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HEART FAILURE
INTRODUCTION
The combination of an aging population and improved treatment of acute cardiac illnesses has
resulted in both an increased incidence of chronic heart failure and an increased number of patients
presenting with acute heart failure. This module will focus on the syndrome of acute heart failure.
Heart failure occurs when the heart is unable to either receive adequate venous return from, or pump
blood into, the arterial system at a sufficient rate to meet the metabolic demands of the body. Acute
heart failure (AHF) is defined as the rapid onset of symptoms and signs secondary to abnormal cardiac
function. It is often life-threatening and requires urgent treatment. It may occur with or without previous
cardiac disease. The cardiac dysfunction can be related to systolic or diastolic dysfunction, to
abnormalities of cardiac rhythm or to preload and afterload mismatch.
AHF presents clinically with non-specific symptoms and signs such as dyspnoea and/or signs of
hypoperfusion. The aim is to recognise these manifestations and to classify the patient into one of the
distinct categories of AHF that will affect the ultimate management and prognosis. The manifestations
include acute heart failure (de novo or as decompensation of chronic heart failure), forward heart
failure, and backward failure, either of left or right heart.
1/ EARLY RECOGNITION AND MANAGEMENT OF THE PATIENT WITH AHF
Acute heart failure is a common problem encountered by intensive care clinicians and can represent a
threat to life. In its severest form, it is a medical emergency that presents with severe pump failure and
symptoms of impaired organ perfusion.
The main goals of acute management of the patient with AHF are to:
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Resuscitate the patient to stabilise the condition and prevent further deterioration.
Assess the severity of the problem so that the patient can be moved to an appropriate
setting that can provide optimal monitoring and support.
Determine the possible aetiology of the acute heart failure. This will enable early
intervention when an acute reversible problem exists.
Immediate assessment and resuscitation
The first line assessment and treatment are closely inter-related and should occur simultaneously.
They include the following tasks:
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Resuscitation of the patient
Institution of basic monitoring
Clinical history
Physical examination
Assessment of severity of AHF
The immediate priorities when treating a patient with acute heart failure are the
same as for any acute illness. Therefore, attention should be paid to ensuring
the ABCs are adequate.
Resuscitation
Airway
Initial assessment of the airway takes only a few seconds. The most likely reason that a patient is
unable to maintain an adequate airway is a reduced level of consciousness. Oral or nasopharyngeal
airways may be sufficient to prevent airway obstruction but endotracheal intubation is required in some
cases. Intubation can sometimes be avoided (preferably) with proper and rapidly acting conservative
therapy.
Breathing
The failing myocardium will be further compromised by hypoxaemia and steps to prevent this
occurrence are essential. Oxygen should be administered in as high a concentration as possible to
maximise tissue oxygenation. The response to oxygen therapy should be assessed by continuous
pulse oximetry and regular blood gas analysis.
How does continuous positive airway pressure (CPAP) help patients with acute heart failure?
If the patient fails to respond to oxygen administered via a face-mask, CPAP or non-invasive mask
ventilation should be considered. This will reduce the work of breathing and therefore oxygen
consumption, minimise pulmonary oedema and improve the functional residual capacity. A reduction in
ventricular transmural pressure is also thought to reduce myocardial work by reducing left ventricular
afterload. Patients in whom poor gas exchange persists may require intubation and invasive
mechanical ventilation.
The reasons for initiating ventilatory support are essentially two-fold. The first reason is to reverse
respiratory muscle fatigue that is secondary to hypoperfusion. The second reason is to reduce the
whole body oxygen requirements in a patient who is in a critical condition, by resting the respiratory
muscles and therefore reducing the oxygen needs of that significant muscle group.
T HINK
about how you institute mechanical ventilation and how you use sedatives for patients with
severe acute heart failure. Evaluate how you utilise these tools to offload the work of breathing
at the same time as improving systemic oxygenation.
Circulation
Therapies aimed at improving the circulatory status are dependent on the pathophysiological
classification of AHF (see Task 2, Pathophysiology ). An appropriate blood pressure and cardiac
output must be obtained in these patients to maintain end organ perfusion and function.
Basic monitoring
These patients can be extremely ill and their clinical condition can fluctuate very quickly. The initiation
of basic monitoring is thus vital to aid in the assessment of the patient's condition as well as to guide
therapy and warn of problems. All patients should have the following parameters monitored:
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Continuous electrocardiogram
Blood pressure
Respiratory rate
Temperature
Continuous oxygen saturation with a pulse oximeter
Clinical history
C OMMUNIC ATI ON
A good clinical history is often difficult to obtain in a patient with severe
acute heart failure. It is important to speak with the patient's family or care
givers as they can often provide the necessary details. See the PACT
modules onCommunication skills and Basic clinical examination
Taking the clinical history is important to:
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Decide - Does this patient have acute heart failure?
Obtain clues to the aetiology of the acute heart failure.
Determine whether the cause of acute heart failure is due to an acute coronary syndrome
that may require immediate intervention.
Avoid potential complications of your acute therapy.
Consider the following items in history-taking:
Key questions in
history-taking
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Definition of DYSPNOEA: breathlessness or dyspnoea is the recognition of an
inappropriate relationship between respiratory work and total body work.
How does dyspnoea present and what is its spectrum of severity?
Dyspnoea is not always a life-threatening problem, however sometimes it can be. The degree or
severity of dyspnoea therefore needs to be rapidly assessed with a detailed history and examination.
When AHF develops, exertional dyspnoea may simply appear to be an aggravation of the
breathlessness that occurs in healthy persons during activity. As left ventricular failure advances, the
intensity of exercise that causes breathlessness progressively declines.
Orthopnoea appears at an early stage of acute heart failure. It is relieved by elevation of the head with
pillows. It is important to evaluate the change in the number of pillows required to ameliorate the
symptom as this describes a worsening of the condition. Orthopnoea may occur in any condition in
which the vital capacity is low. Orthopnoea can occur extremely rapidly when the patient becomes
supine and this is the reason that many patients with AHF cannot lie flat.
