ACUTE CARDIOGENIC PULMONARY OEDEMA

Ns. Ira Rahmawati S.kep, MNSc(EM)

Introduction

Acute pulmonary oedema (APO) is one of the most frequent causes of presenting to
an emergency department (ED). It has high mortality rates with 65 % of the patients
die within one year since being treated for APO (Ekman, Ekstrand & Schoufelberger
2007). APO is defined as an extreme respiratory failure caused by the accumulation
of fluid in the lungs, verified by chest X-ray (Parissis et al. 2010). The underlying
conditions of APO may be cardiac or non-cardiac problems. Blood transfusion, acute
lung injury, and high altitude are some of the non-cardiac precipitating factors. This
essay, however, will focus only on acute cardiogenic pulmonary oedema (ACPO).

Although feeling of being suffocated seems to be the early sign of ACPO, the clinical
manifestations of ACPO might vary amongst the individuals. Furthermore, subjective
feeling of the patients could also influence their clinical presentations (Ekman,
Ekstrand & Schaufelberger 2007). On the other hand, early recognition and
immediate interventions contribute significantly to patients’ prognosis (Williams et al
2013). Therefore, understanding the pathophysiology of ACPO is essential for all ED
nurses in order to provide prompt and accurate treatments.

Search Strategy

CINAHL with full text was explored as the main database. Advanced search was
used as the method and terms used in the search were:

(acute pulmonary oedema OR acute cardiogenic pulmonary oedema) AND

(management* OR treatment* OR assessment* OR approach*) AND (nurse* OR
emergency* OR medic*). 34 articles were found. After that, the search was limited to
academic journals published in 2004 until 2015 which resulted in 22 articles. Then,
13 articles were chosen for the literatures in this essay. One article from Australian
Emergency Nursing Journal published in 1999 was used as a reference in this essay

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because of its relevant content with the topic. Furthermore, this essay used also two
books as secondary resources.

Pathophysiology and clinical manifestations of acute cardiogenic pulmonary

oedema

ACPO may be caused by either systolic heart failure or diastolic heart failure.
Systolic heart failure is a condition in which left ventricle starts to weaken and unable
to maintain adequate cardiac output. Diastolic heart failure refers to the inability of
left ventricle to fully dilate between contractions, causing decreased ventricular filling
which may lead to decreased cardiac output (Stuart & Bament 2013). Many
conditions may lead to heart failure such as hypertension, cardiomyopathy, coronary
artery diseases, and valve dysfunction.

Decreased cardiac output resulted from heart failure stimulates compensatory

mechanisms, which include vasoconstriction and fluid retention. Furthermore, a lack
of oxygen in the tissues stimulates sympathetic nervous systems to cause
vasoconstriction by releasing noradrenaline. Moreover, decrease in blood supply to
the kidney stimulates the renin-angiotensin system which causes systemic
vasoconstriction. In the short term, all these mechanisms will improve cardiac output
(Nicholas 2004; Skinner & McKinney 2011). Nevertheless, the vasoconstriction will
significantly increase the afterload which weakens cardiac function even further.
Furthermore, the increased pressure and volume in left ventricle will eventually
increase the pressure and volume in pulmonary circulation which leads to the
movement of intravascular fluid into the alveolar cells and interstitial spaces (Power
2007). The accumulation of fluid in the lungs diminishes lungs’ compliance and gas
exchange which cause respiratory distress (Skinner & McKinney 2011).

Clinical manifestations of ACPO include severe breathlessness, orthopnoea, and

anxiety because of the suffocating feeling. Patients also present with cold skin and
diaphoresis that indicate inadequate cardiac output, crackles on chest auscultation
and decreased room air oxygen saturation (Curtis, Ramsden & Friendship 2007). A
study conducted in 2013 suggests that shortness of breath accompanied by

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hypertension and crackles over the lungs are the most frequent manifestations of
ACPO identified by paramedics in pre-hospital setting (Williams et al. 2013).

