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Heart failure
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Table of Contents
Preface
Introduction
Early recognition and management of the patient with AHF
Immediate assessment and resuscitation
Diagnostic Category of AHF
Pathophysiology
Specific examples of acute heart failure
Performing Diagnostic Procedures
Further investigations
Managing and treating the patient with AHF in the ICU
Principles of management
Non specific therapy
Managing specific problems
Institution of long term therapy
Conclusion
Self Assessment
Answers to Questions 1 to 11
Type A questions
Type K questions
Old PACT Questions
Old PACT Answers
Patient Challenges
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Heart Failure
Current Status 2017
Awaiting major review
This module is updated and maintained by the Cardiovascular Dynamics section
Latest Update
First Edition
Cardiovascular Dynamics
Chair
Thomas Scheeren , Groningen, The Netherlands
Deputy
Jan Bakker , Department of Intensive Care Erasmus MC Rotterdam, the
Netherlands
ELearning Committee
Chair
Kobus Preller Dr., Consultant, John Farman ICU, Cambridge University Hospitals
NHS Foundation Trust, Cambridge, UK
Deputy
Theodoros Kyprianou Dr., Director, Nicosia General Hospital ICU, Nicosia,
Cyprus
Project Manager
Estelle Pasquier , European Society of Intensive Care Medicine
First Edition 2005
Module Authors
Alexandre Mebazaa , Dept of Anaesthesia & Intensive Care Hôpital Lariboisière
Paris, France
Marco Cavana , Dept of Anaesthesia & Intensive Care Hôpital Lariboisière Paris,
France
Andrew Rhodes , Dept of Intensive Care St George's Hospital London, United
Kingdom
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Rupert Pearse , Dept of Intensive Care St George's Hospital London, United
Kingdom
Module Reviewers
Jayne Fawcett , London, UK
David Porembka , Cincinnati, Ohio, USA
Janice Zimmerman Dr., Dept of Internal Medicine Division of Critical Care The
Methodist Hospital Houston, Texas, USA
Medical Illustrator
Kathleen Brown , Triwords Limited, Tayport, UK
Learning Objectives
After studying this module on Heart failure, you should be able to:
Recognise and initiate early management in the patient with acute heart failure
Comprehend the likely causes and pathophysiology of heart failure
Choose appropriate diagnostic tests and procedures
Manage and treat the patient with acute heart failure in the ICU
eModule Information
Expiry date:
COBATrICe competencies covered in this module:
1. ...
2. ...
Faculty Disclosures:
The authors of this module have not reported any disclosures.
Duration: 7 hours
Copyright©2017. European Society of Intensive Care Medicine. All rights reserved.
ISBN 9789295051782 Legal deposit D/2005/10.772/25
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1. 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 lifethreatening
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 nonspecific 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.
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2. 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:
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.
2. 1. Immediate assessment and resuscitation
The first line assessment and treatment are closely interrelated and should occur
simultaneously. They include the following tasks:
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.
2. 1. 1. Resuscitation
2. 1. 1. 1. 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.
2. 1. 1. 2. Breathing
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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.
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 1
If the patient fails to respond to oxygen administered via a facemask, 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.
Organ specific problems / Heart failure
The reasons for initiating ventilatory support are essentially twofold. 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.
Think
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.
2. 1. 1. 3. Circulation
Therapies aimed at improving the circulatory status are dependent on the
pathophysiological classification of AHF (see later). An appropriate blood pressure and
cardiac output must be obtained in these patients to maintain end organ perfusion and
function.
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2. 1. 2. Basic monitoring Collaboration Site |
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:
Continuous electrocardiogram
Blood pressure
Respiratory rate
Temperature
Continuous oxygen saturation with a pulse oximeter
2. 1. 3. Clinical history
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.
References
PACT modules on Communication skills and Basic clinical examination
Taking the clinical history is important to:
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 historytaking:
Table 1: Definition of DYSPNOEA: breathlessness or
dyspnoea is the recognition of an inappropriate
relationship between respiratory work and total body
work.
Key Questions Principal Reason
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Breathlessness is the most important alter ation due to
Is the patient dyspnoeic? left ventricular failure (either acute or acute on chronic)
and is the main symptom that the patient describes
Has the acute heart failure
This helps to classify the cause of acute is it on top of a
developed de novo or heart
background history
failure of cardiac problems?
