U3 O1 - cardiovascular emergencies Flashcards
What is the function of the cardiovascular system?
The function of the cardiovascular system is to deliver oxygen, nutrients and hormones etc. to all tissues; remove waste products; perform a regulatory role and
protect against infection.
For the cardiovascular system to perform the roles to function, what three basic functions must it carry out?
To perform these roles, the cardiovascular system must perform three basic functions:
- maintenance of normal systemic and pulmonary arterial blood pressure
- maintenance of normal tissue perfusion
- maintenance of normal systemic and pulmonary venous pressures
What is cardiac output?
Cardiac output is the volume of blood that is pumped from the heart each minute. It is the product of the heart rate (HR) and stroke volume (SV).
What is stroke volume?
SV is the volume of blood that is pumped by the heart with each beat.
How do you calculate cardiac output?
Cardiac Output = HR x SV
What three main factors determine stroke volume?
The stroke volume is determined by three main factors:
a. the preload (how much blood is within the ventricles prior to the heart
pumping – i.e. the end-diastolic volume)
b. the afterload (i.e. back pressure caused by resistance within blood vessels
and organs that restricts the volume of blood able to leave the heart)
c. the contractility of the heart itself i.e. the heart’s innate strength and elasticity
producing the contraction.
From this it is apparent that the heart will fail to circulate sufficient blood around the body if any one or more of these factors is significantly altered.
What does decreased cardiac output lead to?
Decreased cardiac output leads to decreased tissue perfusion and oxygen delivery with potentially very
serious consequences.
What is blood pressure?
Blood pressure is the pressure of blood within the systemic arterial system.
What is blood pressure an indicator of?
, it is used as an indicator of blood flow or perfusion
What will normal blood pressure and low blood pressure result in?
Normal blood pressure will generally result in good blood flow (perfusion) whereas low blood pressure will result in decreased tissue perfusion
What is a good analogy for understanding blood pressure?
A good analogy is that of a garden hose pipe- a high pressure is created with the tap on full, due to a large volume of water coming out fast; whereas a low-pressure due to the tap being barely on will result in a gentle trickle.
Again, the analogy of the hosepipe can be used. If the thumb is put over the end of the hosepipe so the outflow is partially occluded, the water will come out faster and travel further. By increasing the resistance to flow to one area, there is increased flow under higher pressure to the other areas.
What does blood pressure depend on?
Blood pressure depends on the cardiac output (volume of blood ejected from the heart per minute) and the systemic vascular resistance (how vasoconstricted the
patient is, or how ‘wide’ the tubing is).
Blood Pressure = Cardiac Output x Systemic Vascular Resistance
What compensatory measures does blood pressure have?
Whilst blood pressure is a fairly good indicator of tissue perfusion, it is essential to be aware that compensatory measures (e.g. peripheral vasoconstriction) will help to
maintain the blood pressure even when there is decreased cardiac output due to e.g. hypovolaemia, haemorrhage.
If a blood pressure reads low in shock what does this indicate?
When the blood pressure drops, this usually indicates
a significant reduction in cardiac output - i.e. the patient is moving from compensated to decompensated shock. Because of effective compensatory mechanisms, reduced arterial blood pressure (ABP) is a late change in cardiovascular dysfunction and reduced perfusion. Decreased ABP does not become evident until there is ~ 30% decrease in cardiac output. So clinical parameters such as pale mucous membranes and weak peripheral pulses are important when assessing the patient in the earlier stages, when ABP may be maintained within the normal range by compensatory
mechanisms.
What is heart failure?
Heart failure is defined as inability of the heart to maintain an effective circulation to tissues.
ttleson (2003) defines heart failure as a clinical syndrome, caused by heart disease, that results in systolic and/or diastolic cardiac dysfunction severe enough to overwhelm the cardiovascular system’s compensatory mechanisms. N.B. the presence of a cardiac defect e.g. mitral valve endocarditis does not mean an animal is in heart failure.
Kittleson (2003) defines heart failure as a clinical syndrome, caused by heart disease, that results in systolic and/or diastolic cardiac dysfunction severe enough to overwhelm the cardiovascular system’s compensatory mechanisms. N.B. the presence of a cardiac defect e.g. mitral valve endocardiosis does not mean an animal is in heart failure.
Heart failure occurs when the condition has progressed to an extent where the heart cannot maintain an adequate circulation to the tissues and the compensatory measures are unable to
remedy this.
How can a patient with heart failure maintain effective circulation?
An effective circulation can generally be maintained by
various means e.g. increased heart rate or force of contraction.
What is an analogy to explain how the heart and blood vessels work?
Using another analogy, the heart can be considered to be a pump and the blood vessels the pipes of a plumbing system. If the pump is not functioning
properly pressure in the pipes (and therefore delivery of blood to tissues) is reduced and will not reach some areas at all.
How can heart failure be classified?
Heart failure can be split into forward (low output) and backward (congestive) heart failure. It can also be classified into location e.g. left-sided vs right-sided, or type e.g. myocardial failure.
A patient with heart failure may present with similar signs as an animal in hypovolaemic shock, What is the difference between the two?
Many of the clinical signs of heart failure are due to decreased cell perfusion and the resulting compensatory mechanisms. The patient with heart disease needs to be assessed with caution as many of the compensatory mechanisms seen on
emergency presentation are the same as those in a patient presenting with hypovolaemic shock e.g. pale mucous membranes, prolonged CRT etc. Unlike a
hypovolaemic patient, however, a patient in heart failure will normally have adequate fluid in the ‘pipes’ (blood volume) - the issue is the ‘pump’ not being able to deliver it effectively.
N.B. it is important to remember that a patient with
heart failure/ cardiogenic shock does not have a lack of blood volume. As previously outlined, it is failure of blood to be circulated effectively that is the issue
What following perfusion parameters should be assessed in all emergency presentations?
The following perfusion parameters should be assessed in all emergency presentations (Davis, 2015). N.B. In a patient presenting with heart disease some of
the signs may be depend on what the underlying heart condition is.
1. Mentation: decreased cerebral perfusion will cause decreased mentation, with lack of interest in the surroundings. In extreme cases, the patient may be stuporous or comatose
2. Mucous membrane colour: this will usually be pale or white secondary to decreased perfusion. It may be red if there is vasodilatory/distributive shock
3. Capillary refill time (CRT): this will often be prolonged/slow (> 2 seconds) unless the patient has vasodilatory shock where it may be too rapid (< 1 second) initially
4. Heart rate: in a dog with heart disease, the heart rate will usually be increased (unless there is an arrhythmia e.g. heart block causing a slow heart rate). A cat with heart disease may be tachycardic or bradycardic depending on how advanced the condition is
5. Pulse quality: the quality of central pulses e.g. femoral may be increased, normal or decreased depending on the compensatory mechanisms.
Peripheral pulses may be absent or decreased due to peripheral vasoconstriction
6. Extremity temperature: this will usually decrease secondary to peripheral vasoconstriction and decreased perfusion. If the toe web temperature is > 4˚
lower than the core temperature, hypoperfusion is likely (Aldridge and O’Dwyer, 2013). With vasodilatory/distributive shock, the extremities may feel
unusually warm.
What 3 clinical findings can be attributed to acute, moderate and chronic compensatory mechanisms when the tissues are being under perfused?
The clinical findings can, in part, be attributed to acute, moderate and chronic compensatory mechanisms
- increased heart rate (** unless cardiac arrhythmia)
- peripheral vasoconstriction (pale mucous membranes, prolonged CRT)
- activation of the renin-angiotensin-aldosterone system (RAAS)
What is cardiogenic shock?
Cardiogenic shock is a serious potential complication of forward or backward heart failure where the cardiac output is so low that it cannot maintain adequate tissue
perfusion and oxygenation
What are the causes of cardiogenic shock?
Causes of cardiogenic shock include cardiac tamponade, serious valvular disease/ rupture of the chordae tendinae, congestive heart failure, dilated or hypertrophic cardiomyopathy and serious arrhythmias
When does forward heart failure occur and what might be an example of this?
Forward failure occurs when the left side of the heart cannot pump sufficient oxygenated blood to the body organs, despite there being adequate blood volume
(e.g. failure of the pump/ myocardial failure). An example of a condition that could cause forward failure is severe dilated cardiomyopathy in a dog. N.B. If the cardiac output in a patient with forward/ low output failure is so low that there is persistent hypotension/ hypoperfusion, resulting in decreased oxygen delivery to cells, it is termed cardiogenic shock.
It is, however, only very end-stage chronic and per-acute cardiac conditions that result in forward failure sufficient to cause cardiogenic shock.
Most animals with valvular endocardiosis will succumb (i.e. go into heart failure) due to the complications of the ongoing compensatory side effects (i.e. congestive heart failure), rather than from forward failure.
What is the aim of the bodys compensatory mechanisms?
the body’s priorities are to preserve arterial blood pressure and tissue perfusion, especially of
the main organs. The previously discussed
compensatory mechanisms exist to support this and are especially adapted to address decreased blood volume
How can compensatory mechanisms be problematic for cardiogenic shock?
Some of the compensatory mechanisms, especially the chronic ones, can cause problems in the
patient with heart failure/ cardiogenic shock e.g. fluid retention.
What can forward heart failure occur secondary to?
Forward failure (low output) can occur secondary to several conditions including -
- Arrhythmias
a. Heart blocks
b. Supraventricular tachycardia
c. Ventricular tachycardia - Dilated cardiomyopathy (DCM)
What clinical signs would you expect to see with forward heart failure?
These will vary depending on the severity of the condition and are often related to compensatory mechanisms. There will usually be respiratory signs as well when there is concurrent congestive heart failure. The patient’s heart rate is often very rapid - even faster than could be expected in a patient with hypovolaemia
Clinical signs may include the following
1. exercise intolerance, syncope or collapse due to decreased cardiac output
2. pale mucous membranes
3. weak pulse +/- pulse deficits
4. prolonged CRT (> 2seconds)
5. cold extremities
6. hypotension
7. altered mentation
8. tachycardia (N.B. cats may have bradycardia)
9. reduced urine output
The patient may have cachexia (weakness and wasting due to chronic illness) if tissue perfusion has been poor for a while. There may also be a cardiac murmur,
arrhythmia and signs of respiratory difficulty/ distress- tachypnoea, orthopnoea, cyanosis, blood- stained frothy liquid from the mouth/ nose, etc. (Tabor, 2016). The respiratory signs are due to chronic/ congestive heart failure where fluid is retained and can lead to pulmonary oedema/pleural effusion.
What monitoring device should be in place on a patient that has inappropriate bradycardia or tachycardia?
Inappropriate bradycardia in a collapsed patient with poor pulse quality should also prompt assessment for an underlying cause (e.g. hyperkalaemia). Any patient
with bradycardia or tachycardia on presentation should have an ECG carried out.
Arrythmias are not always evident on auscultation and, whilst the ECG only gives information about the electrical conduction through the heart and not the heart’s pumping ability, if a treatable arrhythmia is present the cardiac function should improve.
What is cahexia?
cachexia (weakness and wasting due to chronic illness)
What will the mean arterial blood pressure be I compensated, early decompensated and decompensated shock?
In early compensatory shock the systolic blood pressure is often normal or slightly reduced; in the early stages of decompensatory shock the patient is likely to be hypotensive (60-70 mmHg) and in late decompensatory shock there is likely to be marked hypotension (<60 mm Hg) which is not responsive to intravenous fluid therapy
What is the shock index?
Davis (2015) discusses using the shock index as a means of quantifying the severity of the shock and response to treatment in veterinary patients. The shock index is the ratio of the heart rate to systolic blood pressure (HR/SBP) and can be used in the clinical assessment of patients to determine if they are in shock - however this is currently more commonly used in human than veterinary medicine.