Cough, sudden awakening during the night and bronchospasm may be early
signs of AHF.
Cough, especially during semi-recumbency may be the equivalent of orthopnoea. A sudden awakening
of the patient after a couple of hours is defined as an attack of 'paroxysmal nocturnal dyspnoea' and it
is characterised by a feeling of severe anxiety, breathlessness and suffocation. Bronchospasm may
increase ventilatory difficulty and the work of breathing.
This situation can be difficult to distinguish from an acute exacerbation of
asthma ('cardiac asthma').
Additional symptoms
Other symptoms which can be elicited from the patient history:
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None, indeed the patient could be:
o Truly asymptomatic or
 Asymptomatic because of sedentary lifestyle
Fatigue
Weakness
Swelling of ankles
Abdominal pain and/or distension
Palpitations
Syncope or pre-syncope
Central nervous symptoms such as decreased level of consciousness
Fatigue and weakness may be related to poor perfusion of the skeletal muscles in patients
with lowered cardiac output.
Co-morbid conditions
Many of these patients will be suffering from co-morbid conditions that may
help you to understand the cause of the acute heart failure. These can be
conditions such as diabetes mellitus, hypertension, ischaemic heart disease
or atrial fibrillation. Other patients will have had previous admissions to
hospital with acute heart failure. These patients will often have had prior
investigations into their cardiac status and this information can be invaluable
in helping to assess your current patient.
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Relevant co-morbid
conditions can help to
delineate the category of AHF
The main question to be asked at this stage is whether the AHF has arisen de novoor as a
decompensation of a chronic condition. This can be assessed by asking the patient about
other co-morbidities that are associated with a diagnosis of chronic heart failure.
Drug-induced AHF
It is important to get an accurate description of the medication history of the patient. This is because a
number of cardiac as well as non-cardiac medications can precipitate or worsen acute heart failure. It
is also important to realise that in the hospital setting, abrupt stopping of regular cardiac medication
can precipitate an acute heart failure syndrome.
What drugs are used for the treatment of chronic heart failure and therefore will be encountered
in patients presenting with acute heart failure?
Non-cardiac medications can cause an exacerbation of heart failure. Medications for diabetes mellitus
have been reported to increase plasma volume. Non-steroidal anti-inflammatory drugs can promote
sodium and fluid retention, interfere with the pharmacological mechanism of ACE inhibitors and
decrease the effectiveness of loop diuretics. Tricyclic antidepressants, whether used to treat
depression or neuropathy, can produce cardiac conduction delay and increase the risk for ventricular
arrhythmia. Theophylline and β-agonist bronchodilatators may also exacerbate heart failure by
inducing tachyarrhythmias.
In addition, cardiac medications, for instance β-blockers, may precipitate or worsen heart failure. Most
anti-arrhythmic agents can depress myocardial function as well as exacerbate ventricular arrhythmias.
Calcium channel blockers may also depress myocardial function.
Review the prescription chart for the last three patients that have presented with acute
heart failure. You should assess the number of drugs that each patient presents with, the
reason for the patient taking them, their interactions and likely impact on the acute
presentation of the patient's disease.
Physical examination
The purpose of the physical examination is to confirm the symptoms of AHF and to start to understand
the category of AHF that the patient is experiencing. The signs of acute heart failure relate to whether
the patient has a problem with congestion, perfusion or both.
Signs of acute
heart failure
Assessment of severity of AHF
Severity of illness quantification is important as it allows the clinician to make an accurate risk
assessment and to communicate his findings with other colleagues. A rapid assessment should be
made to identify patients who should be transferred to the Intensive Care Unit (ICU) and those who
can be safely managed on a ward setting. The severity of the heart failure can then be quantified in
relation to the patient's chronic condition and current state.
A greater degree of heart failure is suggested by worsening dyspnoea, obtundation, hypotension and
oliguria. These patients will be cyanosed and will have a metabolic acidosis. They will inevitably have a
low stroke volume in association with raised cardiac filling pressures and reduced mixed venous
oxygen saturation.
Which patients with acute heart failure should be transferred to the ICU?
Three scores to describe severity of illness in chronic heart failure patients are:
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New York Heart Association functional classification
'Cold, Warm, Dry, Wet' system
Framingham criteria
The most commonly quoted assessment of heart failure is the New York Heart Association criteria.
This is useful as a quick and easy method of quantifying the baseline state of the patient.
New York Heart
Association
functional
classification
for congestive
heart failure
The 'Cold, Warm, Dry, Wet' system to assess severity: the approach to decompensated heart failure
has been simplified by the consideration of four haemodynamic profiles. Most patients can be
classified into one of these during a two-minute bedside assessment. The two fundamental
haemodynamic abnormalities relate to presence or absence of elevated filling pressures (congestion)
and perfusion that may be adequate or critically limited.
'Cold, Warm, Dry, Wet'
System
You can find further information about the Framingham criteria in the following reference.
Every time you see a patient with acute heart failure you should assess the
severity of their disease with these tools. This will enable you to have a more
objective assessment and make your communication of the patient's problems
to other professionals more precise.
2/ DIAGNOSTIC CATEGORY OF AHF
Acute heart failure often presents with a different clinical picture compared to chronic heart failure due
to the rapid onset preventing development of normal compensatory responses. Thorough
understanding of the likely causes of the heart failure as well as an understanding of the
pathophysiological processes inherent to the condition is therefore necessary, if expedient diagnostic
and therapeutic interventions are to be initiated.
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T HINK
Heart failure should never be the final diagnosis.
about the last few patients you admitted with heart failure and identify the aetiology of
the syndrome and the specific treatments that were necessary.