Does the patient have the
This information is important as it has significant
symptoms of an acute
therapeutic implications
coronary syndrome?
Acute heart failure can be precipitated by a change in
What medications is the
the patient’s medications or noncompliance with their
patient taking?
prescribed regimen.
How does dyspnoea present and what is its spectrum of severity?
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 2
References
Benito S. Causes of breathlessness. In: Webb AR, Shapiro MJ, Singer M,
Suter PM (eds). Oxford Textbook of Critical Care (OTCC). Oxford: Oxford
University Press; 1999. p. 50. ISBN 0192627376
Dyspnoea is not always a lifethreatening 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.
Important
Cough, sudden awakening during the night and bronchospasm may be early
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signs of AHF. Cough, especially during semirecumbency 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.
Important
This situation can be difficult to distinguish from an acute exacerbation of asthma
(‘cardiac asthma’).
2. 1. 3. 1. Additional symptoms
Other symptoms which can be elicited from the patient history:
None, indeed the patient could be:
Truly asymptomaticor
Asymptomatic because of sedentary lifestyle
Fatigue
Weakness
Swelling of ankles
Abdominal pain and/or distension
Palpitations
Syncope or presyncope
Central nervous symptoms such as decreased level of consciousness
Important
Fatigue and weakness may be related to poor perfusion of the skeletal muscles
in patients with lowered cardiac output.
2. 1. 3. 2. Comorbid conditions
Many of these patients will be suffering from comorbid 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.
The main question to be asked at this stage is whether the AHF has arisen de novo or
as a decompensation of a chronic condition. This can be assessed by asking the
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patient about other comorbidities that are associated with a diagnosis of chronic heart
failure.
2. 1. 3. 3. Druginduced 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 noncardiac 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?
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 3
Noncardiac medications can cause an exacerbation of heart failure. Medications for
diabetes mellitus have been reported to increase plasma volume. Nonsteroidal 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 βagonist bronchodilatators may also exacerbate heart failure by
inducing tachyarrhythmias.
In addition, cardiac medications, for instance βblockers, may precipitate or worsen
heart failure. Most antiarrhythmic agents can depress myocardial function as well as
exacerbate ventricular arrhythmias. Calcium channel blockers may also depress
myocardial function.
Challenge
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.
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2. 1. 4. Physical examination Collaboration Site |
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.
2. 1. 4. 1. Signs of heart Failure
Table 2: New York Heart Association functional classification for congestive heart
failure
2. 1. 5. 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?
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 4
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Three scores to describe severity of illness in chronic heart failure patients are:
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.
2. 1. 5. 1. Class I
Patients with cardiac disease but without resulting limitation of physical activity.
Ordinary physical activity does not cause undue fatigue, palpitation, dyspnoea or
anginal pain.
2. 1. 5. 2. Class II
Patients with cardiac disease resulting in slight limitation of physical activity. They are
comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnoea
or anginal pain.
2. 1. 5. 3. Class III
Patients with cardiac disease resulting in marked limitation of physical activity. They
are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitation,
dyspnoea and anginal pain.
2. 1. 5. 4. Class IV
Patients with cardiac disease resulting in inability to carry on any physical activity
without discomfort. Symptoms of cardiac insufficiency or of anginal syndrome may be
present even at rest. If any physical activity is undertaken, discomfort is increased.
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 twominute 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.
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Table 3: ’Cold, Warm, Dry, Wet’ system
Congestion
NO YES
YES DryWarm WetWarm
Adequate Perfussion
NO DryCold WetCold
You can find further information about the Framinghan criteria in the electronic version
and in the following reference.
References
Lloydjones DM. The risk of congestive heart failure: sobering lessons from
the Framingham Heart Study. Curr Cardiol Rep. 2001;3(3):18490 .
Challenge
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.
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3. 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
initialized.
Note
Heart failure should never be the final diagnosis.
Think
about the last few patients you admitted with heart failure and identify the
aetiology of the syndrome and the specific treatments that were necessary.