What information will an ECG give you?
An ECG recording will enable assessment of heart rate and rhythm - it will identify the presence and type of cardiac arrhythmia if present (Unit 1, Outcome 2). It should be noted that an ECG gives information about the electrical conduction system of the heart. On its own it does not indicate how the heart is functioning or whether the patient is in heart failure. It should always be used in combination with physical examination and other diagnostics.
How will testing blood urea nitrogen, specific gravity of urine and measuring urine output give you information about tissue perfusion is shock?
Measurement of blood urea nitrogen (BUN) and creatinine can be used to determine if there is pre-renal azotaemia secondary to poor renal perfusion. Urine output should also be assessed as the patient is likely to be oliguric if there is decreased renal perfusion. N.B. If there is pre-renal azotaemia, the urine specific gravity is like to be normal or increased (> 1.030 dog/ > 1.035 cat) i.e. more concentrated. With renal azotaemia, the urine specific gravity is likely to be decreased (1.008-1.012) as the nephrons are not functioning so cannot concentrate urine. SDMA testing and IRIS staging should be considered if the patient is thought to be concurrently in renal failure, allowing for ongoing monitoring of its status
What blood gas, PH, acid base abnormalities is there likely to be in a patient with shock?
Blood gas, acid-base, pH and electrolyte measurements are of great value in assessing the patient- there is likely to be hypoxaemia, hypercapnia and acidosis.
N.B. the only way to accurately identify hypoxaemia is with the use of arterial blood gas sampling, although this can be technically challenging.
Measuring serum electrolytes may help to identify the cause of a cardiac arrhythmia or potential complications e.g. bradycardia may arise due to hypoadrenocorticism or urethral obstruction (hyperkalaemia).
What use information will a serum lactate should in a patient with shock?
Serial blood lactate assessment is useful to provide information about the patient’s perfusion status and response to treatment. Hyperlactataemia will develop because of anaerobic respiration secondary to decreased cell perfusion and oxygen delivery
What can a POCUS ultrasound help to determine in a patient with shock or heart failure?
FAST/POCUS ultrasound evaluation can demonstrate the presence of abdominal, pleural or pericardial effusion. Short, targeted echocardiographic examination can be performed, in the emergency patient, with the aim of getting specific information
about the heart but without compromising the patient further (Matos and Summerfield, 2018). More comprehensive echocardiography can be performed once the patient is more stable to confirm the diagnosis and assess cardiac structure and
function
What diagnostic tool can be used in a patient with suspected cardiac issues to assess the heart shape and size?
If an underlying cardiac cause is suspected, thoracic radiography could be performed to assess the heart size and shape; and demonstrate signs of congestive
heart failure (engorged pulmonary veins, perihilar pulmonary oedema, pleural effusion etc.). However, radiography should only be performed if the patient is
stable- it is contraindicated if it causes increased patient stress especially in a patient with breathing difficulties.
What are the signs of congestive heart failure on a radiograph?
If an underlying cardiac cause is suspected, thoracic radiography could be performed to assess the heart size and shape; and demonstrate signs of congestive heart failure (engorged pulmonary veins, perihilar pulmonary oedema, pleural effusion etc.).
What nursing care should be carried out on a patient with cardiac failure or cardiogenic shock?
Oxygen supplementation should be provided in the manner least likely to stress the patient whilst also increasing blood oxygen levels. Patient movement should be restricted with the patient supported in sternal recumbency, if possible, in a manner
that does not interfere with its ability to breath. The patient should be cage rested in a quiet area with minimum stress and closely monitored. Intravenous access should be obtained, as soon as possible, on veterinary direction, without stressing the
patient. For most cardiac patients restraint can induce stress and a sensation of panic. This can be mitigated by using fear free techniques and minimal restraint
approaches.
N.B. Medical management will depend on the underlying cause and presenting signs e.g. forward failure/cardiogenic shock or backward failure and will be discussed in the relevant sections.
What medication is commonly used for pulmonary oedema in patients with cardiac failure?
The patient will probably require diuretic therapy (furosemide) for management of pulmonary oedema which has developed secondary to the pump failure
What effects do inotropes have in patients with cardiac failure?
Inotropes - drugs which increase cardiac contractility and systolic output
What is antiarrhythmic medication?
Antiarrhythmics – drugs used to correct an abnormal heart rhythm e.g. lidocaine for ventricular tachycardia
What type of drug is pimobendan?
Pimobendan – this drug has positive inotropic and vasodilator properties - it is called an inodilator. Since becoming available as a licenced intravenous preparation, it has been used as a first line drug in the management of acute congestive cardiac failure and can also be used in a patient with cardiogenic shock, although it is less potent than dobutamine.
What is the first-line drug used in the management of acute congestive heart failure?
Pimobendan
What conditions might dobutamine be used? and how is it administered?
Dobutamine - this can be administered for a short period as a positive inotrope to a patient with cardiogenic shock, heart failure due to systolic
dysfunction or septic shock (BSAVA, 2020). It can also be used provide myocardial support in a hypotensive patient (BSAVA, 2020). It is a shortacting, positive inotrope, titrated to effect, and delivered as a constant rate infusion (CRI). As this drug is a sympathomimetic, the patient should be monitored closely for adverse signs e.g. supraventricular/ ventricular
arrhythmias and hypertension.
What is dopamine useful for in patients with heart failure? What effects occur with low doses and high doses?
Dopamine - this drug has a similar effect to dobutamine and is useful for improving haemodynamic status especially in septic patients - accessing
dopamine can be problematic, however. Dobutamine is preferred for patients in heart failure (BSAVA, 2020). Dopamine is a catecholamine, precursor of
noradrenaline, with sympathomimetic effects (BSAVA, 2020). It has effects on dopaminergic, beta-1 and alpha-1 adrenergic receptors (BSAVA, 2020). It is also a potent, short-acting drug so it is administered as a CRI to patients that are effectively volume resuscitated- the effects of dopamine depend on the dose administered. At low doses, dopamine acts on dopaminergic and
beta receptors- this causes vasodilation, increased force of contraction (positive inotrope) and increased heart rate (positive chronotrope) (BSAVA, 2020). At higher doses, there are more alpha-1 effects which leads to peripheral vasoconstriction. Perivascular administration can cause tissue ischaemia and slough (BSAVA, 2020). Patients should be monitored closely
for adverse signs during administration e.g. tachycardia, arrhythmia and hypertension.
Where does receptor Alpha-1 adrenergic (α-1) act and what effect does it have?
Receptor type
Alpha-1 adrenergic (α-1)
Location
Blood Vessel
effect
Vasoconstriction
Where does receptor Beta- 1 adrenergic (β-1)act and what effect does it have?
Receptor type
Beta- 1 adrenergic (β-1)
Location
Heart
Effect Positive inotrope (increased strength) Positive chronotrope (increased rate)
Where does receptor Beta- 2 adrenergic (β-2) act and what effect does it have?
Receptor type
Beta- 2 adrenergic (β-2)
Location
Blood Vessels
Effect
Vasodilation
Where does receptor Dopamine act and what effect does it have?
Receptor type
Dopamine
Location
Blood vessels
e.g. kidney
Effect
Vasodilation (other effects elsewhere)
(low dose)
Vasoconstriction (high dose)
When might anti-arrhythmic medications be required in cardiac failure?
Anti-arrhythmic medications may be required for specific cardiac rhythm disturbances- especially serious tachydysrhythmias. N.B. Prompt identification and management of underlying electrolyte abnormalities (e.g. hyperkalaemia hypomagnesia) is essential.
What monitoring is required for an animal in cardiac failure?
This should include monitoring patient demeanour, respiration rate and pattern, heart rate and rhythm and perfusion parameters e.g. central and peripheral pulses, temperature (core and peripheral), mucous membrane colour and CRT. Urine output (normal - 1-2ml/kg/hour), blood pressure and pulse oximeter readings. Ideally, blood gases, pH and lactate levels should all be measured regularly if arterial blood
sampling is possible.
It is important to monitor the patient for any adverse signs too e.g. dehydration from excessive diuretic administration or hypotension from over administration of vasodilators. Renal parameters should ideally be monitored alongside electrolyte levels, especially potassium, as furosemide causes increased urine excretion of potassium.
What is backward heart failure?
Backward failure (also called congestive heart/ cardiac failure) is when one or both ventricles is unable to pump all the blood they contain. As well as not meeting the oxygen demands of the tissues, with backward failure there is a progressive build-up of fluid in the heart chambers and blood vessels behind the failing ventricle(s). If the left ventricle is failing, this results in increased pulmonary venous pressure and / or if the right ventricle is failing there is increased systemic venous pressure. The build - up of fluid in the veins results in fluid leaking from capillaries into tissues (e.g. pulmonary oedema) or body cavities (effusion). These changes in hydrostatic pressure can be attributed to Frank Starling’s Law. Frank Starling’s Law is explained by Delicce and Makaryus (2020). This build-up of fluid results in clinical signs of congestive heart failure. It is further compounded by inappropriate stimulation of the compensatory mechanism caused by decreased tissue perfusion
Which cavity is affected with left sided backward heart failure?
In left-sided backward heart failure in dogs, the excess fluid causes pulmonary vein distention which can, in turn, lead to pulmonary oedema developing. In cats, the fluid tends to accumulate in the pleural space instead resulting in a pleural effusion- N.B. remember that by the time a cat displays clinical signs of respiratory difficulty it is already very compromised.
What signs will patients with pulmonary oedema display? Initially what should the nursing considerations be on triage?
Any patient with pulmonary oedema or pleural effusion will have dyspnoea and exercise intolerance. As RVNs who may be triaging these patients, it is especially
important to avoid causing any stress. Oxygen therapy should be provided in a stress-free manner whilst the veterinary surgeon performs additional stabilisation
measures e.g. administration of diuretics or thoracocentesis. Careful assessment and auscultation during the triage process are essential; as well as having a good underpinning knowledge of the risks of handling these very fragile patients
Which cavity is affected with right -sided backward heart failure?
In right sided backward failure, the excess fluid builds up in the venae cavae leading to jugular distention, hepatomegaly and ultimately ascites.
As with patients with forward failure, in a few cases of backward failure, cardiogenic shock will arise if the circulation is insufficient to adequately perfuse the major organs.
N.B. depending on the underlying cardiac abnormality, some patients will have a combination of forward and backward heart failure.
The pathophysiology, however, of right-sided heart failure is similar. Fluid overload of the right side of the
heart results in distention of the cranial and caudal venae cavae, jugular veins and the liver leading to hepatic congestion and hepatomegaly. This in turn can lead to ascites developing in cats and dogs. Subcutaneous oedema may also be present in some cases, although is less common.
What response does an impaired cardiac function - decreased cardiac output and decreased blood pressure cause?
Impaired cardiac function, of any cause, which results in decreased cardiac output and decreased blood pressure, causes a sympatho-adrenal response with
corresponding compensatory mechanisms
What is the main chronic compensatory mechanism?
the main, chronic compensatory mechanism being activated, the renin-angiotensin- aldosterone system
What does the renin-angiotensin-aldosterone system during the chronic compensatory mechanism do?
the main, chronic compensatory mechanism being activated, the renin-angiotensin- aldosterone system (RAAS), sodium, chloride and water are
retained by the kidneys and peripheral vasoconstriction occurs
Why is the renin-angiotensin-aldosterone compensatory mechanism beneficial to the hypovolaemic patient?
