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Canine pericardial effusion — a veterinary nurse's guide

02 May 2018
15 mins read
Volume 9 · Issue 4

Abstract

Pericardial effusion is an emergency that all veterinary nurses (VN) in a variety of roles may encounter. It is the abnormal accumulation of fluid in the pericardium, acute or chronic. There are both acquired and congenital causes, but pericardial effusion is most common in male, large/giant breed dogs. It is paramount that the VN has knowledge of the pathophysiology, presenting clinical signs and management so they can best advise the client, care for the patient (to include triage and monitoring), and assist the veterinary surgeon during pericardiocentesis.

Veterinary nurses (VNs) have a varied and complex role. VNs working in first opinion practices, referral hospitals or as part of a dedicated out of hours clinic may all encounter a patient with pericardial effusion. For this reason it is paramount all VNs have knowledge of its presenting signs and management so they can best advise the client, care for the patient and support the veterinary surgeon (VS). This article aims to provide VNs with a basic overview of the pathophysiology, causes and clinical signs, how to assist with pericardiocentesis and the nursing care of the patient afterwards. The aim is to provide VNs with the knowledge and confidence to assist in emergency situations and to provide patients with the best possible care.

Pathophysiology and cause

The pericardium is a double-layered thin, paper like membrane which is attached to the heart at the base. It forms a protective sac and usually contains 2–10 ml of clear, thin, serous fluid which serves as a lubricant enabling the heart to beat freely (Aspinall and Cappello, 2009; Olcott and Sleeper, 2010a). Pericardial effusion is the abnormal accumulation of fluid within the pericardium; this can be acute or chronic (Laste, 2016). The accumulation of fluid restricts the heart's ability to function resulting in poor circulation and delivery of oxygen and therefore poor tissue perfusion (McDermott, 2015).

Pericardial effusion is commonly associated with cardiac tamponade. Tamponade is the presence of pericardial fluid at increased pressure resulting in compression of the heart and subsequent right sided heart failure (Stepien and Boswood, 2014). Olcott and Sleeper (2010a) expand on this and state tamponade occurs when the intrapericardial pressure exceeds the diastolic right atrial and ventricular pressure. Subsequently, the diastolic right atrium and ventricle collapse inhibiting filling of the right side of the heart. This results in a reduction in cardiac output (CO). Figure 1 shows how CO is affected by heart rate and stroke volume. When tamponade occurs preload is reduced (due to collapse of the right side of the heart and poor filling) and contractility is also affected due to the presence of fluid within the pericardium. If stroke volume is therefore reduced, the body compensates by increasing heart rate (patients often present with tachycardia), however when the body can no longer compensate CO is reduced. As a result blood pressure and delivery of oxygen to tissues (tissue perfusion) is also reduced. Tamponade can occur with both acute and chronic effusions. In acute cases the fluid accumulates quickly and the patient may present with signs of cardiogenic or obstructive shock (weakness, tachycardia, pale mucous membranes with a slow capillary refill time, poor pulses (Stepien and Boswood, 2014)), this is because the pericardium does not have time to stretch resulting in a rapid rise in intrapericardial pressure (Olcott and Sleeper, 2010a). In chronic cases, more commonly seen in veterinary patients (Merck, 2016), the volume of fluid tends to be larger (than in acute cases) as the pericardium has hypertrophied and stretched due to gradual filling. In these cases tamponade occurs due to infiltration and fibrosis of the pericardium which leads to a decreased ability to stretch and therefore accommodate the fluid. Chronic pericardial effusion is also linked to development of right sided congestive heart failure (CHF) (Laste, 2016). Ascites is seen due to activation of the renin-angiotensin-aldosterone system which causes water and sodium to be retained by the kidneys and also due to elevated systemic pressure which results in engorged systemic veins (Olcott and Sleeper, 2010a). Left sided CHF and pulmonary oedema are not commonly associated with pericardial effusion.

Figure 1. Schematic showing factors affecting cardiac output.

Pericardial effusion occurs most commonly in middleaged large/giant breed dogs, and there is a predilection for males. Breeds most commonly at risk include: Boxers, Golden Retrievers, German Shepherd Dogs, Bull Dogs, Pugs and Cocker Spaniels (Laste, 2016).