Table 4: Common causes of acute heart failure
Pressure overload Hepertension Aortic stenosis Pulmonary embolus
Aortic regurgitation High output failure (anaemia,
Volume overload
hyperthyroidism)
Impaired ventricular Mitral stenosis Tamponade Pericardial constriction /
filling restriction
Ischaemic heart disease Myocarditis Metabolic / toxic
Myocardial diseases
disease
Dysrhythmias Ischaemia Brady / tachyarrhythmias
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.
References
Singer M. Pathophysiology of myocardial failure and the systemic circulatory
response. In: Webb AR, Shapiro MJ, Singer M, Suter PM (eds). Oxford
Textbook of Critical Care (OTCC). Oxford: Oxford University Press; 1999. p.
229. ISBN 0192627376
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3. 1. Pathophysiology
The syndrome of acute heart failure develops secondary to one of several
pathophysiological categories:
3. 1. 1. Loss of myocardial contractility
Partial, e.g. coronary artery disease
Generalised, e.g. dilated cardiomyopathy, myocarditis
3. 1. 2. Impediments to cardiac filling and emptying
Pressure, e.g. hypertension
Volume, e.g. excessive intravascular volume
Valvular disease
Pericardial disease
Restrictive disease
3. 1. 3. Abnormal organisation or signalling of cardiac contraction
Tachyarrhythmias
Bradyarrhythmias
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.
3. 1. 4. 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.
3. 1. 5. Forward/backward heart failure
This terminology describes whether the predominant problem is with forward flow
(perfusion) or backward flow (congestion).
3. 1. 6. Systolic and/or diastolic heart failure
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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.
3. 2. Specific examples of acute heart failure
How would a patient with cardiogenic shock present?
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 5
3. 2. 1. Forward (left and right) acute heart failure
Forward acute heart failure may be mildtomoderate 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.
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 6
What is the mechanism of pulmonary oedema in patients with heart failure associated
with normal LVEF?
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3. 2. 2. Left heart backward failure
Left heart backward failure is related to left ventricular dysfunction with varying degrees
of severity from mildtomoderate 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.
Figure 1: Chest Xray 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.
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
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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.
3. 2. 3. Right heart backward failure
Right heart ischaemia is associated with striking increases in the incidence of
haemodynamic compromise, arrhythmias, and inhospital 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 volumedeprived left ventricle,
conspires to further limit LV filling.
References
Mebazaa A, Karpati P, Renaud E, Algotsson L. Acute right ventricular failure
from pathophysiology to new treatments. Intensive Care Med 2004; 30: 185
196. Review. PMID 14618229
How would a patient present if s/he had right heart failure?
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 7
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4. 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.
4. 1. Further investigations
These investigations should be done urgently but should not delay resuscitation and
initiation of definitive therapy.
4. 1. 1. Electrocardiogram
Electrocardiographic changes in patients with heart failure are frequent.
Figure 2:
Note
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 coexist. ECG recordings do not need to be repeated in the absence of
changes of clinical status.
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Note
Collaboration Site |
This chest Xray reveals the patient has had an aortic valve replacement He also
has pulmonary hypertension, left atrial enlargement and evidence of mild
pulmonary oedema.
4. 1. 2. Chest radiograph
A chest Xray 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 abnormal in patients presenting with AHF. The chest radiograph
is able to give you a lot of details about possible comorbidities and the underlying
cardiac status.
Figure 3:
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.
Note
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A high predictive value of Xray findings is only achieved by interpreting the X
ray in the context of clinical findings and ECG abnormalities.
References
PACT module on Clinical imaging
4. 1. 3. Laboratory tests in AHF
The following laboratory tests should be considered in a patient with severe AHF:
Urea and electrolytes
Arterial blood gases
Full blood count
Coagulation profile
Blood glucose
Cardiac troponin
Btype natriuretic peptide (BNP, NTpro BNP)
Liver function tests
4. 1. 4. Cardiac enzymes (troponin)
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 8
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 CKMB (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.
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
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of these biomarkers closely parallel disease severity.
References
PACT module on Acute myocardial ischaemia
4. 1. 5. Btype natriuretic peptide (BNP)
Plasma concentration of certain natriuretic peptides (ANP, BNP and NTpro 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.
4. 1. 6. Echocardiography
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.
Think
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. Invasive haemodynamic
monitoring
Challenge
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.
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.
References
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PACT module on Haemodynamic monitoring
What techniques for monitoring of cardiac output do you know?