Emergency assessment

History and physical assessment

Assessment of every patient presenting to the ED should begin with primary survey
(airway, breathing and circulation). If there is no threat that needs immediate
interventions, physical assessment using four techniques should be done next
(Power 2007). The four techniques include inspection, palpation, percussion, and
auscultation. Other important measurements such as patients’ vital signs, oxygen
saturation, and arterial blood gas (ABG) should be obtained as soon as possible.
Furthermore, patients’ past medical history should be assessed as it plays important
contribution to form a diagnosis.

ACPO is a usual clinical presentation of acute heart failure (Parissi et al. 2010).
Diagnosis of ACPO is made based on patient physical examinations as well as
laboratory and chest radiography results (Bellone et al. 2006). Dyspnoea is the most
common sign of lung oedema. A study conducted in 2010 reveals that 75% of the
patients with ACPO are reported having dyspnoea at rest or exertion (Parissi et al.
2010). The patients should be questioned about the characteristics of the dyspnoea.
Research into ACPO conducted in 2007 reveals that a suffocating feeling is the
commonest symptom reported by patients with ACPO, whereas, patients presenting
chronic obstructive pulmonary disease (COPD) express increased work of breathing
(Ekman, Ekstrand & Schaufelberger 2007). Furthermore, the history investigation
should focus on evaluating the underlying problems associated with ACPO. A history
of orthopnea for instance, may become a clue to rule out cardiac problems (Ware &
Matthay 2005). Hence, the frequent causes of ACPO comprise chronic heart failure
(CHF), ischaemic hearth disease (IHD), and valve dysfunction (Ware & Matthay
2005).

Abnormal cardiac assessment results are often found in patients with ACPO. An S3
gallop indicates left ventricle failure which may lead to ACPO (Ware & Matthay
2005). Auscultations of murmurs indicate mitral regurgitation or aortic stenosis which

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can be the causes of ACPO (Baird 2010; Ware & Matthay 2005). Patients with
ACPO are likely to have cool extremities which indicate inadequate cardiac output.
Furthermore, the lung auscultation reveals crackles or rhonchi resulted from alveolar
and interstitial oedema (Ware & Matthay 2005).

Five vital signs which include pulse, blood pressure, temperature, respiration, and
oxygen saturation should be monitored continuously (Baird 2005). Decrease in room
air oxygen saturation in patients with ACPO is resulted from impaired oxygen
diffusion which is caused by alveolar and interstitial oedema (Curtis, Ramsden &
Friendship 2007).

Laboratory investigation

Troponin level should be checked to rule out infarct myocardium. Patients with
pulmonary oedema resulted from cardiac problems may have an elevated troponin
level (Ware & Matthay 2005). Other pathology tests that should be examined are full
blood count, ABG, electrolytes, liver function tests, urine analysis, and a toxicology
test (Baird 2010; Ware and Matthay 2005).

An elevated brain natriuretic peptide (BNP) level might be a significant sign

indicating ACPO since high BNP level associates with an increase in left ventricle
pressure and pulmonary circulation pressure. High amount of BNP will be secreted
by ventricle muscles when the intracardiac pressure is high. Heart failure is
suggested when a BNP level is higher than 500 pg per millilitre (Ware & Matthay
2005).

Chest Radiography

Although chest x-ray might be very important in distinguishing APO from other
sources of respiratory distress, it could not distinguish non cardiogenic from
cardiogenic pulmonary oedema (Williams et al. 2013). Furthermore, other
radiolucent substances that occupy the lungs such as pus or blood, may result in a
similar x-ray image to that pulmonary oedema (Ware & Matthay 2005). Therefore, a
chest radiographic finding alone is insufficient to diagnose ACPO.

Electrocardiography (ECG) and Echocardiography

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A 12 lead ECG should be done as soon as possible in the ED. ECG findings of
patients with ACPO may reveal myocardial infarction or ischaemia (Baird 2010;
Ware & Matthay 2005). Bedside echocardiography should be done if possible in the
ED. Echocardiography can assess the valvular and ventricular function and
therefore, may help to determine the source of cardiac dysfunction (Ware & Matthay
2005).

Emergency medical management

The management of patients presenting with ACPO should include four fundamental
concepts which consist of respiratory support, preload reduction, afterload reduction
and inotropic administration for patients presenting with hypotension (Stuart &
Bament 2013).