Olcott and Sleeper (2010a) report 0.19% of canine tumours are cardiac in origin. Although rare, cardiac neoplasia is the most common cause of pericardial effusion in canine patients (Aldridge and O'Dwyer, 2013). Haemangiosarcoma and aortic body tumours are the most common neoplastic causes followed by mesothelioma (Olcott and Sleeper, 2010a). In humans a link has been found between exposure to asbestos and development of mesothelioma and early pathological studies suggest this could also be relevant in veterinary patients (Laste, 2016).

Stafford Johnson et al (2004) reported idiopathic haemorrhage/effusion to be the cause of pericardial effusion in 20–75% of cases. Olcott and Sleeper (2010a) state the diagnosis is achieved by excluding other differentials and is most common in Great Danes, St Bernards, Great Pyrenees and Golden Retrievers (Box 1).

Causes of pericardial effusion

  • Idiopathic
  • Inflammatory
  • Secondary to cardiac based tumours:
  • Aortic body tumours e.g. chemodectoma; these originate from chemoreceptors and are more common in brachycephalic breeds
  • Ectopic thyroid carcinoma
  • Haemangiosarcoma (frequently seen in the right atrium); this may not be the primary neoplasm; abdominal ultrasonography should be performed
  • Secondary to infiltrative or diffuse tumours:
  • Mesothelioma
  • Lymphosarcoma
  • Infectious
  • Canine pericardial disease
  • Congenital causes:
  • Partial or total pericardial agenesis
  • Pericardial cysts
  • Peritoneopericardial diaphragmatic hernia (PPDH); this occurs when there is anomalous development of the diaphragm and pleuropericardial membrane which allows abdominal organs to herniate into the pericardial sac
  • (Olcott and Sleeper, 2010a; McDermott, 2015; Laste, 2016)

    Several types of effusion can occur and they are associated with different acquired causes.

  • Transudative:
  • Associated with CHF
  • Hypoalbuminaemia
  • Uraemia.
  • Exudative:
  • Uraemia
  • Infectious due to bacterial, protozoal, fungal and algal sources.
  • Haemorrhagic:
  • Coagulopathy
  • Heart-based tumours
  • Haemangiosarcoma
  • Idiopathic
  • Left atrial rupture (rare) due to trauma or secondary to advanced valvular endocardiosis. Rupture in association with degenerative mitral valve disease is more frequently seen in male Poodles, Cocker Spaniels and Dachshunds, however, any dog with severe degenerative valve disease is at risk
  • Mesothelioma
  • Primary or metastatic cardiac neoplasia (Laste, 2016).
  • Clinical signs

    VNs may be responsible for triaging patients over the phone or on arrival at the veterinary practice. The client may report the following: a history of lethargy, weakness/collapse, exercise intolerance, vomiting and inappetence. Abdominal distension and dyspnoea may be seen in chronic cases (McDermott, 2015; Laste, 2016).

    The clinical signs are fairly non-specific and if presenting in the veterinary practice the VN should perform a physical examination of the three major body systems: cardiovascular, respiratory and neurological. Findings should be reported to the VS; it is important to remember the VN cannot diagnose disease as this is an act of veterinary medicine as detailed in The Veterinary Surgeons Act (1966).

    On clinical examination the patient may present with:

  • A bright, responsive mentation or moribund
  • A pink or pale/muddy mucous membrane colour with a slow, prolonged capillary refill time. Patients with haemorrhagic effusions may have pale mucous membranes and a rapid capillary refill time associated with anaemia
  • Sinus tachycardia; compensatory mechanism for decreased left ventricular stroke volume (see Figure 1)
  • Muffled heart sounds with a pericardial friction rub (an extra heart sound is heard, with three components: one systolic and two diastolic, as a result of friction between the heart and pericardium) and a decreased palpable precordial pulse
  • Dyspnoea and/or tachypnoea. Tachypnoea can occur due to a decreased ability to move the chest wall due to pressure on the diaphragm from ascitic and pleural fluid
  • A cough
  • Arrhythmias; ventricular arrhythmias are common
  • Syncope
  • Hypotension
  • Weak femoral pulses and/or absent peripheral pulses
  • Jugular distension and jugular pulses
  • Pulsus paradoxus; increase in pulse pressure on expiration and decreased pressure on inspiration, this occurs during normal respiration but is accentuated in patients with cardiac tamponade. The variation is palpable
  • Abdominal distension with a fluid thrill; ascites
  • If the patient has peritoneopericardial diaphragmatic hernia (PPDH) there may also be gastrointestinal signs or signs related to the herniated organ, e.g. vomiting, anorexia, diarrhoea. (Rishniw, 2002; Olcott and Sleeper, 2010a; Stepien and Boswood, 2014; McDermott, 2015; Laste, 2016; Merck, 2016).
  • Diagnosis