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 9
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5. Managing and treating the patient with AHF in the ICU
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 bodies’ needs, 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.
Challenge
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.
5. 1. 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.
Note
30 to 40% of cardiac output may be required to support the work of breathing in
a dyspnoeic patient.
5. 1. 1. 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. Betablockers 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%.
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5. 1. 2. Increasing supply Collaboration Site |
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.
5. 2. Nonspecific therapy
5. 2. 1. 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.
5. 2. 2. Ensuring adequate oxygenation
Achieving adequate oxygenation is vital. All of these patients should be given oxygen
therapy. If oxygen via a normal facemask 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.
References
Nava S, Carbone G, DiBattista N, Bellone A, Baiardi P, Cosentini R, et
al.Noninvasive ventilation in cardiogenic pulmonary edema, a multicenter
randomized trial. Am J Respir Crit Care Med 2003;168: 14321437. PMID
12958051
PACT module on Mechanical ventilation
Important
Patients with predominant right ventricular dysfunction tolerate increased
intrathoracic pressures very poorly. The increased pressure can lead to
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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?
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 10
5. 2. 3. 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 later) 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.
References
PACT module on Arrhythmia
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.
Important
Care must be taken when giving sick patients antiarrhythmic drugs as most of
these agents have negative inotropic effects and can worsen myocardial
function.
5. 2. 4. 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
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acute on chronic cardiac failure, may be Collaboration
volume Site |
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.
Important
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.
References
PACT module on Haemodynamic monitoring
5. 2. 5. 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.
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
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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.
5. 2. 6. 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.
5. 3. Managing specific problems
5. 3. 1. 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
30mmHg) and/or low urine output (below 0.5ml/kg/hour) with a pulse rate >60 /minute
with or without evidence of organ congestion.
Important
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, preexisting 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
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from 50% Site |
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.
References
PACT module on Acute myocardial ischaemia
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 11
References
Simoons ML; GUSTO IVACS Investigators. Effect of glycoprotein IIb/IIIa
receptor blocker abciximab on outcome in patients with acute coronary
syndromes without early coronary revascularisation: the GUSTO IVACS
randomised trial. Lancet 2001; 357(9272): 19151924. PMID 11425411
Patients with cardiogenic shock that is not responding to the treatment strategies
described above may benefit from an intraaortic balloon pump (see below). This can
augment coronary perfusion and improve cardiac performance whilst reducing cardiac
work.
5. 3. 1. 1. Intraaortic balloon pump
An intraaortic 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
revascularisation or valve repair.
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5. 3. 1. 2. Ventricular assist devices Collaboration Site |
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.
5. 3. 2. 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 nonischaemic 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.
5. 3. 3. 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
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be difficult to make. Most of the signs described above are nonspecific 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.
Figure 4: 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.
Figure 5: Transthoracic echocardiography, four
cavities view
RV: right ventricle
LV: left ventricle
RA: right atria
LA: left atria
Normal echocardiography, RV diameter should be <0.7 of LV diameter
Dilated cardiomyopathy with central mitral regurgitation
Dilated right ventricle with tricuspid regurgitation
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Important
Collaboration Site |
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.
5. 4. Institution of longterm therapy
Initiating longterm 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. Angiotensinconverting enzyme (ACE) inhibitors, βblockers and
spironolactone may all provide longterm mortality reductions
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6. 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.
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7. Self Assessment
7. 1. Answers to Questions
A1: Application of CPAP can cause pulmonary recruitment and is associated with an
increase in the functional residual capacity. The improved pulmonary compliance,
reduced transdiaphragmatic pressure swings, and decreased diaphragmatic activity
can lead to a decrease in the overall work of breathing and therefore a decreased
metabolic demand from the body.