Respiratory support

Malignant respiratory failure is the commonest presentation of ACPO. Patients are

usually hypoxic and therefore, respiratory support is needed immediately to improve
oxygenation (Stuart & Bament 2013). Oxygen 10 – 15 litres/ minute via Hudson
mask with reservoir bag should be initiated even in patients with COPD (Baird 2010).
Patients may also need ventilator assistance with non-invasive positive pressure
ventilation (NIPPV). In fact, the early use of NIPPV in patients with ACPO may
reduce the need for intubation and lowers mortality rates (Li et al. 2013).

NIPPV can be administered via continuous positive airway pressure (CPAP) or Bi-
level positive airway pressure (BiPAP) (Power 2007). NIPPV has several
advantageous effects including preload and afterload reduction which may help to
increase cardiac output. NIPPV may also reduce work of breathing by preventing
alveolar collapse and enhance gas diffusion (Bellone et al. 2006; Li et al. 2013).
However, the use of NIPPV is contraindicated in patients presenting with
hypotension or shock (Stuart & Bament 2013).

A study conducted in 2009 suggests that compared to conventional oxygen therapy,

CPAP decreased intubation rate, augmented clinical condition and may have
reduced hospital mortality (Mehta, AL-Hashim & Keenan 2009). Meanwhile, trials
that compare BiPAP to oxygen therapy suggest that the use of BiPAP does not lower

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hospital mortality or length of stay but it does lower the need for intubation (Mehta,
Al-Hashim & Keenan 2009). Although some studies suggest the risk of myocardial
infarction on patients receiving BiPAP therapy, there is still no trials or studies that
conclude CPAP is superior over BiPAP or vice versa (Li et al. 2013).

Pharmacological management

The first line drug for ACPO is glyceryl trinitrate (GTN or nitroglycerin). GTN reduces
preload more effectively compared to furosemide or morphine and intravenous GTN
may effectively reduce afterload (Stuart & Bament 2013). 400 µg sublingual GTN
may be given followed by intravenous infusion of 5 – 10 µg/ minute if systolic blood
pressure is above 100 mmHg. The infusion dose may be titrated to improve clinical
conditions (Baird 2010; Stuart & Bament 2013). However, the blood pressure must
be monitored closely and systolic blood pressure to be kept above 100 mmHg.

Diuretic agents such as furosemide have been used as the treatments for ACPO for
decades. Diuretics improve cardiac output by reducing preload and intracardiac
pressure (Skinner & MicKinney 2011). Furthermore, diuretics are known as the most
effective drug for reducing oedema and SOB (Skinner & MicKinney 2011). Three
different kinds of diuretics are available which include potassium sparing diuretics,
loop diuretics, and thiazides. There is no proof suggesting that one category of
diuretics is preferable than the others (Skinner & MicKinney 2011). 20 – 80 mg of
furosemide may be given intravenously followed by IV infusion at 5 – 10 mg/ hour
(Baird 2010).

However, patients with ACPO caused by diastolic dysfunction should not be given
furosemide because fluid overload does not exist in these patients. Furthermore, the
use of diuretics in these patients may only cause hypotension and inadequate
perfusion (Stuart & Bament 2013). Distinguishing systolic heart failure from diastolic
dysfunction is essential to provide accurate treatments for ACPO.

Suffocating feeling encountered by patients with ACPO is very likely to cause panic
or anxiety. Relieving the anxiety is considered one of the most important approaches
in acute stage of ACPO (Sosnowski 2008). Hence, opiates such as morphine have
been encouraged to be used in the management of ACPO. Morphine is known as a
strong anxiolytic drug. Furthermore, morphine causes vasodilatation which leads to
decrease in venous blood return and consequently lowers the preload (Power 2007).

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Indeed, a study conducted in 2007 reveals that almost 25 % of the patients
presenting with ACPO were given IV morphine in the ED (Ekman, Ekstrand &
Schaufelberger 2007).