    Echocardiography

    A definitive diagnosis can be obtained by echocardiography. The VN may assist the VS to perform echocardiography by restraining the patient, usually in lateral recumbancy and administering oxygen therapy (if tolerated). Echocardiography will reveal an echo free space — fluid between the heart and pericardium (Figure 2). If experienced in performing echocardiography the VS may also be able to identify a possible cause, e.g. a mass (Figure 3), or in the case of left atrial rupture, a clot (a hypoechoic structure in the pericardial space). Cardiac tamponade may also be observed in which the right atrium and/or ventricle collapse during diastole (Olcott and Sleeper, 2010a; Laste, 2016).

    Figure 2. Echocardiography demonstrating a pericardial effusion (echo free space on left hand side of image).
    Figure 3. Echocardiography demonstrating a mass.

    Radiography

    In some cases radiographs may be taken on admittance dependent on the patient's demeanour and condition, however, in many cases radiographs may not be performed until the patient has been stabilised as stress can cause the patient to deteriorate. The decision to perform radiographs, their interpretation and diagnosis is the role of the VS, but it is useful for VNs to have knowledge of what may be observed.

    In acute cases the cardiac silhouette may appear normal, however in chronic cases the heart may appear enlarged and globoid (Mazzaferro, 2005). In addition, due to poor CO and possible tamponade the lungs may be hypoper-fused and the pulmonary vessels small. Distention of the caudal vena cava, pleural effusion and/or peritoneal effusion may also be observed. An atypical cardiac silhouette may suggest a tumour. Olcott and Sleeper (2010a) report some heart-based tumours may cause deviation of the trachea. Evidence of metastasis may also be seen (inflated thoracic views, right and left lateral and dorsoventral are recommended under general anaesthesia), this is common with cardiac haemangiosarcoma and mesothelioma.

    In cases of PPDH the peritoneum and pericardium will overlap and abdominal viscera may be seen within the pericardium, sternal deformities are also common (Laste, 2016).

    Abdominal ultrasonography

    The VN may assist the VS to perform abdominal ultrasonography by restraining the patient, ideally in lateral recumbancy and by providing oxygen therapy to the patient if tolerated. Abdominal ultrasonography is recommended if a cardiac mass is not found. Stepien and Boswood (2014) advise this is useful to screen for a primary mass, for example a splenic haemangiosarcoma. Distension of the hepatic vein and the presence of ascites indicates increased systemic pressure which is often seen in patients with cardiac tamponade.

    Electrocardiography (ECG)

    An ECG should be attached to the patient to enable monitoring, this should be attached prior, during and after pericardiocentesis if tolerated. The patient is likely to have a sinus tachycardia and the ECG may show ST segment elevation (McDermott, 2015). The ST segment is the isoelectric section between the end of the S wave and start of the T wave, which represents the interval between ventricular depolarisation and repolarisation (Burns, 2016). Electrical alternans (Figure 4) may also be seen in which the amplitude of the R wave varies beat to beat as the heart swings in the fluid filled pericardium. Electrical alternans usually occurs when the effusion is large; a study by Sacks and Widman (1993) suggested occurrence was most likely when the heart rate is 90–144 beats per minute (bpm). Olcott and Sleeper (2010a) reported that the R wave may also have a decreased amplitude due to increased fluid insulation between the heart and electrodes. Ventricular premature complexes (VPCs) may also be observed and appear as wide and bizarre QRS complexes (Figure 5).

    Figure 4. Electrocardiogram (ECG) trace showing electrical alternans.
    Figure 5. Ventricular premature complexes.