Multiple extra-cardiac pathologies may result in acute heart failure by changing
the cardiac loading conditions e.g. high output states due to sepsis in a patient
with poor physiological reserve
Common causes
of acute heart
failure
The aetiology of heart failure and the presence of exacerbating factors or other diseases that may
have an important influence on management should be carefully considered in all cases. The extent to
which the cause of heart failure should be pursued by further investigation will depend on the
resources available and the likelihood that a diagnosis will influence management. The causes of AHF
are wide and varied. It is important to recognise which of the causes are more common for your own
clinical practice. This will vary depending on the patient population you are treating. The commonest
primary cardiac cause of acute heart failure in the Western world is ischaemic heart disease.
Pathophysiology
The syndrome of acute heart failure develops secondary to one of several pathophysiological
categories.
Pathophysiological
categories of heart
failure
The terminology that is commonly used to describe the pathophysiological and clinical disturbances is
not all encompassing and complete. However it does provide a basis for understanding the patient's
condition and overall status. The terms that are commonly attributed to patients with heart failure are
forward/backward, systolic/diastolic or whether the predominant problem is on the right or left side of
the heart.
Right and/or left heart failure
This terminology describes the side of the heart the predominant problem is on. The clinical picture will
vary dramatically depending on whether the patient has a predominantly left or right sided problem.
Forward/backward heart failure
This terminology describes whether the predominant problem is with forward flow (perfusion) or
backward flow (congestion).
systolic and/or diastolic heart failure
As ischaemic heart disease is the commonest cause of heart failure in industrialised societies, most
cases of heart failure are associated with evidence of left ventricular systolic dysfunction, although
diastolic impairment at rest is a common if not universal accompaniment. Diastolic heart failure is often
presumed to be present when symptoms and signs of heart failure occur in the presence of preserved
left ventricular systolic function. Predominant diastolic dysfunction is relatively uncommon in younger
patients, but increases in importance in the elderly, especially in combination with systemic
hypertension.
Specific examples of acute heart failure
How would a patient with cardiogenic shock present?
Forward (left and right) acute heart failure
Forward acute heart failure may be mild-to-moderate with only effort fatigue, up to severe with
manifestations of reduced tissue perfusion at rest with weakness, confusion, drowsiness, pallor with
peripheral cyanosis, cold clammy skin, low blood pressure, filiform pulse, and oliguria, culminating in
the full blown presentation of cardiogenic shock. The aetiology of this syndrome is diverse, but
common causes include acute myocardial infarction, acute myocarditis, acute valvular dysfunction,
pulmonary embolism and cardiac tamponade.
An 82-year-old female patient was admitted to the emergency department for acute pulmonary
oedema (APE). Her past medical history showed a long-standing history of hypertension.
Echocardiography during the episode showed left ventricular ejection fraction (LVEF) 56% and left
ventricular hypertrophy (LVH).
What is the mechanism of pulmonary oedema in patients with heart failure associated with normal
LVEF?
Left heart backward failure
Left heart backward failure is related to left ventricular dysfunction with varying degrees of severity
from mild-to-moderate with only exertional dyspnoea, to pulmonary oedema presenting with shortness
of breath (dry cough, sometimes with frothy sputum), pallor or even cyanosis, cold clammy skin, and
normal or elevated blood pressure. Pathology of the left heart is often responsible for this syndrome.
Cardiac pathologies responsible for this syndrome include acute ischaemic events, acute valvular
problems and arrhythmias. The syndrome can also commonly present as a result of an acute elevation
in blood pressure causing an excessive left ventricular afterload and therefore the left ventricle to fail.
This sudden presentation of acute pulmonary oedema is often referred to as 'flash' pulmonary
oedema.
Chest X-ray showing
cardiogenic pulmonary
oedema
Acute cardiogenic pulmonary oedema usually presents in elderly women with a long history of
hypertension that has been inadequately treated. They usually present with the clinical signs of acute
pulmonary oedema and uncontrolled hypertension. Assessment of these patients is predominantly with
a chest radiograph, electrocardiogram and cardiac enzymes. Management consists of oxygen,
symptom control, nitrates, vasodilators for hypertension and loop diuretics. The priority in treating
these patients is to achieve rapid control of the blood pressure. Response to treatment is usually rapid
and mortality is low. Further investigations in terms of invasive monitoring or echocardiography should
be reserved in the acute setting to patients who fail to respond to the baseline therapy.
Right heart backward failure
Right heart ischaemia is associated with striking increases in the incidence of haemodynamic
compromise, arrhythmias, and in-hospital mortality. The classical cause of acute right ventricular
failure is an acute pulmonary embolism. On the ICU, this syndrome can be seen as acute cor
pulmonale when high intrathoracic pressures are used to aid mechanical ventilation. This syndrome
can often be diagnosed clinically with the onset of acute tricuspid regurgitation and the presence of 'V'
waves on the central venous pressure trace. Although haemodynamic manifestations develop in less
than half of cases, right ventricular infarction may result in cardiogenic shock characterised by a
disproportionate elevation of the right heart filling pressures with hypotension and a low cardiac output
despite preserved LV systolic function. The pathophysiologic mechanisms contributing to
haemodynamic compromise with severe right ventricular infarction are now well documented.
Right coronary occlusions proximal to the RV branches reduce RV free wall perfusion, resulting in
depressed global RV performance, which diminishes transpulmonary delivery of LV preload, leading to
decreased cardiac output despite intact LV contractility. Acute RV dilation results in elevated
intrapericardial pressure, which together with increased RV diastolic pressure shifting the
interventricular septum towards the volume-deprived left ventricle, conspires to further limit LV filling.
How would a patient present if s/he had right heart failure?
3/ PERFORMING DIAGNOSTIC PROCEDURES
Task 1 briefly described how a patient with acute heart failure could be
recognised from physical history and examination. This section expands on the
tests that should be performed on the patient to both confirm the physical
findings but also to provide a clinical diagnosis.
Further investigations
These investigations should be done urgently but should not delay resuscitation and initiation of
definitive therapy.