A2: Dyspnoea may appear with a progressively increasing severity which limits the
exercise capacity. The severity of dyspnoea can be characterised in five steps:
Step 1 Exertional dyspnoea
Step 2 Orthopnoea and cough
Step 3 Paroxysmal nocturnal dyspnoea
Step 4 Dyspnoea at rest
Step 5 Associated with acute pulmonary oedema
A3: Patients presenting with AHF are commonly on a number of drugs that are used for
the treatment of chronic heart failure. These are important as they can give information
about the underlying state of the patient but also can contribute to the acute
presentation. These drugs include:
Betablockers
Spironolactone and/or loop diuretics
ACE inhibitors
Angiotensin II antagonists
Nitrates
Digoxin
A4: Intensive care is appropriate only for the severest forms of acute heart failure in
patients who are thought to have a likelihood of surviving. These are patients who:
Have failure of other organ systems apart from the heart
Need protection of their airway or mechanical ventilatory assistance
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Are not responding to basic medical treatment
A5:
Oliguria
Clouded sensorium
Cool, mottled extremities
Systolic blood pressure B90 mmHg for at least 30 minutes
Heart rate is usually L90 beats per minute
Reduced cardiac index: B2.2 l/min/m2
Elevated pulmonary capillary occlusion pressure: L15 mmHg.
Cardiogenic shock state is the most advanced clinical situation in which a patient may
arrive either through a chronic congestive heart failure or dramatically within a few
hours after an acute myocardial infarction.
A6: Increased LV filling pressures may be related to several mechanisms including a
decrease in LV relaxation and/or LV compliance and/or a structural defect in the heart
leading to mitral regurgitation or a ventricular septal rupture. Pulmonary oedema is
related to an increase in left ventricular filling pressure that leads to a steep increase in
pulmonary venous and hence pulmonary capillary pressure inducing exudation of fluid
from the intravascular compartment into the lung interstitium and alveoli, resulting in
the heart failure symptoms.
A7: The patient often appears malnourished or even cachectic; s/he can exhibit signs
of air hunger and anxiety; a chronic marked elevation of systemic venous pressure
produces exophthalmos, tricuspid regurgitation and may lead to visible pulsation of the
eyes and of the neck veins. Central cyanosis and icterus may be present in patients
with severe heart failure.
A8: Troponin levels have been found to be increased in a number of conditions
unrelated to acute myocardial infarction. They have been found to be increased in
shock, renal failure, sepsis and hypovolaemia. Care must be exercised in these
conditions not to attribute troponin rises to acute myocardial ischaemia unless there is
either clinical or electrocardiographic evidence to corroborate this.
A9: There are a number of techniques used to monitor or measure cardiac output.
These include:
Pulmonary artery catheterisation
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Pulse contour analysis
Oesophageal doppler
Echocardiography
A10: High intrathoracic volumes can precipitate right ventricular failure (acute cor
pulmonale) in patients with borderline right ventricular function. This is particularly
common in patients following right coronary artery myocardial infarction or patients with
ARDS
A11: Adequate heart rate and rhythm
Optimisation of preload
Increasing cardiac output
Afterload reduction
Table of contents:
7. 1. 1. Old PACT Questions
Which clinical sign(s) in a patient with acute heart failure reflect a
problem with congestion rather than perfusion?
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 1
A: Parasternal lift
B: Hypotension
C: Decreased level of consciousness
D: Raised jugular venous pressure
E: Hepatomegaly
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Which of the following statements regarding acute right heart failure
is/are true?
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 2
A: Right heart failure is rarely associated with haemodynamic compromise
B: The mortality from right heart failure is low
C: Right heart failure can lead to reduced cardiac output despite preserved left
ventricular contractility
D: Right heart failure rarely leads to high levels of lactate
E: Right heart failure is a consequence of reduced diastolic perfusion pressures
Which of the following drugs can exacerbate acute heart failure?
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 3
A: Indomethacin
B: Amitripyline
C: Gliclizide
D: Theophylline
E: Salbutamol (albuterol)
Common causes of acute left heart backward failure include:
Answer can be found in this eModule's Self Assessment Section:
Answer ID: 4
A: Acute mitral regurgitation
B: Severe hypertension
C: Acute tricuspid regurgitation
D: Acute myocardial infarction
E: Atrial fibrillation
Drugs that increase the contractile state of the myocardium include:
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Answer can be found in this eModule's Self Assessment Section:
Answer ID: 5
A: Amiodarone
B: Levosimendan
C: Adrenaline
D: Milrinone
E: Ramipril
7. 1. 2. Old PACT Answers
A1:
A True
B False
C False
D True
E True
A2:
A False
B False
C True
D False
E True
A3:
A True
B True
C True
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D True
E True
A4:
A True
B True
C False
D True
E True
A5:
A False
B True
C True
D True
E False
Table of contents:
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