This compensatory mechanism is beneficial in the hypovolaemic patient (e.g. blood loss), as the fluid retention helps to increase the stroke volume and cardiac output by increasing cardiac preload i.e. more fluid is returned to the heart.
Why is the renin-angiotensin-aldosterone compensatory mechanism not beneficial to the heart failure patient?
However, in a patient with a failing heart, the decreased cardiac output is due to heart failure rather than decreased blood volume. The patient has sufficient blood volume but poor pumping ability. In addition, because of peripheral vasoconstriction,
there will be increased resistance to blood flow, further compounding the problem for the ‘pump’. In the patient with heart failure, chronic activation of RAAS leads to
progressive increase in fluid volume in the circulatory system. This is called congestive heart failure. The fluid progressively backs-up behind the left ventricle (in
left-sided failure) with the resulting, increased hydrostatic pressure in the pulmonary veins leading to pulmonary oedema or pleural effusion, as previously outlined.
What secondary conditions may lead to backward congestive heart failure?
Backward (congestive) heart failure may arise secondary to conditions including:
- endocardiosis / myxomatous mitral valve disease (dogs- common)
- hypertrophic cardiomyopathy (cats- common)
- dilated cardiomyopathy (dogs- quite common)
- congenital defects (relatively rare)
- endocarditis (rare)
What are the clinical signs of congestive heart failure?
Congestive cardiac failure is usually a chronic condition but a patient may present as an emergency with dyspnoea, if pulmonary oedema or pleural effusion has developed to such an extent that the patient is now compromised. It is important to note that these patients may have been showing indications of an issue for some time. They may not have been checked, however, as often exercise intolerance and lethargy are attributed to aging. There may be a cough which the client has been monitoring. When taking a telephone call or triaging such a patient, it is important to
be aware that even if the patient is already diagnosed/ on medication, even a minor change in the its condition may indicate decompensation. Some of the clinical signs of a patient presenting with backward failure are like those of a patient presenting with forward failure, especially in severe cases with cardiogenic shock:
1. exercise intolerance or collapse
2. altered mentation
3. rapid, weak pulses
4. tachycardia (N.B. a cat may have bradycardia)
5. cold extremities
6. pale or cyanotic mucous membranes
7. prolonged CRT
8. hypotension
Additional signs may include cough, lethargy, inappetence, vomiting/ diarrhoea and
cachexia.
What are the differences between clinical signs in dogs and cats with congestive heart failure?
Dogs with congestive heart failure will typically be tachycardic due to the sympathoadrenal response, which increases the heart rate in an attempt to maintain cardiac output. Heart rate and rhythm are less reliable indicators of congestive cardiac failure in cats- their clinical findings are more variable. An affected cat may have tachycardia, a normal heart rate, or reflex bradycardia. Thoracic auscultation may reveal a heart murmur and/or arrhythmia e.g. gallop rhythm in a cat with hypertrophic cardiomyopathy. Crackles may be heard on pulmonary auscultation if pulmonary
oedema is present; or lung sounds may be quiet if there is a pleural effusion. A cat may have clinical signs of an underlying condition e.g. hyperthyroidism with weight loss, hair loss, goitre etc. With right-sided heart failure, jugular distension, ascites and, occasionally, subcutaneous oedema may be present. A cat in congestive heart failure may be hypothermic.
What may thrombo or aortic embolisms be caused by and what are the nursing considerations for these patients?
Cats, and dogs less commonly, may present as emergencies due to aortic thromboembolism (ATE) - cardiac disease (3.1.7). Pulmonary thromboembolism (PTE) is another rare but serious complication of heart disease that may occur in dogs and cats. PTE may also be a complication of Angiostrongylus vasorum infection in some canine patients. Patients that present with thromboembolic disease need to be assessed carefully. The outcome for these patients is often poor.
However, treatment of the underlying process, if possible, is key to patient recovery.
While the underlying disease will need to need appropriate treatment high quality nursing care is vital for the recovery of these patients. During hospitalisation, these patients require intensive care nursing, on a 1:1 basis, with close monitoring of
cardiovascular and respiratory function and monitoring for signs of improvement or deterioration. Pain management, recumbency care and respiratory system function are additional important considerations
What signs may a patient show that has presented with a sudden onset of pulmonary oedema from congestive heart failure?
Sometimes a patient with congestive cardiac failure presents as a serious emergency- collapsed, distressed and profoundly dyspnoeic due to fulminant (severe / sudden onset) pulmonary oedema. There may be blood-stained, watery fluid coming from the oral/ nasal cavity; the mucous membranes will be pale, probably cyanotic, with prolonged CRT; the tongue may appear cyanosed; central pulses will be rapid and weak and the heart sounds may be muffled by harsh, crackles from the lung fields. These patients require urgent attention to relieve suffering.
How do you perform acute stabilisation of congestive heart failure?
Acute stabilisation of congestive heart/ cardiac failure (CHF/ CCF), as advised in the ACVIM Consensus Statement (2009) cited by Matos and Summerfield (2018), includes hospitalisation for strict rest and monitoring; oxygen therapy; opioid sedation if anxious/ agitated; furosemide IV (or IM); and appropriate cardiovascular drugs e.g. vasodilators, positive inotropes. Thoracocentesis may be indicated if the
patient has a pleural effusion. N.B. It should be noted that abdominocentesis is rarely indicated in a patient with ascites due to the potential serious complications. If ascites is affecting a patient’s ability to ventilate properly, a small volume may rarely need to be removed but only enough alleviate pressure on the diaphragm. In addition to the risk of infection, if a large volume of ascitic fluid is removed from the
abdomen acute changes in intra-abdominal pressure, potential acid-base and electrolyte disturbances and alteration in proteins can all lead to complications.
What should the initial stabilisation of a dyspnoeic patient include?
Initial stabilisation of the dyspnoeic patient consists of decreasing oxygen requirements (by limiting activity and stress – an initial hands-off approach) and
providing oxygen therapy by the means that causes least stress to the patient. If the patient is collapsed and unconscious, it will require to be intubated and ventilated.
Opioid administration may decrease stress and relieve anxiety thereby, hopefully, improving patient breathing and allowing for examination. Handling should be kept to a minimum and the patient should be in a quiet, low-stress environment. An intravenous catheter should ideally be placed as soon as possible to ensure IV
access should the patient ‘crash’. The decision on whether to place an intravenous catheter should be made, however, with consideration of the patient’s condition- a risk to benefit assessment should be made, and each patient considered individually.
For example, if attempting to place an IV catheter causes stress it could seriously worsen the patient’s condition. Veterinary guidance should be sought prior to placement of an IV catheter in such cases.
How is congestive heart failure initially managed?
If the patient has signs of congestive heart failure, a diuretic, usually furosemide will be required via the intravenous or intramuscular route. Administration by oral or subcutaneous routes is not advised, in the emergency patient, as absorption will be significantly reduced in the patient with congestive heart failure. Furosemide, a loop diuretic, is the main diuretic used in the management of CHF/ CCF (Matos and
Summerfield, 2018). It has a rapid onset of action after IV administration- with an effect often being apparent as soon as five minutes after IV treatment but certainly
within the first hour. Instead of, or following, bolus treatment, a furosemide CRI may be administered. Close monitoring of the patient’s respiratory rate is an effective way of monitoring the response to diuretic treatment
If the patient has a pleural effusion, thoracocentesis will be required rather than treatment with diuretics.
inotropes may be used in the management of
cardiogenic shock and forward heart failure. Brown and Willis (n.d.) outline the management of the canine patient presenting with acute congestive heart failure.
Because pimobendan has both positive inotropic and vasodilator activity, it is often used with furosemide as first-line treatment.
What should a patient receiving diuretic therapy be monitored for?
A patient receiving diuretic therapy must be closely monitored for signs of dehydration, pre-renal
azotaemia and electrolyte abnormalities. Animals receiving diuretic therapy will have increased fluid loss, so it is sensible to measure ins and outs and calculate fluid balance over 4-6hrs, as well as regular bodyweight checks.
It is important to consider that these patients are often middle aged to older patients and may have concurrent disease processes which can affect the treatment options in some cases
Why might vasodilators be useful in the treatment of backward heart failure?
Other vasodilators (venodilators, arteriodilators or mixed) may be used as second line treatment (Swift, 2018). These help to expand the storage capacity of blood vessels, especially veins. This decreases the cardiac preload which is useful in backward heart failure and can decrease pulmonary and systemic congestion.
Why might arteriodilators be useful in the treatment of forward cardiac failure?
Arteriodilators reduce the afterload, which can make it easier for the heart to pump blood especially in forward failure. They also help to re-establish a blood supply to
the periphery. Vasodilators, especially arterial dilators, lead to decreased systemic resistance allowing ‘…. rapid ‘unloading’ of the ventricle’ (Matos and Summerfield,
2018) and can be extremely helpful in patients with severe pulmonary oedema.
What is sodium nitroprusside? What is it used to treat? How should it be administered? What is the potential side effects?
Sodium nitroprusside is a very rapid acting and potent vasodilator that may be used in the management of
severe, acute congestive cardiac failure. It must be administered as a CRI and titrated to effect. A patient receiving sodium nitroprusside should have its blood
pressure closely monitored, ideally direct arterial, as
hypotension is a potential risk (Matos and Summerfield, 2018). It is less likely to be used now for cost reasons.
What is Glyceryl trinitrate and what is it used to treat? How must it be handled and why?
Glyceryl trinitrate/ nitro-glycerine (e.g. Percutol™) is a potent vasodilator which can be used in the short-term emergency management of acute, cardiac pulmonary oedema (BSAVA, 2020) ‘although its efficacy is debatable’. It is applied topically- the person applying the product MUST wear gloves and avoid handling the area of application to prevent a sudden vasodilatory effect which would cause a sudden drop in blood pressure. This could cause the individual to faint/collapse.
Once a patient with cardiac failure has been stabilised what further assessment should be carried out?
Once the patient has been stabilised a more thorough cardiovascular assessment should be performed (auscultation, pulse assessment, BP recording, echocardiography, radiography etc.) A heart murmur may be audible in a patient with e.g. valvular disease or cardiomyopathy.
Diagnostics should only be performed once the patient has been stabilised sufficiently to allow safe handling. By this stage the function of the patient’s cardiovascular and respiratory system should have improved sufficiently to be able to tolerate an increase in heart rate, respiratory rate and oxygen requirement without decompensating. Ongoing supplemental oxygen therapy should be provided in a or POCUS/FAST thoracic/ abdominal ultrasound scans can be performed cage/ kennel side and require minimal restraint/ patient positioning.
Specific information can be gained from these e.g. cardiac chamber size, degree of ventricular contractility, presence of pericardial effusion with targeted echocardiography (Matos and Summerfield, 2018); presence of pleural effusion,
abdominal effusion, pneumothorax and/or pericardial effusion with POCUS/FAST scans. Thoracocentesis may be required for emergency management and
diagnostics in the case of a patient with pleural effusion. The patient should not be positioned for radiography whilst still dyspnoeic, due to the risk of deterioration. The only relatively safe view for a dyspnoeic patient is the dorso-ventral view - however
careful risk versus benefit assessments need to be carried out. Radiography is generally not indicated in the dyspnoeic patient as the required information can
generally be obtained using other safer diagnostic techniques. Cats/ small dogs may sometimes sit on a cassette for a dorso-ventral view; or can be X-rayed through the oxygen tent/cage. Thoracic radiographs of a patient with congestive cardiac failure may reveal pulmonary oedema, cardiomegaly, tracheal elevation, left atrial enlargement and pulmonary vein distension.
If a patient has a heart murmur what should be noted?