Electrocardiogram
Electrocardiographic changes in patients with heart failure are
frequent.
The negative predictive value
of a normal ECG to exclude
LV systolic dysfunction
exceeds 90%
The electrocardiogram (ECG) describes the electrical heart state and this is crucial data to eliminate
either conduction abnormalities (blocks; arrhythmias: atrial fibrillation with a rapid ventricular response,
ventricular tachycardia, bradycardia) or myocardial ischaemic lesions (acute coronary syndrome). On
the other hand, the presence of anterior Q waves and a left bundle branch block in patients with
ischaemic heart disease are good predictors of a decreased ejection fraction (EF). ECG signs of left
atrial overload or left ventricular hypertrophy may be associated with systolic as well as isolated
diastolic dysfunction, but they have a low predictive value. The diagnostic contribution of ECG
anomalies markedly increases if clinical symptoms and signs of heart failure co-exist. ECG recordings
do not need to be repeated in the absence of changes of clinical status.
Chest radiograph
A chest X-ray should be performed early for all patients with AHF to evaluate pre-existing chest or
cardiac conditions (cardiac size and shape) and also to determine the presence of pulmonary
congestion.
In patients with heart failure an increased cardiac size as judged by a cardiothoracic ratio >0.50, and
the presence of pulmonary venous congestion are useful indicators of abnormal cardiac function with a
decreased ejection fraction and/or elevated left ventricular filling pressure.
A chest radiograph is often abnormal in patients presenting with AHF. The chest radiograph is able to
give you a lot of details about possible co-morbidities and the underlying cardiac status.
This chest X-ray reveals the
patient has had an aortic
valve replacement
He also has pulmonary
hypertension, left atrial
enlargement and evidence of
mild pulmonary oedema
Interstitial and alveolar pulmonary oedema are also reliable and important signs of severe left
ventricular dysfunction. However, in individual patients the radiographic findings alone do not allow a
reliable estimation of the pulmonary capillary pressure and are therefore not suitable as the only basis
for therapeutic decisions. There may also be interobserver variations in the interpretations of chest Xray changes. The relationship between radiological signs and haemodynamic signs may depend on
the duration as well as the severity of cardiac dysfunction.
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A high predictive value of X-ray findings is only achieved by interpreting the Xray in the context of clinical findings and ECG abnormalities.
See the PACT module on Clinical imaging for further information on chest X-rays.
Laboratory tests in AHF
The following laboratory tests should be considered in a patient with severe AHF:
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Urea and electrolytes
Arterial blood gases
Full blood count
Coagulation profile
Blood glucose
Cardiac troponin
B-type natriuretic peptide (BNP, NT-pro BNP)
Liver function tests
Cardiac enzymes (troponin)
Apart from the acute coronary syndromes what other conditions can cause increases in the
troponin enzymes?
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The most recently described and preferred biomarker for myocardial damage is cardiac
troponin (I or T), which has nearly absolute myocardial tissue specificity, as well as high
sensitivity, thereby reflecting even microscopic zones of myocardial necrosis. Because cardiac
troponin values may remain elevated for seven to ten days or longer after myocardial necrosis,
care should be exercised in attribution of elevated cardiac troponin levels to very recent clinical
events. If cardiac troponin assays are not available, the best alternative is CK-MB (measured by
mass assay). This is less tissue-specific than cardiac troponin, but the data documenting its
clinical specificity for irreversible injury are more robust. In most situations, elevated values for
biomarkers should be recorded from at least two successive blood samples to classify acute
coronary syndromes.
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Several studies have shown that cardiac troponin T (cTnT) and cardiac troponin I (cTnI) are
increased in patients with advanced heart failure and that the concentrations of these
biomarkers closely parallel disease severity. See the PACT module on Acute myocardial
ischaemia for more information.
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B-type natriuretic peptide (BNP)
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Plasma concentration of certain natriuretic peptides (ANP, BNP and NT-pro BNP) can be
helpful in the diagnostic process. BNP has been proposed as a tool to distinguish acute heart
failure from other causes of acute dyspnoea. These peptides may be most useful clinically as a
'rule out' test due to consistent and very high negative predictive values. Plasma levels of ANP
and BNP increase in accordance with the severity of the heart failure.
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Echocardiography
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Echocardiography is an essential tool for the evaluation of the functional and structural changes
underlying or associated with AHF, as well as in the assessment of acute coronary syndromes.
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Early echocardiographic evaluation is warranted to define global and regional cardiac function
and detect any mechanical problem such as severe valvular lesion (progressive mitral
regurgitation) or septal or free wall rupture leading to AHF. Echocardiography may show atrial
or ventricular dilatation and signs of hypertrophy. The most important parameter of heart
function is the LV ejection fraction for distinguishing patients with cardiac systolic dysfunction
and those with preserved systolic function. One of the most important reasons for the
widespread use of echocardiography to determine EF is that a clear association between EF
and prognosis has been demonstrated.
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Invasive haemodynamic monitoring
In the next five patients that you treat for acute heart failure, note the methods of cardiac
output monitoring and assess what information this gives you to help to manage the
patient.
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All patients with severe AHF should be monitored in an intensive care or coronary care unit with
invasive arterial and central venous lines. Pulmonary artery catheterisation should be withheld
for only the very severest form of AHF: patients who are not responding to therapy or who need
assessment of left sided filling pressures or with concurrent cardiac and pulmonary diseases.
See the PACT module onHaemodynamic monitoring for more information.
What techniques for monitoring of cardiac output do you know?
4/ MANAGING AND TREATING THE PATIENT WITH AHF IN THE ICU
P RACTICE
The immediate goals for the management of patients with acute heart failure are to
stabilise the haemodynamic condition and at the same time to improve symptoms. The
symptoms can be directly attributed to a combination of an insufficient oxygen delivery
for the needs of the body, raised pulmonary or systemic venous pressures and
peripheral vasoconstriction. Management requires a sound understanding of the
aetiology of the condition and its related pathophysiology in order for an effective
management plan to be formulated.