    Laboratory tests

    Where possible, it is recommended to perform a coagulation profile including a prothrombin time prior to pericardiocentesis; this is of particular importance if it is suspected the patient may have a haemorrhagic pericardial effusion secondary to rodenticide toxicity (Mazzaferro, 2005). This may not be possible in all veterinary practices, and the VS will carefully assess the patient's history and clinical condition before performing pericardiocentesis.

    Haematology and biochemistry profiles may reveal prerenal azotaemia, schistocytosis (fragments of red blood cells seen in patients with haemangiosarcoma) and hypoxaemia in acute cases. In chronic cases blood tests may be unremarkable, however in severe cases the patient may have a pre-renal azotaemia and a dilutional hypokalaemia and hyponatraemia secondary to CHF due to activation of the renin-angiotensin-aldosterone system (Rishniw, 2002; Olcott and Sleeper, 2010a).

    How to assist with pericardiocentesis

    It is vital that informed consent is obtained from the client before progressing to pericardiocentesis, as there are several associated complications including: ongoing bleeding; severe ectopy (disturbance of the electrical conduction system resulting in the beat originating from heart tissue which is not usually responsible for impulse transmission); and fatal arrhythmias leading to cardiac arrest and possible death. Conversations of this nature are usually conducted by the VS, but it is important for VNs to have an understanding of the complications and importance of informed consent (Paul, 2016). Figure 6 shows a pericardiocentesis kit prepared for use (Box 2).

    Figure 6. Pericardiocentesis kit prepared for use.

    Equipment

  • Clippers with clean intact clipper blade (No. 40)
  • Skin preparation solution, e.g. chlorhexidine or povidone iodine
  • Swabs
  • Surgical spirit
  • 2% lidocaine
  • 25G ¾ inch needle
  • 2.5 ml syringe
  • Sterile gloves
  • Sterile drape
  • Scalpel blade
  • 14G 5 inch angiocatheters or 16G 6 inch over the needle catheter with additional fenestrations for large dogs, 16–18G 2.5 inch for small dogs
  • 60 ml syringe
  • Three way tap
  • Intravenous fluid extension line
  • Sample tubes; EDTA and serum
  • Kidney dish/collecting jug
  • Crash box
  • Intravenous catheter equipment; suitable size peripheral catheter, tape, bandage material, heparinised saline to check patency
  • Monitoring equipment: electrocardiogram, pulse oximeter, blood pressure
  • Supplemental oxygen and methods of administration: face mask, nasal prongs, flow-by using an anaesthetic circuit
  • If possible, two non-sterile assistants
  • (Olcott and Sleeper, 2010b; Stepien and Boswood, 2014; McDermott, 2015; Merck, 2016)

    Patient preparation

    A peripheral intravenous catheter should be placed to enable the administration of fluid therapy and emergency drugs as directed by the VS (Olcott and Sleeper, 2010b). Some patients may require sedation unless severely compromised. Paul (2016) states if the patient is active or anxious then sedation is advised. Careful consideration of the sedative drugs is necessary; those that result in cardiovascular depression such as phenothiazines (acepromazine) and alpha-2 agonists (medetomidine) should be avoided (McDermott, 2015), however some sources advocate acepromazine can be used at low doses in conjunction with an opioid such as butorphanol (Swift, 2011), this is the decision of the VS.

    Many sources recommend the patient is positioned in left lateral recumbancy (Mazzaferro, 2005; McDermott, 2015). Laste (2016) states that the patient can also be positioned in sternal recumbancy if lateral is not tolerated. Olcott and Sleeper (2010a) concur a left lateral approach can be conducted, but in addition also suggest right lateral. When a significant pericardial effusion is present, distension of the pericardium pushes the lungs dorsally, this results in a ‘cardiac notch’. Positioning of the patient is at the discretion of the VS and the VN should position the patient according to their advice. In general a left lateral approach (e.g. pericardiocentesis performed on the right side which is uppermost) is recommended for the following reasons:

  • The risk of lacerating a major coronary artery is reduced as there are fewer coronary arteries on the right side (Paul, 2016)
  • Recognition of iatrogenic puncture of the left ventricle is easier to detect than the right ventricle as the blood is oxygenated and bright red in colour, which is in contrast to the colour of most effusions — port red
  • The high pressure of the left ventricle makes puncture of it obvious as the blood is at a high velocity so rapid flashback in the catheter hub is seen
  • The left ventricle is thicker than the right so it is less easy to penetrate
  • Presence of a ‘cardiac notch’ between the right cranial and caudal lung lobes means the risk of iatrogenic puncture to the lungs is reduced (Olcott and Sleeper, 2010a).
  • The VN should clip a 10 cm2 patch caudal to the point of the elbow on the right hand side (if performing pericardiocentesis on this side) of the chest using clippers with a no. 40 clean, intact blade. The area should then be aseptically prepared (Mazzaferro, 2005; Olcott and Sleeper, 2010b).