It is good practice to describe the stage of
the cardiac cycle where the murmur is heard e.g. systole or diastole; describe the anatomic location where it is most audible and grade it based on how loud it is
What cardiac phase do most murmurs occur?
Most murmurs occur during systole.
Where will a murmur be the loudest when a patient has mitral valve disease?
A murmur due to mitral valve disease will usually be
loudest over the left thorax at the 5th
- 6 th intercostal spaces.
Where will a murmur be the loudest when a patient has tricuspid valve disease?
a murmur due to tricuspid valve disease which will be loudest on the right thorax at the 3 rd - 5th intercostal spaces
Where will a murmur be the loudest when a patient has aortic stenosis?
The murmur from aortic stenosis can be heard on both
the right and left thorax at the 2nd - 4th intercostal spaces.
When
Diagnostics should only be performed once the patient has been stabilised sufficiently to allow safe handling. By this stage the function of the patient’s
cardiovascular and respiratory system should have improved sufficiently to be able to tolerate an increase in heart rate, respiratory rate and oxygen requirement without decompensating. Ongoing supplemental oxygen therapy should be provided in a
What is an ECG helpful at identifying?
Electrocardiography (ECG) is especially useful in the acute cardiac presentation – it demonstrates heart rate and rhythm and is useful for identifying arrhythmias,
especially if they are intermittent. Holter monitors may be used for longer recordings.
ECG is helpful in identifying arrhythmias associated with electrolyte abnormalities e.g. hyperkalaemia, however, it does not give any information about heart function.
What is an echo ultrasound valuable at identifying?
A more detailed ultrasound examination of the heart, echocardiography/ ‘echo’, is valuable at identifying the cause of the heart disease (e.g. DCM and HCM) and recognising complicating factors (e.g. smoke signal in cats with ATE). Congenital structural abnormalities of the heart e.g. atrial septal defect (ASD), ventricular septal defect (VSD) and patent ductus arteriosus (PDA) may be identified. Echo can also demonstrate cardiac function e.g. how effective ventricular contraction is; and will also demonstrate any abnormal, regurgitant blood flow such as that seen with valvular disease, HCM and pulmonary hypertension.
How can ongoing assessment of a patients oxygenation status of a cardiac failure dog be performed?
Ongoing assessment of patient oxygenation status should be performed. This can be done using pulse oximetry but arterial blood gas analysis is more accurate and thus preferred. Venous blood gas analysis can be performed in a patient who cannot
have an arterial catheter placed.
What blood test monitoring should continue for a patient with heart failure?
Blood gases, pH and acid-base status; serum
electrolytes; lactate and renal biochemical parameters should be monitored to assess effectiveness of treatment and identify any potential side-effects e.g. prerenal azotaemia due to dehydration caused by excessive diuretic administration.
What blood test can help to determine if there has been myocardial damage?
Serum troponin levels can be assessed as an indicator of myocardial damage
What tests can be performed to confirm Angiostrongylus vasorum?
Confirmation of Angiostrongylus vasorum, as a cause of cardiorespiratory disease, may be done by identifying L1 larval stages in faeces; or by using Elisa SNAP tests
What are the side effects of furosemide and what should be monitored when a patient receives this?
a loop diuretic, it increases urine production, fluid and potassium loss. The patient should be monitored closely for evidence of dehydration, oliguria,
hypokalaemia and pre-renal azotaemia.
How do angiotensin converting enzyme (ACE) inhibitors work to help treat heart failure and what are the potential adverse effects of these?
orally administered angiotensin converting enzyme (ACE) inhibitors (ACE-i) e.g. benazepril may be used in the ongoing management of congestive cardiac failure. By inhibiting angiotensin converting enzyme (ACE) which normally converts angiotensin I to angiotensin II, the renin- angiotensin- aldosterone system (RAAS) is interrupted. The effects of angiotensin II e.g. peripheral vasoconstriction and release of aldosterone are
partially blocked by ACE-i. By causing vasodilation of arteries and veins, ACE-i reduce both the pre-and afterload on the heart. As they decrease aldosterone
release, they also decrease sodium and chloride resorption in the distal convoluted tubules of the kidneys and the accompanying water retention- thus helping to decrease congestion. Potential adverse effects include hypotension, hyperkalaemia
(especially if used with potassium sparing diuretics e.g. spironolactone) and azotaemia
What cardiac condition should pimobendan not be used to treat?
Pimobendan should not be used in animals with
hypertrophic cardiomyopathy
What is Pimonedan and what is it used to treat?
Pimobendan is a phosphodiesterase, inhibitor with both inotropic and vasodilator effects- it is commonly used in the management of heart failure in animals with valve insufficiency or dilated cardiomyopathy.
The EPIC study has evaluated the use of pimobendan in dogs with stage B2 myxomatous mitral valve disease
In the mergency patient what do arrhythmias tend to arise secondary to? Why is it important to identify this early on?
In most cases, they are not due to primary heart disease but tend to arise secondary to another problem which affects the conducting system in the heart e.g. hyperkalaemia causing bradycardia. They will often accompany or develop in response to other emergency conditions with electrolyte abnormalities e.g. GDV. If an arrhythmia is newly detected in an ECC patient, it is important to report this promptly- it may decrease cardiac output further, seriously complicating
the underlying condition and possibly causing myocardial ischaemia
What information do ECG’s provide?
An ECG recording is the best way of confirming that an arrhythmia is present. As this could arise at any time in an ECC patient and could be intermittent, ECG recording is an important part of patient monitoring. ECGs provide no information about myocardial and valve function but can be used to calculate the patient’s heart rate, assess the heart rhythm and the morphology of complexes. An ECG can confirm the presence and type of arrhythmia – enabling the veterinary surgeon to decide whether emergency treatment is required and what this should be. Often management of the primary underlying condition e.g. intravenous fluid therapy in the case of hypovolaemic shock or analgesics in the case of acute abdominal pain eliminates the arrhythmia.
Do all arrhythmias require treatment?
Not all arrhythmias require emergency treatment and it is important to be aware that any drug used to treat an arrhythmia has the potential to cause another arrhythmia i.e. they are proarrhythmic
What conditions can arrhythmias develop in association with?
Arrhythmias can develop in association with conditions such as - hypoadrenocorticism, GDV, urethral obstruction, DCM and hyperthermia. RVNs should be able to recognise abnormal patterns present on an ECG and know their significance and the importance of prompt reporting to a veterinary surgeon. This is
not a diagnosis but a significant clinical finding / observation.
What colour ECG electrode goes to what limb on the patient?
To get the best information from an ECG recording it is important to set the machine
up, calibrate it and attach the electrodes correctly. Electrodes should be placed
according to the following table (UK/ European lead convention). N.B. The USA
uses a different lead colour system
Electrode
Red
Limb
Right forelimb
Green
Left hind limb
Yellow
Left forelimb
Black (reference) (if
present)
Right hind limb
When setting up an ECG why should the speed of tracing be noted and what speed to do standard machines record at?
When setting up the ECG, the speed of the tracing should be noted so that the heart rate can be calculated- standard machines record at 50mm / second or 25mm / second
What lead is generally run when performing an ECG on a patient?
Lead II is generally the easiest to interpret although other recordings can also be obtained. When analysing Lead II, each normal heartbeat should have a
corresponding P wave, a QRS complex and a T wave
What does the P wave on an ECG correspond to?
the P wave corresponds to contraction of the atria
What does the QRS wave on an ECG correspond to?
the QRS complex is contraction of the ventricles
What does the T wave on an ECG correspond to?
the T wave is repolarisation prior to the next contraction
When examining an ECG what should be assessed?
When examining an ECG-
• the rate and rhythm of contractions should be assessed
• the P, QRS, T waves should all look the same
• all expected waves (P, QRS and T) should be present i.e. there should be a QRS and T wave corresponding to each P wave and vice versus.
• the height (or depth) of waves should be measured
• the shape of the complexes should be assessed-are they normal or are they wide and bizarre?
• the presence and frequency of any abnormalities should be recorded – this becomes an important factor in the decision to treat some arrhythmias
alongside patient assessment.
What different type of arrhythmias should be recognised and assessed by veterinary nurses?
The underlying disease process is not likely to be diagnosed from an ECG recording alone- it is important that veterinary nurses can, however, recognise and identify the type of arrhythmia. • Tachyarrhythmias or bradyarrhythmia? • Regular or irregular arrhythmia? • P wave for every QRS complex? • QRS complex for every P wave? • Morphology of QRS complex? • Morphology of T wave? • Ventricular or supraventricular (above the ventricles e.g. atria) in origin?
What two different categories are arrhythmias classified as?
Arrhythmias are classified as ventricular or supraventricular in origin.
Where do ventricular arrhythmias arise in the heart and how does this appear on an ECG?
Ventricular arrhythmias arise in the ventricles. Because the normal conduction pathway is not
followed the QRS complexes appear wide and bizarre
Where do supraventricular arrhythmias arise in the heart? How does this appear on an ECG?
Supraventricular arrhythmias arise in the atria, at a point other than the sino-atrial node (SA node), and then conduct via the atrio-ventricular node (AV node) to the ventricles. The QRS complexes appear more like normal complexes although they are often tall and thin.
The arrhythmia may cause the heart rate to be too slow (bradyarrhythmia) or too fast
(tachyarrhythmia).
What is atrial fibrillation?
Atrial fibrillation is an abnormal heart rhythm characterised by rapid and irregular
beating of the atria.
What can fibrillation be described as?
Fibrillation can be described as rapid, irregular contractions –
‘quivering’ rather than normal coordinated chamber contractions
What species is atrial fibrillation most common in?
This is a quite common arrhythmia in dogs but is rare in cats.
What condition do many dogs have that present with atrial fibrillation?
Many dogs with atrial fibrillation have dilated cardiomyopathy (DCM) - the arrhythmia develops secondary to left atrial stretching. Atrial fibrillation may be the first indication of occult DCM in giant breed dogs e.g. Irish Wolfhounds with no previous clinical signs of heart disease. It also occasionally arises in giant breed dogs with no underlying heart
disease. In some patients it will be a coincidental finding such as in a large breed dog with a GDV who has an ECG assessment prior to surgery.
What are the symptoms of atrial fibrillation?
Many dogs with atrial fibrillation have dilated cardiomyopathy (DCM) - the arrhythmia develops secondary to left atrial stretching. Atrial fibrillation may be the first indication of occult DCM in
giant breed dogs e.g. Irish Wolfhounds with no previous clinical signs of heart disease. It also occasionally arises in giant breed dogs with no underlying heart disease. In some patients it will be a coincidental finding such as in a large breed
dog with a GDV who has an ECG assessment prior to surgery.
What are the typical ECG findings when a patient has atrial fibrillation?
The typical ECG findings are- supraventricular QRS complexes (narrow and upright); irregularly irregular rhythm with low ventricular rates and no visible P waves – as these abnormal contractions do not arise from the SA node. Fibrillation (‘f’ waves) are present instead. The heart rate may be normal but is often tachycardic.
What type of medications may be used for the management of dilated cardiomyopathy?
If the dog has DCM and congestive cardiac failure, diuretics, inotropes and ACE inhibitors may be used in the management. Additional drugs that might be used are calcium channel blockers e.g. diltiazem or beta-blockers e.g. sotalol to slow the heart rate. Digoxin may also be used to slow the ventricular rate
and act as a positive inotrope (Stephenson, 2011). More recently drugs such as amiodarone have been used (Mills, 2015). There are a few reports of efforts to use transthoracic biphasic electrical cardioversion techniques in dogs with atrial fibrillation and then maintaining them on amiodarone. These cases are, however, few although the results have been promising
What is the aim of treatment for atrial fibrillation?