Review the protocols for managing patients with acute heart failure in your
hospital. Assess the important points and then compare them to the main points
in this Task.
Principles of management
The aim is to preserve an adequate oxygen supply/demand balance for both the myocardium and the
body as a whole. The principles of management are therefore to reduce the metabolic demand of the
myocardium whilst at the same time increasing the delivery of oxygen to the tissues.
Reducing demand
It is vitally important to reduce the cardiac work and therefore
decrease the metabolic imbalance in the failing heart. This entails
reducing the heart rate and the ventricular afterload to reasonable
limits. This can be achieved by relieving anxiety with reassurance
and anxiolytics, and preventing or treating pain with analgesics.
Tachycardia can be reduced by ensuring there is an adequate
preload with cautious fluid challenges to maximise stroke volume.
Beta-blockers may be helpful in treating tachycardia in patients with
primarily diastolic dysfunction. Afterload can then be reduced with
vasodilators and if the patient is volume overloaded, diuretics.
Oxygen demand can be further reduced in the ICU setting by
sedating the patient and instituting mechanical ventilation. This
diminishes the work of breathing and can reduce the oxygen
requirements by up to 40%.
30 to 40% of cardiac output
may be required to support
the work of breathing in a
dyspnoeic patient
Increasing supply
Quite often the steps taken above to reduce the myocardial work will be all that is necessary to
alleviate the symptoms and stabilise the haemodynamics. In some patients, however, the systemic
demand for oxygen will still be higher than its delivery. In these patients, oxygen delivery will need to
be increased further. The first step to achieve this aim should always be through the addition of a
vasodilator if possible. Further treatments include the transfusion of blood to increase the oxygen
carrying capacity of blood and the judicious use of inotropic agents to increase myocardial contractility.
Care must be taken with the use of inotropic agents, however, as these can increase the myocardial
work and compromise a brittle oxygen supply/demand balance in the myocardium.
Non-specific therapy
General care
General care of patients with acute heart failure should include measures appropriate in every critically
ill patient such as thromboprophylaxis, adequate nutrition and correction of electrolyte imbalances.
Septic complications are common in this patient group and should be identified and treated
immediately.
Ensuring adequate oxygenation
Achieving adequate oxygenation is vital. All of these patients should be given oxygen therapy. If
oxygen via a normal face-mask fails to improve the oxygen saturation of haemoglobin, then noninvasive ventilation via either CPAP or biphasic positive airway pressure (BIPAP) can be tried. These
positive pressure modes of ventilation have the added benefit of reducing the work of breathing,
increasing the number of recruitable lung units and avoiding intubation. Some patients will need to be
sedated and receive mechanical ventilation via an endotracheal tube. See the following reference and
the PACT module onMechanical ventilation
Patients with predominant right ventricular dysfunction tolerate increased
intrathoracic pressures very poorly. The increased pressure can lead to
increased right ventricular afterload and frank right ventricular failure.
In which patients might acute right ventricular failure and increases in intrathoracic pressures be
an issue?
Obtaining an adequate heart rate and rhythm
Tachycardias are undesirable as they lead to an increased oxygen requirement from the myocardium.
It is preferable to ensure the heart rate is less than 100 beats per minute in this patient group. The first
step with these patients is to relieve anxiety, stress and/or pain. The second step is then to ensure that
the circulating volume is appropriate (see T4 Optimisation of Preload) and that the patient is in sinus
rhythm. Atrial fibrillation is particularly common in this patient group and cardioversion to sinus rhythm
is a priority if possible. This is rarely achieved when the atrial fibrillation is longstanding but should be
actively sought if it has occurred acutely. This is best done first by ensuring there is an adequate
circulating volume, then correcting any electrolyte abnormalities. If this does not succeed in obtaining
sinus rhythm, then either DC cardioversion or chemical cardioversion are warranted. If conversion to
sinus rhythm is not possible, then control of the heart rate can be achieved with agents such as
diltiazem or digoxin. See the PACT module on Arrhythmia for more information.
Bradycardias and heart block lead to a reduced cardiac output. These need to be treated in critically ill
patients especially if there is evidence of a global oxygenation deficit. Temporary transcutaneous or
transvenous pacing can be a lifesaving procedure in patients presenting with shock and complete
heart block.
Care must be taken when giving sick patients anti-arrhythmic drugs as most of
these agents have negative inotropic effects and can worsen myocardial
function.
Optimisation of preload
The achievement of an adequate circulating volume is a vital part of the management for this group of
patients. Most of these patients will be volume deficient and will therefore respond to a fluid challenge.
Some of the patients, especially those with acute on chronic cardiac failure, may be volume
overloaded. These will be better treated with diuresis. This situation is especially common in patients
who develop acute heart failure whilst on the ICU. These patients then quite commonly have an
increased circulating volume and high filling pressures.
It is a common misconception that the pulmonary oedema in acute de novo heart failure is the result of
excessive blood volume. This is not generally the case, in fact many such patients respond favourably
to fluid challenges. The elevation of venous pressure observed in many patients is the result of
reduced forward flow, which causes congestion in the venous circulation. The role of loop diuretics in
the management of acute heart failure seems to contradict this. In fact the beneficial effect of
frusemide (furosemide) is often the result of its vasodilator effect rather than diuresis.
It is common to see large doses of diuretics given to patients with acute
pulmonary oedema irrespective of whether they are hypervolaemic. This can
often lead to subsequent hypotension secondary to hypovolaemia.
The identification of appropriate levels of preload can be very difficult in critically ill patients with heart
failure. It is for this reason that sophisticated methods of monitoring the circulation are required. Fluid
challenges can then be dosed directly according to, or guided by, stroke volume, cardiac filling
pressures or cardiac volumes. See the PACT module on Haemodynamic monitoring for more
information.