    Many sources advocate infusing 1 mg/kg 2% lidocaine into the skin and intercostal muscles between the 5th and 6th intercostal space (or at the anticipated site) dorsal to the sternum prior to performing pericardiocentesis (Figure 7) (Mazzaferro, 2005; Olcott and Sleeper, 2010b; Laste, 2016). Laste (2016) advises this should be administered just below the costo-chondral junction at the cardiac notch in the lungs. Stepien and Boswood (2014) also recommend performing a local anaesthetic nerve block to innervate the intercostal space in which centesis will be performed. Administration of local anaesthetics should be performed by the VS. A full surgical skin prep should then be conducted (usually performed by the VN) and once the VS has donned sterile gloves the area should be draped (Olcott and Sleeper, 2010b).

    Figure 7. Administration of local anaesthetic prior to pericardiocentesis.

    Pericardiocentesis technique and the nurses role

    Where staffing levels allow it is useful to have two VNs to assist with pericardiocentesis; one to monitor the patient and one to assist the VS (Olcott and Sleeper, 2010b).

    Laste (2016) recommends using a pericardiocentesis catheter rather than an over the needle catheter, as a fenestrated over the needle catheter may lead to incomplete drainage or spillage of the effusion into the thoracic cavity.

    The VS should identify the anatomical landmarks prior to making an incision to minimise the likelihood of lacerating the coronary artery (Rishniw, 2002; McDermott, 2015). A small cutaneous incision should be made using a scalpel blade. The catheter can then be advanced slowly through the skin and thoracic wall, a pop may be felt when it enters the pleural space. The catheter is advanced further in the direction of the opposite scapula (Olcott and Sleeper, 2010b; McDermott, 2015). It is vital the VN closely monitors the ECG during this stage for changes in heart rate or rhythm. As the catheter is introduced a flash of blood will be observed in the catheter hub, this is usually port wine coloured. The stylet should be removed and the catheter connected to extension tubing and the three way tap and 60 ml syringe (Figure 8) (Mazzaferro, 2005). While the VS holds the catheter in place the VN will be required to put gentle negative pressure on the syringe to remove the effusion. The fluid should constantly be checked to ensure it is not clotting. Fluid removed from the pericardium should not clot as it has already undergone fibrinolysis. If the fluid clots this indicates an active bleed, acute haemorrhage or could be as a result of iatrogenic trauma to the ventricular lumen;, and the pericardiocentesis should be stopped (Olcott and Sleeper, 2010b). The total volume of fluid removed should be recorded.

    Figure 8. Removal of a pericardial effusion using a pericardiocentesis catheter and syringe with gentle negative pressure.

    Samples should be collected for bacterial culture and cytology, these should be placed in an EDTA and serum tube (Laste, 2016). Diagnosis of a neoplastic cause can be difficult during cytological examination as reactive mesothelial cells can be present in benign effusions, despite this cytology is recommended particularly if an inflammatory cause is likely (Olcott and Sleeper, 2010a). McDermott (2015) also recommends checking the packed cell volume of the sample.

    When monitoring the patient it is vital an ECG is attached (Mazzaferro, 2005). When the catheter is introduced ventricular arrhythmias such as VPCs may be observed, this can occur if the tip of the catheter touches the epicardium, the VS should withdraw the catheter slightly. The ECG should be monitored closely throughout the procedure. A decrease in heart rate indicates relief of cardiac tamponade (Laste, 2016). Removal of small volumes of fluid is often sufficient to improve ventricular preload and therefore CO (see Figure 1) (Mazzaferro, 2005).