Treatment of atrial fibrillation is aimed at decreasing the heart rate and increasing cardiac output- unlike horses and people where treatment tries to convert the heart back to normal rhythm.
What is a supraventricular arrhythmia?
A supraventricular beat occurs when an abnormal electrical impulse starts at an ectopic site that it is above (‘supra’) the AV node- i.e. atrial in origin rather than ventricular. There may be a re-entrant rhythm. With a re-entrant rhythm, depolarisation starts in one part of the heart, spreads to the atria, through an accessory pathway, before re-entering the ventricles via the AV node. The ectopic beat occurs prior to normal sino-atrial depolarisation and is therefore ‘premature’ (i.e. it occurs earlier than expected). This ectopic beat is therefore called an atrial premature contraction (APC).
What is an APC?
Atrial premature contraction
What is it called when there are 3 or more atrial premature contractions?
If there are 3 or more APCs in a row, the arrhythmia is called supraventricular tachycardia (SVT).
How do atrial premature contractions appear on an ECG?
The QRS complexes of APCs/ SVT are almost like normal QRS
complexes, often narrow and upright, rather than the wide and bizarre looking
complexes seen with ventricular premature contractions (VPCs) or ventricular
tachycardia. There may or may not be associated P waves. The rate of SVT can be
170-350 bpm.
What conditions are supraventricular usually associated with?
SVT in dog is usually associated with underlying cardiac disease, or sometimes systemic disease, (e.g. toxicity, hypovolaemia, ischaemia) but it is occasionally a primary condition
How do you treat supraventricular tachycardia?
If frequent, with associated clinical signs, weakness/collapse, treatment will be required. The first line of treatment is to treat the underlying cause where possible (e.g. hypovolaemia). Initial emergency management of SVT may involve mediating the vaso-vagal reflex using ocular pressure. If unsuccessful, medication such as beta blockers or calcium
channel blockers may be required.
What is a bradyarrhythmia?
This is when a patient has bradycardia associated with an arrythmia
What is a sinus bradyarrhythmia?
This is when the sinus rhythm is inappropriately slow for the breed
What are bradyarrhythmia’s likely to be secondary to?
Rather than being a primary cardiac problem, it is likely to be secondary to some other disease which increases vagal tone e.g. increased intracranial pressure or brachycephalic obstructive airway disease or electrolyte
abnormalities e.g. hyperkalaemia It may arise due to a problem with the sino-atrial (SA) node or secondary to
other conditions e.g. hypothyroidism, hypoadrenocorticism, hypocalcaemia or vasovagal reaction
When might a bradyarrhythmia be a normal finding?
It may be a ‘normal’ finding in e.g. older, brachycephalic dogs secondary to high vagal tone- greyhounds may also be affected
What is considered a slow heart rate for a dog?
On ECG, a normal sinus rhythm is seen with a slow heart rate (<60 bpm dog).
What does a brady arrhythmia look like on an ECG?
a 1:1 ratio of P: QRS i.e. each P wave has a corresponding QRS
What clinical signs are usually associated with bradyarrhythmia?
weakness, exercise intolerance and/or lethargy
How do you treat bradyarrhythmia?
Treatment is dictated by the underlying cause and whether the patient is showing clinical signs
due to the arrhythmia e.g. managing hyperkalaemia in a patient with hypoadrenocorticism. However, the bradycardia may be temporarily managed using
an anticholinergic depending on the cause and the effect it is having on the patient’s cardiovascular status e.g. atropine sulphate or glycopyrrolate. If this is unsuccessful, positive inotropes e.g. dopamine, dobutamine may be required.
What is sick sinus syndrome?
This is where a problem arises with the sino-atrial (S-A) node (or A-V node) where it fails to discharge – it is a degenerative condition. It is almost exclusively dog that are affected although the cause is generally unknown.
Due to the decreased S-A output, the heart rate will be abnormally slow or there will be periods of asystole- the S-A node normally starts functioning again, but
this condition is likely to be recurrent.
What breed and age dogs does sick sinus syndrome usually affect?
Breeds which are predisposed include West Highland White Terriers, Cocker Spaniels and Miniature Schnauzers- it is usually older animals that are affected (~ 6-10 years)
What clinical signs are associated with sick sinus sydrome?
The dog may have episodes of collapse/fainting during the asystole although some cases are asymptomatic.
Asystole can be present for several seconds
How does sick sinus syndrome appear on an ECG?
During sinus arrest no impulses are generated by the S-A node so no P waves will be seen. After a period of asystole, a ventricular escape beat/complex may be seen this is generated by a ventricular pacemaker when there is no S-A node activity.
The ECG will show periods of bradycardia or no electrical activity (asystole) due to sinus arrest; this may be followed by paroxysmal supraventricular tachycardia and no associated P wave. Patients often respond poorly to medical treatment e.g. atropine so may need a pacemaker to be fitted.
What is a heart block/atrioventricular block?
With a heart block, there is a delay or complete blockage of the impulse from the SA
node going through the AV node
Why might a atrioventricular block occur?
This may arise due to a disease or a drug-related
effect at the AV node.
How does an atrioventricular block appear on an ECG?
Delayed conduction through the AV node is called a first-degree block- the ECG will show a longer interval between the P wave and corresponding QRS complex. With a second-degree heart block, there is a longer conduction delay- some P waves will not have a corresponding QRS i.e. there are dropped beats. With a third-degree heart block, there is a complete lack of conduction through the AV node. In cases of
3 rd degree block, ventricular ‘escape beats/ complexes’ occur which permit the heart to still beat- without these escape beats the animal would die. The rate of the ventricular escape beats is typically 20-40 beats per minutes.
A tracing of a 2nd degree AV block is shown. Note the presence of some P-waves with no associated QRS complexes. Those complexes that do occur are normal in morphology- this shows that this is a 2
nd degree block (there has been conduction through the AV node so the QRS complex has a normal shape).
What clinical signs are associated with an atrioventricular block?
The patient will show clinical signs associated with decreased cardiac output e.g.
lethargy, syncope and collapse
How do you manage/ treat atrioventricular blocks?
Management of the underlying condition (e.g.
hypoadrenocorticism may resolve the AV block. If not vagolytic drugs, such as atropine sulphate and glycopyrrolate, may be tried. In cases of severe second or third-degree block, implantation of a pacemaker is typically required.
What is atrial asystole?
This is a lack of atrial activity (i.e. no atrial contraction) due to failure of atrial myocardial cell depolarisation, even though the S-A node has created an impulse.
What is atrial asystole caused by?
It could be caused by atrial muscle myopathy but is often due to hyperkalaemia.
Atrial asystole may be secondary to cardiac pathology but is commonly associated with hyperkalaemia secondary to e.g. hypoadrenocorticism or urethral obstruction.
Generally, the heart sounds and pulses are normal but slow. Typically, dogs with hyperkalaemia have bradycardia although cats may have tachycardia.
What happens to the heart in atrial asystole?
The ventricles continue to function. The impulse, created by the SA node, does reach the
AV node, despite no atrial muscle depolarisation. This then results in ventricular depolarisation and contraction- this is called sino-ventricular rhythm.
How will atrial asystole appear on an ECG?
The ECG show a lack of P waves. The heart rate is regular but normally slow (< 60 bpm in dogs) because of the escape rhythm. The QRS complexes can appear
normal or may be slightly wide.
How cn atrial asystole caused by hyperkalaemia be treated?
A patient with hyperkalaemia should have appropriate fluid resuscitation as appropriate to stimulate diuresis and excretion of potassium. If additional treatment is
required, hyperkalaemia may be treated with intravenous soluble/neutral insulininsulin causes movement of glucose and potassium from the extracellular space into cells. Dextrose is also administered to avoid hypoglycaemia. Half the dextrose can be given as a bolus with the rest administered over 4-6 hours (BSAVA, 2020)).
Injections of 10% calcium gluconate (over 15 minutes) may help protect the myocardium from the arrhythmogenic effects of the hyperkalaemia. IV calcium should be given slowly, whilst an ECG is being recorded, due to the risk of cardiac arrest. Treatment of the underlying cause of the hyperkalaemia is essential
How can bicarbonate therapy assist with hyperkalaemia?
Bicarbonate therapy can very rarely be used in the treatment of severe hyperkalaemia but it has to be administered with care due to the risk of serious sideeffects- the risks are greater if it is administered rapidly (Poli, 2017). Adverse effects of bicarbonate administration are metabolic alkalosis and hypocalcaemia – therefore it should only be used when acid-base status can be measured. Both insulin and
bicarbonate treatments encourage potassium ions to move into the intracellular space. It should be noted that whilst bicarbonate is mentioned in many sources for reducing potassium levels the focus should be on appropriate fluid resuscitation, restoring urine output and stabilising the patient’s condition appropriately. Only when other techniques have failed should bicarbonate be considered due to the potentially
fatal side effects.
What is a tachyarrhythmia?
This is when a patient has an arrythmia causing tachycardia. It may be supraventricular e.g. of atrial origin
What are some examples of tachyarrhythmias and how do these appear on an ECG?
Examples of supraventricular tachycardia include atrial tachycardia, atrial flutter and atrial fibrillation. Ventricular tachycardia and ventricular fibrillation are examples of tachyarrhythmias of ventricular origin. If
there is a supraventricular arrythmia, on ECG, the QRS complexes usually appear relatively normal although they may be taller and narrower than normal. If the
tachyarrhythmia is of ventricular origin, the QRS complexes usually appear wide and bizarre as they have originated directly within the ventricles rather than via the conduction mechanism.
What is a ventricular arrhythmia and how does this appear on an ECG?
With a ventricular arrhythmia, the SA node no longer controls the ventricular contractions. Another area in the ventricles takes over the pacemaker role. As the
normal electrical pathway is not followed, the appearance of these complexes is unusual e.g. usually wide and bizarre and without a corresponding P wave indicating atrial involvement.
What condition might a ventricular dysrhythmia arise from?
A ventricular dysrhythmia may arise as a serious complication of another condition e.g. GDV and it is important to be aware of this possibility when
monitoring patients.
What are ventricular premature contractions and how do these appear on an ECG?
Ventricular beats occur when an abnormal electrical impulse starts at an ectopic site that it is below the AV node (i.e. ventricular in origin, not atrial).
The ectopic beat occurs prior to normal sino-atrial depolarisation - thus the beat is ‘premature’ (i.e. it occurs before it is expected). Therefore, they are called
ventricular premature contractions (VPCs). The VPC/beat starts at an aberrant/unusual location in the ventricles and therefore does not follow the normal
conduction pathway. As it takes longer for the conduction to occur, the complex appears wider on ECG and there is no associated P wave.
When can ventricular premature contractions occur?
VPCs can sometimes be present in low numbers in healthy animals without being a problem. They can also arise secondary to other problems e.g. GDV/Splenectomy or surgery.
Sometimes VPCs occur in patterns e.g. every second beat or every third beat is a VPC
What is the phenomenon called when a ventricular premature contraction occurs on a downward slope?
If a VPC occurs on the downward slope of the previous T wave (i.e. right at the end of the previous normal contraction) – this is called R-on -T phenomenon. If
present, this is potentially very serious- the end of the T wave is ‘a vulnerable period’ and anything abnormal at this period can predispose a patient to ventricular
fibrillation
What is an accelerated idioventricular rhythm?
When there are 3 or more VPCs together but the heart rate is not much more than usual (~ 140 - 170 per minute in a dog), the ECG rhythm is termed an accelerated idioventricular rhythm (AIVR). This heart rate is not fast enough to be considered true ventricular tachycardia
What is ventricular tachycardia?