Increasing cardiac output
If all of the measures above fail to restore tissue oxygenation, it may be warranted to increase
systemic oxygen delivery. In practice this means either increasing the contractility state of the heart
with a positive inotropic agent or reducing the systemic vascular resistance. Of these two options,
when possible, vasodilatation is preferable as this will lead to a reduced work of the heart at the same
time as increasing systemic oxygen delivery.
N OTE
Care must be taken when giving intravenous vasodilators to ensure an adequate
perfusion pressure for the coronary arteries exists. If the systemic diastolic
pressure falls too much, coronary artery perfusion will be compromised and
myocardial ischaemia and failure may ensue.
The mechanism of action and physiological effects of the various inotropic agents are diverse. The
correct choice of treatment requires a good understanding of basic physiology and biochemistry. The
use of cardiac output monitoring and/or central or mixed venous oxygen saturations is recommended
to confirm the need for inotropes (as opposed to vasopressors), to choose the most suitable agent and
to guide dose adjustment.
Review the common inotropic agents that are used in the ICU. Assess the
differences between these agents and work out where they will be most
appropriately used.
Correction of structural problems
Some patients with acute heart failure will present secondary to a structural problem. This may be a
valvular abnormality or could be a defect in the intraventricular septum as a consequence of an acute
myocardial infarction. Other common issues include pericardial tamponade following cardiac surgery,
aortic dissection or free wall rupture. Whatever the cause, specialist opinion should be rapidly sought
as it is uncommon for the heart failure to resolve without definitive therapy for the structural deficit.
Managing specific problems
Forward (left and right) acute heart failure
Severe left ventricular failure will result in hypotension with failure of tissue perfusion. This pattern of
heart failure has a high mortality. The most severe form of this problem is known as cardiogenic shock.
Cardiogenic shock is defined as evidence of tissue hypoperfusion induced by heart failure after
correction of preload. It is characterised by a reduced blood pressure (SBP <90 mmHg or a drop of
mean arterial BP >30mmHg) and/or low urine output (below 0.5ml/kg/hour) with a pulse rate >60
/minute with or without evidence of organ congestion.
Cardiogenic shock is diagnosed after documentation of myocardial dysfunction
and exclusion or correction of factors such as hypovolaemia, haemorrhage,
sepsis, pulmonary embolism, tamponade, aortic dissection, pre-existing valvular
disease, hypoxia and acidosis.
Treatment of cardiogenic shock comprises supportive therapy following the principles described above
as well as correcting or treating the underlying cause. The most common cause of cardiogenic shock
is extensive acute myocardial infarction. Recent estimates of the incidence of cardiogenic shock range
from 5% to 10% of patients with myocardial infarction and the mortality rate from 50% to 80%. In
patients presenting with cardiogenic shock secondary to acute myocardial infarction, reperfusion of the
compromised coronary artery is vital.
The extent of myocardial salvage from reperfusion treatment decreases exponentially with time to reestablishing coronary flow. A number of strategies that centre on reducing the time to effective
treatment may help decrease the incidence of shock. These include public education to decrease the
time to hospital presentation, triage and early transfer of high risk patients to selected centres, and
early primary percutaneous coronary intervention or rescue PTCA for failed thrombolysis in high risk
patients. See the PACT module on Acute myocardial ischaemia for more information.
What are the principles involved with improving the circulation in cardiogenic shock?
Patients with cardiogenic shock that is not responding to the treatment strategies described above may
benefit from an intra-aortic balloon pump (see below). This can augment coronary perfusion and
improve cardiac performance whilst reducing cardiac work.
Intra-aortic balloon pump
An intra-aortic balloon pump is inserted percutaneously via the femoral artery into the descending
aorta. The balloon inflates during diastole to improve coronary and cerebral blood flow and deflates
immediately prior to systole resulting in a reduction in afterload. The balloon pump is used most
commonly following cardiac surgery in patients with poor ventricular function but also has a role in the
management of severe cases of heart failure where the underlying cause may be corrected e.g. by
coronary re-vascularisation or valve repair.
Ventricular assist devices
Ventricular assist devices are only available in a few specialist centres. These are small mechanical
pumps that are placed in the arterial tree or between the ventricle and the descending aorta. Their
original role was to support the circulation of patients awaiting transplant but it is now recognised that
their use in some patients with acute heart failure facilitates a recovery of the myocardium. In many
cases the recovery has been so impressive that the device has been removed and the patient has
recovered without the need for heart transplant. It is therefore recognised now as a bridge to recovery
in certain causes of heart failure e.g. myocarditis.
Left heart backward failure
When pulmonary oedema is suspected, a brief medical history and direct physical examination are
generally sufficient to initiate therapy. Early in the initial evaluation of patients with acute pulmonary
oedema, the physician must determine whether an acute coronary syndrome is present. At this stage,
this determination is based on clinical assessment and the electrocardiogram (ECG). Evidence of
acute coronary syndrome should raise consideration of urgent myocardial reperfusion therapy.
Echocardiography should be used to elucidate the aetiology. Treatment of this condition is
predominantly with oxygen, diuretics and vasodilators in the form of nitrates.
Patients often present with extremely high systemic blood pressure resulting in acute pulmonary
oedema and AHF. In such cases a reduction in afterload is the most important aspect of treatment.
The aim should be to reduce systemic blood pressure by 30% rather than to normal values. The
sublingual administration of nitroglycerine (0.4 to 0.6 mg, repeated every 5 to 10 minutes four times as
needed) is of value. Nitroglycerine is effective in patients with acute cardiogenic pulmonary oedema
due to both ischaemic and non-ischaemic causes. If systemic blood pressure is acceptable
nitroglycerine can be administered intravenously (0.3 to 0.5 µg/kg/min) as well. Frusemide
(furosemide, 20 to 80 mg intravenously) should be given shortly after the diagnosis of acute pulmonary
oedema is established. Morphine sulphate (3 to 5 mg intravenously) is effective in ameliorating many
of the symptoms of acute pulmonary oedema and can be safely administrated to most patients in this
condition.