    Nursing care

    Monitoring of the patient post pericardiocentesis is the same for any patient recovering from a sedation. One to one care and monitoring is recommended where possible. The following parameters should be monitored: temperature, heart rate and pulse rate/quality, respiratory rate and effort, mucous membrane colour, capillary refill time, blood pressure and level of consciousness (Lamb, 2009; McDermott, 2015). An ECG should also be monitored for the first 12–24 hours post pericardiocentesis either continuously or intermittently depending on what the patient will tolerate (Lamb, 2009; Laste, 2016). The patient should be monitored closely for signs of pain and discomfort (McDermott, 2015), completion of a pain score may aid the VS in deciding whether pain relief is required and if when administered it is sufficient. The author recommends the use of the modified Glasgow Composite pain scale as this is easy to use and interpret (Figure 9). Standard nursing care should also not be overlooked; a holistic care plan can be completed and implemented following discussion with the owner about the patient's normal routines. Provision of a comfortable, absorbent bed to prevent scalds and decubitus ulcers, carefully tempting the patient to eat and providing TLC are all important for patient recovery.

    Figure 9. The Modified Glasgow Composite Pain Scale for Canine Patients.

    The site of pericardiocentesis should also be monitored closely for signs of haemorrhage (McDermott, 2015). Some VS may place a skin staple or suture across the skin incision. It is vital the VS is informed of any wound complications so prompt treatment can be given.

    Administration of fluid therapy is at the discretion of the VS and is dependent on the patient's haemodynamic status (Laste, 2016). Merck (2016) recommends the use of parenteral fluid therapy before, during and after pericardiocentesis particularly in patients with obstructive/cardiogenic shock and/or hypovolaemic shock (Stepien and Boswood, 2014).

    Some sources advocate the use of diuretics, e.g. furosemide, to remove the fluid, if blood pressure is stable. However, Olcott and Sleeper (2010a) state the use of diuretics may worsen the patient's clinical condition as it reduces cardiac preload and therefore CO (Figure 1). In a patient whose CO is already reduced this can be life threatening. In patients with a chronic effusion and right-sided CHF, Rishniw (2002) asserts diuretics may be of benefit following pericardiocentesis to evacuate any ascitic fluid, however, usually this fluid is mobilised within 48 hours without administration of a diuretic. Kittleson (2007) concurs that diuretics may be useful in patients that are uncomfortable or dyspnoeic. If there is a large pleural effusion then thoracocentesis is advised.

    The patient should be monitored closely for signs of reoccurrence, these may include a return of previous clinical signs, a change in ECG trace, e.g. arrhythmias, tachycardia, muffled heart sounds and pale mucous membranes (Mazzaferro, 2005; Laste, 2016). If monitoring of central venous pressure (CVP) is available (this requires placement of a central line which is contraindicated in patients with coagulopathies), then an increase in CVP (normal is 0–5 cm/H2O) will be seen if the pericardial effusion reoccurs (McDermott, 2015). Repeat echocardiography enables the VS to identify subclinical reoccurrence, this should be performed where possible to enable rapid identification of reoccurrence before clinical signs occur and subsequent patient discomfort (Olcott and Sleeper, 2010a).

    Complications associated with pericardiocentesis include: death, reoccurrence, thickening of the pericardium due to repeated drainage, infection, pneumothorax, haemothorax and iatrogenic damage to the heart and/or lungs (McDermott, 2015). Laceration of a coronary artery can result in infarction or death (Olcott and Sleeper, 2010b).

    Conclusion

    Pericardial effusion and tamponade is an emergency which VNs in a variety of roles may encounter. Through understanding of the pathophysiology, presenting signs, management and nursing care, VNs should have the confidence and knowledge to support the VS and provide patients with the best possible care.

    KEY POINTS

  • Pericardial effusion is the abnormal accumulation of fluid within the pericardium, this can be acute or chronic and is most common in male, large or giant breed dogs.
  • Cardiac tamponade is the presence of pericardial fluid at increased pressure resulting in compression of the heart and subsequent right sided heart failure.
  • It is vital veterinary nurses have knowledge of the pathophysiology, clinical signs and management so they can best advise the client, care for the patient and assist the veterinary surgeon.
  • Pericardiocentesis is the removal of fluid from the pericardium.
  • The veterinary nurse requires knowledge of pericardiocentesis including the risks and complications, and the care of the patient afterwards.