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