Right heart backward failure
Right heart failure is characterised by elevation of the right heart pressures transmitted backwards into
the portal vein circulation. Dyspnoea is not prominent because of the initial absence of pulmonary
congestion. Clinical signs include ascites with tender, congestive hepatomegaly. The latter may occur
rapidly, sometimes with, particularly in the presence of considerable tricuspid regurgitation, systolic
pulsation of the liver, anasarca and hepatojugular reflux. Clinical manifestations include anorexia,
bloating, nausea and constipation. In critically ill patients the diagnosis of right heart failure can be
difficult to make. Most of the signs described above are non-specific and occur in other sick patients
without heart failure. The diagnosis is therefore one of exclusion and requires a high index of
suspicion.
The principles of management are exactly the same as for other causes of heart failure. However, care
must be taken with intravenous volume therapy, or a vicious circle of harm develops.
Circle of Harm
RAP = right atrial
pressure
RVEDP = right
ventricular
end diastolic
pressure
RVEDV = right
ventricular end
diastolic volume
In this cycle further volume challenges will lead to dilatation of the right ventricle and tricuspid
regurgitation. This leads to systemic and portal congestion which compromises venous return, but is
also an impediment to the left ventricle secondary to the intraventricular coupling.
Transthoracic
echocardiography, four
cavities view
RV: right ventricle
LV: left ventricle
RA: right atria
LA: left atria
1. Normal echocardiography, RV diameter should be <0.7 of LV diameter
2. Dilated cardiomyopathy with central mitral regurgitation
3. Dilated right ventricle with tricuspid regurgitation
The right ventricle is particularly afterload dependent, so even a minor increase
in pulmonary vascular pressures can have a dramatic effect on right ventricular
function. The aims of treating right ventricular failure are therefore to reduce
right ventricular afterload without affecting systemic blood pressure and
therefore the systolic and diastolic perfusion of the heart.
Specific therapy depends on the underlying cause. The most common cause of this problem in general
ICU patients is pulmonary embolism. If severe pulmonary hypertension is the cause of right ventricular
failure, then specific therapy designed to reduce pulmonary artery pressures (and therefore resistance)
can be given. This can be attempted with the use of specific pulmonary vascular vasodilators such as
inhaled nitric oxide or sildenafil.
Institution of long-term therapy
Initiating long-term therapy for heart failure is worthwhile and advisable before the patient leaves the
ICU. This allows safe commencement of therapy in a monitored environment, more rapid dose
adjustment and may facilitate weaning from mechanical ventilation. Angiotensin-converting enzyme
(ACE) inhibitors, β-blockers and spironolactone may all provide long-term mortality reductions.
CONCLUSION
Acute heart failure is a syndrome with a high mortality. There are a large number of causes of this
syndrome and it can present in a number of differing patterns that depend on the underlying
pathophysiology. It often presents with a different clinical picture compared to chronic heart failure.
Treatment is a combination of supportive measures and definitive therapy that depends on the
aetiology.
PATIENT CHALLENGES
An 86-year-old female is admitted for elective total knee replacement surgery. Her past medical
history includes hypertension and supraventricular arrhythmia. At the age of 82, she had a posterior
myocardial infarction, resulting in New York Heart Association (NYHA) II functional status.She had no
history of cerebrovascular accidents, and cardiopulmonary examination was normal, BP 160/90
mmHg, HR 84 bpm.The patient was receiving treatment with aspirin, amiodarone, nitrates and
captopril. All drugs were continued up to surgery except for aspirin which was replaced by low
molecular weight heparin.A pre-operative chest X-ray showed cardiac enlargement and apical
emphysema (below).
Learning issues
Heart failure functional class
Immediate assessment of AHF
Using chest radiographs
Cardiac enlargement
The pre-operative ECG was as follows.
How would you interpret this pre-operative ECG?
Learning issues
Diagnosing rhythm disturbances
PACT module on Arrhythmia
Echocardiography showed a left ventricular end-diastolic diameter of 55 mm with a posterior wall
thickness of 14 mm, inferobasal akinesia and a left ventricular ejection fraction of 63%. The systolic
pulmonary arterial pressure was approximately 30 mmHg.
How would you interpret this pre-operative echocardiogram (please give the normal values of the
echocardiographic parameters mentioned above)?
In the operating room, an arterial line was inserted in the radial artery after the induction of
anaesthesia. Intra-operative bleeding was estimated to be 1000 ml. The patient was not transfused.
Throughout the intervention, systolic blood pressure remained >100 mmHg and diastolic >50 mmHg.In
the recovery room, the patient was extubated and oxygen saturation remained at 98% on 2 l/min. Initial
postoperative haemoglobin was 10.4 g/dl.The ECG at admission to the recovery room is shown below.
Twelve hours later, lab tests show haemoglobin 8.2 g/dl, troponin I 1.1 µg/l (normal value <0.4). There
is significant postoperative bleeding 1400 ml/12 hours. The patient receives two units of red blood cells
over the next six hours. Bleeding in the drains stops.One hour later, the patient starts to complain of
dyspnoea, blood pressure 130/65 mmHg, heart rate 114 bpm. The patient does not complain of
precordial pain but becomes tachypnoeic (25 breaths/ min). Pulmonary auscultation reveals bilateral
rales and a fourth heart sound is audible on cardiac auscultation. She is immediately admitted to your
ICU.
Learning issues
Implications of increased troponin
What diagnostic tests would you rapidly perform in order to confirm a diagnosis and assess the
mechanism(s)?
Learning issues
Diagnostic procedures
What mechanism(s) may explain tachycardia?
You order a chest X-ray, ECG and laboratory tests which reveal the following:
Chest X-ray at ICU admission
ECG at ICU admission
The lab tests show haemoglobin 8.8 g/dl, troponin I 14.7 µg/l, B-type natriuretic peptide (BNP) 872
pg/ml (normal value <200).