If there are 3 or more VPCs in a run and the heart rate
is significantly increased (~ > 170/180bpm), this is called ventricular tachycardia
Why might an idioventricular rhythm occur and how do you treat it?
An accelerated idioventricular rhythm may occur for the same reasons as ventricular tachycardia (see below). It is often secondary to non-cardiac disease in hospitalised patients e.g. GDV, pyometra, post-trauma, pancreatitis etc. but is generally considered to be benign rhythm because at this rate, there is unlikely to be decreased cardiac output, haemodynamic compromise or hypotension. Treatment is
usually not required for AIVR however the patient and ECG should be closely monitored for progression to ventricular tachycardia.
What is ventricular tachycardia and how might this appear on an ECG?
This is demonstrated by three or more ventricular premature contractions occurring at a high heart rate (typically greater than 170/180 bpm but often around 220 bpm or more). The origin of the electrical impulse is from the ventricle rather than the sinoatrial node. The QRS complexes are therefore wide and bizarre with no associated p-wave. This is an example of ventricular tachycardia
What primary cardiac disease causes Ventricular arrhythmias/dysrhythmias in dogs?
Primary cardiac disease
o Structural - e.g. dilated cardiomyopathy (DCM)
o Arrhythmogenic right ventricular cardiomyopathy in Boxers
How can Abnormal autonomic activity cause Ventricular arrhythmias/dysrhythmias in dogs?
Abnormal autonomic activity
o High sympathetic tone
▪ e.g. pain
How can electrolyte disturbances cause Ventricular arrhythmias/dysrhythmias in dogs?
Electrolyte disturbances
o Hypercalcaemia
What drugs causes Ventricular arrhythmias/dysrhythmias in dogs?
Drugs/hormones/toxins
o Caffeine
o Cocaine
o Cardiac glycosides
What conditions can cause ischaemia leading to Ventricular arrhythmias/dysrhythmias in dogs?
Ischaemia
o Hypovolaemia
o Anaemia
o Thromboembolic disease
What type of neoplasia causes Ventricular arrhythmias/dysrhythmias in dogs?
Neoplasia
o Lymphosarcoma
o Haemangiosarcoma
What are the different causes for Ventricular arrhythmias/dysrhythmias in dogs?
Inflammation/inflammatory mediators Trauma Ischaemia Drugs Electrolyte disturbances Primary cardiac disease Abnormal autonomic activity
What would the heart rate be if a patient has ventricular tachycardia? How would this affect the patient? What signs would you likely see? What monitoring is required?
With very rapid heart rates (> 250-300 bpm), there is likely to be decreased cardiac filling and therefore there will be decreased cardiac output and associated signsrelated to hypoperfusion e.g. exercise intolerance, syncope or collapse. Although as these patients may already be hospitalised due to serious conditions, they may already be recumbent and inactive. Therefore, it is also essential to monitor perfusion parameters. Signs of haemodynamic compromise in a patient with ventricular tachycardia include altered mentation, pale mucous membranes, prolonged CRT, weak or absent peripheral pulses (‘pulseless V Tach’)., hypotension,
hypothermia decreased urine output etc
What haemodynamic serious consequences are associated with ventricular tachycardia?
Serious consequences of ventricular tachycardia, associated with haemodynamic compromise, include:
• Decreased systemic tissue perfusion (cardiogenic shock)
• Decreased cardiac perfusion
• Development of a malignant arrhythmia (i.e. ventricular fibrillation)
• Development of myocardial failure if prolonged tachycardia
• Sudden death may also occur.
How do you treat ventricular tachycardia? What heart rate would prompt treatment?
Ventricular tachycardia is a serious arrhythmia although it does not always require treatment. Treatment may not be effective and can have adverse effects. Generally,
if the patient’s heart rate is extremely rapid (> 250-300 bpm) treatment will be required to prevent ventricular fibrillation and sudden death, although other sources state that treatment might be required above ~ 160-
200 bpm. Whether treatment is required is case dependent and will depend on the degree of haemodynamic compromise and the underlying cause in each case.
Patients with underlying heart disease (e.g. dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and hypertrophic cardiomyopathy) are more likely to require treatment due to the risk of cardiac arrest.
The main priority for a patient with ventricular tachycardia is to ensure the underlying disease process, if present, is being managed appropriately e.g. IVFT for hypovolaemia, dehydration; monitoring oxygenation, electrolytes and blood gas status and treating accordingly.
Intravenous lidocaine is usually the first choice of treatment for ventricular tachycardia– it is usually started as a bolus and continued as a CRI. If there is a poor response to the first bolus, this can be repeated 2-3 times over a 10-minute period if required. N.B. Once a bolus of lidocaine has been administered there is usually a rapid response. If the response is appropriate, the patient is most likely to have ongoing CRI treatment rather than repeated boluses.
Other treatment options could be tried if lidocaine is ineffective- however, if the response to lidocaine is poor the patient’s general condition should be reassessed. It is more likely that the underlying disease process is responsible for the poor response e.g. hypokalaemia.
Other drugs that might be used in the management of ventricular tachycardia, depending on the underlying cause, include procainamide, beta-blockers, magnesium, sotalol and amiodarone
What are the signs of lidocaine toxicity?
It is essential to monitor the patient for signs of lidocaine toxicity, especially if repeated boluses are administered. Signs of toxicity can be neurological e.g.
seizures, cardiac e.g. bradycardia and/or gastrointestinal e.g. vomiting. Cats are much more sensitive to the toxic effects than dogs. If
toxicity does arise then intra-venous lipid emulsion can be administered. However, care must be taken not to volume overload the patient.
Why is it important to treat ventricular fibrillation?
Ventricular Fibrillation: this is a very serious condition which will result in patient death unless instantly recognised and treated- it is considered to be a ‘pre-terminal’ condition. Because there are no effective ventricular contractions, they are all chaotic, there is no cardiac output
How will ventricular fibrillation appear on an ECG?
The ECG shows an irregular, wavy baseline with no
recognised complexes.
How do you treat ventricular fibrillation?
The patient will require immediate CPR and defibrillation – this is a shockable rhythm. N.B. it is important to ensure that the ECG leads are
correctly attached – poor skin contact can cause a similar appearance.
Matos and Summerfield (2018) state that electrical defibrillation is the only effective
treatment option for ventricular fibrillation.
What is pulseless electrical activity?
Pulseless Electrical Activity (PEA) in this condition, there are electrical impulses within the heart but no corresponding contractions. Pulseless electrical activity is the condition in which, despite a normal heart rate and rhythm on ECG, there is an absence of myocardial contractions so no cardiac output. It is a type of asystole.
There are no audible heart beats or palpable pulses as there is no cardiac output but there is normal or slow electrical activity visible on the ECG. The patient will be
collapsed. In addition to CPR, adrenaline, atropine or an inotrope may be used.
What is asystole and how is it treated?
This is the most common arrest arrythmia in dogs and cats-there are no contractions and so no cardiac output. It can develop with any end-stage disease e.g. cardiac or pulmonary. It can also be caused occasionally by very high vagal tone. Generally, it has an extremely poor prognosis.
Prompt cardiopulmonary resuscitation (CPR) in accordance with the RECOVER guidelines is the only treatment option for asystole and PEA
What will treatment of an arrhythmia depend on?
Treatment of an arrhythmia will depend on multiple factors. The first (and probably the most important) is whether there are clinical signs associated with the
arrhythmia. If a patient is ‘clinical’ – i.e. showing signs of cardiogenic shock then it requires treatment. Treatment of any underlying condition is the priority and some
arrhythmias will resolve when this is addressed e.g. GDV patient. If the animal is clinically normal, then emergency treatment is less likely to be required although the patient should be monitored closely and an underlying cause identified, where possible. The second consideration is the ECG rhythm and morphology of the complexes. The heart rate, the complex morphology and whether the arrhythmia is
sustained are all important factors. Treatment will be decided by the veterinary surgeon responsible for the case- there are no hard and fast rules but the following
provides pre-treatment guidance
When should treatment of an arrhythmia be considered?
When to treat
- Clinical signs consistent with poor perfusion ( hypoperfusion)
a. Pulse quality/ lack of peripheral pulse
b. Pale mucous membranes
c. Prolonged capillary refill time
d. MENTATION- decreased - Objective data consistent with poor perfusion
a. Increased lactate
b. Low blood pressure - High heart rate - How high is high?
a. There is no set value but many vets will treat if significantly increased
(> 160 if cardiac pathology or > 250 bpm if no cardiac pathology). Important to monitor trends and ensure the veterinary surgeon is
promptly alerted to any abnormal rhythm irrespective of the rate. - Multiform complexes
a. When all the ventricular complexes look different. - ‘R on T’ (VT only)
a. When the R of the complex appears above the previous T. As discussed previously, this is a very fast rhythm which may progress to ventricular fibrillation.
What is the treatment for supraventricular tachycardia?
Treatment involves managing the causal disease where possible – treat the treatable prior to the administration of any drugs. The medical treatment of any supraventricular tachycardia (including atrial fibrillation) is based upon slowing down the heart rate. This is typically achieved with a calcium channel blocker (e.g. diltiazem) or a beta blocker (e.g. atenolol). Some drugs such as sotalol have multiple effects including beta-blocking and potassium channel block that slows repolarisation.
What is the treatment for ventricular tachycardia?
Treatment involves managing the causal disease where possible. For example, if a dog is significantly anaemic, then the anaemia should be corrected prior to
administration of anti-arrhythmic medication which could have a proarrhythmic effect.
Medical treatment of ventricular tachycardia may result in conversion of the electrical rhythm into sinus rhythm or may just slow the heart rate down. A reduction in heart rate from 220 to 140, even if an abnormal ventricular rhythm remains, would still be considered successful. Ideally, though, the rhythm will be converted back to into sinus rhythm again.
Lidocaine is typically the first line agent in dogs with ventricular tachycardia- a bolus is administered slowly IV over 1-3 minutes followed by an intravenous CRI.
Lidocaine is a sodium channel blocker that should be administrated intravenously as it has low bioavailability. It has a short half-life and so should be given as a constant rate infusion. As discussed previously other drugs may be used if there is a poor response to lidocaine.
What is the pericardium and what does it do?
The pericardium is a thin-walled sac surrounding the heart which normally contains a volume of fluid to aid lubrication and reduce friction.
What species does pericardial effusion affect the most and what is it commonly caused by?
Pericardial effusion is a relatively common cause of emergency presentations, especially in dogs, due to signs of right-sided forward heart failure which develops secondary to the presence of fluid accumulation in the pericardium. Occasionally the
signs are caused by a soft-tissue mass e.g. tumour within the pericardial sac.
Pericardial effusion occurs in the cat but is less common than in dogs.
What is cardiac tamponade and how does it affect the heart?
Cardiac tamponade is a serious form of pericardial effusion where the fluid in the pericardium compresses the heart to such an extent that cardiac filling is significantly impeded. If cardiac filling is reduced to this extent, less blood will enter the ventricles during diastole resulting in significantly decreased cardiac output during ventricular contraction (systole). With cardiac tamponade the pericardial pressures exceed right atrial pressures.
The abnormal presence of fluid in the pericardium puts pressure on the thin-walled right atrium, causing it to, partially or completely, collapse. As the right ventricle is
also relatively thin walled it can also be prevented from expanding by the pericardial effusion. This means that the right ventricle cannot fill sufficiently with blood during diastole (decreased diastolic function). If the chambers are unable to fill with blood (preload) then there is a decreased amount for the heart to pump when it contracts.
As a result, the stroke volume, and thus the cardiac output, is decreased. If the cardiac output is insufficient to maintain a blood supply to the tissues, the animal will show signs of cardiogenic or obstructive shock – cardiac tamponade. Cardiac tamponade is rare in cats
What are the causes of a pericardial effusion?
