Clinical Practice Guidelines: Respiratory/Acute pulmonary oedema

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Date April, 2017

Purpose To ensure consistent management of patients with Acute pulmonary oedema.

Scope Applies to all QAS clinical staff.

Author Clinical Quality & Patient Safety Unit, QAS

Review date April, 2019

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URL https://ambulance.qld.gov.au/clinical.html

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Acute pulmonary oedema

Acute pulmonary oedema (APO) refers to the rapid buildup of fluid in the alveoli and lung interstitium that has extravasated out of the pulmonary circulation. As the fluid accumulates, it impairs gas exchange and decreases lung compliance, producing dyspnoea and hypoxia.[1] The pathophysiological mechanisms are traditionally categorised into two primary causes:

Cardiogenic

Cardiogenic APO occurs when cardiac output drops despite an increased systemic resistance, so that blood returning to the left atrium exceeds that leaving the left ventricle (LV). As a result, pulmonary venous pressure increases, causing the capillary hydrostatic pressure in the lungs to exceed the oncotic pressure of the blood, leading to a net filtration of protein poor fluid out of the capillaries.[1,2]

Examples include:

• Left ventricular failure (LVF):

- Acute Coronary Syndromes (ACS)- Arrhythmia- Pericarditis, myocarditis or endocarditis- Valve dysfunction (e.g. aortic stenosis, mitral regurgitation)

• Increased intravascular volume:

- Fluid overload- Non-compliance with fluid restriction or diuretics- Renal failure

• Pulmonary venous outflow obstruction:

- Mitral valve stenosis

Non-cardiogenic

Pathological processes acting either directly or indirectly on the pulmonary vascular permeability are thought to cause this form of APO. As a result, proteins leak from the capillaries, increasing the interstitial oncotic pressure, so that it exceeds that of the blood and fluid is subsequently drawn from the capillaries.[1,2]

Examples include:

• High output states

- Septicaemia- Anaemia- Thyrotoxicosis

• Systemic increase of vascular permeability

- Pancreatitis- Eclampsia- Disseminated Intravascular Coagulation (DIC)- Burns

• Toxins/environmental

- Immersion/submersion- Toxic inhalation- High Altitude Pulmonary Oedema (HAPE)

& decompression illness

• Other

- Head Injury/intracranial haemorrhage- Drugs (e.g. NSAIDs, calcium channel blockers and naloxone)- Pulmonary embolus

April, 2017

Figure 2.46

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Risk assessment

Clinical features

• Regardless of the aetiologies between

cardiogenic and non-cardiogic pulmonary

oedema the presenting features of dyspnoea

and tachycardia remain the same.[3]

• Sudden onset of extreme breathlessness,anxiety, and the feeling of drowning

• Profuse diaphoresis

• Crackles are usually heard at the bases first;as the condition worsens, they progress tothe apices.

• Cough is a frequent complaint that suggestsworsening pulmonary oedema in patientswith chronic LV dysfunction.

• Pink, frothy sputum may be present in patientswith severe disease.

• Tachypnoea and tachycardia

• Hypertension is often present because of thehyperadrenergic state.

• Hypotension indicates severe left ventricularand cardiogenic shock.

• Cyanosis (late sign)

• Raised jugular venous pressure

Additional information

• Cardiogenic pulmonary oedema patients often havea history of cardiac hypertrophy/Acute MyocardialInfarction (AMI) and/or LVF.

• The primary goal in the treatment of cardiogenicpulmonary oedema is reduction in preload andafterload with nitrates.

• All patients with APO should be given supplementaloxygen as required to meet their physiological needsand reduce hypoxia.

• Patients with cardiogenic shock and concurrentrespiratory failure from APO require CCP supportwhere available. These patients may have a fluid deficit,therefore cautious fluid bolus (250 – 500 mL maximum)resuscitation should be titrated against haemodynamicsand clinical effect. Inotropic support may be required toincrease cardiac output.

• Non-cardiogenic APO requires respiratory support(with lung protection ventilation strategies)and treatment of the underlying cause.[3,4]

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172

Transport to hospitalPre-notify as appropriate

Determine cause of oedema

Consider:

• Oxygen• Aspirin• GTN• 12-Lead ECG

Appropriate positioning

Cardiogenic?

Note: Officers are only to perform procedures for which they have received specific training and authorisation by the QAS.

CPG: Paramedic SafetyCPG: Standard Cares

Non-cardiogenic?

• IPPV• PEEP• CPAP

Manage as per:

• CPG: Relevant dysrhythmia• CPG: Acute coronary syndrome

Is the patient hypotensive?

Manage as per:

• CPG: Cardiogenic shock

Consider:

• Oxygen• 12-Lead ECG• IPPV• PEEP• CPAP

Manage as per:

• CPG: Burns• CPG: Post submersion• CPG: Head injury• CPG: Spinal injury• CPG: Relevant toxicology/toxinology

Oxygen OxygenAspirinGTN

NY

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