthesia brachycephalic dogs and cats. This is associated with some stress for us, given the peculiarities of the breed. In this article I will try to briefly present the main key points in the anesthesia of brachycephalic breeds, which has gained great popularity in recent years. Will pay attention to their anatomical and physiological features, which are a prerequisite for complications during anesthesia, and how to avoid them and reduce the risk.

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The main specificity of them is the so-called brachycephalic syndrome ( BOAS). It may include narrowed nostrils, a long soft palate, a hypoplastic trachea, or an inverted laryngeal sac. It can be re-applied and used for prolonged trauma to the pharyngeal soft tissues and trachea, which can cause soft tissue outflow or tracheal collapse. This trauma most often occurs when the animal is intubated. Gastroesophageal reflux should not be forgotten, also high vagal tone.

In severe cases of BOAS, airway obstruction may benefit from the development of pulmonary edema. The pathophysiology of post-obstructive pulmonary edema includes the effect of negative intrathoracic pressure on fluid distribution and subsequent hypoxia. High negative intrathoracic pressure causes an increase in venous return to the right atrium, which increases the pulmonary artery, while left ventricular function is reduced and afterload is increased. The end result is increased hydrostatic pressure, which aids in the movement of fluids from the capillaries in the interstitium and thus causes pulmonary outflow. Rapid recognition of this condition and taking temporary measures, such as maintaining airway patency, adequate oxygen supply and, if necessary, PPV administration. Diuretics may also be used, but it should be anticipated that hypovolaemia and hypoperfusion may occur during anesthesia and clinical delivery should be considered. And because of the risk of soft tisuue and pulmonary oedema, it’s beneficial to add an corticosteroid in low dose, as prevention. Unless there are a serious contraindications. There are different anaesthesia protocols with dexamethason or methylprednisolon, it’s a matter of personal choice.

Deep sedation in these patients is performed with excessive relaxation of the pectoral muscles and aggravation of airway obstruction. Even if the patient is aggressive, it is good to adhere to lower doses of premedication. The most commonly used combination is of a sedative component, for example an alpha-2-agonist and an opioid. A tranquilizer such as acepromazine and benzodiazepines such as diazepam or midazolam may also be used. Accordingly, the doses are at the discretion and according to the desired effect and treatment.  In the table below I quote some of the most commonly used pre- anaesthetic drugs with the value of the dose. There are no restrictions and contraindications to the use of narcotic drugs in this breed. For induction you can use a different combinations, as benzodiazepine+ propofol or benzodiazepine+ ketamine. Your choice mainly depends on what the end result you whant. In brachycefalic breeds it is recommended the induction to be smooth and fast, so the most suitable drug in this case is propofol.

Given the peculiarity of the birth, it is very important to monitor the brachycephalic patient during the pre-aesthetic period, as relaxation of the pectoral muscles further complicates breathing, reduces the number of respiratory movements and the appropriate patient does not fall into hypoxia. It is recommended that the patient be preoxygenated during the pre-anesthetic period. The administration of 100% oxygen before induction of anesthesia prolongs the time to the onset of arterial hypoxemia.

When intubating a brachycephalic patient, prepare several tube sizes, apparently up to two sizes smaller than you think would be appropriate. It will be useful if you use a laryngoscope, especially when your patient has a long soft palate, as it will help ensure good visibility to the airways.

It is common practice to maintain the patient under inhalation anesthesia during the operation. Isoflurane is most commonly used for this purpose. It should be borne in mind that, like other inhaled anesthetics, it produces a dose-dependent reduction in myocardial contractility, systemic vascular resistance and cardiac preload, followed by a reduction in mean arterial pressure (MAP) and cardiac output in a dose-dependent manner; therefore, the evaporator settings should be kept as low as possible while maintaining an adequate depth of anesthesia.

In brachycephalic breeds, there is a very strong vasovagal tone, which can cause bradycardia, which in turn can lead to AV block or even cardiac arrest. The most common reason for increased vagal tone is severe pain. Advice on this reason for good pain relief of this breed is extremely important. However, if the patient develops severe bradycardia, a use of anticholinergic in an appropriate emergency dose is indicated.

As mentioned earlier, another common complication is gastroesophageal reflux, which can occur at any stage of anesthesia. This can lead to airway obstruction and aspiration pneumonia. Advice for this reason is recommended in the anesthesia protocol to include antiemetics, unless there are serious contraindications. It is recomended to be applied proton pump inhibitors as omeprasole, 4 hours before the planed anaesthesia.

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The recovery period is also not to be underestimated. Here it is important to constantly monitor the patient and be extubated, when we are sure that all reflexes have returned. Especially the swallowing one. The best time to extubate is when our patient has muscle tone in the lower jaw and tries to cough up the endotracheal tubus itself or even better if the patient is tring to chews it. It is important to be positioned in a sternal position with appropriate continuous monitoring.

The anaesthesia of these specific breeds is not so complicated, if know their features and for what to watch out for. With more carefulness and knowinge there is nothing to be afraid of.

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Tabl. Most commonly used pre- anaesthetic drugs

Drug Benefit Side effects Peak onset/duration of action IM dose
Dexmedetomidine,

Medetomidine

Profound sedation, reversible, some analgesic properties, drug sparing (reduction in induction drugs needed) Dose dependent bradycardia 5-15 min IM

2- 3 min IV

Dexmedetomidine 5-15 µg/  kg

 

Medetomidine

3- 10 µg/ kg

Butorphanol Mild analgesia, good sedation Poor analgesia and should not be used for surgical patients 10–15min/lasts for 60–90min 0.1–0.4mg/kg
Buprenorphine Moderate analgesia, mild sedation Moderate analgesia 10- 15 min IV

15-30min IM

/can be given q 6–8 h

0.01–0.04mg/kg
Methadone Good analgesia If given too fast, IV can cause bradycardia and respiratory depression 30min/can be given q 4 – 6 h 0.1–0.4mg/kg
Acepromazine Good anxiolytic, sedation improved when administered with an opioid Hypotension, unreliable sedation when used alone, not reversible 35–40min IM

10- 15 IV

/can be given q 4–6h

0.01–0.05mg/kg