Causes of pericardial effusions include:
- Haemorrhage
a. Neoplasia e.g. haemangiosarcoma
b. Coagulopathy
c. Idiopathic
d. Trauma (rare)
e. Left atrial tear (very rare) - Pericarditis (often idiopathic)
- Congestive heart failure (cats)
- Infection e.g. FIP/toxoplasmosis in cats
- Neoplasia e.g. chemodectoma, mesothelioma
What are the clinical signs of a pericardial effusion?
The clinical signs depend upon the volume of fluid present in the pericardial sac and the rate at which it develops. With an acute effusion (short time-course), serious clinical signs can result from a relatively low volume effusion; however, with a chronic effusion (longer time-course) a large volume effusion might have built up before signs are apparent due to the gradual stretching of the pericardium. Depending on the severity of the effusion and the rate it develops, a patient may present with non-specific signs varying from lethargy, anorexia, cough, GI signs to collapse especially if acute onset. With a chronic pericardial effusion, there may be a history of lethargy, exercise intolerance and progressive abdominal distention. More serious clinical signs are seen with a rapid accumulation of a large volume effusion.
What clinical signs is a patient likely to have if they have cardiac tamponade?
If the animal has tamponade it will have signs consistent with decreased cardiac output (cardiogenic shock) and hypoperfusion. Clinical findings of hypoperfusion include tachycardia, pale mucous membranes, prolonged CRT, absent peripheral pulses +/- weak central pulses etc.
➢ Beck’s triad is likely to be present in a patient with cardiac tamponade- low
arterial blood pressure, distended jugular veins and muffled heart sounds.
What signs might be present in chronic cases of pericardial effusion?
In chronic cases, there may be signs of right-sided, forward heart failure including hepatomegaly, ascites and jugular vein distension, often with a pronounced jugular pulse as the return of blood back to the right side of the heart is impeded. Thoracic auscultation will reveal muffled (or absent) heart sounds; and if there is pleural effusion (secondary to right sided heart failure) the lung sounds will also be quiet.
What is pulsus paradoxicus?
Pulsus paradoxicus may also be present if a patient has tamponade- the quality of the pulse alters with respiration. With pulsus paradoxicus, the arterial blood pressure decreases during inspiration. This is because the increased intrathoracic pressure during inspiration increases venous return to the right side of the heart causing it to enlarge. The combination of the enlarged right heart and the tamponade further compress the left side of the heart so decreasing the stroke volume meaning that the pulse is weaker during inspiration.
What is involved in the initial stabilisation of a patient with pericardial effusion?
Initial stabilisation of a patient presenting with signs of hypoperfusion, +/- respiratory distress, will include supplementary oxygen, by the means most accepted by the patient and strict cage rest in a minimal stress environment. An intravenous catheter should be placed on veterinary direction as soon as the patient will tolerate it.
However, the patient may be severely dyspnoeic and so precautions need to be taken to minimise increased oxygen demand during the stabilisation period. The
definitive management of this condition is pericardiocentesis which should be performed as soon as possible. Whilst intravenous fluids are sometimes given in these circumstances, as with other cases of cardiogenic shock, hypovolaemia is not the problem. Although IVFT may provide some short-term relief (by increasing intravascular volume) the problem is impaired ventricular filling secondary to cardiac tamponade, not hypovolaemia - inappropriate IVFT may lead to clinical signs associated with over infusion.
Emergency administration of diuretics are unlikely to be indicated with pericardial effusion despite the signs of right-sided failure that might be present e.g.
hepatomegaly, jugular distention and ascites. They could cause the patient to become dehydrated leading to hypovolaemia and thus further decreased ventricular
filling leading to a worsening of the clinical signs. As soon as the cardiac tamponade is alleviated (from pericardiocentesis) the signs of right-sided failure should resolve.
What is the most sensitive, specific and easiest way to diagnose a pericardial effusion?
The most sensitive, specific and easiest way, to confirm the presence of a pericardial effusion is with ultrasound/ echocardiography. This can be performed rapidly and with minimal to no stress to the patient. Anechoic fluid
will be visible within the pericardial sac. In addition, the presence of a pleural effusion and ascites if present, can be confirmed. Ultrasound can confirm the presence of
tamponade which would require urgent treatment. It can also identify any abnormal masses within the pericardium
Is radiography suitable for diagnosing a pericardial effusion?
Radiography can be performed but is insensitive for a diagnosis of pericardial effusion. It may demonstrate an enlarged, globoid cardiac silhouette. However, because fluid and soft tissue cannot be differentiated
radiographically, it is not possible to differentiate pericardial effusion from other causes of cardiomegaly e.g. DCM. In addition, obtaining radiographs will be more stressful for the animal- thus ultrasound is the diagnostic modality of choice.
What may be seen on an ECG if a patient has a pericardial effusion?
Electrocardiography (ECG) may show tachycardia, small complexes, occasional escape beats. There will be a changing electrical axis as the heart swings about
within the fluid of the pericardial sac. This can result in an ECG appearance called electrical alternans – the QRS complexes alternate in height with each beat.
Why should clotting times be checked if a patient has a pericardial effusion?
Clotting times (PT, aPTT, ACT) should be assessed prior to pericardiocentesis to ensure that the pericardial effusion has not occurred secondary to a coagulopathy (e.g. anticoagulant rodenticide intoxication). Pericardiocentesis is contraindicated if there is a coagulopathy. In that scenario stabilising the coagulopathy will lead to resolution and re-absorption of the pericardial effusion.
Why is it important that blood pressure is monitored when a patient has a pericardial effusion?
Arterial blood pressure should also be monitored. Hypotension could indicate severe cardiac tamponade and therefore the need for prompt emergency treatment pericardiocentesis
How does a pericardiocentesis benefit a patient with a pericardial effusion?
Pericardiocentesis removes fluid from the pericardial space reducing the pressure on the cardiac chambers, thereby enabling increased ventricular filling (increased
preload) during diastole. This in turn will lead to increased stroke volume during systole so a return to normal cardiac output.
The fluid type can also be analysed so pericardiocentesis is also diagnostic.
Does a patient require a sedation for a pericardiocentesis?
Unless the patient is collapsed, it is likely to be sedated for the procedure to ensure it is still and to minimise discomfort. A cardiovascularly sparing sedation protocol is required e.g. an opiate (butorphanol) and benzodiazepine (midazolam) combination.
Whilst, pericardiocentesis is not a particularly painful procedure, it is important to be aware that the patient may have concurrent illness, such as osteo-arthritis, that might elicit pain that could be worsened with handling and restraint. Drugs such as acepromazine and alpha-2 agonists should be avoided due to their hypotensive
effects.
What equipment is required for a pericardiocentesis?
Equipment for pericardiocentesis Clippers Surgical scrub to prepare sterile site Commercial pericardiocentesis kits are available Or 14 – 18 gauge over the needle catheter of a suitable length for the patient Three-way tap IV extension tubing 50-60ml syringe Kidney dish Local anaesthetic Sterile gloves Scalpel blade Sample pots (EDTA, plain) and slides Ultrasound ECG
How do you perform a pericardiocentesis?
Pericardiocentesis may be performed on the left or right side of the thorax although a right sided approach is preferred by many. There is a ‘cardiac notch’ between the right cranial and caudal lung lobes which decreases the risk of iatrogenic lung puncture; and there are fewer coronary vessels on the right side (Olcott, 2010).
There are, however, potential risks associated with either left or right sided pericardiocentesis.
The patient can be positioned in sternal or left lateral recumbency - however sternal is likely to be better tolerated in the very compromised patient. The lateral thorax is clipped upwards from the sternum to the mid-thorax from ~ rib 3 to rib 9 and surgically prepared. A ‘window’ into the pericardial effusion can be detected with the use of ultrasound. The area of the chest to be penetrated (usually 4th to 6th intercostal space just below the costo-chondral junction) is infiltrated with local anaesthetic 5-10 minutes prior to the procedure. It is important to have ECG leads attached during this procedure to identify ventricular premature complexes (VPCs) that will occur if the catheter touches the epicardium. Ideally the procedure is performed with ultrasound guidance. The catheter is attached to the IV extension tubing, three-way tap and syringe A small skin incision is made with the scalpel blade. One operator advances the catheter through the incision and into the pericardial sac whilst the other gently pulls back on the syringe plunger to aspirate the free fluid. Initially a small amount of the fluid should be placed in a plain tube to see if it clots- if it does clot then there is a concern that it is fresh blood that has been
aspirated from the heart. In this case, the catheter should be removed, and the procedure started again. Samples of the pericardial fluid, which is generally
sanguinous in appearance, should be collected into plain and EDTA tubes for analysis. The PCV should be checked and compared with venous blood. It would be
expected to be lower than the peripheral blood unless there has been a recent, acute pericardial haemorrhage. If there is ongoing active
pericardial bleeding, pericardiocentesis is contraindicate. A smear should be made to
look for evidence of neoplastic cells or schistocytes that may be associated with haemangiosarcoma of the heart base- a common cause of haemopericardium.
Some fluid can be sent for culture and sensitivity testing. Thereafter the rest of the effusion should be drained - progress can be monitored using ultrasound to determine if all the fluid has been removed. The effusion should be drained slowly to allow adequate re-filling of cardiac chambers and avoid dramatic changes in pressure.
What should happen when fluid is removed from the pericardium when a patient has a pericardial effusion?
Once the fluid has been removed, the patient’s perfusion parameters should start to improve e.g. the heart rate should return to normal, although arrhythmias may persist for a bit longer. The patient should be much brighter once the sedation has worn off, as normal perfusion has been restored. Ongoing nursing care should focus on monitoring for any complications of the procedure (e.g. haemorrhage, pneumothorax, arrhythmias); as well as monitoring for recurrence of the effusion (e.g. recurrence of tachycardia and signs of poor perfusion.
What species does aortic thromboembolism usually affect and how does it usually present?
Affected cats usually present acutely and in distress with a thromboembolism affecting at least one limb- it is a condition with high morbidity and mortality. Commonly owners will report the patient being normal in the time up to presentation where they are commonly found collapsed, in extreme pain and unable to use hind limbs.
How does an aortic thromboembolism usually occur?
FATE occurs most commonly occurs secondary to hypertrophic or restrictive cardiomyopathy in cats although there is often no previous history of
cardiac disease. Left atrial enlargement occurs secondary to the heart disease and blood movement within this chamber is turbulent. This can lead to micro-thrombi and thrombus formation within the left atrium. Emboli from these thrombi break off and
enter the systemic circulation via the aorta. Depending on their size, these typically lodge at the aortic trifurcation, or just beyond it, restricting or completely cutting off blood flow to one or both hind limbs. A thrombus can lodge elsewhere including
forelimb arteries, cerebral arteries and even the renal arteries. Sometimes a thrombus only causes a partial obstruction, initially, but it will continue to enlarge.
Mortality is high with this condition- many cats die soon after the condition develops or are euthanased on humane grounds.
What are the signs of an aortic thromboembolism?
The signs will depend on location of the thrombus; and whether the obstruction is complete or incomplete- the patient shows signs of severe pain and distress due to ischaemia. There will be paresis or paralysis of the affected limb (s) - if the clot lodges and completely obstructs the caudal aorta the cat will be unable to use both hind legs. There may be a previous history of heart disease but often here is none.
Affected cats usually present with per-acute, sudden onset extreme distress, difficulty moving and are often yowling. The presenting signs can be
like those of trauma or acute neurological conditions.