Learning
issues
Laboratory tests
What information do you extract from chest X-ray, ECG and lab tests performed at ICU
admission?
The echocardiogram demonstrates a left ventricular ejection fraction of 50%, with a normal diameter
and slight hypertrophy of the left ventricular wall. There is no evidence of valvular dysfunction. Right
ventricular function is normal.
Knowing the above-described results of the tests you performed, how would you characterise
heart function? What mechanism(s) is (are) involved?
Learning issues
Pathophysiology: systolic and/or diastolic heart failure
What would be your immediate therapeutic management?
Learning issues
Management of systolic and diastolic heart failure
The patient is discharged from ICU two days later, BNP 312 pg/ml. A coronary angiography performed
one week later showed multiple lesions in all three coronary arteries.
A 30-year-old man is returned to the ICU from the operating theatre following replacement of his
aortic arch and aortic valve. He is a known Marfan's syndrome and was otherwise completely well. The
operation was uneventful and involved replacing the ascending aorta together with the valve and reimplantation of the coronary arteries.On return to the ICU he was sedated and ventilated and in a good
overall clinical condition. He was warm and well perfused. His heart rate was 86/minute and his arterial
blood pressure was 120/85 mmHg. His central venous pressure (CVP) was 9 mmHg.Six hours later he
becomes tachycardic (heart rate 125/min), hypotensive (BP 70/50 mmHg) and his CVP increases to
20 mmHg with a tricuspid regurgitant trace. He is cool to touch and has a pansystolic murmur best
heard at the apex of the heart. Clinical examination is otherwise normal. His arterial lactate has
increased from 2 mmol/l to 9 mmol/l.
Learning issues
Causes of acute heart failure
What are the initial steps that you should take in assessing this patient?
Learning issues
Immediate assessment of AHF
Resuscitation
PACT module on Airway management
How would you characterise the haemodynamic status of this patient?
Learning issues
Signs of low cardiac output
What is the likely cause of the shock?
Learning issues
Right ventricular dysfunction
Further clinical examination shows a positive hepatojugular reflex, suggesting a clinical diagnosis of
right ventricular failure.
Learning issues
Physical signs of AHF
What diagnostic tests would you perform in order to confirm what is going on?
Learning issues
Diagnostic procedures
N OTE
If an echo is not readily available, then pulmonary artery catheterisation could be
performed to understand the specifics of the haemodynamic disturbance.
The electrocardiogram, at that time, shows a complete right bundle branch block and a 4 mm ST
elevation in the inferior leads (II, III, aVF) and a mirror image in the lateral leads (I, aVL, V5, V6).
Echocardiography demonstrates:





No evidence of a pericardial effusion
Severe dilatation of the right heart cavities in an already hypokinetic RV, in both systole and
diastole
Hypertrophied left ventricle, apparently rather empty, with 'normal' contraction
Dilated inferior vena cava (20 mm) without changes with ventilation
Tricuspid insufficiency
Learning issues
The role of echocardiography
Implications of increased troponin
What is the significance of the ECG changes?
How would you resuscitate this patient?
Learning issues
Early management of AHF
Afterload reduction
After resuscitation has commenced what would you do next?
The patient is transferred to the operating theatre where coronary angiography shows a complete
obstruction of the proximal end of the re-implanted right coronary artery. A right coronary bypass with
venous graft is performed on cardiopulmonary bypass.
What would be the best method of providing continuous data with regards to right ventricular
performance?
Learning issues
Right ventricular failure
Invasive haemodynamic monitoring
A pulmonary artery catheter was inserted in the operating theatre. It showed physiological PAP values:
21/14/16 mmHg and a low capillary wedge pressure: 7 mmHg. The cardiac index was 1.15
l/min/m2 and the mixed venous oxygen saturation is 45%. These results confirm the severe right
ventricular problem and provided continuous data on which to dose therapy.Following surgery this
patient still had residual right ventricular dysfunction. However with appropriate treatment this gradually
improved and he was able to make a full recovery.
On reflection, these two cases presented with the clinical signs of acute heart failure, however with
appropriate investigations each had a specific category of cardiac dysfunction that directed further therapy.
Acute heart failure should never be the final diagnosis as it is always caused by another disease state. It is this
disease state that dictates therapy and ultimate prognosis. Echocardiography is the pivotal tool for
understanding the pathophysiological basis of the cardiac dysfunction.
Q1. Which clinical sign(s) in a patient with acute heart failure reflect a problem with congestion rather
than perfusion?
A. Parasternal lift
True
False
B. Hypotension
True
False
C. Decreased level of consciousness
True
False
D. Raised jugular venous pressure
True
False
E. Hepatomegaly
True
False
Q2. Which of the following statements regarding acute right heart failure is/are true?
A. Right heart failure is rarely associated with haemodynamic compromise
True
False
B. The mortality from right heart failure is low
True
False
C. Right heart failure can lead to reduced cardiac output despite preserved left ventricular
contractility
True
False
D. Right heart failure rarely leads to high levels of lactate
True
False
E. Right heart failure is a consequence of reduced diastolic perfusion pressures
True
False
Q3. Which of the following drugs can exacerbate acute heart failure?
A. Indomethacin
True
False
B. Amitripyline
True
False
C. Gliclizide
True
False
D. Theophylline
True
False
E. Salbutamol (albuterol)
True
False
A. Acute mitral regurgitation
True
False
B. Severe hypertension
True
False
C. Acute tricuspid regurgitation
True
False
D. Acute myocardial infarction
True
False
E. Atrial fibrillation
True
False
Q4. Common causes of acute left heart backward failure include:
Q5. Drugs that increase the contractile state of the myocardium include:
A. Amiodarone
True
False
B. Levosimendan
True
False
C. Adrenaline
True
False
D. Milrinone
True
False
E. Ramipril
True
False