However, a retrospective study conducted in 1999 discovers that the use of

morphine in patients with ACPO increases the need for intubation by five times and
the need for ICU care by three times (Sacchetti et al. 1999; Sosnowski 2008).
Another study has also revealed that the use of morphine as a treatment for ACPO is
correlated with high mortality rates (Fiutowski et al. 2003; Sosnowski 2008).
Administration of morphine causes drowsiness, depressed respiratory function and
low blood pressure that do not provide significant beneficial effects for patients with
ACPO (Sosnowski 2008). Therefore, the use of morphine as a treatment for ACPO
should be avoided and benzodiazepines may be given instead to reduce the anxiety
(Sosnowski 2008).

Severe hypotension may eventually develop in patients with grave systolic failure
which requires the administration of inotropes (Stuart & Bament 2013). A study
conducted in 2007 discovers that almost 40% of the patients presenting with ACPO
required inotropic infusion to maintain their blood pressure (Parissis et al. 2010).
Inotropic agents that can be used include dopamine, dobutamine, adrenaline and nor
adrenaline.

Emergency Nursing Management

Nursing care for patients presenting with ACPO should focus on relieving the
symptoms, improving the oxygenation and reducing the anxiety. Initial nursing
assessment should include the primary survey which ensuring that the patients have
a patent airway, adequate breathing and adequate circulation. The ED nurse should
also obtain patients’ baseline vital signs, a 12 lead ECG, oxygen saturation, ABG
and cardiac monitoring. Assessment of cardiopulmonary system should be
performed promptly and continuously. IV access should be obtained and pathology
tests should be done. The findings of these examinations may provide an idea about
the underlying cause of ACPO (Power 2007).

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Positioning is an important approach to help reduce dyspnoea in patients with ACPO
(Nicholas 2004). Patients encountering ACPO should be placed in upright position,
except for patients presenting with cardiogenic shock or unconsciousness which
should be placed in supine position (Baird, 2010).

High flow oxygen should be given via Hudson mask with reservoir bag. If available,
NIPPV should be considered and may be given using CPAP or BiPAP provided
there are no contraindications such as hypotension, pneumothorax or elevated
intracranial pressure. Furthermore, the use of NIPPV in patients with ACPO has
been encouraged by the British Thoracic Society (Skinner & McKinney 2011). ED
nurses should be familiar with NIPPV because nurses are those who observe the
patients’ conditions and the effectivity of the treatment. The British Thoracic Society
suggests that NIPPV should be run by skilled nursing staff (The British Thoracic
Society 2002; Skinner & McKinney 2011).

NIPPV has beneficial effects on respiratory functions as well as cardiac systems.

CPAP may prevent atelectasis and reduce work of breathing. Furthermore, the
positive pressure in intrathoracic space may improve CO by reducing the afterload
(Skinner & McKinney 2011). However, problems associated with NIPPV
administration may arise such as gastric distention, agitation and discomfort.
Therefore, continuous observation of the patients’ conditions is needed. This
includes monitoring patients’ vital signs, patients’ complaints such as nausea or
vomiting, ABG results, oxygen saturation, and level of consciousness (Skinner &
McKinney 2011).

The patients’ responses to the pharmacology therapies should be assessed. The

administrations of diuretics may lead to over diuresis, therefore fluid balance should
be closely monitored. Blood pressure should be frequently checked as the patients
receive vasodilators such as nitrates. If the patients have low systolic blood
pressure, IV nitrates should be stopped (Kelly 1999). Furthermore, if the patients are
treated by morphine, the signs and symptom of the respiratory centre depression
should be monitored.

Psychological support is very important for patients encountering a life threatening

illness such as ACPO. Explaining every procedures to the patients may reduce their
anxiety and improve their wellbeing (Kelly 1999).

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Conclusion

Apart from cardiogenic shock, acute cardiogenic pulmonary oedema is the most
severe presentation of heart failure which may lead to death. Patients commonly
present to the ED with extreme breathlessness and fluid overload. Early diagnosis
and accurate treatments contribute significantly to the patients’ outcomes. The ED
nurses play significant roles in managing patients with ACPO. Therefore, it is
important that ED nurses have sufficient knowledge about the pathophysiology and
management of ACPO.

References

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