They will often be open mouth breathing and tachypnoeic due to stress and pain rather than cardiac signs.
They are likely to have all or some of the five P’s- paralysis, paresis, pain, lack of pulse, pallor (or cyanotic pads) and polar (cold) distal limbs/ extremities.
If the cat has pre-existing congestive cardiac failure, there may additionally be signs associated with that e.g. dyspnoea secondary to pleural effusion.
What might be found on the primary assessment of a patient with feline aortic thromboembolism?
The cat will be very painful and may be crying out. It may resent any handling - it is important not to cause any further distress as this may cause cardiac arrest. It is likely to be tachypnoeic due to pain and distress. It may be dyspnoeic from concurrent congestive heart failure. Auscultation of the thorax may reveal
tachycardia, a gallop rhythm or decreased heart sounds if pleural effusion is present.
Palpation of the affected limbs, usually hind-limbs, will reveal decreased or absent femoral pulses (one or both) - the affected limbs will be cold with pale or cyanotic pads. There will be diminished or no neurological function in the hind-limb (s) - the
cat will have paresis or complete paralysis and will be dragging the affected limb,
usually hind limbs. The rectal temperature may be decreased due to lack of blood
flow and the sympatho-adrenal response.
What would initial stabilisation of a patient with aortic thromboembolism involve?
Opioid analgesia is the main initial priority. Handling
of the patient should be kept to a minimum and the cat placed into a comfortable kennel where movement can be restricted. Oxygen therapy is indicated if the cat is
dyspnoeic. Fentanyl and methadone have a rapid onset of action and are commonly used to manage pain in these patients. Buprenorphine, as a partial agonist indicated for mild to moderate pain, would not generally be sufficient for a patient with ATE.
What diagnostics can be performed to diagnose an aortic thromboembolism?
The absence of a (hind-limb) pulse can be confirmed with Doppler. Stress-induced hyperglycaemia and azotaemia may be present. Comparison of the serum glucose and lactate levels from affected and unaffected limbs can be performed. Due to anaerobic respiration, glucose will be low and lactate high in the compromised limbs compared to the normal limbs. Echocardiography will demonstrate the underlying cardiac disease (e.g. hypertrophic or restrictive cardiomyopathy). The left atrium will likely be enlarged and there may be a thrombus in the left atrium or ‘smoke sign’
which is consistent with formation of micro-thrombi. Thoracic radiography can be performed (if/ when the patient can tolerate this) - this may reveal cardiomegaly +/- signs of congestive heart failure.
ECG can also be useful in diagnosing arrythmias.
How do you manage aortic thromboembolism?
The current advised regime is to manage pain and prevent further clot formation using thromboprophylaxis/ anticoagulation therapy.
Treatment of the underlying heart disease (+/- congestive heart failure) will also be necessary- e.g. furosemide and ACE inhibitors as discussed previously.
Supportive therapy should be aimed at maintaining body temperature as many patients are hypothermic on presentation; hydration and nutritional status. IVFT may be required but it is essential to avoid over infusion in a cat with congestive cardiac failure.
What use is aspirin or clopidogrel in patients with aortic thromboembolism?
Aspirin or clopidogrel can be used to inhibit platelet aggregation thus preventing further clot formation. They do not have any effect on pre-existing clots
Is heparin used in the treatent of aortic thromboembolism?
Heparin (either unfractionated or, more recently, low molecular weight) may be used to prevent further clot formation by blocking the coagulation cascade. However, there is some debate as to its efficacy
Why is thrombolysis not recommended for aortic thromboembolism?
Thrombolysis (breaking down the clot) is not currently recommended. There is a high risk of reperfusion injury and increased mortality associated with thrombolysis.
Is physiotherapy recommended for patients with aortic thromboembolism?
Physiotherapy
In mild cases, limb manipulation and massage may facilitate blood flow if the cat can tolerate handling. Physiotherapy will be important for the longer-term management and recuperation process.
What monitoring should be carried out on a patient with an aortic thromboembolism?
The cat will need to be monitored closely for signs of pain, using a validated pain scoring method, with the analgesic plan being reviewed as required. Ongoing
monitoring of the circulation to the affected area is important. Increasing levels of pain can be seen despite adequate analgesia and multi modal techniques are
needed.
The cat may also be in congestive heart failure (or at risk of) and should be monitored for signs of dyspnoea. Whilst limb movement will sometimes return, it may take a long time and may not be complete. Appropriate nursing and management of the neurological signs will be required. Because clots may also embolise to the kidneys, renal values should be monitored- especially as heart medication may also affect these.
Affected cats are at risk of reperfusion injury within a few days of the thromboembolic event. As the blood supply returns to the affected limbs, waste products and electrolytes that have accumulated from damaged cells enter the systemic circulation. This can result in severe hyperkalaemia and metabolic acidosis
What nursing care should be carried out on a patient with an aortic thromboembolism?
Nursing care for these patients is focused on pain management and a validated pain scoring scale must be used. Knowledge of the side effects of medications
administered to manage pain is necessary for effective monitoring of these patients.
As they are commonly on oxygen therapy for longer periods of time, ocular lubrication, especially for a patient receiving pure mu opioids, is indicated to stop the corneas drying.
Recumbency care should focus on maintaining comfort, maximising ventilation, preventing lung atelectasis and pressure sores from lying in one position for too long.
Patients should be positioned in sternal as much as possible. However, if this is not tolerated, placing in left lateral for two hours, then into sternal for two hours then into right lateral for two hours can be helpful. The patient can be placed in a padded trough to facilitate maintaining in sternal recumbency. Bladder management becomes an important part of recumbency care. Although there is no reason for this
patient not to be able to urinate, they will often be unable to access a litter tray due to the paresis; and therefore need wicking bedding and regular hygiene checks. If the cat is long haired, clipping hair around the perineum may help prevent urine scald. In some patients an indwelling urinary catheter and closed collection system may be required.
Physiotherapy and gentle application of heat are beneficial but must be performed on the direction of the veterinary surgeon. 12-24 hours following the initial
presentation, it can be useful, if the patient tolerates it, to apply a gentle heat source for 10 minutes every 2 hours to encourage mild vasodilation. However, these
patients should not be placed on a static heat source due to their inability to move and the significant risk of burns.
Nutritional support is important – often due to the severe pain associated with this condition, these patients will not eat voluntarily. The main focus will be pain management; however, a feeding tube may need to be considered for short term support.
The cat is also at risk of a further thromboembolic event so close monitoring should be performed for this.
Because of this the long-term prognosis is usually poor. Some cats may be euthanased soon after presentation, on humane grounds, or if they fail to respond to treatment
What is systemic hypertension?
Systemic hypertension is the pathological syndrome due to elevated systemic arterial blood pressure. The importance of systemic hypertension as a condition in
animals is increasingly recognised, especially in cats
What can be the cause of systemic hypertension?
It can be a primary condition or is often secondary to other conditions. Potential secondary
causes include phaeochromocytomas, renal failure, diabetes mellitus, hyperthyroidism (cats) and hyperadrenocorticism (dogs). Animals will also present
with severe hypertension secondary to raised intra cranial pressure (ICP; Cushing’s reflex- discussed further in unit 5)
Why is systemic hypertension problematic in patients?
Elevation of systemic blood pressure can lead to tissue damage especially nervous, ocular and renal. This can result in neuron damage/cerebral haemorrhage; retinal or intraocular haemorrhage/retinal detachment; or kidney damage. Sudden development of clinical signs secondary to systemic hypertension may be a
reason for an emergency presentation e.g. sudden onset blindness, ataxia, signs of vestibular disease etc.
What organ damage (if at all) would a systolic of <150 and a diastolic of <95 have and what would the blood pressure substage be?
none or minimal
BP substage AP0
What organ damage (if at all) would a systolic of 150-159 and a diastolic of 95-99 have and what would the blood pressure substage be?
Low
BP substage AP1
What organ damage (if at all) would a systolic of 160-179 and a diastolic of 100-119 have and what would the blood pressure substage be?
Moderate
BP substage AP2
What organ damage (if at all) would a systolic of 1≥180 and a diastolic of ≥120 have and what would the blood pressure substage be?
High
BP substage AP3
What is pulmonary hypertension?
Pulmonary hypertension is caused by elevated pulmonary artery blood pressure.
Pulmonary arterial hypertension (PAH) is a rare, but increasingly recognised condition, characterised by an increase in pulmonary vascular resistance which
leads to right ventricular failure ‘cor pulmonale’ (Williams, 2011). The increase in pulmonary arterial pressure (PAP) can result from left sided heart disease,
pulmonary over-circulation, chronic pulmonary disease or vascular obstruction e.g. due to Angiostrongylus vasorum. Pulmonary pressures can be measured by
pulmonary arterial catheterisation or more commonly by using echocardiography.
What signs do patients with pulmonary hypertension have?
Affected animals are typically exercise-intolerant and have episodes of collapse.
Ultimately, right-sided failure or (ascites etc.) cardiac arrhythmias may develop.
What is the treatment of pulmonary hypertension?
Treatment is aimed at the underlying cause (e.g. furosemide, ACEi if left sided heart disease); parasiticide therapy for Angiostrongylus vasorum; and pulmonary vasodilators that will reduce the pulmonary pressures. Sildenafil is a phosphodiesterase (V) inhibitor that enhances nitric oxide (NO)-mediated pulmonary vasodilation (BSAVA, 2020). It has been shown to reduce pulmonary arterial pressures, increase exercise tolerance and improve quality of life in dogs with PAH. Pimobendan can also be used in dogs with PAH.
State five parameters that should be monitored in a patient with cardiogenic shock
Peripheral and central pulses Mentation Body Temperature- core and peripheral Urine output ( should be 1-2 ml/hr) Blood Pressure Respiratory Rate CRT ( should be 1-2 seconds) Blood gases Blood Lactate
Which of the following conditions is most likely to cause pulmonary oedema in a dog?
Select one:
a. Forward heart failure
b. Backward heart failure
c. Cardiogenic shock
d. Hypotension
The correct answer is: Backward heart failure
A rapid, irregular heart rhythm and pulse deficit is most likely to be present with which condition?
Select one:
a. Pericardial effusion
b. Ventricular septal defect
c. Atrial fibrillation
d. Hypertrophic cardiomyopathy
The correct answer is: Atrial fibrillation
Which of the following drugs is a calcium channel blocker?
Select one:
a. Sotalol
b. Atropine
c. Diltiazem
d. Lidocaine
The correct answer is: Diltiazem
Which of the following can be used in the management of hyperkalaemia?
Select one:
a. Insulin
b. Glucose
c. Calcium gluconate
d. All of the above
The correct answer is: All of the above
A dog is to undergo pericardiocentesis. What area should be clipped and surgically prepared?
Select one:
a. 7th-11th intercostal spaces from the sternum to the mid-thoracic region
b. 2nd to 5th intercostal spaces from the mid-thorax to dorsal spinous processes
c. Intercostal spaces 2-8 from sternum to the mid-thoracic region
d. 8th-12th intercostal spaces from mid-thorax to dorsal spinous processes
The correct answer is: Intercostal spaces 2-8 from sternum to the mid-thoracic region
Which of the following medications is an anti-platelet medication that might be used in the management of a cat with aortic thromboembolism?
Select one:
a. Heparin
b. Insulin
c. Fentanyl
d. Clopidogrel
The correct answer is: Clopidogrel
Which of the following diagnostic tests should be performed in a dog prior to performing pericardiocentesis?
Select one:
a. Blood smear examination
b. PT/aPTT or Activated clotting time
c. Slide agglutination test
d. Coombs test
The correct answer is: PT/aPTT or Activated clotting time
